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© 2001, 2006 Informa Healthcare, an imprint of Informa UK Ltd First edition published in the United Kingdom in 2001 by Isis Medical Media Ltd. Second edition published by Informa Healthcare, an imprint of Informa UK Ltd, 2 Park Square, Milton Park, Abingdon, Oxon OX14 4RN Tel: +44 (0)20 7017 6000 Fax: +44 (0)20 7017 6699 Email:
[email protected] Website: www.tandf.co.uk/medicine All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior permission of the publisher or in accordance with the provisions of the Copyright, Designs and Patents Act 1988 or under the terms of any licence permitting limited copying issued by the Copyright Licensing Agency, 90 Tottenham Court Road, London W1P 0LP. Although every effort has been made to ensure that all owners of copyright material have been acknowledged in this publication, we would be glad to acknowledge in subsequent reprints or editions any omissions brought to our attention. Although every effort has been made to ensure that drug doses and other information are presented accurately in this publication, the ultimate responsibility rests with the prescribing physician. Neither the publishers nor the authors can be held responsible for errors or for any consequences arising from the use of information contained herein. For detailed prescribing information or instructions on the use of any product or procedure discussed herein, please consult the prescribing information or instructional material issued by the manufacturer. A CIP record for this book is available from the British Library. Library of Congress Cataloging-in-Publication Data Data available on application ISBN10: 1-84184-358-X ISBN13: 978-1-84184-358-2 Distributed in North and South America by Taylor & Francis 6000 Broken Sound Parkway, NW, (Suite 300) Boca Raton, FL 33487, USA Within Continental USA Tel: 800 272 7737; Fax: 800 374 3401 Outside Continental USA Tel: 561 994 0555; Fax: 561 361 6018 Email:
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[email protected] Composition by Phoenix Photosetting UK Printed and bound in Singapore by Kyodo Printing Co (S’pore) Pte Ltd Chapter title image courtesy of Geoffrey W Cundiff md facog Cover image courtesy of Science Photo Library (photographer: Cristina Pedrazzini)
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Contents List of Contributors Foreword Preface
x xix xx
VOLUME 1
Volume 1, Section 1 – 1 History of urogynecology and female urology Background Jane A Schulz, Jack R Robertson, Harold P Drutz Section Editor: 2a Epidemiology: USA CORNELIUS J Kelleher Brandon S Rubens, William D Tissot, Ananias C Diokno 2b Epidemiology: South America Paulo Palma, Miriam Dambros 2c Epidemiology: Europe Ian Milsom 2d Epidemiology: Australia Richard J Millard 2e Epidemiology: Asia Peter H C Lim, Marie Carmela Lapitan 3 Quality of life and urinary incontinence Cornelius J Kelleher, Stephen Radley 4 Tackling the stigma of incontinence – promoting continence worldwide David Fonda, Diane K Newman 5a The roles of the continence nurse specialist Ellie Stewart 5b The roles of the continence nurse specialist – global perspective Diane K Newman 6 The role of the pelvic physical therapist Bary Berghmans
Volume 1, Section 2 – 7 Basic Science: Structure and Function of 8 Lower Urinary and Ano- Rectal Tracts in women 9 Section Editor: Jacek L Mostwin 10 11
Anatomy John O L DeLancey Embryology of the female urogenital system with clinical applications Jenny Lassmann, Stephen A Zderic Clinical physiology of micturition Jacek L Mostwin Pharmacology of the bladder Karl-Erik Andersson Classification of voiding dysfunction in the female patient David Staskin, Alan J Wein
Volume 1, Section 3 – 12 Diagnostic Evaluation, Incontinence and Prolapse 13 Section Editor: Sender Herschorn 14 15 16
History and examination Vikram Khullar, Lesley K Carr Voiding diary Matthew Parsons Pad tests Marie-Andrée Harvey Uroflowmetry Jean-Jacques J M Wyndaele Cystometry Hashim Hashim, Paul Abrams
3 13 23 31 39 51 63 75 81 91 99 115 127 141 157 173 185 197 205 215 225
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Textbook of Female Urology and Urogynecology
17 18 19 20 21 22 23 24 25 26 27
Pressure–flow plot in the evaluation of female incontinence and postoperative obstruction Philippe Zimmern, Jason P Gilleran Urethral pressure measurements Gunnar Lose Leak point pressures Edward J McGuire Electromyography David B Vodušek, Clare J Fowler Clinical neurophysiologic conduction studies David B Vodušek, Clare J Fowler Videourodynamics Sender Herschorn, Jerome Green, Dudley Robinson Ambulatory urodynamics Stefano Salvatore, Vikram Khullar, Linda Cardozo Radiologic imaging Andrea Tubaro, Antonio Carbone, Alberto Trucchi Magnetic resonance imaging (MRI) and the female pelvic floor Lennox Hoyte Pelvic floor ultrasound Hans P Dietz Endoscopy Geoffrey W Cundiff, Gary E Lemack
Volume 1, Section 4 – 28 Natural history and prevention of incontinence and prolapse Non-Surgical treatment Robert M Freeman of Incontinence, Prolapse 29 Outcomes of conservative treatment and related conditions Don Wilson Section Editor: Eric S Rovner 30a Outcome measures in women with lower urinary tract symptoms: overactive bladder Catherine E DuBeau, Eboo Versi 30b Outcome measures in women with lower urinary tract symptoms: stress incontinence Richard C Bump, Ilker Yalcin 30c Outcome measures in women with lower urinary tract symptoms: pelvic organ prolapse Peggy A Norton 31 Behavioral therapies and management of urinary incontinence in women Kathryn L Burgio 32 Physiotherapy for urinary incontinence Jeanette Haslam 33 Drug treatment of voiding dysfunction in women Alan J Wein, M Louis Moy 34 Pessaries and devices for non-surgical treatment of pelvic organ prolapse and stress incontinence Ingrid E Nygaard 35 Catheters; pads and pants; appliances Kate Anders, Su Foxley
235 251 265 277 289 301 313 325 339 355 377 393 407
429
449
459
467 475 485
533 541
vi
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Contents
Volume 1, Section 5 – Associated Disorders Section Editor: Philip Toozs-Hobson
Volume 1, Section 6 – Appendices
36 37 38 39 40 41 42 43 44 45 46 47 48 49
Neurologic disorders Ricardo R Gonzalez, Renuka Tyagi, Alexis E Te Non-neurogenic voiding difficulty and retention Amitabha Majumdar, Philip Toozs-Hobson Painful bladder syndrome Deborah R Erickson The neuropathology of chronic pelvic pain Ursula Wesselmann Lower urinary tract infections – simple and complex James Gray, Dudley Robinson The overactive bladder syndrome Philip Toozs-Hobson, Matthew Parsons Vaginitis Brian G Wise, Gopalan Vijaya Sports and fitness activities Kari Bø Problems associated with sexual activity Andrew Hextall, Nicholas Christofi Nulliparous women Katharine H Robb, Philip Toozs-Hobson Pregnancy and childbirth and the effect on the pelvic floor Charlotte Chaliha Menopause Andrew Hextall, Dudley Robinson Anal incontinence Michael Walker, Simon Radley Constipation Jason Goh, Iqbal Khan
50 The purpose of standardization of terminology and methods in patients with lower urinary tract dysfunction Anders Mattiasson 51a The standardization of terminology of lower urinary tract function: Report from the Standardization Subcommittee of the International Continence Society (ICS) Paul Abrams, Linda Cardozo, Magnus Fall, Derek Griffiths, Peter Rosier, Ulf Ulmsten, Philip van Kerrebroeck, Arne Victor, Alan J Wein 51b The standardization of terminology of lower urinary tract function recommended by the ICS 2002 Samih Al-Hayek, Paul Abrams 52 The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction Richard C Bump, Anders Mattiasson, Kari Bø, Linda P Brubaker, John O L DeLancey, Peter Klarskov, Bob L Shull, Anthony R B Smith 53 Good urodynamic practices: uroflowmetry, filling cystometry, and pressure-flow studies Werner Schaefer, Paul Abrams, Limin Liao, Anders Mattiasson, Francesco Pesce, Anders Spangberg, Arthur M Sterling, Norman R Zinner, Philip van Kerrebroeck Index
565 583 593 605 613 631 643 655 663 673 681 695 711 721
737
745
759
771
783
I-1
vii
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Textbook of Female Urology and Urogynecology
VOLUME 2 Volume 2, Section 7 – 54 The assessment of outcomes used for incontinence interventions Surgery for Urinary in women Incontinence Emily E Cole, Harriette M Scarpero, Roger R Dmochowski Section Editor: 55 Peri- and postoperative care Roger R Dmochowski Maria Vella, John Bidmead 56 Synthetic materials for pelvic reconstructive surgery Mark Slack 57 Biologic materials for reconstructive surgery Harriette M Scarpero, Emily E Cole, Roger R Dmochowski 58 Urethral injections for incontinence Rodney A Appell 59 Abdominal and transvaginal colpourethropexies for stress urinary incontinence Michelle Y Morrill, Karl M Luber 60 An overview of pubovaginal slings: evolution of technology Emily E Cole, Harriette M Scarpero, Roger R Dmochowski 61 Pubovaginal fascial sling for the treatment of all types of stress urinary incontinence: surgical technique and long-term outcome Jerry G Blaivas, David Chaikin 62 Tension-free vaginal tape procedure for treatment of female urinary stress incontinence Carl Gustaf Nilsson 63 SPARC – midurethral sling suspension system David Staskin, Renuka Tyagi 64 Other sling variants Kristie A Blanchard, J Christian Winters 65a Transobturator midurethral sling technique for stress urinary incontinence Jonathan S Starkman, Harriette M Scarpero, Roger R Dmochowski 65b Transobturator approach Calin Ciofu, Francois Haab 66 The artifical urinary sphincter for treatment of stress urinary incontinence in women Emily E Cole, Harriette M Scarpero, Roger R Dmochowski 67 New technologies for stress urinary incontinence Jay-James R Miller, Peter K Sand 68 Diagnosis and treatment of obstruction following incontinence surgery – urethrolysis and other techniques Chad Huckabay, Victor W Nitti Volume 2, Section 8 – 69 Surgery for Urogenital Prolapse 70 Section Editor: Bernhard Schuessler 71 72 73 74
Classification and epidemiology of pelvic organ prolapse Steven Swift Anterior vaginal wall prolapse Mark D Walters Enterocele Kaven Baessler, Bernhard Schuessler Rectocele – anatomic and functional repair William A Silva, Mickey M Karram Vaginal approach to fixation of the vaginal apex May Alarab, Harold P Drutz Abdominal approach to fixation of the vaginal apex Wesley Hilger, Jeffrey Cornella
801 825 835 845 859
865 879
907
917 925 935
945 955
961 971
981 999 1009 1023 1035 1053 1067
viii
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Contents
Volume 2, Section 9 – Laparoscopy Section Editor: Anthony R B Smith
Volume 2, Section 10 – Complex problems Section Editor: Rodney A Appell
75 76 77 78 79 80
Preservation of the prolapsed uterus Vasiliki Varela, Adam Magos Urinary incontinence following prolapse surgery Brigitte Fatton, Bernard Jacquetin, Rufus Cartwright Episiotomy and perineal repair Ranee Thakar, Christine Kettle Primary repair of obstetric anal sphincter injury Abdul H Sultan Surgery for fecal incontinence Klaus E Matzel, Manuel Besendörfer Combined genital and rectal prolapse Vanessa Banz, Jürg Metzger, Bernhard Schuessler
81 82 83 84 85 86 87
The role of laparoscopic surgery Anthony R B Smith Pelvic anatomy through the laparoscope Edmund Edi-Osagie Laparoscopic treatment of pelvic pain Christopher Sutton, Richard Dover Laparoscopic colposuspension and paravaginal repair Rohna Kearney, Alfred Cutner Laparoscopic sacrocolpopexy Marcus P Carey Other laparoscopic support procedures Peta Higgs Prevention, recognition, and treatment of complications in laparoscopic pelvic floor surgery Christopher Maher
88 89 90 91 92 93 94 95 96 97 98
Urogenital fistulae – surgical Paul Hilton Urogenital fistulae – obstetric Andrew Browning Urethral diverticulum and fistula Kenneth C Hsiao, Kathleen C Kobashi Electrical stimulation of the lower urinary tract Firouz Daneshgari Complex reconstructive surgery Christopher R Chapple, Richard T Turner-Warwick Gynecologic developmental abnormalities Melissa C Davies, Sarah M Creighton Pediatric urogynecology Andrew J Kirsch, Howard M Snyder Complications of surgery for stress incontinence Walter Artibani, Maria Angela Cerruto, Giacomo Novara The effect of hysterectomy (simple and radical) on the lower urinary tract Heinz Koelbl Recognition and management of urologic complications of gynecologic surgery Kevin R Loughlin Cosmetic vaginal surgery James Balmforth, Linda Cardozo
Index
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1077 1089 1099 1111 1121 1135 1151 1153 1165 1179 1193 1205
1211 1223 1239 1251 1275 1289 1317 1329 1345
1363
1367 1377 I-1
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Contributors Paul Abrams md frcs Professor of Urology, Bristol Urological Institute, Southmead Hospital, Bristol, UK May Alarab mb chb mrcog mrcpi Department of Obstetrics and Gynecology, University of Toronto, Toronto, ON, Canada Samih Al-Hayek md lmssa lrcp(lond) lrcs(eng) mrcs Bristol Urological Institute, Southmead Hospital, Bristol, UK Kate Anders rgn bsc Nurse Specialist in Urogynaecology, Surrey, UK Karl-Erik Andersson md phd Department of Clinical and Experimental Pharmacology, Lund University Hospital, Lund, Sweden Rodney A Appell md frcs Professor of Urology and Chief, Division of Voiding Dysfunction and Female Urology, Baylor College of Medicine, F. Brantley Scott Chair in Urology St. Luke’s Episcopal Hospital, Houston, TX, USA Walter Artibani md Professor of Urology, Chief of Urology Department, University of Padova Via Giustiniani, Padova, Italy Kaven Baessler md Department of Obstetrics and Gynecology, Cantonal Hospital, Lucerne, Switzerland James Balmforth mrcog Department of Urogynaecology, Kings College Hospital, Denmark Hill, London, UK Vanessa Banz md Department of Surgery, Cantonal Hospital, Lucerne, Switzerland Bary Berghmans phd msc rpt Health Scientist, Epidemiologist, AZM University Hospital Maastricht, The Netherlands Manuel Besendörfer md Chirurgische Klinik mit Poliklinik der Universität Erlangen, Germany John Bidmead mb bs mrcog Research Fellow, Department of Urogynaecology, King’s College Hospital, London, UK Kristie A Blanchard md Department of Urology, Ochsner Clinic Foundation, New Orleans, LA, USA Jerry G Blaivas md Clinical Professor of Urology, Cornell Medical Center, UroCenter of New York, New York, NY, USA Kari Bø phd Professor, Norwegian University of Sport and Physical Education, Oslo, Norway Andrew Browning mb bs mrcog Gynecologist, Addis Ababa Fistula Hospital, Ethiopia, Addis Ababa, Ethiopia Linda P Brubaker md facog facs Professor and Director, Section of Urogynecology and Reconstructive Plastic Surgery, Loyola University Medical Center, Maywood, IL, USA Richard C Bump md Eli Lilly and Company Corporate Center, Indianapolis, ID, USA
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Contributors
Kathryn L Burgio phd Department of Veterans Affairs Medical Center, Birmingham/Atlanta Geriatric Research, Education and Clinical Center, Birmingham, AL, USA Antonio Carbone Associate Professor of Urology, Department of Urology, I.C.O.T. Hospital, Rome, Italy Linda Cardozo md frcog Professor of Urogynaecology, Department of Urogynaecology, King’s College Hospital, London, UK Marcus P Carey mb bs franzcog Director of Urogynaecology, Royal Women’s Hospital, Melbourne, Australia Lesley K Carr md frcs Division of Urology, Sunnybrook and Women’s College Health Science Centre, Toronto, ON, Canada Rufus Cartwright ma mb bs Department of Urogynaecology, King’s College Hospital, London, UK Maria Angela Cerruto md Assistant Professor, Department of Urology, University of Verona, Verona, Italy David Chaikin md Clinical Assistant Professor, Department of Urology, Cornell Medical Center, New York, NY; Associate Attending Urologist, Morristown Memorial Hospital, Morristown, NJ, USA Charlotte Chaliha ma mb bchir mrcog Sub-specialist trainee in Urogynaecology, St Mary’s Hospital, London, UK Christopher R Chapple bsc md frcs Urology Department, Royal Hallamshire Hospital, Sheffield, UK Nicholas Christofi mb bs Fellow in Urogynaecology, St Albans City Hospital, West Hertfordshire Hospitals NHS Trust, St Albans, UK Calin Ciofu md Urology Department, Tenon Hospital, Paris, France Emily E Cole md Fellow, Department of Urology, Vanderbilt University Medical Center, Nashville, TN, USA Jeffrey Cornella md Chair, Pelvic Reconstructive Surgery, Associate Professor, Mayo Medical School Mayo Clinic Scottsdale, Department of Gynecology, Scottsdale, AZ, USA Sarah M Creighton md frcog Consultant Gynaecologist, Elizabeth Garrett Anderson Hospital, University College Hospitals, London, UK Geoffrey W Cundiff md Professor, Department of Gynecology and Obstetrics, Johns Hopkins School of Medicine, Baltimore, MD, USA Alfred Cutner md mrcog Consultant Gynaecologist, University College London Hospitals NHS Foundation Trust, London, UK Miriam Dambros md phd Urogynaecology Research, Division of Urology, State University of Campinas, UNICAMP, São Paulo, Brazil Firouz Daneshgari md Glickman Urological Institute, The Cleveland Clinic Foundation, Cleveland, OH, USA
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Melissa C Davies mrcs Clinical Research Fellow, Academic Department of Obstetrics & Gynaecology, University College London, London, UK John O L DeLancey md Normal F Miller Professor of Gynecology, Director, Pelvic Floor Research Group Director, Fellowship in Female Pelvic Medicine and Reconstructive Surgery, Ann Arbor, MI, USA Hans P Dietz Associate Professor in Obstetrics and Gynaecology, Western Clinical School, University of Sydney, Penrith, NSW, Australia Ananias C Diokno md facs Department of Urology, William Beaumont Hospital, Royal Oak, MI, USA Roger R Dmochowski md facs Professor, Department of Urology, Vanderbilt University Medical Center, Nashville, TN, USA Richard Dover mb bs Consultant Obstetrician and Gynaecologist, Royal North Shore Hospital, Sydney, Australia Harold P Drutz md Professor and Head Division of Urogynecology, Department of Obstetrics and Gynecology, University of Toronto, Toronto, ON, Canada Catherine E DuBeau Section of Geriatrics, University of Chicago, Chicago, IL, USA Edmond Edi-Osagie md mrcog Consultant Gynaecologist, St. Mary’s Hospital, Manchester, UK Deborah R Erickson md Professor of Surgery, Division of Urology, University of Kentucky College of Medicine, Lexington, KY, USA Magnus Fall md phd Professor of Urology, Senior Consultant, Department of Urology, Sahgrenska University Hospital, Göteborgs, Sweden Brigitte Fatton Gynaecologic Surgeon, Maternité de l’Hotel-Dieu, Centre Hospitalier Universitaire, France David Fonda mb bs bmed sci fracp fafrm Associate Professor of Medicine, Monash University, Consultant Geriatrician, Cabrini Medical Centre, Malvern, VIC, Australia Clare J Fowler mb bs msc frcp Department of Uro-Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London, UK Su Foxley rgn dip ns Nurse Consultant Incontinence, King’s College Hospital, London, UK Robert M Freeman md frcog Consultant, Urogynaecology Unit, Directorate of Obstetrics and Gynaecology, Derriford Hospital, Plymouth, UK Jason P Gilleran md Assistant Professor, Division of Urology, 4980 University Hospital Clinics, Columbus, OH, USA Jason Goh md GI Unit, University Hospital Birmingham, UK Ricardo R Gonzalez md Instructor in Urology, Weill Cornell Medical College, New York, NY, USA xii
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Contributors
James Gray mrcpath Department of Microbiology, Birmingham Women’s Hospital, Birmingham, UK, Department of Urogynaecology, King’s College Hospital, London, UK Jerome Green md frcsc Fellow in Urodynamics, Sunnybrook and Women’s College Health Sciences Centre, Toronto, ON, Canada Derek Griffiths md Geriatric Continence Unit, Montefiore Hospital, Pittsburgh, PA, USA Francois Haab md Urology Department, Tenon Hospital, Paris, France Marie-Andrée Harvey md sc(epi) frcsc faclog Assistant Professor of Obstetrics, Gynaecology and Urology, Queen’s University, Kingston, ON, Canada Hashim Hashim mb bs mrcs Urology Research Registrar, Bristol Urological Institute, Southmead Hospital, Bristol, UK Jeanette Haslam MPhil Grad Dip Phys mcsp Senior Visiting Fellow, University of East London, Honorary Visiting Lecturer, University of Bradford, Bradford, UK Sender Herschorn bsc mdcm frcsc Division of Urology, Sunnybrook and Women’s College Health Sciences Centre, Toronto, ON, Canada Andrew Hextall md mrcog Consultant Urogynaecologist, West Hertfordshire Hospitals NHS Trust, St Albans, UK Peta Higgs mb bs franzcog Urogynaecology Department, Royal Women’s Hospital, Melbourne, Australia Wesley Hilger md Fellow, Female Pelvic Medicine and Reconstructive Surgery, Mayo Clinic Scottsdale Department of Gynecology, Scottsdale, AZ, USA Paul Hilton md frcog Consultant Gynaecologist, Royal Victoria Infirmary, Newcastle upon Tyne, Senior Lecturer in Urogynaecology, University of Newcastle upon Tyne, UK Lennox Hoyte md mseecs facog Assistant Professor of Obstetrics/Gynecology and Radiology, Harvard Medical School, Director of Clinical Research in the Division of Urogynecology, Dept of Obstetrics/Gynecology, Senior Clinical Research Scientist, Surgical Planning Laboratory, Dept of Radiology, Brigham and Womens Hospital, Boston, MA, USA Kenneth C Hsiao md Fellow, Female Urology, The Continence Center at Virginia Mason Medical Center, Seattle, WA, USA Chad Huckabay md Fellow, Department of Urology, New York University School of Medicine, New York, NY, USA Bernard Jacquetin md Head, Department of OBGYN, Maternité de l’Hotel-Dieu, Centre Hospitalier Universitaire, France Mickey M Karram md Division of Urogynecology and Pelvic Reconstructive Surgery, Department of Obstetrics and Gynecology, Good Samaritan Hospital, Cincinnati, OH, USA
xiii
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Rohna Kearney mrcog mrcpi Subspecialty Trainee Urogynaecology, University College London Hospitals NHS Foundation Trust, London, UK Cornelius J Kelleher md mrcog Consultant Physician, Department of Obstetrics and Gynaecology, Guy’s and St Thomas’s Hospital Trust, London, UK Christine Kettle srn scm dip mid phd Professor of Women’s Health, Academic Unit of Obstetrics & Gynaecology, University Hospital of North Staffordshire & Staffordshire University, UK Iqbal Khan phd GI Unit, University Hospital Birmingham, UK Vikram Khullar bsc mrcog Department of Reproductive Science and Medicine, Division of Paediatrics, Obstetrics and Gynaecology, Mint Wing, St Mary’s Campus, Imperial College London, South Kensington Campus, London, UK Andrew J Kirsch md faap facs Clinical Professor of Urology, Emory University School of Medicine, Director Pediatric Urology Fellowship, Georgia Urology, Private Practice Peter Klarskov md phd Department of Neurology, Glostrup Hospital, Glostrup, Denmark Kathleen C Kobashi md Co-Director, The Continence Center at Virginia Mason Medical Center, Seattle, WA, USA Heinz Koelbl md Department of Obstetrics and Gynecology, Johannes-Gutenberg University, Mainz, Germany Jenny Lassmann md Fellow in Pediatric Urology, The Children’s Hospital Philadelphia, Philadelphia, PA, USA Marie Carmela Lapitan md Asia Pacific Continence Advisory Board, Gleneagles Hospital Singapore, Philippine General Hospital, Manila, Philippines Gary E Lemack md Associate Professor and Residency Program Director Holder of the Rose, Mary Haggar Professorship in Urology, University of Texas Southwestern Medical Center, Dallas, TX, USA Limin Liao md Professor of Urology, Chairman of Department of Urology, China Rehabilitation Research Center, Beijing, China Peter H C Lim am mb bs mmed durol fams(urol) miurol (hon) Senior Consultant Urological Surgeon, Andrology, Urology and Continence Centre, Gleneagles Hospital, Singapore Gunnar Lose md dmsc Chief Gynecologist, Department of Gynecology, Glostrup Hospital, Glostrup, Denmark Kevin R Loughlin md Division of Urology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA Karl M Luber md Department of Obstetrics and Gynecology, Division of Female Pelvic Medicine and Reconstructive Surgery, Southern California Permanenete Medical Group, San Diego, CA, USA Adam Magos bsc md frcog Consultant Gynaecologist, Minimally Invasive Therapy Unit and Endoscopy Training Centre, University Department of Obstetrics and Gynaecology, Royal Free Hospital, London, UK xiv
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Contributors
Christopher Maher franzcog Royal Women’s and Mater Urogynaecology, Brisbane, Queensland, Australia Amitabha Majumdar mb bs Research Fellow, Department of Urogynaecology, Birmingham Women’s Hospital, Birmingham, UK Anders Mattiasson md Department of Urology, University Hospital, Lund, Sweden Klaus E Matzel md Chirurgische Klinik mit Poliklinik der Universität Erlangen, Erlangen, Germany Edward J McGuire md Professor of Urology, The University of Michigan, Ann Arbor, MI, USA Jürg Metzger md Head of Department Visceral Surgery, Cantonal Hospital of Lucerne, Switzerland Richard J Millard mb bs frcs fracs Associate Professor and Head, Department of Urology, Prince of Wales Hospital, Randwick, Sydney, NSW, Australia Jay-James R Miller md Evanston Continence Center, Feinberg School of Medicine, Northwestern University Evanston, IL, USA Ian Milsom md phd Professor of Obstetrics and Gynecology, Department of Obstetrics and Gynecology, Sahlgrenska Academy at Göteborg University and Consultant Gynecologist at Sahlgrenska University Hospital, Göteborg, Sweden Michelle Y Morrill md Senior Fellow, Female Pelvic Medicine and Reconstructive Surgery, University of California, San Diego, USA Assistant Professor, Division of Urology, University of Pennsylvania Health System, PA, USA Jacek L Mostwin md dphil Professor of Urology, James Buchanan Brady Urological Institute, Johns Hopkins Medical Institutions, Baltimore, MD, USA M Louis Moy md Attending Surgeon, Division of Urology, Hospital of the University of Pennsylvania, PA, USA Diane K Newman rnc msn crnp faan Co-Director, Penn Center for Continence and Pelvic Health, Division of Urology, University of Pennsylvania Medical Center, Philadelphia, PA, USA Carl Gustaf Nilsson md phd Department of Obstetrics and Gynecology, Helsinki University Central Hospital, Finland Victor W Nitti md Associate Professor and Vice Chairman, Department of Urology, New York University School of Medicine, New York, NY, USA Peggy A Norton md Professor of Obstetrics and Gynecology, Chief of Urogynecology and Reconstructive Pelvic Surgery, University of Utah School of Medicine, UT, USA Giacomo Novara md University of Padova, Padova, Italy Ingrid E Nygaard md Professor, University of Iowa, Department of Obstetrics and Gynecology, Iowa City, IA, USA xv
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Paulo Palma md phd Head, Division of Urogynaecology, Department of Urology, State University of Campinas, UNICAMP, São Paulo, Brazil Matthew Parsons mrcog Urogynaecology Fellow, King’s College Hospital, London, UK Francesco Pesce md Specialist in Urology and Neurology, University of Verona, Italy Simon Radley md frcs Consultant Surgeon, University Hospital Birmingham, Edgbaston, Birmingham, UK Stephen Radley mb bs frcs ed mrcog Senior Registrar in Obstetrics and Gynaecology and Research Fellow in Urogynaecology, Royal Hallamshire Hospital, Urology Research, Sheffield, UK Katharine H Robb mrcog Research Fellow in Urogynaecology, Birmingham Women’s Hospital, Birmingham, UK Jack R Robertson md Urogynecologist and Professor Emeritus, University of Nevada Medical School, Reno, NV, USA Dudley Robinson mrcog Department of Microbiology, Birmingham Women’s Hospital, Birmingham UK, Department of Urogynaecology, King’s College Hospital, London. UK Peter Rosier md Department of Urology, UMC Utrecht, Heidelberglaan, Utrecht, The Netherlands Eric S Rovner md Assistant Professor of Urology, Division of Urology, Department of Surgery, Hospital of the University of Pennsylvania, PA, USA Brandon S Rubens md House Officer in Urology, William Beaumont Hospital, Royal Oak, MI, USA Stefano Salvatore md Divisione di Ginecologia Chirurgica, Ospedale Bassini, Università di Milano, Milan, Italy Peter K Sand md Evanston Continence Center, Feinberg School of Medicine, Northwestern University Evanston, IL, USA Harriette M Scarpero md Assistant Professor, Department of Urology, Vanderbilt University Medical Center, Nashville, TN, USA Werner Schaefer di Associate Professor of Medicine, Director, Continence Research Unit, University of Pittsburgh, Montfiore Hospital, Pittsburgh, PA, USA Bernhard Schuessler md Department of Obstetrics and Gynecology, Cantonal Hospital, Lucerne, Switzerland Jane A Schulz md Urogynecologist and Associate Professor, Department of Obstetrics and Gynecology, University of Alberta, Edmonton, Canada Bob L Shull md Vice-Chairman, Scott & White Women’s Health Center, Temple, TX, USA William A Silva md Division of Urogynecology and Pelvic Reconstructive Surgery, Department of Obstetrics and Gynecology, Good Samaritan Hospital, Cincinnati, OH, USA
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Contributors
Mark Slack mmed mrcog Simms Black Professor of Gynaecology , Head of Urogynaecology, Addenbrooke’s Hospital, Cambridge, UK; Lead Clinician, Department of Urogynaecology, Addenbrooke’s Hospital University of Cambridge NHS Foundation Trust, Cambridge, UK Anthony R B Smith mb chb frcog md Consultant Gynaecologist, St Mary’s Hospital for Women & Children, Manchester, UK Howard M Snyder md Division of Pediatric Urology, Children’s Hospital of Philadelphia, PA, USA, Clinical Professor of Urology, Emory University School of Medicine, Director Pediatric Urology Fellowship Georgia Urology, Private Practice Anders Spangberg md phd Urologist, Consultant, Department of Urology, University Hospital, Linkoping, Sweden Jonathan S Starkman md Department of Urologic Surgery, Vanderbilt University Medical Center, Nashville, TN, USA David Staskin md Head, Section of Female Urology, New York Presbyterian Hospital, Cornell Associate Professor of Urology, Weill-Cornell Medical College, New York, NY, USA Ellie Stewart rgn dip ns Clinical Nurse Specialist Urogynaecology, Guys and St Thomas NHS Trust, London, UK Abdul H Sultan mb chb md frcog Mayday University Hospital, Croydon, Surrey, UK Christopher Sutton md Professor of Gynaecological Surgery, University of Surrey, Honorary and Emeritus Consultant, Royal Surrey County Hospital, Guildford, Emeritus Consultant, Chelsea and Westminster Hospital, London, UK Steven Swift md Department of Obstetrics and Gynecology, Medical University of South Carolina, Charleston, SC, USA Alexis E Te md Associate Professor of Urology, Weill Cornell Medical College, New York, NY, USA Ranee Thakar md mrcog Academic Unit of Obstetrics and Gynaecology, University Hospital of North Staffordshire and Staffordshire University, UK William D Tissot md House Officer in Urology. William Beaumont Hospital, Royal Oak, MI, USA Philip Toozs-Hobson mb bs mrcog Consultant Urogynaecologist, Birmingham Women’s Hospital, Birmingham, UK Alberto Trucchi md febu Assistant Professor of Urology, Department of Urology, Sant’Andrea Hospital, Rome, Italy Andrea Tubaro md febu Associate Professor of Urology, Department of Urology, Sant’Andrea Hospital, Rome, Italy Richard T Turner-Warwick md Emeritus Surgeon, The Middlesex Hospital, London, UK Renuka Tyagi md Associate Professor of Urology, Weill Cornell Medical College, New York, NY, USA Ulf Ulmsten† Philip van Kerrebroeck md phd fellow ebu Professor of Urology, University Hospital Maastricht, The Netherlands xvii
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Vasiliki Varela md Visiting Clinical Fellow, Minimally Invasive Therapy Unit & Endoscopy Training Centre, University Department of Obstetrics and Gynaecology, Royal Free Hospital, London, UK Maria Vella mrcog Clinical Research Fellow, Department of Urogynaecology, King’s College Hospital, Denmark Hill, London Eboo Versi md phd Department of Obstetrics and Gynecology, United Medical and Dental School, New Brunswick, NJ, USA Arne Victor md Medical Product Agency, Uppsala, Sweden Gopalan Vijaya mrcog Specialist Registrar, Department of Obstetrics and Gynaecology, Medway Maritime Hospital, Kent, UK David B Vodusˇek md Medical Director, Division of Neurology, University Medical Center, Ljubljana, Slovenia Michael Walker bsc mb chb mrcs Specialist Registrar in General Surgery, Department of Surgery, University of Birmingham, Birmingham, UK Mark D Walters md Head, Section of General Gynecology, Urogynecology and Pelvic Reconstructive Surgery, The Cleveland Clinic Foundation, Department of Obstetrics and Gynecology, Cleveland, OH, USA Alan J Wein md Professor and Chief of Urology, Hospital of the University of Pennsylvania, Urology Division, Philadelphia, PA, USA Ursula Wesselmann md phd Departments of Neurology, Neurological Surgery and Biomedical Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD, USA Don Wilson md frcs franzcog cu Professor of Obstetrics and Gynaecology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand J Christian Winters md facs Department of Urology, Ochsner Clinic Foundation, New Orleans, LA, USA Brian G Wise mb bs md mrcog Consultant Urogynaecologist, William Harvey Hospital, Ashford, Kent, UK Jean-Jacques J M Wyndaele md Department of Urology and Center for Urological Rehabilitation, University Hospital Antwerp, Belgium Ilker Yalcin phd Eli Lilly and Company Corporate Center, Indianapolis, ID, USA Stephen A Zderic md Professor of Surgery, University of Pennsylvania, School of Medicine, Attending Surgeon, Division of Urology, The Childrens Hospital of Philadelphia, Philadelphia, PA, USA Philippe Zimmern md Department of Urology, University of Texas Southwestern Medical Center, Dallas, TX, USA Norman R Zinner md ms facs Medical Director, Western Clinical Research Inc, Torrance, CA, USA
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Foreword Female urology / urogynecology is a blooming subspecialty. We owe our gratitude to the prior outstanding masters from multiple disciplines who have contributed to a solid foundation of practical knowledge from the past. Fortunately, a unique multi-disciplinary culture has flourished over the last decade, and even in the early evolution of this collaborative effort we have embraced a new approach that incorporates the entire ‘pelvic floor’. This core approach will continue to be a catalyst from which current and future generations can generate new information and novel techniques based on creativity, innovation, and evidence based analysis of the results. This new and updated edition of the Textbook of Female Urology and Urogynecology continues a tradition from the first volume which is already considered a classic in the field. The text provides the reader with a comprehensive high-quality and inclusive review of the subject of female urology and urogynecology. This book is a vital and important reflection of the standardised and validated approach put forth for the management of female pelvic floor disorders, following the pathways indicated by the International Continence Society (ICS), the Society of Urodynamics and Female Urology (SUFU), the International Urogynecological Association (IUGA) and the International Consultation on Incontinence (ICI). This book should be listed as a must in the personal library of those interested and involved in female urology and urogynecology. Reading, incorporating and referring to the various chapters of the book will be a pleasure and enrichment both for beginners as well as for experts. Walter Artibani md Chief of Urology Department University of Padova
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Preface Our decision to produce a second edition of this textbook, a formidable undertaking, is due to the many rapid advances which have occurred in urogynecology/ female urology. The first edition was well received by readers and we had an overwhelmingly favorable response from the contributors to update and where necessary re-write their chapters. In addition, a number of new authors have taken on the task of creating new chapters relating to topics which had not previously been covered and enhancing many areas covered in the previous edition. We are truly grateful to all those whose hard work has resulted in this finished product, of which we can all be very proud. Our vision was, once again, to assemble an international group of experts as authors, but on this occasion we have been able to recruit the invaluable help of section editors who have guided the authors and prevented too much “overlap” from occurring in the various chapters of the book. Because our authors represent both gynecologists and urologists, as well as some non-medical clinicians, with a true international perspective, we have been able to avoid the polarization of ideas which occurs in many textbooks as a natural product of geography and the training and interests of the contributors. So a muchísimas gracias - grazie infinite - danke sehr – merci beaucoup to our section editors, the authors from the first edition and the new authors who have brought fresh ideas and new areas of interest to this textbook. As previously our mission was to produce a comprehensive textbook which would chronicle past contributions, document the present state of the art, and serve as a foundation, preparing the reader for future developments in the field. The text is arranged in sections enabling the reader to access areas of interest with an extensive bibliography intended to facilitate further study of this fascinating and rapidly changing subject. The section on surgery has been formatted to serve as both evidence based text and an atlas which should provide information pertaining to the decision making process as well as the technical aspects of the surgical procedures. We do however recognize that as this text goes to press, it is impossible to cover all aspects of female urology and urogynecology comprehensively and that the rapid pace of advances makes it difficult to be completely up to date. We will to try to amend any deficiencies in our 3rd edition! As editors we are truly grateful to all those authors who have contributed. Researching and writing demands a considerable amount of time and effort and is often a thankless task. We are really grateful to the individuals who sacrificed much of their “quality time and family life” outside of their required hours of clinical and scientific work, to make this project a reality. Once again we would like to thank the publishers for producing a well illustrated book of high quality which should enhance the minds, practices and book shelves of those who own it. Finally, we recognize the contribution from our patients who place their trust in all of us, and without whom this work would be futile. We hope that the textbook contributes to their quality of care and to the ability of those who care for them today and in the future. Linda Cardozo David Staskin
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Section 1 background Section Editor Cornelius J Kelleher
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1 History of urogynecology and female urology Jane A Schulz, Jack R Robertson, Harold P Drutz
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IntroductIon As we move into the new millennium, accompanied by many new advances in the field of urogynecology and reconstructive pelvic surgery, it is appropriate to take time to reflect on the events of the last century, and to make suggestions for future directions. With the significant increase in our postmenopausal female population, there is a growing demand for improved quality of life and management of pelvic floor dysfunction. No longer do we contemplate whether women will grow older but, rather, how they will grow older. The life expectancy for women has almost doubled through the 20th century. In 1923, Professor Sir Arthur Keith, in his Hunterian Lecture on ‘Man’s Posture: Its Evolution and Disorders’1 stated: Every movement of the arms, cough or strain sets going a multitude of ‘water hammers’ within the abdominal and pelvic cavities. Every impulse sets the bladder knocking at the vaginal exit ... it is the continual repetition of small forces, more frequently than the sudden application of a great effort, which wear down the vaginal defense.
Although it has long been recognized that factors such as childbearing and chronic increases in intraabdominal pressure contributed to pelvic floor prolapse, only recently has there been growing demand to manage all of the resulting problems. Urinary incontinence is now the most common reason for admission to long-term institutionalized centers in Canada and the United States. Billions of dollars are spent every year on diaper (nappy) and pad products, but this does nothing to correct the underlying problem of incontinence. Since the inception of medical writing, gynecologic and urologic conditions have been reported. The Kahun papyrus, circa 2000 BC, described diseases of women, including diseases of the urinary bladder. The Ebers papyrus, 1550 BC, classified diseases by systems and organs. Section 6 includes a prescription for the cure of a woman suffering from disease of her urine, as well as her womb. Urinary fistula is an example of the intimate relationship of the urinary and genital systems in women. Henhenit lived in the court of Menuhotep II, about 2050 BC. Her mummy, found in 1935, revealed by radiography an extensive urinary fistula.2 Reviewing the last century of progress in the new subspecialty of urogynecology and reconstructive pelvic surgery proved to be a tremendous, and somewhat daunting, task. Perhaps the quotation that best summarizes the events that have occurred is the opening sentence from Charles Dickens’ A Tale of Two Cities: ‘It was the best of times, it was the worst of times’. Undoubtedly,
we have made tremendous progress in this burgeoning new field; however, a political battlefield was perpetuated with the division of the female pelvic floor between urologists, urogynecologists, gynecologists, and colorectal surgeons. This political feud is cleverly illustrated in the article of Louis Wall and John DeLancey with its well-known drawing of the competing urologist, gynecologist, and colorectal surgeon.3 This is one of the many challenges that must be overcome in providing overall women’s healthcare as we move into the 21st century. A multidisciplinary approach to managing female pelvic floor dysfunction must be advocated to provide women with appropriate care in the areas of urinary and fecal incontinence, urogenital aging, conservative management, and reconstructive pelvic surgery. Voltaire, the French philosopher of the ‘age of enlightenment’, said: ‘These truths are not for all men nor for all times.’ From this we must humbly accept the concept that the truths we believe in today regarding our management of women with pelvic floor disorders must be constantly reassessed and modified with scientific advancements and research. Similarly, the epigram by Alphonse Karr (189) – ‘plus ça change plus c’est la même chose’ (the more things change, the more they stay the same) – also reflects the changes during the past century, especially in the field of surgical intervention, where in many cases we have continued to reinvent the wheel. We will now review the significant events in this field over the last century.
HIstory of tHe InternatIonal urogynecology assocIatIon At the International Federation of Gynecology and Obstetrics (FIGO) meeting in Mexico City in 1976, two medical friends, Professor Axel Ingelman-Sundberg, of Stockholm, Sweden, and Jack Rodney Robertson, of California, USA, met. It was time to form a new society. The objective was to further the urinary health of females. Both physicians were deeply involved in this work. Axel Ingelman-Sundberg, renowned for his research, his pioneering work in gynecologic surgery, and his teaching at the Karolinska Institute in Stockholm, Sweden, was the catalyst. Sweden had been a founding member of FIGO. Axel tried to persuade FIGO to inaugurate an International Urinary Incontinence subcommittee, but they declined. In his capacity as Vice President of FIGO, Axel reserved a special room for the formation of the International Urogynecologic Association (IUGA). He was elected the first president, to serve 5 years (1976–1980), by the colleagues who registered as
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members. They were: Abbo Hassan Abbo, MD (Sudan); Wolfgang Fisher, MD (East Germany); Bozo Kralj, MD (Yugoslavia); Oscar Contreras Ortiz, MD (Argentina); Donald R. Ostergard, MD (USA); Eckard Petrie, MD (West Germany); Jack Robertson, MD (USA); Stuart Stanton, MD (UK); Ulf Ulmsten, MD (Sweden); and David W. Waller, MD (UK). Ulf Ulmsten, then professor of obstetrics and gynecology in Aarhus, Denmark, was chosen secretary. The next meeting was held in Sheffield, UK, in July 1977, in connection with the local gynecologic meeting. At Bergen, Norway, in 1978, IUGA met along with the Scandinavian Congress of Obstetrics and Gynecology. In 1979 in Tokyo, Japan, IUGA met again with FIGO; this time IUGA was a special section of the program. In October, 1980, IUGA met in New Orleans, USA, organized by Jack Robertson, in connection with the newly formed Gynecological Urology Society (GUS), later to become the American Urogynecological Society (AUGS). The fifth IUGA meeting was held in Stockholm, Sweden in September, 1981 at the Wenner-Gren Center, famous for Nobel Prize presentations. The banquet was at the Royal Opera House, with a special program by the famous Swedish opera singer, Kerstin Dellert. Jack Robertson was elected president, and served until 1986. Peter Sand, of Chicago, USA, became the general secretary. During this time the association was growing in membership. In the USA, Jack Robertson had found that women were being treated as second-class citizens, being examined with male instruments for their incontinence problems. An alarming number of women were incontinent after their hysterectomy surgeries. Robertson devised a system of viewing the bladder, using carbon dioxide instead of water. In 1968, he went to Germany and convinced the famous endoscope maker, Karl Storz, who had recently acquired the technique of fiber optics, to produce a female urethroscope to Robertson’s specifications. Storz immediately liked the idea of not using water, and made the first Robertson female urethroscope. Instead of just resting their instruments upon it, this was the first time doctors could view the female urethra and its pathology. This was the beginning of a pioneering path with Robertson giving seminars to physicians anxious to learn about the female urinary tract, a subject that had not been included in their gynecologic training. The immediate result was a sharp rise in the diagnoses of urethral diverticula. 1982 saw the meeting in Santa Barbara, USA, organized by Jack Robertson, and combined with the Gynecological Urology Society, organized by Don
Ostergard. An ‘Old West’ rodeo and barbeque at Jack Robertson’s nearby Santa Ynez ranch fostered a lively interchange of ideas among the attendees. In 1983, IUGA met in Mainz, Germany, with wine tasting at the Cloisters of Eberbach, followed by a sunny sail up the Rhine to another meeting in Aachen. In 198, IUGA was at the famous Breakers Hotel in West Palm Beach, USA. At the 1985 meeting in Budapest, Hungary, physicians came from behind the Iron Curtain. It was vital for them to present their work at the meeting, as they would rise in professional and, most importantly, pay level as a result. When one group from Poland presented a problem, the audience asked why ultrasound had not been used, which at that time would have been the obvious method of treatment. The physicians from Poland replied simply, ‘We do not have ultrasound.’ Donald Ostergard was elected the third president and presided at the 1986 meeting at Yale University, USA organized by Ernest Kohorn. Don’s memories include ‘a lot of work organizing individuals to take the financial risks to hold a meeting’. An important event occurred at the 1986, Yale meeting – the International Urogynecology Journal was born. Oscar Contreras Ortiz was nominated Editor in Chief. Donald Ostergard became the first Managing Editor and later, Editor in Chief. He was followed by Linda Brubaker, and, now, Mickey M. Karram. The first issue, Volume 1, was printed in September 1989 and contained the abstracts of the Riva del Garda meeting. The Associate Editors, Section Editors, and Editorial Board represent countries from around the world. The 1987 meeting was in Ljubljana, Yugoslavia, organized by Bozo Kralj of Slovenia, with 200 members worldwide. Bozo became the fourth president at the memorable 1988 meeting at Iguazu Falls, Argentina, hosted by Oscar Contreras Ortiz, who – Hans van Geelen says – ‘made every effort, and succeeded in strengthening social ties’. In 1989, Rudolfo Milana hosted the meeting in Riva Del Garda, Italy. Next elected as president was Eckhard Petri of Germany (1990–1992), inaugurated at the Stockholm, Sweden, meeting organized by Ulf Ulmsten. Peter Dwyer says of this meeting: One of the most low key of all the meetings, it was possibly one of the most enjoyable. It was basic but had good science. The chairman’s dinner was held in Ulf’s department at the Uppsala University cafeteria.
The 16th annual IUGA meeting was held in Sydney, Australia, in 1991, with Jim and Peggy Gibson as host and hostess. They had a fabulous chairman’s reception 5
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which was held at the farm they owned at the time, called Stanton Hall. In 1992, IUGA combined with AUGS in Boston, USA, with a lobster bake party at the famous Aquarium. James Gibson of Australia, was elected sixth president. He presided at the 1993 meeting in Nimes, France, which was coordinated with the International Continence Society (ICS) in Rome. Gibson persuaded Organon to give IUGA $10,000 each year for 5 years for the best presentation at each meeting. He also hosted the Kuala Lumpur meeting in 1995 at which Harold Drutz presided. In 199, Harold Drutz hosted the meeting in Toronto, Canada, at which he was elected the seventh president. Harold Drutz also presided at the Kuala Lumpur meeting in 1995, hosted by Jim Gibson, which, he says, was one of the first meetings to make a profit. In September 1996, the meeting was held in Vienna, Austria, organized by Paul Riss. This was a glorious site at which Oscar Contreras Ortiz, of Argentina, was elected eighth president. The 1997 meeting occurred in Amsterdam, arranged with the combined efforts of Hans van Geelen, Harry Vervest, and Mark Vierhout. The meeting location was planned in Europe as FIGO was in Copenhagen. In 1998, Buenos Aires, Argentina, was the venue for IUGA, hosted by Oscar Contreras Ortiz. Linda Cardozo, of the UK, was elected ninth president. In 1999, in Denver, USA, Willy Davila organized IUGA with Rick Schmidt of ICS to allow the first combined meeting of the two societies. The 2000 IUGA meeting in Rome, Italy, organized by Mauro Cervini, chose Hans van Geelen, of the Netherlands, as president. The widely attended meeting was enlivened by an audience with Pope John Paul II, celebrating the millennium year. The Pope blessed the International Urogynecology Association in his Papal Address during the meeting. Hans van Geelen recalls that at an early IUGA meeting the attendance was so small, the members could sit around one table, discussing the clinical relevance of urodynamics. He, too, says: ‘In the beginning, hosting a meeting was a delicate task.’ In 2001, the IUGA meeting moved to the southern hemisphere again with Peter Dwyer as host in Melbourne, Australia, combined with the Australian Continence Foundation. There Axel Ingelman-Sundberg was awarded a lifetime achievement award, via a live television connection. The 2002 meeting was held in Prague, Czech Republic, with Michael Halaska as organizer. The River Moldau flooded the inner town, and Professor Halaska had to change the venue of the gala dinner, and take out new insurance. In Prague, Peter Dwyer, of Australia, was elected president. Peter comments that IUGA
became not only a scientific society, but developed a true camaraderie of friendship. He says that the young urogynecologists appreciated the emphasis on the clinical rather than the basic science (rats). Peter writes: ‘Presenting our own research internationally and getting ideas for our next projects was also very important, and the meetings were great fun.’ In 2003, IUGA was back in Buenos Aires, Argentina again organized by Oscar Contreras Ortiz. August 200 saw a spectacular meeting of IUGA in Paris, France, combined for the second time with the ICS. The Chairman’s dinner, held at Maxim’s Restaurant, honored Jack Robertson with a lifetime achievement award. The Palais Versailles was the unbelievable site of the gala dinner, all hosted by Bernard Jacquetin for IUGA and Francois Haab for ICS. Paul Riss of Austria, was elected to serve as president from 200 to 2006. Copenhagen, Denmark, was the site of the August 2005 IUGA meeting, organized by Gunnar Lose. The two old friends – Axel Ingelman-Sundberg and Jack Robertson – met in Munich, Germany, in August 200. They plan, God willing, to attend the Copenhagen meeting.
Progress In tHe 20tH century treatment Marion Sims, in the USA, was one of the first to establish the relationship of urology and gynecology. Determined to cure vesicovaginal fistulae, he finally used silver wire and announced in 1852 the cure of 252 out of 320 attempts. Howard A. Kelly, the first professor of gynecology at Johns Hopkins Medical School, believed that gynecology and urology were so closely related that no physician in either field could ignore the other. In 1893, he invented a cystoscope, and was the first person to insert ureteral catheters under direct vision. Kelly’s successor – Guy Hunner – described Hunner’s ulcer, which today is called interstitial cystitis. Succeeding Hunner was Houston Everett, whose contribution was the relationship of the urinary tract to cervical cancer. In 191, Latzko perfected the cure of posthysterectomy vesicovaginal fistula. Next, Richard TeLinde added water endoscopy to the Hopkins female urology program. Most teaching programs at the time gave little or no exposure to female urology.2 In 1892, Poussan proposed the concept of urethral advancement for the management of urinary incontinence.5 He suggested ‘introducing a bougie into the urethra, resecting the external meatus and portion of
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the urethra, and then after torsion of the canal to one hundred and eighty degrees, it is transplanted to a point just below the clitoris’. By the turn of the century, four main treatments for stress urinary incontinence were outlined:
• • • •
injection of paraffin into the region of the urethra; massage and electricity; torsion of the urethra; advancement of the external urethral meatus.
A century later, we are still trying to identify the best urethral bulking agent. Although it is no longer paraffin, research with Teflon (polytetrafluoroethylene), silicone, collagen, autologous fat, carbon particles, and various co-polymers has failed to identify an ideal medium. In his landmark paper in 1913, Kelly outlined operations for managing urinary incontinence in women.6 These included:
• puncture of the bladder and insertion of a catheter; • closing the urethra and creating a vesicoabdominal • • • •
fistula; closing the vagina and creating a rectovaginal fistula; compression of the urethra with an anterior colporrhaphy; periurethral injection of paraffin; advancement of the urethral meatus to the clitoris.
Kelly suggested that ‘the torn or relaxed tissues of the vesical neck should be sutured together using two or three vertical mattress sutures of fine silk linen passed from side to side’. In his first publication, he described 16 patients as being well and four patients in whom the procedure was not successful, giving a success rate of 80%. However, further evaluation has revealed that long-term success, using only these sutures to correct 7 stress incontinence, falls to roughly 60%. This decline is possibly related to gradual postoperative elongation of the smooth muscle in which the sutures were placed.8 With coincident suburethral plication of the pubourethrovaginal ligaments of the urogenital diaphragm, the long-term results of a Kelly plication are significantly better.9 Sling procedures were pioneered in the early 1900s by three European physicians. Goebell first suggested transplantation of the pyramidalis muscle in 1910.10 This was followed by Frankenheim who, in 191, recommended using the pyramidalis or strips of rectus muscle as a suburethral sling, by attaching the muscle to overlying fascia.11 In 1917, Stoeckel suggested combining the techniques of Goebell and Frankenheim and adding
plication of the vesical neck.12 Throughout the 20th century, many variations of sling procedures were described in the literature. In 1907, Giordano suggested the use of gracilis muscle by wrapping it around the urethra.13 Shortly thereafter, in 1911, Souier described the use of levator ani muscles by placing them between the vagina and urethra1 and, in 1923, Thompson recommended the use of strips of rectus muscle, surrounded by fascia, to be passed in front of the pubic bones and around the urethra.15 The next key event in the development of surgery to the anterior compartment was the development of the bulbocavernosus muscle fat pad graft by Martius in 1929.16 This has found wide use in fistula repairs and reconstruction of the anterior vaginal wall. In 1968, John Chasser Moir17 introduced the concept of the gauze hammock operation as a modification of the original Aldridge18 sling procedure described in 192. Chasser Moir recognized that: ‘Operations of this type do no more than support the bladder neck and urethrovesical junction and so prevent the undue descent of parts when the woman strains or coughs.’ In 1923, Victor Bonney19 stated: ‘Incontinence depends in some way upon a sudden and abnormal displacement of the urethra and urethrovesical junction immediately behind the symphysis.’ This was followed in 192 by a description from B.P. Watson20 of ‘the muscle sheet that normally supports the base and neck of the bladder’ and his statement that: ‘So far as the incontinence of urine is concerned, the important sutures are those which overlap the fascia at the neck of the bladder and so restore it to its normal position.’ A review of Watson’s work with anterior colporrhaphy shows that he was able to obtain ‘perfect control’ in 65.7% of cases, ‘improvement’ in 21.9%, and ‘no success’ in 12.%.20 These figures are in keeping with others that have been reported for anterior colporrhaphy. Therefore, it was apparent that hypermobility of the bladder neck was an issue, and that anterior colporrhaphy was not a satisfactory operation for stress incontinence. The next landmark in genitourinary surgery occurred in 199 with the publication of the paper of Marshall, Marchetti, and Krantz entitled, ‘The correction of stress incontinence by simple vesicourethral suspension.’ They suggested that this operation was ‘particularly valuable for patients whose first procedure failed’. In their first patients they described 82% of patients with excellent results, 7% with improvement, and an 11% failure rate.21 Shortly thereafter, in 1950, H.H. Fouracre Barns described the ‘round ligament sling operation for stress incontinence’; this technique was popularized by Paul Hodgkinson.22 7
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In 1961, John Burch first described his modification of the Marshall–Marchetti–Krantz procedure which involved a retropubic colpourethropexy that attached the anterolateral aspects of the vault of the vagina to Cooper’s ligament.23 Burch recognized the potential complications of this procedure if performed alone, including the creation of an enterocele or rectocele, the development of ventral/incisional hernias, and even the possibility of a vesicovaginal fistula.
diagnosis and investigation As the number of procedures offered for the treatment of stress incontinence increased, there were also significant advances in the urogynecologic diagnostic procedures available. In 1882, Mosso and Pellacani described cystometry using a smoked drum and a water manometer.2 An aneroid barometer for cystometric evaluation was developed by Lewis in 1939.25 Jeffcoate and Roberts, in 1952, introduced the concept of radiographic changes in the posterior urethrovesical angle.26 These changes were further modified in 1956 by Bailey in England, who described seven variations in the urethrovesical angle on radiographic studies.27 Later modifications were performed by Tom Green in the United States in 1962, when he described Green types 1 and 2 incontinence.28 Identification of the posterior urethrovesical angle by lateral bead chain cystography was introduced by Hodgkinson in 1953.29 By 1956, Von Garrelts had introduced the concept of uroflowmetry.30 In 196, Enhorning, Miller and Hinman combined cystometry with radiographic screening of the bladder;31 this was followed in 1969 by Brown and Wickham’s introduction of urethral pressure profilometry.32 Another landmark occurred in 1971, when Patrick Bates, Sir Richard Turner-Warwick and Graham Whiteside introduced synchronous cine pressure–flow cystography, with pressure and flow studies.33 This was the beginning of the field of videourodynamics. Equipment was further expanded by Asmussen and Ulmsten in 1975 with the introduction of the microtip transducer for measuring urethral closure pressure.3 Further investigational advances occurred in the latter part of the 20th century. These included the introduction of the Urilos monitor in 197 by James, Flack, Caldwell and Smith.35 This device allowed evaluation of the symptom of dampness to determine whether the fluid lost was urine. In 1981, Sutherst, Brown and Shawer developed the pad-weighing test as an objective measure of the severity of urinary incontinence.36 In 1961, Enhorning suggested that ‘surgical treatment for stress incontinence is probably mainly beneficial
because it restores the neck of the bladder and the upper part of the urethra to the influence of intra-abdominal pressure’.37 This introduced the concept of pressure transmission ratios, and the idea that successful operations for stress urinary incontinence worked by restoring the urethrovesical junction to an intra-abdominal position. In 1956, Jeffcoate added further interpretation of our investigative techniques when he attempted to caution gynecologists, stating: ‘The absence of the posterior urethrovesical angle is merely a sign of incompetence of the internal sphincter. The presence of an angle is a function of the involuntary muscle at the urethrovesical junction, not of the muscle of the pelvic floor.’38 Thus the simplistic approach of static cystourethrograms began to be questioned. Green had suggested that if one saw a radiographic diagnosis of type 1 incontinence this could readily be repaired with an anterior colporrhaphy; type 2 stress incontinence required a retropubic urethropexy. A number of authors, including Drutz et al. in 1978,39 have confirmed the limited accuracy of static cystourethrograms. By 1953, Paul Hodgkinson had recommended that: ‘If, on anteroposterior straining radiograph, the urethrovesical junction is depressed cm below the lower border of the symphysis, I believe the objective of the operation can be accomplished through anterior colporrhaphy.’29 A decade later Hodgkinson commented on the frequency of detrusor dyssynergia, with grade 1 defining this as a detrusor contraction in response to coughing and heel bouncing; grade 2 was spontaneous automatic detrusor contractility when recumbent. Hodgkinson recognized the importance of discovering this condition prior to performing any surgery for stress urinary incontinence.0
success rates As we approached the 1970s, we began to recognize that operative failures in the treatment of stress urinary incontinence involve three areas,1 as follows:
• incorrect diagnosis and the fact that bladder • •
instability (and not just simple stress incontinence) may have been the cause of the incontinence; the wrong operation may have been chosen, and some operations probably give better long-term results; technical failure.
We recognized that the vaginal approach to primary stress incontinence only gave a 50–60% success rate, whereas the suprapubic approach gave success rates of
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at least 80%. J. E. Morgan, in 1973, discussed indications for primary retropubic urethropexy; these included minimal pelvic floor relaxation, chronic chest disease, occupations involving heavy lifting, patients who were heavily involved in athletics, and obesity.2 In 1970, Paul Hodgkinson stated that ‘the most durable operation for stress incontinence is a retropubic urethropexy and the least durable is a vaginal repair’. Hodgkinson quoted a 92.1% success rate with his own 0 patients that had a retropubic urethropexy.1 The other movement in the 1970s was of urologists and gynecologists toward endoscopic bladder neck suspensions such as the Pereyra, Raz, and Stamey suspensions; numerous variations including the Gittes and Cobb-Raagde were described in the literature. By the 1990s, we realized that the long-term results of these needle suspension procedures were also not as good as the retropubic procedures. The 1990s also saw the advent of minimally invasive sling procedures for stress urinary incontinence. The first of these – the tension free vaginal tape and the concomitant integral theory of the pathophysiology of incontinence – were described by Ulmsten and Petros in the early 1990s.3, There are now multiple variations of this procedure, including the new transobturator approach. Success rates are reported to be similar to that of the Burch repair.5 The great champion of pelvic floor exercises, Arnold Kegel, reported pre- and postoperative benefits of properly performed exercises.6 Unfortunately, many patients are placed on this regimen only after an unsuccessful surgical procedure. In 200, Robertson, with Bergman and Elia, described an enhancement of Kegel’s exercise, when done in a magnetic field, combined with DeLancey’s ‘knack procedure’, to give support to the urethra when it is most needed.7
education
tHe Way aHead
New pharmacologic agents continue to be produced; well-designed, placebo-controlled trials are mandatory for their evaluation. Neurophysiology is another developing area; work is being done to determine if there are certain factors in labor that lead to irreversible changes to the pelvic floor. Other questions that have been raised include whether abnormalities in the electromyographic patterns predict success or failure of different treatments. We continue to develop new modes of conservative management, including behavior modification and devices; further studies are needed to clarify the specific areas of use for these therapies.
At the outset of the 21st century, we must consider what lies ahead. The main fields of responsibility of urogynecologists and reconstructive pelvic surgeons include:
• • • • • • • •
education; surgery; uropharmacology; neurophysiology; behavior modification; connective tissues (such as collagen); ultrasonography/magnetic resonance imaging (MRI); quality of life.
We need to focus on education of our colleagues in obstetrics and gynecology, family practice, geriatrics and community healthcare, allied health professionals such as nursing and physiotherapy, as well as the public. Awareness that incontinence is not a normal effect of aging must be increased; the many myths, including ‘everyone gets it’ and ‘it cannot be treated’, must be dispelled. Urogenital aging must be stressed as part of menopause management, and conservative management in the community should be promoted. The other aspect of education is the training of new subspecialists in the field of urogynecology and reconstructive pelvic surgery. Board certification is now available in Australia, and board recognition has been established in the United States. The IUGA is establishing international standards of training in conjunction with FIGO and the World Health Organization.
surgery Within the field of surgery for pelvic floor problems, we need to re-evaluate what we do. Over 200 operations have been described for stress incontinence. Randomized controlled trials, with adequate patient numbers and follow-up of at least 2 years, are required for evaluation of new and existing procedures. The role of bulking agents is still controversial, and the ideal medium has yet to be discovered. A variety of fascia and mesh are available for use in pelvic floor reconstructive procedures; however, the long-term durability and consequences of these are still unknown.
uropharmacology, neurophysiology and behavior modification
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connective tissues The role of collagen in pelvic floor disorders is a fascinating area. We need both effective qualitative and quantitative assays to determine whether there are certain defects of collagen in patients with pelvic floor dysfunction. Also, we need to establish whether there may be potential genetic markers that may be screened for to determine certain ‘at-risk’ patients. Perhaps there exists a select group of patients that should be counseled to have delivery by cesarean section; this group may also require the use of synthetic materials in reconstruction of their pelvic floor. We need to look at the relationship of collagen to estrogen and the general effects of urogenital aging to see if they are independent factors.
ultrasonography/MrI We are in the midst of a revolution in imaging and diagnostic technology. The development of 3-dimensional ultrasound8 and the progress with MRI has allowed a new approach to evaluating defects associated with stress urinary incontinence and pelvic floor disorders. Progress in the field of ultrasound has been hampered by a lack of standardization of terminology; this was recognized by the German Association of Urogynecology, which attempted to make recommendations for standardization of methodology.9 The fact that different methods are used (such as abdominal, perineal, introital, vaginal, and rectal) has further impeded progress in this field. Recent papers have investigated the urethra and surrounding tissues with intraurethral ultrasonography; the authors have proposed that sphincter measurements can be a prognostic factor in patients who underwent operations for stress urinary incontinence.50 Beco stated that ‘Doppler and colour studies will play an increasing role in the evaluation of urethrovesical disorders’.51 With new developments in MRI, and especially dynamic MRI, these techniques will also play a growing role in investigation and research. New ways of investigating urethral function are also appearing, with the introduction of the MoniTorr device and measurement of urethral retroresistance.52
conclusIons At the International Continence Society Meeting in 1986, Sir Richard Turner-Warwick gave an address in which he defined the urogynecologist as ‘neither the general urologist nor the general obstetrician and gynecologist, but someone who has special training and expertise in genitourinary problems in women’.53 Today, we should expand this definition to include urogynecology and reconstructive pelvic surgery. Such a description implies a surgeon with specialized training in the conservative and surgical management of women with urinary or fecal incontinence, persistent genitourinary complaints, and disorders of pelvic floor supports. As Marcel Proust said: ‘We must never be afraid to go too far, for the truth lies beyond.’ We must humbly accept that the ‘truths’ we identify today will certainly have to be changed in the future. However, if we work collaboratively to produce well-designed scientific research, we should be able to establish truths that stand the test of time in our ongoing quest to improve the quality of life for women with pelvic floor problems.
acknoWledgMent This chapter includes major segments of text adapted from the IUGA Presidential Address given by Professor Harold Drutz at the 21st Annual Meeting of the International Urogynecological Association held in Vienna in 1996. The text was later published: Drutz HP. The first century of urogynecology and reconstructive pelvic surgery: where do we go from here? Int Urogynecol J 1996;7:38–53.
references 1. Keith A. Man’s posture: its evolution and disorders. Br Med J 1923;II:51–. 2. Robertson JR. Genitourinary problems in women. Springfield, IL: CC Thomas, 1978; 6–12. 3. Wall LL, DeLancey JOL. The politics of prolapse: a revisionist approach to disorders of the pelvic floor in women. Perspect Biol Med 1991;3:86–96. . Nager CW, Kumar D, Kahn M, Stanton SL. Management of pelvic floor dysfunction. Lancet 1997;350:1751. 5. Poussan. Arch Clin Bord 1892. No. 1.
Quality of life There is an increasing focus on quality of life tools as a research outcome. National and international societies must continue to promote and support research in the field to advance pelvic floor health for women.
6. Kelly HA. Incontinence of urine in women. Urol Cutan Rev 1913;17:291. 7. Bergman A, Elia G. Three surgical procedures for genuine stress urinary incontinence: five year follow-up of a prospective randomized study. Am J Obstet Gynecol 1995;173(1):66–71.
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8. Wall LL, Norton PA, DeLancey JOL. Practical Urogynecology. Baltimore: Williams and Wilkins 1993; 153–90.
der in urinary stress incontinence. Am J Obstet Gynecol 1953;65:560–75.
9. Nichols DH, Randall CL. Vaginal Surgery. Baltimore: Williams and Wilkins 1996; 218–56.
30. Von Garrelts B. Analysis of micturition: a new method of recording the voiding of the bladder. Acta Chir Scand 1956;112:326–0.
10. Goebell R. Zur operativen Besierigung der angeborenen Incontinentia vesical. Z Gynäk Urol 1910;2:187. 11. Frankenheim P. Zentral Verhandl. d. Deutsch. Geseusch Chir 191;3:19. 12. Stoeckel W. Über die Verwändung der Musculi Pyramidales bei der opeutinen Behandlung der Incontinentia Urinae 1917;1:11. 13. Giordano D. Twentieth Congress Franc de Chir. 1907; 506. 1. Souier JB. Med Rec 1911;79:868. 15. Thompson R. Br J Dis Child 1923;20:116. 16. Martius H. Sphincter und Harndöurenplastic aus dem Musicailus Bulbocavernosus. Chirurgie 1929;1:769. 17. Chasser Moir J. The gauze-hammock operation (a modified Aldridge sling procedure). J Obstet Gynaecol Br Commonw 1968;75:1–9.
31. Enhorning G, Miller E, Hinman F Jr. Urethral closure studied with cine roentgenography and simultaneous bladder–urethral pressure recording. Surg Gynaecol Obstet 196;118:507–16. 32. Brown W, Wickham JEA. The urethral pressure profile. Br J Urol 1969;1:211–7. 33. Bates CP, Whiteside CG, Turner-Warwick R. Synchronous cine/pressure/flow cystography: a method of routine urodynamic investigation. Br J Radiol 1971;:–50. 3. Asmussen M, Ulmsten U. Simultaneous urethrocystometry and urethral pressure profile measurements with a new technique. Acta Obstet Gynaecol 1975;5:385–6. 35. James ED, Flack F, Caldwell KP, Smith. Urine loss in incontinence patients: how often, how much? Clin Med 197;:13–7.
18. Aldridge AH. Transplantation of fascia for relief of urinary stress incontinence. Am J Obstet Gynecol 192;:398–11.
36. Sutherst JL, Brown M, Shawer M. Assessing the severity of urinary incontinence in women by weighing perineal pads. Lancet 1981;1:1128–30.
19. Bonney V. On diurnal incontinence of urine in women. J Obstet Gynecol Br Emp 1923;30:358–65.
37. Enhorning G. Simultaneous recording of intravesical and intraurethral pressure: a study of urethral closure pressures in normal and incontinent women. Acta Chir Scand 1961;276(Suppl):1.
20. Watson BP. Imperfect urinary control following childbirth and its surgical treatment. Br Med J 192;11:566. 21. Marshall VF, Marchetti AA, Krantz KE. The correction of stress incontinence by simple vesicourethral suspension. Surg Gynecol Obstet 199;88:509–18. 22. Fouracre Barns HH. Round ligament sling operation for stress incontinence. J Obstet Gynaecol Br Emp 1950;57:0–7. 23. Burch JC. Urethrovaginal fixation to Cooper’s ligament for correction of stress incontinence, cystocele and prolapse. Am J Obstet Gynecol 1961;81:281–90. 2. Mosso A, Pallacani P. Sur les fonctions de la vessie. Arch Ital Biol 1882;1:97. 25. Lewis LG. New clinical recording cystometer. J Urol 1939;1:638–5. 26. Jeffcoate TNA, Roberts H. Stress incontinence. J Obstet Gynaecol Br Emp 1952;59:865–720. 27. Bailey KV. A clinical investigation into uterine prolapse with stress incontinence: treatment by modified Manchester colporrhaphy. Part II. J Obstet Gynaecol Br Emp 1956;63:663. 28. Green TH Jr. Development of a plan for the diagnosis and treatment of urinary stress incontinence. Am J Obstet Gynecol 1962;83:632–8. 29. Hodgkinson CP. Relationship of female urethra and blad-
38. Jeffcoate TNA. Bladder control in the female. Proc R Soc Med 1956;9:652–60. 39. Drutz HP, Shapiro BJ, Mandel F. Do static cystourethrograms have a role in the investigation of female incontinence? Am J Obstet Gynecol 1978;130:516–20. 0. Hodgkinson CP, Ayers MA, Drukker BH. Dyssynergic detrusor dysfunction in the apparently normal female. Am J Obstet Gynecol 1963;87:717–30. 1. Hodgkinson CP. Stress urinary incontinence. Am J Obstet Gynecol 1970;1:111–68. 2. Morgan JE. The suprapubic approach to primary stress incontinence. Am J Obstet Gynecol 1973;9:37–2. 3. Petros PE, Ulmsten UI. An integral theory and its method for the diagnosis and management of female urinary incontinence. Scand J Urol Nephrol Suppl 1993;153:1–93. . Ulmsten U, Petros P. Intravaginal slingplasty (IVS): an ambulatory surgical procedure for treatment of female urinary incontinence. Scand J Urol Nephrol 1995;29(1):75–82. 5. Ward KL, Hilton P. UK and Ireland TVT Trial Group. A prospective multicenter randomized trial of tension-free vaginal tape and colposuspension for primary urodynamic
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stress incontinence: two-year follow-up. Am J Obstet Gynecol 200;190(2):32–31. 6. Kegel AH, Powell TH. The physiologic treatment of stress incontinence. J Urol 1950;63:808. 7. Bergman J, Robertson JR, Elia G. Effects of a magnetic field on pelvic floor muscle function in women with stress urinary incontinence. Altern Ther Health Med 200;10(3):70–2. 8. Khullar V, Salvatore S, Cardozo LD, Hill S, Kelleher CJ. Three dimensional ultrasound of the urethra and urethral sphincter: a new diagnostic technique. Neurourol Urodyn 199;13:352–3. 9. Shaer G, Koelbl H, Voigt R et al. Recommendations of the German Association of Urogynecology on functional
sonography of the lower female urinary tract. Int Urogynecol J 1996;7:105–8. 50. Hermans RK, Klein HM, Muller U, Schafer W, Jakse G. Intraurethral ultrasound in women with stress incontinence. Br J Urol 199;7:315–8. 51. Beco J. Personal communication, November 1996. 52. Slack M, Culligan P, Tracey M, Hunsicker K, Patel B, Sumeray M. Relationship of urethral retro-resistance pressure to urodynamic measurements and incontinence severity. Neurourol Urodyn 200;23(2):109–1. 53. Turner-Warwick R. International Continence Society Proceedings. Boston, MA, 1986.
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2a Epidemiology: USA Brandon S Rubens, William D Tissot, Ananias C Diokno
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IntroductIon Epidemiology is defined as the study of the relationships of various factors determining the frequency and distribution of diseases in a community.1 The epidemiologic study of urinary incontinence (UI) has advanced over the past several years. However, most of these studies are cross-sectional. A need exists for more longitudinal studies to evaluate the incidence, remission, risk factors, and prevention of this disease process. The methodologies to evaluate the epidemiology of UI vary greatly. Furthermore, there is no consensus on the definition of UI among investigators dealing with this subject. As a consequence, there is conflicting information, especially in the prevalence rates. Another major issue in studying UI is the fact that incontinence itself is a condition with many varied types, occurring in many different segments of the population. Students of the epidemiology of UI must therefore account for all these variables when evaluating data from these studies.
Prevalence of urInary IncontInence The prevalence of UI is defined as the probability of being incontinent within the defined population group within a specific period of time. The first comprehensive epidemiologic study of incontinence in the United States was conducted by Diokno et al.2 in 1983 in Washtenaw County, Michigan. The Medical, Epidemiologic, and Social Aspects of Aging (MESA) study showed the prevalence of incontinence among women 60 years and older living in the community to be 38%. Other more recent studies have agreed with this prevalence rate, such as the data reported by Fultz et al. A 14-item questionnaire was returned by 29,903 people, of whom 37% reported incontinence in the past 30 days.3 The prevalence of UI in women increases with age. A postal survey was conducted by Thomas et al.4 to selected table 2a.1.
health districts in the London boroughs and neighboring health districts in the late 1970s. In that survey, incontinence was defined as involuntary excretion or leakage of urine in inappropriate places or at inappropriate times twice or more a month, regardless of the quantity of urine lost. Incontinence was further subdivided into regular UI for a loss twice or more per month, and occasional for less than twice per month. The response rate was excellent at 89%. Table 2a.1 shows the prevalence rates for regular and occasional incontinence in women aged 15 to more than 85 years. Three age tiers to the prevalence of regular incontinence in women were noted: tier 1 (15–34 years) showed a prevalence of 4–5.5%, tier 2 (35–74 years) showed a prevalence of 8.8–11.9%, and tier 3 (75 years and older) showed a prevalence of 16–16.2%. Several studies have investigated incontinence in women of different races and found intriguing results. Lower rates of stress and mixed incontinence were reported by African–American women when compared with white women.5 Hispanic and Asian–American women have been shown to have equivalent genuine stress incontinence rates to white women, whereas the African–American women had higher rates of detrusor instability than the other three groups.6 African– American women were found to have statistically significant smaller bladder capacities, smaller maximum cystometric capacities, and higher maximum urethral closure pressures compared to Caucasians.7
IncIdence and remIssIon Incidence is the probability of becoming incontinent during a defined period of time. Determining the incidence of a condition or disease is helpful in determining the onset of the condition as well as in understanding the risk factors of the condition. The MESA survey estab-
Prevalence of urinary incontinence (UI) in women
Age group (years)
Regular UI (%)
Occasional UI (%)
Total UI (%)
15–24
4.0
11.9
15.9
25–34
5.5
20.0
25.5
35–44
10.2
20.7
30.9
45–54
11.8
21.9
32.9
55–64
11.9
18.6
30.5
65–74
8.8
14.6
22.4
75–84
16.0
13.6
29.6
> 85
16.2
16.2
32.4
Data adapted from ref. 4.
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lished the incidence rate of UI in the United States.8 The incidence rate among women who were continent during the initial baseline interview and became incontinent a year later was 22.4%. For those who remained continent at the 1-year follow-up visit, the incidence in the second year of follow-up was 20.2%. Hagglund et al., reporting on a Swedish community of 10,500 inhabitants aged between 22 and 50 years, found a mean 4% annual incidence rate of UI.9 An annual incidence rate of 6.3% for people ≥40 years old was found in the study by McGrother et al. in the UK.10 In rural Iowa, 2025 women older than 65 years were evaluated by Nygaard and Lemke. The 3-year incidence rates for urge and stress incontinence were 28.5% and 28.6%, respectively.11 The MESA survey also analyzed the remission rate for urinary incontinence. The remission rate – i.e. women who were incontinent at the baseline (first) interview and became continent during the second interview a year later – was 11.2%. A similar rate (13.3%) of incontinent respondents at the second interview reported being continent a year later at the third interview. Hagglund et al. reported a 4% mean annual remission rate in the same Swedish community as above.9 Nygaard and Lemke’s 3-year remission rates for urge and stress incontinence were 22.1% and 25.1%, respectively.11
tyPes and severIty of urInary IncontInence
and urge incontinence was 61 years old.12 Luber et al. evaluated 642 incontinent women and discovered that stress incontinence was more common in younger women aged 30–49 years (78%) versus those 50–89 years of age (57%). Urge incontinence predominates in the older population (67%) versus women under the age of 50 years (56%).13 According to Nygaard and Lemke, the rate of urge incontinence tends to rise with age, while the rate of stress incontinence decreases somewhat in the oldest age groups, possibly due to lower activity levels11 (Fig. 2a.1). The MESA survey conducted by Diokno et al.2 reported the prevalence of the types of clinical incontinence encountered among their respondents. The most common type reported by those women aged 60 years and older was the mixed stress and urge type (55.5%), followed by the stress type (26.7%), then the urge (9.0%) and other (8.8%) types. A meta-analysis of published studies of urinary incontinence epidemiology throughout the world suggested that stress incontinence is the most common form.14 Stress incontinence accounted for almost half of the total worldwide prevalence of urinary incontinence, and mixed incontinence constituted 29% of the total prevalence. The analysis showed that urge incontinence was less common, consistent with US and European surveys.
In epidemiologic studies, as in clinical investigations, the type of UI must be defined. In general, incontinence is considered to be of the stress type when the urine loss was experienced at the time of physical exertion (such as coughing, laughing, sneezing, etc.). Urge incontinence is defined as involuntary loss of urine preceded by a sudden urge to void. When the urine loss is associated with both stress and urge, it is considered to be of the mixed type. Because of the difficulty in identifying the overflow type, when the urine loss is associated with neither the stress nor the urge type, the incontinence is labeled ‘other’. However, when the survey respondents were taken one step further into urodynamic testing, the type of incontinence has been classified into the various urodynamic types according to the pathophysiologic abnormality. The age of onset may be an important factor in the type of UI experienced. Kinchen et al. found the median age of American women reporting stress incontinence was 48 years old, mixed incontinence was 55 years old,
Prevalence (%)
Prevalence and incidence of types of uI 100 90 80 70 60 50 40 30 20 10 0 66
Either
Urge
69
Stress
72
75
78 Age
81
84
87
Figure 2a.1. Prevalence of incontinence by age groups at baseline. Each age represents the midpoint of a 3-year age range. Because of the small number of women above age 90, the graph ends with age range 86–88. ‘Urge’ and ‘stress’ refer to women who answered affirmatively to the urge and stress incontinence questions, respectively. ‘Either’ refers to women who reported any incontinence (either urge or stress). (Data adapted from ref. 11.) 15
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Prevalence and incidence of severity of uI In epidemiologic studies, severity has been categorized by the frequency of incontinent episodes, by the volume of urine loss or by the frequency of difficulty in controlling the flow of urine. The Diokno MESA study2 reported the severity of UI among its 60-yearold respondents in terms of the number of days per year that urine loss was experienced and the volume of urine loss per day. As shown in Table 2a.2, if severe or significant UI is considered to be the loss of at least a quarter cup of urine per day on 50 or more days/year, or frequency of incontinence is 300 or more days/ year, then 20.4% of women respondents aged 60 years and older at the time of the MESA survey had severe incontinence. The patterns of change in the severity of UI in the MESA survey were also analyzed.8 Based on the severity levels described in Table 2a.2, continent respondents who became incontinent were most likely to develop a mild form of incontinence. About half of those who were classified originally as mildly incontinent remained so and very few became severely incontinent. Among those who reported moderate incontinence, most remained moderately incontinent or changed to mildly incontinent, with very few advancing to severe incontinence. Among women who were severely incontinent at baseline, most remained severely incontinent. Kinchen et al. revealed that over 50% of incontinent respondents have urine loss at least once per week.12 The severity of incontinence symptoms influences a woman’s willingness to discuss the symptoms with a physician. Fewer than 20% of women report discussing incontinence with a physician within the past year when
symptoms are mild. The proportion increases to 42% of women when symptoms are severe.15
Prevalence of voiding frequency The prevalence of voiding frequency is receiving greater attention as more and more studies are being conducted for conditions related to bladder dysfunction. For example, pharmacologic interventions as well as behavioral techniques aimed at improving bladder function usually affect the frequency of voiding day and night. It is therefore imperative that a comparative standard is available on which to base any observations related to frequency of voiding prior to, during and after an intervention. The MESA study has established the distribution of voiding frequency among the elderly (60 years and older) living in a community, who are likely to be the subjects of pharmacologic and behavioral interventions aimed at controlling abnormal voiding.2 It appears that the normal daily frequency of urination in this age group is no more than eight times, as 88% of all our asymptomatic respondents reported that range. To be more specific, 47.3% of asymptomatic women reported that they voided six to eight times, 34.8% voided four to five times, and 5.5% voided one to three times daily. FitzGerald et al. re-evaluated the definition of urinary frequency by evaluating 300 asymptomatic women aged 18–91 (median 40 years) who volunteered from a large metropolitan community. These women completed a 24-hour log of fluid intake and volumes voided. They found a median of 8 voids in 24 hours, with 95% of subjects recording less than 13 voids per 24 hours. Their conclusion was that using ≥8 voids per 24 hours as the definition of ‘frequency’ may be inappropriate, sug-
table 2a.2. Percentage of severe incontinence, as judged by volume and frequency of urine loss, in 60-year-old women Volume of urine lost in 24 hours
No. of days with urine loss 1–9
10–49
Drops < ½ tsp
16.1
11.6
5.6
3.0
36.3 (135)
½ tsp – < 1 tbsp
9.7
9.7
7.5
3.2
30.1 (112)
1 tbsp – < ¼ cup
4.6
4.6
5.4
3.2
17.8 (66)
¼ cup or more
2.4
2.4
4.3
6.7
15.8 (59)
Total *
32.8 (122)
28.3 (105)
50–299
22.8 (85)
300–365
16.1 (60)
Total percentage*
100.0 (372)
Respondents with mild incontinence were those who reported low frequency (1–9 days/year) and/or small volume (<½ teaspoon/day for <300 days/year); those with severe incontinence were those who reported high frequency (≥300 days/year) and/or large volumes (>¼ cup/day on ≥50 days/year); those respondents with intermediate volume and/or frequency were considered to have moderate incontinence. *Number of patients in parentheses. Data adapted from ref. 2.
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gesting that ‘frequency’ may be ≥13 voids in 24 hours.16 Since the information came from a self-selected group of volunteers that reside in a large metropolitan area, their findings may not represent the true frequency of voiding in the general community. In terms of nocturia – defined as the frequency of being awakened from sleep and getting up to void – 93% of asymptomatic women voided no more than twice at night. In contrast, 25% of women with irritative symptoms and 24% of women with difficulty in emptying the bladder voided three or more times each night.2 These data suggest that abnormal bladder function has a significant effect on the frequency of voiding. Incontinent women are voiding much more frequently than continent women. FitzGerald et al.16 recorded night-time voids in 44% of their population: 36% voided once during the night while 8% voided greater than or equal to two times per night. The number of night-time voids was dependent only on patient age.
QualIty of lIfe Urinary incontinence has a significant impact on a woman’s quality of life. Fultz et al. examined 174 respondents who were moderately to extremely bothered by stress incontinence symptoms. Of these women, 54.4% reported that their symptoms had a moderate to extreme impact on physical activities, 42.7% perceived such impact on confidence, 38.6% on daily activities, and 36.5% on social activities.3 The odds of moderate-to-extreme bother/burden decreased with age and increased with symptom severity. According to Thom et al., the relative risk of admission to a nursing home is two times greater for incontinent women.17 Over half of all female nursing home residents are reported to have ‘difficulty controlling urine’, and over half need assistance in using the toilet.18
Prevalence of urodynamIc measures among contInent and IncontInent elderly women To establish the urodynamic characteristics of both continent and incontinent elderly women living in a community, a series of urodynamic tests were conducted on those MESA respondents who volunteered to undergo such tests.19,20 This study provided information on the prevalence of the various parameters in the urodynamic tests that are of interest in the evaluation of incontinent patients but for which there are no well-established data from control subjects. The MESA survey data established the sensitivity and specificity of the various
urodynamic tests, from which it was concluded that such tests – including uroflow, cytometrography, static urethral profilometry, and stress cystography – should be used, not to screen and diagnose UI but, rather, to confirm clinical manifestation. Urodynamic testing, by virtue of its ability to identify various mechanisms of UI, is believed to be helpful not only in determining the category of therapeutic approach but also in assessing outcomes of therapy. The MESA survey studied a random sample of noninstitutionalized ambulatory elderly women, both continent and incontinent; an initial clinical evaluation was followed by a series of urodynamic evaluations. A total of 258 self-reported continent and 198 self-reported incontinent women underwent the clinical evaluation comprising history taking, physical examination (including pelvic examination), and urinalysis. From these groups, 67 continent and 100 incontinent women underwent urodynamic testing, including an initial noninstrumented uroflow test, followed by catheterized post-void volume measurements, and subsequently by filling cystometry, static and dynamic urethral profilometry, provocative stress test, and lateral stress resting and straining cystogram.
uroflowmetry The uroflow measures of peak flow rate (PFR) and average flow rate (AFR) were analyzed according to the voided volume at increments of 100 ml. When volume was controlled, the mean PFR and AFR did not differ significantly between respondents who were continent and those who were incontinent. The flow rates did not differ between women with competent sphincters and those with urethral incompetence. The continuity of the urinary stream was not associated with continence status or with the clinical type of incontinence (i.e. urge, stress, etc.).
Post-void residual volume A post-void residual volume of 0–50 ml was found in 78.1% of continent and 86.5% of incontinent women; 9.7% and 8.4% had residuals of 51–100 ml; 2.4% and 1.6% had residuals of 101–150 ml, and 9.7% and 3.5% had residuals of 151 ml or more, respectively. There was no statistical difference between continent and incontinent women with regard to prevalence of a residual urine volume greater than 50 ml. These data give rise to questions regarding the post-void residual volume in relation to the diagnosis of overflow incontinence: the determining factor for overflow incontinence may be 17
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the same factor as for urge and/or stress incontinence, and the abnormal post-void residual volume may be coincidental or a contributory factor rather than a primary reason for the incontinence.
Bladder capacity Among the women volunteers, 79% of continent volunteers and 64% of incontinent volunteers had a bladder capacity of 300 ml or more; however, this difference in bladder volume between continent and incontinent subjects was not significant. The mean cystometric bladder capacities among continent and incontinent subjects, respectively were:
• • • • •
60–64 years: 381.8 and 442.7 ml; 65–69 years: 421.6 and 370.0 ml; 70–74 years: 410.3 and 414.2 ml; 75–79 years: 350.3 and 426.8 ml; 80+ years: 318.3 and 408.3 ml.
These results refute the notion that the bladder capacity of the elderly is smaller than normal, if we consider a bladder capacity of 300 ml or more to be normal.
uninhibited detrusor contraction The diagnosis of uninhibited detrusor contraction was based on the definition by the International Continence Society. The overall prevalence of uninhibited detrusor contraction in women was 7.9%; the prevalence of uninhibited detrusor contraction among continent respondents was 4.9%, whereas for incontinent subjects it was 12.2%. The difference between the two prevalence rates was not significant. However, comparison of the bladder capacity between female respondents showed that the capacity in women with uninhibited detrusor contraction was 364 ml, whereas in those without uninhibited contractions it was 404 ml; the difference was statistically significant at p<0.05. This may explain the increased frequency, urgency, and smaller voided volumes of patients with detrusor instability.
static and dynamic urethral pressure profilometry (uPP) The mean functional urethral length (FUL) did not change significantly as the age of the subjects increased, but the values of the maximum urethral pressure (MUP) and the maximum closure pressure (MCP) showed a significant progressive reduction as age increased (p=0.002 and p=0.0003, respectively). This progressive reduc-
tion of MUP and MCP reinforces the belief that elderly women are more predisposed to stress urine loss. The parameters of UPP for supine subjects did not show any significant difference between continence and incontinence. However, for standing subjects, significant differences were observed between continent and incontinent groups with respect to MUP, which was significantly (p=0.0025) lower in the incontinent compared with the continent group. Likewise, the MCP and the FUL were significantly reduced in standing but not in supine incontinent subjects when compared with the continent group. The results of dynamic profilometry were reported as either positive (zero or positive reading), corresponding to incontinence, or negative (corresponding to continence). There was no significant difference between incontinent and continent subjects in the supine position, but there was between the groups in the standing position. Despite this significant difference, there was a great deal of overlap between the results for the continent and incontinent groups, invalidating a diagnosis based on this test alone.
lateral stress cystography Comparison between continent and incontinent subjects and between those with different types of incontinence with regard to urethral axis, posterior urethrovesical (PUV) angle, and distance of urethrovesical junction to the urogenital diaphragm (UGD) showed that incontinent respondents had a significantly (p=0.001) wider PUV angle than did continent respondents; however, no significant difference was observed between stress and non-stress types of incontinence. There was no difference in the urethral axis and the position of the bladder neck in relation to the UGD between the groups according to continence status or clinical type of incontinence. There was a significantly greater mean PUV angle among incontinent subjects with an incompetent sphincter than among continent subjects with a competent sphincter (p=0.004); however, neither the measurements of the urethral axis nor the location of the UGD differed between these two groups.
Provocative stress test A provocative cough stress test was found to be significantly correlated to continence and incontinence status and, more specifically, to the stress type of urine loss with or without urge loss (p≤0.0005). The result of the stress cystogram, when correlated with the stress test,
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showed a strong association (p=0.009). A urethral axis of 30 degrees or more is more likely to give rise to a positive stress test than is an axis less than 30 degrees. The stress test can be performed as part of the initial office evaluation and does not require special equipment: there is no morbidity, it is inexpensive, and (more importantly) it has extremely high specificity; it should be a part of everyone’s initial evaluation. However, a negative test in someone who is experiencing UI does not rule out its existence, as sensitivity of the test often is only 40%.
medIcal correlates of urInary IncontInence Several medical conditions have been associated with urinary incontinence in women. Difficulties with physical mobility, lower urinary tract symptoms, bowel problems, and diabetes are more common in women with incontinence. Other factors associated with urinary incontinence include a family history of incontinence, vaginal childbirth, and estrogen hormone use. Many of these associations were identified through the MESA survey.21 Patients who used wheelchairs or walking aids, who had a diagnosis of arthritis or who had fallen in the past year were defined as having mobility difficulties in the MESA survey. In women with mobility problems, urge incontinence was more common than any other type. Regarding urinary tract and bowel problems, women with urinary incontinence had a history of more urinary tract infections, dysuria, hesitancy, urgency, and slow stream than continent women. In addition, those who had more fecal incontinence or constipation had a higher rate of urinary incontinence. Women with stress incontinence were the least likely of all urinary incontinent patients to lose control of their bowels. Diabetes affects more than 12% of adults older than 40 and the prevalence increases to 19% of adults older than 60.22 Diabetic women have a 30–70% increased risk of urinary incontinence.21,23,24 The risk of urge incontinence was increased about 50% among women with diabetes, whereas they had no increased risk of stress urinary incontinence.25 The mechanism for the incontinence is unclear. Possibilities include hyperglycemia26 and microvascular complications causing altered innervation to the bladder.27 Most prior studies on diabetic people with incontinence were conducted on elderly patients with type 1 diabetes who may have had other neurologic or urologic reasons for their incontinence. In addition, these studies were small and observational, and not adjusted for other confounding factors such as parity, stroke, age or body weight.
Therefore, there are no well-established risk factors for urinary incontinence, no trials of interventions to reduce the risk, and no prospective studies of early diabetic disease that have included incontinence as an outcome. Females with incontinence more often reported a parent or sibling with UI than continent women. It was also noted that UI patients had a higher rate of personal UI during adolescence versus continent patients. There is an increased risk of later urinary incontinence after a vaginal delivery, even after the first delivery.28 An increased risk of surgery for the stress urinary incontinence is also seen after a vaginal delivery.29 During pregnancy there is an increased prevalence of incontinence, especially in the third trimester, which usually resolves shortly after delivery.30 Possible etiologies are hormonal changes during pregnancy, damage to the pelvic muscles, and nerve injury during labor and delivery.31 It is difficult to identify the specific parturition risk factors as there are many potential interrelated factors that occur during a single pregnancy and delivery. Most observational studies have demonstrated that cesarean sections are protective against incontinence versus vaginal deliveries. However, less is known about the cesarean section timing (before labor, in labor but without pushing, or in labor and pushing) and its effect on incontinence. Historically, estrogen (either vaginal or oral) was thought to improve incontinence episodes in postmenopausal women. The trigone and urethra are covered by non-keratinized squamous epithelium and these tissues contain estrogen receptors32 and respond to estrogen.33 There have been many uncontrolled trials demonstrating subjective improvement in incontinence, whereas the few randomized controlled trials showed no significant difference between control and treatment groups.34,35 Recently, the Heart and Estrogen/Progestin Replacement Study (HERS) found that a regimen of conjugated estrogen and medroxyprogesterone acetate resulted in increased urinary incontinence compared to placebo.36 They concluded that the effect of estrogen may be cancelled by the progesterone, as progestin has been shown to decrease intraurethral closing pressure. Numerous studies have demonstrated an association between obesity and stress urinary incontinence. The additional weight results in higher pressures on the bladder and causes an increase in urethral hypermobility. Those women with a median body mass index (BMI) of 28.2 had a higher incidence of urinary incontinence than those with a BMI of 25.5 (normal range).37 19
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Patterns of rePortIng of urInary IncontInence According to a nationwide, two-staged, cross-sectional postal survey conducted by the NFO Worldgroup,38 41.6% of incontinent women believed their incontinence was a natural part of growing older and 47.0% accepted it as a part of their life. Approximately 86% of women reported being bothered by symptoms of UI, with 25.6% reported being moderately bothered, 14.5% very bothered, and 8.5% extremely bothered. Only 44.9% of these incontinent women had ever talked to a physician about their UI symptoms. Those who were more bothered by their symptoms were more likely to have talked to a physician (not bothered 25.2%, slightly bothered 37.1%, moderately to extremely bothered 56.5%). Older women were also more likely to talk to a physician than younger women (53.5% versus 39.8%). Of the incontinent women who spoke with a physician, 42.9% first talked with a family practitioner, 35.1% with an obstetrician/gynecologist, 10.9% with an internist and 4.4% with a urologist. Of all women who initially spoke with an internist or family practitioner, 19.0% were later referred to a urologist and 17.3% to a gynecologist.
coPIng strategIes to control urInary IncontInence Patient self-care practices were also evaluated by the NFO Worldgroup.38 Of all the women surveyed (bothered and non-bothered by UI), 42.1% currently used panty liners, 33.5% used the toilet frequently, even when they did not have an urge to urinate, and 29.5% sought out a toilet immediately upon arriving at an unfamiliar location. Of the incontinent women, 23.3% limited their fluid intake, and pelvic floor muscle exercises were performed by 19.9% of all UI women and by 20.3% of women with stress symptoms only. Only 6.3% of all the women are currently being treated with prescription medications and 2.1% have had surgery for their UI.
contInent surgery and Its outcomes An estimated 126,000 continence surgeries are performed annually in the United States.39 A review of the literature demonstrates that the median proportion of women cured or improved by surgery at 1–2 years was 78% for anterior repair, 86% for retropubic suspension, and 91% for sling procedures.40 However, the NFO Worldgroup panel evaluated the prevalence and outcomes of continence surgery in community-dwelling
women via a postal survey.41 Four percent of communitydwelling women and 8% of women 60 years or older had a history of continence surgery. The initial satisfaction of surgery was high, but then decreased as time progressed. Of those who had surgery within the past 3 years, 64% were currently satisfied, whereas only 41% were satisfied if their surgery was 3–5 years ago. Seventy-three percent of the women who had surgery reported incontinence in the preceding month, 58% in the preceding week, and 53% used pads. Of those with recurrent UI, 83% complained of stress incontinence. A third of the women had their surgery within the last 5 years.
Prevalence of PelvIc organ ProlaPse Pelvic organ prolapse is often a concurrent problem with urinary incontinence. The prevalence of pelvic prolapse was evaluated by Hendrix et al. in 2002 by analyzing women who enrolled in the Women’s Health Initiative Hormone Replacement Therapy Clinical Trial.42 They found that, in women with a uterus, the rate of uterine prolapse was 14.2%, cystocele was 34.3%, and rectocele was 18.6%. For the women who had a hysterectomy, the rate of a cystocele was 32.9% and a rectocele was 18.3%. Hispanic women had the highest risk for uterine prolapse and African–Americans had the lowest risk. Finally, parity and obesity were strongly associated with an increased risk of uterine prolapse, cystocele, and rectocele.
economIc Burden of urInary IncontInence The direct and indirect financial impact of urinary incontinence on our healthcare system is significant. Hu et al. estimated the total cost of urinary incontinence was $19.5 billion (year 2000 dollars):43 $14.2 billion was due to community residents and $5.3 billion to institutional residents. The direct costs for community residents, which included absorbent products, laundry, treatment, and consequences (UTIs etc.), were $13.66 billion. Indirect costs (which involved lost productivity secondary to missing work) for community residents was estimated to be $553 million, with a $394 million loss for women and $159 million loss for men. For institutionalized individuals, the direct cost is $5.32 billion.
conclusIon Urinary incontinence is a prevalent condition that can affect women of all ages. The incidence is especially high in the elderly population. UI is associated with many medical conditions. Urodynamic testing can help
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explain the mechanism of UI. Many women with UI think that it is a part of the normal aging process and do not talk to their physicians about this condition. Despite the advancement in medical and surgical treatment of UI, many women’s satisfaction rate with the treatment is not as high as some physicians perceive it to be.
references 1. Dorland’s Illustrated Medical Dictionary, 26th ed. Philadelphia: WB Saunders, 1985; 451. 2. Diokno AC, Brock BM, Brown MB et al. Prevalence of urinary incontinence and other urological symptoms in the noninstitutionalized elderly. J Urol 1986;136:1022–5. 3. Fultz NH, Burgio K, Diokno AC et al. Burden of stress urinary incontinence for community-dwelling women. Am J Obstet Gynecol 2003;189:1275–82. 4. Thomas TM, Plymat KR, Blannin J et al. Prevalence of urinary incontinence. Br Med J 1980;281:1243–5. 5. Brown JS, Grady D, Ouslander J et al. Prevalence of urinary incontinence and associated risk factors in postmenopausal women. Heart & Estrogen/Progestin Replacement Study (HERS) Research Group. Obstet Gynecol 1999;94:66–70. 6. Duong TH, Korn AP. A comparison of urinary incontinence among African American, Asian, Hispanic and white women. Am J Obstet Gynecol 2001;184:1083–6. 7. Graham CA, Mallet VT. Race as a predictor of urinary incontinence and pelvic organ prolapse. Am J Obstet Gynecol 2001;185:116–20. 8. Herzog AR, Diokno AC, Brown MB et al. Two-year incidences, remissions and change patterns of urinary incontinence in noninstitutionalized older adults. J Gerontol 1990;45:67–74. 9. Hagglund D, Walker-Engstrom ML, Larsson G et al. Changes in urinary incontinence and quality of life after four years. A population-based study of women aged 22–50 years. Scand J Prim Health Care 2004;22:112–7. 10. McGrother CW, Donaldson MM, Shaw C et al. Storage symptoms of the bladder; prevalence, incidence and need for services in the UK. BJU Int 2004;93:763–9. 11. Nygaard IE, Lemke JH. Urinary incontinence in rural older women; prevalence, incidence, and remission. J Am Geriatr Soc 1996;44:1049–54. 12. Kinchen K, Gohier J, Obenchain R et al. Prevalence and frequency of stress urinary incontinence among community-dwelling women. Eur Urol 2002;40(Suppl 1):85. 13. Luber KM, Boero S, Choe JY et al. The demographics of pelvic floor disorders: current observations and future projections. Am J Obstet Gynecol 2001;184:1496–1501; discussion 1501–3. 14. Hampel C, Wienhold D, Benken N et al. Definition of
overactive bladder and epidemiology of urinary incontinence. Urology 1997;50(6A Suppl):4–14. 15. Herzog AR, Fultz NH, Normolle DP et al. Methods used to manage urinary incontinence by older adults in the community. J Am Geriatr Soc 1989;37:339–47. 16. FitzGerald MP, Stablein U, Brubaker L. Urinary habits among asymptomatic women. Am J Obstet Gynecol 2002;187:1384–8. 17. Thom DH, Haan MN, Van Den Eeden SK. Medically recognized urinary incontinence and risks of hospitalization, nursing home admission and mortality. Age Ageing 1997;26:367–74. 18. Nygaard I, Thom DH, Calhoun EA. Urinary incontinence in women. In: Litwin MS, Saigal CS (eds) Urologic Diseases in America. Washington DC: US Government Publishing Office, 2004; 71–103 (Table 22). 19. Diokno AC, Brown MB, Browk BM et al. Clinical and cystometric characteristics of continent and incontinent noninstitutionalized elderly. J Urol 1988;140:567–71. 20. Diokno AC, Normalle DP, Brown MB et al. Urodynamic tests for female geriatric urinary incontinence. Urology 1990;36:431–9. 21. Diokno AC, Brock BM, Herzog AR et al. Medical correlates of urinary incontinence in the elderly. Urology 1990;36:129–38. 22. Harris MI, Flegal KM, Cowie CC et al. Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in US adults: the Third National Health and Nutrition Examination Survey, 1988–1994. Diabetes Care 1998;21:518–24. 23. Brown J, Seeley D, Fong J et al. Urinary incontinence in older women: who is at risk? Obstet Gynecol 1996;87:715–21. 24. Wetle T, Scherr P, Branch LG et al. Difficulty with holding urine among older persons in a geographically defined community: prevalence and correlates. J Am Geriatric Soc 1995;43:349–55. 25. Brown JS, Grady D, Ouslander J et al. Prevalence of urinary incontinence and associated risk factors in postmenopausal women. Heart and Estrogen/Progestin Replacement Study (HERS) Research Group. Obstet Gynecol 1999;94:66–70. 26. Belis J, Curley R, Lang C. Bladder dysfunction in the spontaneously diabetic male Abyssinian-Hartley guinea pig. Pharmacology 1996;53:66–70. 27. Ellenberg M. Development of urinary bladder dysfunction in diabetes mellitus. Ann Intern Med 1980;92:321–3. 28. Milsom I, Ekelund P, Molander U et al. The influence of age, parity, oral contraception, hysterectomy and menopause on the prevalence of urinary incontinence in women. J Urol 1993;149:1459–62. 29. Persson J, Wolner-Hanssen P, Rydhstroem H. Obstetric risk factors for stress urinary incontinence: a population based study. Obstet Gynecol 2000;96:440–5.
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30. Viktrup L, Lose G, Rolgg M et al. The symptom of stress incontinence caused by pregnancy or delivery in primiparas. Obstet Gynecol 1992;79:945–9. 31. Smith AR, Hosker GL, Warrell DW. The role of partial denervation of the pelvic floor in the aetiology of genitourinary prolapse and stress incontinence of urine: a neurophysiological study. Br J Obstet Gynaecol 1989;96:24–8. 32. Iosif CS, Batra S, Ek A et al. Estrogen receptors in the human female lower urinary tract. Am J Obstet Gynecol 1981;141:817–20. 33. Van der Kinden MC, Gerretsen G, Brandhorst MS et al. The effect of estriol on the cytology of urethra and vagina in post-menopausal women with genitourinary symptoms. Eur J Obstet Gynecol Reprod Biol 1993;51:29–33. 34. Fantl JA, Bump RC, Robinson D et al. The Continence Program for Women Research Group. Efficacy of estrogen supplementation in the treatment of urinary incontinence. Obstet Gynecol 1996;88:745–9. 35. Jackson S, Shepherd A, Brooks S et al. The effect of estrogen supplementation in treatment of urinary stress incontinence: a double blind placebo-controlled trial. Br J Obstet Gynaecol 1999;106:711–18. 36. Grady D, Brown S, Vittinghoff E et al. HERS Research Group. Postmenopausal hormones and incontinence:
The Heart and Estrogen/Progestin Replacement Study. Obstet Gynecol 2001;97:116–20. 37. Elia G, Dye TD, Scariati PD. Body mass index and urinary symptoms in women. Int Urogynecol J 2001;12:366–9. 38. Diokno AC, Burgio K, Fultz NH et al. Medical and self-care practices reported by women with urinary incontinence. Am J Manag Care 2004;10:69–78. 39. Brown JS, Waetjen LE, Subak LL et al. Pelvic organ prolapse surgery in the United States, 1997. Am J Obstet Gynecol 2002;186:712–16. 40. Leach GE, Dmochowski RR, Appell RA et al. Female stress urinary incontinence clinical guidelines panel summary report on surgical management of female stress urinary incontinence. J Urol 1997;158:875–80. 41. Diokno AC, Burgio K, Fultz NH et al. Prevalence and outcomes of continence surgery in community dwelling women. J Urol 2003;170:507–11. 42. Hendrix SL, Clark A, Nygaard I et al. Pelvic organ prolapse in the Women’s Health Initiative: gravity and gravidity. Am J Obstet Gynecol 2002;186:1160–6. 43. Hu TW, Wagner TH, Bentkover JD et al. Costs of urinary incontinence and over active bladder in the United States: a comparative study. Urology 2004;63:461–5.
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2b Epidemiology: South America Paulo Palma, Miriam Dambros
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Introduction World wide, urinary incontinence (UI) is a common problem which can affect 17–45% of adult women. The high cost in terms of personal well-being1 and financial expenditure for both individuals and society2 makes this syndrome a major public health concern. The most prevalent type is stress incontinence, being responsible for 48% of all cases.3 Next to stress incontinence, urge incontinence is the second most prevalent cause of incontinence (17%).3 Mainly due to shame, taboo, and unawareness of treatment possibilities, only a minority of women suffering from incontinence seek professional help. In daily practice, patients usually seek help only when urine loss leads to significant mental, physical, and social problems, as well as discomfort, often after many years of suffering. The prevalence of UI is the probability of being incontinent within a defined population at a defined point in time, estimated as the proportion of incontinent respondents identified in a cross-sectional survey.4 The World Health Organization (WHO) defines health not only as the absence of disease, but also a ‘state of physical, emotional and social well being’.5 According to the old International Continence Society (ICS) definition, UI causes hygienic and social problems,6 and results in quality of life impairment, depression, and sexual problems.7 Urinary incontinence has a significant impact on the quality of life of 20% of women.8 Epidemiologic studies dealing with UI are sparse and methodologies varied. In South America very little research has been done on this subject, and, as a consequence, there is conflicting information, especially in respect to South American prevalence rates.
Etiologic factors It is generally believed that the main etiologic factor leading to UI is one or more vaginal deliveries, with an increase in risk with greater parity.9 Possible etiologies for UI include distension or disruption of the muscles, ligaments, and nerves responsible for bladder control that occurs during vaginal delivery.10 Other authors, however, have found that the occurrence of UI during pregnancy in nulliparous women has a stronger association with persistent incontinence after delivery than with parity.11 This would suggest a more significant effect from pregnancy itself that the process of vaginal delivery. Women who are not exposed to vaginal childbirth by having all their babies by cesarean section (CS) offer the opportunity to check the relative relevance of pregnancy itself, as compared with vaginal delivery, as a risk factor for UI.
A cross-sectional study was carried out in our institution (Hospital das Clínicas, Universidade Estadual de Campinas, UNICAMP, Brazil) in order to evaluate if avoiding vaginal delivery by having babies only by CS is effective in preventing UI. The survey was conducted among women consulting at the gynecology outpatient clinic.12 That study identified a group of 91 women who had signs and symptoms of either stress or urge incontinence, or both (Fig. 2b.1). Stress incontinence was defined as the involuntary loss of urine during stress, such as coughing, bending down or lifting weights. ‘Urge incontinence’ was defined as a sudden need to urinate, followed by loss of urine before the woman has time to get to the toilet. The risk of having UI was not significantly greater among women of 45 years or older compared to those aged 35–44 years. There were no differences due to ethnicity or employment status. Apart from a relative risk of 1.5 of having UI in women who had history of recurrent urinary infection, there were no differences in the risk of UI according to smoking habits, chronic cough, diabetes or previous use of hormonal replacement therapy (Table 2b.1). The risk of having UI was approximately five times greater among women who had one or two pregnancies, but it did not increase with three or more pregnancies. The risk of UI among parous women who had all their deliveries by CS was 3.5, and was significantly higher than among nulliparous women. The risk of those with one or more vaginal deliveries was only slightly higher (Table 2b.2). The prevalence of UI among women who delivered vaginally (58%) was higher than among those who had only cesarean sections (48%), but the sample was too small to verify whether this difference was statistically significant. The result of that study helps to confirm that pregnancy is the most important determinant of permanent UI, a conclusion that Beck and Hsu reached some 40 years ago.13 While these results confirm that pregnancy is more important than vaginal delivery as a determinant of permanent UI, the sample size does not have enough power to eliminate a possible effect of route of delivery.
23 Pure stress incontinence symptoms Pure urgency incontinence
3 72
Mixed incontinence symptoms
Figure 2b.1. Distribution of patients according to their symptoms (values correspond to the number of patients).
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Table 2b.1. Prevalence ratio of urinary incontinence according to medical history Urinary incontinence Characteristics
Yes (n=98)
No (n=91)
Prevalence ratio
No
84
76
1.00
Yes
14
15
0.92
No
88
88
1.00
Yes
9
3
1.50
No
89
86
1.00
Yes
9
5
1.26
No
90
87
1.00
Yes
8
4
1.31
Non-users
58
54
1.00
Users
40
37
1.00
Smoking
Recurrent urinary infection
Chronic cough
Diabetes
History of hormonal replacement therapy
Data adapted from ref. 12.
Table 2b.2. Risk of having urinary incontinence according to obstetric history Urinary incontinence History
Yes
No
Prevalence ratio
0
2
15
1.00
1–2
30
17
5.43
≥3
66
59
4.49
Nullipara
3
19
1.90
Only cesarean sections
11
12
3.51
One or more vaginal deliveries
84
60
4.28
Number of gestations
Route of delivery
Data adapted from ref. 12.
Latin America has one of the highest rates of CS in the world, with a tendency towards a further increase. Recent estimates indicate that the incidence of CS varies between 16.8 and 40% in most Latin American countries,14 and that this rate is higher in private hospitals than in public hospitals. In addition, the incidence of CS is greater in those Latin American countries with a higher per capita gross domestic product. Although strategies to reduce CS rates have been proposed, very few have been assessed through randomized controlled trials.
Urinary Incontinence, quality of life and sexual function Recently, many studies have measured the quality of life in incontinent patients, using a number of different selfadministered condition-specific and generic quality-oflife questionnaires. The impact of UI on patients’ lives does not appear to be directly related to the volume of urine loss, although it does appear to be related to the overall burden of symptoms.15 25
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An open prospective study was carried out at our institution, enrolling patients with UI. The aim was to look at the relationship of UI and quality-of-life issues, particularly with respect to altered sexual function. The study population consisted of 30 women aged between 31 and 51 years (mean 43 years). The duration of symptoms ranged from 12 to 53 months. All the patients were multiparous and 60% of women had incomplete elementary education. Two sexual function questionnaires were completed by respondents. The Female Sexual Function Index (FSFI) identifies problems related to sexual response and possible dysfunctions, as well as issues related to libido, excitement, lubrication, orgasm, pleasure, and pain. The Impact of Urinary Incontinence on the Sexual Response/RJ (IIURS-RJ) questionnaire16,17 identifies the effects of UI on sexual function, social problems, and self-esteem. It also evaluates adaptive changes to cope with urinary symptoms, and sexual behavior before and after the onset of urinary incontinence. Of the 30 women participating in the study, 26 (86%) were married and all had only one partner; 19 (63%) were catholic, and 18 (60%) had incomplete elementary education. Concerning the effects of UI on daily life (Table 2b.3), the major problems identified were the bad smell caused by urinary leakage, the need to use pads for 13 patients (43%), and the involuntary loss and wetness for 12 (40%). In addition to the results in Table 2b.3, the study also showed that there were significant effects of UI on selfesteem, 11 patients (37%) having the feeling of being less valued, with 17 (57%) women having a worsening of their sexual lives as a result of their urinary symptoms. Twenty-three patients (76%) related that they had urinary loss during sexual intercourse. Among these, 17 (74%) claimed it as a negative influence on their sexual life. Of the 23 patients, 6 (26%) did not complain, 2 (9%) considered it a mild interference, 4 (17%) evalu-
Table 2b.3. Most frequent problems identified in urinary incontinence Problem
Frequency (%)
Bad smell and use of tampon
13 (43)
Involuntary loss and wetness
12 (40)
Surgery indication
2 (07)
Stress incontinence
1 (03)
Urinary frequency
1 (03)
Urine loss in the presence of the husband
1 (03)
ated it as moderate, and 11 (48%) indicated it as a severe interference. Regarding the frequency of sexual intercourse before and after the onset of incontinence, 17 patients (57%) expressed altering patterns. Sexual activity changed from weekly to monthly in seven patients (41%), from daily to weekly in five (29%), from daily to monthly in three (18%), from monthly to annual in one (6%), and from weekly to no relationship in one (6%). Differences in sexual function before and after the onset of incontinence were established. Ten variables related to sexuality were studied: desire, excitement, vaginal lubrication, general caresses, genital caresses, oral sex in the partner and in the patient, vaginal penetration, anal penetration, and orgasm. Six variables were significantly different following the onset of urinary leakage, with a worsening of sexual desire, genital caresses and general caresses, vaginal penetration, anal penetration, and orgasm. Abdo and colleagues studied the sexual lives of 1502 healthy Brazilian women and concluded that in 34.6% the greatest complaint was a lack of desire and in 29.3% was orgasmic dysfunction.18 These results demonstrated a reasonable degree of sexual dysfunction amongst the general Brazilian population although this appears to be greater in the presence of UI.
Prevalence of climacteric, urogenital and sexual symptoms in a population of Brazilian women A cross-sectional, descriptive, population-based study19 was also carried out at our institution on 456 women aged 45–60 years, living in Campinas, SP, Brazil, in 1997. Data were collected via home interviews, using structured validated questionnaires. The results showed that climacteric symptoms in the population were highly prevalent and similar to those described in developed Western countries. Figure 2b.2 shows the most prevalent symptoms identified. Hot flushes, sweating and insomnia as expected were significantly more prevalent in peri- and postmenopausal women. The severity of vasomotor and psychological symptoms did not vary according to the menopause phase. Decreased libido was the most frequent sexual complaint. It was observed that some climacteric complaints were interrelated.
Prevalence of stress urinary incontinence and its associated factors in perimenopausal women A descriptive, exploratory, population-based study with secondary analysis of a population-based household
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Vaginal dryness Dyspareunia Urinary incontinence Sweating Irritability Headache Hot flushes Nervousness 0
10 20 30 40 50 60 70 80 90 Percentages
Figure 2b.2. The most climacteric and urogenital prevalent symptoms found in the study of Pedro et al.19
survey on the perimenopause and menopause was conducted among women living in a Brazilian city.20 Through a sampling process, 456 women between 45 and 60 years old were selected. Thirty-five percent of the interviewees complained of stress urinary incontinence (SUI). None of the sociodemographic factors studied was associated with the risk of SUI (Table 2b.4). In addition, parity did not significantly alter SUI risk (Table 2b.5). Other factors, such as previous gynecologic surgeries, body mass
index, smoking habits, menopausal status, and hormone replacement therapy, were not associated with the prevalence of SUI. There were no racial variations in the prevalence of SUI. In the international literature, most prevalence studies are conducted amongst Caucasian women and only few studies have assessed racial differences in the prevalence of UI. In the few studies which have included other racial groups, a significantly larger percentage of Caucasian women appear to report UI compared to African–American or Hispanic females.21 Urodynamic diagnosis showed that SUI was more frequent in Caucasian women compared to African–Americans. However, more research with regard to racial differences in the prevalence of UI is necessary to make significant conclusions regarding inter-racial differences in incontinence.
Conclusion Urinary incontinence is a highly prevalent condition in South America, as it is in many other parts of the world. Very few studies have concentrated on South American populations alone but those that have show a significant impact of urinary incontinence on the quality of life of sufferers.
Table 2b.4. Background data for all patients assessed by Guarisi et al.20 Stress urinary incontinence Most times or sometimes (n=160) Never (n=295)
Prevalence ratio
n
%
n
%
45–49
69
40.4
102
59.6
Reference
50–54
50
34.7
94
65.3
0.8
55–60
41
29.3
99
70.7
0.7
Caucasian
96
37.4
161
62.6
Reference
Black, brown
46
36.8
79
63.2
1.0
Others
18
24.7
55
75.3
0.6
Literate
28
38.9
44
61.1
Reference
Incomplete elementary school
81
33.3
162
66.7
0.9
Complete elementary school
32
39.5
49
60.5
1.0
High school, college
19
32.2
40
67.8
0.8
Age (years)
Race
Literacy
Data adapted from ref. 20.
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Table 2b.5 Obstetric history for all patients assessed by Guarisi et al.20 Stress urinary incontinence Most times or sometimes (n=160)
Never (n=295)
Prevalence ratio
n
%
n
%
0
9
34.6
17
65.4
Reference
1 or 2
24
26.4
67
73.6
0.8
≥3
127
37.6
211
62.4
1.1
0
11
34.4
21
65.6
Reference
1 or 2
40
32.8
82
67.2
1.0
≥3
109
36.2
192
63.8
1.0
≤10
14
48.3
15
51.7
Reference
11–20
64
38.1
104
61.9
0.8
≥30
70
31.5
152
68.5
0.7
Number of gestations
Delivery
Time after the last delivery (years)
Data adapted from ref. 20.
REFERENCES 1. Thomas TM, Plymat KR, Blannin J, Meade TW. Prevalence of urinary incontinence. Br Med J 1980;281:1243–5. 2. Hu TW. Impact of urinary incontinence on health-care costs. J Am Geriatric Soc 1990, 38:292–5. 3. Norton PA, MacDonald LD, Sedgwick PM, Stanton SL. Distress and delay associated with urinary incontinence, frequency, and urgency in women. Br Med J 1988;297:1187– 9. 4. Hunskaar S, Burgio K, Dioko AC, Herzog AR, Hjälmas K, Lapitan MC. Epidemiology and natural history of urinary incontinence. In: Abrams P, Cardozo L, Khoury S, Wein A (eds) Incontinence, 2nd ed. Plymouth: Plymbridge Distributors, 2002; 165. 5. Corcos J, Beaulieu S, Donovan J et al. Quality of life assessment in men and women with urinary incontinence. J Urol 2002;168:896–905. 6. Blaivas JG, Appell RA, Fantl JA et al. Standards of efficacy for evaluation of treatment outcomes in urinary incontinence: recommendations of the Urodynamic Society. Neurourol Urodyn 1997;16:145–7.
childbirth, and obstetrics techniques. Am J Public Health 1999;89:209–12. 10. Allen RE, Hosker GL, Smith ARB, Warrell DW. Pelvic floor damage and childbirth: a neurophysiological study. Br J Obstet Gynaecol 1990;97:770–9. 11. Viktrup L, Lose G, Rolff M, Barfoed K. The symptom of stress incontinence caused by pregnancy or delivery in primiparas. Obstet Gynecol 1992;79:945–9. 12. Faúndes A, Guarisi T, Pinto-Neto AM. The risk of urinary incontinence of parous women who delivered only by cesarean section. Int J Gynecol Obstet 2001;72:41–6. 13. Beck RP, Hsu N. Pregnancy, childbirth, and the menopause related to the development of stress incontinence. Am J Obstet Gynecol 1965;91:820–3. 14. Osis MJD, Pádua KS, Duarte GA, Souza TR, Faúndes A. The opinion of Brazilian women regarding vaginal labor and cesarean section. Int J Gynecol Obstet 2001;75:S59– 66. 15. Wyman JF, Harkins SW, Choi SC et al. Psychosocial impact of urinary incontinence in women. Obstet Gynecol 1987;70:378–81.
7. Hafner RJ, Stanton SL, Guy LA. A psychiatric study of women with urgency and urgency incontinence. Br J Urol 1977;49:211–4.
16. Rezende RCA. A Influência da Incontinência Urinária na Resposta Sexual Feminina. Rio de Janeiro: Mestrado em Sexologia da Universidade Gama Filho, M2000. Masters Degree, University of Rio de Janeiro, Brazil.
8. Burgio KL, Matthews KA, Engel BT. Prevalence, incidence and correlates of urinary incontinence in healthy middleaged women. J Urol 1991;146:1255–9.
17. Palma PCR, Thiel RRC, Thiel M et al. Impacto da incontinência urinária na qualidade de vida e sexualidade feminina. Urodinamica Uroginecologai 2003; 71–76
9. Foldspang A, Mommsen S, Djurhuus JC. Prevalent urinary incontinence as a correlate of pregnancy, vaginal
18. Abdo CHN, Oliveira WM Jr, Moreira ED et al. Perfil sexual da população Brasileira: Resultados do Estudo de Com-
28
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portamento Sexual (ECOS) do Brasileiro. Rev Brasileira de Medicina 2002;59(4):250–7.
Brazilian women: household survey. Rev Saúde Publica 2001;35:428–35.
19. Pedro AO, Pinto-Neto AM, Costa-Paiva LHS, Osis MJD, Hardy EE. Climacteric syndrome: a population-based study in Brazil. Rev Saúde Publica 2003;37:735–42.
21. Sze EHM, Jones WP, Ferguson JL, Barker CD, Dolezal JM. Prevalence of urinary incontinence symptoms among Black, White and Hispanic women. Obstet Gynecol 2002;99:572–5.
20. Guarisi T, Pinto-Neto AM, Osis MJ, Pedro AO, Paiva LHC, Faúndes A. Urinary incontinence among climacteric
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2c Epidemiology: Europe Ian Milsom
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Urinary incontinence is one of the most important health problems confronting modern society.1 It is a symptom with widespread human and social implications, causing discomfort, shame, and loss of self-confidence, and may negatively affect the woman’s quality of life.1–3 Millions of women throughout the world are afflicted. Population studies have demonstrated that urinary incontinence is more common in women than in men and that approximately 10% of all women suffer from urinary incontinence. Prevalence figures increase with increasing age and, in women aged ≥70 years, more than 20% of the female population is affected. Inappropriate leakage of urine is perceived by many women but is not always reported to the doctor. However, an increasing awareness of the problem in recent years has prompted more patients to seek advice. In elderly women, urinary incontinence may lead to possible rejection on the part of a relative and may be an important factor in the decision whether or not to institutionalize an elderly person. Urinary incontinence not only causes considerable personal suffering for the individual afflicted but is also of immense economic importance for the health service. The annual cost of urinary incontinence in Sweden, for example, has been reported to account for approximately 2% of the total healthcare budget.1
Thomas et al.5 investigated the prevalence of urinary incontinence in two London boroughs by a postal survey (Fig. 2c.1). The reported prevalence of urinary incontinence increased from 5.1% in girls aged 5–14 years to 16.2% in 85-year-old women. There was, however, little or no change in prevalence rates up to 35 years of age. The prevalence rates then increased to approximately 10% in the 35–44 years age group. There was no significant increase at the time of the menopause but a further increase to approximately 16% occurred in women ≥75 years. On the other hand, Iosif et al.6 and Jolleys13 (Fig. 2c.1) reported a maximum prevalence of urinary incontinence at the time of the menopause. Hannestad et al.,26 in a large Norwegian study, demonstrated an increased prevalence during the perimenopausal years, with prevalence rates being lower both before and after the time of the menopause (Fig. 2c.2a). Conditions in Sweden are extremely favorable for epidemiologic studies, in particular longitudinal stud-
16
Thomas et al.5
14 12 Percentage
INTRODUCTION
10 8 6
PRevaleNCe
4
This chapter describes the results of epidemiologic studies performed in Europe. The reported prevalence of urinary incontinence in women has varied considerably in different studies. Possible explanations for this wide variation are that different populations of women have been studied, in some cases highly selected subgroups of the total population. In addition, different definitions of urinary incontinence have been applied. Urinary incontinence has been defined by the International Continence Society (ICS) as any involuntary leakage of urine.4 However, some authors have chosen to restrict prevalence figures according to the frequency of involuntary urinary leakage – for example, based only on daily, weekly, monthly or annual urinary leakage. Thus, for the reasons given above, it is difficult to compare the results of different population studies. However, when reviewing the literature, there is considerable evidence to support the theory that the prevalence of urinary incontinence in women increases with age, but there are divergent opinions regarding the pattern of this increase.5–28 The epidemiology of urinary incontinence in women has been described in detail in three recent reviews.29–31
2 0
5–14 15–24 25–34 35–44 45–54 55–64 65–74 75–84 85+
Age range (years) Jolleys et al.13 60
Percentage
50 40 30 20 10 0
–25
25–34 35–44 45–54 55–64 65–74 75–84
85+
Age range (years)
Figure 2c.1. Comparison of the prevalence of female urinary incontinence in two British studies. The study by Thomas et al.5 was performed in 9323 British women and the study by Jolleys et al.13 was performed in 833 British women.
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Prevalance rate
Epidemiology: Europe
45 40 35 30 25 20 15 10 5 0
20–24
25–29
30–34
35–39
40–44
45–49
50–54
a
55–59
60–64
65–69
70–74
75–79
80–84
85–89
90+
Age (years)
Other
MUI
SUI
UUI b
Figure 2c.2. Prevalence of urinary incontinence in Norwegian women grouped (a) by age, and (b) type of incontinence. (MUI, mixed urinary incontinence; SUI, stress urinary incontinence; UUI, urge urinary incontinence.) (Based on data from ref. 26.) 16 Samuelsson et al.24
14
Simeonova et al.25
Percentage
12 10 8 6 4 2 0
20–29
30–39 40–49 Age (years)
a
50–59
30 Women
25 Percentage
ies. The Swedish Population Register, with its personal number system, provides up-to-date information on the total population and can be used to obtain random and, in some cases, representative subgroups of the total population for the purpose of epidemiologic studies. There are several large population-based studies from Sweden describing the prevalence of urinary incontinence in women. Figure 2c.3a illustrates the results from two independent studies of urinary incontinence in women. In both studies, prevalence was restricted to women who had urinary leakage at least once per week. Although the study performed by Samuelsson and co-workers24 was undertaken in a rural area and that by Simeonova et al.25 was carried out in an inner city, there are strong similarities between the results of the two studies, with a linear increase in the prevalence of urinary incontinence which continues over the perimenopausal years. In contrast, another Swedish population study22 (Fig. 2c.3b) failed to demonstrate any increase in the prevalence of urinary incontinence between women aged 46 and 56 years of age (prevalence 12% for both cohorts). The majority of 46-year-old women were premenopausal whereas the majority of 56-year-old women were postmenopausal. There were no differences in prevalence rates between pre- and postmenopausal women within the respective birth cohorts (Fig. 2c.4a). Thus there was no evidence to suggest that the prevalence of urinary incontinence increased at the time of the last menstrual
Men
20 15 10 5 0
b
46
56
66 Age (years)
76
86
Figure 2c.3. Comparison of the prevalence of urinary incontinence: (a) in two population-based studies of Swedish women in a rural area (Samuelsson et al.24) and in an inner city (Simeonova et al.25); (b) in two population-based Swedish studies in women (n=7459) 22 and men (n=7763)34 of the same ages. 33
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Percentage
Textbook of Female Urology and Urogynecology
Percentage
a
b
14 12 10 8 6 4 2 0
Age 46 Age 56
Pre-MP
18 16 14 12 10 8 6 4 2 0
Post-MP
Age 46 Age 56
0
1
Percentage
35 30
Hysterectomy
25
No hysterectomy
Parity
2
3
20 15 10 5
c
0
Age 66
Age 71
Age 76
Age 81
Age 86
All
Figure 2c.4. Prevalence of urinary incontinence: (a) in a random sample of 46- and 56-year-old women grouped according to menopausal (MP) status; (b) in a random sample of 46- (n=1530) and 56-year-old (n=1638) women grouped according to parity; (c) in a random sample of 66- 71-, 76-, 81- and 86-year-old women grouped according to history of hysterectomy. (Data from ref. 22.)
this chapter have been performed by means of postal questionnaires. In several of the studies, attempts have been made to determine the proportion of women suffering from the different types of urinary leakage, i.e. stress urinary leakage (SUI), urge urinary leakage (UUI), and mixed urinary leakage (MUI). The distribution of the various types of incontinence in the large Norwegian study by Hannestad et al.26 is shown in Figure 2c.2b. In the literature, stress urinary leakage tends to dominate among younger women while the number of women with urge incontinence and mixed incontinence increases with age. In recent years increasing attention has been devoted to the condition known as the overactive bladder. The overactive bladder has been defined by the ICS as urgency with or without urge incontinence and usually with frequency and nocturia. Thus, some women with symptoms of an overactive bladder will suffer from urge incontinence while others will experience no urinary leakage. The prevalence of overactive bladder symptoms was estimated in a large European study involving more than 16,000 individuals.35 Data were collected using a population-based survey (conducted by telephone or face-to-face interview) of men and women aged ≥40 years, selected from the general population in France, Germany, Italy, Spain, Sweden, and the United Kingdom using a random, stratified approach. The main outcome measures were:
• prevalence of urinary frequency (>8 micturitions/24 hours), urgency and urge incontinence;
• proportion of participants who had sought medical advice for overactive bladder symptoms;
• current or previous therapy received for these symptoms.
period. However, this is not necessarily synonymous with the fact that the reduction in circulating estrogens is not associated with an increase in the prevalence of urinary incontinence in women after the menopause. Falconer et al. have demonstrated the importance of the paraurethral connective tissue in the etiology of stress urinary incontinence and have demonstrated the influence of estrogens and the changes associated with the menopause on collagen formation.32,33 The prevalence of urinary incontinence in women has been compared with the prevalence in men of the same age in two large Swedish studies (Fig. 2c.3b).22,34 As can be seen from the results illustrated in Figure 2c.3b, there is a higher prevalence of urinary incontinence in women than in men in all the age groups studied. In general, the prevalence of urinary incontinence is approximately three times more common in women than in men. The majority of the population studies referred to in
The main results of this study are illustrated in Figure 2c.5a with the prevalence of overactive bladder symptoms grouped according to age and sex, and in Figure 2c.5b grouped according to age, sex and nationality. Thus, in summary, when reviewing the literature, there is considerable evidence to support the theory that the prevalence of urinary incontinence increases in a linear fashion with age as shown in Figure 2c.6 which includes pooled data from 19 epidemiologic studies where urinary incontinence was reported to occur at least once per week.36
Factors influencing the prevalence of urinary incontinence Risk factors described in the literature are shown in Table 2c.1.29–31,36,37 For the majority of these risk factors
34
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Epidemiology: Europe
Percentage
45 40
Men
35
Women
30 25 20 15 10 5
a
0
40–44
45–49
50–54
55–59
60–64
65–69
70–74
75+
25 Men Women
Percentage
20 15 10 5 0
Percentage
b
France
45 40 35 30 25 20 15 10 5 0
Germany
Italy
Spain
Sweden
UK
All
Table 2c.1.
0
10
20
30
40 50 60 Age (years)
70
80
90
Figure 2c.6. Prevalence of female urinary incontinence (≥1/week) which affected the woman's way of life (summary of 19 population studies, based on ref. 36). there are at present no controlled trials demonstrating that intervention reduces the incidence, prevalence or degree of severity of urinary incontinence. The influence of various factors on the prevalence of urinary incontinence was evaluated by means of a postal questionnaire in women aged 46–86 years resident in the city of Gothenburg, Sweden.22 Age, parity, and a history of hysterectomy were all correlated to the prevalence of urinary incontinence which increased in a linear fashion from 12.1% in women 46 years of age to 24.6% in women aged 86 years of age (Fig. 2c.3). The prevalence of uri-
• • • • • • • • • •
Figure 2c.5. Prevalence of overactive bladder symptoms: (a) grouped according to age and sex; (b) in a random sample of the total population aged ≥40 years from six European countries. (Adapted from ref. 35.) Risk factors for urinary incontinence in women
Age Sex Smoking Chronic bronchitis, asthma Ethnic group Obesity Pregnancy Vaginal delivery Collagen defect Hysterectomy
• • • • • • • •
Dementia Stroke, Parkinson's disease, etc. Physical activity Medication Constipation Diuretics Enuresis Chronic illness
nary incontinence was greater in parous women compared to nulliparous women, and prevalence increased with increasing parity (Fig. 2c.4b). Urinary incontinence was more prevalent in women who had undergone a hysterectomy (Fig. 2c.4c). The prevalence of urinary incontinence was unaffected by the duration of previous oral contraceptive usage and there was no evidence to suggest that the prevalence of urinary incontinence increased at the time of the last menstrual period.
SOCIOeCONOmIC CONSIDeRaTIONS The economic consequences of urinary incontinence in Sweden in 1990 were assessed by Milsom et al.38 35
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The estimated annual cost for urinary incontinence in Sweden at that time was 1.8 billion Swedish Crowns. The Swedish Health Care budget for 1990 amounted to 93 billion Crowns. Based on the results of this evaluation, the annual costs of urinary incontinence in Sweden accounted for approximately 2% of the total healthcare costs. The mean life expectancy of women in Sweden is at present 83 years, which is higher than in many other Western countries, and 19% of all persons are at present ≥65 years of age.38 The proportion of elderly women in many Western countries is currently increasing, and it is estimated that in many European countries there will be a substantial increase in the number of women aged ≥65 years by the year 2025.39 Thus, the number of women requiring treatment for urinary incontinence is expected to increase in the future. Another important factor to consider, apart from the numerical increase in the number of elderly women, is the fact that many elderly women of today suffer in silence, accepting these symptoms as a normal part of the aging process. Women who are at present 30 and 40 years of age have other demands on their physical condition and will undoubtedly not accept what their older counterparts accepted later in life.
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Ekelund P, Grimby A, Milsom I. Urinary incontinence: social and financial costs high. Br Med J 1993;306:1344.
2.
Hunskaar S, Vinsnes A. The quality of life in women with urinary incontinence as measured by the sickness impact profile. J Am Geriatr Soc 1991;39:378–82.
3.
4.
Grimby A, Milsom I, Wiklund I et al. The influence of urinary incontinence on the quality of life in elderly women. Age Ageing 1993;22:82–9. Abrams P, Cardozo L, Fall M et al. Standardisation Subcommittee of the International Continence Society. The standardisation of terminology of lower urinary tract function: report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 2002;21:167–78.
5.
Thomas TM, Plymat KR, Blannin J et al. Prevalence of urinary incontinence. Br Med J 1980;281:1243–5.
6.
Iosif S, Henriksson L, Ulmsten U. The frequency of disorders of the lower urinary tract, urinary incontinence in particular, as evaluated by a questionnaire survey in a gynecological health control population. Acta Obstet Gynecol Scand 1981;60:71–6.
7.
Vetter NJ, Jones DA, Victor CR. Urinary incontinence in the elderly at home. Lancet 1981:ii;1275–7.
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Iosif C, Bekassy Z. Prevalence of genito-urinary symp-
toms in the late menopause. Acta Obstet Gynecol Scand 1984;63:257–60. 9.
Campbell AJ, Reinken J, McCosh L. Incontinence in the elderly: prevalence and prognosis. Age Ageing 1985;14:65–70.
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Samsioe G, Jansson I, Mellström D et al. The occurrence, nature and treatment of urinary incontinence in a 70 year old population. Maturitas 1985;7:335–42.
11.
Vehkalahti I, Kivelä S-L. Urinary incontinence and its correlates in very old age. Gerontology 1985;31:391–6.
12.
Berg G, Gottqall T, Hammar M et al. Climacteric symptoms among women aged 60–62 in Linkö ping, Sweden, in 1986. Maturitas 1988;10:193–9.
13.
Jolleys J. Reported prevalence of urinary incontinence in women in a general practice. Br Med J 1988;296:1300–2.
14.
Elving LB, Foldspang A, Lam GW et al. Descriptive epidemiology of urinary incontinence in 3,100 women aged 30–59. Scand J Urol Nephrol 1989;(Suppl 125):37–43.
15.
Hellström L, Ekelund P, Milsom I et al. The prevalence of urinary incontinence and incontinence aids in 85year-old men and women. Age Ageing 1990;19:383–9.
16.
Molander U, Milsom I, Ekelund P et al. An epidemiological study of urinary incontinence and related urogenital symptoms in elderly women. Maturitas 1990;12:51–60.
17.
O’Brien J, Austin M, Parminder S et al. Urinary incontinence: prevalence, need for treatment, and effectiveness of intervention by nurse. Br Med J 1991;303:1308–12.
18.
Mäkinen JI, Grönroos M, Kiilholma PJA et al. The prevalence of urinary incontinence in a randomized population of 5247 adult Finnish women. Int Urogynecol J 1992;3:110–13.
19.
Rekers H, Drogendijk AC, Valenburg H et al. Urinary incontinence in women 35 to 79 years of age: prevalence and consequences. Eur J Obstet Gynaecol Reprod Biol 1992;43:229–34.
20.
Brocklehurst JC. Urinary incontinence in the community: analysis of a MORI poll. Br Med J 1993;306:832–4.
21.
Lagace EA, Hansen W, Hickner LM. Prevalence and severity of urinary incontinence in ambulatory adults: an UPRNet Study. J Fam Pract 1993;36:610–4.
22.
Milsom I, Ekelund P, Molander U et al. The influence of age, parity, oral contraception, hysterectomy and the menopause on the prevalence of urinary incontinence in women. J Urol 1993;149:1459–62.
23.
Seim A, Sandvik H, Hermstad R et al. Female urinary incontinence – consultation, behaviour and patient experiences: an epidemiological survey in a Norwegian community. Fam Pract 1995;12:18–21.
24.
Samuelsson E, Victor A, Tibblin G. A population study of urinary incontinence and nocturia among women 20–59 years. Prevalence, well-being and wish for treatment. Acta Obstet Gynecol Scand 1997;76:74–80.
36
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25.
Simeonova Z, Milsom I, Kullendorff M et al. The prevalence of urinary incontinence and its influence on the quality of life in women from an urban Swedish population. Acta Obstet Gynecol Scand 1999;78:546–51.
32.
Falconer C, Blomgren B, Johansson O et al. Different organization of collagen fibrils in stress-incontinent women of fertile age. Acta Obstet Gynecol Scand 1998;77:87–94.
26.
Hannestad YS, Rortveit G, Sandvik H et al. A community-based epidemiological survey of female urinary incontinence: the Norwegian EPINCONT Study. J Clin Epidemiol 2000;53:1150–7.
33.
Falconer C, Ekman-Ordeberg G, Blomgren B et al. Paraurethral connective tissue in stress-incontinent women after menopause. Acta Obstet Gynecol Scand 1998;77:95–100.
27.
Hunskaar S, Lose G, Sykes D et al. The prevalence of urinary incontinence in women in four European countries. BJU Int 2004;93:324–30.
34.
28.
Hannestad YS, Lie RT, Rortveit G et al. Familial risk of urinary incontinence in women: population based cross sectional study. BMJ 2004;329:889–91.
Malmsten UG, Milsom I, Molander U et al. Urinary incontinence and lower urinary tract symptoms: an epidemiological study of men aged 45 to 99 years. J Urol 1997;158:1733–7.
35.
Milsom I, Abrams P, Cardozo L et al. How widespread are the symptoms of an overactive bladder and how are they managed? A population-based prevalence study. BJU Int 2001;87:760–6.
36.
Milsom I. Prevalence and risk factors. In: Treatment of urinary incontinence. The Swedish Council on Technology Assessment in Health Care Report on Urinary Incontinence. Stockholm: SBU, 2000.
37.
Rortveit G, Daltveit AK, Hannestad YS et al. Norwegian EPINCONT Study. Urinary incontinence after vaginal delivery or cesarean section. N Engl J Med 2003;348:900–7.
38.
Milsom I, Fall M, Ekelund P. The cost of urinary incontinence. Läkartidningen 1992;89:1772–4.
39.
WHO Report. Population statistics. Geneva: WHO, 1993.
29.
Hampel C, Wienhold D, Benken N et al. Definition of overactive bladder and epidemiology of urinary incontinence. Urology 1997;(6A Suppl):4–14.
30.
Hunskaar S, Burgio K, Diokno A et al. Epidemiology and natural history of urinary incontinence in women. Urology 2003;62(4 Suppl 1):16–23.
31.
Brown JS, Nyberg LM, Kusek JW et al. National Institute of Diabetes and Digestive Kidney Diseases International Research Working Group on Bladder Dysfunction. Proceedings of the National Institute of Diabetes and Digestive and Kidney Diseases International Symposium on Epidemiologic Issues in Urinary Incontinence in Women. Am J Obstet Gynecol 2003;188:S77–88.
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2d Epidemiology: Australia Richard J Millard
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IntroductIon In geographical terms, Australia is the driest continent on earth; regrettably the same cannot be said of its inhabitants. The Australian population is multicultural, having been derived largely from waves of immigrants from Britain and the Mediterranean and Balkan countries for much of its 200 year post-colonization history, and from Asian and Central European countries more recently. Studies show that 5–6% of adult Australians have regular or severe urinary incontinence, a prevalence remarkably similar to that reported from other basically Caucasian populations.1,2 Data regarding prevalence in Australia have been available since a study in Sydney in 1983.3,4 No systematic study of general prevalence has been conducted since that time. However, the longitudinal Women’s Health Australia study, involving over 40,000 women,5 has provided new data on prevalence in women6 and may yield further data on the incidence of incontinence over the next 10–20 years as the cohorts age. The problem with all surveys aimed at assessing the prevalence of incontinence is how to define urinary incontinence. Do we wish to know only how many people have regular and severe incontinence, assuming that we could even define what we meant by this term? Alternatively, is it relevant to know about all levels of urinary incontinence that occur in the community? Is whether the individual chooses to wear an incontinence pad or appliance a good indicator of significant incontinence? To circumvent these issues, the 1983 Sydney survey attempted to ascertain the prevalence of all past and present urinary incontinence and to stratify the type, severity, and frequency of occurrence of the incontinence problems discovered in the study population. The study was designed to ascertain the prevalence of urinary incontinence in Australia. Prevalence was correlated with age, gender, and socioeconomic stratification. An attempt was made to define at-risk groups, types and severity of incontinence, and use of protective appliances. A detailed, 38-question, self-report questionnaire was devised and tested for comprehensibility in small focus groups before distribution. A multistage clustersampling technique was used to target 3000 adults in 1000 homes, randomly selected from 100 postal districts. All 3000 were telephoned to increase compliance and to check data received, and a total of 1256 completed questionnaires were analyzed. Three hospitals (1666 beds) and 15 nursing homes (1631 beds) were also surveyed by questionnaires sent to staff, and the data from these establishments were analyzed separately.
A total of 293 individuals admitted to some degree of present urinary incontinence or leakage by day, and 51 also had some loss of urine at night. In all, 301 persons (24%) – 13% of the male and 34% of the female respondents – had some degree of urinary loss. Eight people were incontinent only at night. The male-to-female ratio among those with urinary leakage was 1:2.7, with females accounting for 73% of sufferers. The frequency of urinary loss is shown in Table 2d.1. Leakage was more common in members of bluecollar families (27%) than in members of white-collar families (25%). Students and those in full-time employment tended to have half the prevalence of incontinence (13% and 16%, respectively) reported by the other groups (30–34%). Housewives had the highest prevalence of incontinence overall (40%). The mean duration of all leakage problems was 8.8 years; 18% reported leakage for less than a year, whereas 23% had had problems for 15 or more years; 17% could not specify the duration of their problem. The 293 positive respondents were asked to specify circumstances under which they experienced leakage (more than one answer was allowed) (Table 2d.2). All 293 individuals who reported some current degree of leakage were asked to quantify the severity of the urine loss (Table 2d.3). Severe incontinence was twice as common in bluecollar as in white-collar families, but minor degrees of leakage were equally prevalent. The type of incontinence was correlated with severity and frequency of leakage episodes as shown in Table 2d.4. In most cases, incontinence occurred infrequently and was of minor severity. What stands out is the relatively more frequent nature of the leakage of the quiet dribbling incontinence type, which occurs without warning or provocation.
table 2d.1.
Frequency of incontinence episodes Percentage of respondents
Frequency
Male
Often wet
2
4
3
Once a day
2
4
3
Once a week
1
3
2
Once or twice a month
0
4
2
Rarely
8
18
13
87
66
76
Never wet
Female
Overall
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table 2d.2.
Circumstances in which respondents experienced leakage
table 2d.3.
Percentage of respondents Males (n=79)
Quantification of severity of urinary loss in 293 respondents Percentage of respondents
Females (n=214)
Urinary loss
Male (n=79)
Female (n= 214)
Overall
Coughing or sneezing
5
61
Always wet
0
2
2
Straining or lifting
5
12
Flooding
0
2
1
Urge
27
35
8
5
5
Giggle
9
30
Moderate loss
No warning or provocation
1
7
Slight loss
25
41
37
Just a spot
66
49
54
Postmicturition dribble
59
8
With urinary infections
8
10
Other
8
9
Total*
122
172
* Respondents may have more than one type of incontinence.
table 2d.4.
Percentage frequency and severity of leakage in 293 respondents wet by day* Frequency
Type of incontinence
Often
1/day
Coughing
15
12
Strain
31
Urge
1/week
2/month
Rarely
9
12
52
7
7
14
41
20
11
8
10
50
Giggle
15
13
7
8
56
No warning
38
19
6
6
31
Postmicturition
22
15
4
11
48
Other
12
15
4
19
50
Slight
Drops
Severity Always
Flood
Moderate
Coughing
1
2
2
46
48
Strain
7
3
10
38
41
Urge
1
3
7
35
52
19
6
6
38
19
Postmicturition
2
2
2
27
69
With UTI
–
–
7
37
56
Other
4
4
8
50
35
No warning
* A patient may have more than one type of incontinence. UTI, urinary tract infection.
nocturnal incontinence
treatment experience
Incontinence at night was reported by 51 (26 female and 25 male) individuals, a prevalence of 4% of the population over the age of 10 years. The frequency of nocturnal incontinence is shown in Table 2d.5, correlated with sex and age group.
Perhaps reflecting the minor nature of the problem for the majority of the positive respondents, 70% of the 301 with leakage had never sought any treatment. However, 31% of the women and 26% of the men had sought help from general practitioners (24%), from specialists (14%) 41
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table 2d.5.
Frequency of nocturnal incontinence, correlated to sex and age group No. and sex
Frequency
Overall percentage
M
Age group (years) F
10–29
30–44
45–59
60–74
75+
Most nights
8
2
2
2
0
1
1
0
Once a month
4
2
0
1
0
1
0
0
Occasionally
16
5
3
6
1
1
0
0
Rarely
73
16
21
19
7
8
0
3
28
8
11
1
3
1
8
Percentage wet in age group
or from other health professionals (1%). (Respondents may have sought help from more than one healthcare professional.) Those most likely to seek help were over 60 years of age, and either blue-collar or unemployed persons. This may be explained by the fact that it is the elderly and those from blue-collar families who have the highest prevalence of urinary leakage and also the more severe degrees of incontinence. At the time of the study, 93 people were having treatment for incontinence, representing 31% of the 301 with current leakage. This is similar to the treatment rate reported by Thomas et al.1 The types of treatment being received were pharmaceutical agents in 33%, appliances in 8%, bladder/muscle training in 13%, and surgery in 24% of patients.
relatIonshIp between IncontInence and age group The prevalence of incontinence and its relationship to age group and gender is shown in Figure 2d.1 and in Table 2d.6. The increased prevalence seen with increasing age is particularly prominent in men over 60 years of age. The normal female preponderance is lost in old age, with a consequent rise in overall prevalence. The high (40%+) prevalence rate in the over-60 age groups is similar to that found in other studies7 and to the prevalence of incontinence found in nursing homes.8 Those over 60 years of age reported more severe and more frequent episodes of incontinence than did younger people. Even young women have a higher prevalence of incontinence than young men, and this trend is accentuated after 30 years of age, possibly as a result of pregnancy and childbirth. This was particularly apparent in the rates of stress urinary incontinence, which increased from 7% in the 10–29 year-old group to 26% in 30- to 44-year-old women and to 36% in the 45- to 60-year-old group. These data are similar to those obtained from
5.6
2.3
4.4
the Women’s Health Australia study.6 The relationship between incontinence type and age group is shown in Table 2d.7, which emphasizes the rising prevalence of urge incontinence in the elderly and the high rate of simple stress incontinence in middle age.
precIpItatIng Factors The 301 individuals who were ‘wet day or night’ were requested to identify the ‘cause’ of their leakage problem (Table 2d.8). Hysterectomy was blamed for incontinence in 7% of the women, mostly by women from blue-collar families or those off the workforce, compared with only 1% of the women from white-collar families. Incontinence associated with urinary tract infection was also twice as common in women from blue-collar families. The association between incontinence and hysterectomy and other pelvic surgery has been observed in other studies by Foldspang et al.9 and Parys et al.10 The relationship between incontinence and number of children is shown in Figure 2d.2. The first child and pregnancy virtually doubled the prevalence of incontinence in women from 20% to about 40%. There was no change then until the fourth child, when the prevalence rose to 56%. The effect of parity has been noted from other studies.1,2,7,11 Women from blue-collar families were more likely than others to blame childbirth for their incontinence. A recent study of incontinence during pregnancy was reported by Chiarelli and Campbell.12 In a crosssectional descriptive study using a five-item structured interview, 336 women were approached and 304 participated (90%): overall, 64% reported stress urinary incontinence during pregnancy; in the last month of pregnancy 57% reported stress incontinence (with or without urge incontinence) while 42% had urge incontinence (with or without stress incontinence). Among the 195 women experiencing incontinence, 25% lost only a few drops, 57% lost sufficient to dampen the under-
42
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60
4+ children
Recurrent UTI 50
Locomotor problems
Prevalence (%)
Pregnant
40
Median of female
30 20 Median of male
10 0
10–29
table 2d.6.
30–44
45–59 Age (years)
60–74
Figure 2d.1. Prevalence of incontinence according to age and sex (— female [n=214]; — male [n=79]).
75+
Prevalence of incontinence, and its relationship to age group and gender Age group (years)
No. of individuals
10–29
30–44
45–59
60–74
75+
Overall
Sample total
498
354
250
117
37
1256
Female
243
194
129
64
21
651
47
75
64
19
9
214
(19)
(39)
(50)
(30)
(43)
(33)
255
160
121
53
16
605
Wet* Male Wet*
25
20
16
11
7
79
(10)
(13)
(13)
(21)
(44)
(13)
* Percentages in parentheses.
table 2d.7.
Relationship between incontinence type and age group Percentage in age group (years)
Incontinence
Percentage female
Cough/sneeze
97
25
53
63
33
Strain/lift
86
7
13
12
7
Urge
78
31
29
28
Giggle
90
29
25
24
No warning
94
6
5
Postmicturition
37
26
24
With UTI
78
11
12
Other
77
14
10
No./group size
72/498
97/354
78/250
30/117
16/37
Prevalence (%)
14
27
31
26
43
30
150
171
161
143
150
159
Percentage of responses/sufferers*
10–29
30–44
45–59
60–74
75-plus
Overall percentage
44
46
–
10
50
56
33
13
19
24
6
3
6
5
18
23
6
22
4
7
13
9
5
7
6
9
* A patient may have more than one type of incontinence. UTI, urinary tract infection.
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table 2d.8.
Cause of leakage identified by 301 individuals who were ‘wet day or night’. Percentage of individuals
Cause
Male
Female
5
13
Hysterectomy
–
7
Childbirth/pregnancy
–
31
Menopause
–
5
Prostatectomy
5
–
Other operation
4
2
Miscellaneous
13
32
No cause identified
69
32
Prevalence of incontinence (%)
Urinary tract infection
60 50 40 30 20 10 0
n=220 Nil
n=41 1
n=135 2
n=97 3
n=55 4
Number of children
Figure 2d.2. Relationship between incontinence and number of children.
wear or pad, and 18% reported severe loss. The leakage had started during the first trimester in 8%, in 18% in the second trimester, and in 47% in the last trimester of the most recent pregnancy, whereas, for 20%, leakage had begun in a previous pregnancy, in 6% it began after the birth of a previous child, and only 3% indicated that they had been incontinent before any of their pregnancies. For 49%, leakage was not at all bothersome, 31% found it a little bothersome, 16% quite bothersome and 4% extremely bothersome. Chi-square analysis showed four factors to be significantly associated with continence status: previous delivery mode, parity, chronic cough, and bouts of sneezing. Women who had previous vaginal deliveries were 2.5 times more likely to be incontinent than those who had no previous delivery or had only cesarean section. Those who reported previous forceps delivery were 10 times more likely to be incontinent than those with no prior delivery. Only 8% of the women had had their pelvic floor muscles tested during their pregnancy.12
rIsk Factors InFluencIng IncontInence An analysis of potential risk factors was undertaken. The groups found to be associated with higher rates of incontinence are shown in Table 2d.9. The association between incontinence and cystitis has been noted by Mommsen et al.,13 who found a six-fold increase in experience of incontinence. A more detailed analysis of risk factors in women has emerged from the Women’s Health Australia project6 (Table 2d.10). This longitudinal study involved three cohorts of women: young (age 18–23 years), middleaged (age 45–50 years) and older (70–75 years) at the time of the baseline survey. The women were selected randomly5 from the Australian Medicare database covering all women resident in Australia. During 1996, 14,761 young women, 14,070 middle-aged women, and 12,893 older women completed baseline surveys (respectively, 48, 54 and 41% of those of each group invited to take part). The baseline questionnaire consisted of 252, 285 and 260 items, respectively, for each of the age cohorts. Participants were asked whether they had leaked urine in the last month ‘never’, ‘rarely’, ‘sometimes’ or ‘often’: responses other than ‘never’ were taken as indicating incontinence. The advantages of this study were its large sample size and the representative nature of the sample. The limitation was the use of a single non-validated question about leaking urine which fails to differentiate between different types of incontinence. The prevalence of leaking urine in young women was 12.8% (95% confidence interval [CI] 12.2–13.3); in middle-aged women it was 36.15% (CI 35.2–37.0), and in older women 35.0% (CI 34.1–35.9).6 These figures are similar to those reported by the earlier Australian prevalence study.
table 2d.9.
Groups found to be associated with higher rates of incontinence
Risk factor
Percentage incontinence in group
Percentage incontinence in remainder
Diabetes
36
24
Cerebrovascular accident
25
24
Neurologic disorder
29
24
Locomotor difficulty
45
24
Over 75 years of age
43
24
Recurrent urinary tract infection
55
24
Pregnancy
45
34
Four (or more) children
56
34
44
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table 2d.10.
Adjusted odds ratios for variables associated with leakage of urine in women Odds ratio (95% confidence intervals)
Variable
Young (18–23 years)
Middle-aged (45–50 years)
Older (70–75 years)
Parity 0
1.00
1
2.82 (2.37–3.35)
1.58 (1.29–1.93)
0.88 (0.71–1.0)
2
2.59 (1.86–3.61)
1.66 (1.41–1.95)
1.14 (0.96–1.36)
3 or more
4.84 (2.54–9.20)
1.81 (1.54–2.12)
1.16 (0.98–1.36)
Constipation Never
1.00
Rarely
2.13 (1.86–2.42)
2.46 (2.24–2.71)
2.67 (2.38–2.99)
Sometimes
2.86 (2.43–3.36)
2.16 (1.94–2.40)
2.05 (1.82–2.31)
Often
2.66 (2.07–3.40)
2.31 (1.84–3.35)
2.21 (1.87–2.61)
Body mass index <19.9 1.00
Underweight Ideal
20–24.99 1.08 (0.94–1.23)
1.31 1(1.10–1.55)
1.19 (1.00–1.40)
Overweight
25–29.99 1.34 (1.13–1.60)
1.47 (1.23–1.75)
1.39 (1.16–1.65)
30–40 2.09 (1.67–2.61)
2.05 (1.70–2.46)
1.82 (1.49–2.23)
>40 1.82 (1.07–3.09)
2.49 (1.84–3.35)
3.29 (2.05–5.29)
Obese Very obese Burning and stinging* Never
1.00
Rare
2.94 (2.59–3.33)
2.17 (1.96–2.42)
2.45 (2.18–2.76)
Sometimes
4.19 (3.56–4.93)
2.71 (2.35–3.14)
2.99 (2.62–3.41)
Often
4.93 (3.60–6.74)
4.29 (2.85–6.45)
7.97 (5.71–11.12)
* Indicative of a history of urinary tract infection. Data provided by P. Chiarelli; personal communication and ref. 6.
Parity was significantly associated with the prevalence of incontinence in young women but was less strongly correlated in the other age groups. There was a strong association between any degree of constipation and urinary leakage. In middle-aged women, those with high body mass index (BMI >25) and constipation were those most likely to experience leakage of urine. Hysterectomy alone had a lower odds ratio (OR) for leakage, whereas women who reported a prolapse repair, either alone or with a hysterectomy, were more likely to leak. Neither current use of hormone replacement therapy nor duration of use was associated with leaking urine. In the older cohort, the effect of parity was obscured. Pelvic surgery of any kind had a positive association with incontinence. Those with high BMI and those with a history suggestive of urinary tract infection (burning and stinging) were more likely to report incontinence.
At all ages, women who reported leaking urine had lower scores on the physical and mental component of the Swedish Short Form 36 (SF36) inventory, suggesting a lower quality of life for these women compared with continent women. In a follow-up study reported in 2003,14 the cohorts had aged by 5 years. The majority of all age groups reported mixed incontinence, most commonly mixtures of stress and urge leakage, almost 80% of wet women over 50 years of age having mixed urinary incontinence (Table 2d.11). The severity of incontinence was as high as or worse than that in older women. Incontinence severity was associated with BMI and this effect involved women with stress urinary incontinence or urge urinary incontinence. Other risk factors identified for severity included number of deliveries but there were insufficient numbers of women with large babies for a significant difference to be attributed to the size of the baby. Smoking >20 cigarettes per day was a risk factor 45
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table 2d.11.
Proportion of incontinent women in age cohorts who reported symptoms of stress, urge or ‘other’ incontinence Age at time of study
Type of incontinence
Young (21–26 years) (n=187)
Stress only (%)
10.7
6.4
2.0
Urge only (%)
2.7
1.3
6.1
Other only (%)
0.0
0.0
0.8
Mixed (%)
Middle-aged (48–53 years) (n=389)
Older (73–79 years) (n=358)
86.6
92.3
91.1
Stress, urge and ‘other’
63.6
65.3
60.9
Stress and urge
18.2
26.0
26.8
3.2
0.8
2.5
Stress and ‘other’ Urge and ‘other’
1.6
0.3
0.8
Any stress symptoms
95.7
98.5
92.2
Any urge symptoms
86.1
92.8
94.7
Any ‘other’ symptoms
68.4
66.3
65.1
Data from ref. 14.
(OR 3.34, 95% CI 1.6, 6.98) in even young women in contrast to other studies that have only shown this association in older cohorts. Urine that burns or stings was often associated with higher adjusted odds ratios in all age cohorts. Adolescents with chronic lung disease and cystic fibrosis aged 12–19 years have been reported to have a high incidence of incontinence.15 Of 55 adolescents, 47% had ever experienced urinary incontinence (UI) and 22% had UI at least twice a month. Median age of onset was 13 (range 7–16 years) and most had leakage associated with coughing (84%) or laughing (64%). Importantly, 42% reported that it sometimes prevented them from doing effective physiotherapy and 33% said their social life had been affected. Only 58% had told anyone about their problem and only 2 of 26 girls had talked to their doctor.
past experIence oF IncontInence IF no problem at present The 955 respondents who denied any degree of urinary leakage at the present time were asked to report if they had ever experienced urinary leakage since they were 17 years of age. Replies showed that 16% of men and 30% of women had had previous experience of leakage: in 6% leakage had occurred occasionally and in 17% it had been experienced only rarely. The pattern of previous incontinence was similar to that found among those who admitted to present leakage.
chIldhood IncontInence and relatIve rIsk Of the whole group of 1256 respondents, 21% (269) recalled having problems as a child with bedwetting. The occurrence of this problem was equal in males and females. In addition, 9% (114 respondents, 67% female) recalled having had urinary leakage at school. Bedwetting was apparently more common in whitecollar families (25% of whom were affected) than in bluecollar families (where only 20% recalled problems). Childhood nocturnal enuresis was recalled by 269 individuals. As adults, 11% of these individuals still wet the bed while 32% had diurnal incontinence. Childhood bedwetters accounted for 57% of all those currently wet at night and 30% of all those wet by day (Table 2d.12). Childhood bedwetters appeared to carry a five-fold increased risk of nocturnal incontinence in adult life compared with non-bedwetters. They were also at higher risk of developing some degree of urinary incontinence by day, with 1.7 times the prevalence rate of non-bedwetters. Of 114 respondents (9%) wet at school, 39% were wet by day at the time of the survey, accounting for 15% of all those now wet; 7% of the group now suffer from table 2d.12.
Present incontinence among those recalling nocturnal enuresis as a child
Current
Childhood bedwetter
Childhood non-bedwetter
Percentage wet at night now
11
2
Percentage wet by day now
32
19
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incontinence at night and account for 16% of all those now wet at night (Table 2d.13). Individuals with incontinence in childhood at school carry a three-fold risk of night-time incontinence as an adult and twice the risk of diurnal incontinence than their fellows who had been dry at school. The epidemiology of childhood enuresis in Australia has been independently studied by Hawkins16 in 1962 and by Bower et al.17 in 1996. The former took a sample of 1000 children in one general practice only and found a prevalence of nocturnal enuresis (of one or more nights per week at school age) of 18%; daytime incontinence was not evaluated. The 1996 study by Bower and colleagues17 used a self-administered questionnaire distributed to parents with children 5–12 years of age at the eight largest polling stations of three electorates. Voting is compulsory in Australia and these electorates were selected to represent voters of high (9000), middle (7600), and lower (9000) socioeconomic classification. Of the 3111 parents approached, 2292 (74%) responded. The prevalence rate was 15% for nocturnal enuresis, 2% for isolated day wetting and 4% for combined day and night wetting; overall, 79% of children were dry, 18.9% had nocturnal enuresis, and 5.5% had daytime incontinence. Whereas daytime wetting did not show a gender bias, 60% of children with enuresis were male, regardless of whether the enuresis was primary or secondary (Table 2d.14). The families of only 33.8% of enuretic children had sought professional help for the problem. Family strategies used were reward charts table 2d.13.
Incontinence among those wet at school
Current
Wet at school Dry at school
Percentage wet at night now
7
2
Percentage wet by day now
39
19
table 2d.14.
Prevalence (%) of enuresis
Type
Male (n=277)
Nocturnal enuresis
11.3
7.6
18.9
2.7
2.8
5.5
Daytime wetting
Female (n=181)
Overall
(16%), waking the child to void (30%), fluid restriction (43%), and waiting for maturity (51%). Non-enuretic children woke spontaneously to void at night in 80% of cases; by contrast, enuretic children woke only 49% of the time. There was a significant difference in the incidence of a positive family history between enuretic and dry children: among dry children, 55.5% had no family history, whereas only 30.6% of enuretics had no known family history. These figures corroborate the findings of the earlier general population study,3,4 suggesting that 100,000 children wet the bed each night in Australia.
prevalence oF sIgnIFIcant IncontInence In the populatIon The results detailed above indicate that some urinary incontinence is experienced by many people. The problem has been identification of the rate of troublesome and significant leakage from most of the infrequently wet individuals. Using computer analysis, the entire sample was filtered to exclude all those with rare episodes of leakage and those who had ‘just a spot’ or slight loss of urine only, on infrequent occasions; patients who had leakage only with urinary infections were also excluded. The remainder were considered as having ‘significant’ urinary incontinence: of these 85 people, 10 were men and 75 were women. The frequency with which they experienced incontinence is shown in Table 2d.15. Infrequent urinary incontinence was rare in those women over 65 years of age, whereas frequent leakage was unusual in patients under 35 years of age. The degree of wetness experienced is detailed in Table 2d.16. Minor leakage volumes were rare over 65 years of age. Whereas those ‘always wet’ tended to be younger (<64 years old), the elderly tended to have ‘moderate loss’ or ‘flooding’. Of this group, only 40% of both sexes had ever sought treatment: 30% of each sex had seen their general practitioner, and specialists had seen 30% of the men but only 17% of the women. This low percentage of people seeking treatment reflects the fact that about
table 2d.15.
Frequency of significant urinary incontinence in 10 men and 75 women
Total
14
10.4
Frequency
Night
Day
Every day
2.4
0.6
Frequency of incontinence
Male
Female
2+/week
2.7
0.8
Often wet
50
25
30
27
20
25
–
23
Percentage
1/2 weeks
0.9
0.3
Once a day
1/month
1.8
0.4
Once a week
11.1
3.4
Once or twice a month
<1/month
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table 2d.16.
Degree of wetness in respondents with significant urinary incontinence Percentage
Degree of wetness
Male
Female
Always wet
0
4
Flooding
0
4
Moderate loss
30
11
Slight loss
70
48
Just a spot
0
33
40% of each sex needed to wear protective underwear; the remainder managed by hygienic measures alone. The pattern of incontinence reported by those who were deemed to have significant incontinence is shown in Table 2d.17. Among the men with frequent incontinence, smallvolume postmicturition loss was most commonly a complaint of younger men; older men suffered from urge incontinence (especially in the 75+ age group, in which this occurred in 20%). By contrast, females tended to have more than one cause of leakage, with stress incontinence predominant (particularly in middle-aged women). Urge incontinence in women appeared to be equally prevalent at all ages, but its severity grew with advancing years; flooding urinary loss was reported only by those over 50 years of age.
urInary IncontInence In people In InstItutIons
Pattern of incontinence reported by those deemed to have significant incontinence Percentage
Incontinence type
Male
Female
Coughing or sneezing
–
67
Straining or lifting
–
17
Urge
50
43
Giggle
10
27
No warning or provocation
10
12
Postmicturition dribbling
40
11
110
177
Total*
* More than one response was allowed.
Incontinence in nursing homes The staff of 15 of the larger nursing homes across the city were asked to fill out profiles of their patients’ continence status (Table 2d.18). Among the 1631 residents of these nursing homes, 596 were incontinent, a prevalence rate of 37%. Most of those who were incontinent were over 70 years of age. The ratio of males to females was close to 1:1, but females outnumbered males in the homes by 2.6:1; as a result there were more wet women than men. Wet men tended to be slightly younger than wet women. The degree of incontinence reported in this group is shown in Table 2d.19, correlated with mobility status. There was no significant difference between the degree of incontinence found in men and women in nursing homes. Residents who were chair-bound tended to have the highest rates of incontinence. Another Sydney study of 1659 residents of nursing homes found UI affected 77%, and that 25% of nursing staff time was spent dealing with urinary leakage.18 The long-term care of looking after such residents was estimated at AUS$45,000 per annum or $450 million a year. If the prevalence found in this survey (37%) is applied to the population of all nursing homes in Australia, an estimated 22,000 incontinent individuals might be expected to be found in these establishments.
Incontinence in hospitals
A parallel study was conducted to determine the prevalence of incontinence among those in institutional care: 15 nursing homes in the Sydney area were surveyed; one
table 2d.17.
public hospital (824 beds) and two private hospitals (842 beds) were also investigated.
In order to assess the prevalence of incontinence, the staff of one large public hospital and two small private hospitals were asked to make a count of incontinence among their patients. In the public hospital, 3.4% of the 824 patients had incontinence known to the nursing staff and 71% of these were over 71 years of age. This may be an underestimate in that many patients who table 2d.18.
Continence status of patients in 15 of the larger nursing homes in Sydney Percentage
Degree of wetness
Male
Female
Overall
Always wet
39
40
39
Flooding
15
13
13
Moderate loss
31
35
34
Slight loss
13
10
11
194
394
596
n
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table 2d.19.
Degree of incontinence analyzed by patient mobility Percentage of patients incontinent
Mobility
Always wet
Flooding
Slight
Overall
10
11
20
44
18
Chair-bound
76
64
54
27
61
8
16
3
–
6
Bedridden Mobile aided n
6
9
23
27
15
234
80
200
66
596
were able to manage their own incontinence may not have been known to the ward nursing staff. In the two small private hospitals, the prevalence of incontinence was 13 and 22%, respectively. There was a high proportion of psychiatric patients, of whom 15% were incontinent; 40% of the geriatric patients in these hospitals were incontinent.
prevalence oF IncontInence In australIa Among adult Australians, 24% of individuals admit to having some urinary loss and 6% of the population have significant or frequent urinary leakage. Of those who currently have no incontinence (76%), 23% have experienced some urinary leakage in their past adult life. Of those who currently suffer some form of leakage, 73% are female, but women account for 88% of those with severe incontinence (M:F ratio = 1:7.5). The female predominance disappears over the age of 60. A summary of the prevalence of incontinence is shown in Table 2d.20. If the figures for significant present incontinence are applied to the census figures, it can be estimated that as many as 960,000 adults in Australia may experience regular or severe incontinence; however, fewer than half of these ever seek professional help. Conversely, if prevalence figures of 24% of all women over 18 years are used and applied to current census data, a figure table 2d.20.
Moderate
Ambulant
Summary of prevalence of incontinence in Australia Percentage of individuals
Incontinence
Male
Female
Overall
Childhood enuresis
21
21
21
Past incontinence (in adult life)
16
30
23
All present incontinence
13
34
24
Ever incontinent as an adult
28
53
41
Significant incontinence now
2
11
6
closer to 2 million incontinent individuals would be more appropriate. What then is prevalence? Should we only be interested in severe incontinence, or should we screen individuals in the community for lesser degrees of UI which might be amenable to interventions by the family practitioner, thereby perhaps avoiding more major problems later in life? A simple Incontinence Screening Questionnaire (ISQ) was evaluated and correlated with 48-hour pad test data, resulting in only five discriminating questions19 (Table 2d.21). With an aging population we can anticipate an increase in the probability of UI and in its severity. In addition, with aging comes a change from stress incontinence to urge incontinence and co-morbidity. UI has a considerable financial impact on individuals and the healthcare system. In Australia the total annual cost of UI was estimated at AUS$710 million in 1998 for the 1,835,628 community-dwelling incontinent women over 18 years of age. This represents $387 per incontinent woman, comprising $338.47 million in treatment costs and $371.97 million in personal costs. These costs will escalate to AUS$1.27 billion per annum by 2018.20 These figures do not include indirect or intangible costs, neither do they include the costs of nursing home care mentioned above. table 2d.21.
Predictive validity of incontinence screening questionnaire PPV (%)
Have you leaked urine when: • coughing/laughing/sneezing • on the way to the toilet • waiting to use the toilet • going to the toilet urgently when first feeling the need • going to the toilet ‘just in case’
64 68 67 67 68
Data from ref. 19.
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We cannot afford to ignore the prevalence of incontinence; it is going to cost us or our children dearly. There is a need to emphasize to primary care physicians the importance of identifying at-risk women or those with minor degrees of UI, for which conservative options (pelvic floor exercise programs for stress urinary incontinence, or bladder training/drug therapy) may be restorative or may prevent deterioration. Clearly, the cost–benefit of early intervention needs to be evaluated in anticipation of the flood of incontinence with which the profession will be inundated as our population ages.
reFerences 1. Thomas TM, Plymat KR, Blannin J, Meade TW. Prevalence of urinary incontinence. Br Med J 1980;281:1243–5. 2. Jolleys JV. Reported prevalence of urinary incontinence in women in general practice. Br Med J 1988;296:1300–2. 3. Millard RJ. The incidence of urinary incontinence in Australia. Br J Urol 1985;57:98–9. 4. Millard RJ. The prevalence of urinary incontinence in Australia: a demographic study in the Sydney area in 1983. Aust Continence J 1988;4:92–9. 5. Brown WJ, Bryson L, Byles J et al. Women’s Health Australia: recruitment for a national longitudinal cohort study. Women’s Health 1998;28:23–40. 6. Chiarelli P, Brown W, McElduff P. Leaking urine – prevalence and associated factors in Australian women. Neurourol Urodyn 1999;18;567–77. 7. Milsom I, Ekelund P, Molander U et al. The influence of age, parity, oral contraception, hysterectomy and menopause on the prevalence of urinary incontinence in women. J Urol 1993;149:1459–62. 8. Ouslander JG. Urinary incontinence in nursing homes. J Am Geriatr Soc 1990;38:289–91.
9. Foldspang A, Mommsen S, Elving L, Lam GW. Parity as a correlate of adult female urinary incontinence prevalence. J Epidemiol Community Health 1992;46:595–600. 10. Parys B, Haylen B, Hutton J, Parsons K. The effects of simple hysterectomy on vesicourethral function. Br J Urol 1989;64:594–9. 11. Mommsen S, Foldspang A, Elving L, Lam GW. Association between urinary incontinence in women and a previous history of surgery. Br J Urol 1993;72:30–7. 12. Chiarelli P, Campbell E. Incontinence during pregnancy: prevalence and opportunities from continence promotion. Aust N Z J Obstet Gynaecol 1997;37:66–73. 13. Mommsen S, Foldspang A, Elving L, Lam GW. Cystitis as correlate of female urinary incontinence. Int Urogynaecol J Pelvic Floor Dysfunct 1994;5:135–40. 14. Miller YD, Brown WJ, Russell A, Chiarelli P. Urinary incontinence across the lifespan. Neurourol Urodyn 2003;22:550–7. 15. Nixon GM, Glazener JA, Martin JM, Sawyer SM. Urinary incontinence in female adolescents with cystic fibrosis. Pediatrics 2002;110:e22. 16. Hawkins DN. Enuresis: a survey. Med J Aust 1962;23:979–80. 17. Bower WF, Moore KH, Shepherd RB, Adams RD. The epidemiology of childhood enuresis in Australia. Br J Urol 1996;78:602–6. 18. Steel J, Fonda D. Minimising the cost of urinary incontinence in nursing homes. PharmacoEconomics 1995;7:191–7. 19. Gunthorpe W, Brown W, Redman S. The development and evaluation of an Incontinence Screening Questionnaire for Female Primary Care. Neurourol Urodyn 2000;19:595–607. 20. Doran CM, Chiarelli P, Cockburn J. Economic costs of urinary incontinence in community dwelling Australian women. Med J Aust 2001;174:456–8.
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2e Epidemiology: Asia Peter H C Lim, Marie Carmela Lapitan
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INTRODUCTION Urinary incontinence has been increasingly recognized as a significant problem in the past decade in all parts of the world. Most, if not all, studies on the epidemiology of urinary incontinence have been conducted on Western (i.e. American and European) populations. In this light, the Asia–Pacific Continence Advisory Board conducted an Asian-wide epidemiologic survey on urinary incontinence to determine the magnitude of the problem in the region. The Philippines, Singapore, Malaysia, Thailand, and Indonesia were among the participating countries. This study aimed to establish the prevalence of urinary incontinence, identify the demographic factors related to its occurrence and ascertain the determinants for seeking help for this condition among the female population of Southeast Asia.
METHODS A comprehensive questionnaire was designed to determine presence of urinary incontinence, defined as the inappropriate leakage of urine, its associated symptoms and the resulting degree of bother, and the action taken to address the condition. The questionnaire used was a 34-item multiple-choice type. This questionnaire was translated into the local dialects and was validated in each country. In the survey proper, the questionnaire was administered by medically trained personnel to randomly selected women consulting at outpatient clinics for non-urologic or non-gynecologic problems. The survey was conducted in a total of ten centers: two in the Philippines, one in Singapore, two in Malaysia, one in Indonesia, and four in Thailand. The first part of the questionnaire included queries on population demographics such as age, civil status, parity, educational attainment, occupation, monthly family income, and place of residence. The general voiding pattern was established by noting the normal daytime and nocturnal voiding frequencies. The main body of the questionnaire focused on establishing the presence of voiding dysfunction, particularly urinary incontinence and overactive bladder through extensive inquiry on the different symptoms associated with these conditions. The presence of urinary incontinence was ascertained by a positive response to the question of ever having leaked urine inappropriately before reaching the toilet. Incontinence was classified as stress if the respondent reported urine loss with coughing, sneezing or other physical exertion. Urge incontinence was recorded if urinary loss was associated with a sudden strong desire
to void. If symptoms of both stress and urge were present, incontinence was labeled as mixed. Incontinence as a problem was assessed according to the degree of bother it caused the subject using a scoring system of 0–5 (0 as none, 5 as severe). In addition, the need for leakage protection was also determined. It was also noted whether the subject sought help for her condition. The relationships between the occurrence of urinary incontinence and age, parity, number of vaginal deliveries, occupation, family income, type of toilet used, family history, and place of residence were also analyzed.
RESULTS Study population demographics A total of 2422 female respondents were included in the survey. Table 2e.1 shows the distribution of the study population per country. While each age group was well represented (Table 2e.2), the population studied was relatively young, with the majority aged below 60 years old and more than 50% younger than 40 years. Fortyfour percent of the study population was nulliparous. Among the parous respondents, the majority had had Table 2e.1.
Urinary incontinence: frequency distribution of study population according to country n
Percentage
Philippines
682
28.2
Singapore
228
9.4
Malaysia
351
14.5
Indonesia
257
10.6
Thailand
904
37.3
2422
100.0
Total
Table 2e.2.
Urinary incontinence: frequency distribution of study population according to age n
Percentage
18–28
726
30.0
29–39
676
27.9
40–49
474
19.6
50–59
324
13.4
60–69
153
6.3
64
2.6
5
0.2
2422
100.0
≥70 Not indicated Total
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at least two deliveries (Table 2e.3). Most of the women were doing office work (Table 2e.4). There was a high literacy rate, with more than 85% of the population having had at least a secondary level of education (Table 2e.5). The study population was evenly distributed among the income groups (Table 2e.6), and at least 60% resided in the urban area (Table 2e.7).
The majority voided fewer than eight times during the day, with half of this population voiding between four and eight times. Almost all voided fewer than three times during the night, with nearly one-third not voiding at all at night time. Around 72% of the study population voided fewer than eight times per 24 hours.
Prevalence of urinary incontinence General voiding pattern The voiding pattern of the study population was analyzed according to the frequency of urination (Table 2e.8). Table 2e.3.
Urinary incontinence: frequency distribution of survey population according to parity n
Percentage
0
1059
43.7
1
273
11.3
2–4
786
32.5
5–8
260
10.7
>8
40
1.7
4
0.2
2422
100.0
Not indicated Total
Table 2e.4.
Urinary incontinence: frequency distribution of survey population according to occupation n
Manual labor Office work
The prevalence of urinary incontinence in the study population was 14.8% (359/2422). Nearly half of the incontinent individuals (47.9%) presented with the mixed type. Eighty-one women (22.6%) had stress incontinence while less than 10% presented with urge incontinence (Table 2e.9).
Incontinence as a problem The majority of the population who experienced incontinence in this survey were not bothered or, if so, were only mildly bothered by their condition (Table 2e.10). However, a major portion (157/359 or 43.7%) felt that protection from leakage was necessary. Of the 359 affected individuals, 150 (41.8%) sought help for their condition.
Table 2e.6.
Percentage
Urinary incontinence: frequency distribution of survey population according to monthly income n
Percentage
296
12.2
A
316
13.0
1105
45.6
B 100–199
310
12.8
Others
904
37.3
C 200–399
493
20.4
Unemployed
117
4.8
D 400–599
322
13.3
2422
99.9
E 600–799
424
17.5
F ≥800
375
15.5
Not indicated
182
7.5
2422
100.0
Total
Table 2e.5.
Urinary incontinence: frequency distribution of survey population according to educational attainment n
Never went to school
Percentage
Total
Table 2e.7.
84
3.5
Primary school
293
12.1
Secondary school
582
24.0
Pre-university
380
15.7
Urban
University
652
26.9
Professional education
414
17.1
17
0.7
2422
100.0
Not indicated Total
Urinary incontinence: frequency distribution of survey population according to place of residence n
Percentage
1473
60.8
Semi-urban
676
27.9
Rural
230
9.5
Not indicated Total
43
1.8
2422
100.0
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Table 2e.8.
Urinary incontinence: frequency distribution of survey population according to voiding frequency n
Percentage
Daytime frequency 1
Table 2e.10.
Frequency distribution of incontinent population according to degree of bother
Bother score
n
Percentage
0 – none
130
36.2
1 – very mild
94
26.2
2 – mild
54
15.0
74
3.1
2–4
917
37.9
3 – moderate
23
6.4
4–8
1217
50.2
4 – severe
14
3.9
>8
167
6.9
5 – very severe
18
5.0
47
1.9
Not indicated
26
7.2
2422
100.0
359
99.9
0
628
2509
1
1027
4204
Not indicated Total
Total
Night-time frequency
2–3
667
27.5
>3
73
3.0
Not indicated
27
1.1
2422
99.9
Total
2.
24-hour frequency <8
1737
71.7
≥8
638
26.3
47
1.9
2422
99.9
Not indicated Total
Table 2e.9.
Type
Frequency distribution of incontinent population according to type of incontinence n
Percentage
Stress
81
22.6
Urge
31
8.6
Mixed
172
47.9
75
20.9
359
100.0
Undetermined Total
3.
4.
5.
Factors related to the occurrence of urinary incontinence Age, parity, mode of delivery or childbirth, number of vaginal deliveries, occupation, family history, and family income were found to be significantly related to the occurrence of urinary incontinence. The type of toilet used and the place of residence were not found to be related to the occurrence of the condition (Table 2e.11). 1. Age. Increasing age was found to be significantly related to the occurrence of incontinence. By the age of 40 years, the risk for incontinence was found
6.
7.
to be increased by 2.5 times (95% CI 2.0–3.1). The odds progressively increased to 2.8 times and 3.4 times at ages 50 and 60 years, respectively. Parity. The majority of the incontinent population was parous. There was a significant correlation between increasing prevalence of incontinence with higher parity. A woman who has delivered at least once was found to be 2.1 times (95% CI 1.6–2.7) at risk for incontinence compared to the nulliparous. With a parity of more than four, the odds increased to 2.5 times. Mode of delivery. There was a higher prevalence of incontinence among those who delivered vaginally, by forceps extraction or a combination of both, a woman who has given birth vaginally having twice the risk of urinary incontinence than one who has delivered abdominally. Number of vaginal deliveries. Taking into account vaginal deliveries (including forceps delivery), there was a significant relationship of increasing prevalence of incontinence with a higher number of deliveries. Having delivered more than once vaginally increased a woman’s risk for incontinence to 2.0 times (95% CI 1.6–2.6). The odds increased to 2.6 times when the number of deliveries reached five. Occupation. The prevalence of incontinence was highest among those doing manual labor (see Table 2e.4). This was found to be statistically significant, with a woman doing manual labor 1.6 times (95% CI 1.3–2.1) at risk of having incontinence. Family history. The family history of incontinence was significantly related to the occurrence of the condition. A woman with a positive family history was 2.4 times (95% CI 1.9–3.0) at risk of having the condition compared to one without. Family income. A higher prevalence of incontinence was found among those from the lower income group, which was found to be statistically significant.
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Table 2e.11.
Demographic factors and their relation with the occurrence of urinary incontinence
Factor Age 18–28 29–39 40–49 50–59 60–69 >70 Parity 0 1 2–4 5–8 >8 Mode of delivery Vaginal only Cesarean only Forceps only Combination None Number of vaginal deliveries 0 1 2–4 5–8 >8 Occupation Manual Labor Office Work Others Monthly income A B C D E F Family history Yes No Type of toilet used Sitting Squatting Both Place of residence Urban Semi-urban Rural
Incontinence* Yes No
p-value
Odds ratio
95% confidence interval
58 82 76 69 49 24
661 587 397 248 103 40
<0.001
2.466 (<40 vs. ≥40) 2.766 (<50 vs. ≥50) 3.391 (<60 vs. ≥60)
1.959–3.105 2.178–3.512 2.491–4.615
104 38 133 69 14
943 232 646 191 26
<0.001
3.391 (0 vs. ≥1) (<5 vs. ≥5)
1.648–2.685
197 26 3 25 104
813 160 18 94 945
<0.001
2.067 (vaginal/forceps vs. cesarean/none)
131 34 108 69 13
1111 183 531 181 24
<0.001
2.025 (≤1 vs. >1)
1.613–2.541
62 139
231 958
<0.001
1.645 (manual labor vs. office work/ others)
1.284–2.108
152
752
30 56 82 54 43 69
286 253 406 264 377 302
<0.001
1.367 (
1.021–1.831 1.303–2.171
174 104
631 1056
<0.001
2.411
1.924–3.021
239 109 9
1345 595 86
NS
NA
NA
210 107 35
1249 566 194
NS
NA
NA
* Counts may not total to 2422 because category ‘not available’ was not included in the analysis. NA, not applicable; NS, not significant.
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A woman earning less than ‘E’ had a 1.7 times risk (95% CI 1.3–2.2) of having incontinence.
Factors associated with seeking help for urinary incontinence Forty-two percent of the incontinent population sought help for their condition, consulting either a specialist or a general practitioner (Table 2e.12). Among the factors studied in relation to the likelihood of seeking help for urinary incontinence, only age and degree of bother were noted to be significant (Table 2e.13). Increasing age positively influenced the likelihood of seeking a consult. A woman of at least 50 years of age is 2.4 times more likely to seek help for her condition compared to a younger woman. This likelihood increases to 2.5 times by age 60 years. The incontinent female who is moderately bothered (score of at least 3) is 3.7 times (95% CI 2.0–6.9) more likely to seek consultation for her condition compared to one who is less affected. A severe condition increases this likelihood to 5.1 times (95% CI 2.5–10.4).
DISCUSSION Prevalence – comparison with world figures The prevalence of urinary incontinence in this Asian survey is comparable to the Western figures1–4 and demonstrates the fact that while the condition may not present as a significant problem, urinary incontinence is prevalent Table 2e.12.
Frequency distribution of incontinent females who sought help according to person consulted
Person consulted
n
Percentage
Herbalist/traditional medical practitioner (TMP)
19
12.7
General practitioner (GP)
34
22.7
Primary healthcare center (PHCC)
17
11.3
Specialist (SP)
37
24.7
Nurse
16
10.7
Others
9
6.0
TMP + GP
5
3.3
TMP + GP + SP
3
2.0
GP + SP
3
2.0
TMP + PHCC
6
4.0
Not indicated
1
0.7
150
100.1
Total
in the Southeast Asian population. Additionally, this puts into question the presumed fact that urinary incontinence is more common in those with European versus Pacific ancestry. Thus, it is worthwhile investing time and effort to study the problem, its causes and its management.
Types of incontinence – comparison with world figures The proportion of females having stress incontinence in relation to the other types appears to be relatively low compared to previous studies citing numbers as high as 50%. This may be due to the fact that the population surveyed is relatively young while stress incontinence is more associated with advancing age. Thus, closer attention to the problem of mixed incontinence may be necessary, it being the more prevalent type among Asian females.5–7 It must be recognized, however, that the classification of incontinence used in this survey is based mainly on symptoms alone and not on any objective parameter. The authors realize this limitation of the study which is inherent in its design. Previous studies have noted that symptoms alone do not accurately classify incontinence. Therefore, further studies must be done to verify the discrepancy in the distribution of the different types of incontinence among Asian females compared to their Western counterparts. The factors found to be related to the occurrence of incontinence were not unexpected. Older age, higher parity, higher number of vaginal deliveries, and the increased physical strain associated with manual labor and the use of a sitting toilet have all been cited and accepted as contributing to the weakness of the pelvic floor leading to incontinence.8 Aging has been associated with the loss of striated muscles at the area of the urethra leading to impaired continence. The change in the hormonal milieu brought about by aging also affects the ability of the urethral submucosal layer to provide the watertight closure of the female urethra. Childbearing, childbirth,9 and physical straining have been found to cause hypermobility, innervation injuries,10 and connective tissue changes11 to the pelvic floor leading to loss of support.
Family history, family income and the occurrence of incontinence The significant relation between a positive family history of urinary incontinence and its occurrence may be indicative of a possible hereditary component to the disease. A congenital predisposition to urinary incontinence has been proposed, citing a common collagen
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Table 2e.13.
Urinary incontinence: demographic factors and their relation with seeking help Sought help*
Factor
Yes
No
p-value
Odds ratio
95% confidence interval
0.001
2.438 (<50 vs. ≥50)
1.578–3.766
2.562 (<60 vs. ≥60)
1.513–4.339
NS
NA
NA
NS
NA
NA
NS
NA
NA
<0.001
3.740 (<3 vs. ≥3)
2.009–6.961
5.139 (<4 vs. ≥4)
2.528–10.448
Age 18–28
15
43
29–39
34
48
40–49
23
53
50–59
34
35
60–69
29
20
>70
15
9
Never went to school
13
10
Primary
31
35
Secondary
37
45
Pre-university
27
42
University
30
39
Professional
12
38
A
13
17
Education
Monthly income B
24
33
C
37
46
D
25
31
E
17
32
F
21
38
Urban
79
131
Semi-urban
49
59
Rural
21
14
0 – none
38
93
1 – very mild
41
53
2 – mild
25
28
3 – moderate
17
6
4 – severe
10
4
5 – very severe
11
7
Place of residence
Degree of bother
* Counts may not total 359 because category ‘not available’ was not included in the analysis. NA, not applicable; NS, not significant.
makeup of the pelvic floor found among the affected group. However, a more likely explanation is the tendency of the members of one family to be exposed to the same type of work and physical stresses that predispose an individual to urinary incontinence. It is difficult to explain the reason behind the relationship between family income and the occurrence of
incontinence. This factor may be related to parity, with those belonging in the lower income bracket having a higher parity. In addition, the lower income group tends to do more manual labor. Thus, it may be necessary to test the interdependence of these factors to see the true relationship between income and urinary incontinence. 57
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Factors related to seeking help – possible explanations The proportion of the incontinent population seeking help is higher than most study investigators expected since this condition has been regarded as a rare clinical entity among Asians. While this observation is an interesting realization, this high figure may be due to the fact that this survey is institution-based and the population surveyed may be those who are motivated to seek a medical consult for any disease condition. Therefore, a community-based survey must be undertaken in order to verify this finding. It is interesting to note that almost one-fifth of those seeking help do so by seeing a traditional medical practitioner. This underscores the high regard the Asian patient still gives to traditional medical science despite decades of Western medicine with its advances. Further studies must be conducted to determine why this is so. This is important in the creation of efficient and effective programs that aim to encourage the affected population to find the solution to their problem. It is apparent that demographic data are inadequate to fully explain the occurrence of urinary incontinence and why an affected individual seeks help for the condition. A more objective assessment and a clinical study of the disease must be undertaken to completely understand its pathophysiology. In addition, a deeper and more exhaustive analysis of the attitude of the population toward the disease and the reasons for seeking consult is warranted. Knowledge gained from this will be valuable in future programs and campaigns to increase awareness of urinary incontinence and to encourage the affected population and the caregivers to address the problem and pursue its solution.
ADDENDUM: OvERACTIvE bLADDER AMONg FEMALES IN ASIA INTRODUCTION As overactive bladder (OAB) has a very different implication, a separate study was later conducted and added to establish the prevalence of OAB among the female population in Asia. It was also intended to describe OAB in terms of symptom presentation, the resulting degree of bother, and the rate at which help is sought to address the condition. The study also aimed to identify the factors related to the occurrence of OAB.
METHODS An epidemiologic survey was performed in 11 countries in Asia. A questionnaire of 34 multiple-choice-type queries on the presence and severity of the different symptoms of overactive bladder was formulated by a panel of experts. A demographic profile of the subjects was also included. The questionnaire was administered randomly to females consulting at outpatient clinics for non-urologic and non-gynecologic diseases in 28 centers. Prevalence of OAB was computed based on the presence of at least one of the symptoms of frequency, urgency, and urge incontinence. A chi-square test for independence to analyze the relationship between demographic data and the occurrence of OAB was performed.
Table 2e.14.
Overactive bladder: frequency distribution of study population according to nationality n
Percentage
Taiwan
653
11.9
CONCLUSION
Thailand
904
16.4
The prevalence of urinary incontinence among Southeast Asian females appears comparable to worldwide figures. As such, it is a significant and common problem requiring attention. The incontinent female in Southeast Asia is most likely to be older, of higher parity, have delivered vaginally, does manual labor, earns less, has a positive family history for the disorder, uses a squatting toilet, and resides in a rural area. A significant portion of the incontinent population has been noted to seek help. This is most likely composed of the older age group and those who suffer from the condition to a greater degree.
India
649
11.8
Philippines
682
12.4
Malaysia
351
6.4
Pakistan
621
13.1
Hong Kong
416
7.6
Indonesia
257
4.7
South Korea
442
8.0
China
199
3.6
Singapore
228
3.6
7871
100.4
Total
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RESULTS A total of 5502 females were included in the study. The overall prevalence of OAB was 53.1%. The most common presenting symptom of OAB was urgency (65.4%), while frequency was present in 55.4%. Twenty-one percent of the OAB population presented with incontinence, giving a prevalence of 11.4% for urge incontinence among Asian females. Frequency of OAB with respect to nationality is shown in Table 2e.14. Frequency according to age is indicated in Table 2e.15. The distribution in the female population according to parity appears in Table 2e.16. Occupational factors are listed in Table 2e.17. Frequency of OAB occurring within various levels of educational attainment appear on Table 2e.18. Frequency distribution of the condition according to monthly income is listed in Table 2e.19. The relationship between OAB and place of residence appears on Table 2e.20. The distribution of the population with overactive bladder according to symptoms is presented on Table 2e.21. The frequency of overactive bladder according to the degree of bother reported appears on Table 2e.22. The majority (75.4%) were not significantly bothered by the condition. Frequency distribution of females with overactive bladder who sought help according to person consulted is indicated in Table 2e.23. Only 21.1% sought Table 2e.15.
Overactive bladder: frequency distribution of study population according to age n
Table 2e.17.
Overactive bladder: frequency distribution of survey population according to occupation n
Manual labor
630
11.5
2242
40.7
22 983
41.7
337
6.1
5502
100.0
Office work Others Unemployed Total
Table 2e.18.
Percentage
Overactive bladder: frequency distribution of survey population according to educational attainment n
Percentage
Never went to school
463
8.4
Primary school
706
12.8
Secondary school
1184
21.5
Pre-university
1069
19.4
University
1238
22.5
779
14.2
63
1.1
5502
99.9
Professional education Not indicated Total
Table 2e.19.
Percentage
Overactive bladder: frequency distribution of survey population according to monthly income n
Percentage
18–28
1501
27.3
29–39
1521
27.6
A
919
16.7
958
17.4
40–49
1159
21.1
B 100–199
50–59
754
13.7
C 200–399
857
15.6
60–69
368
6.7
D 400–599
549
10.0
≥70
176
3.2
E 500–799
23
0.4
F ≥800
5502
100.0
Not indicated Total
Not indicated Total
Table 2e.16.
Overactive bladder: frequency distribution of female population according to parity n
Table 2e.20.
Percentage
0
2005
36.4
1
738
13.4
2–4
2018
36.7
Urban
5–8
590
10.7
>8 Not indicated Total
697
12.7
1098
20.0
424
7.7
5502
100.1
Overactive bladder: frequency distribution of survey population according to place of residence n
Percentage
3770
68.5
Semi-urban
980
17.8
670
12.2
82
1.5
5502
100.0
114
2.1
Rural
37
0.7
Not indicated
5502
100.0
Total
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Table 2e.21.
Frequency distribution of population with overactive bladder according to symptoms present
Urgency alone Frequency alone Urge incontinence alone
Table 2e.23.
Frequency distribution of females with overactive bladder who sought help according to person consulted
n
Percentage
Person consulted
1098
37.6
754
25.8
Herbalist/traditional medical practitioner
58
2.0
General practitioner Primary healthcare center
n
Percentage
89
14.2
203
33.1
47
7.7
159.9
25.9
7
1.1
Urgency + frequency
444
15.2
Frequency + urge incontinence
197
6.7
Specialist
Urgency + urge incontinence
144
4.9
Nurse
Frequency + urgency + urge incontinence
226
7.7
Others/combination
94
15.3
Not specified
14
2.3
613
99.6
Total
Table 2e.22.
2921
99.9
Frequency distribution of population with overactive bladder according to degree of bother
Bother score
n
Percentage
0 – none
2204
75.4
1 – very mild
300
10.3
2 – mild
188
6.4
3 – moderate
97
3.3
4 – severe
61
2.1
5 – very severe Total
71
2.4
2921
99.9
help for their condition. Finally, demographic factors and their relationship with the occurrence of overactive bladder are shown in Table 2e.24. Using the chi-square test for independence, older age, multiparity, a positive family history, residence in rural areas, and the use of a sitting-type of commode were found to be associated with a greater occurrence of OAB.
CONCLUSION The study has shown that the problem of overactive bladder among females in Asia is significant and warrants closer attention.12 It has also highlighted the low treatment-seeking rate among those suffering from the condition.13 This is the first report on the epidemiology of overactive bladder among Asians.
ACKNOWLEDgEMENTS In this second study on overactive bladder, the following contributed to the epidemiologic survey and credit
Total
is hereby given accordingly: Y. Yong, S. Bo (China), M.F. Leung, T.F. Kwok (HK), H. Pathak, S. Nagasubramanyan, P.J. Urvashi (India), R. bin Sumardi, R. Yuwana (Indonesia), J.Y. Hong, J.G. Lee, H.Y. Kwon (Korea), R.M. Sahabudin, C.S. Loh (Malaysia), M. Sheikh, K. Waheed, S. Asif, K.J. Noorani (Pakistan), E.R. Gatchalian, D.T. Bolong (Philippines), P. Lim (Singapore), A.C. Wang, C.H. Huang, H.S. Chiang (Taiwan), P. Bunyaratavej, D. Watanachote, K.R. Olarn, A. Tantiwong (Thailand).
REFERENCES 1. Thomas TM, Plymat KR, Blannin J, Meade TW. Prevalence of urinary incontinence. Br Med J 1980;281:1243–5. 2. Jolleys JV. Reported prevalence of urinary incontinence in women in a general practice. Br Med J 1988;296:1300–2. 3. Vetter NJ, Jones DA, Victor CR. Urinary incontinence in the elderly at home. Lancet 1981;I:1275–7. 4. Molander U, Milsom I, Ekelund P, Mellstrom D. An epidemiological study of urinary incontinence and related urogenital symptoms in elderly women. Maturitas 1990;12:51–60. 5. Sommer P, Bauer T, Nielson KK et al. Voiding patterns and prevalence of women. A questionnaire survey. Br J Urol 1990;66:12–5. 6. Burgio KL, Matthews KA, Engel BT. Prevalence, incidence and correlates of urinary incontinence in healthy, middleaged women. J Urol 1991;146:1255–9. 7. Payne CK. Epidemiology, pathophysiology and evaluation of urinary incontinence and overactive bladder. Urology 1998;51(Suppl 2A):3–10. 8. Shershan S, Ansari RL. The frequency of urinary incontinence in Pakistani women. J Pak Med Assoc 1989;39:16–7. 9. Allen RE, Hosker GL, Smith ARB, Warrell DW. Pelvic floor damage and childbirth: a neurophysiological study. Br J Obstet Gynaecol 1990;97:770–9.
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Table 2e.24.
Demographic factors and their relation with the occurrence of overactive bladder Overactive bladder*
Factor
Yes
No
p-value
Odds ratio
95% confidence interval
<0.001
Age 18–28
727
742
1.275 (<40 vs. ≥40)
1.199–1.356
29–39
733
749
1.626 (<50 vs. ≥50)
1.468–1.803
40–49
610
522
1.877 (<60 vs. ≥60)
1.574–2.237
50–59
469
268
2.121 (<70 vs. ≥70)
1.525–2.950
60–69
247
117
>70
121
48
0
1019
928
1.539 (0–1 vs. >1)
1.467–1.616
1
376
350
1.161 (0–2 vs. >2)
1.086–1.241
2
528
470
1.182 (0–4 vs. >4)
1.072–1.302
3
330
245
4
228
163
5–8
347
238
>8
77
37
361
258
Office work
1143
1042
Others
1255
994
A
448
459
B
501
438
C
470
373
D
301
242
E
386
300
F
591
462
Parity <0.001
Occupation Manual labor
<0.001
1.063 (manual vs. non-manual) 1.002–1.1127
NS
NA
NA
<0.001
1.616
1.422–1.837
<0.001
1.322
1.178–1.484
1.236
1.115–1.370
Monthly income
Family history Yes
888
558
No
1479
1502
1934
1471
878
883
1938
1790
Semi-urban
547
409
Rural
400
245
Type of toilet used Sitting Squatting
(sitting vs. squatting)
Both Place of residence Urban
<0.001
(rural vs. non-rural)
* Counts may not total to 7871 because category ‘not indicated’ was not included in the analysis. NA, not applicable; NS, not significant.
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10. Snooks SJ, Swash M, Setchell M, Henry MM. Injury to innervation of pelvic floor sphincter musculature in childbirth. Lancet 1984;ii:546–50.
12. Lapitan MC, Chye PLH. The epidemiology of overactive bladder among females in Asia: A questionnaire survey. Int Urogynecol J 2001;12:226–31.
11. Eldabawi A, Yalla SV, Resnick NM. Structural basis of geriatric voiding dysfunction. III. Detrusor overactivity. J Urol 1993;150:1650–6.
13. Kobelt G, Kirchberger I, Malone-Lee J. Quality of life aspects of the overactive bladder and the effect of treatment with tolterodine. Br J Urol 1999;83:583–90.
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3 Quality of life and urinary incontinence Cornelius J Kelleher, Stephen Radley
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Introduction Impairment of quality of life is the inevitable consequence of lower urinary tract dysfunction and, from the patient’s perspective, forms both the basis upon which medical intervention is sought and upon which the success of treatment is measured. Urinary incontinence is a complex problem resulting from many different causes and for which many different approaches to treatment exist. It is also complex because of the different ways and varying severity with which it affects the lives of sufferers. Urinary symptoms affect different people in different ways and have a variable influence on their physical, psychological, social, domestic, and interpersonal lifestyles. These are modified by other factors, which include age, race and culture, personal goals and experience, interpersonal relationships, general physical and mental health, and life expectancy. Assessing the impact of urinary problems on the quality of life (QoL) of patients is therefore not straightforward, although it has been recognized by the International Continence Society, among other learned societies, as an essential outcome measure in both clinical trials and clinical practice. The severity of urinary incontinence and improvement after treatment has traditionally been measured in terms of improvement in urodynamic parameters, urinary diary variables and symptom scores. While these measures are of important clinical value, and the key to the diagnosis of the cause of urinary symptoms, they fail to measure how patients feel about their condition, how it affects their lives, and how their lives are improved by treatment. At the time of publication of the last edition of this textbook, the concept of QoL assessment of patients with urinary symptoms was in its relative infancy. It had been recognized that although validated generic QoL questionnaires (e.g. Short Form 36) were in existence, they were insensitive to the assessment of QoL impact among patients with urinary symptoms and therefore had little value in clinical trials of continence care or indeed in clinical practice. Condition-specific questionnaires had evolved to fill the void and many different condition-specific questionnaires, each of individual merit, were in circulation.1 Several questionnaires stood out from the rest and were widely adopted in clinical trials and clinical practice, and were translated into different language formats for inclusion in multinational clinical trials. The recommended questionnaires from this and the more recent triennial International Consultation on Incontinence are discussed later in this chapter.
Since that time, computer-generated questionnaires using a patient–computer interface have been developed, the interpretation of questionnaire scores has evolved with the concept of minimal important difference (MID) assessment, questionnaires have been modified to generate quality adjusted life year scores (QALYS) for health economic analysis, and – under the aegis of Professor Paul Abrams and the International Consultation on Incontinence (ICI) – a unifying format for questionnaires (ICIQ modular questionnaire), including the best of those currently available, has evolved. Each of these new concepts will be discussed later in this chapter. Of great importance in the development and widespread use of QoL assessment – or, as it is frequently now called, patient derived outcome measures (PDO) – has been the overactive bladder (OAB) syndrome. This subjectively defined symptom complex (described in detail in later chapters of this book) has proven an ideal condition for assessment by patient-derived subjective measures.2 Even greater impetus to the use of such measures was provided by a recent British Medical Journal editorial and paper which questioned the value of antimuscarinic treatment for unstable bladder conditions on the basis of statistically significant but questionably clinically significant symptom improvement reported in clinical trials.3 Clinicians treating OAB were suitably alarmed that the value of treatments which appear to them to improve the quality of life of patients with OAB was questioned, but understood that it was beholden on them to prove that these therapies did indeed work, and that patients felt and functioned better as a consequence. Many large scale short- and long-term multinational studies of antimuscarinic therapy for OAB have since reported favorable QoL outcomes for patients consistent with significant symptom improvements. The initial part of this chapter introduces the concept and value of QoL assessment for women with urinary incontinence, and explains how this is measured using a number of different validated QoL questionnaires.
What is Quality of Life? There is no consensus definition of quality of life, although it is linked to the World Health Organization (WHO) definition of health as being ‘not merely the absence of disease, but complete physical, mental, and social wellbeing’.4 It is a multidimensional concept, and has come to mean a combination of patient-assessed measures of health, including physical function, role function, social function, emotional or mental state, burden of symptoms, and sense of well-being.5
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How to measure Quality of Life Quality of life is usually measured with questionnaires completed by the patient or their carer, and although many different questionnaires are now available, each conforms to the same basic structure. The questionnaires consist of a variable number of domains (or sections), usually 1–7, which gather information focused on particular aspects of health and quality of life6 (Table 3.1).
Applications of Quality-of-life measures in Urogynecology Perhaps the most obvious use for standardized health measurement profiles is as outcome measures in clinical trials, where the quality of life of patients taking an active treatment can be shown to be superior to that of a placebo treatment.7,8 This approach is commonly used in the study of drug treatment of lower urinary tract dysfunction. Such approaches are also of value for the comparison of treatments with little apparent difference in objective clinical outcome, but where patient morbidity is reduced for one treatment compared to another, with obvious QoL benefits. An example would be the comparison of established and new surgical procedures for the correction of urodynamic stress incontinence.9 An additional value of QoL measures is their ability to determine the significance to patients of changes in objective clinical parameters which, although they may achieve statistical significance, may be clinically irrelevant. An example could be a change in nocturia from six to five voids per night which, while generating significant p values in clinical studies, may confer little if any QoL improvement to the patient. Another example may be the assessment of a new surgical procedure for the treatment of urodynamic stress incontinence (USI) whereby USI is cured but at the expense of voiding difficulties and detrusor overactivity and consequently poorer QoL.9 In addition to these obvious clinical applications, QoL assessment may prove to be important for health services research and the allocation of financial resources within an already overutilized and underfunded health Table 3.1. Dimensions of quality of life
• • • • • • •
Physical function (e.g. mobility, self care, exercise) Emotional function (e.g. depression, anxiety, worry) Social function (e.g. intimacy, social support, social contact, leisure activities) Role performance (e.g. work, housework, shopping) Pain Sleep/nausea Disease-specific symptoms
service. Although costs are difficult to calculate and are undoubtedly underestimated, research data in the United States have estimated the cost of continence care to be in excess of $16 billion.10 This can be expected to increase further with the present shift towards a larger elderly population. QoL assessment is of value in health economic evaluations as it is a desired outcome of all medical treatments and therefore an important measure of the success of all interventions. Calculating the value of QoL improvements following different medical treatments allows those which improve the lives of patients the most to be supported to a greater extent and the cost per unit QoL improvement to be maximized. In order for QoL instruments to be useful for costeffectiveness analysis, a single composite questionnaire score is required. Once the healthcare expenditure required to produce a certain level of improvement in QoL is known, this can be used to compare the effects of expenditure in other areas of continence care or be compared to other conditions. An example of this form of calculation would be the use of quality adjusted life years (QALY) which is a measure incorporating both QoL and survival obtained by multiplying life years by a weight reflecting the QoL of that year.10 The level of willingness to pay for a reduction in incontinence problems is another form of cost–utility analysis and may be an indication of both the physical and psychological burden of patients with urinary incontinence. Willingness-to-pay questionnaires ask women the amount they are willing to spend to achieve a specified improvement in their clinical condition. A study in Sweden has shown that the severity of symptoms of urge incontinence, expressed as frequency and leakage episodes, is correlated with patients’ quality of life, as well as the amount that they are willing to pay for a given percentage reduction in their symptoms.10 It is unclear whether this form of hypothetical analysis would be applicable in populations where healthcare is entirely free, and the costs of delivering health are rarely considered by patients. The ultimate aim for QoL assessment is the inclusion of short and meaningful questionnaires into routine clinical practice, but unfortunately as yet no single questionnaire is either short enough, or widely enough accepted to fulfill this role. Recent work has focused on the development of simple patient self-assessment tools which allow patients to assess the severity of their urinary symptoms and to determine, before seeking medical help, whether their symptoms bother them sufficiently and whether the symptoms would benefit from medical consultation. The Bladder Health Questionnaire (BHQ) is an example of 65
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such a questionnaire designed for the rapid screening of populations to determine the prevalence and impact of overactive bladder syndrome.11 A list of some of the potential applications for QoL questionnaires is shown in Table 3.2.
Predictors of quality-of-life impairment for incontinent women Urinary incontinence results in impairment in many aspects of the quality of life of sufferers, yet it is impossible to predict, on the basis of urinary symptoms and urodynamic diagnosis alone, the degree of this impairment. Little is known about the effect of age on the subjective severity of urinary incontinence. Gjorp and colleagues12 found that 72% of a sample of 79 elderly women with genitourinary symptoms felt them to be normal for elderly people. In addition, Norton et al. have shown that elderly women tend to present later for the assessment and treatment of urinary incontinence, although there is insufficient evidence to support the assumption that their urinary symptoms are less troublesome.13 It is possible that the earlier presentation of younger women reflects a greater knowledge about incontinence and its treatment, as neither symptom severity nor diagnosis affected presentation to the same degree. It is also possible that urinary incontinence may affect the young and old differently. For example, incontinence often results in sexual dysfunction and exercise restriction which may be more problematic for younger women.14,15 Although it would be expected that the duration of symptoms and severity of leakage are major predictors of QoL impairment, symptom duration and severity of urinary incontinence per se do not appear to correlate well with quality of life. At present it is unclear whether QoL deteriorates with a longer duration of urinary symptoms, as prospective studies are difficult to perform. This would, however, be particularly interesting to ascertain for women with detrusor overactivity where it has been shown that those with a poorer QoL are less likely to respond to conventional treatments.16 The reaTable 3.2. Applications of quality of life measures
• • • • • • •
Screening and monitoring for psychosocial problems in individual patient care Population surveys of perceived health problems Medical audit Outcome measures in health services or evaluation research Clinical trials Cost–utility analyses An adjunct to the clinical interview
son for this may be that urinary symptoms are of greater severity and therefore less likely to improve,17 although it would be important to determine if earlier intervention would prevent inevitable QoL deterioration and improve the chance of successful treatment. This would also encourage the wider availability of community continence clinics and improve the initial management of urinary symptoms in primary care. The urodynamic diagnosis appears to be a major factor predicting QoL impairment. It has been shown by a number of studies that women with detrusor overactivity have a greater QoL impairment than those with genuine stress incontinence.18,19 Wyman et al. attributed this to the fact that women with detrusor overactivity are less able to predict incontinent episodes, have more precipitating factors, more severe leakage, and therefore have less feeling of control over their bladder symptoms than those with urodynamic stress incontinence.20 In addition, interpersonal and sexual problems appear to be particularly common among urinary incontinent women, and are greater for women with detrusor overactivity than for those with urodynamic stress incontinence.21 Undoubtedly, targeting treatment towards women with greater QoL impairment and isolating particular problem areas in the management of urinary incontinence would be of great benefit to continence carers, and ultimately improve our treatment of incontinent women.
Relationship of quality of life with clinical measures On the whole, few and weak relationships have been found between the presence of urinary symptoms (including incontinence) and clinical measures such as urodynamics. Lower urinary tract symptoms are diagnostically disappointing and additional information from urodynamic evaluation is needed in order to make an accurate diagnosis and propose specific and effective therapies.22,23 Assessing the impact of urinary incontinence on the well-being of individuals can be accomplished using a symptom impact evaluation, or a QoL questionnaire which addresses symptom bother. Symptom impact questionnaires measure the degree to which a patient is bothered by the presence of a symptom, rather than measuring whether a symptom is present or absent. Such a system is used in several of the condition-specific QoL questionnaires designed for the assessment of urinary incontinent patients, such as the King’s Health Questionnaire.21 Comparing symptom impact and symptom presence is an important concept. In one study by Jolleys et al.,24
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the prevalence of symptoms did not correlate with their ‘degree of bothersomeness’. For example, while only 14% of patients had nocturia (more than one episode), 67% found it bothersome. In contrast, 78% of patients had terminal dribbling but only 19% found it bothersome. Individual patients’ views of bothersomeness vary significantly, and are modified by many different factors. The objective degree of symptom severity such as the number of pads worn or the amount of urine lost is therefore less important than an individual’s overall outlook on the problem. This is an important concept when assessing condition-specific questionnaires which address the impact of specific symptoms. If the impact of symptoms is to be used to compare individuals with different urinary problems, then a system of weighting the significance of the individual symptoms is essential in order to make any valid comparisons between different diagnostic groups. It would, for example, be difficult to compare the symptom impact for women with predominantly irritative bladder symptoms to that of women with predominantly stress symptoms when both are scored on the same scale. This is particularly important when questionnaires are used as outcome measures in clinical trials and the type of symptoms changes. In this context, the assessment of quality of life – or rather the impact of the presence of any symptoms on various aspects of the lifestyle of patients – allows for more meaningful and stable comparison both between patients and for the same patient before and after treatment.
Quality-of-life studies of Urinary Incontinent women A number of studies have attempted to measure the QoL of incontinent women. They vary in their design, methodology, the criteria used for the diagnosis of urinary incontinence, and (where stated) the definition of QoL and the means by which QoL is measured. Incontinence has, however, been shown to reduce social relationships and activities, impair emotional and psychological well-being, and impair sexual relationships. In addition, embarrassment and diminished selfesteem are common reactions to incontinent episodes.
Quality of life questionnaires Two major types of QoL questionnaire are available: generic and disease specific. Irrespective of their type, all questionnaires have been previously validated and reliability tested to ensure their psychometric value for the assessment of quality of life. Questionnaires which
have not been through this lengthy design process have unproven value and should not be used in clinical studies where QoL is a stated outcome measure.
Generic QoL questionnaires Generic questionnaires (e.g. Nottingham Health Profile,25 UK Short Form 36 (SF36) health status questionnaire,26 Sickness Impact Profile,27 Psychosocial Adjustment to Illness Scale28) are designed as general measures of QoL, applicable to a wide range of different populations and clinical conditions, and are not specific to a particular disease, treatment or age group. They allow comparisons to be made between different patient groups, and between patients with and without medical complaints. Extensive previous research using these questionnaires has provided comparative and normative data which are of value in QoL studies. Normative values are obtained from large population surveys of people without medical complaints, and the results are usually available in the instruction manuals provided with properly validated questionnaires. Normative data are stratified by age, social class, and sex. Many studies include a generic QoL questionnaire, either alone or in combination with a condition-specific measure. The most frequently used is the SF36 health status questionnaire which has been both extensively validated and used elsewhere in QoL studies of other medical complaints. This questionnaire is both sufficiently short to be used in conjunction with other measures, and has greater sensitivity to change than other short questionnaires such as the Nottingham Health Profile. Inevitably, one of the major reasons for choosing one questionnaire in preference to another is their popularity among other investigators and their use in previous similar studies. Hunskaar and Vinsnes used the Sickness Impact Profile (SIP) – a lengthy, validated 136-item questionnaire – to assess 70 women attending a self-referral center for incontinent patients.18 Women were divided on the basis of age into two groups (middle aged; 40–60 years, and elderly; over 70 years), and on the basis of symptom questionnaires into stress and urge symptom subgroups. Women were asked to respond to SIP items only if they considered them attributable to their bladder symptoms. Mean scores on the SIP were low for both groups, but the study concluded that the impact of urinary incontinence on QoL was both age and symptom dependent. Younger women scored significantly higher on the SIP as did women with urge symptoms. Sleep, rest, emotional behavior, mobility, social interaction, and recreational activities were most commonly affected. 67
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The study unfortunately lacked objective urodynamic assessment, the sample sizes were small, and no account was taken of the women’s age in the comparison of QoL scores. Similarly, the practice of encouraging women to respond to questionnaire items only if attributable to their urinary symptoms may introduce inaccuracies in both the scoring and interpretation of QoL measures. This is particularly problematic in an elderly population who may be unsure as to the cause of their QoL impairment, and which problems are attributable to urinary incontinence and which to other co-morbid conditions. Grimby et al.19 examined the Nottingham Health Profile scores from 120 elderly women (65–84 years) with urinary incontinence compared to 313 76-yearold women without urinary symptoms. Their data were obtained from a large population study of 6000 women living in the city of Göteborg in Sweden and the overall response rate to this parent study was 70.1%. Elderly women (>70 years of age) with subjectively reported urinary incontinence were subdivided into those with urge incontinence (48 women, 40%), stress incontinence (34 women, 28.3%) or both (38 women, 31.7%) on the basis of a pad test, urinary diary, a cough provocation test, and a clinical history, but without the benefit of urodynamic investigations. The mean age of the incontinent group was 75.4 years and that of the continent control group 76 years. Unfortunately, the total number of incontinent women in the parent study was not stated and the women included in this study were merely the first 120 women in whom incontinence could be demonstrated by either a pad or cough provocation test. No attempt was made to determine incontinence in the control group by similar tests and continence was assumed on the basis of their lack of admission to this symptom. Ideally, for a true control group, a cough provocation test and pad test should also have been performed on these women, and the number of women in the test and control groups matched. Using the Nottingham Health Profile, Grimby et al. showed a significantly higher level of both emotional impairment and social isolation among the incontinent women.19 They also showed a higher level of emotional disturbance among women with urge and mixed incontinence than among those with stress incontinence. Women with urge incontinence had significantly greater sleep disturbance than the control women. Sand et al.29 were among the first to use the SF36 health status questionnaire to assess the quality of life of urinary incontinent women in the context of a clinical trial. They assessed the efficacy of treatment for women with urodynamic stress incontinence entered into a prospective, randomized, double-blind, placebo-controlled
trial comparing the use of an active pelvic floor stimulator to a sham device: 35 women used the active device and 17 the sham device, the latter acting as controls. A significant benefit of the active device was demonstrated by both objective (pad testing, urinary diary, vaginal muscle strength) and subjective (urinary symptom questionnaire, severity of urinary incontinence visual analog scale) measures, although no significant improvement was seen in SF36 scores. It is highly likely that this result was attributable to the small number of women entered into the study, and that results would have been different had a disease-specific measure been used. The SF36 has been integrated into two large willingness-to-pay surveys in Sweden and in the United States of patients with urge and mixed incontinence.30,31 It has also been used in clinical studies comparing tolterodine with oxybutynin and placebo, both in the UK and the US.32,33 Scores at baseline were used to compare the QoL of patients with urinary symptoms to published normative values of an age- and sex-matched cohort of the normal population. In all of the studies, most of the domains of the questionnaire showed a poorer QoL among patients with urinary symptoms compared to those of the normal population. An analysis of the different age groups showed that the impact of symptoms is greater in younger patients although the data were not controlled for co-morbidity. Despite the fact that treatment intervention tended to improve QoL measured by the SF36, improvements were not found to be statistically significant, and reflect the limited sensitivity of generic questionnaires as a whole when used to assess patients with urinary symptoms. Unfortunately, generic questionnaires necessitate non-specific questioning, and scoring systems applicable to widely varying states of health, and therefore lack sensitivity when applied to women with non-life-threatening conditions such as urinary incontinence. This is particularly important in respect of their inability to detect clinically important improvement in QoL when incorporated into clinical trials of continence care. Disease-specific questionnaires aim to overcome this problem and are designed to assess, with greater complexity and accuracy, the impact of specific medical complaints. A number of different condition-specific questionnaires have been designed for the assessment of urinary incontinent women. Only questionnaires of published validity and reliability are discussed in this chapter.
Disease-specific quality of life assessment of urinary symptoms QoL is an important outcome in clinical trials of continence care, and the International Continence Society
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(ICS) has recommended that QoL measurements be included in all studies of urinary incontinence as a complement to clinical measures.34 In recognition of the limited sensitivity of generic questionnaires, a number of different condition-specific QoL questionnaires have been developed, or are at various stages of development. A list of selected condition-specific QoL questionnaires recommended by the last triennial report of the International Consultation on Incontinence is shown in Table 3.3. These questionnaires have been extensively reported on in the International Consultation of Incontinence triennial report where grading and recommendation for usage based on peer-reviewed published data have also been reviewed.1 Questionnaires are those recommended to assess symptoms and/or quality of life by the ICI committee. The questionnaires differ in several important respects. Some questionnaires – for example, the Bristol Female Lower Urinary Tract Symptoms (BFLUTS)35 – are essentially an assessment of the impact of urinary symptoms. In contrast to a traditional symptom scale, questions focus on the degree of bother caused to patients by a particular symptom, rather than whether the symptom is present, absent or of varying severity. Those questionnaires designed along the lines of a more traditional QoL questionnaire assess the impact of a patient’s urinary symptoms as a whole. This is achieved using questions focusing on the major domains of QoL but phrased specifically to apply to urinary incontinent patients and to avoid measuring QoL impairment attribTable 3.3. Recommended condition-specific questionnaires Questionnaires to assess symptoms 1. King’s Health Questionnaire (KHQ)21 2. Bristol Lower Urinary Tract Symptoms (BFLUTS)35 3. UDI-636 4. Urge – UDI37 5. Incontinence severity index38 6. Urogenital Distress Inventory (UDI)39 7. Symptom Severity Index (SSI)40 Questionnaires for QoL assessment 1. Men and women • King's Health Questionnaire (KHQ)21 • Quality of life in persons with urinary incontinence (I-QoL)41 2. Women only • Incontinence Impact Questionnaire (IIQ)42 • IIQ-736 • Urge – IIQ37 Copies of each of these questionnaires can be obtained from their authors upon request.
utable to other co-morbid conditions. Both types of questioning have their merits. Assessment of the bother of individual urinary symptoms identifies which symptoms are most problematic to patients, and how both the symptoms and their relative impact change as a result of treatment. What this fails to measure is the complex way in which the overall burden of symptoms impacts on various aspects and therefore quality of an individual’s life. One questionnaire – the King’s Health Questionnaire (KHQ)21 – uses both methods of assessment and has sections covering both aspects of questioning. The KHQ therefore is applicable to both men and women with lower urinary tract dysfunction, and consists of both a symptom bother and QoL impact questionnaire. The KHQ also has over 30 linguistic validations, making it ideal for multinational multicenter clinical trials. The majority of the linguistically validated versions of the KHQ can be obtained from www.Mapi.fr. The content of the KHQ is detailed in Table 3.4. The printed version of the questionnaire used in clinical studies and the scoring system can be obtained from the authors via
[email protected] or
[email protected]. The questionnaire takes approximately 10 minutes to complete and is used in many institutions as an adjunct to the clinical interview in addition to its role as a QoL assessment tool. The KHQ has been used widely for the assessment of men and women with lower urinary tract dysfunction and has been shown to be a sensitive measure to QoL improvement after the treatment of both overactive bladder and urodynamic stress incontinence.7–9,43–45 Malone Lee et al. used the SF36 and the KHQ to compare tolterodine and oxybutynin for the treatment of both men and women with detrusor instability. Although no significant improvement was seen in SF36 scores, significant improvements were seen in KHQ scores for both men and women using oxybutynin and tolterodine.46 For both treatments all domains other than personal relationships and general health perceptions improved significantly after 10 weeks of treatment with either medication. The ICIQ and ICIQ-SF There are many disease-specific QoL questionnaires to choose from but only a few which have the recommendation of the International Consultation on Incontinence. Ultimately, however, to make studies of continence care understandable by the wider scientific community, a few standardized and widely accepted measures of assessment are required. In order to achieve this goal, the modular ICIQ questionnaire was developed under 69
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Table 3.4. King’s Health Questionnaire PART I General health perception 1. How would you describe your health at present? Incontinence impact 2. How much do you think your bladder problem affects your life? PART II Role limitations 3a. To what extent does your bladder problem affect your household tasks (e.g. cleaning, shopping, etc.)? 3b. Does your bladder problem affect your job, or your normal daily activities outside the home? Physical limitations 4a. Does your bladder problem affect your physical activities (e.g. going for a walk, run, sport, gym, etc.)? 4b. Does your bladder problem affect your ability to travel? Social limitations 4c. Does your bladder problem restrict your social life? 4d. Does your bladder problem limit your ability to see/visit friends? Personal relationships 5a. Does your bladder problem affect your relationship with your partner? 5b. Does your bladder problem affect your sex life? 5c. Does your bladder problem affect your family life? Emotions 6a. Does your bladder problem make you feel depressed? 6b. Does your bladder problem make you feel anxious or nervous? 6c. Does your bladder problem make you feel bad about yourself? Sleep/energy 7a. Does your bladder problem affect your sleep? 7b. Do you feel worn out or tired? Severity measures Do you do any of the following; if so, how much? 8a. Wear pads to keep dry? 8b. Be careful how much fluid you drink? 8c. Change your underclothes when they get wet? 8d. Worry in case you smell? 8e. Get embarrassed because of your bladder problem? PART III We would like to know what your bladder problems are and how much they affect you. From the list below choose only those problems that you have at present. Leave out those that do not apply to you. • Frequency Going to the toilet very often • Nocturia Getting up at night to pass urine • Urgency A strong and difficult to control desire to pass urine • Urge incontinence Urinary leakage associated with a strong desire to pass urine • Stress incontinence Urinary leakage with physical activity, e.g. coughing, sneezing • Nocturnal enuresis Wetting the bed at night • Intercourse incontinence Urinary leakage with sexual intercourse • Frequent waterworks infections • Bladder pain • Difficulty passing urine • Other (Please specify)
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the aegis of Paul Abrams and the ICI Quality of Life Committee. The aim of this new questionnaire is to provide a set of modules to cover all of the major aspects of the assessment of incontinence and its impact on quality of life in detail. The modules incorporate the recommended questionnaires of the ICI and include an ICIQ-KHQ module for use among men and women with lower urinary tract dysfunction. The modules are linked by the ICIQ-SF which precedes the recommended questionnaire and which includes six basic questions relating to frequency of leakage, bothersomeness, protection use and type, perceived quantity of leakage (usually and at worst), and interference with daily life, social life and sex life. The questionnaire has now been published and has ICI recommendation for use in trials of continence care. The development and validation of the questionnaire is detailed in the last ICI consultation report as an appendix to Chapter 6.1 This is an important unifying step for advancement of QoL research in the area of lower urinary tract dysfunction.
Minimal important difference (MID) assessment of QoL questionnaire scores Ultimately, in all clinical studies which employ QoL assessment, it is important not only to establish whether there is statistically significant improvement in QoL following an intervention but also whether the improved QoL is sufficient to be both noticeable to the patient and of clinical relevance. MID assessment is a method of determining what degree of improvement in QoL score is clinically as well as statistically significant. The statistical methods employed are complex but a widely used method of calculating a MID score is known as the anchor-based approach. This uses an anchor, most commonly a global question measuring treatment effect and well-being, to compare with improvements in QoL domain scores and determine what improvement in QoL score is likely to be meaningful to the patient. The technique has been described in detail for the assessment of MID scores for the KHQ, and the expected scores for a meaningful small, moderate, and large improvement in QoL have been calculated.47 Using this method, it can be shown that the improvements in QoL as measured by the KHQ which are shown to be statistically significant following the treatment of OAB with tolterodine are also clinically meaningful to the patient. The technique provides an understanding of the magnitude of QoL improvement expected for patients attaining a small, medium, and large improvement in their urinary symptoms as a result of treatment. In essence, a five-point improvement in KHQ score rep-
resents a meaningful improvement at the patient level with respect to symptoms and clinical well-being.
Computerization of QoL assessment In order to evaluate QoL questionnaire scores, the responses to individual questions are entered into a computer database and the results analyzed using a statistical package. The evolution of computer technology, in particular the development of patient–computer interfaces, has allowed the direct completion of questionnaires by patients using a touchpad screen. Work has shown that electronic questionnaires which prompt patients to answer questions prior to proceeding to the next computer screen have lower levels of missing data without being unduly arduous for patients to complete.48 A purpose-designed computer-based questionnaire has been developed by Radley and Jones in Sheffield (UK) for the assessment of pelvic floor and urinary symptoms and QoL impact. The electronic pelvic floor symptoms assessment questionnaire (e-PAQ) appears to be easy and quick to complete and is used in routine clinical practice by the developers.49 It is likely that with further development of clinic computerization within the health service in the UK such questionnaires and patient assessment formats will become more widespread.
Simple global scoring systems In clinical practice, everybody measures some aspect of the QoL of their patients. Whether the patient is asked simply whether their problem affects them in an adverse way or whether they feel better as a consequence of treatment, some aspects of QoL have been measured. In busy clinical practice this is often felt to be enough, although in the clinical trial setting this would be considered unstructured, not reproducible, and a far too crude means of patient assessment. Increasingly, however, there is a demand for simple (albeit structured and validated) global assessment questionnaires measuring the patient’s perception of their condition, certain aspects of their condition (e.g. urgency), and the response of their condition to specific treatments. An example would be the perception of bladder condition questionnaire. This is a straightforward six-point questionnaire assessing the impact of the patient’s bladder symptoms and, although simple, this questionnaire is often used either in isolation or alongside more complex QoL assessment tools in clinical practice. The items of the questionnaire are outlined in Table 3.5. 71
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Table 3.5. Patient perception of bladder condition questionnaire50 Patients are asked to rate the severity of problems caused by their bladder problems on a six-point scale: 1. No problems 2. Very minor problems 3. Minor problems 4. Moderate problems 5. Severe problems 6. Many severe problems
The simplicity of scales such as these is the reason for their obvious appeal although they convey little information regarding the areas impacted by the bladder problems and no information regarding the general well-being of the patient which may be indirectly affected by the bladder problem or the treatment used to improve it. Recently, two further condition-specific global scales have been validated for use in lower urinary tract research.51 One (the Patient Global Impression of Severity, or PGI-S Scale) is a single-state severity rating scale, whereas the other (the Patient Global Impression of Improvement, or PGI-I Scale) is a transitional improvement rating scale. These two scales were modeled after scales that were described previously and used successfully in psychopharmacologic research.52 These scales are shown in Table 3.6. Although it is likely that the use of simple global rating scales will increase due their simplicity, it should be
Table 3.6. Condition-specific global scales for use in lower urinary tract research Patient Global Impression of Severity (PGI-S) Scale Check the one number that best describes how your urinary tract condition is now: 1. Normal 2. Mild 3. Moderate 4. Severe Patient Global Impression of Improvement (PGI-I) Scale Check the one number that best describes how your urinary tract condition is now, compared with how it was before you began taking medication in this study: 1. Very much better 2. Much better 3. A little better 4. No change 5. A little worse 6. Much worse 7. Very much worse
recommended that they be used alongside a validated QoL and symptom bother measure.
Conclusion There has been considerable advance in quality of life assessment since the previous edition of this textbook was published. QoL now forms one of the major important outcomes of continence care, and to the patient is perhaps the single most important outcome following treatment. There are now available several validated reliable questionnaires designed specifically to assess men and women with lower urinary tract dysfunction. These questionnaires have been shown to be of value in both clinical trials and clinical practice and may play a major future role in health economic assessment and resource allocation. Interpretation of improvements in QoL scores has created some confusion among researchers who have proven statistically significant improvement in questionnaire scores but questioned the clinical significance of such improvements. Advances in questionnaire score analysis, and particularly the introduction of minimal important difference analysis, allows us to understand when score improvements are indicative of meaningful improvement in clinical condition. The Short Form 36 has become the standard generic QoL questionnaire included in the majority of studies of urinary incontinence because of its credibility, established validity, reliability, and inevitably its general popularity. At present, the selection of a single conditionspecific questionnaire is not universally agreed, despite the obvious advantages this would confer. The ICI has recommended those questionnaires which appear to best measure the QoL of patients with lower urinary tract dysfunction and which have published peer review data to substantiate this claim. Many of these questionnaires are available in many different language formats, making them ideal for multinational clinical trials. As a unifying concept, the ICIQ and its modular format is attractive and incorporates those questionnaires such as the KHQ which are already in widespread use. Ultimately, there is a need for simplicity in clinical practice and a number of global assessment scales and patient self-assessment scales have been developed. These are likely to be increasingly used in clinical studies and clinical practice. In the future, much of the acquisition of data from patients may be computer based and this would also be applicable to QoL assessment. There are a number of advantages of such an approach, although at present it is not widely available in many clinical settings.
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Ultimately, QoL and other patient-derived outcome measures will play a pivotal role in the assessment of patients with lower urinary tract dysfunction. Without understanding the impairment caused by urinary problems and the improvement after treatment we cannot hope to meaningfully improve the lives of affected individuals.
REFERENCES 1. Donovan JL, Badia X, Corcos J et al. Symptom and quality of life assessment. In: Abrams P, Cardozo L, Khoury S, Wein A (eds) Incontinence. Proceedings of the Second International Consultation on Incontinence, Paris 2001. Amsterdam: Elsevier, 2001, 267–91. 2. Abrams P, Kelleher CJ, Kerr LA, Rogers RG. Overactive bladder significantly affects quality of life. Am J Managed Care 2000;6(11 Suppl):S580–90. 3. Herbison P, Hay-Smith J, Ellis G, Moore K. Effectiveness of anticholinergic drugs compared with placebo in the treatment of overactive bladder: systematic review. Br Med J 2003;326:841–4. 4. World Health Organization. Definition of health from preamble to the constitution of the WHO basic documents, 28th ed. Geneva: WHO, 1978, 1. 5. Coulter A. Measuring quality of life. In: Kinmonth AL, Jones R (eds) Critical Reading in General Practice. Oxford: Oxford University Press, 1993. 6. Streiner DL, Norman GR. Health measurement scales: a practical guide to their development and use. Oxford: Oxford Medical Publications, 1993. 7. Kelleher CJ, Cardozo L, Chapple CR, Haab F, Ridder AM. Improved quality of life in patients with overactive bladder treated with solifenacin. BJU Int 2005;95(1):81–5. 8. Kobelt G, Kirchberger I, Malone-Lee J. Quality of life aspects of the overactive bladder and the effect of treatment with tolterodine. Br J Urol 1999;83:583–90. 9. Bidmead J, Cardozo L, McLellan A, Khullar V, Kelleher C. A comparison of the objective and subjective outcomes of colposuspension for stress incontinence in women. BJOG 2001;108(4):408–13. 10. Kobelt G. Economic considerations and outcome measurement in urge incontinence. Urology 1997;50(6A):100–7. 11. Payne CK, Stewart W, Wein A, VanRooyen J. The bladder health questionnaire (BHQ): the first clinically validated screening tool for bladder health problems. Poster presentation, ICI, Paris 2001. 12. Gjorp T, Hendriksen C, Lund E, Stromgard E. Is growing old a disease? A study of the attitudes of elderly people to physical symptoms. J Chron Dis 1987;40(12):1095–8. 13. Norton PA, MacDonald LD, Sedgwick PM, Stanton SL. Distress and delay associated with urinary incon-
tinence, frequency and urgency in women. Br Med J 1988;297:1187–9. 14. Sutherst JR. Sexual dysfunction and urinary incontinence. Br J Obstet Gynaecol 1979;86:387–8. 15. Kelleher CJ, Cardozo LD. Sexual dysfunction and urinary incontinence. J Sexual Health 1994;3(7):186–91. 16. Moore KH, Hay DM, Imrie AH. Oxybutynin chloride (3 mg) in the treatment of women with idiopathic detrusor instability. Br J Urol 1990;66:479–85. 17. Moore KH, Richmond DH, Sutherst JR, Manasse P. Is severe wetness associated with severe madness in detrusor instability? Neurourol Urodyn 1992;11(4):460–1. 18. Hunskaar S, Vinsnes A. The quality of life in women with urinary incontinence as measured by the sickness impact profile. J Am Geriatr Soc 1991;39:378–82. 19. Grimby A, Milstrom I, Molander U, Wiklund I, Ekelund P. The influence of urinary incontinence on the quality of life of women. Age Ageing 1993;22:82–9. 20. Wyman JF, Harkins S, Choi S, Taylor J, Fantl JA. Psychosocial impact of urinary incontinence in women. Obstet Gynecol 1987;70:378–80. 21. Kelleher CJ, Cardozo LD, Khullar V, Salvatore S. A new questionnaire to assess the quality of life of urinary incontinent women. Br J Obstet Gynaecol 1997;104:1374–9. 22. Versi E, Cardozo L, Anand D, Cooper D. Symptoms analysis for the diagnosis of genuine stress incontinence. Br J Obstet Gynaecol 1991;98(8):815–9. 23. Bergman A, Bader K. Reliability of the patient’s history in the diagnosis of urinary incontinence. Int J Gynecol Obstet 1990;32:255–9. 24. Jolleys JV, Donovan JL, Nanchahal K, Peters TJ, Abrams P. Urinary symptoms in the community: how bothersome are they? Br J Urol 1994;74:551–5. 25. Hunt SM, McEwen J, McKenna SP. Measuring health status. A new tool for clinicians and epidemiologists. J R Coll Gen Pract 1985;35:185–8. 26. Jenkinson C, Coulter A, Wright L. Short Form 36 (SF-36) health survey questionnaire. Normative data for adults of working age. Br Med J 1993;306:1437–40. 27. Bergner M, Bobbitt R, Carter W, Gibson B. The sickness impact profile: development and final revision of a health status measure. Med Care 1981;19:787–805. 28. Derogatis LR, Derogatis MF. The Psychosocial Adjustment to Illness Scale (PAIS and PAIS SR). Administration, Scoring and Procedures Manual-II. Towson, MD: Clinical Psychometric Research, 1990. 29. Sand PK, Richardson DA, Staskin DR et al. Pelvic floor stimulation in the treatment of genuine stress incontinence: a multicentre placebo controlled trial. Neurourol Urodyn 1994:13:356–7. 30. Johannesson M, O’Connor RM, Kobelt G, Mattiason A. Willingness to pay for reduced incontinence symptoms. Br J Urol 1997;80:557–62.
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31. O’Connor RM, Johannesson M, Hass S, Kobelt G. Urge incontinence: quality of life and patients’ valuation of symptom reduction. Pharmacoeconomics 1998;14:153–9.
42. Wyman JF, Harkins SW, Taylor JR, Fantl AJ. Psychosocial impact of urinary incontinence in women. Obstet Gynecol 1987;70(3):378–81.
32. Malone-Lee JG, Eriksson M, Olofsson S, Lidberg M. UK/Eire Tolterodine versus Oxybutynin Study Group. The comparative tolerability and efficacy of tolterodine 2 mg bd versus oxybutynin 2.5/5 mg bd in the treatment of the overactive bladder. Proceedings of the ICS 1998;220:163–4.
43. Reese PR, Pleil AM, Okano GJ, Kelleher CJ. Multinational study of the reliability and validity of the KHQ in patients with overactive bladder. Qual Life Res 2003;12(4):427–42.
33. Appell RA. Clinical efficacy and safety of tolterodine in the treatment of overactive bladder. A pooled analysis. Urology 1997;50:90–6.
44. Kelleher CJ, Kreder KJ, Pleil AM, Burgess SM, Reese PR. Long term health related quality of life of patients receiving extended release tolterodine for overactive bladder. Am J Managed Care 2002;8(19 Suppl):S616–30.
34. Blaivas JG, Appell RA, Fantl JA et al. Standards of efficacy for evaluation of treatment outcomes in urinary incontinence: recommendations of the Urodynamic Society. Neurourol Urodyn 1997;6:145–7.
45. Kelleher CJ, Reese PR, Pleil AM, Okano GJ. Health related quality of life of patients receiving extended release tolterodine for overactive bladder. Am J Managed Care 2002;8(19 Suppl):S608–15.
35. Jackson S, Donovan J, Brookes S, Eckford S, Swithinbank L, Abrams P. The Bristol Female Lower Urinary Tract Symptoms questionnaire: development and psychometric testing. Br J Urol 1996;7:805–12. 36. Uebersax JS, Wyman JF, Shumaker SA, McClish DK, Fantl AL. Short forms to assess life quality and symptom distress for urinary incontinence in women. The Incontinence Impact Questionnaire and the Urogenital Distress Inventory. Neurourol Urodyn 1995;14:131–9. 37. Lubeck DP, Prebil LA, Peebles P, Brown JS. A health related quality of life measure for use in patients with urge urinary incontinence: a validation study. Qual Life Res 1999;1999:337–44. 38. Sandvik H, Hunskaar S, Seim A, Hermstad R, Vanvik A, Bratt H. Validation of a severity index in female urinary incontinence and its implementation in an epidemiological survey. J Epidemiol Comm Health Med 1993;47:497–9. 39. Shumaker SA, Wyman JF, Uerbersax JS, McClish D, Fantl JA. Health related quality of life measures for women with urinary incontinence. The Urogenital Distress Inventory and the Incontinence Impact Questionnaire. Qual Life Res 1994;3:291–306. 40. Black N, Griffiths J, Pope C. Development of a symptom severity index and a symptom impact index for stress incontinence in women. Neurourol Urodyn 1996;15:630–40. 41. Wagner TH, Patrick DL, Bavendam TG, Martin ML, Buesching DP. Quality of life in persons with urinary incontinence: development of a new measure. Urology 1996;47(1):67–72.
46. Malone-Lee JG, Eriksson M, Olofsson S, Lidberg M. UK/Eire Tolterodine versus Oxybutynin Study Group. The comparative tolerability and efficacy of tolterodine 2 mg bd versus oxybutynin 2.5/5 mg bd in the treatment of the overactive bladder. Proceedings of the ICS 1998;220:163–4. 47. Kelleher CJ, Pleil AM, Reese PR, Burgess SM, Brodish PH. How much is enough and who says so. The case of the King’s Health Questionnaire and overactive bladder. Br J Obstet Gynaecol 2004;111:605–12. 48. Velikova G, Wright EP, Smith AB et al. Automated collection of quality of life data: a comparison of paper and computer touch screen questionnaires. J Clin Oncol 1999;17:998–1007. 49. Radley SC, Jones GL. Measuring quality of life in urogynaecology. BJOG 2004;111(Suppl 1):33–6. 50. Freeman R, Hill S, Millard R, Slack M, Sutherst J. Reduced perception of urgency in treatment of overactive bladder with extended release tolterodine. Obstet Gynecol 2003;102(3):605–11. 51. Yalcin I, Bump RC. Validation of two global impression questionnaires for incontinence. Am J Obstet Gynecol 2003;189:98–101. 52. Guy W. ECDEU assessment manual for psychopharmacology. Rockville, MD: National Institute of Mental Health, US Department of Health, Education, and Welfare, 1976, 218–22.
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4 Tackling the stigma of incontinence – promoting continence worldwide David Fonda, Diane K Newman
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introduction It is estimated that a quarter of a billion people worldwide suffer from urinary incontinence (UI) of varying degrees. This is an underreported condition that has a profound impact on the life and well-being of the individual sufferer as well as their families.1–3 There has been extensive research documenting the success of various forms of conservative, pharmacologic, and surgical treatment but reality is that less than 50% of persons with UI seek help.3,4 Many more, especially in less developed countries, do not have help available. The psychological consequences of incontinence are well documented and include stigma, shame, embarrassment, isolation, and depression. This is besides the physical and economic consequences of being incontinent. One method to promote understanding about the problem of incontinence is through public awareness.
the basis of stigma It is possible to understand the longstanding stigma surrounding incontinence by considering the potential health consequence of incontinence on society. We can find references as far back as biblical times that reflect a prevailing societal need: If there be among you any man, that is not clean by reason of that which chanceth him by night, then shall he go abroad out of the camp, he shall not come within the camp…Thou shalt have a place also outwith the camp, whither thou shalt go abroad: and thou shalt have a shovel among thy weapons; and it shall be, when thou sittest down abroad thou shall dig therewith, and shalt turn back and cover that which cometh from thee: for the Lord thy God walketh in the midst of thy camp…therefore shall thy camp be holy; that he see no unclean thing in thee, and turn away from thee. Deuteronomy 23, verses 10–14.
While this probably did not reflect stigma in its true sense, presumably it represented the need to protect the community from being surrounded by excrement. Throughout the entire evolution of mankind, and in fact the entire animal world, living beings make all reasonable efforts to distance themselves from their excrement. It is not surprising therefore that negative attitudes, and ultimately stigma, evolve around people who are unable to achieve this most basic process. The word stigma has been defined in different ways. In the Collins Dictionary it is referred to as ‘…distinguishing mark of social disgrace...’ while Mosby’s Medical Dictionary defines it as ‘a moral or physical blemish that serves to identify a disease or condition’. The key feature
associated with stigma is that often the stigmatized person and society represent extreme positions of the condition. Ignorance and lack of tolerance by and of others is common, leading frequently to anger and withdrawal. Whether the condition is visible or apparent to others (e.g. disfigurement) or concealed (e.g. colostomy or incontinence) does not change the way the person with the condition feels or reacts. The stigma associated with incontinence is similar to the stigma in other conditions and is associated with public ignorance and lack of awareness. The ‘stigma’ surrounding bladder and bowel control problems, and the fact that people have many misconceptions about these conditions, prevents patients from seeking care.5 The traditional medical model of care is very much focused at ‘treatment’ but is not empowering to the sufferer to actually develop strategies to cope with what is often a lifelong condition. The way people react to a person with incontinence is influenced by many factors. The further the person is connected from the sufferer, the more negative attitudes become, as shown in Figure 4.1. As the condition becomes more severe, the more obvious it becomes to others, and often, therefore, the more the person is likely to be stigmatized.6 In addition, attitudes and reactions of both the person with incontinence and those in society who interact with that person may vary according to the age of the person. At the extreme is the newborn child, where incontinence is regarded as a norm, through to childhood bedwetting, all the way to a frail old person in a nursing home. Depending on the age, sex, and social situation of the person, the reaction may well be different. Table 4.1 shows some of the factors that will modify response and attitude to incontinence.
More negative Sufferer
Figure 4.1. table 4.1.
• • • • •
Family
Carers
Friends
Culture Society
Attitudes through society. Modifiers of attitude and response
Condition Socioeconomic Severity Culture Religion
• • • • •
Sex Age Ignorance Prejudice Education
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We also see a common phenomenon in that conditions which have greater stigma (and often are less life threatening) tend to take a much longer time to be declared to the doctor and even longer to family, friends and others. Figure 4.2 illustrates this schematically. Breast cancer is a good example where now it is common for a woman to go immediately to a doctor when she identifies a breast lump and to share this finding with family and friends even before the diagnosis is confirmed. Cancer in the past was very much a taboo subject but in the past 10 years we have more public figures coming forward with their health-related issues to give greater insight into cancers such as prostate, colon, etc. While infertility in the past was regarded with shame by the infertile couple, people now know when friends or acquaintances are on an in vitro fertilization (IVF) program. Mental health conditions (particularly depression), HIV and the AIDS epidemic are gaining more and more acknowledgement in society. Public figures are stepping forward and putting their face and name to such conditions. It is important to understand how attitudes and stigma changed for these conditions. An important component is breaking the cycle of public and personal ignorance through education and public awareness programs.2,3 For this to be successful, there needs to be a partnership between healthcare professionals, governments, and industry groups with a vested interest to work together to break the cycle of ignorance and negative attitude.2 Central to this is the availability of funds, either in allocated dollars or ‘in kind’ (e.g. access to advertisements), that represents an ongoing funding source. In the sections below we see examples of how this process is being tackled locally and internationally in order to raise awareness of incontinence, bring a greater opportunity to help, and improve the plight of hundreds of millions of people around the world.
Onset of condition
Disclosure to doctor family/friend
B
D
Breast lump Depression
Tonsillitis
Alzheimer’s
Epilepsy
HIV
A,H
I
Incontinence
Figure 4.2. Response time to an illness. D, Diabetes; A, Alzheimer’s; H, Hypertension; B, Breast Cancer; I, Incontinence.
results of a survey of national organizations The Continence Promotion, Prevention, Education and Organization (CPPEO) committee of the International Consultation on Incontinence (ICI) published the results of a 2003 survey from 24 organizations in 19 countries (67.7% response rate).7 Some of the aims of the survey were to determine organization funding sources, membership specifics, and programs developed and executed on continence promotion. The survey indicated that more than 50% of these organizations have been in existence for more than 10 years and that membership includes both professionals and the public. The results demonstrated that those organizations which have been in existence for more than 10 years are very active in educating both consumers and even professionals (principally primary care physicians) about incontinence. These organizations have oversight from advisory boards consisting of consumers (lay public) and healthcare professional members. In addition to consumer advocacy, organizations have developed medical guidelines for continence care which represent solo efforts by the organization or in collaboration with the medical community and the government. The survey ascertained that funding is an ongoing challenge for most of these organizations. Very few receive government funds, and most rely on support from industry or manufacturers of drugs and products for specific projects developed for consumers. These organizations are promoting continence awareness generally to a public that has ‘very little’ to ‘no understanding’ of incontinence. Attempts are made to publicize the magnitude of the problem of incontinence, but the media (e.g. print, television) is an obstacle, as most journalists and the media in general are uncomfortable or not interested in the subject matter. In many cultures, one of the best vehicles to reaching the public is through an informed journalist. Journalists often use a ‘media hook’ – an interesting story that will take priority over other news on the television, radio or newspaper. Having a spokesperson with the problem or finding a celebrity who is willing to speak for the cause can help.5 These individuals can act as ‘influence leaders’. Organizations have identified education about incontinence as the most important method to decrease the perceived stigma associated with the disease. A successful method to educate has been through public awareness campaigns, health promotion projects, or health fairs. Examples of the programs are found in Table 4.2. However, these outreach programs have not been evaluated to determine the effectiveness of their messages. 77
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Another source of information is provided on the internet through websites developed by each organization. These websites provide useful information on incontinence, what it is, and how it can be managed, treated, and cured. They provide frequently asked questions (FAQs) as well as useful links to other continencerelated websites. A needed service that has been identified by several organizations concerns the management or containment of urine leakage through the use of products and devices. A guide to continence products has been developed by many organizations and is available to the members as well as healthcare professionals. This is aimed at providing useful information about the range of different products available. Another service available through several of these organizations was a ‘directory’ of healthcare professionals who have expertise in the area of incontinence and its management. Certain organizations have this directory available through their website.
the role of national organizations Continence promotion involves informing and educating the public that incontinence is not inevitable or shameful, but is treatable or at least manageable.8 In the past 15 years, national organizations have been formed under various auspices to tackle issues to do with incontinence awareness, education, and promotion. Table 4.3 provides a list of countries that have national organizations, the organization’s name and table 4.2.
• • • • • • • • • • • • • • • • • •
Examples of national continence organizations’ initiatives
Australia – Helpline promotion Belgium – GP and incontinence Canada – Incontinence awareness month Hong Kong – Continence promotion Indonesia – GP seminars India – Public awareness exhibition Japan – Let’s talk and think about continence Korea – Incontinence awareness campaign New Zealand – National bladder awareness week Poland – National billboard campaign Singapore – Women’s health issues and healthy aging Taiwan – A dry and comfortable spring UK, Continence Foundation – Continence awareness week UK, ERIC – Bed-wetting awareness in schools UK, Incontact – Healthy bladder campaign USA, IFFGD – Irritable Bowel Syndrome (IBS) awareness month USA, NAFC – Women’s forum on lifelong bladder health USA, SFC – Stigma in healthcare
websites or contact details. While each organization is unique in its mandate, what they have in common is their commitment to improve the situation for persons with incontinence. Continence promotion is a most challenging endeavor. Although the ratio between affected patient populations and continence national organization funding has not been formally studied, anecdotal information suggests that continence promotion is among the most difficult of medical problems for which to obtain funding. In view of all these challenges, the proliferation of new national continence organizations, especially in Asia, is a validation of both the need for continence promotion and the dedication of those who have recognized and are addressing this need. National organizations which promote continence are as diverse as the cultures they serve. They represent a wide diversity of models, including consumer-led, company sponsored, professionals only, and organizations which have deliberately set about trying to bring together all relevant stakeholders in a relatively democratic model.7 In every part of the world these organizations play a dynamic role in building both public and professional awareness of this underserved and underreported condition. Most continence organizations are poorly capitalized, being either under- or unfunded (i.e. run by volunteers) and are held together initially by either a dedicated patient advocate or an energized healthcare professional. In most cases this professional is a urologist or nurse whose patient population includes persons with UI. However, despite this limitation, these organizations often provide their country with the first wake-up call that incontinence is common.
continence foundation of australia – model for partnerships An organization that is well funded typically has strong support from the government. The National Foundation for Continence in the US has attempted to create a coalition with government health agencies and consumer-based foundations to further common goals.9 The Continence Foundation (UK) has also been successful in partnering with government for funding, as well as guideline development and consumer awareness. However, the most successful organization appears to be the Continence Foundation of Australia (CFA), a non-profit organization established in 1989 which has lobbied and worked very closely with the Australian Government. In 1998 the Government funded a 4-year, $15 million AUD National Continence Management Strategy (NCMS).10 Following its success, a further $16
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table 4.3.
• • • • • • • • • • • • • • • • • • • • • • • • • • • • • •
National continence organizations
Australia – Continence Foundation of Australia Ltd: www.continence.org.au Austria – Medizinischen Kontinenzgesellschaft Österreich: www.inkontinenz.at Belgium – U-Control vzw (Belgian Association for Incontinence): www.sosincontinence.org Brazil – Brazilian Foundation for Continence Promotion:
[email protected] Canada – The Canadian Continence Foundation: www.continence-fdn.ca China – Hong Kong Continence Society:
[email protected] Colombia – Instituto de Urologia Especializada: www.urologiacali.com Denmark –
[email protected] France – Femmes pour toujours: www.femsante.com Germany – Gsellschaft fur Inkontinenzhilfe e.V. (GIH): www.gih.de Hungary – Inko Forum: www.inkoforum.hu India – Indian Continence Foundation: www.indiancontinencefoundation.org Indonesia – Indonesian Continence Society:
[email protected] Israel – National Center for Continence:
[email protected] Italy – Fondazione Italiana Continenza (The Italian Continence Foundation): www.continenza-italia.org; Associazione Italiana Donne Medico (AIDM): www.donnemedico.org; The Federazione Italiana Incontinenti (FINCO):
[email protected] Japan – Japan Continence Action Society: www.jcas.or.jp Korea – Korea Continence Foundation:
[email protected] Malaysia – Continence Foundation:
[email protected] Netherlands – Pelvic Floor Netherlands: www.pelvicfloor.nl; Pelvic Floor Patients Foundation (SBP): www.bekkenbodem.net; Vereniging Nederlandse Incontinentie, Verpleegkundigen (VNIV): www.vniv.nl New Zealand – New Zealand Continence Association: www.continence.org.nz Norway – NORFUS (Norwegian Society for Patients with Urologic Diseases
[email protected] Philippines – Continence Foundation of the Philippines:
[email protected] Poland – NTM (INCO) Forum (The Polish Continence Organization): www.ntm.pl Singapore – Society for Continence: www.sfcs.org.sg Spain – Associacion Nacional de Ostomizados e Incontinentes (ANOI): www.coalicion.org Sweden – Swedish Urotherapists:
[email protected]; Sinoba: www.sinoba.se Taiwan – Taiwan Continence Society: www.tcs.org.tw Thailand –
[email protected] United Kingdom – Association For Continence Advice (ACA): www.aca.uk.com; The Continence Foundation, UK: www.continence-foundation.org.uk; Incontact: www.incontact.org; Enuresis Resource and Information Centre (ERIC): www.eric.org.uk United States – American Urological Association Foundation, Inc: www.afud.org; International Foundation for Functional Gastrointestinal Disorders: www.aboutincontinence.org; National Association For Continence: www.nafc.org; Simon Foundation for Continence: www.simonfoundation.org
million AUD over 3 years was provided. The CFA website can be accessed at www.continence.health.gov.au. The NCMS initiatives have been extensive and farreaching. A free telephone helpline is staffed by experienced continence nurse advisers. A common complaint by patients with overactive bladder is ‘toilet mapping’. The NCMS addressed this complaint through the Public Toilet Map, a popular initiative that identifies public toilet facilities in Australian towns and cities on 21 major travel routes. It provides information on the opening hours of toilets and access for people with disability. Developed to assist people with incontinence to travel more confidently, it is accessible to the public through the internet (www.toiletmap.gov.au). Currently over 13,000 public toilets throughout Australia have been identified. The NCMS is committed to providing UI information to all Australians despite cultural and language barriers. Because Australia is made up of people of many culturally
diverse backgrounds, it is difficult for people to access linguistically and culturally appropriate services. It is further complicated by various cultural backgrounds that make seeking help by itself difficult. In recognition of the indigenous Aboriginal and Torres Strait Island people, the NCMS has funded a series of projects to develop culturally and linguistically sensitive material for these various groups. The NCMS has produced 14 different pamphlets that have been produced in 15 different languages. These pamphlets can be downloaded from the website and printed out for ready distribution. This seems to be a great contribution to people worldwide. At the outset it was recognized that, with such a diverse range of projects that are likely to be funded, it would be difficult to evaluate the effectiveness of these individual projects as well as the strategy overall. An independent evaluator was therefore appointed by the Australian Government, their role being to provide advice and 79
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guidance to projects to ensure consistency and quality in evaluation for all funded projects.
the role of the international continence society (ics) Professionals (e.g. urologists, urogynecologists, nurses, physiotherapists, continence advisers) and professional organizations have been instrumental in promoting awareness of continence. The International Continence Society (ICS) established the Continence Promotion Committee (CPC) to promote awareness through its members, as well as to provide a forum to support the formation of individual consumer-based organizations in interested countries. The CPC has a multinational, multidisciplinary representation which aims to identify broad issues through this international forum that can facilitate translation at a local national level. The website for the CPC, established in 1997, can be found at www.continenceworldwide.org.9,11 In 1998, the CPC became an official committee of the ICS. The principal aims of the CPC are to:
• look at opportunities for networking across various countries;
• increase awareness amongst ICS members of • • •
continence-related issues; facilitate development of continence organizations; facilitate interchange of information about continence awareness and promotion; identify opportunities for continence promotion strategies.
A visit to the CPC website will provide details of the CPC, its relationship to the ICS, and its committee membership, as well as copies of its various activities including its annual newsletter Continence Worldwide. Each year at the ICS, the CPC has held workshops around various themes that have a broad national focus such as prevention, general practitioner education, and promotional strategies. Its relevance, as is the case with each of the national organizations, is to recognize the interface between continence management and continence awareness and promotion. The role of national organizations is even more relevant because of the underreporting of this problem.
of healthcare professionals, governments, and industry. This process must continue in order for incontinence to be removed from the list of conditions with stigma so that people can and will seek help. Continence awareness is growing worldwide. The ICI CPPEO committee recommended the formation of a worldwide resource center, preferably through the ICS. The center should update educational materials and verify best practice experiences or activities while ensuring efficient sharing and optimum use of resources for promoting continence, especially for countries with fewer resources. Continence organizations should have the outcomes and cost-effectiveness of their consumerbased UI awareness programs and activities independently evaluated.
references 1. Fonda D. Leading article: Taking the ‘in’ out of incontinence. Med J Aust 1990;153;245–7. 2. Fonda D. Promoting continence as a health issue. Eur Urol 1997;32:28–32. 3. Fonda D, Ouslander J, Norton C. Continence across the continents. J Am Geriatr Soc 1994;42:109–12. 4. Kinchen KS, Burgio K, Diokno A et al. Factors associated with women’s decisions to seek treatment for urinary incontinence. J Women’s Health 2003;12:687–98. 5. Garcia JA, Crocker J, Wyman JF. Breaking the cycle of stigmatization. J Wound Ostomy Continence Nurs 2005;32(1):38–52. 6. Norton NJ. The perspective of the patient. Gastroenterology 2004;126(Suppl 1):S175–9. 7. Newman DK, Denis L, Gruenwald I et al. Continence promotion: prevention, education and organisation. In: Abrams P, Cardozo L, Khoury S, Wein A (eds). Incontinence. Proceedings from the Third International Consultation on Incontinence. Plymouth, MA: Health Publication, 2005. 8. Newman DK, Denis L, Gartley CB et al. Promotion, education and organization for continence care. In: Abrams P, Cardozo L, Khoury S, Wein A (eds) Incontinence. Proceedings from the Second International Consultation on Incontinence. Plymouth, MA: Health Publication, 2002, 937–64. 9. Mueller N. What the future holds for continence care. Urol Nurs 2004;24(3):181–6.
recommendations
10. National Continence Management Strategy, Australian Government. Personal communication, Kerry Markoulli, 2004. Online. Available: www.continence.health.gov.au.
Around the world, there has been an increase in promoting awareness of incontinence through partnerships
11. Lim PHC, Fonda D. The CONTInet of the International Continence Society. Neurourol Urodyn 1997;16:609–16.
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5a The roles of the continence nurse specialist Ellie Stewart
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INTRODUCTION Urinary incontinence (UI) is a devastating condition that affects between 2.5 and 4 million people in the UK.1 There have been many studies, using various methodologies, to estimate the prevalence of urinary incontinence in different populations. Currently the best information suggests that the prevalence is: For people living at home:
• between 1 in 20 and 1 in 14 women aged 15–44 • • • •
years; between 1 in 13 and 1 in 7 women aged 45–64 years; between 1 in 10 and 1 in 5 women aged 65 years and over; over 1 in 33 men aged 15–64 years; between 1 in 14 and 1 in 10 men aged 65 years and over. For people living in institutions:
• 1 in 3 in residential homes; • nearly 2 in every 3 in nursing homes.2 In 1998 the estimated cost of caring for incontinent patients in the NHS in the UK was £423,467,000 annually. This equates to roughly 0.85% or 1/20th of the total budget of the NHS.3 Nazarko estimated the cost of nursing time, laundry, and incontinence pads for an incontinent individual in a nursing home to be £15 a day or £105 a week.4 Very few people with continence problems will seek help and when they do it is often far down the line when the problem is much harder to treat. This may be related to feelings of embarrassment or shame, or to a belief that the condition is hopeless and occurs naturally with aging.5 The impact of incontinence on a patient’s quality of life can be huge. It can:
nence is inevitable and irreversible. This perception is held by most health workers as well as patients and the general public. As a result, many individuals turn to the use of products such as absorbent pads and supportive aids without having the condition properly diagnosed or treated.7 Over the past few years the nursing profession has come to the forefront as one of the primary healthcare providers for people with UI. Continence advisors, district nurses, nurse specialists in urology and gynecology, and physiotherapists are now widely involved in the diagnosis, treatment, and management of incontinence.
The ROle Of The CONTINeNCe NURse The post of nurse specialist for continence care or continence advisor began in the 1980s in the United Kingdom.8 It evolved more in relation to the source of funding rather than the needs of the local population. There was soon a need for the principal functions of the continence advisor to be identified. The Royal College of Nursing Continence Forum identified these functions as:
• self-education and educating other professionals (Figure 5a.1);
• providing a quality comprehensive continence advisory service;
• meeting the needs of the consumer; • having knowledge of research evidence and applying it to continence care.9
• lead to bullying at school, and to emotional and behavioral problems in childhood;
• restrict employment, education, and leisure • •
activities; lead to social exclusion and embarrassment; often result, in the case of the elderly, in admission to nursing and residential homes.
A study examining reasons for institutionalization found that 44% of family members reported that UI was a significant factor in placing a relative in long-term care.6 One of the greatest obstacles to effective management of incontinence is the perception that inconti-
Figure 5a.1. There is considerable literature available for incontinence sufferers.
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Assessment All patients presenting with incontinence should be offered an initial assessment by a suitably trained individual – this could be by a practice nurse, district nurse or ward nurse who has had basic training in continence assessment. This assessment should be in addition to the usual general patient assessment in respect of mobility, mental health, and underlying conditions. The key components of an initial nursing assessment are shown in Table 5a.1. Once the initial assessment is completed, it may be necessary for the advanced practitioner – continence advisor, nurse specialist or physiotherapist – to augment the assessment. An advanced practitioner would be expected to add extra competencies to ensure a thorough assessment had been undertaken (Table 5a.2). Not all patients need to undergo these further investigations. As well as advanced assessment skills, it is vital for the continence nurse to have the following aptitudes:
• • • • • •
Compassion; Diplomacy; Accountability; Competency; Empathy; Assertiveness.
It may have taken the patient a long time to present with their symptoms, so a sympathetic practitioner who is able to empathize with the patient will be more likely to get the required results. A number of recent publications have helped to bring the management of incontinence to the fore in all specialties in the NHS; for example:
• Good Practice in Continence Services (2000);2 • Essence of Care: Patient Focused Benchmarks for Clinical • •
Governance (2003);10 Essence of Care: Benchmarks for Continence and Bladder and Bowel Care (2003);11 National Service Framework for older people (2001).12
Types Of URINARy INCONTINeNCe stress urinary incontinence Stress urinary incontinence (SUI) is the most common cause of incontinence in women.13 It is defined as the involuntary loss of urine when the intravesical pressure
Table 5a.1.
Initial nursing assessment
Obtain a focused health history to include: 1. The presence of risk factors for urinary incontinence (UI) and the medical conditions that may be contributing to UI, i.e. parity, weight, menopause, smoking, obesity 2. Confirming the presence of UI 3. A detailed exploration of the symptoms including symptoms of leakage, frequency, urgency, nocturia, and voiding difficulties/retention 4. Medication review including non-prescription drugs as these can also affect control of urine 5. Bowel pattern 6. Functional, environmental, social, and cognitive factors that may contribute to or result in UI Obtain an intake and output chart that includes: 1. Voiding records over a period of 24 hours, recording episodes of leakage, urgency, and amount voided 2. An intake record with 24-hour pattern of fluid intake including amount, type, and frequency of intake Obtain diagnostic measures to detect any urine infection or possible causes of incontinence: 1. Urinalysis – to detect leukocytes, nitrites, hematuria, pyuria, bacteriuria, glycosuria or proteinuria 2. Send a sample for culture and sensitivity 3. Perform a post-void residual (PVR) Conduct a basic physical examination: 1. Perform a rectal examination to detect the presence or absence of fecal impaction, tone, and perineal sensation 2. Confirm the presence of UI by performing the cough test 3. Functional assessment including mobility, self-care ability, cognitive ability, and communication patterns Initiate basic nursing interventions which may include: 1. Education – fluids, weight loss, bowel management, dietary advice, smoking and alcohol reduction 2. Implementing scheduled toileting programs and evaluating their success 3. Identifying patients who may benefit from assistive devices to maintain continence or containment devices to manage incontinence 4. Recommending topical therapy for prevention and management of perineal skin breakdown 5. Implementation of basic treatments, i.e. pelvic floor exercises, bladder retraining 6. Identifying patients who may need to be referred to other physicians or healthcare professionals
exceeds the maximum urethral closure pressure in the absence of detrusor activity.14 Patients complain of leaking urine when they cough, sneeze, undertake exercise or lift objects. SUI is usually caused by:
• • • • •
an incompetent urethral sphincter; pregnancy and childbirth; obstetric trauma; laxity of the pelvic floor; prolapse; 83
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Table 5a.2.
Augmenting the initial nursing assessment
1. Physical examination • Abdominal examination to detect masses • Neurologic examination • Pelvic examination to evaluate muscle strength, perineal structure, perineal skin status, and signs of prolapse • Rectal examination to evaluate presence or absence of reflexes, resting anal sphincter tone, anorectal sensation, and sphincter function • Provocative stress testing • Urodynamic testing – uroflowmetry, cystometry, simple cystometry, videourodynamics, and interpretation of urodynamic data 2. Evaluation of assessment findings • Identifying patients who may need further referrals or tests/investigations 3. Implementing behavioral continence programs • Bladder retraining • Pelvic floor muscle exercises – this may be augmented by the use of vaginal cones, biofeedback, and electrical stimulation • Education of caregivers regarding specifics of prompted toileting and other scheduled regimes • Intermittent self-catheterization and development of bladder management programs • Individualizing a plan that incorporates drug management 4. Evaluate individual patient outcomes on a regular basis 5. Develop management programs for chronic, long-term incontinence to include the use of alternative measures and supportive devices
• • • •
atrophy of the pelvic supports; estrogen depletion; obesity; chronic constipation.
Urge incontinence/detrusor overactivity The woman complains of a leakage of urine with an urgent desire to void associated with frequency and nocturia. This is normally caused by detrusor instability and sensory urgency.
Mixed urge and stress incontinence The woman complains of symptoms of pure stress or urge incontinence, or a mixture of both. This is normally due to an incompetent sphincter and detrusor overactivity.
Overflow incontinence The patient complains of frequency, nocturia, passive
dribbling, incomplete emptying of the bladder, and symptoms of a urinary tract infection (UTI). This may be due to uterine or vaginal prolapse, urethral stricture, infection or atonic bladder, or may be present in a person with neurologic voiding dysfunction (e.g. multiple sclerosis or a cerebrovascular accident).
MANAGeMeNT Of sTRess URINARy INCONTINeNCe Conservative treatment The conservative therapies detailed in Table 5a.3 may be used to treat women with SUI, but must only be used under the supervision of a competent continence nurse or physiotherapist.15 The patients must be followed up regularly, given encouragement, and their progress monitored. It is possible to use a combination of conservative measures as pelvic floor exercises alone may not improve the symptoms. If conservative therapy fails and the patient and doctor are considering surgery, then urodynamics must be performed to confirm the diagnosis of genuine stress incontinence.16 Videourodynamics should be performed if the patient has a complicated history or has had previous surgery to the bladder.13
Pelvic floor exercises Strengthening of the pelvic floor muscles by regular exercise is the best form of therapy for mild to moderate stress incontinence, in the absence of marked prolapse of the anterior vaginal wall. Pelvic floor exercises have been described as ‘repetitive selective voluntary contraction and relaxation of specific pelvic floor muscles’.17 To achieve a successful outcome, it is imperative that the patient is well motivated and sufficiently mentally alert to carry out an exercise program. Exercising the pelvic floor muscles can help to strengthen them so that they provide good support,
Table 5a.3.
• • • • • •
Conservative therapies for stress urinary incontinence
Pelvic floor exercises Biofeedback Electrical stimulation Vaginal cones Devices, e.g. Neen pelvic floor educator, continence guards, Contiform, perineometers Education on diet, smoking, bowels, fluids
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helping to improve bladder control and improve or stop the leakage of urine. Like any other muscles in the body, the more they are used and exercised, the stronger they will become, so it is vital that patients are aware of how to do pelvic floor exercises correctly. The grade, strength and duration of muscle contraction can be assessed using the modified Oxford grading system.18 The scale is as follows: 0 = nil 1 = flicker 2 = weak 3 = moderate 4 = good 5 = strong. It is essential that the exercises are taught and performed correctly. Bo et al.19 found that pelvic floor exercises are the most effective treatment for genuine stress incontinence – more effective than vaginal cones, electrical stimulation or no treatment. How pelvic floor assessment is performed is outlined in Table 5a.4.
Biofeedback Patients frequently need assistance to perform these exercises correctly. The use of biofeedback therapy assists the patient in identifying and isolating the pelvic floor muscles with visual and auditory cues displayed on a monitor. EMG, pressure probes (vaginal or rectal) or perianal EMG surface electrodes are used to display the patient’s pelvic floor muscle strength, duration, relaxation, and isolation on a monitor viewed by the patient. EMG surface electrodes can be placed on the abdomen to monitor accessory muscle activity during the pelvic floor muscle contraction.7
Table 5a.4.
The examination should only be performed by a practitioner who is competent to do so.15 The patient must give their informed consent for any physical examination to be performed. Without this, the examination must not be undertaken. Consent must be documented on the assessment form.
• •
• •
•
• • •
•
Electrical stimulation Electrical stimulation is described by Abrams et al.17 as ‘the application of electrical current to stimulate the pelvic viscera or their nerve supply’. When there is no voluntary movement of the pelvic floor detected on digital examination, treatment should begin with electrical stimulation. In the past, this was in the domain of the physiotherapist20 but now such treatments are available as pre-programmed home devices. There are three forms of electrical stimulation treatment: interferential, faradism, and maximal electrical stimulation (MES). The difference between the three types of stimulation allows slightly different applications of the treatment.21 Pelvic floor stimulation units are available for hire or for purchase.
How to assess the pelvic floor
•
•
The patient should be examined in a supine position with her knees bent up and abducted laterally. The presence of any cystocele (prolapse of the anterior vaginal wall) or rectocele (prolapse of the posterior vaginal wall) should be noted. If either of these is severe, or if there is any degree of uterine descent, the chances of success from the exercises may be diminished. Even if surgery is contemplated, the exercises should still be tried as they will improve the tone and blood supply locally, thus improving postoperative healing. The presence of excoriation may give an indication of the severity of the incontinence. Examination of the introitus and distal vagina will identify the presence of vaginitis, which appears as a red, dry area instead of moist, pink tissue. This is more common in postmenopausal women and often mirrors the state of the urethra. Urethritis may cause frequency, urgency, and dysuria. Ask the patient to cough. The assessor should observe for urinary leakage during the cough and record the outcome. There may also be demonstrable perineal descent, the vagina may bulge and gape, and there may be movement of any prolapse. The pelvic floor should be examined by inserting a gloved, lubricated finger into the vagina. Two fingers can be used to assess the strength, endurance, and coordination of the pelvic floor. The patient is asked to squeeze, lift, hold, and relax.18 The examiner should feel the fingers being gripped and pulled inwards. Many women cannot do this at the first try, or tend to bear down or contract the abdominal muscles or buttocks. The strength of the muscle squeeze is noted using the Oxford grading system as a guide. The length of time that the muscle is contracted is recorded in seconds. The woman must be in control of the relaxation of the muscles so it should be noted at what point the contraction has faded away. It is futile to tell a woman to contract for 6 seconds when she is only able to contract for 4. It is then important to assess muscle endurance by getting the patient to contract, hold, and release the muscle as many times as she can. This assesses the slow twitch muscles, which are responsible for endurance and strength qualities.20 The 'quick twitch' movement of the muscle should then be assessed and recorded. This part of the exercise re-educates the part of the muscle responsible for reflex activity. It should be noted how many such movements can be done before fatigue sets in.20
The correct exercise program should then be developed.
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Vaginal cones Vaginal cones are used in the treatment of SUI (Figure 5a.2). These plastic cones are inserted into the vagina with varying weights inside. They provide proprioceptive biofeedback where the weight of the cone on the superior surface of the perineal muscles provides the woman with the sensation to contract her pelvic floor muscles to retain the cone in the vagina. They help to strengthen the pelvic floor to prevent muscle weakness, or to treat symptoms of stress incontinence. When used correctly, cones provide a positive feedback of muscle progress, thus giving a sense of achievement.20 Compared to conventional exercises, the use of cones requires very little professional teaching time, and therefore represents a very cost-effective option for the conservative management of stress incontinence.22 It is important to mention that due to fatigue of the pelvic floor muscles during the day, many patients can retain heavier weights in the morning than in the evening. Due to the variation in vaginal secretions, which affect cone retention, patients may demonstrate ‘good’ and ‘bad’ days. Pelvic floor muscles may appear weaker premenstrually and this may be a progesterone effect.18
tinence which they are unable to account for and seems to ‘just happen’. Patients with a bladder dysfunction other than an unstable bladder are less likely to benefit from bladder training (symptoms of stress incontinence, or retention with overflow incontinence). This highlights the need for a thorough assessment and accurate diagnosis prior to the implementation of any treatment program. The aim of bladder training is to restore the patient with frequency, urgency, and urge incontinence to a more normal and convenient micturition pattern.23 It aims to restore the individual’s confidence in the bladder’s ability to hold urine. The objective is that voiding should occur only every 3–4 hours or longer without any urgency or urge incontinence. The patient must be cognitively intact and motivated to comply with the treatment, since it may take 3–4 months to restore continence. When the bladder is known or thought to be unstable, drug therapy is often combined with the bladder training. Tips and techniques for successful bladder retraining are outlined in Table 5a.5. Timed voiding and habit training are forms of behavioral modification; however, unlike bladder retraining, they control incontinence, but do not normalize bladder function. The goal is to keep the patient dry by regular toileting. With timed voiding, the patient’s daytime voids are scheduled at fixed intervals, such as every 2 hours, or
Table 5a.5.
• • • Figure 5a.2. There are various different types of vaginal cone available
BehAVIORAl MODIfICATION Behavioral modifications include bladder retraining, urge inhibition, timed toileting, habit training, prompted voiding, fluid management, and elimination of bladder irritants. Bladder retraining programs are most suitable for people with symptoms of urgency, frequency, and urge incontinence, with or without an underlying unstable detrusor muscle, and for those with non-specific incon-
• • • • •
Useful tips when teaching bladder retraining
Patients must be warned that they may leak more at the beginning of the bladder training schedule as the bladder is being stretched when it is holding onto larger volumes of urine. They must be warned that they will not notice changes immediately. Their bladder has taken time to get into the bad habit and will take time to get back into a good habit. They should regularly fill in a bladder diary to monitor their progress. They should be followed up regularly, every 4–6 weeks initially, to maintain enthusiasm and motivation. They should be given lots of positive feedback when the baseline charts are compared and improvements are noted. Patients should be advised to drink seven to eight cups of fluid a day. They should be advised about the effect of caffeine on their bladder, and encouraged to reduce the number of caffeinated drinks they consume. They should be advised on the importance of keeping their bowels regular and eating a healthy, well-balanced diet.
The aims of bladder retraining are for the patient to hold on, to void less often, and to pass larger volumes at a time.
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only on even hours. In habit training, the patient voids in accordance with the times of voiding indicated on the voiding chart. Advice on the amount and type of fluids to drink in a 24-hour period is essential information that should be given to all women attending the clinic. It is widely recommended that patients should drink 8 cups/1.5 liters/2.7 pints of fluid a day to flush the bladder regularly to remove waste products and other irritants.24 It is common for people with bladder dysfunction to reduce their oral intake, which can in turn impact on already existing symptoms. It is also important for women to have regular bowel movements as straining associated with constipation can cause pelvic floor muscle weakness. Advice on diet, position on the toilet, and fiber intake can help to ease/solve any existing constipation problems. Chronic chest problems associated with smoking may result in stress incontinence if the pelvic floor muscles are weak. The woman should be encouraged to give up smoking.25 Symptoms may worsen if the woman develops a urinary tract infection. Advice should be given on hygiene, not using perfumed soaps, not wearing nylon knickers, and drinking cranberry juice.
MeDICATION Pharmacotherapy is used to treat both stress urinary incontinence and detrusor overactivity. Prescription of medications and monitoring of effects are integral to a continence nurse/advisor role. Collaboration with a physician is essential if nurses are unable to prescribe the medications themselves. Drug therapy for the treatment of overactive bladder and stress incontinence are outlined in a separate chapter of this text.
DeVICes Devices have been developed which block urinary leakage at the external urethral meatus. Several devices have either adhesive or mild suction to occlude urinary loss at the urethral meatus (Figure 5a.3). One example of an intraurethral device is a disposable catheter-like product sized for women’s urethral length. This device is inserted in the urethra and a retention air balloon is inflated to prevent urine loss during physical activity. A metal tab at the opposite end prevents the device migrating into the bladder. The device is inserted to prevent urine loss during increases in intra-abdominal pressure and is worn until the urge to void is present as a result of normal bladder filling.7
Figure 5a.3. Contrelle intravaginal device for the management of stress urinary incontinence.
Intravaginal devices are also used; these help by supporting the bladder neck. Traditional tampons, pessaries, and specifically designed intravaginal devices are used.26 Contrelle Activguard (previously known as Conveen Contiguard) and an expanding polyvinyl alcohol sponge have been used. One of the easiest devices available on the market for women to purchase is the tampon-like sponge that can be inserted into the vagina. It is first moistened with water and squeezed to reduce its size. Once inserted into the vagina, it expands, applying external pressure to the urethra and bladder neck. It should only be used for short periods of time, as the absorbable properties tend to make the vagina dry and sore.20
pADs Disposable continence pads are the most common method of dealing with bladder and bowel problems27 but patients often comment that pads ‘rustle’ when they move or walk and they are very self-conscious about this noise. Several manufacturers have now introduced a ’cotton feel’ back to some products in their portfolio – mainly the small shaped pads and the pull-up pants (Figure 5a.4). There is a wide range of disposable continence pads for women which manufacturers are continually improving for comfort and efficacy.28 Visiting professional exhibitions to see the latest developments in disposable pads is a good way of keeping up to date with what is available as there are too many to detail here. When assisting the patient in the choice of appropriate protective products to manage incontinence, it is 87
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Table 5a.6.
• • • • • • • • • •
Considerations in the choice of continence aid
Size and shape Reliability Quantity of urine held Odor Concealability Comfort and skin irritability Price Accessibility/supply Disposable/reusable Ease of use/changing21
Figure 5a.4. Examples of different types of pad and pants for the management of ‘heavy’ urinary incontinence. important to consider their physical, psychological, and financial concerns (Table 5a.6) Active women with moderate to severe urinary incontinence may not wish to wear a ‘diaper-like’ pad because of its similarity to a diaper (nappy) even though it may be the best product available to them. Some people may not be able to afford to buy pads and may prefer to change a piece of toilet paper in their knickers every time they wet themselves. Some women use panty liners and pads designed for periods to manage their incontinence as they are cheaper, easier to obtain, and are not embarrassing to buy as they tend not to be associated with incontinence. Incontinence pads have a role in the management of incontinence but should not be a substitute for seeking professional help to treat the condition of urinary incontinence.
urethra or cystostomy to drain urine (Figure 5a.5) and 5a.6. The patient may be required to perform the task as a result of a neurologic defect that impairs bladder emptying (e.g. multiple sclerosis, stroke) or as a result of temporary retention postoperatively. A nurse who can demonstrate competence in the skill and procedure is able to teach ISC. Under no circumstances should a nurse undertake male/female catheterization unless competent to do so.15 It is essential that the patient is cognitively intact, motivated, and has adequate manual dexterity to perform the procedure as reduced cognition and motivation can be limiting factors.29 ISC is a simple task where the only equipment needed is a hydrophilic catheter and some tap water. Most of the manufacturers now make ISC catheters which either have their own supply of water as part of the catheter or as part of the packaging, thus allowing patients to perform ISC in a public toilet without having to worry about getting a supply of water to lubricate the catheter. These catheters are single-use only and should be disposed of after use. Initially a patient may want to learn how to carry out ISC with a mirror to help find the urethral meatus, but after time and experience, they will often perform ISC as a ‘blind’ procedure.21 Once they have been performing ISC for a period of time, the patient will also be able to change the number of times a day they catheterize depending upon how much fluid they have consumed in a day. Urethral catheterization with an indwelling urethral catheter is an option for intractable incontinence, once all other avenues have been explored, as it comes with its risks and complications (e.g. UTI, blocking, reduced
CATheTeRs Intermittent self-catheterization (ISC) involves the patient inserting a catheter into the bladder via the
Figure 5a.5. Differentent catheters used for intermittent self catheterisation.
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ject of incontinence becomes less taboo amongst the general public. Continence nurses would not be able to perform their job as successfully without the support of colleagues on the wards and in the community as incontinence is a problem that is present at all levels and specialties throughout the NHS.
RefeReNCes 1. Royal College of Physicians. Report of a Working Party. Incontinence – causes, management and provision of services. London: RCP, 1995. 2. Department of Health. Good practice in continence services. London: DOH, 2000.
Figure 5a.6. Examples of self retaining catheters, valves and a collecting bag.
3. Continence Foundation. Making a case for investment in an integrated continence service. London: Continence Foundation, 2000.
bladder capacity, life restrictions).20 A thorough assessment of the patient is required to ensure that the most appropriate catheter and drainage system is selected. For example, catheter valves allow for natural bladder filling and emptying, but the patient must have the dexterity and cognitive awareness to be able to empty the urine regularly.30 The position of the catheter would also need to be considered, i.e. suprapubic or urethral, depending upon whether the patient is sexually active, wheelchair bound, obese, etc. Urethral catheters are often more uncomfortable and traumatic for long-term use and more prone to catheter-related urinary tract infections. Catheters can also be used as a temporary measure to help heal excoriated perineal skin as a result of longterm urinary and/or fecal incontinence. District nursing staff would need to be involved to provide support and backup in the community to ensure that the patient is caring for their catheter correctly.
4. Nazarko L. Cited by ACA Continence Resource Pack for Care Homes. London: Association for Continence Advice, 1995; 3.
CONClUsION The continence nurse is capable of providing assessment, diagnosis, treatment, and management options for patients with urinary incontinence. This care can be provided as an outpatient in a specially designated continence clinic, with the full support of a clinician, or as an inpatient with the support of the nursing staff and clinicians on the ward. The continence nurse has to wear a number of hats and have a number of skills, including educator (for patients, carers, and colleagues), counselor and practitioner in order to attain maximum success for these patients. The role of the continence nurse is continuing to develop and is becoming more high profile as the sub-
5. Wagner TH. Economic costs of urinary incontinence. Urology 1998;51:355–61. 6. Johnson MJ, Werner C. We have no choice: a study of familial guilt feelings surrounding nursing home care. J Geront Nursing 1982;8:641–5; 654. 7. Gallo ML, Newman DK, Sasso KC. The evolution of continence nurse specialists. In: Cardozo L, Staskin D (eds) Textbook of Female Urology and Urogynaecology. London: Martin Dunitz, 2001; 66–80. 8. Getliffe K, Dolman M. Promoting Continence – A Clinical Research Resource. London: Baillière Tindall. 9. Roe BH, Addison R, Clayton J. The Role of the Continence Advisor. London: RCN Care Forum, 1994. 10. Modernisation Agency. Essence of care: patient focused benchmarks for clinical governance London: DOH, 2003. 11. Modernisation Agency. Essence of care: benchmarks for continence and bladder and bowel care. London: DOH, 2003. 12. Department of Health. National Service Framework for older people. London: TSO, 2001. 13. Shah J, Leach G. Urinary Incontinence, 2nd ed. Oxford: Health Press, 2001. 14. Dolman M. Mostly female. In: Getliffe K, Dolman M (eds) Promoting Continence – A Clinical and Research Source. London: Baillière Tindall, 1997. 15. Nursing and Midwifery Council. Code of professional conduct. London: NMC, 2002. 16. Abrams P. Urodynamics, 2nd ed. London: SpringerVerlag, 1999.
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17. Abrams P, Cardozo L, Fall M et al. The standardisation of terminology in lower urinary tract function: report from the Standardisation Sub-Committee of the ICS. Urology 2003;61(1):37–9. 18. Laycock J. Pelvic floor re-education for the promotion of continence. In: Roe BH (ed) Clinical Nursing Practice: The Promotion and Management of Continence. London: Prentice Hall International, 1994 19. Bo K, Talseth T, Holme I. Single blind randomised trial of pelvic floor exercises, electrical stimulation, vaginal cones and no treatment in the treatment of genuine stress incontinence. Br Med J 1999;318:487–93. 20. Getliffe K, Dolman M. Promoting Continence – A Clinical and Research Resource, 2nd ed. London: Baillière Tindall, 2003. 21. Tooz-Hobson P, Cardozo L. Understanding Female Urinary Incontinence. Poole: Family Doctor Publications, 1999. 22. Haken J, Benness C, Cardozo L, Cutner A. A randomised trial of vaginal cones and pelvic floor exercises in the management of genuine stress incontinence. Neurourol Urodyn 1991;10(4):393–4.
23. Stewart E. Pelvic floor disorders. In: Hamilton-Fairley D, Holloway D (eds) Clinic Handbook of Women’s Health. Oxford: BIOS Scientific Publishers, 2003. 24. Addison R. Practical procedures for nurses No. 37.1. Fluid intake and continence care. Nursing Times 1999;95(49). 25. Addison R. Practical procedures for nurses Nos 35.1 and 35.2. Assessment of stress incontinence 1 and 2. Nursing Times 1999;95(45–46). 26. Abrams P, Cardozo L, Khoury S, Wein A. Incontinence: 2nd International Consultation on Incontinence. Conservative Treatment in Women. Plymouth: Health Publication, 2002; 571. 27. Evans D. Lifestyle solutions for men with continence problems. Nursing Times 2005;101(2):61–64. 28. Dolman M. Mostly female. In: Getliffe K, Dolman M (eds) Promoting Continence – A Clinical and Research Resource, 2nd edn. London: Baillière Tindall, 2003; 93. 29. Haslam C. Managing bladder symptoms in people with MS. Nursing Times 2005;101(2):48–52. 30. Addison R. Catheter valves – a special focus on the bard flip flo catheter valve. Br J Nursing 1999;8(9):576–80.
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5b The roles of the continence nurse specialist – global perspective Diane K Newman
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INTRODUCTION Throughout the world, care of individuals with urinary incontinence (UI), particularly containment or collection of urine, has traditionally been seen solely as a nursing care problem, with little interest or input from other members of a multidisciplinary medical team. Nurses have often been more closely involved in continence care and management than physicians or allied health professionals. Education and clinical training has enabled nurses to expand their practice to provide comprehensive and specialized services relating to incontinence and pelvic floor disorders. The International Consultation on Incontinence has published an extensive review of the role of nurses worldwide in the care of patients with incontinence.1 In countries such as the UK, Australia, Singapore, Canada, and Germany, government-regulated health systems have supported fairly well-developed systems of continence care.2,3 In countries where there are well-developed continence care programs there is funding for preventive efforts. In the USA, advanced practice nurses (APNs) have become increasingly interested, knowledgeable, and informed about the assessment, diagnosis, and treatment of patients suffering with UI.4 Like nurses in other countries, these nurses are developing a nursing subspecialty in the care of individuals with incontinence to meet the rising demands of this growing population. However, as the USA does not have well-developed government funding of continence nurse services, growth in this area is nurse dependent. Despite considerable advances in the management of UI in recent years, many nurses, irrespective of experience, lack sufficient knowledge about incontinence upon which informed nursing practice should be based. This chapter will outline the role of the nurse in various countries, the growth of the ‘continence nurse specialist’ as a leader of healthcare services for incontinence worldwide, and review current nursing education for UI. Nurses are instrumental in helping the patient and the patient’s family and caregivers, where relevant, to cope effectively with the physical, psychological, social, and economic consequences of UI. In the long-term care, acute care, and home care setting, the nurse may be the only healthcare professional who detects and begins the assessment and treatment of incontinence.5 In most institutional healthcare settings, nurses not only provide direct patient care, but are also responsible for the philosophy, standard, and policy of care while supervising the performance of other nursing staff members.6 Because of this lead role, the nurse needs to have a thorough knowledge of all aspects of this condition in order to provide systematic assessments and appropri-
ate and informed interventions. Nurses who specialize in the area of incontinence patient services can serve as expert clinical support for other nurses who have incontinent patients, as catalysts for improved care and coordination of services, and as educators and researchers.6 They can also be major change agents for eliminating negative perceptions of this problem as many patients become socially marginalized and are reluctant to seek healthcare.7 In some situations, rivalries and competition between disciplines and medical specialties is evident. This may be because of competition for patients and revenue or because of disputes over the demarcation of the scope of different disciplines (such as the boundary between urology and gynecology, or between nursing and physiotherapy).1
A GLOBAL PERSPECTIVE OF THE CONTINENCE NURSE SPECIALIST The scope and extent of nursing services for UI differ throughout the world. Two models that have been comprehensively used in countries such as Australia, New Zealand, and the UK are the continence nurse advisor (CNA) and the nurse continence advisor (NCA), both of whom are registered (generalist) nurses with specialized training in urinary incontinence.1 In the past several years, particularly in the UK, USA, and Australia, nurses with additional nursing education (graduate or doctorate level) have evolved into the continence nurse practitioner (CNP).1,2
Continence nurse advisor The primary role of the CNA has been to act as a liaison, integrate services, and guide individuals through the referral route most appropriate to their individual needs. This model originated in the UK with the goal to use a nurse as the reference point on the subject of incontinence, both urinary and fecal. Multiple branches of the government fund these nurse specialists and assign them to a geographic location, usually a district health authority, and determine the scope of practice.8 Initially, the growth was slow; however, as manufacturing companies developed disposable products, many health authorities saw the need for an advisor to assist with their use. Through publications and experience, CNAs and physicians throughout the UK have contributed greatly to the expansion of knowledge about the assessment and treatment of patients with UI. In addition, many physicians developed specialty continence assessment clinics, and promoted the role of the CNA as a major contribu-
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tor in the British healthcare system. Currently, the CNA has four main areas of responsibility: 1. clinical – involving patient assessment, management and treatment; 2. administrative – including monitoring supplies, protocols and the budget for incontinence in their specific health district; 3. education – for patients, consumers, and other nurses; 4. research. This specialty of incontinence nurses has evolved into a national professional organization – the Association for Continence Advice (ACA) –that includes both nurses and physical therapists who deal with individuals with incontinence.
Nurse continence advisor The NCA has evolved into a more independent nurse role. NCAs are usually associated with community/area health centers, where they may have variable professional support from general practitioners (GPs) and family physicians. NCAs often work in both hospital and community, and the service is focused on primary care assessment of patients and organization of free incontinence product delivery to the home. An additional number of studies support the efficacy of the NCA in the delivery of community continence care.9–12 One Australian study compared outcomes in 145 women presenting with stress UI, with or without urge UI, randomly allocated to a standardized regime with the NCA or treatment by a urogynecologist.13 The treatment by the NCA took a median of 160 minutes, but cost AUD59.20 compared with 90 minutes of gynecologist time at a cost of AUD189.70. At 2.5 years, 29% of the NCA group and 41% of the other group were dry. The authors concluded that similar results were achieved at lower cost using the NCA.
Continence nurse practitioner The third nursing model that has evolved, especially in the UK, USA, and Australia, is that of the CNP. Research has shown that CNP assessment has the potential to assign patients to the correct conservative treatment, thereby shortening waiting times for urodynamics and specialist assessment.14 In a series of studies performed in Leicestershire, UK, the short- and long-term outcomes of a new CNP-led service for urinary symptoms were examined and evaluated.15,16 The CNP-led service had a 10% higher cure rate
than standard care, with statistically and clinically significant reductions in urinary urgency, frequency, nocturia, and UI. In addition, quality of life (QoL) improvements were greater in users of the CNP-led service, and higher levels of patient satisfaction were achieved.
Advanced practice nurse In the USA, nurses at all levels provide aspects or levels of incontinence care (Table 5b.1). However, there is a group of nurses in the USA – advanced practice nurses (APNs) – who are coming to the forefront as primary providers for individuals with UI. APNs are nurse practitioners or clinical nurse specialists – registered (generalist) nurses who have received graduate or doctorate education and training in nursing. They can be compared to the CNP model seen in other countries. They are clinicians who are knowledgeable about a wide range of medical health conditions, and work closely with a physician collaborator to maximize patient outcomes in acute, primary, home, outpatient, and long-term care settings.6,17–22 Despite great diversity among client populations, practice setting, and specific function, all APNs have the same role as practitioner, consultant, educator, researcher, administrator, and leader.17,23 The APN role is growing in the USA due to an increase in nursing graduate programs, research that demonstrates the cost effectiveness of APNs, and the expansion of innovative practice and consultation models.2,24–26 The APN ‘continence nurse specialist’ provides assessment and non-surgical treatment, including the ability to prescribe medication and provide pelvic floor muscle rehabilitation.6 However, the most significant growth in the use of the APN to provide healthcare services has been the direct payment of services by both government and private medical insurers. In the USA, many experts feel there is a niche in advanced practice nursing for those providing continence care and research.2,27 Although no educational program in the USA provides continence care as part of the prescribed curriculum, the basic knowledge of health assessment and applied research is incorporated in the APN’s graduate nursing education.2 An example of a curriculum is found in Table 5b.2. They may receive ‘on-the-job’ training from a practicing physician, such as a urologist, urogynecologist or gynecologist, whose background and interests lie in the care of women with voiding dysfunction, from nurse preceptorships available from physicians, other APN continence experts, and/or attendance at instructional seminars/conferences on continence care.28 Regardless of the method used to obtain continence care knowledge, the APN is currently 93
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Table 5b.1.
Identification of nurses, educational preparation and incontinence-related care
Nurse
Education/licensure
Incontinence-related care
Registered Nurse (RN)
Diploma
Identification of UI Basic assessment of UI to include history, physical examination and baseline urologic assessment Education and counseling of patients/families and caregivers Nursing interventions to include: • scheduled toileting programs • bladder retraining • behavior modification • implementation of the use of devices, catheters and products Supervision of non-professional staff Bladder health promotion strategies
Associate degree in nursing Bachelor’s degree in nursing or outside nursing
Advanced Practice Nurse (APN)
Master of Science in Nursing Master of Science
Nurse Practitioner (NP)
Certification through the American Nurses Credentialing Center or American Academy of Nurse Practitioners
Clinical Nurse Specialist (CNS)
Meets individual State requirements for advanced practice nurse
Identification of UI Basic assessment of UI to include comprehensive history, mental, functional and environmental assessment Complete physical examination to include assessment of pelvic organ prolapse with fitting of pessary Baseline urologic assessment Complex urodynamics with interpretation of data Additional studies such as laboratory Identification of patients who need referral to other medical specialists Education and counseling of patients/families and caregivers Nursing interventions to include: • scheduled toileting programs • bladder retraining • behavior modification • pelvic floor muscle rehabilitation with biofeedback therapy and interpretation of data • neuromuscular pelvic floor muscle stimulation • implementation of the use of devices, catheters and products Prescribes pharmacological intervention Supervision of non-professional staff Bladder health promotion strategies
Adapted from ref. 23.
active in providing this much-needed service. There are programs through the Wound, Ostomy, and Continence Nurses Society (WOCN) that allow registered nurses to become certified as ‘continence nurses’. The Society of Urologic Nurses and Associates (SUNA) certifies different levels of nurses in the area of urology. A 2000 study in the USA demonstrated significantly improved outcomes for three clinical problems – urinary incontinence, depression, and pressure ulcers – when advanced practice gerontologic nurses (APNs) worked with nursing home (NH) staff to implement scientifically based protocols.21 In addition to working with nursing homes to provide resident evaluation as physician
extenders, this research indicates that this service model using an APN can be an effective link between current research-based knowledge about clinical problems and NH staff. This study also showed that consistent educational efforts with staff and NH residents demonstrated that interventions could improve or stabilize the level of UI in these individuals.
EDUCATION FOR THE CONTINENCE NURSE SPECIALIST The key to nursing care for incontinence is education. A common theme that has run through the international
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Table 5b.2.
Curriculum outline for continence nurse practitioner
Topic
Content
Urinary incontinence
Overview • History • Current state of prevalence, impact risk factors • Management guidelines (AHCPR, AMDA, AUA, CMS Tag F315 guidance)
Genitourinary system
Anatomy and physiology • Kidneys, bladder, urethra, pelvic floor Voiding physiology • Structure, function, age-related changes Pathophysiology • Transient versus established causes of UI • Neurologic causes
Assessment
History • Identification of UI Mental status, functional, environmental Physical examination • General, neurologic, abdomen, pelvic/genitalia, rectal Diagnostics • Urinalysis, post-void residual, blood studies, radiology Urodynamics • Simple, office based • Advanced/video Indications for referral to specialist
Management
Behavioral modification (lifestyle changes, toileting programs, bladder refraining) Pelvic floor muscle rehabilitation • Use of adjuncts – biofeedback, pelvic floor stimulation Drug therapy Surgical intervention Use of containment devices, catheters and products
Clinical skills
Psychomotor (e.g. external catheter application, pelvic floor muscle exercise teaching)
Documentation
Documentation (setting appropriate, reimbursement/coding requirements)
Goals of management
Patient versus provider
AHCPR, Agency for Health Care Policy and Research; AMDA, American Medical Directors Association; AUA, American Urological Association; CMS, Centers for Medicare & Medicaid Services. Adapted from ref. 2.
nursing literature over the past two decades is that nurses recognize a lack of knowledge of incontinence and indicate that they would like further training.29–31 In 2002, a national symposium, The State of the Science on Urinary Incontinence, was held in the United States to discuss the future of continence nursing care.24 This symposium raised concerns that although continence care is within the scope of nurses, many do not assess patients for urinary symptoms. In 2004, an International Nursing Summit convened incontinence nurse clinicians and researchers to a symposium to identify that knowledge deficit by practicing nurses is one of the main barriers to optimal continence nursing care.27 This symposium acknowledged the significant gaps in knowledge and clinical practice adoption related to both UI and fecal incontinence, although
nurses worldwide have played a major role in developing new information and testing interventions. Despite the fact that nursing interventions for patients with UI are effective, most individuals in the USA do not report this condition to their healthcare provider. In most cases, once the UI is reported, providers do not assess or treat accurately. This is not surprising, as most nurses do not receive basic training in this field. To help remedy this neglect, in 1992 the US Department of Health and Human Services, Agency for Health Care Policy and Research (AHCPR) recommended that ‘first and foremost, information about UI be included in the curricula of undergraduate and graduate health professional schools’.32 However, Colling33 notes that more than half the faculty who teach geriatric content in nursing programs lack any formal education specifically related 95
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to UI. Information about the evaluation and treatment of incontinence is more likely to be learned in fragments, or ‘on-the- job’ training, when confronted with a patient with skin breakdown associated with UI. Educational courses on incontinence are available for nurses in the UK, USA, Europe, Australia, and Canada, and are beginning to appear in Asia, notably Hong Kong and Singapore.1,34 These courses vary from 2–4 weeks of face-to-face didactic courses to distance learning courses lasting 4–6 months that lead to a post-basic nursing certificate. Research in the UK has shown improvements in both knowledge and attitudes of nurses who undertook a specially designed full-time, 3-month program that included a continence module.31 Internationally, there is inconsistency in the provision of nurse specialist education to prepare nurses to practice as experts in the field of incontinence. Programs of study are developed, but rarely fully evaluated. The need for innovative web-based learning programs incorporating modern information and communication technology (e-learning) may offer one way of providing standardized programs of study to practitioners.35,36 The internet also offers education courses: continuing medical education (CME) accredited courses and NCA distance education packages for nurses. Standard setting has been one method by which general nurses can acquire skills to meet set standards of practice. In Australia, for example, since government funding to nursing homes is dependent upon their reaching certain standards in continence assessment and management, educational resources for nurses working in elder care have been developed.37 The use of continence care pathways has been evaluated among generalist nurses. It was found that the use of such pathways has aided the identification of reversible causes of incontinence (e.g. UTI, medication, fluid intake, constipation, dexterity and mobility issues), and addressed poor quality of life and bothersomeness issues.38,39 By using care pathways, patients could be referred to CNPs more appropriately for specific treatment beyond the scope of the generalist nurse, or when they failed to respond to first line therapy. The care pathway not only identified the needs of the patient, and directed simple investigation and primary therapy, but also identified the resources needed by the nurses (e.g. urine testing dipsticks, lists of drugs, frequency/volume charts). The pathway could be modified according to the equipment and expertise locally available. Educating large numbers of general nurses to follow a simple pathway with basic continence-care competencies40 may allow better use of specialist nursing time
and specialized skills.41 Nursing education for elderly patients is a significant need as several studies have demonstrated the lack of formal education in this area.42,43 However, the real challenge remains in not only increasing knowledge, but also translating that knowledge into improvements in clinical practice.44 Guidelines have been developed to improve nursing practice for UI.12,32 In the USA, nurses have used the AHCPR32 recommendations more effectively than physicians, incorporating them into curricula, evidence-based clinical practice, and care pathways.20,26,45,46 In the USA, although many nurses have great expertise in caring for incontinent patients – and a growing number of nurses who are developing such expertise – there are no academic or clinical proficiency requirements in order to be considered a ‘continence nurse practitioner or specialist’. The norm is that most nurses in the USA obtain their knowledge and skill through self-motivated activities. A survey of nurses attending a national nursing conference on UI asked about educational preparation related to this condition.28 Respondents reported that less than half (40%) received academic education including course work in accredited post-baccalaureate or graduate programs related to UI. However, most nurses (76%) obtained instruction at professional conferences, continence clinics supervised by nurse practitioners or physicians, ‘on-the-job’ training, self-study, or in-service programs. In another UK study of general nurses’ knowledge of UI, a clinical handbook was evaluated using a preand post-test design with an experimental and a control group.47 This study showed that the use of the handbook, which consisted of a decanted, user-friendly, researchbased resource on continence care, improved nurses’ knowledge of incontinence. A significant improvement in reported clinical practice was found for 86% of variables in the experimental group compared to a 59% improvement in controls. However, only 54% of those approached agreed to enter the study, suggesting a general lack of interest and motivation. As with physicians, it is unlikely that improving nursing knowledge alone will translate into improved clinical practice, or into the ultimate goal of improved patient outcomes. In the USA, specialty nursing organizations, such the Wound, Ostomy, and Continence Nurses Society (WOCN Accreditation Policy and Procedure Manual, 2003), provide certification education programs to develop knowledge and experience in urinary incontinence care nurses. The Society of Urologic Nurses and Associates does not provide formal education programs on incontinence but will provide certification to general
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(registered) and advanced practice nurses in urology nursing (ww.suna.org).
CONCLUSION The nurse is capable of providing assessment, diagnosis, and treatment and management options for patients in need of continence care. The CNP or APN is an important resource to the patient in need of continence care, and acts as an educator, counselor, and practitioner. Worldwide, nursing models for care of individuals with incontinence are evolving. Areas that need further development are the specifics of nursing care and the expansion of knowledge into nursing education and training programs.
REFERENCES 1. Newman DK, Denis L, Gruenwald I et al. Promotion, education and organization for continence care. In: Abrams P, Cardozo L, Khoury S, Wein A (eds) Incontinence: Proceedings from the 3rd International Consultation on Incontinence. Plymouth: Health Publication, 2005; 35–72. 2. Rogalski NM. A graduate nursing curriculum for the evaluation and management of urinary incontinence. Educ Gerontol 2005;31:139–59. 3. Milne JL, Moore KN. An exploratory study of continence care services worldwide. Int J Nurs Stud 2003;40:235–47. 4. Ebersole PR. Continence care pioneers: Thelma Wells, RN, PhD, FAAN, FRCN and Joyce Colling, RN, PhD, FAAN. Geriatr Nurs 1998;19(2):103–5. 5. Du Moulin, MFMT, Hamers JPH, Paulus A, Berendsen C, Halfens R. The role of the nurse in community continence care: a systematic review. Int J Nurs Stud 2005;42:479–92. 6. Newman DK. Managing and Treating Urinary Incontinence. Baltimore: Health Professions Press, 2002. 7. Norton C. Nurses, bowel continence, stigma, and taboos. J Wound Ostomy Continence Nurs 2004;31(2):85–94. 8. Thomas S, Billington A, Getliffe K. Improving continence services – a case study in policy influence. J Nurs Manag 2004;12:252–7. 9. Borrie MJ, Bawden ME, Kartha AS et al. A nurse/physician continence clinic triage approach for urinary incontinence: a 25 week randomised trial. Neurourol Urodynam 1992;11:364–5. 10. O’Brien J, Long H. Urinary incontinence: long tern effectiveness of nursing intervention in primary care. Br Med J 1995;311:1208. 11. Saltmarche A, Reid DW, Harvey R, Linton L. A community nurse continence service delivery model – a demonstra-
tion project. Proceedings of the International Continence Society Meeting, Halifax, Nova Scotia. 1992, 274. 12. Button D, Roe B, Webb C, Frith T, Colin-Thome D, Gardner L. Consensus guidelines for the promotion and management of continence by primary health care teams: development, implementation, and evaluation. J Adv Nurs 1998;27:91–9. 13. Moore KH, O’Sullivan RJ, Simons A, Prashar S, Anderson P, Louey M. Randomised controlled trial of nurse continence advisor therapy compared with standard urogynaecology regimen for conservative incontinence treatment: efficacy costs and two year follow-up. Br J Obstet Gynaecol 2003;10:649–57. 14. Matharu GS, Assassa RP, Williams KS et al. Continence nurse treatment of women’s urinary symptoms. Br J Nurs 2004;13:140–3. 15. Williams KS, Assassa RP, Smith NKG et al. Development, implementation and evaluation of a new nurse-led continence service: a pilot study. J Clin Nurs 2000;9:566–73. 16. Shaw C, Williams KS, Assassa RP. Patients’ views of a new nurse-led continence service. J Clin Nurs 2000;9:574–82. 17. Carcio H. Comprehensive continence care: the nurse practitioner’s role. Adv Nurse Pract 2003;11(10):26–36. 18. Klay M, Marfyak K. Use of a continence nurse specialist in an extended care facility. Urol Nurs 2005;20(10):1–4. 19. Cooper G, Watts E. An exploration of acute care nurses’ approach to assessment and management of people with urinary incontinence. J Wound Ostomy Continence Nurs 2003;30(6):305–13. 20. Watson NM, Brink CA, Zimmer JG, Mayer RD. Use of the Agency for Health Care Policy and Research urinary incontinence guideline in nursing homes. JAGS 2003;51:1779–86. 21. Ryden MB, Snyder M, Gross CR et al. Value-added outcomes: the use of advanced practice nurses in long-term facilities. Gerontologist 2000;40:654–62. 22. Cacchione PZ, Decker SA. Caring for the incontinent elder: advanced practice nursing concepts. Clin Geriatr Med 2004;20:489–97. 23. Gallo ML, Newman DK, Sasso KC. The evolution of continence nurse specialists. In: Cardozo L, Staskin D (eds) Textbook of Female Urology and Urogynaecology. London: Martin Dunitz, 2001; 65–80. 24. Mason D, Newman D, Palmer M. State of the science on urinary incontinence. Am J Nurs 2003;3(Suppl):7. 25. Newman DK, Palumbo MV. Planning an independent nursing practice for continence services. Nurse Pract Forum 1994;5(3):190–3. 26. Newman DK, Parente CA, Yuan JR. Implementing the Agency for Health Care Policy and Research urinary incontinence guidelines in a home health agency. In: Harris MD (ed) Handbook of Home Health Care Admin-
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istration, 2nd ed. Gaithersburg, MD: Aspen Publications, 1997; 394–403.
timely? Is it accurate? J Wound Ostomy Continence Nurs 2001;27:1–9.
27. Wyman JF, Bliss DZ, Dougherty MC et al. Shaping future directions for incontinence research in aging adults. Nurs Res 2004;53(6S):S1–10.
37. Hunt S. Promoting Continence in the Nursing Home. Parkville, Victoria: Continence Foundation of Australia, 1993.
28. Jacobs M, Wyman JF, Rowell P, Smith D. Continence nurses: a survey of who they are and what they do. Urol Nurs 1998;18(1):13–20.
38. Bayliss V, Cherry M, Locke R, Salter E. Pathways for continence care: development of pathways. Br J Nurs 2000;9:1165–72.
29. Morishita L, Uman G, Pierson C. Education on adult urinary incontinence in nursing school curricula: can it be done in two hours? Nurs Outlook 1994;42:123–9.
39. Bayliss V, Salter L. Pathways for evidence-based continence care. Nurs Stand 2004;19(9):45–51.
30. McConnell ES, Lekan-Rutledge D, Nevidjon B, Anderson R. Complexity theory: a long-term care specialty practice exemplar for the education of advanced practice nurses. J Nurs Educ 2004;43(2):84–7. 31. Williams KS, Assassa RP, Smith NK, Shaw C, Carter E. Educational preparation: specialist practice in continence care. Br J Nurs 1999;8:1198–1207. 32. Fantl JA, Newman DK, Colling J et al. Urinary Incontinence in Adults: Acute and Chronic Management Clinical Practice Guideline No. 2, 1996 Update. Rockville, MD: US Department of Health and Human Services. Public Health Service, Agency for Health Care Policy and Research, AHCPR Publication No. 96–0682, 1996. 33. Colling J. Educating nurses to care for the incontinent patient. Nursing Clinics of North America 1988;23:279–89. 34. Collette C, Leclerc G, Tu LM. Effectiveness of a geriatric urinary incontinence educational program for nursing staff. Can J Nurs Leadersh 2003;16(4):99–109. 35. Boyington AR, Dougherty MC, Yuan-Mei L. Analysis of interactive continence health information on the web. J Wound Ostomy Continence Nurs 2003;30(5):280–6. 36. Diering C, Palmer MH. Professional information about urinary incontinence on the World Wide Web: Is it
40. Jirovec MM, Wyman JF, Wells TJ. Addressing urinary incontinence with educational continence-care competencies. Image J Nurs Sch 1998;30:375–8. 41. Hall C, Castleden CM, Grove GJ. Fifty six continence advisers, one peripatetic teacher. Br Med J 1988;297:1181–2. 42. Cheater FM. Nurses’ educational preparation and knowledge concerning continence promotion. J Adv Nurs 1992;17:328–38. 43. Connor PA, Kooker BM. Nurses’ knowledge, attitudes and practices in managing urinary incontinence in the acute care setting. Medsurg Nurs 1996;5(2)87–92. 44. Rigby D. The value of continence training: does it change clinical practice? Br J Nurs 2003;12(8):484–92. 45. Sampselle CM, Burns PA, Dougherty MC, Newman DK, Thomas KK, Wyman JF. Continence for women: evidence-based practice. J Obstet Gynecol Neonatal Nurs 1997:26(4):375–85. 46. Sampselle CM, Wyman JF, Thomas KK, Newman K, Gray M, Dougherty M, Burns PA. Continence for women: a test of AWHONN’s evidence-based protocol in clinical practice. J Obstet Gynecol Neonatal Nurs 2000;29:18–26. 47. Williams KS, Crichton NJ, Roe B. Disseminating research evidence. A controlled trial in continence care. J Adv Nurs 1997;25:691–8.
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6 The role of the pelvic physical therapist Bary Berghmans
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INTRODUCTION Worldwide, urinary incontinence is a common problem. In Western countries approximately 5% of the population suffer from incontinence.1 Among nursing home residents this increases to over 50%.2 Incontinence is predominantly a problem among women: 9% of women suffer from incontinence compared to ‘only’ 1.6% of all men.3 Male incontinence is usually seen only in the elderly.4 Mainly due to shame, taboo, and unawareness of treatment possibilities, only a minority of people suffering from incontinence seek professional help.5 In daily general practice, patients usually go for help when the loss of urine leads to mental, physical or social problems, or discomfort for the patient or their social environment. Several forms of incontinence – such as stress incontinence, mixed incontinence, and incontinence due to detrusor overactivity – can be differentiated.6 Symptoms of detrusor overactivity are urgency, frequent micturition or frequency, nocturia and/or urgency incontinence.6 The most prevalent form in women is stress incontinence, being responsible for 48% of all cases.7 Next to stress incontinence, detrusor overactivity is the second most prevalent cause of incontinence (17%).7 A patient suffering from stress incontinence usually has a normal voiding frequency (≤8 times in 24 hours) and bladder volume, with mean micturitions between 200 and 400 cc/void, but with neither urgency nor nocturia. The patient complains of losing small amounts of urine, i.e. drops or spurts, during exertion. A patient with urgency incontinence usually loses more urine (up to the complete content of the bladder) than a patient with stress incontinence. On the other hand, the patient may lose less than 150 ml urine during micturition, suggesting a reduced functional capacity of the bladder. Combinations of the aforementioned symptoms of stress and urgency incontinence are considered to reflect mixed incontinence.8 Incontinence has several treatment options such as pelvic physical therapy, drug treatment, and surgical procedures. Pelvic physical therapy focuses on the prevention and the treatment of all types of functional disorder of the abdominal, pelvic and low back region in women, men, children, and the elderly. The bony structures of the pelvis, the suspensory ligaments (e.g. pubourethral ligaments), connective tissue (e.g. arcus tendineus fasciae pelvis), the pelvic floor, and the pelvic organs all have mutual influence on each other. A problem in one part can provoke problems in other parts of the pelvic floor and can lead to functional health difficulties such as uri-
nary incontinence. In many countries in the developed world pelvic physical therapy is easily accessible for most incontinent patients and can therefore play an important role in the diagnosis and treatment of this type of disorder. The pelvic physical therapist is specialized in conservative (i.e. non-surgical, non-pharmacologic) interventions for the bladder and pelvic floor, and is considered to be a valued member of anti-incontinent multidisciplinary teams involving paramedical and medical specialists such as urologists, gynecologists, gastroenterologists, colorectal surgeons, sexual therapists, general practitioners, and incontinence nurses. The non-invasive and low key nature of pelvic physical therapy puts the physical therapist in the front line of the wide range of healthcare providers that assess patients with functional health problems of bladder and pelvic floor. The armamentarium of the pelvic physical therapist is based on specific knowledge and skills, and contains interventions such as physiotherapeutic diagnostics, education and information, pelvic floor muscle training (PFMT), bladder training (BlT), training with vaginal cones, electrical stimulation, biofeedback, rectal balloon training, etc. With pelvic physical therapy most patients can be treated to a satisfactory level.9 Guidelines have been published in several countries.10–14 However, little is known about the implementation of these guidelines and their use in daily practice.9 For patients with incontinence, physical therapy is generally considered first line therapy, due to its noninvasive character, the results in terms of symptom relief, the possibility of combining physical therapy with other treatments, the low risk of side-effects, and the moderate to low costs. Important restrictions are that success depends on the motivation and perseverance of both the patient and the physical therapist and the time needed for therapy.12 In this chapter we review and discuss the role of pelvic physical therapy, and its diagnostic and therapeutic possibilities for stress urinary incontinence, detrusor overactivity, and mixed urinary incontinence.
MEDICAL DIAGNOSIS When referring a patient to a pelvic physical therapist, as accurate a medical diagnosis as possible is important in determining the impact of the complaints of the patient and in estimating the likely success or failure of pelvic physical therapy.15 For the general practitioner (GP), who in many countries throughout the world is the first physician for patients to consult, it may be difficult to find the exact
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cause of urinary incontinence. Specialists, like the urologist or the gynecologist, may fall back on specific diagnostic tests such as urodynamic evaluation. GPs usually have no access to such tests and therefore must rely on their history taking and physical examination. For GPs, urodynamic tests are – by and large – only needed if there is doubt about the type of incontinence and, consequently, about the necessity and choice of treatment. Under optimal conditions (after GP training), the sensitivity and specificity of the GP’s history taking and physical examination to detect genuine stress incontinence is 78% and 84%, respectively, with a positive predictive value of 87%.16 Unfortunately, in daily practice with busy GPs, such optimal conditions cannot usually be met over a prolonged period of time. Moreover, the symptoms of incontinence are often vague and less clear-cut than depicted in textbooks. Altogether, this may impair the reliability of history taking and physical examination.9 Simple tools such as a standardized questionnaire for history taking, and a voiding diary (to assess drinking habits, voiding pattern, type/pattern of urine loss and impact; Fig. 6.1) filled in by the patient, may help the GP.2,16,17
However, to find out the nature and extent of a health problem, early and adequate initiation of proper diagnostics (including differential diagnosis, analysis, and evaluation) is mandatory. For instance, detrusor overactivity has a greater impact on quality of life than stress incontinence, probably because of its unpredictable prognosis.18 Younger people in particular regard detrusor overactivity as very distressing.19 After childbirth, stress incontinence sometimes goes together with a total denervation of the pelvic floor musculature or with extensive damage to surrounding connective and structural tissue. In such cases, physical therapy usually has little or no effect. In addition, in patients with detrusor overactivity as a result of an infection or a neurologic problem, physical therapy is unlikely to be helpful.20 In men, a transurethral, transvesical or (in particular) radical prostatectomy can cause both stress and urgency incontinence.21 Incontinence can also develop as a result of prostate hypertrophy, a neurologic problem, trauma or a birth defect. For many, the pathophysiologic character of the health problem determines the prognosis and results of treatment.22 Other etiologic and prognostic factors – such as age, hysterectomy, estrogen depletion during the menopause, chronic diseases (e.g. diabetes mellitus), immobility, obesity, the number of exercise repetitions, their duration and mode of delivery – play a role in incontinence.23 If, and to what extent, there is an association or causal relationship between these factors and the incidence of incontinence is not yet clear.23
PHYSIOTHERAPEUTIC DIAGNOSTIC PHASE
Figure 6.1.
Voiding diary.
Based on the medical diagnosis of the referring physician, the physical therapist starts the physiotherapeutic diagnostic process. The aim is to assess, analyze and evaluate the (often unclear12) nature and severity of the urinary incontinence problem and to determine if and to what extent a physiotherapeutic intervention can be effective. What is the nature of the underlying pathology, are there any local or general obstructing factors for recovery and improvement, and to what extent can these factors be influenced by physiotherapy? Using the International Classification of Functions, Disability and Health (ICF)24 (Table 6.1), the physical therapist tries to influence the consequences of the health problem on three different levels: organ level (impairment level, e.g. urine loss while coughing), person level (disability level, e.g. sanitation) and social–societal level (restriction of participation, e.g. social isolation). 101
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Table 6.1.
•
• •
Definitions of the ICF terms impairment, disability and handicap
Impairment: Loss or abnormality of psychological, physiologic, or anatomic structure or function at organ level. With respect to the classification of disorders in the storage and voiding of urine and feces, this means the impairment of stress incontinence or detrusor overactivity. Disability: Restriction or loss of ability of a person to perform functions/activities in a normal manner. With respect to the classification of disabilities of voiding and stool, this means the disability of involuntary loss of urine. Restriction in participation (handicap): Disadvantage due to impairment or disability that limits or prevents fulfillment of a normal role (depends on age, sex, sociocultural factors) for the person.
Modified from ref. 24.
due to the complaint, and Body image as a result of the urine loss are the five elements of the PRAFAB-score. With such questionnaires it is possible to illustrate the degree of incontinence in a reproducible manner.27 In patients with stress incontinence a pad test can be particularly useful to test the extent and severity of the involuntary loss of urine.28 The objectives of physical examination are to understand:
• the functionality of the pelvic floor in rest and • •
Systematic history-taking aims to establish and record:
• the severity of the health problem by noting • • • •
impairment(s), disability(ies), and restrictions in participation; the likely nature of the underlying pathology by noting causal factors (e.g. in stress incontinence trauma during vaginal delivery(ies)); local factors which may prevent recovery and improvement (e.g. prolapsed uterus); general or systematic factors which may prevent recovery and improvement (e.g. diabetes mellitus) personal factors (e.g. what efforts does the patient make to alleviate stress or urgency incontinence).
A physical examination of the patient is important in order to verify and support the profile gained from the patient’s history. To conduct the physical examination, a number of diagnostic tests are available to the physiotherapist. The severity of the stress, urgency or mixed incontinence depends not only on the condition of the pelvic floor and the bladder, but also on the patient’s posture, respiration, and movement, as well as general physical and psychological condition.25,26 Information on the severity of the stress, urgency or mixed incontinence can also be obtained by studying the voiding diaries mentioned above with relevant data about incontinence. Subjective self-report, standardized quality-of-life questionnaires and/or symptom questionnaires, such as the PRAFAB-score (which combines the most important objective and subjective elements of the degree of urinary incontinence) are helpful;27 PRotection (use of pads), Amount of urine loss, Frequency of the complaint, Adjustment in behavior
during activities in terms of coordination, tonus, endurance, and strength; the possibility and degree of contraction (with or without awareness) of the pelvic floor muscles; the influence of other parts of the body on the function of the pelvic floor, by inspection at rest and while moving.
Analysis of the results of diagnosis and relevant medical data will complete this process. The diagnosis of the referrer can be stated and the indication for physiotherapy ascertained. To this end, answers to the following questions should be sought:
• Is the referral diagnosis the right one for the • • • • • •
• •
patient's condition? Are there any urinary incontinence-related health problems? What is the nature of the stress incontinence, detrusor overactivity or mixed incontinence? What is the severity and the extent of the health problem? Is there a dysfunction of the pelvic floor? What caused this dysfunction? Are there any local factors which may prevent recovery or improvement, and can physiotherapeutic intervention have an influence on these factors? Are there any general factors which may prevent recovery or improvement? Is physiotherapy indicated?
A given severity of the health problem at referral has impact on the prognosis and the evaluation of the likely effect of the physiotherapeutic intervention. It is important to also take into account other prognostic and patient variables, such as age, obesity and vaginal childbirth, which will have an impact on the process of intervention. A flowchart of the referral and physiotherapeutic diagnostic process is outlined in Table 6.2.
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Table 6.2.
Referral and physiotherapeutic process
Referral for physiotherapy intervention 1. Specialist • Medical diagnosis (urodynamics) • Referral diagnosis • Referral data 2. General practitioner • Medical diagnosis (?) (no urodynamics) • Referral diagnosis • Referral data Physiotherapy Patient education and information 1. Anatomy, physiology • pelvic floor, bladder • toilet behavior/regime Process of diagnosis 1. History taking 2. Physical examination • general examination • local examination 3. Relevant data from: • Subjective self-report a. questionnaires (e.g. PRAFAB) b. diaries (e.g. voiding diary) • Functional tests (e.g. pad test) • Observation • Palpation: vaginal/anal • Physiotherapist's diagnosis • Inventory of health problem (e.g. genuine stress incontinence) a. nature b. severity c. obstructing factors 4. Conclusion: indication for physiotherapy → continue with treatment plan; no indication for physiotherapy → back to referring physician Formulation of treatment plan 1. Treatment objectives 2. Treatment strategy 3. Treatment procedures 4. Expected outcome 5. Prognosis of treatment duration in terms of total time and number of treatment sessions
INTERVENTION PHASE As a general rule, the least invasive and the least troublesome treatment procedure should be considered as first line therapy. After analysis and evaluation, the physical therapist formulates the treatment plan, estimating whether full recovery can be achieved or only compensation of the complaint is possible. The physical therapist should also determine the strategy, procedure, and methods of treatment to reach the goal, and whether or not they have the skills and capability to do the job.
Approach and treatment modalities will be different for patients with stress incontinence, detrusor overactivity or mixed incontinence, but all these low-risk interventions involve educating the patient and providing positive reinforcement for effort and progress.13 Patient education embraces all relevant concepts (e.g. what is the function of the bladder?) and information for the patient. Comprehension on the part of the patient will promote the motivation to start on other stages of treatment. The interplay between patient and physicaltherapist is very important in this process. Before starting the specific therapy modalities of the pelvic floor, it is important for the patient to know and appreciate the position and the function of the pelvic floor and how to contract and relax the pelvic floor muscles. To achieve satisfactory results from intervention (in the long term), information and supervision by the physical therapist throughout the intervention phase are essential, especially concerning the adequate use of the pelvic floor muscles and the process of micturition.
Stress incontinence Physiotherapeutic treatment modalities for stress urinary incontinence are PFMT (with or without biofeedback), electrical stimulation, and/or vaginal cones.
Pelvic floor muscle training (PFMT) The biologic rationale for PFMT in the management of stress incontinence is that a strong and fast pelvic floor muscle (PFM) contraction will clamp the urethra, increasing the urethral pressure, to prevent leakage during an abrupt increase in intra-abdominal pressure.20 DeLancey has also suggested that an effective PFM contraction may press the urethra against the pubic symphysis, creating a mechanical pressure rise.20 PFM contraction also supports the pelvic organs.20 Timing might also be important; Bø has suggested that a well-timed, fast and strong PFM contraction may prevent urethral descent during intra-abdominal pressure rise.29 PFMT is especially focused on strength improvement and coordination of the periurethral and the pelvic floor muscles. Appropriate treatment with PFMT should always include an assessment of PFM contraction and relaxation, because the effect of PFMT is dependent on whether the contractions and relaxations are performed correctly.30 Repeated correct contractions of the pelvic floor, strengthening the PFM in a regular, intensive and long-lasting training program, are essential for an effective improvement through PFMT.30–32 Extrapolation of exercise prescription guidelines suggests that PFMT should include short- and long103
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duration exercises, based on diagnostic findings, as both type I and type II muscle fibers need to be exercised with overload strategies. The frequency and the number of repetitions of exercises should be selected following assessment of the PFM. Daily regimes of increasing repetitions to the point of fatigue seem to be recommended (8–12 maximal PFM contractions, three times a day for at least 6 months32). It is important to select relevant starting positions, tailored to the individual patient, and training and functional activities must be incorporated into the training program as soon as possible.23 Improvement of absolute power and endurance of the pelvic floor do not guarantee correct function of the continence mechanism. A process of patient awareness of isolated contractions to fully automatic controlled function of the pelvic floor during multiple complex tasks is required.12 An individually tailored home exercise program focused on incorporation of activities of daily living is essential.30 Meanwhile, there is sufficient evidence that PFMT is effective in the reduction of involuntary loss of urine in patients with stress incontinence by the end of the training program and also in the long term.33,34 In general, intensive training shows better results than a low intensity program.23 Twenty-five percent of females are still dry after 5 years, while two-thirds indicate by follow-up that they are very satisfied with their present state and that they wish no further treatment.
Biofeedback Biofeedback is the technique whereby information regarding ‘hidden’ physiologic processes, in this case PFM contractions and relaxations, is displayed in a form understandable to the patient to permit self-regulation of these events.35 This technique can be applied either by the use of electromyography signals (EMG) or manometry (pressure), or a combination of both. Biofeedback is based on operant conditioning and a cognitive learning process. An incontinent patient can be taught, with the aid of biofeedback, to be selective in the use of the pelvic floor muscles. Through registration by means of an intravaginal or intrarectal electrode the patient can see on a monitor if and to what extent contraction and relaxation of the PFM is possible and adequate (Fig. 6.2). Usually, at the outset of therapy with biofeedback, the first measurement is of the motor unit activity (EMG) or the intravaginal/anal pressure of the PFM (manometry) at rest, during a maximal PFM contraction (Pmax), and relaxation after Pmax. For the treatment of stress incontinence, biofeedback in combination with PFMT seems as equally effective
Figure 6.2. Biofeedback equipment for urinary incontinence. as PFMT only.28 Nevertheless, in patients with urinary incontinence who have insufficient or no awareness of the PFM, and therefore are not able to voluntarily contract or relax their PFM, or have very poor quality (intensity) of contraction at initial assessment, biofeedback is suggested to be an important strategy to speed up and restore this awareness.23,28,29,36 However, in order to prove this hypothesis, further large, high quality, randomized clinical trials (RCTs) are required.23,28,29
Electrical stimulation Electrical stimulation is provided by clinic-based mains powered machines (i.e. those that need to be plugged into a wall socket) or portable battery-powered stimulators (Fig. 6.3). Although the biologic rationale underpinning the application of electrical stimulation for the treatment of stress urinary incontinence has been poorly reported,23 the aim of electrical stimulation here appears to be to improve the function of the pelvic floor muscles, whereas
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EMG vaginal probe
EMG anal probe
Pressure vaginal probe
for patients with urgency incontinence the objective seems to be to inhibit detrusor muscle overactivity. For stress incontinence, electrical stimulation is focused on the restoration of reflexivity through stimulation of the fibers of the pudendal nerve to create a contraction of the PFM.37 Electrical stimulation is believed to instigate a motor response by patients for whom a voluntary contraction is not possible as a result of insufficient PFM, provided the nerve is intact.29 Although electrical stimulation appears to be better than placebo, its effect in stress incontinence is, as yet, insufficiently demonstrated as a result of inconsistency in protocols.23 There are many differences in clinical application that have not yet been investigated. For example, some clinicians suggest that ‘active’ electrical stimulation (i.e. the patient voluntarily contracts the PFM during stimulation) is better than ‘passive’ electrical stimulation but the effect of these two approaches has not yet been evaluated.23 Equally, it may be that some populations or subgroups of patients benefit from electrical stimulation more than others. Although there is still insufficient evidence to date, in clinical practice we suggest that in patients with stress incontinence, who – during initial assessment – were not capable of performing an active voluntary contraction of the PFM, the following parameters of electrical stimulation be used as a starting point:
• • • • • •
pulse shape: bipolar rectangular square wave; frequency: 50 Hz; pulse duration: 200/sec; duty circle: ratio 1:2; intensity of current: patient’s maximal tolerance; timing: twice a week office-bound, twice a day at
Pressure anal probe
Figure 6.3. Office-bound and home devices for electrical stimulation.
home, until voluntary contraction by the patient is possible and adequate.
Vaginal cones In women with stress incontinence, weighted vaginal cones (Fig. 6.4) are sometimes used in combination with PFMT. All cones are identical in size, but have increasing weight. The idea is that the stronger the pelvic floor muscles become, the higher the weight of a cone must be to stimulate the PFM to hold the cone inside the vagina. A review by Herbison et al.38 provided some evidence that weighted vaginal cones are better than no active treatment but on the other hand add no benefit to a PFM training program.23
Figure 6.4.
Vaginal cones. 105
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Because of the lack of evidence about their efficacy, widespread use of vaginal cones is not recommended.39
Table 6.3 provides an algorithm of the process of therapy for stress incontinence in women.
Guidelines for stress urinary incontinence In the Royal Dutch Foundation of Physiotherapy (KNGF) guidelines for stress incontinence, the following problem areas were identified:12 1. Stress incontinence with a dysfunction of the pelvic floor • with awareness of the pelvic floor; • without awareness of the pelvic floor; • the function of the pelvic floor is compromised by dysfunctions in the respiratory or the locomotive system. 2. Stress incontinence without a dysfunction of the pelvic floor. 3. Stress incontinence (with or without a dysfunction of the pelvic floor) in combination with general factors that inhibit or delay improvement or recovery.
Stress incontinence with a dysfunction of the pelvic floor The primary aim of treatment is to obtain a good awareness of the PFM. During treatment the following techniques are used: digital palpation either by the patient herself or by the physical therapist, and electrical stimulation and/or biofeedback in combination with PFMT. If the patient is aware of contraction and relaxation of the PFM, the therapy continues with the use of PFMT only. If a pelvic floor dysfunction coexists with dysfunctions of the respiratory or the locomotive system, or with inadequate toilet behavior, these issues also need to be addressed. The ultimate aim of the treatment is a complete restoration of the functionality of the pelvic floor.
Stress incontinence without a dysfunction of the pelvic floor Without a dysfunction of the pelvic floor, an intrinsic sphincter deficiency is likely. Here, pelvic floor training can only achieve compensation at the most; a complete cure is not possible.
Stress incontinence in combination with general factors that inhibit or delay improvement or recovery In this case, physical therapy will aim at the reduction of these negative general factors. Avoiding specific situations by the patient, impaired social participation and feelings of shame related to involuntary urine loss can be reduced by the physical therapist using relevant information, education, counseling, and care.
Table 6.3.
Process of therapy for stress incontinence in women
Therapeutic training/management to distinguish problem areas USI + dysfunction pelvic floor + no awareness of pelvic floor 1. Digital palpation by patient and/or physiotherapist 2. Electrical stimulation (intravaginal/extravaginal) + PFMT 3. Biofeedback + PFMT • Objective: restoration of awareness of the pelvic floor • if awareness is restored → see GSI + dysfunction pelvic floor + awareness of the pelvic floor below • unsatisfactory results → back to referring physician USI + dysfunction pelvic floor + awareness of the pelvic floor 1. PFMT + home exercises; isolated contractions of the pelvic floor with awareness of pelvic floor, single tasks → double tasks → multiple tasks → automatic controlled tasks; optional: vaginal cones • Objective: total recovery (of the functionality of the pelvic floor) • unsatisfactory results → back to referring physician USI + dysfunction pelvic floor + function pelvic floor malinfluenced by respiratory or locomotive disorders, toilet regime, toilet behavior 1. PFMT + home exercises 2. Exercises to achieve adequate respiration, postural exercises, relaxation exercises, instruction on lifting procedures • Objective: reduction or elimination of malinfluence disorders, improvement in functionality of pelvic floor • unsatisfactory results → back to referring physician USI + no dysfunction of the pelvic floor 1. PFMT + home exercises; optional: vaginal cones • Objective: compensation. Expectation: total recovery is not likely • unsatisfactory results → back to referring physician USI + general obstructing factors • Objective: maximal possible reduction of these negative factors • unsatisfactory results → back to referring physician Evaluation 1. Treatment results, i.e. (changes in) patient’s health status 2. Course of action by physiotherapist Conclusion 1. Conclude treatment period 2. Report to referring physician GSI, genuine stress incontinence; PFMT, pelvic floor muscle training.
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Detrusor overactivity In this condition, the patient has no or insufficient control over involuntary detrusor muscle contractions, which can result in involuntary urine loss.40 Physical therapy for detrusor overactivity consists of patient information and education, toilet training, bladder (retraining) or behavioral therapy, PFMT (with or without biofeedback), and electrical stimulation. All physiotherapeutic modalities can be used alone or in combination with each other or in combination with medication.
Patient information and education This is provided about lower urinary tract function, the function of the pelvic floor, and the way to contract and relax the pelvic floor.
Toilet training Toilet training aims to change inadequate toilet behavior and regimes, i.e. the aspects of the micturition process itself.
Bladder training/re-training Bladder (re-)training (BlT) consists of four components:
tion of the pelvic floor muscles. PFMT consists of pelvic floor muscle exercises and general or specific relaxation exercises. Different from the mechanism in stress incontinence, in patients with detrusor overactivity selective contractions of the PFM during the therapy are focused on the inhibition of involuntary detrusor contractions (reflex inhibition).41 Many patients with detrusor overactivity have a concurrent high PFM tonus.42 The level of activation is so high43 that selective contraction of the pelvic floor muscles in order to achieve reciprocal inhibition of the bladder is very difficult or impossible. Teaching selective contraction and relaxation of the pelvic floor muscles is then an important first step. Once this is achieved, selective contraction of the pelvic floor muscles focuses on facilitation of the DIR. After testing a patient’s ability to hold contractions for at least 20 seconds by digital palpation by the physiotherapist, patients are instructed to do so, followed by a relaxation period of 10 seconds. A more functional training program (pelvic floor exercises during activities of daily living) completes the exercise program. Combinations of bladder (re-)training and PFMT are also used in patients with detrusor overactivity. In the study of Berghmans et al. 44 this kind of program was termed lower urinary tract exercises (LUTE).
Biofeedback 1. an educational program that addresses lower urinary tract function; 2. training to inhibit the sensation of urgency and to postpone voiding; 3. to urinate according to a timetable in patients with an interval of less than 2 hours between two consecutive micturitions in order to reach an interval of at least 3 hours between two consecutive voidings and to reach larger voided volumes; 4. reinforcement of patient motivation by the physical therapist. In those patients whose functional capacity of the bladder is too small, a bladder (re-)training program can provide normalization of bladder capacity. The efficacy of bladder training in women with detrusor overactivity varies from 12 to 90%.23 If there is no reduction in incontinent episodes after 3 weeks of bladder training, the International Consultation of Incontinence (ICI) recommends re-evaluation and the consideration of other treatment options.23
Pelvic floor muscle training (PFMT) Specific PFMT most likely facilitates and restores the detrusor inhibition reflex (DIR) by selective contrac-
As in patients with stress incontinence, in patients with detrusor overactivity with insufficient or no awareness of the pelvic floor, biofeedback can be used to learn to control muscle functions28 such as reduction of increased muscle activity or a better timing and coordination of contraction or relaxation. Wyman et al. suggested that a combination of biofeedback, PFMT and bladder training was more effective immediately after the therapy than separate application of each treatment modality.45
Electrical stimulation In patients with detrusor overactivity, electrical stimulation theoretically stimulates the DIR and pacifies the micturition reflex, resulting in a decrease in overactive bladder dysfunction.37 Through selective stimulation of afferent and efferent nerve fibers in the pelvic floor, resulting in contraction of the para- and periurethral musculature (either direct or via spinal reflexes), electrical stimulation aims to inhibit involuntary detrusor muscle contractions.44 Although external electrodes have been used on occasion, electrical stimulation is mostly applied vaginally or anally through plug-mounted electrodes (Fig. 6.5).16,23 The patient is instructed to use the maximum tolerable level during stimulation. In recent studies the 107
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•
programs (with or without biofeedback) in patients with detrusor overactivity.16,23,44 Recent studies show that acute and chronic electrical stimulation, both office- and home-based, is effective in 70% of all cases.44,46,47 This treatment modality may be the treatment of first choice in patients with detrusor overactivity.44,46,47
Mixed incontinence
Figure 6.5. Vaginal, rectal, and external electrical stimulation probes. following treatment characteristics were used: frequency modulation of 0.1-second trains of rectangular biphasic 200 µsec44,46 or 400 µsec47 long pulses which varied stochastically between 4 and 10 Hz43 or with a fixed frequency of 10 Hz.46,47 Acute electrical stimulation (mostly once or twice a week for 20 minutes) or chronic electrical stimulation (daily at home, e.g. every 6 hours for 20 minutes) can be applied. As well as office-based electrical stimulation, portable electrical stimulation devices for use by patients at home have been developed44 (Fig. 6.6). In assessing the evidence for the different treatment modalities for detrusor overactivity (Fig. 6.7.), the following conclusions can be made:
• The efficacy of bladder training in women with •
detrusor overactivity is still pending and varies from 12 to 90%.23 Despite a positive trend in several studies,44,47 with reported success of around 45–50%, there is still insufficient evidence for the efficacy of PFMT
The physiotherapeutic diagnostic and therapeutic process focuses on the predominant factors of mixed urinary incontinence. If the symptoms of urgency/frequency appear to be dominant, the principal aim will be to reduce and improve these factors. If the physical therapist starts with the stress component, this can provide a negative influence on the urgency component, perhaps introducing more severe urgency/frequency. Reduction or improvement of the latter symptoms will provide a solid base for the subsequent treatment of the stress component. The choice of therapy modality depends on the nature, extent, and severity of the health problem, and is based on the analysis and evaluation of the physiotherapeutic diagnostic process.
Physical therapy in men Until recently, in only a few non-controlled studies, were investigations carried out into the effect of physical therapy in men with incontinence as a consequence of prostatectomy.48 Recently, in a well-designed RCT, Van Kampen et al. showed that an adequate program of pelvic floor re-education after radical prostatectomy decreased the duration and extent of incontinence and improved the quality of life.49 This physiotherapeutic program consisted of a weekly or 2-weekly session of individual treatment, including education and information, PFMT (with and without biofeedback), together with bladder training in those cases of apparent urgency. If required, electrical stimulation was applied to improve the proprioception of the pelvic floor and to create PFM contractions. Treatment was continued as long as necessary to restore continence.
Patient education in physical therapy practice
Figure 6.6. Portable electrical stimulation device for self-care at home.
In order to achieve a permanent positive result from physical therapy, patients have to incorporate the newly acquired abilities into daily life. In our opinion, the physical therapist is the most important mentor in this behavioral modification. Patient education is a very
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Efficacy of therapy modalities 01.00 0.90 0.80 0.70 0.60 0.50 0.40 0.30 0.20
Baseline DAI
0.10
Endline DAI
00.00 n=
14 14 18 18 Controls LUTE
17 17 19 19 FES Combination
THERAPY MODALITY
Effect of therapy on self-professed impact 3.00 100 2.50
90 80
2.00 1.50 1.00 IQ7 baseline .50 0.00 n=
13 13 13 17 17 17 15 15 15 16 16 16 Controls LUTE FES Combination
Percentage
70 60
No change/worse
50
Improved
40
Cured
30
IQ7 endline
20
IQ7 endline+3m
10 0
ES
BBSO
BBSO+ES
Controls
THERAPY MODALITY
Figure 6.7. Proven overactive bladder. (BBSO, pelvic floor muscle exercises; DAI, detrussor activity index; ES, electrical stimulation; FES, functional electrical stimulation; IIQ7, Impact Incontinence Questionnaire (short form); LUTE, lower urinary tract exercises.) important aspect of this kind of care and a professional attitude towards providing patient education is required. Van der Burgt and Verhulst50 developed a model for allied health professions as a tool for patient education. This model is a combination of the ASE model and the so-called steps model of Hoenen et al.,51 developed for individual patient education.50 In the ASE model the premise is that the interplay between Attitude, Social influence and the patient’s own Efficacy determines the willingness to modify behavior (Fig. 6.8). In the model of Van der Burgt and Verhulst,50 a number of stages are distinguished, such as thinking, feeling, and doing. In patients with urinary incontinence this model can be transformed into an exchange of information and explanation (thinking), in awareness and feeling of the pelvic floor, posture and movement (feeling), and in training of the pelvic floor and promotion of short- and long-term compliance (doing). The stan-
dardized patient education model of van der Burgt and Verhulst can be seen as an example of how to facilitate best practice and thus can provide physical therapists with a framework upon which to base patient education in urinary incontinence.
A S E
Be open Understand
Barriers E Behavior Intention Skills Will Can Do
E
Maintenance of behavior
Keep doing
Figure 6.8. Parallels between the ASE model and the steps model. (Adapted from ref. 49.) 109
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Specific and non-specific effects of pelvic physical therapy
2. Valk M. Urinary incontinence in psychogeriatric nursing home patients. Prevalence and determinants [Dissertation]. Utrecht: Universiteit Utrecht, 1999.
Adequate physical therapy has a mixture of specific and non-specific elements. In that sense, precisely controlled exercises, devices for biofeedback, electrical simulation, and vaginal cones are examples of specific elements of therapy. If a researcher wishes to evaluate and analyze the real effects of each specific element on its own, it is necessary to take out or keep exactly under control all non-specific elements such as the physical therapist’s assessment, motivational support and guidance of the patient. As in drug trials, where the exact pharmacologic properties of a drug can be studied, our researcher is eager to find out what, for example, electrical stimulation within certain specified parameters (e.g. in women with detrusor overactivity) does precisely. The researcher is interested in whether or not the chosen parameters stimulate the pudendal nerve and to what extent this influences the involuntary detrusor muscle contractions. So far, so good! However, in physical therapeutic clinical practice, the impact of the non-specific effects – here often falsely called placebo effects – on the result of physical therapy is also desirable and important. The combined nonspecific and specific elements of therapy must be considered as unbreakable parts of the physical therapist’s strategy to reach the defined goals. In other words, these elements are needed to improve or cure the patient’s underlying health problem. So, to assess the real effect of physical therapy as a whole, all elements and effects of the intervention need to be incorporated in the final conclusion about success or failure.
3. Newman DK. How much society pays for urinary incontinence. Ostomy Wound Manage 1997;43:18–25.
CONCLUSION Pelvic physical therapy is clearly of benefit to many patients with urinary incontinence. A thorough assessment, careful selection and individualization of treatment, and continued reinforcement and motivation are the keys to success. As pelvic physical therapy has no significant adverse effects, it should be considered as a first line or adjunctive therapy for the majority of patients presenting with lower urinary tract dysfunction.
REFERENCES 1. Rekers H, Drogendijk AC, Valkenburg H et al. Urinary incontinence in women from 35 to 79 years of age: prevalence and consequences. Eur J Gynecol Reprod Biol 1992;43:229–34.
4. Schulman C, Claes H, Matthijs J. Urinary incontinence in Belgium: a population-based epidemiological survey. Eur Urol 1997;32:315–20. 5. Lagro-Janssen ALM, Smits AJA, van Weel C. Women with urinary incontinence: self perceived worries and general practitioners’ knowledge of the problem. Br J Gen Pract 1990;40:331–4. 6. Abrams P, Cardozo L, Fall M et al. The standardization of terminology of lower urinary tract function. Neurourol Urodyn 2002;21:167–78. 7. Hunskaar S, Arnold EP, Burgio K et al. Epidemiology and natural history of urinary incontinence. In: Abrams P, Khoury S, Wein A (eds) Incontinence. Plymouth, UK: Health Publication, 1999; 206. 8. ICS Pelvic Floor Clinical Assessment Group. Terminology of pelvic floor function and dysfunction. Bristol: International Continence Society, 2001. 9. Gezondheidsraad. Urine-incontinentie. Den Gezondheidsraad, 2001; publicatie nr 2001/12.
Haag:
10. Lagro-Janssen ALM, Breedvelt Boer HP, van Dongen JJA et al. NHG-standaard Incontinentie voor urine. Huisarts Wet 1995;38(2):71–80. 11. Klomp MLF, Gercama AJ, de Jong-Wubben JGM et al. NHG-standaard Bemoeilijkte mictie bij oudere mannen (eerste herziening). Huisarts Wet 1997;40(3):114–24. 12. Berghmans LCM, Bernards ATM, Bluyssen AMW et al. KNGF-richtlijn Stress urine-incontinentie. Ned Tijdschr Fysiother 1998;108(4 Suppl):1–35. 13. Fantl JA, Newman DK, Colling J et al. Urinary incontinence in adults: acute and chronic management. Rockville, MD: US Department of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research; March 1996. AHCPR publication 96-0682 Clinical Practice Guideline No. 2, 1996 Update. 14. Abrams P. Assessment and treatment of urinary incontinence. Lancet 2000;355:2153–8. 15. DeLancey JOL. Genuine stress incontinence: where are we now, where should we go? Am J Obstet Gynecol 1996;175:311–19. 16. Lagro-Janssen ALM, Debruyne FMJ, Smits AJA et al. The effects of treatment of urinary incontinence in general practice. Fam Pract 1992;9(3):284–9. 17. Berghmans LCM, Hendriks HJM, De Bie RA et al. Conservative treatment of urge urinary incontinence in women: a systematic review of randomized clinical trials. BJU Int 2000;85:254–63. 18. Grimby A, Milson I, Molander U, Wiklund I, Ekelund P.
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The influence of urinary incontinence on the QoL of elderly women. Age Ageing 1993;22:82–9. 19. Norton P, MacDonald L, Sedgwick P et al. Distress and delay associated with urinary incontinence, frequency, and urgency in women. Br Med J 1988;297:1187–9. 20. DeLancey JOL. Structural aspects of urethrovesical function in the female. Neurourol Urodyn 1988;7:509–19. 21. Van Kampen M, De Weerdt W, Van Poppel H et al. Urinary incontinence following transurethral, transvesical and radical prostatectomy. Acta Urol Belg 1997;65:1–7. 22. Van Kampen M, De Weerdt W, Van Poppel H et al. Prediction of urinary continence following radical prostatectomy. Urol Int 1998;60:80–4. 23. Wilson PD, Berghmans B, Hagen S et al. Conservative treatment in adults. In: Abrams P, Cardozo L, Khoury S, Wein A (eds) Incontinence. Plymouth, UK. Health Publication, 2005; 855–964. 24. World Health Organization. International Classification of Impairments, Activities and Participation: a Manual of Dimensions of Disablement and Functioning. Geneva: WHO, 1997. 25. Wells TJ, Brink CA, Diokno AC, Wolfe R, Gillis GL. Pelvic muscle exercise for stress urinary incontinence in elderly women. J Am Geriatr Soc 1991;39:785–91. 26. Tapp AJS, Hills B, Cardozo LD. Randomized study comparing pelvic floor physiotherapy with the Burch colposuspension. Neurourol Urodyn 1989;8:356–57. 27. Mulder AFP, Vierhout ME. De Inco-test. Medicus 1990:264. 28. Berghmans LCM, Frederiks CMA, De Bie RA et al. Efficacy of biofeedback, when included with pelvic floor muscle exercise treatment, for genuine stress incontinence. Neurourol Urodyn 1996;15:37–52. 29. Bø K. Pelvic floor muscle exercise for the treatment of stress urinary incontinence: an exercise physiology perspective. Int Urogynecol J Pelvic Floor Dysfunct 1995;6:282–91. 30. Bø K. Physiotherapy to treat genuine stress incontinence. Int Cont Surv 1996;6:2–8. 31. DiNubile NA. Strength training. Clin Sports Med 1991;10:33–62. 32. Bø K, Hage RH, Kvarstein B et al. Pelvic floor muscle exercise for the treatment of female stress urinary incontinence. III. Effects of two different degrees of pelvic floor muscle exercises. Neurourol Urodyn 1990;9:489–502. 33. Berghmans LCM, Hendriks HJM, Bø K et al. Conservative treatment of stress urinary incontinence in women: a systematic review of randomized clinical trials. BJU Int 1998;82:181–91. 34. Hay-Smith EJC, Bø K, Berghmans LCM et al. Pelvic floor muscle training for urinary incontinence in women (Cochrane Review). In: The Cochrane Library, Issue 4, 2003. Chichester: Wiley, CD001407.
35. Krebs DE. Biofeedback in therapeutic exercise. In: Basmajian JV, Wolf SL (eds) Therapeutic Exercise. Baltimore: Williams and Wilkins, 1990. 36. Wall LL, Davidson TG. The role of muscular re-education by physical therapy in the treatment of GSI. Obstet Gynecol Surv 1992;47:322–31. 37. Eriksen BC. Electrostimulation of the pelvic floor in female urinary incontinence [Thesis]. Norway: University of Trondheim, 1989. 38. Herbison P, Plevnik S, Mantle J. Weighted vaginal cones for urinary incontinence (Cochrane Review). Chichester: Wiley, 2002. 39. Bø K. Vaginal weight cones. Theoretical framework, effect on pelvic floor muscle strength and female stress urinary incontinence. Acta Obstet Gynecol Scand 1995;74:87–92. 40. Van Waalwijk van Doorn ESC, Ambergen AW. Diagnostic assessment of the overactive bladder during the filling phase: the detrusor activity index. BJU Int 1999;83(Suppl 2):16–21. 41. Bø K, Berghmans LCM. Nonpharmacologic treatments for overactive bladder – pelvic floor exercises. Urology 2000;55(Suppl 5a):7–11. 42. Houston KA. Incontinence and the older woman. Clin Geriatr Med 1993;9:157–71. 43. Messelink EJ. The overactive bladder and the role of the pelvic floor muscles. BJU Int 1999;83(Suppl 2):31–5. 44. Berghmans LCM, Van Waalwijk van Doorn ESC, Nieman FHM et al. Efficacy of physical therapeutic modalities in women with proven bladder overactivity. Eur Urol 2002;41(6):581–8. 45. Wyman JF, Fantl JA, McClish DK et al. Comparative efficacy of behavioural interventions in the management of female urinary incontinence. Continence Program for Women Research Group. Am J Obstet Gynecol 1998;179:999–1007. 46. Yamanishi T, Yasuda K, Sakakibara R et al. Randomized, double blind study of electrical stimulation for urinary incontinence due to detrusor overactivity. Urology 2000;55:353–7. 47. Wang AC, Wang YY, Chen MC. Single-blind, randomized trial of pelvic floor muscle training, biofeedback-assisted pelvic floor muscle training, and electric stimulation in the management of overactive bladder. Urology 2004;63(1):61–6. 48. Ceresoli A, Zanetti G, Trinchieri A et al. Stress urinary incontinence after perineal radical prostatectomy. Arch Ital Urol Androl 1995;67:207–20. 49. Van Kampen M, De Weerdt W, Van Poppel H et al. The effect of pelvic floor re-education on duration and degree of incontinence after radical prostatectomy: a randomised controlled study. Lancet 2000;355(9198):98–102.
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50. Van der Burgt M, Verhulst F. Doen en blijven doen. In: van der Burgt M, Verhulst F (eds) Gedragsmodellen. Houten: Bohn Stafleu Van Loghum, 1996; 31. 51. Hoenen JA, Tielen LM, Willink AE. Patiëntenvoorlichting
stap voor stap: Suggesties voor de huisarts voor de aanpak van patiëntenvoorlichting in het consult. Rijswijk, the Netherlands: Uitgeverij voor gezondheidsbevordering, Stichting O&O; 1988.
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Section 2 Basic science: structure and function of lower urinary and ano-rectal tracts in women Section Editor Jacek L Mostwin
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7 Anatomy John O L DeLancey
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FUNCTIONAL ANATOMY OF THE LOWER URINARY TRACT The inseparable relationship between structure and function in living organisms is one of the common themes found in biology. The anatomy and clinical behavior of the lower urinary tract exemplify this immutable link. The following descriptions are intended to offer a brief overview of some clinically relevant aspects of lower urinary tract structure that help us understand the normal and abnormal behavior of this system. Because of the importance of the pelvic floor to lower urinary tract function, comments on the structure of the lower urinary tract organs are followed by a section describing the structure of the pelvic floor as it relates to micturition, continence, and pelvic organ support. The lower urinary tract can be divided into the bladder and urethra. At the junction of these two continuous, yet discrete, structures lies the vesical neck. This hybrid structure represents that part of the lower urinary tract where the urethral lumen traverses the bladder wall before becoming surrounded by the urethral wall. It contains portions of the bladder muscle, and also elements that continue into the urethra. The vesical neck is considered separately because of its functional differentiation from the bladder and the urethra. The spatial relationships of this region are illustrated in Figure 7.1 and described in Table 7.1.
Two prominent bands on the dorsal aspect of the bladder form one of the prominent landmarks of detrusor musculature.1 They are derived from the outer longitudinal layer and pass beside the urethra to form a loop on its anterior aspect, called the detrusor loop. On the anterior aspect of this loop, some detrusor fibers leave the region of the vesical neck and attach to the pubic bones and pelvic walls; these are called the pubovesical muscles and are discussed below.
Trigone Within the bladder there is a visible triangular area known as the vesical trigone. The two ureteral orifices and the internal urinary meatus form its apices. The
Bladder The bladder consists of the detrusor muscle, covered by an adventitia and serosa over its dome, and lined by a submucosa and transitional cell epithelium. The muscular layers of the detrusor are not discrete; nevertheless, in general, the outer and inner layers of the detrusor musculature tend to be longitudinal, with an intervening circular–oblique layer.
Table 7.1.
Figure 7.1. The lower urinary tract, including the striated urogenital sphincter muscle.
Topography of urethral and paraurethral structures*
Approximate location†
Region of the urethra
Paraurethral structures
0–20
Intramural urethra
Urethral lumen traverses the bladder wall
20–60
Midurethra
Sphincter urethrae muscle Pubovesical muscle Vaginolevator attachment
60–80
Perineal membrane
Compressor urethrae muscle Urethrovaginal sphincter muscle
80–100
Distal urethra
Bulbocavernosus muscle
* Smooth muscle of the urethra was not considered. † Expressed as a percentage of total urethral length. Reproduced from ref. 4 with permission.
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Anatomy
base of the triangle, the interureteric ridge, forms a useful landmark in cystoscopic identification of the ureteric orifices. This triangular elevation is caused by the presence of a specialized group of smooth muscle fibers that lie within the detrusor, and arise from a separate embryologic primordium. They are continuous above with the ureteral smooth muscle;2 below, they continue down the urethra. In addition to their visible triangular elevation, these muscle fibers form a ring inside the detrusor loop at the level of the internal urinary meatus3 (Fig. 7.2). Some fibers continue down the dorsal surface of the urethra and lie between the ends of the U-shaped striated sphincter muscles of the urethra. These smooth muscle fibers of the trigone are clearly separable from those of the detrusor by the smaller size of their fascicles and greater density of surrounding connective tissue. The mucosa over the trigone frequently undergoes squamous metaplasia and therefore differs from that in the rest of the bladder. The circumferential distribution of the trigonal ring fibers at the vesical neck might contribute to closure of the lumen of the vesical neck in this area, but its role has yet to be fully elucidated.
Urinary trigone
Trigonal ring Detrusor loop 0 20 Pubic symphysis
Vagina 40
60
Sphincter urethrae
80
100 Urethrovaginal sphincter Compressor urethrae
Figure 7.2. Striated urogenital sphincter muscle and trigonal musculature within the bladder base and urethra (cut in sagittal section). The ruler indicates the locations of structures along the urethral length.
Urethra The urethra holds urine in the bladder and is therefore an important structure that helps determine urinary continence. It is a complex tubular viscus extending below the bladder. In its upper third it is clearly separable from the adjacent vagina, but its lower portion is fused with the wall of the latter structure. Embedded within its sub-
a
b
stance are a number of elements that are important to lower urinary tract function; their locations are summarized in Table 7.1.4
Striated urogenital sphincter The outer layer of the urethra is formed by the muscle of the striated urogenital sphincter (Figs 7.3, 7.4) which is
c
Figure 7.3. Striated urogenital sphincter muscle seen from below after removal of the perineal membrane (a) and pubic bones (b, c). (B, bladder; CU, compressor urethrae; IR, ischiopubic ramus; SM, smooth muscle; TV, transverse vaginal muscle; U, urethra; US, urethral sphincter; UVS, urethrovaginal sphincter; V, vagina; VW, vaginal wall.) (Reproduced from ref. 30 with permission.) 117
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found from approximately 20% to 80% of the total urethral length (measured as a percentage of the distance from the internal meatus to the external meatus). In its upper two-thirds, the sphincter fibers lie in a primarily circular orientation; distally, they leave the confines of the urethra and either encircle the vaginal wall as the urethrovaginal sphincter or extend along the inferior pubic ramus above the perineal membrane (urogenital diaphragm) as the compressor urethrae. This muscle is composed largely of slow-twitch muscle vfibers,5 which are well suited to maintaining the constant tone exhibited by this muscle. In addition, voluntary muscle activation increases urethral constriction during times when increased closure pressure is needed. In the distal urethra, this striated muscle compresses the urethra from above; proximally, it constricts the lumen. Studies of skeletal muscle blockade suggest that this muscle is responsible for approximately one-third of resting urethral closure pressure.6
Urethral smooth muscle The smooth muscle of the urethra is contiguous with that of the trigone and detrusor, but can be separated from these other muscles on embryologic, topographical and morphologic grounds.3,7 It has an inner longitudinal layer, and a thin outer circular layer, with the former being by far the more prominent of the two (Fig. 7.5). The layers lie inside the striated urogenital sphincter muscle, and are present throughout the upper fourfifths of the urethra. The configuration of the circular muscle suggests a role in constricting the lumen, and the longitudinal muscle may help to shorten and funnel the urethra during voiding.
Submucosal vasculature Lying within the urethra is a surprisingly well-developed vascular plexus that is more prominent than one would expect for the ordinary demands of so small an organ.8 These vessels have been studied in serial reconstruction by Huisman,3 who has demonstrated the presence of several specialized types of arteriovenous anastomosis. They are formed in such a way that the flow of blood into large venules can be controlled to inflate or deflate them. This would assist in forming a watertight closure of the mucosal surfaces, and offer the possibility of rapid increases in their filling from the pressure on the abdominal vessels that supply them. Occlusion of the arterial inflow to these venous reservoirs has been shown to influence urethral closure pressure.6 In addition, these appear to be hormone sensitive,3 which may help to explain some individuals’ response to estrogen supplementation.
Figure 7.4. Sagittal section from a 29-year-old cadaver, cut just lateral to the midline and not quite parallel to it. The section contains tissue nearer the midline in the distal urethra where the lumen can be seen at the vesical neck. (BM, bladder mucosa; CMU, circular smooth muscle of the urethra; CU, compressor urethrae; D, detrusor muscle; LMU, longitudinal smooth muscles of the urethra; PB, perineal body; PS, pubic symphysis; PUL, pubourethral ligament; PVM, pubovesical muscle; R, rectum; T, trigonal ring; UL, urethral lumen; US, urethral sphincter; UVS, urethrovaginal sphincter; V, vagina.) (Reproduced from ref. 4 with permission.)
Mucosa The mucosal lining of the urethra is continuous above with the transitional epithelium of the bladder and below with the non-keratinizing squamous epithelium of the vestibule. This mucosa shares a common derivation from the urogenital sinus with the lower vagina and vestibule. Like these other areas, its mucosa is hormonally sensitive and undergoes significant change, depending on its state of stimulation.
Connective tissue In addition to the contractile and vascular tissue of the urethra, there is a considerable quantity of connective tissue interspersed within the muscle and the submucosa. This tissue contains both collagenous and elastin fibers. Studies that have sought to abolish the active aspects of urethral closure have suggested that the non-contractile
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Therefore, it is sometimes considered as part of the bladder musculature, but it also contains the urethral lumen studied during urethral pressure profilometry. It is a region where the detrusor musculature, including the detrusor loop, surrounds the trigonal ring and the internal urinary meatus. The vesical neck has come to be considered separately from the bladder and urethra because it has unique functional characteristics. Specifically, sympathetic denervation or damage of this area results in its remaining open at rest;10 when this happens in association with stress incontinence, simple urethral suspension is often ineffective in curing this problem.11 Figure 7.5. Axial midurethral actin immunoperoxidase histologic section for smooth muscle (a) and mirrored Mallory trichrome histologic section (b) from the same specimen. A few small spots are identified in the submucosa (SM). The longitudinal (LMU) and circular (CMU) smooth muscle of the urethra, the pubovesical muscle (PVM) and the smooth muscle layer of the anterior vaginal wall (AV) are easily identified on the actin-stained immunoperoxidase preparation whereas the striated urogenital sphincter muscle (SUG) does not stain with actin. (ATFP, arcus tendineus fasciae pelvis; LA, levator ani muscles.) elements contribute to urethral closure.3 However, it is difficult to study the function of these tissues because there is no specific way to block their action pharmacologically or surgically.
Glands A series of glands are found in the submucosa, primarily along the dorsal (vaginal) surface of the urethra.9 They are most concentrated in the lower and middle thirds, and vary in number. The location of urethral diverticula (which are derived from cystic dilation of these glands) follows this distribution, being most common distally and usually originating along the dorsal surface of the urethra. In addition, their origin within the submucosa indicates that the fascia of the urethra must be stretched and attenuated over their surface, and indicates the need for its approximation after diverticular excision.
Vesical neck The term ‘vesical neck’ is both a regional and a functional one, as previously discussed. It does not refer to a single anatomic entity; it denotes that area, at the base of the bladder, where the urethral lumen passes through the thickened musculature of the bladder base.
Functional terms A number of terms have been used to describe functional units within the vesicourethral unit, based upon radiographic observations of the activities of these viscera. The term ‘extrinsic continence mechanism’ or ‘external sphincteric mechanism’ usually refers to that group of structures that respond when an individual is instructed to stop the urine stream. The two phenomena observed during this effort are a constriction of the urethral lumen by the striated urogenital sphincter and an elevation of the vesical neck, caused by contraction of the levator ani muscles, as described below. The intrinsic continence mechanism then consists of the structures which lie within the vesical neck, and which are not specifically activated by contraction of the voluntary muscles. It is this system that fails in patients whose vesical neck can be seen to be open at rest.
PELVIC FLOOR The position and mobility of the bladder and urethra are recognized as important to urinary continence.12 Because these two organs are limp and formless when removed from the body, they must depend upon attachments to the pelvic floor for their shape and position. Fluoroscopic examination has shown that the upper portions of the urethra and vesical neck are normally mobile structures, whereas the distal urethra remains fixed in position.13,14 The pelvic floor muscles and fasciae determine these aspects of support and fixation. The term ‘pelvic floor’ is used in different ways by different authors. Sometimes, especially in the colorectal field, the term is used to refer to the levator ani muscles. In this chapter, it will be given its broader interpretation because the anatomic term ‘pelvic diaphragm’ serves to identify levator ani muscles and their covering fascia, leaving the term ‘pelvic floor’ to identify the complex 119
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structural unit that lies at the bottom of the abdominal cavity. The pelvic floor consists of several components lying between the pelvic peritoneum and the vulvar skin. These are (from above downwards) the peritoneum, viscera and endopelvic fascia, levator ani muscles, perineal membrane, and external genital muscles. The eventual support for all of these structures comes from their connection to the bony pelvis and its attached muscles. The viscera are often thought of as being supported by the pelvic floor; however, they are actually a part of it. Through such structures as the cardinal and uterosacral ligaments and the pubocervical fascia, the viscera have an important role in forming the pelvic floor.
Endopelvic fascia
Figure 7.6. Supportive tissues of the cervix and upper vagina. Bladder has been removed above the vesical neck.
The viscerofascial layer The top layer of the pelvic floor is provided by the endopelvic fascia that attaches the pelvic organs to the pelvic walls, thereby suspending the pelvic organs.15–17 Because this layer is a combination of the pelvic viscera and the endopelvic fascia, it is referred to here as the viscerofascial layer. It is common to speak of the fasciae and ligaments alone, separate from the pelvic organs as if they had a discrete identity; however, unless these fibrous structures have something to attach to (the pelvic organs), they can have no mechanical effect. On each side of the pelvis the endopelvic fascia attaches the uterus and vagina to the pelvic wall (Figs 7.6–7.8). This fascia forms a continuous sheet-like mesentery, extending from the uterine artery at its cephalic margin to the point at which the vagina fuses with the levator ani muscles below. The part that attaches to the uterus is called the parametrium and that which attaches to the vagina, the paracolpium. The parametria are made up of what are clinically referred to as the cardinal and uterosacral ligaments.18,19 Although the cardinal and uterosacrals are termed ‘ligaments’ and ‘fasciae’, they are not the same type of tissue as that seen in the ‘fascia’ of the rectus abdominis muscle or in the ligaments of the knee, both of which are composed of parallel collagen fibers forming dense, regular, connective tissue. The cardinal ligament consists of blood vessels, nerves, and fibrous connective tissue, and can be thought of as mesenteries that supply the genital tract bilaterally. The uterosacral ligament contains a specific body of smooth muscle not contained in the cardinal ligament that attaches to the dorsal surface of the cervix. The ridge formed by these tissues when the uterus is elevated is visible when the cul de sac is viewed from above and is the most familiar view of this
Figure 7.7. Vagina and supportive structures drawn from dissection of a 56-year-old cadaver after hysterectomy. The paracolpium extends along the lateral wall of the vagina. (Reproduced from ref. 17 with permission.) structure, but looks entirely different when the uterus is drawn downward, the action that demonstrates its supportive function. The structural effect of the cardinal and uterosacral ligaments is most evident when the uterine cervix is pulled downwards with a tenaculum, as occurs during dilation and curettage, or pushed downwards, as during laparotomy. After a certain amount of descent within the elastic range of the fascia, the parametria become tight and arrest the further cervical descent. Similarly, downward descent of the vaginal apex after hysterectomy is resisted by the paracolpia. The fact that these ligaments do not determine the position of the uterus in normal healthy women is attested to by the observation that the cervix may be pulled down to the level of the hymen with little difficulty.20
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Figure 7.8. Level I (suspension) and level II (attachment). In level I the paracolpium suspends the vagina from the lateral pelvic walls. Fibers of level I extend both vertically and posteriorly towards the sacrum. In Level II, the vagina is attached to the arcus tendineus fasciae pelvis and superior fascia of levator ani. (Reproduced from ref. 17 with permission.) Although it is traditional to focus attention on the ligaments that suspend the uterus, the attachments of the vagina to the pelvic walls are equally important and are responsible for normal support of the vagina, bladder, and rectum, even after hysterectomy. The location of damage to these supports determines whether a woman has a cystocele, rectocele, or vaginal vault prolapse; understanding the different characteristics of this support helps in the understanding of the different types of prolapse that can occur. After hysterectomy the upper two-thirds of the vagina is suspended and attached to the pelvic walls by the paracolpium.17 This paracolpium has two portions (see Fig. 7.8): the upper portion (level I) consists of a relatively long sheet of tissue that suspends the vagina by attaching it to the pelvic wall; in the mid-portion of the vagina, the paracolpium attaches the vagina laterally and more directly to the pelvic walls (level II). This attachment stretches the vagina transversely between the bladder and rectum and has functional significance. The structural layer that supports the bladder (‘pubocervical fascia’) is composed of the anterior vaginal wall and its attachment through the endopelvic fascia to the pelvic wall. It is not a layer separate from the vagina, as sometimes suggested, but is a combination of the anterior vaginal wall and its attachments to the pelvic wall. Similarly, the
posterior vaginal wall and endopelvic fascia (rectovaginal fascia) form the restraining layer that prevents the rectum from protruding forwards, blocking formation of a rectocele. In the distal vagina (level III) the vaginal wall is directly attached to surrounding structures without any intervening paracolpium: anteriorly it fuses with the urethra, posteriorly with the perineal body and laterally with the levator ani muscles. Damage to the upper suspensory fibers of the paracolpium causes a type of prolapse that differs from damage to the mid-level supports of the vagina: defects in the support provided by the mid-level vaginal supports (pubocervical and rectovaginal fasciae) result in cystocele and rectocele, whereas loss of the upper suspensory fibers of the paracolpium and parametrium is responsible for development of vaginal and uterine prolapse. These defects occur in varying combinations and this variation is responsible for the diversity of clinical problems encountered within the overall spectrum of pelvic organ prolapse. Loss of level II support occurs because of detachment of the arcus tendineus from the ischial spine rather than from the pubic bone.21 This allows the trapezoidalshaped anterior vaginal wall to swing downward, resulting in the characteristic cystocele seen clinically. There is also some failure of the midline vaginal wall in these patients and the relationship between these two defects remains to be clarified.
Pelvic diaphragm Subjecting connective tissue to constant force will stretch any such tissue within the body. Skin expanders used in plastic surgery stretch the dense and resistant dermis to extraordinary degrees, and flexibility exercises practiced by dancers and athletes elongate leg ligaments with as little as 10 minutes of stretching a day. Both of these observations underscore the malleable nature of connective tissue when subjected to force over time. If the ligaments and fasciae within the pelvis were subjected to the continuous stress imposed on the pelvic floor by the great weight of abdominal pressure, they would stretch; this stretching does not occur because the pelvic floor muscles close the pelvic floor and carry the weight of the abdominal and pelvic organs, preventing constant strain on the ligaments. Below the viscerofascial layer is the levator ani group of muscles22 (Fig. 7.9). They have a connective tissue covering on both superior and inferior surfaces, known as the superior and inferior fasciae of the levator ani, respectively. When these muscles and their fasciae are considered together, the combined structure is termed 121
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the pelvic diaphragm. Although there have been disagreements about the terminology for this muscle, recent review of the literature shows good unanimity regarding anatomy, and a consistent nomenclature based on standardized anatomic terminology is possible.23 The levator ani consists of two portions: the pubovisceral muscle and the iliococcygeal muscle.24,25 Laterally, the iliococcygeus arises from a fibrous band on the pelvic wall (arcus tendineus levator ani; ATLA) and forms a relatively horizontal sheet that spans the opening within the pelvis and provides a shelf on which the organs may rest. The muscle inserts into the iliococcygeal raphe that is connected to the inner surface of the coccyx and sacrum. The pubovisceral muscle is a thick U-shaped muscle, the ends of which arise from the pubic bones on either side of the midline, and inserts into, or forms a sling around, the urethra, vagina, and rectum. This portion includes both the pubococcygeus and puborectalis portions of the levator ani. The pubococcygeus muscle lies medial to the puborectalis. It has several identifiable portions, each with a specific insertion point; the puboperineal muscle attaching to the perineal body, the pubovaginal muscle where the fibers of the levator attach to the elevator ani muscle as they pass by its lateral margin, and the puboanalis part where fibers insert into the space between the internal and external anal sphincter. The puborectalis muscle
a
originates near the pubic bone, possibly from the superior surface of the perineal membrane, and forms a sling dorsal to the anorectal angle, just cranial to the external anal sphincter. The opening within the levator ani muscle through which the urethra and vagina pass (and through which prolapse occurs) is called the urogenital hiatus of the levator ani. The rectum also passes through this opening; however, because the levator ani muscles attach directly to the anus, it is not included in the name of the hiatus. The hiatus, therefore, is bounded ventrally (anteriorly) by the pubic bones, laterally by the levator ani muscles and dorsally (posteriorly) by the perineal body and external anal sphincter. The normal baseline activity of the levator ani muscle keeps the urogenital hiatus closed: it squeezes the vagina, urethra and rectum closed by compressing them against the pubic bone and it lifts the floor and organs in a cephalic direction. The levator ani muscles have constant activity,26 like that of other postural muscles. This continuous contraction is similar to the continuous activity of the external anal sphincter muscle and closes the lumen of the vagina in a way similar to that by which the anal sphincter closes the anus. This constant action eliminates any opening within the pelvic floor through which prolapse could occur and forms a relatively horizontal shelf on which the pelvic organs are supported.27,28
b
Figure 7.9. (a) The levator ani muscles from below after the vulvar structures and perineal membrane have been removed showing the arcus tendineus levator ani (ATLA), external anal sphincter (EAS), puboanal muscle (PAM), perineal body (PB) uniting the two ends of the puboperineal muscle (PPM), iliococcygeal muscle (ICM), and puborectal muscle (PRM). The urethra and vagina have been transected just above the hymenal ring. (b) The levator ani muscle seen from above looking over the sacral promontory (SAC) showing the pubovaginal muscle (PVM; other abbreviations as in Fig. 7.9a). The urethra, vagina and rectum have been transected just above the pelvic floor. (Note: the internal obturator muscles have been removed to clarify levator muscle origins.) (Reproduced from ref. 23 with permission. ©DeLancey 2003.) 122
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Interaction between muscle and connective tissue The interaction between the pelvic floor muscles and the supportive ligaments is critical to pelvic organ support. As long as the levator ani muscles function properly, the pelvic floor is closed and the ligaments and fascia are under no tension; the fasciae simply act to stabilize the organs in their position above the levator ani muscles. When the pelvic floor muscles relax or are damaged, the pelvic floor opens and the vagina lies between the high abdominal pressure and low atmospheric pressure; in this situation it must be held in place by the ligaments. Although the ligaments can sustain these loads for short periods of time, if the pelvic floor muscles do not close the pelvic floor then the connective tissue must carry this load for long periods and will eventually fail to hold the vagina in place. This support of the uterus has been likened to a ship in its berth, floating on the water attached by ropes on either side to a dock.29 The ship is analogous to the uterus, the ropes to the ligaments, and the water to the supportive layer formed by the pelvic floor muscles. The ropes (ligaments) function to hold the ship (uterus) in the center of its berth as it rests on the water (pelvic floor muscles). If, however, the water level were to fall so far that the ropes would be required to hold the ship without the support of the water, the ropes would break. The analogous situation in the pelvic floor involves the pelvic floor muscles supporting the uterus and vagina that are stabilized in position by the ligaments and fasciae: once the pelvic floor musculature becomes damaged and no longer holds the organs in place, the connective tissue fails because of significant overload.
Perineal membrane and external genital muscles In the anterior portion of the pelvis, below the pelvic diaphragm, is a dense triangular membrane containing a central opening called the perineal membrane (urogenital diaphragm). This lies at the level of the hymenal ring and attaches the urethra, vagina, and perineal body to the ischiopubic rami. Just above the perineal membrane are the compressor urethrae and urethrovaginal sphincter muscles, previously discussed as part of the striated urogenital sphincter muscle. The term ‘perineal membrane’ replaces the old term ‘urogenital diaphragm’, reflecting more accurate recent anatomic information.30 Previous concepts of the urogenital diaphragm show two fascial layers, with a transversely orientated muscle between them (the deep transverse perineal muscle). Observations based on serial histology
and gross dissection, however, reveal a single connective tissue membrane, with these muscles and the levator ani muscles lying immediately above. The correct anatomy explains the observation that pressures during a cough are greatest in the distal urethra,31,32 where the compressor urethrae and urethrovaginal sphincter can squeeze the lumen in anticipation of a cough.33
Position and mobility of the urethra When the importance of urethral position to determining urinary continence was recognized, anatomic observations revealed an attachment of the tissues around the urethra to the pubic bones. These connections were referred to as the pubourethral ligaments34 and were found to be continuous with the connective tissue of the perineal membrane.35 Further studies33,36,37 have expanded these observations and revealed several separate structural elements contained within these tissues that have functional importance to urinary continence. As mentioned earlier in this chapter, urethral support is dynamic rather than static. Fluoroscopic and topographic observations13,14 suggest that urethral position is determined both by attachments to bone and by those to the levator ani muscles. The role of the connection between the ureteral supports and those to the levator ani is probably more important than previously thought, for the following reasons:
• The resting position of the proximal urethra is high
•
•
•
within the pelvis, some 3 cm above the inferior aspect of the pubic bones38 (Fig. 7.10) and above the insertion of the ‘posterior pubourethral ligaments’ which attach near the lower margin of the pubic bones.34 Maintenance of this position would be best explained by the constant muscular activity of the levator ani. In addition, the upper two-thirds of the urethra is mobile13,14,39 and under voluntary control. At the onset of micturition, relaxation of the levator ani muscles allows the urethra to descend and obliterates the posterior urethrovesical angle (Fig. 7.10). Resumption of the normal tonic contraction of the muscle at the end of micturition returns the vesical neck to its normal position.
The anterior vaginal wall and urethra arise from the urogenital sinus and are intimately connected. The support of the urethra does not depend on attachments of the urethra itself to adjacent structures, but on the connection of the vagina and periurethral tissues to the muscles and fasciae of the pelvic wall. Surgeons are most familiar 123
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3 cm
Perineal membrane
Figure 7.10. Topography and mobility of the normal proximal urethra and vesical neck based upon resting () and voiding ( ) in nulliparae.
with seeing this anatomy through the space of Retzius, and this view is also helpful in understanding urethral support (Fig. 7.11). On either side of the pelvis, the arcus tendineus fasciae pelvis (ATFP) is found as a band of connective tissue attached at one end to the lower one-sixth of the pubic bone, 1 cm from the midline, and at the other end to the ischial spine. The anterior portion of this band lies on the inner surface of the levator ani muscle that arises some 3 cm above the ATFP. Posteriorly, the levator ani arises from a second arcus, the ATLA, which fuses with the ATFP near the ischial spine. The layer of tissue that provides urethral support has two lateral attachments: a fascial attachment and a muscular attachment (Fig. 7.12). The fascial attachments of the urethral supports connect the periurethral tissues and anterior vaginal wall to the ATFP and have been termed the paravaginal fascial attachments.36 The muscular attachment connects these same periurethral tissues to the medial border of the levator ani muscle. These attachments allow the normal resting tone of the levator ani to maintain the position of the vesical neck, supported by the fascial attachments (Fig. 7.13). When the muscle relaxes at the onset of micturition, it allows the vesical neck to rotate downwards to the limit of the elasticity of the fascial attachments; at the end of micturition, contraction allows it to resume its normal position. Also within this region are the pubovesical muscles, which are extensions of the detrusor muscle.1,40,41 They lie within connective tissue; when both muscular and fibrous elements are considered together they are termed the pubovesical ligaments, in much the same
Figure 7.11. Space of Retzius (drawn from cadaver dissection). Pubovesical muscle (PVM) can be seen going from vesical neck (VN) to arcus tendineus fasciae pelvis (ATFP) and running over the paraurethral vascular plexus (PVP). (ATLA, arcus tendineus levator ani; B, bladder; IS, ischial spine; LA, levator ani muscles; OIM&F obturator internus muscle and fascia; PS, pubic symphysis; U, urethra.) (Reproduced from ref. 41 with permission.)
Figure 7.12. Relationship of the supportive tissues of the urethra (USu) to the pubovesical muscles (PVM). Crosssection of the urethra (U), vagina (V), arcus tendineus fasciae pelvis (ATFP) and superior fascia of levator ani (SFLA) just below the vesical neck (drawn from cadaver dissection). The PVM lie anterior to the urethra, and anterior and superior to the paraurethral vascular plexus (PVP). The USu (‘the pubourethral ligaments’) attach the vagina and vaginal surface of the urethra to the levator ani (LA) muscles (MAt, muscular attachment) and to the superior fascia of the LA (FAt, fascial attachment). (R, rectum; RP, rectal pillar; VM, vaginal wall muscularis.) (Reproduced from ref. 41 with permission.)
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way that the smooth muscle of the ligamentum teres is referred to as the round ligament (see Figs 7.4, 7.5, 7.11, 7.12). Although the terms ‘pubovesical ligament’ and ‘pubourethral ligament’ have sometimes been considered to be synonymous, the pubovesical ligaments are different structures from the urethral supportive tissues. Fibers of the detrusor muscle are able to undergo great elongation, and these weak tissues are, therefore, not suited to maintain urethral position under stress. In addition, they run in front of the vesical neck rather than underneath it, where one would expect supportive tissues to be found. It is not surprising, therefore, that these detrusor fibers do not differ, in stress-incontinent patients, from those in patients without this condition.42 The tissues that support the urethra are separated from the pubovesical ligaments by a prominent vascular plexus, and are easily parted from them. Rather than supporting the urethra, the pubovesical muscles may be responsible for assisting in vesical neck opening at the onset of micturition by contracting to pull the anterior vesical neck forwards, as some have suggested.43 This mechanism influences incontinence by determining how the urethra is supported, not by how high or low the urethra is in the pelvis. In examining anatomic specimens, simulated increases in abdominal pressure reveal that the urethra lies in a position where it can be compressed against the supporting hammock by rises in abdominal pressure (Fig. 7.13). In this model, it is the stability of this supporting layer under the urethra rather than the height of the urethra that determines stress continence. In an individual with a firm supportive layer, the urethra would be compressed between abdominal pressure and pelvic fascia (Fig. 7.14) in much the same way that the flow of water through a garden hose can be stopped by stepping on and compressing it against underlying paving. If, however, the layer under the urethra becomes unstable and does not provide a firm backstop against which the urethra can be compressed by abdominal pressure, the opposing force that causes closure is lost and the occlusive action is diminished. This latter situation is similar to an attempt to stop the flow of water through a garden hose by stepping on it while it lies on soft soil. The structural and functional aspects of the body must always be in agreement. As new functional observations are made of the lower urinary tract, it will be necessary to re-examine our anatomic concepts; doubtless, some of the structural arrangements described in this chapter will be corrected, expanded upon, and improved. This will continue to enhance our ability to understand the variety of patients with lower urinary tract dysfunction, and will improve our ability to restore normal urinary control.
Endopelvic fascia Anterior vaginal wall Rectum External anal sphincter
Arcus tendineus fasciae pelvis Levator ani Urethra Perineal membrane
Figure 7.13. Lateral view of the pelvic floor structures related to urethral support, seen from the side in the standing position cut just lateral to the midline. Note that windows have been cut in the levator ani muscles, vagina and endopelvic fascia, so that the urethra and anterior vaginal walls can be seen.
Figure 7.14. Lateral view of pelvic floor with the urethra, vagina and fascial tissues transected at the level of the vesical neck, drawn from three-dimensional reconstruction indicating compression of the urethra by downward force (arrow) against the supportive tissues indicating the influence of abdominal pressure on the urethra (arrow).
REFERENCES 1. Gil Vernet S. Morphology and Function of the Vesico-prostato-urethral Musculature. Italy: Edizioni Canova Treviso, 1968. 2. Woodburne RT. The ureter ureterovesical junction and vesical trigone. Anat Rec 1965;151:243–9. 3. Huisman AB. Aspects on the anatomy of the female ure-
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thra with special relation to urinary continence. Contrib Gynecol Obstet 1983;10:1–31.
24. Lawson JON. Pelvic anatomy. I. Pelvic floor muscles. Ann R Coll Surg Engl 1974;54:244–52.
4. DeLancey JOL. Correlative study of paraurethral anatomy. Obstet Gynecol 1986;68:91–7.
25. Lawson JON. Pelvic anatomy. II. Anal canal and associated sphincters. Ann R Coll Surg Engl 1974;54:288–300.
5. Gosling JA, Dixon JS, Critchley HOD, Thompson SA. A comparative study of the human external sphincter and periurethral levator ani muscles. Br J Urol 1981;53:35–41.
26. Parks AG, Porter NH, Melzak J. Experimental study of the reflex mechanism controlling muscles of the pelvic floor. Dis Colon Rectum 1962;5:407–14.
6. Rud T, Anderson KE, Asmussen M et al. Factors maintaining the intraurethral pressure in women. Invest Urol 1980;17:343–7.
27. Berglas B, Rubin IC. Study of the supportive structures of the uterus by levator myography. Surg Gynecol Obstet 1953;97:677–92.
7. Dröes JTPM. Observations on the musculature of the urinary bladder and urethra in the human foetus. Br J Urol 1974;46:179–85. 8. Berkow SG. The corpus spongiosum of the urethra: its possible role in urinary control and stress incontinence in women. Am J Obstet Gynecol 1953;65:346–51. 9. Huffman J. Detailed anatomy of the paraurethral ducts in the adult human female. Am J Obstet Gynecol 1948;55:86–101. 10. McGuire EJ. The innervation and function of the lower urinary tract. J Neurosurg 1986;65:278–85. 11. McGuire EJ. Urodynamic findings in patients after failure of stress incontinence operations. Prog Clin Biol Res 1981;78:351–60. 12. Hodgkinson CP. Relationships of the female urethra in urinary incontinence. Am J Obstet Gynecol 1953;65:560–73. 13. Muellner SR. Physiology 1951;65:805–10.
of
micturition.
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Urol
14. Westby M, Asmussen M, Ulmsten U. Location of maximum intraurethral pressure related to urogenital diaphragm in the female subject as studied by simultaneous urethrocystometry and voiding urethrocystography. Am J Obstet Gynecol 1982;144:408–12. 15. Ricci JV, Thom CH. The myth of a surgically useful fascia in vaginal plastic reconstructions. Q Rev Surg Obstet Gynecol 1954;2:261–3. 16. Uhlenhuth E, Nolley GW. Vaginal fascia a myth? Obstet Gynecol 1957;10:349–58. 17. DeLancey JOL. Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 1992;166:1717–28. 18. Range RL, Woodburne RT. The gross and microscopic anatomy of the transverse cervical ligaments. Am J Obstet Gynecol 1964;90:460–7. 19. Campbell RM. The anatomy and histology of the sacrouterine ligaments. Am J Obstet Gynecol 1950;59:1–12. 20. Bartscht KD, DeLancey JOL. A technique to study cervical descent. Obstet Gynecol 1988;72:940–3. 21. DeLancey JOL. Fascial and muscular abnormalities in women with urethral hypermobility and anterior vaginal wall prolapse. Am J Obstet Gynecol 2002;187:93–8.
28. Nichols DH, Milley PS, Randall CL. Significance of restoration of normal vaginal depth and axis. Obstet Gynecol 1970;36:251–6. 29. Paramore RH. The uterus as a floating organ. The Statics of the Female Pelvic Viscera. London: HK Lewis, 1918; 12–5. 30. Oelrich TM. The striated urogenital sphincter muscle in the female. Anat Rec 1983;205:223–32. 31. Hilton P, Stanton SL. Urethral pressure measurement by microtransducer: the results in symptom-free women and in those with genuine stress incontinence. Br J Obstet Gynaecol 1983;90:919–33. 32. Constantinou CE. Resting and stress urethral pressures as a clinical guide to the mechanism of continence in the female patient. Urol Clin North Am 1985;12:247–58. 33. DeLancey JOL. Structural aspects of the extrinsic continence mechanism. Obstet Gynecol 1988;72:296–301. 34. Zacharin RF. The anatomic supports of the female urethra. Obstet Gynecol 1968;21:754–9. 35. Milley PS, Nichols DH. Relationship between the pubourethral ligaments and the urogenital diaphragm in the human female. Anat Rec 1971;170:81–3. 36. Richardson AC, Edmonds PB, Williams NL. Treatment of stress urinary incontinence due to paravaginal fascial defect. Obstet Gynecol 1981;57:357–62. 37. DeLancey JOL. Structural support of the urethra as it relates to stress urinary incontinence: the hammock hypothesis. Am J Obstet Gynecol 1994;170:1713–20. 38. Noll LE, Hutch JA. The SCIPP line – an aid in interpreting the voiding lateral cystourethrogram. Obstet Gynecol 1969;33:680–9. 39. Jeffcoate TNA, Roberts H. Observations on stress incontinence of urine. Am J Obstet Gynecol 1952;64:721–38. 40. Woodburne RT. Anatomy of the bladder and bladder outlet. J Urol 1968;100:474–87. 41. DeLancey JOL. Pubovesical ligament: a separate structure from the urethral supports (pubo-urethral ligaments). Neurourol Urodyn 1989;8:53–62.
22. Dickinson RL. Studies of the levator ani muscle. Am J Dis Women 1889;22:897–917.
42. Wilson PD, Dixon JS, Brown ADG, Gosling JA. Posterior pubo-urethral ligaments in normal and genuine stress incontinent women. J Urol 1983;130:802–5.
23. Kearney R, Sawhney R, DeLancey JO. Levator ani muscle anatomy evaluated by origin-insertion pairs. Obstet Gynecol 2004;104:168–73.
43. Power RMH. An anatomical contribution to the problem of continence and incontinence in the female. Am J Obstet Gynecol 1954;67:302–14.
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8 Embryology of the female urogenital system with clinical applications Jenny Lassmann, Stephen A Zderic
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IntroductIon The first aim of this chapter is to provide the reader with an overview of the embryologic steps that lead to formation of the upper and lower urinary tract. Since normal lower urinary tract development in the female cannot be discussed in isolation from that of rectum, anus, and vagina, a good deal of attention will be focused on the embryology of the perineum. Traditional embryology writings were highly descriptive anatomic treatises; the modern world of developmental biology is changing this rapidly. Therefore a second aim is to briefly discuss the recurring theme of cell–cell communication that occurs as these complex structures develop, and to offer a basic introduction to some of the genes and signaling molecules involved in this embryology. A third aim of this chapter is to provide several clinical examples of malformations that arise as deviations occur from this path of normal development.
Early EmbryogEnEsIs Following conception, the resulting zygote undergoes a series of cell divisions, and the resulting embryo becomes implanted within the endometrial wall of the uterine cavity. Via unknown molecular mechanisms, this collection of ultimate stem cells begins to differentiate into three basic germ layers. By 22 days of gestation, the embryo is a disk-shaped structure containing the three germ cell layers: the ectoderm lined amniotic cavity, the mesoderm, and the endoderm arising within the yolk sac. At the cranial and caudal ends the ectoderm and endoderm are in direct contact, and these bilaminar areas are described as the oropharyngeal and cloacal membranes (Fig. 8.1a).1 With further growth this disk folds progressively, both craniocaudally and laterally, resulting in yolk sac invagination. Over the ensuing 6 weeks the yolk sac tubularizes and differentiates into the stomach, small intestine and large intestine, completing this process by week 10 of embryonic development.1 During the course of this yolk sac tubularization, the intestines are extruded from the abdominal cavity by means of the incompletely developed anterior abdominal wall. Simultaneously with the abdominal wall closure, the developing intestines return to the abdominal cavity, and in doing so undergo a 245-degree anticlockwise rotation about the superior mesenteric artery. This process is complete by 10 weeks of age, and explains why the cecum is found in the right lower quadrant. The development of the ureters, bladder, and urethra starts at the caudal end of the embryo at the cloacal membrane and within the adjacent mesenchyme. It is via differential growth rates of the adjacent mesenchyme
Figure 8.1. (a) Sagittal section of the discoid 22-day-old embryo, showing the relationship of the yolk sac to the neural and mesenchymal layers prior to the folding. The arrows show the direction of the subsequent folding that takes place by day 28. The oropharyngeal and cloacal membranes are already developing at the cranial and caudal ends of the neural tube. (b) Sagittal section of the embryo at day 28, showing the residual yolk sac contained within the developing umbilical cord. The second smaller extension of the yolk sac into the cord (which forms the basis of the allantois) can be seen. The cloacal membrane is just to the right of the umbilical cord. (Reproduced with permission from ref. 2.) that the distal primitive hindgut begins to form a dilated chamber known as the cloaca. To appreciate the development of the lower urinary tract and female perineum, one must understand the transition from the 4 mm (4week) to the 36 mm (10-week) embryo as the cloaca is partitioned into anterior (urogenital) and posterior (rectal) components.
dIvIsIon of thE cloaca Following invagination of the yolk sac at day 28, the primitive hindgut begins to form a dilated chamber,
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Figure 8.2. (a) Undivided internal cloaca at the 4 mm stage of development. The developing urorectal septum separates the allantois from the hindgut. The allantoic extension to the left leads to the umbilical cord and the future navel; this extension forms the basis of the urachal remnant. (b) Division of the internal cloaca is completed in this sequence, and the cloacal membrane has now ruptured, allowing for communication between the internal and external cloacal chambers. (c) With further growth, the external cloaca is partitioned by an extension of the urorectal septum and an ingrowth of the genital folds. (d) Fusion of the genital folds in the midline completes the separation of the urethra anteriorly from the rectum posteriorly. (Reproduced with permission from ref. 2.) referred to as the cloaca. From this develops a ventral outgrowth oriented towards the umbilicus referred to as the allantois (Fig. 8.2a). At this stage, the cloacal membrane which separates the internal cloaca (lined with endoderm derived from the yolk sac) from the external cloaca (composed of ectoderm) remains intact.2 Part of the allantois will contribute to bladder development; those portions closest to the umbilicus will atrophy forming the urachus. However, in order for these structures to form, the internal cloaca must be partitioned into the ventral (urogenital) and dorsal (rectal) cloaca. This division of the cloaca, which is first recognized within the
upper portions of the chamber, begins during the 5th week, and is completed during the 7th week of gestation with resulting rupture of the cloacal membrane (Fig. 8.2b). The exact mechanisms are still debated. Rathke3 claimed that this partition takes place by median fusion of two lateral ridges of the cloacal wall in a caudal direction, whereas Torneaux4 described a descending septum fusing with the cloacal membrane. In contrast, more recent studies described this process as a fusion of the surrounding mesoderm of the incorporated parts of the yolk sac and allantois.5,6 Irrespective of the exact mechanism, by the beginning of the 8th week of gestation the cloaca has been divided into anterior (ventral) and posterior (dorsal) components, and there is free communication between the internal and external cloaca due to the rupture of the cloacal membrane. The molecular basis for cloacal differentiation is better understood today thanks to the tools of modern molecular biology. Using a murine model of fetal exposure to all trans retinoic acid on the 9th day of conception, Sasaki et al.7 demonstrated that all fetal survivors had a short tail and imperforate anus. In females this was manifest as a common cloaca in which the urethra, vagina, and rectum all merged (Fig. 8.3). The process of normal cloacal differentiation appears to be under the control of the sonic hedgehog (Shh) signaling pathway. Shh immunoreactivity was prominent in the rectal, urethral, and bladder epithelium in normal mice, but was absent in those with anorectal malformations (ARM). Bone morphogenic protein type 4 (BMP-4) immunoreactivity was noted in the mesenchyme below the epithelium staining for Shh expression in normal mice, but was absent in the population with ARM. In a second model using a knockout mouse model for Shh, Sukegawa et al. demonstrated that Shh signaling is critical to the concentric development of the hindgut.8 It is becoming increasingly clear that complex epithelial mesenchymal interactions are critical to normal cloacal differentiation. Simultaneously with the septation of the internal cloaca, the external cloaca also undergoes partitioning in order for the normal perineum to develop and the process of external sexual differentiation begins. Partitioning of the external cloaca begins in part as a distal extension of the urorectal septum (Fig. 8.2c) coupled to an inward migration of the genital folds to create the short female perineal body and median raphe (Fig. 8.2d). In contrast, the perineal body in males is elongated, and there is an anterior deflection of the proximal urethra, a process that is regulated by androgens. This phase also marks the onset of müllerian differentiation in the female embryo. 129
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Normal perineal and external genital development also arises from a complex epithelial mesenchymal interaction. While androgens are critical to the resulting male phenotype, genital patterning is initiated 2 weeks prior to testosterone synthesis, in part by a program that is Shh dependent. These concepts are nicely demonstrated in a mouse with a deletion of Shh expression; external genitalia are absent and a primitive cloaca develops instead (Fig. 8.3).9 It appears that with Shh deletion, there is also a concomitant downregulation of BMP2, BMP4, Fgf8, Fgf10, and Wnt5a, and there is enhanced apoptosis within the genitalia.9 Clearly, some of the pathways leading to genital development must be androgen dependent, of which Ephrin B signaling in the developing urethral seam is one such example.10
müllErIan dIffErEntIatIon By week 6 the müllerian ducts form from intermediate cell masses located laterally from the wolffian ducts. They begin as solid cords which tubularize, probably on the basis of apoptosis during their differentiation. Proximal parts of these ducts form the fallopian tubes; distally, they fuse in the midline producing the uterus, cervix, and proximal two-thirds of the vagina.11 By week 7, the caudal ends of the müllerian ducts migrate through the urorectal septum to penetrate the posterior aspect of the urethra at the müllerian tubercle between the two openings of the wolffian ducts (Fig. 8.4). With growth, the urethra and müllerian structures terminate in the common urogenital sinus (Fig. 8.4b) prior to the separation of the urethra and vagina that takes place by differential growth (Fig. 8.4c) and an anterior turn of the distal urethra (Fig. 8.4d). Failures in such distal migration of the müllerian ducts to form the urogenital sinus may result in distal vaginal atresia.
A
It is important to appreciate the interaction between the wolffian and müllerian systems leading to formation of the urogenital sinus. The wolffian ducts serve to guide the müllerian ducts to the urogenital sinus, and are carried towards the perineum in the lateral walls of the vagina and undergo involution in the course of normal differentiation. If they fail to involute completely, they can remain as small cysts within the lateral vaginal wall or the cervix. Occasionally, these remnants become larger and infected, and present clinically as Gartner’s duct cysts. This embryology is also clinically relevant because the ureteral buds arise from the wolffian system, meaning that the lateral walls of the vagina may be a site for the rare insertion of an ectopic ureter.
smooth musclE dIffErEntIatIon The female urothelium arises from endoderm derived from the ventral chamber created by the division of the cloaca by the urorectal septum.12 The connective tissue and smooth muscle are subsequently derived from adjacent mesenchyme. The developing urethra and bladder contain no muscle in the early stages of development and the endoderm of the urogenital sinus remains a single layer of epithelium up to the 7th week and then gradually assumes the appearance of transitional epithelium in the third month. The earliest muscle layers arise within the bladder, and the urethral smooth muscle layers are induced 1 week later, implying that these smooth muscle bodies are distinct entities despite their close approximation at the bladder neck. This should not be particularly surprising given the pharmacologic differences and functional demands between these two bodies of smooth muscle. The mechanism by which epithelial mesenchymal interactions induce smooth muscle development has been described. Using fetal rat primitive mesenchyme
B
Figure 8.3. (A) Midsagittal section taken through a mouse embryo with a deletion of Shh expression shows a persistent cloaca covered by a thin cloacal membrane (cm). The bladder (b) and hindgut (h) are partially separated by the urorectal septum (urs). The proximal portion of the tail (t) can be seen. (B) In comparison, a midsagittal section taken through a wild-type embryo showing almost complete separation of the bladder and urogenital sinus from the rectum (r). (Reproduced with permission from ref. 9.) 130
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dEvElopmEnt of thE sphInctErs Little has been written about the development of the internal or smooth muscle sphincter, i.e. the bladder neck. In contrast, more efforts have been expended in trying to better characterize the development of the striated external sphincter. There is some evidence to support the notion of transdifferentiation from smooth to striated muscle which could then account for the development of the external sphincter.16 As an alternative explanation, anatomic observations in female fetal specimens confirm that, by 9 weeks of gestation, there is a condensation of undifferentiated mesenchyme immediately adjacent to the urethra. By 10 weeks of gestation this mesenchyme had differentiated into striated muscle which formed the omega-shaped external sphincter.17,18 In this study, there was no evidence for concentric development of this striated muscle group followed by a selective loss of muscle to produce the omega shape characteristic of this sphincter. Similar observations were reported by Yucel and Baskin19 who also noted that this striated sphincter is always distinct from the levator muscle group, and commented on the innervation of this sphincter by both myelinated fibers and neurons that stained positively for neuronal nitric oxide synthase (nNOS).20 Figure 8.4. (a) The Müllerian ducts migrate to and penetrate the posterior urethra at week 7. The müllerian ducts are guided to this point in the posterior urethra by the wolffian ducts. (b) The ducts migrate caudally, and the urogenital sinus becomes a shallow channel. At this point there is a good separation between the urethra and vagina. (c) With continued growth the urogenital sinus disappears, as both the urethra and vaginal introitus are now at the perineal surface. The distal vagina is formed from sinus epithelium which streams into the vaginal vault. (d) With continued growth, the urethra turns anteriorly to reach its final location. (Reproduced with permission from ref. 11.) transferred below the renal capsule in nude mice, Baskin et al. demonstrated that a transformation of this mesenchyme into smooth muscle was possible only if urothelium was also implanted simultaneously.13,14 The growth factors secreted by such epithelial surfaces are powerful driving forces for differentiation of the adjacent mesenchyme, i.e. the process of cell–cell interaction. This concept was also described in another murine model, when it was observed that urethral urothelium implanted in a primitive limb bud could induce additional digits to develop.9 Further morphologic growth of smooth muscle development is accompanied by complex serial changes in musclespecific protein expression and cell turnover, as shown in a detailed study of mouse detrusor development.15
dEvElopmEnt of thE trIgonE and uppEr urInary tract The pronephros develops at the 4th week and differentiates into the mesonephric ducts and the mesonephros. The mesonephros consists of primitive glomeruli and tubules, which open into the mesonephric (wolffian) ducts that are derived from the pronephric ducts. The mesonephric ducts extend caudally and drain into the cloaca,1 and an outgrowth of the ducts near their insertion at the cloaca gives rise to the ureteric buds (Figs 8.5, 8.6).21,22 The ureteric buds grow cranially until they contact the metanephric mesenchyme, at which point a series of complex reciprocal interactions between the bud and the mesoderm result in differentiation to the metanephros and ultimately a functioning kidney; fetal urine production is evident by the 9th week of gestation. The takeoff point of the ureteric bud is critical for formation of the trigone, development of a normal vesicoureteral junction, and ultimately for the formation of a normal kidney. The embryologic development of the trigone continues to be a source of some debate. The trigone was traditionally thought to be of mesodermal origin. In order for the ureteric bud to become incorporated into the developing urogenital sinus, the common excre131
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Figure 8.5. Stages of the renal branching morphogenesis: (A) Ureteric bud outgrowth from the wolffian duct is induced by signals from the metanephric mesenchyme. (B, C) Invasion of the metanephric mesenchyme by the ureteric bud results in branching. (D) At the tips of the branches, the epithelium induces the mesenchyme to form pretubular aggregates, which are stimulated to undergo mesenchymal to epithelial transformation through the formation of comma-shaped (E) and S-shaped (F) bodies to form components of the nephron. (G) The renal tubules merge with the epithelial and vascular components of the glomerulus. (Reproduced with permission from ref. 21.) tory duct must become absorbed into this sinus. Thus it would stand to reason that at least part of the trigone is of mesodermal origin. However, recent studies using transgenic mice suggest that in fact the trigone is of endodermal origin.23 The kidney develops as a result of complex reciprocal signaling between the ureteric bud and the primitive metanephric mesenchyme.21 Once this signaling is initiated, the bud elongates to penetrate the blastema, and the process of branching begins. In order for the final form of a single human kidney to have 500,000 to 1 million nephrons, the ureteral bud must undergo branching morphogenesis (Fig. 8.5).21 Iterative branching of the ureteral bud must occur about 15 times during human development in order to lead to this number of nephrons. As this division of the terminal ureteral
bud takes place to produce a tree-like structure, lateral branches differentiate into terminal bifid branches. In these terminal bifid branches, the ureteral bud tip will attach itself to a nephron, and remove itself from further bifurcations. This attachment of bud to a primitive nephron then initiates the formation of the full nephron. Critical to this view is the notion that the final population of nephrons is ultimately determined by the branching and proper functioning of the ureteral bud, a view espoused by Mackie and Stephens over 30 years ago (Fig. 8.7).24 Equally critical to establishing normal renal function is the acquisition of the renal artery(ies) and subsequent vascular development (for a complete review of renal development, see Shah et al.21). With current methods of molecular biology, the complex chemistry underlying these reciprocal inter-
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Figure 8.6. Visualization of the three stages of ureter maturation in vivo in Hoxb7-GFP mice that express green fluorescent protein in epithelia of the fetal excretory system. (a–c) Ureteric bud formation and outgrowth: the distal ureter (ur) remains attached to the wolffian duct (wd). The distal ureter starts to separate from the primitive bladder (ugs) by a terminal wolffian duct segment, the common nephric duct (cnd). (d–f) Vertical displacement: distal ureter descends and contacts the urogenital sinus. The yellow arrow indicates the common nephric duct. Broken yellow arrow shows downward movement of the ureter towards the urogenital sinus. Yellow and green arrows indicate final position of distal ureter and wolffian duct. (g–i) Lateral displacement: the distal ureter separates from the wolffian duct and moves to the final position at the bladder base. Yellow and green arrows mark the position of distal ureter and wolffian duct before and after separation. Double-headed yellow arrow indicates epithelial wedge, an epithelial outgrowth, which facilitates the separation. Color code for c,f,i: wolffian duct and trigonal wedge: green; urogenital sinus: grey; müllerian duct (md): pink; common nephric duct: red; kidney (ki) and ureter: blue. (Reproduced with permission from ref. 22.) actions is being clarified, and several examples are offered here. In vitro studies have shown that glial derived neurotrophic factor (GDNF) secreted by the metanephric mesenchyme serves to induce ureteric budding.25 This is supported by the observation that the ureters and kidney do not develop in GDNF knockout mice. It has also been shown that gene products that antagonize GDNF expression such as FOXc1 (Fig. 8.8)25 or BMP-426 can result in multiple bud formation and duplex collecting systems. There is also a role for retinoic acid-mediated signaling in the development of the ureteral buds and trigone as shown in a model using targeted deletion of the retinoic acid receptors.22 Abnormal vesicoureteral development has also been demonstrated in the presence of targeted RET overexpression27 or the deletion of the type 2 angiotensin receptor.28
clInIcal ExamplEs urogenital sinus Persistence of the urogenital sinus can occur as an isolated malformation or in association with intersex conditions such as adrenogenital syndrome. In these patients the urethra and the vagina converge in a short common channel, and the convergence is close to the perineum. In some cases the voided urine is trapped within the vagina, resulting in hydrocolpos. These patients may present with a palpable pelvic mass requiring decompression, an infection of trapped urine, or with overflow incontinence. The rectum is often displaced anteriorly, but it functions normally. (A review of Figure 8.4 should allow the reader to understand the embryologic basis for this anomaly.) The distal müllerian ducts fuse with the 133
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adequate vaginal introitus. A urogenital sinus with a low confluence can be managed with a ‘cutback’ operation, together with an inverted U-flap to prevent introital stenosis.29 When the common channel exceeds 3 cm, the modified total urogenital sinus mobilization is the preferred approach.30,31 Depending on the length of the common channel and related anatomic malformations, a more complex surgical repair may be necessary.32,33 a
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Figure 8.7. The ureteral bud hypothesis described by Mackie and Stephens.24 (a, b) Normal kidney development: single ureteral bud is induced and grows into the nephric mesenchyme (small dots). The caudal end of the wolffian duct is incorporated into the developing bladder (red arrow). The yellow marked region contributes to the trigone, the green to the urethra and blue for the lateral bladder. (c, d) Ectopic ureter development: a second ectopic ureteral bud is induced more anteriorly than normal (green region at wolffian duct), interacts with the adjacent nephrogenic mesenchyme giving rise to a duplex system. This ectopic ureter opens into the urethra with abnormal outflow and development of hydroureter. (Reproduced with permission from ref. 25.)
Case: A 1-day-old female was noted to have a palpable mass in her lower abdomen, and sonography revealed distended fluid-filled collections in her pelvis. On physical examination her lower abdomen was filled with a tense mass, the rectum was normally placed, but no vaginal introitus could be appreciated. Via the one opening near her introitus, a genitogram was performed (Fig. 8.9), demonstrating a common urogenital sinus with a bifurcation leading to the bladder and a dilated vagina. A subsequent endoscopic examination revealed the anatomy shown in Figure 8.9, and allowed for a plan of reconstruction to be developed. Using a posterior sagittal approach, the urethrovaginal trifurcation was divided, and the urogenital sinus was converted into the urethra. The vaginas were then mobilized, and moved down into the perineum with a perineal skin flap being used to complete the vaginoplasty.
common cloaca Rarely, patients may present with a common cloaca in which the urethra, vagina, and rectum converge into one common sinus that exits at the perineum. An example of this may be found in patients with the VATER syndrome. Many of these patients often present with the associated findings of spinal cord tethering and a neurogenic bladder.
congenital vaginal anomalies urethra and then migrate caudally during normal perineal development. Arrest of this distal migration at any point will result in a urogenital sinus as the fused urethra and vagina drain into a common channel. On physical examination the vaginal introitus is absent with a single opening in the urethral position, although the labia majora and minora might be normal in appearance. The diagnosis is confirmed radiographically with a retrograde contrast injection, i.e. a genitogram (Fig. 8.9). Depending on the length of the common channel and the complexity of related malformations, different surgical procedures are available. The objectives of the surgical repair are separation of urinary and genital tracts, allowing normal voiding and creation of an
Though rare, a variety of congenital vaginal anomalies have been described in the urologic and gynecologic literature. Such anomalies may include vaginal duplication and/or associated atresias. As seen in Figure 8.4, there is an association with the wolffian ducts and the distal müllerian ducts fusing with the posterior urethra. Thus it is not surprising that there might be a condition in which ipsilateral and/or bilateral vaginal agenesis or stenosis is associated with unilateral renal agenesis which is the classic description of the Mayer–Rokitansky–Küster–Hauser syndrome.11 Increasingly this diagnosis may be made in the neonatal period because of the widespread use of prenatal sonography which would attract attention by virtue
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Figure 8.8. Kidney and ureter abnormalities in mice homozygous for Foxc1ch. (a, b) Wild-type and mutant (a) in male: hydroureter (asterisks) and testes (arrows) located more anteriorly in mutant type compared to wild-type. (b): In female with hydroureter (asterisks) and normal ureter (white arrow) behind, and mutant ovaries located more anteriorly (arrowhead). (c, d) Section of wild-type (c) and mutant (d) kidneys with a duplex kidney in the mutant and clear boundary of the peripheral metanephrogenic mesenchyme (arrow). The upper part of the kidney connects to the hydroureter (asterisk). Dorsal view of mutant kidney with normal ureters (arrows) and ectopic hydroureter (asterisks). (e, f) Sections showing abnormal position of hydroureters in mutants (f) in male: hydroureter (arrow) does not connect to bladder (b). (g) In female: hydroureter (arrow) ends blindly, while normal ureter (arrowhead) connects to bladder (b). (Reproduced with permission from ref. 25.) of the solitary kidney. In contrast, other vaginal anomalies may become manifest only with the onset of puberty. Case: A 12-year-old healthy and normally developed female presented with multiple 1-week episodes of abdominal pain occurring on a monthly basis; she was amenorrheic. Breast development was present as was pubic hair, and the urethra was normally placed above a blind-ending vaginal introitus. Further imaging with ultrasound and MRI revealed a huge hematocolpos with dilated fallopian tubes on both sides (Fig. 8.10) without any other malformations of the upper or lower urinary tract. Evaluation under anesthesia revealed a complete distal atresia of the vagina; the vaginal to perineal surface
distance was measured at 10 cm. She was managed with a combined laparoscopic mobilization of the vagina, with a simultaneous perineal exploration and vaginal pull-through in combination with a perineal skin flap. The normal urethral development seen in this case illustrates the concept that there was most likely a failure of fusion between the distal müllerian ducts and the urethra (Fig. 8.4). Subsequently, urethral migration proceeded distally, leaving the distal müllerian remnants in a position far from the perineal body. Normal urethral migration to the perineum is also seen in patients with androgen resistance syndromes, despite the absence of the upper two-thirds of the vagina, uterus, and fallopian tubes. 135
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Ectopic ureter
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Figure 8.9. (a) Genitogram demonstrating a common urogenital sinus (arrow) dividing into bladder (b) and dilated vagina (v). (b) Summary of the anatomy as revealed by endoscopic examination. (c) Postoperative result after reconstruction and conversion of the urogenital sinus into urethra.
A ureter that opens anywhere but into the trigone is considered ectopic and is the result of a displaced ureteric bud. Ureteric buds that develop very low along the mesonephric duct will be sited in a laterocranial ectopic position, often associated with a significant vesicoureteral reflux. In contrast, if a bud develops high along the mesonephric duct, it bypasses the trigone and inserts within the urethra, vestibule or vagina. An ectopic ureter can drain a single system,34 but about 70% are associated with complete ureteral duplication, with the ectopic ureter draining the upper moiety of a complete pyeloureteral duplication. Complete ureteral duplication occurs when two separate ureteral buds arise independently from the mesonephric duct. A duplex kidney is induced when these two buds meet the metanephric blastema. During the development of the trigone, the most cranial ureter that drains the upper moiety of the duplex kidney rotates inwardly on its long axis and crosses the lower pole ureter. A normal duplex kidney develops if the two ureters originate close to each other and both ureteral orifices terminate on the trigone. However, if the ureteral buds arise from widely separate positions on the mesonephric duct, the upper pole ureter is incorporated into the urogenital sinus at a later stage of development, and the resulting orifice is situated in an ectopic position, inferior to the trigone. This accounts for the Meyer Weigert law which states that the upper pole ureter shall always be found distal to that ureter which drains the lower renal unit (Fig. 8.7). Mackie and Stephens24 have postulated that induction of the metanephric blastema either too caudally or too cranially will result in renal dysplasia. This is the reason for impaired function of the renal unit draining into an ectopic ureter, whereas refluxing ureters most often drain normally functioning renal units. If the ureter opens below the internal sphincter, the ectopia becomes clinical with incontinence. If the ureteric bud arises very high along the mesonephric duct, it fails to become incorporated into the lower urinary tract and remains confluent with the mesonephric duct. These vestiges of the mesonephric system track along the lateral vagina wall and may become clinically manifest as Gartner’s duct cysts. This also provides an embryologic basis for the rare vaginal ectopic ureter. Approximately one-half of female patients with ectopic ureters frequently present with continuous dribbling of urine, despite normal bladder emptying, due to a normally situated ipsilateral or contralateral ureter.34,35 If the ectopic ureter is draining a dysplastic or hypoplastic kidney or upper pole, infection or vaginal
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B
A
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Figure 8.10. (A) Pelvic ultrasound (sagittal) demonstrating the blood filled vagina (v) behind the bladder (b). (B) MRI furthermore revealed dilated fallopian tubes (f) on both sides (u, uterus). (C) MRI in coronal view.
discharge may be the only complaint. Today, most of these cases are diagnosed by prenatal ultrasound, since most ectopic ureters are associated with significant hydronephrosis. On occasion this diagnosis is not established before toilet training and some patients are mistakenly diagnosed as enuretics and treated as such for many years. The traditional imaging workup included a cyclic vesicoureterogram (VCUG) which demonstrates reflux into the ectopic ureter in 70–80% of cases, and an intravenous urogram or CAT scan. More recently the application of MRI urography has provided a global view of the malformation, including the renal dysplasia and dilated ureter, even in the presence of diminished renal function.36 Depending on renal function, the treatment varies from ureter–ureterostomy in duplicated systems, upper pole resection (with or without ureterectomy), various ureteroneocystostomy procedures, or nephroureterectomy. Case: A 3-month-old female was hospitalized with a febrile urinary tract infection and she failed to improve clinically following 3 days of antibiotic therapy. A renal
bladder ultrasound revealed evidence of a right duplex kidney and a dilated distal ureter with an extension past the bladder neck (Fig. 8.11). Cystoscopy and retrograde pyelography revealed a right upper pole ureter that was ectopic to the right periurethral meatus. A temporizing cutaneous ureterostomy was performed, and the infant was afebrile within 24 hours. This ureter was subsequently reimplanted 1 year later. It is important to note that, in this particular instance, prenatal sonography had not been performed. In rare instances, bilateral ureteral budding may occur high along the mesonephric duct and the result is bilateral ectopic ureters. These patients present with total urinary incontinence, a deficient internal sphincter, and a non-compliant bladder with small capacity. These cases serve to illustrate the importance of bladder cycling to the acquisition of normal capacity and compliance, a concept that has been confirmed in fetal experimental models.37 For these patients, urinary continence will require complex surgery, most often consisting of a bladder neck reconstruction, ureteral reimplantation, and augmentation. 137
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a
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Figure 8.11. (A) Renal ultrasound demonstrating the dilation of the right upper pole (k) collecting system. (B) Sagittal pelvic ultrasound demonstrating the dilated ureter (u) extending behind the bladder (b) neck. (C) Retrograde pyelogram of the dilated upper pole ureter.
ureterocele A ureterocele is a cystic dilation of the lower end of the ureter which protrudes into the bladder. The origin of the defect begins in the 8th week of gestation, and may result from obstruction or, more likely, a failure of Chwalle’s epithelial membrane to regress during the incorporation of the ureteral bud into the developing trigone.38 Ureteroceles are associated with duplex systems in 80% of cases, and girls are affected four times more frequently than boys.39,40 Since most ureteroceles are associated with hydronephrosis, the vast majority of these patients are now being diagnosed in utero by sonography.41 Prenatal diagnosis and management of duplex system ureteroceles are important in the endeavor to decrease morbidity and potential adverse outcomes related to infection.42 Clinically, ureteroceles are the most common cause of retention in female infants.43 The initial workup of these patients must include a VCUG to detect whether there is associated reflux, and a renal scan to determine the functional contribution of the system (especially in the case of the rare single system ureterocele). A large number of options exist for management of these patients: complete upper and lower urinary tract reconstruction, upper pole heminephrectomy (simplified approach) and ureterocele decompres-
sion and observation, and endoscopic incision.44–47 While endoscopic decompression may be definitive treatment for intravesical ureteroceles, partial nephrectomy appears to be more curative for extravesical ureteroceles. Other groups advocate primary endoscopic puncture, even for patients with ectopic and duplex ureteroceles, because a third of patients are definitively treated and early decompression is presumed to reduce the risk of pyelonephritis.46 Incontinence may be seen after the initial treatment of ectopic ureteroceles and was thought to be related to iatrogenic bladder neck or external urinary sphincter injury at surgery. However, Husmann et al. observed that, in patients treated by partial nephrectomy alone, 10% subsequently developed urinary stress incontinence, despite the absence of any bladder neck surgery.48 It seems that large ureteroceles are capable of significantly distorting the developing bladder neck and urethra, which will not become apparent until the system is decompressed by whatever means used. In a more recent study,49 the authors concluded that children with ectopic ureteroceles presenting with incontinence are at high risk for a high capacity bladder with incomplete emptying and bladder dysfunction following bladder neck procedures. They concluded that this was not related to the surgery per se, but rather to an integral part of the disorder.
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Case: An 11-year-old continent girl presented with recurrent febrile urinary tract infections. Sonography revealed duplications of both kidneys and a large ectopic ureterocele draining the upper moiety of the right kidney. The VCUG demonstrated right-sided reflux into both moieties on the right side. An endoscopic examination revealed a ureterocele that extended into the bladder neck and upper third of the urethra. An endoscopic puncture and decompression of the ureterocele was performed. Postoperatively the patient experienced moderate stress incontinence that she had not manifested preoperatively and a VCUG revealed persisting right high grade reflux. A right-sided common sheath reimplant, ureterocele excision, and bladder neck reconstruction were performed. Five years later she remains continent, free of infections and off antibiotic prophylaxis. This clinical evidence would suggest that once a large ectopic ureterocele is deflated, function of the bladder neck and urethra may be impaired due to distortion of these structures by the longstanding distension.
rEfErEncEs 1. Moore KL. The Developing Human: Clinically Oriented Embryology, 5th ed. Philadelphia: Saunders, 1993; 71–92. 2. Stephens FD, Smith ED, Hutson JM. Normal Embryology of the Cloaca, 2nd ed. Congenital Anomalies of the Kidney, Urinary and Genital Tract. London: Martin Dunitz, 2002; 3–12.
signaling from the urethral epithelium controls external genital development. Dev Biol 2002;247(1):26–46. 10. Lorenzo AJ, Nguyen MT, Sozubir S et al. Dihydrotestosterone induction of EphB2 expression in the female genital tubercle mimics male pattern of expression during embryogenesis. J Urol 2003;170(4 Pt 2):1618–23. 11. Stephens FD, Smith ED, Hutson JM. Müllerian and Wolffian Anomalies, 2nd ed. Congenital Anomalies of the Urinary and Genital Tracts. London: Martin Dunitz, 2002; 50–62. 12. Parrot TS, Gray SW, Skandalakis JE. The Bladder and Urethra, 2nd ed. Embryology for Surgeons: The Embryological Basis for the Treatment of Congenital Anomalies. Baltimore: Williams and Wilkins, 1994; 671–8. 13. Baskin LS, Hayward SW, Young PF et al. Role of mesenchymal–epithelial interactions in normal bladder development. J Urol 1996;156(5):1820–7. 14. Baskin L, DiSandro M, Li Y et al. Mesenchymal–epithelial interactions in bladder smooth muscle development: effects of the local tissue environment. J Urol 2001;165(4):1283–8. 15. Smeulders N, Woolf AS, Wilcox DT. Smooth muscle differentiation and cell turnover in mouse detrusor development. J Urol 2002;167(1):385–90. 16. Borirakchanyavat S, Baskin LS, Kogan BA, Cunha GR. Smooth and striated muscle development in the intrinsic urethral sphincter. J Urol 1997;158(3 Pt 2):1119–22. 17. Sebe P, Schwentner C, Oswald J et al. Fetal development of striated and smooth muscle sphincters of the male urethra from a common primordium and modifications due to the development of the prostate: an anatomic and histologic study. Prostate 2005;62(4):388–93.
3. Rathke H. Abhandlungen zur Bildungs – und Entwicklungsgeschichte der Tiere. Leipzig, 1832.
18. Ludwikowski B, Oesch Hayward I, Brenner E, Fritsch H. The development of the external urethral sphincter in humans. BJU Int 2001;87(6):565–8.
4. Tourneaux F. Sur les premiers developpements du cloaques du tubercule genital et de l’anus chez l’embryon de mouton. J Anat 1888;24:503–17.
19. Yucel S, Baskin LS. An anatomical description of the male and female urethral sphincter complex. J Urol 2004;171(5):1890–7.
5. Vermeij-Keers C, Hartwig NG, van der Werff JF. Embryonic development of the ventral body wall and its congenital malformations. Semin Pediatr Surg 1996;5(2):82–9.
20. Yucel S, De Souza A Jr, Baskin LS. Neuroanatomy of the human female lower urogenital tract. J Urol 2004;172(1):191–5.
6. Nievelstein RA, van der Werff JF, Verbeek FJ, Valk J, Vermeij-Keers C. Normal and abnormal embryonic development of the anorectum in human embryos. Teratology 1998;57(2):70–8.
21. Shah MM, Sampogna RV, Sakurai H et al. Branching morphogenesis and kidney disease. Development 2004;131(7):1449–62.
7. Sasaki Y, Iwai N, Tsuda T et al. Sonic hedgehog and bone morphogenetic protein 4 expressions in the hindgut region of murine embryos with anorectal malformations. J Pediatr Surg 2004;39(2):170–3; discussion 170–3. 8. Sukegawa A, Narita T, Kameda T et al. The concentric structure of the developing gut is regulated by Sonic hedgehog derived from endodermal epithelium. Development 2000;127(9):1971–80. 9. Perriton CL, Powles N, Chiang C et al. Sonic hedgehog
22. Batourina E, Choi C, Paragas N et al. Distal ureter morphogenesis depends on epithelial cell remodeling mediated by vitamin A and Ret [erratum appears in Nat Genet 2002;32(2):331]. Nat Genet 2002;32(1):109–15. 23. Thomas JC, Demarco RT, Pope JC. Molecular biology of ureteral bud and trigonal development. Curr Urol Rep 2005;6(2):146–51. 24. Mackie GG, Stephens FD. Duplex kidneys: a correlation of renal dysplasia with position of the ureteral orifice. J Urol 1975;114(2):274–80.
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25. Kume T, Deng K, Hogan BL. Murine forkhead/winged helix genes Foxc1 (Mf1) and Foxc2 (Mfh1) are required for the early organogenesis of the kidney and urinary tract. Development 2000;127(7):1387–95. 26. Miyazaki Y et al. Bone morphogenetic protein 4 regulates the budding site and elongation of the mouse ureter. J Clin Invest 2000;105(7):863–73.
EJ. Response of the fetal sheep bladder to urinary diversion. J Urol 2003;169(2):735–9. 38. Chwalle R. Eine bemerkenswerte Anomalie der Harnblase bei einem menschlichen Embryo von 32,5mm. 1927;[A]263:632. 39. Coplen DE, Duckett JW. The modern approach to ureteroceles. J Urol 1995;153(1):166–71.
27. Yu OH, Murawski IJ, Myburgh DB, Gupta IR. Overexpression of RET leads to vesicoureteric reflux in mice. Am J Physiol Renal Physiol 2004;287(6):F1123–30.
40. Gonzales E. Anomalies of renal pelvis and ureter. In: Kelalis P, King L, Belman AB (eds) Clinical Pediatric Urology, 3rd ed. Philadelphia: WB Saunders, 1992.
28. Ichikawa I, Kuwayama F, Pope JC IV et al. Paradigm shift from classic anatomic theories to contemporary cell biological views of CAKUT. Kidney Int 2002;61(3): 889–98.
41. Barthold JS. Individualized approach to the prenatally diagnosed ureterocele [comment]. J Urol 1998;159(3): 1011–12.
29. Fortunoff S, Lattimer JK, Edson M. Vaginoplasty technique for female pseudohermaphrodites. Surg Gynecol Obstet 1964;118:545–8. 30. Pena A. Total urogenital mobilization – an easier way to repair cloacas. J Pediatr Surg 1997;32(2):263–7; discussion 267–8. 31. Ludwikowski B, Oesch Hayward I, Gonzalez R. Total urogenital sinus mobilization: expanded applications. BJU Int 1999;83(7):820–2. 32. Domini R, Rossi F, Ceccarelli PL, De Castro R. Anterior sagittal transanorectal approach to the urogenital sinus in adrenogenital syndrome: preliminary report. J Pediatr Surg 1997;32(5):714–6. 33. Pena A, Filmer B, Bonilla E, Mendez M, Stolar C. Transanorectal approach for the treatment of urogenital sinus: preliminary report. J Pediatr Surg 1992;27(6):681–5. 34. Ahmed S, Barker A. Single-system ectopic ureters: a review of 12 cases. J Pediatr Surg 1992;27(4):491–6. 35. Fernbach SK, Feinstein KA, Spencer K, Lindstrom CA. Ureteral duplication and its complications. Radiographics 1997;17(1):109–27. 36. Avni FE, Nicaise N, Hall M et al. The role of MR imaging for the assessment of complicated duplex kidneys in children: preliminary report. Pediatr Radiol 2001;31(4): 215–23. 37. Matsumoto S, Kogan BA, Levin RM, Howard PS, Macarak
42. Upadhyay J, Bolduc S, Braga L et al. Impact of prenatal diagnosis on the morbidity associated with ureterocele management. J Urol 2002;167(6):2560–5. 43. Merlini E, Lelli Chiesa P. Obstructive ureterocele – an ongoing challenge. World J Urol 2004;22(2):107–14. 44. Chertin B, Fridmans A, Hadas-Halpren I et al. Endoscopic puncture of ureterocele as a minimally invasive and effective long-term procedure in children. Eur Urol 2001;39(3):332–6. 45. Chertin B, de Caluwe D, Puri P. Is primary endoscopic puncture of ureterocele a long-term effective procedure? J Pediatr Surg 2003;38(1):116–9; discussion 116–19. 46. Cooper CS, Passerini-Glazel G, Hutcheson JC et al. Longterm followup of endoscopic incision of ureteroceles: intravesical versus extravesical. J Urol 2000;164(3 (2 of 2)):1097–1100. 47. Husmann D, Strand B, Ewalt D et al. Management of ectopic ureterocele associated with renal duplication: a comparison of partial nephrectomy and endoscopic decompression. J Urol 1999;162(4):1406–9. 48. Husmann DA, Ewalt DH, Glenski WJ, Bernier PA. Ureterocele associated with ureteral duplication and a nonfunctioning upper pole segment: management by partial nephroureterectomy alone. J Urol 1995;154(2 Pt 2):723–6. 49. Abrahamsson K, Hansson E, Sillén U et al. Bladder dysfunction: an integral part of the ectopic ureterocele complex. J Urol 1998;160(4):1468–70.
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9 Clinical physiology of micturition Jacek L Mostwin
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The Bladder CyCle: an InTroduCTIon The bladder cycle is a simple, practical concept of micturition that can help clarify clinical understanding of lower urinary tract function and help plan and interpret objective studies in women with incontinence and lower urinary tract symptoms. The concept of bladder cycle incorporates all major elements of bladder function and continence into a single, continuous, repeating physiologic event. The physiologic basis of most components of the bladder cycle is understood, but the application of this understanding to clinical evaluation is not always as direct as it might seem. In the normal adult, one can make the following generalizations about the bladder cycle: the bladder fills steadily with urine, and the bladder spends most of its time storing urine, emptying only periodically. There is conscious awareness of filling as intravesical volume increases, and eventually, a need to void is felt. Furthermore, as bladder volume increases, there is a subliminal guarding against involuntary leakage by recruitment of external sphincter activity until voluntary micturition is initiated. Once micturition begins, there is sphincteric relaxation and a sustained bladder contraction. These two events are coordinated by a set of reflexes mediated by spinal pathways. Clinical urodynamic testing to evaluate bladder function begins at one part of this cycle, usually with an empty bladder at the start of filling, and progresses to the point where urine is discharged by normal or abnormal means (including clinical incontinence). An experienced urodynamic examiner can study only selected elements of the bladder cycle yet still emerge with a comprehensive understanding of the patient’s function. In addition to a physiologic approach, mastery of urodynamic practice also requires an understanding of lower urinary tract musculature and the major neuroanatomic pathways regulating it. This chapter reviews the important experimental and clinical work that has given rise to modern concepts of bladder function. The selections have been chosen for their relevance to clinical work. Anatomic concepts relevant to understanding lower urinary tract function are also reviewed, and finally, essential clinical events of the bladder cycle are described. The most recent report of the World Health Organization Third International Consultation on Incontinence (ICI) provides the most up-to-date summary of existing information on neuroanatomy, clinical physiology, and pathophysiology in the field.1
early PhysIologIC sTudIes: exPerImenTal work Early physiologic studies looked at the spontaneous resting activity of the bladder, reflexes affecting voiding physiology elicited by bladder filling or urethral manipulation, and also considered the relative roles of the sympathetic and parasympathetic nervous system in affecting these reflexes. These early studies laid the foundation for further experimental work, tracing neuronal pathways in the central nervous system (CNS), and clinical studies of bladder function in the setting of neurologic illness or injury. These early studies are not much discussed today, but form the cornerstones upon which modern urodynamic concepts are based. At the end of the 19th century, Sherrington first showed that the musculature of the bladder was spontaneously active at rest, governed by a rhythmic pacemaker activity that could be influenced by stimulation of spinal nerve roots. When Sherrington did his experiments, it was already known that the mammalian bladder had a parasympathetic motor innervation arising from anterior sacral roots 2, 3 and 4 that was carried in the pelvic nerves, and a sympathetic motor innervation arising from the mid-lumbar roots carried in the hypogastric nerves. Both pelvic and hypogastric nerves merged pre-sacrally to form a pelvic plexus from which postganglionic fibers were distributed to lower pelvic viscera. Sherrington2 was the first to study the effect of nerve stimulation on the bladder by the volumetric methods developed previously by two clinicians, Mosso and Pellicani,3 a precursor to a modern filling cystometrogram. The former method of determining bladder contraction was by visual inspection of the bladder muscle after nerve stimulation. Sherrington knew that Mosso and Pellicani had previously recorded spontaneous fluctuations of intravesical pressures in conscious patients. He observed that stimulating either group of roots resulted in a distinctly unilateral contraction of the bladder that varied in strength and character depending upon which roots were stimulated: sacral roots caused rapid, powerful contractions of brief duration; lumbar roots produced a weaker, longer lasting contraction of longer latency. He noted that lumbar root stimulation produced a contraction difficult to distinguish from spontaneously occurring rhythmic contraction. He tried to abolish spontaneous activity by cutting the spinal cord, its roots and peripheral nerves in various combinations. Regardless of the neural lesion, spontaneous bladder activity always persisted. Even after the bladder was removed from the animal and placed in a warm
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saline bath at intravesical pressures of 2–4 cmH2O, activity persisted. Sherrington finally distinguished between the effects of lumbar and sacral efferent stimulation by eliminating spontaneous activity with large doses of morphine and chloralose. He concluded: It seems therefore justifiable to suppose that here… just as… in the middle third of the ureter... the rhythmic action of the monkey’s bladder arises in its own muscular wall. Its ‘beat’, like that of the heart, is of intrinsic origin.
For many years, the spontaneous activity of the bladder was felt to be a factor in the genesis of the normal bladder contraction during micturition, as well as the deployment of overactive bladder dysfunction. However, although spontaneous bladder activity continues to play a role in experimental work, it has still not found a place in clinical neurourologic practice. The first thorough description of reflex bladder activity was provided by Barrington in a series of papers spanning over 25 years.4–6 He studied volumetric changes produced in the urethra and bladder of the cat in response to nerve stimulation, and described seven reflexes: 1. a hindbrain reflex evoked by distending the bladder, producing contraction of the bladder, having afferent and efferent paths in the pelvic nerves; 2. a hindbrain reflex evoked by running water through the urethra, producing bladder contraction, having afferent paths in pudendal and efferent paths in pelvic nerves; 3. a spinal reflex evoked by distending the proximal urethra, producing slight transient contraction, having afferent and efferent paths in hypogastric nerves; 4. a spinal reflex evoked by running water through the urethra, producing relaxation of the urethra, having afferent and efferent paths in the pudendal nerve; 5. a spinal reflex evoked by bladder distension, producing urethral relaxation, having afferents in pelvic and efferents in pudendal nerves; 6. a spinal reflex evoked by bladder distension, producing relaxation of the proximal urethra, having afferents and efferents in pelvic nerves; 7. a spinal reflex evoked by running water through the urethra, producing bladder contraction, having both paths in the pelvic nerves. Barrington’s reflexes form the core of most modern thinking about clinical neurourology, and are of particular interest to the clinician dealing with women’s
incontinence. Reflexes 2, 3 and 7, in particular, suggest a physiologic means by which urine forcing its way into the urethra can lead to a desire to void and/or a detrusor contraction. In women suffering from stress urinary incontinence, in whom there is some element of intrinsic urethral dysfunction preventing complete closure of the urethra during all periods of storage, one could speculate that urine entering the urethra before the time of convenient voiding could lead to a bladder contraction and evoke symptoms of urgency and urge incontinence. (Whether the sense of urgency is due to the detrusor contraction or the presence of urine in the urethra, or both, is no longer as apparent as once thought.) Barrington’s reflexes 2, 3 and 7 may explain why so many women with stress urinary incontinence may have urgency or urge incontinence and be classified as showing so-called mixed urinary incontinence. More recent animal experiments have reinforced and expanded upon Barrington’s observations and made suggestions that urethral afferent activity can induce detrusor overactivity in women with stress incontinence.7 Clinical evidence for urethral activation of detrusor contraction has also been obtained using electrical stimulation.8 Langworthy et al.9 experimentally localized the voiding center to the brainstem. They created stereotactically controlled thermal lesions in the cat brain, recorded voiding behavior, bladder and urethral function, and then performed postmortem examinations to correlate physiologic behavior with locations of the brain lesions. Various areas of the cortex and cut brainstem were also stimulated. The most vigorous contraction of the bladder and the greatest associated intravesical pressure rise was produced by stimulating areas just lateral to the posterior commissure, and anterior and lateral to the aqueduct of Sylvius. They concluded: We have localized areas of the cerebral cortex of cats which on stimulation produced or stopped micturition. The bladder becomes hyperirritable to stretch stimuli after removal of the motor cortices. Reflex mechanisms in the midbrain appear to control tone in the vesical muscle.
It would take many years for Langworthy’s observations to be accepted into general neurourologic practice, replacing the widely held opinion that the voiding center was located in the sacral cord. Two additional important studies of bladder function were performed in conscious subjects prior to World War II. Denny-Brown and Robertson10 studied voiding events of and bladder volume changes in relation to sphincter activity. They identified spontaneous waves of pressure in the bladder during filling. As these increased in ampli143
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tude, subjective sensations of fullness or urinary urgency developed in the subjects. The subjects, when asked, could voluntarily suppress the summation of these pressure waves. Among their conclusions, they noted: Apart from a faint background of maintained tonic activity, spontaneous vesical activity takes the form of waves of contraction appearing in rhythmical progressions. Willed effort to micturate can evoke powerful contractions of the bladder with very brief latency of development. These contractions in their form and rhythm differ in no way from the spontaneous reaction of the viscus. Voluntary restraint of micturition has a direct effect on the contraction of the bladder, so that spontaneous nervous discharges responsible for vesical contractions can be completely inhibited with ease. Relaxation of the musculature of the perineum appears to be inseparably associated with the voluntary development of micturition. The internal (involuntary) sphincter contracts and relaxes in reciprocal relationship with the detrusor muscle of the wall of the bladder.
Denny-Brown and Robertson’s work reinforced Sherrington’s findings of spontaneous activity and suggested that summation of this activity gradually led to bladder contraction. They did not, however, draw any specific conclusions regarding the relationship of urgency to spontaneous or increasing intravesical pressure change. This implied relationship came about as a result of the work of the Middlesex Hospital group in London (cf. below) and led to a general paradigm regarding clinical bladder physiology that persisted until very recently, i.e. the symptoms of urgency and frequency were in some fundamental way associated with the findings of overactive bladder activity during filling cystometry. Today, even though the symptoms of urgency and frequency are considered to be among the lower urinary tract symptoms (LUTS), it is no longer widely accepted that these symptoms are caused by overactive bladder activity seen during filling cystometry. In fact, it is not clear what the relationship of these symptoms is to overactive bladder activity. This is an important consideration in applying urodynamic techniques to the study of incontinence in women, because it means that urgency and overactive bladder activity during cystometry are not one and the same thing. The second major contribution before World War II was that of Learmonth,11 an Irish surgeon working at the Mayo Clinic. He observed the effects of direct hypogastric nerve stimulation and division on the urinary tract of conscious patients undergoing open pelvic opera-
tions. Unilateral stimulation resulted in contraction of the ipsilateral ureteral orifice, tightening of the trigone, contraction of the internal sphincter, and contraction of the musculature of the prostate, seminal vesicles, and ejaculatory ducts. Sectioning the hypogastric nerve produced relaxation of the ureteral orifice and trigone, and relaxation of the internal sphincter with no appreciable effect on the dome or the lateral walls of the bladder. He cited two cases of low spinal cord injury in which the pelvic nerve supply to the bladder had been interrupted and voiding could not be accomplished until division of the hypogastrics had been performed. He concluded: … the results of sympathetic neurectomy in the two cases cited in which inability to empty the bladder resulted from functional impairment of the parasympathetic system, the sympathetic system remaining intact, seems to me almost to force acceptance of the hypothesis that sympathetic influences act as a brake on contractions of the detrusor.
Learmonth’s studies were consistent with more modern findings of α-adrenergic receptors in the bladder neck, trigone, proximal urethra, and prostate. His nerve interruption operations achieved surgically what is today done by administration of α-adrenergic blocking medication, a cornerstone of medical treatment of prostatic symptoms in men, and, occasionally, urinary retention in women. These historical studies treated the urinary bladder as an organ for the storage and expulsion of urine, much as a modern urodynamicist would do, concentrating on hydrodynamics and the general integrity of central and peripheral reflexes. Several conclusions emerged from these early studies, however, they remain valid today:
• the bladder muscle was capable of rhythmic and spontaneous contraction in vivo and ex vivo;
• there was reciprocal innervation of the component
•
parts of micturition mediated by sympathetic, parasympathetic, and somatic pathways, and stimulation of each of the pathways produced effects specific for certain regions of the lower urinary tract; the sensory events of micturition were represented at the cortical level and overall coordination and facilitation of voiding was regulated by the higher centers of the central nervous system.
Later studies reinforced and extended these early observations. Plum et al.12,13 confirmed the persistence of autonomous bladder activity in animals and patients under general and spinal anesthesia even with pharmacologic ganglionic blockade. El-Badawi and other anatomists14–17
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identified an extensive intramural network of ganglia in the various layers of the bladder, and deGroat and co-workers described local ganglionic responses to sensory stimulation of the bladder, identifying several reflex pathways by electrophysiologic techniques.18,19 Most interestingly, in view of Learmonth’s observations on spinally injured patients, they demonstrated that stimulation of bladder wall afferents resulted in a reciprocal sympathetic inhibition of pelvic nerve efferent firing until a certain threshold of sensory stimulation was reached.
early urodynamIC sTudIes: ClInICal PhysIology The need to manage a large population of injured war veterans surviving with spinal cord injury after World War II led to many detailed studies using water cystometry, radiography, and clinical examination. Such studies led to the comprehensive classification of Bors and Comarr20 in which bladder dysfunction was classified by clinical signs and symptoms, correlated with whatever lesions were known to be present. Bors and Comarr borrowed the terms ‘upper motor neuron’ and ‘lower motor neuron’, used to describe skeletal muscle behavior in high and low spinal injury, to describe two characteristic patterns of bladder activity that emerged after the period of spinal shock. ‘Upper motor neuron’ lesions, frequently associated with suprasacral injury, were characterized by a spastic bladder of small capacity, responding to filling with strong involuntary contractions, usually resulting in incontinence and often associated with simultaneous spastic, obstructing contractions of the external sphincter. ‘Lower motor neuron’ lesions, frequently associated with sacral cord injury or pelvic crush injury, were associated with a larger flaccid bladder, or a thickened poorly compliant bladder incapable of generating contraction, as well as a patulous internal and a relaxed external sphincter that resulted in overflow incontinence. The ‘spastic’ and ‘flaccid’ nature of the two patterns of injury resulted in an appealing but incorrect analogy with skeletal muscle behavior in similar conditions. It became generally assumed that a sacral cord micturition center was responsible for the voiding reflex, subject only to conscious inhibition by higher centers. The idea was much popularized in urology.21 In this paradigm, the release of cortical inhibition by suprasacral injury resulted in an ‘uninhibited bladder’ (now called overactive bladder, or OAB) in much the same way as skeletal muscle spasticity was due to damage to corticospinal tracts. Destruction of the sacral center resulted in a flaccid bladder, much as lower cord or peripheral nerve injury resulted in flaccid skeletal muscle injury.
Anatomically, the terms ‘upper motor neuron’ and ‘lower motor neuron’ were misnomers. Only pudendal nerves carry the axons of true motor neurons that are involved in control of micturition. The cell bodies of these axons are in the anterior spinal horn. Pudendal nerves provide afferent and efferent pathways only to the external sphincter. (Poliomyelitis, in which anterior horn cells are damaged, is not generally associated with bladder dysfunction.) The motor supply to the bladder originates from neurons having their cell bodies in the intermediolateral cell column. These are part of the parasympathetic nervous system. Nonetheless, the concept of a sacral micturition center under the inhibition of higher centers and ‘upper motor neuron’ and ‘lower motor neuron’ lesions were popular in urology from the 1950s to the mid-1970s.
modern clinical urodynamics The era of modern clinical urodynamics began with the work of Hinman and colleagues in the 1950s.22,23 These investigators studied voiding in normal persons, not neurologically injured patients. They measured intravesical and intraurethral pressure and urinary flow rate and simultaneously observed cineradiographic changes in the bladder and urethra. They showed that a fall in urethral pressure and a radiographic sign of opening of the posterior urethra was the first event in normal voiding. In some women, they could see that a fall in urethral pressure alone was sufficient to achieve voiding. In men, higher intravesical pressures were required to overcome urethral resistance. These techniques were successfully adopted at the Middlesex Hospital in London to study a large variety of patients with assorted voiding complaints.24,25 Patterns of dysfunctional voiding, such as those with urinary outflow obstruction from benign prostatic hyperplasia or bladder neck contracture, were identified in patients without overt neurologic disease. Bladder overactivity found in patients without overt neurologic disease was termed ‘idiopathic detrusor instability’. The Middlesex group widely disseminated the urodynamic approach for the investigation and management of many patients with voiding complaints and was successful in focusing attention on the role of clinical urinary tract physiology in everyday urology. In the United States, urodynamic techniques were used by several groups to study adults26,27 and children.28 Of particular interest were studies of children with no neurologic abnormalities but with functional noncoordination of bladder and sphincter.29 Urodynamic techniques were applied to the study of children with 145
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non-neurologic abnormalities such as posterior urethral valves, which could lead to prenatal and neonatal obstruction, and could result in eventual voiding abnormalities based on permanent bladder changes even after surgical relief of obstructing valves.30 Studies such as these emphasized the importance of obstruction alone as a cause of bladder overactivity and dysfunction. Voiding dysfunction in other congenital anomalies such as prune belly syndrome31 and bladder exstrophy32 have also been studied. These investigations have resulted in a growing appreciation by clinicians of the integration of the various components of micturition and their clinical abnormalities.
ConTemPorary sTudIes The most recent studies of bladder function have focused on the distribution and pharmacology of autonomic receptors in the urinary tract, their significance in the control of motility, the function of the smooth muscle of the bladder itself, the cellular and molecular control of voiding reflexes, and the details of the function and integration of neuroanatomic pathways. Extensive work has shown that most mammalian bladder, urethral, and prostate tissue is invested with homogeneously distributed muscarinic receptors, but that adrenergic receptors are unevenly distributed.33,34 The bladder neck (internal sphincter) and urethra (especially in males) have a dense distribution of α-adrenergic receptors, and the bladder dome contains β-adrenergic receptors in a lesser density than alpha. There has been great interest in the plasticity of these receptor populations and reflexes as they are affected by obstruction, aging, and other sources of pathology. These findings have been utilized in several ways: 1. Krane and Olsson35,36 were the first to demonstrate that the bladder neck in spinal cord injury patients behaves autonomously, is dependent on αadrenergic stimulation, is related to the syndrome of ‘autonomic dysreflexia’, and is possible to control by pharmacologic α-adrenergic blockade. 2. Caine et al.37 first studied the role of α-adrenergic receptors in the prostate and bladder neck. This work has led to very successful treatment of prostatic obstruction and acute urinary retention38,39 and forms a cornerstone of modern management of prostatic obstruction. 3. Receptor populations may change after trauma or hormonal manipulation.40 Increased α-adrenergic bladder innervation after spinal injury or obstruction may contribute to bladder instability.
Experimental spinal cord injury and models of chemical cystitis have shown increased unmyelinated C-afferent fiber activity which may be associated with lower thresholds for bladder reflex activation.41–43 4. Neural populations regulating reflex bladder function may undergo changes under the influence of urethral outflow obstruction or neural degeneration.44 Hyperreflexia in patients with obstruction or lower urinary tract symptoms can be due in part to changes in these reflexes and may require pharmacologic treatment specific for neurotransmission.45 5. For the last 25 years, these developments have formed the scientific basis for a widely utilized neurourologic pharmacopoeia1,46–48 to enhance or diminish contractility in bladder or urethra. These historical, urodynamic, and pharmacologic studies form the basis of our current concepts of urinary tract motility as presented in the major urologic textbooks and monographs dealing with this subject.48–53 The degree of control theoretically predicted by urodynamic, physiologic, and pharmacologic studies, however, has progressed slowly and is considered by many to be disappointing.47,54 With rare exception, the primary approach to pharmacologic management of bladder dysfunction is blockade of muscarinic receptors. The only other major pharmacologic development in the treatment of incontinence has been the development of duloxetine, a selective serotonin reuptake inhibitor (SSRI) used to stimulate activity at Onuf’s nucleus in the sacral spinal cord for increasing extrinsic striated sphincter activity. Clinical studies tend to lag considerably behind the experimental ones on which most drug recommendations are based. Many clinicians consider the results of pharmacologic treatment of voiding disorders disappointing. Attempts to surgically denervate or pharmacologically control, in particular, the overactive bladder have met with only partial success.55 Manipulation of sacral spinal cord reflexes by implantable nerve root stimulation has shown promise in the management of lower urinary tract symptoms, specifically urgency and urge incontinence, and is gradually replacing augmentation as a more conservative method of managing intractable urge incontinence. Among the reasons put forward for limited therapeutic success are lack of understanding of normal physiologic events associated with voiding, and lack of understanding of basic pathophysiologic changes in abnormal voiding. Some emerging concepts regarding mechanisms underlying pathophysiology include the following:
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1. Possible contributions of unknown non-adrenergic, non-cholinergic (NANC) neurotransmitters. Candidates for such transmitters include adenosine triphosphate (ATP), vasoactive intestinal polypeptide (VIP), prostaglandins, and, most recently, nitric oxide56,57 2. Changes in the neuronal population from Aδmyelinated afferent fibers to unmyelinated C-afferent fibers. DeGroat et al. had initially suggested that maturation of the voiding reflex in kittens required the myelination of Aδ-fibers.58 Experimental interstitial cystitis and spinal cord injury have shown similar emergence of C-fiber activity41,43,59 which can be stimulated by nerve growth factor.42
sTruCTural FeaTures relevanT To FunCTIon The bladder is composed primarily of interdigitating smooth muscle fibers,60 which can stretch to almost four times their resting length without increasing their linear tension. This creates a hollow muscular viscus capable of storing increasing amounts of urine for prolonged periods of time at continuously low pressure until evacuation can be conveniently initiated. In contrast to intestinal smooth muscle, however, bladder smooth muscle is not organized into distinct inner longitudinal and outer circular layers except in the region of the urethra. These vesical smooth muscle bundles act as interdigitating slings originating near the urethra, traversing the spherical dimensions of the bladder, and coursing back again to the urethra. The narrow portion of the internal urethral meatus, or bladder neck, provides sphincteric closure of the urethra by its very muscular arrangement. At the proximal urethra, which is the region of highest intraluminal pressure and, hence, continence at rest, one finds an inner longitudinal arrangement of muscular fibers, representing direct continuation of these muscle bundles, and a sleeve of outer circular muscle. In addition, there is a sleeve of circular striated muscle surrounding the urethra at this point, forming the external sphincter (rhabdosphincter). This striated muscle provides tonic closure of the urethra and most likely helps to resist passage of urine during increases in intraabdominal pressure. The mass of this rhabdosphincter has been shown to decrease with menopause and may play a role in the emergence of intrinsic sphincteric deficiency during this stage of life. The arrangement of smooth muscles at the internal urethral meatus, or proximal urethra, favors tonic closure at rest.60–62 While it is known that a fall in urethral pressure and radiographic signs of opening of the proximal urethra are the earliest signs of the initiation of
normal micturition,51 there is no general agreement on whether this takes place because the urethra is ‘pulled open’, i.e. the longitudinal fibers extending into the urethra from the bladder shorten, pulling apart the circular fibers while the sphincter relaxes, or whether the urethral muscles themselves cease tonic activity. Various NANC transmitters, including nitric oxide,56 have been proposed as mediators of this activity. Thickness and suppleness of muscle fibers and the collagen composition of the bladder interstitium also affect storage compliance. Obstruction and neuropathic conditions such as myelodysplasia are associated with increased collagen deposition in the interstitium, most likely secreted by the smooth muscle cells themselves in response to injury or obstruction.63,64 The increasing presence of collagen may affect the stretch characteristics (compliance) of the bladder at higher filling volumes, and may explain a loss of compliance and higher intravesical pressures at the end of filling on cystometry. This kind of loss of compliance can overwhelm an already compromised sphincter (as in myelodysplasia or with severe intrinsic sphincter deficiency), and can lead not only to vesicoureteral reflux but also to increased urgency or the triggering of unstable contractions. Muscle thickness increases in lower cord myelodysplasia and hypertrophy develops following obstruction. Thicker muscle bundles are less distensible and less compliant and may also lead to the same difficulties as stiffness due to collagen deposition.
The Bladder CyCle At birth, the bladder stores and discharges urine in a rhythmic manner independent of cortical control. This pattern gradually comes under voluntary control sometime during the first 5 years of life. The development of voluntary control probably requires a number of maturational developments:
• there must be sufficient strength and maturity of pelvic somatic musculature;
• cortical appreciation of proprioceptive signals
•
regarding bladder fullness must be achieved through myelination and maturity of somatosensory pathways; cortical recognition and regulation of somatosensory pathways and the ability to link the inhibition of voiding to voluntary contraction of the external urinary sphincter must develop.
When parental supervision is added to this ‘toilet training’ infrastructure, the basic elements for early biofeed147
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back training are in place. Similar methods are used in biofeedback and behavioral training programs for incontinent adults to re-educate and restore these same reflexes. The technique of sacral stimulation of somatosensory pathways in the pudendal nerve for treatment of urge incontinence also relies on this form of reflex inhibition. The lower urinary tract spends almost all of its time in a storage (or diastolic) phase. Its main functions during this period are low-pressure storage of urine, gradual warning to the CNS that intravesical volume is reaching a threshold of voiding, and prevention of leakage until voluntary micturition is desired. The voiding (or systolic) phase represents only a brief fraction of the overall bladder cycle. During this phase the main function is adequate coordinated relaxation of the sphincter, and emptying of the bladder by a mixture of gravity, activation of the bladder contraction or an increase in intra-abdominal pressure. The events of emptying need to be sustained until they have been carried to the point of completion. Clinical urodynamic testing is capable of examining each of these aspects of bladder function, which will now be reviewed in detail.
Bladder cycle I – diastole: the filling phase The bladder cycle consists mostly of time spent storing urine, accommodating to an increasing volume at low pressure, and inhibiting contraction by giving rise to gradual awareness of filling, activating a reciprocal guarding reflex by rhabdosphincter contraction, and generating reciprocal inhibition of bladder parasympathetic stimulation. The important clinical elements of the filling phase that can be measured during urodynamic testing are sensation, stability, compliance, capacity and (although not usually considered much) recruitment of external sphincter activity. Each of these elements can vary independently and each may be studied by conventional clinical urodynamic techniques.
Sensation Bladder sensation consists of several different sources of nervous information. Proprioception, the sensation of visceral distension, is transmitted by long latency myelinated Aδ-fibers in parasympathetic afferents traveling in the pelvic nerves to sacral segments 2, 3 and 4. It is then carried along the dorsal columns to the pons where it is integrated into processing centers supplying the cortex with a conscious sensation of bladder filling. Nociception, under normal conditions, transmits information about temperature and pain from the bladder mucosa.
Somatosensory perception transmits information through sacral segments 2, 3 and 4 via the pudendal nerve about the state of the external sphincters and distension or movement of fluid through the urethra. For recent detailed reviews of pharmacologic and neuroanatomic aspects of afferent mechanisms in the bladder, see the reviews by Andersson45 and Morrison et al.65,66 In the normal adult, bladder sensation is never painful, it distinguishes warm from cold, and leads to an increasing conscious awareness of filling that is related to intravesical volume, but is independent of intravesical pressure. Conventional urodynamic testing distinguishes four distinct sensory phases during filling, although these may be thought of as markers along a continuum of increasing sensation: 1) a first desire to void; 2) a sense of fullness; 3) a strong desire to void; and 4) a sense of imminent voiding or urgency. Throughout this increasing awareness of voiding, the bladder should store urine at low pressures and there should be no leakage. Other than studies by evoked cortical potential, there is no objective way to evaluate sensation except by direct contact with the subject during a urodynamic test. Bladder filling is not a purely passive phenomenon. Electromyographic recording (needle or surface) from the pelvic floor or the external sphincter shows gradual recruitment of muscle activity, the so-called ‘guarding reflex’. This indicates that cortical activity is taking place during filling, activating somatosensory pathways that increase sphincter contraction, increasing sphincteric resistance and also activating reciprocal inhibitory pathways that reduce bladder muscle contractility. Sensation can be diminished selectively by disease such as diabetic or alcoholic neuropathy, tabes dorsalis, or subacute combined deficiency (vitamin B12 and folate deficiency). Pain or dysesthesia can be produced by inflammation, bladder stone, infection, radiation or interstitial cystitis. Abnormal sensation may be produced by altered spinal cord reflexes, learned behavior or pelvic muscle spasm, none of which directly involves the bladder itself, but all of which can lead to urgency, urge incontinence, pain or reduced storage capacity. This particular area of disordered sensation is an important area of contemporary research. Cortical lesions affecting sensation (brain tumor, stroke, Alzheimer’s disease) may reduce cortical awareness and thus, inhibition, and permit incontinence despite a normal lower urinary tract. Among the particularly important abnormalities that can be elicited during filling cystometry in women with stress incontinence, particularly elderly women, is delayed or precipitant urgency. These patients feel very little during filling until capacity is reached or leakage
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has begun, or is about to begin. These patients most likely have a loss of Aδ visceral proprioceptive sensation, but the source of their sudden delayed urgency is not clear. There is evidence that some of their urgency may be due to the emergence of unmyelinated C-fiber afferent signaling. In some patients with diminished or even absent visceral bladder sensation, it is possible that the only physical event giving rise to urgency is the passage of urine through the urethra. In this case, it is the actual sensation of leaking that the patient experiences as a desire to void, although bladder emptying has already commenced and may be only partially related to intrinsic bladder activity.
Stability and overactivity Absence of involuntary bladder contraction during filling is considered a hallmark of normal adult function. During filling, bladder capacity is normally reached with increasing awareness of fullness but without phasic increases in bladder pressure. Phasic increases in bladder pressure can occur with or without the individual’s awareness that something is happening in the bladder. Involuntary contractions may occur with or without a sensation of urgency or impending urination, during the filling phase or only at capacity, and with or without associated changes in bladder compliance. The International Continence Society has arbitrarily decided that phasic contractions ≥15 cm water may be defined as overactive bladder contraction. In clinical practice this number serves only as a guideline, and many problems related to stability remain unsolved. Instability can be produced or elicited by rapid filling of the bladder (>100 ml/min) or the use of gas or cold (including room temperature) water as a filling medium. More common causes are obstruction and neurologic injury/illness. As discussed above, one of the great problems in clinical neurourology is how to relate the findings of stability during cystometry to the clinical presence of urgency and urge incontinence. Many patients with urge incontinence are presumed to have bladder overactivity and unstable contractions, even if testing conditions fail to demonstrate them, an observation which should stimulate further investigation of this relationship. There is a significant problem relating the sensory symptom of urgency and urge incontinence to the urodynamic finding of instability/overactivity. Exactly how urgency and motor overactivity are related is not clear. Here we should digress to consider the historical background of how this conceptual relationship evolved. Bladder instability was first characterized in male patients with spinal injury. Since these men often suffered
from urgency and urge incontinence, it was assumed that instability and urgency were related. The Middlesex group then showed that prostatic obstruction was associated with urgency and urodynamic evidence of bladder instability, which could resolve in up to 75% of affected patients after prostatectomy.25 These types of observation led to the hypothesis that urgency is a symptom of underlying unstable contractions: as bladder pressure rises, the patient experiences an impending need to void, sometimes with expulsion of urine – urge incontinence. Animal experiments also supported this hypothesis: partial urethral obstruction, similar to prostatic obstruction, resulted in bladder muscle hypertrophy and unstable contractions during cystometry in vivo.67 Later animal work, however, showed that experimental urethral obstruction created new neurologic reflexes associated with increased frequency of voiding and evidence of unstable contractions on cystometry. In a rat model of partial urethral obstruction, Steers and his coworkers showed that the number of sensory nerve cell bodies in the dorsal ganglia increased, as did the neurologic events associated with reflex voiding.68 Nerve growth factor secreted by the smooth muscle cells of the bladder after obstruction may have initiated the proliferation of sensory and sympathetic neurons and the development of these increased reflexes.69 It has therefore been suggested that the emergence of new spinal reflexes may lead to urgency and frequency in the absence of direct bladder muscle abnormalities. Further experimental evidence continues to reinforce this hypothesis.70 Afferent pathways are modulated by serotonergic pathways in the CNS. Pharmacologic intervention in these CNS pathways is an active area of investigation for treatment of urgency and bladder overactivity.71 It is therefore very important for the clinician to keep separate the two phenomena of cystometrically demonstrated motor bladder overactivity/instability and the clinical symptoms of urgency, frequency, and urge incontinence (belonging to the LUTS syndrome).72 Their exact relationship remains unclear. In summary, there is ample experimental evidence that instability can be due to either sensory or motor changes in the bladder. During filling cystometry, it is not possible to distinguish between the two; that is why it is essential for the clinician to determine whether bladder contractions are associated with abnormal sensation.
Compliance Compliance is a measure of bladder elasticity or tone, mathematically described as instantaneous change in volume with respect to pressure. During normal filling, bladder pressure remains low until capacity is reached. 149
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A bladder showing decreased compliance during filling is described as hypertonic. The term -tonic is used to distinguish these changes from the phasic changes more typically seen in neurogenic bladder overactivity. Phasic changes can be superimposed on tonic changes. The compliance of a normal bladder is almost infinite until capacity is reached: graphic representation of pressure as a function of volume (the cystometrogram) is essentially flat. The flatness of this curve is due to: 1) reciprocal inhibitory pathways; 2) anatomic arrangement and great stretching potential of the smooth muscle of the bladder; and 3) absence of restriction by collagen. Disturbance of any of these three can significantly alter compliance, increasing pressure during filling. Increased pressure during filling at lower volumes is a clinical finding of extreme importance. At resting intravesical pressures greater than 40 cmH2O, for example, the ability of the ureters to propel urine from the renal pelvis is compromised, hydrostatic pressures are transmitted to the upper tracts and renal deterioration commences.73 Increased intravesical pressures at lower volumes may also work against a sphincter that is compromised by intrinsic deficiency or poor support, increasing the chances of incontinence due to sphincteric opening at a volume lower than would be seen otherwise. Causes of reduced compliance include bladder muscle hypertrophy that results from bladder outlet obstruction, most typically seen in adult men with prostatic obstruction and boys with posterior urethral valves. In adult women it is most likely to be seen following iatrogenic obstruction from stress incontinence surgery. Hypertrophied muscle is less elastic than normal detrusor smooth muscle and it has also synthesized increased amounts of collagen, further increasing stiffness. Decentralization of the bladder from the CNS, as in myelodysplasia or spinal cord injury, or after such operations as cytolysis, may also lead to hypertrophic musculature and increased collagen deposition. Age alone may lead to a partial replacement of bladder smooth muscle by collagen. All of these factors can affect compliance. Changes in compliance and stability may be found together in the presence of neurologic injury or disease, physical damage to the bladder by radiation or fibrosis, or after prolonged catheter drainage leading to decreased compliance. In this setting, the phasic changes of instability are superimposed upon the rising slope of tonicity. Thus a bladder may be both hypertonic and hyperactive.
Capacity Capacity is the volume to which the bladder will fill until voiding commences voluntarily or involuntarily
due to contraction, sphincteric relaxation, sphincteric incompetence or rising intravesical pressure that overcomes sphincteric resistance (overflow incontinence). Absolute capacity is limited to a maximum by the viscoelastic properties of the bladder, the physical limits of smooth muscle stretch, and the resistance of the outflow. Relative functional capacity can be affected by sensation, stability or decreased compliance. A residual urine can alter functional capacity by providing a ‘dead space’ that limits the amount of urine the bladder will store during the voiding interval. A large bladder, which may hold 1000 ml or more, may only empty 200 ml at a time, so that the functional capacity is only 200 ml. Normal values for capacity in adults have not been determined. Generally accepted values range between 280 and 600 ml but should always be interpreted within a clinical context.
Bladder cycle II – systole: the emptying phase The important elements of the emptying phase are: 1) urethral opening and sphincteric coordination; 2) sources of power for bladder emptying; 3) urinary flow rate and pattern, and voiding pressure; and 4) completeness of emptying.
Urethral opening Young and Wesson, after watching men void through the cystoscope, suggested that the trigonal muscle contracted and appeared to flatten the elevated ridge of bladder neck muscle. They proposed this as a mechanism of urethral opening.74 Hutch studied anatomic dissections of trigone and proximal urethra and observed voiding under fluoroscopy. He proposed that voiding commenced when the trigone flattened and the urethra funneled to permit passage of urine.61 Hutch’s observation was remarkably similar to later observations by Jeffcoate and Roberts of women with stress incontinence, studied with lateral cystourethrograms. They concluded: The most characteristic anatomical change, present in four out of five cases of incontinence, is loss of the posterior vesico-urethral angle so that the urethra and the trigone tend to come into line.75
Hinman et al.,22,23 as described earlier, observed that opening of the urethra was the first event in normal bladder emptying. McGuire51 also reported that opening of the bladder neck (proximal urethra) was the first videourodynamic sign of normal voiding or bladder contraction. Urethral opening is usually associated with
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cessation of electrical activity of the sphincter. These findings are remarkably consistent with Barrington’s observation, made more than 50 years ago. While it is generally agreed that the urethra opens during the first phase of normal micturition, there is no agreement about whether this is an active or passive phenomenon. Innervation and relaxation of the proximal urethra independent of bladder contraction was suggested by earlier studies of Tanagho in which bladder neck and proximal urethra were surgically separated from the bladder body.60 The presence and pharmacologic response of α-adrenergic receptors in the smooth muscle of the trigone and proximal urethra of both men and women would suggest a role for these receptors in the initiation of normal voiding. However, men who have undergone sympathectomy after retroperitoneal lymph node dissection for testis tumor and have lost seminal emission do not show voiding dysfunction. Ample evidence now suggests that nitric oxide may mediate active relaxation of proximal urethral smooth muscle.76,77 A purely mechanical explanation for urethral opening by bladder contraction has been suggested by the anatomic arrangement of smooth muscle of the urethra. The interdigitating bundles of the bladder form more distinct longitudinal bundles continuous with the urethra. The proximal urethra and the bladder form one organ. The proximal urethral portion, surrounded by skeletal muscle fibers of the voluntary sphincter, is the very area that shows opening on videourodynamic studies. Relaxation of a contracted external sphincter associated with shortening of the detrusor muscle might explain the sort of events that are seen during the initiation of voiding. The relative roles of this kind of passive opening of the urethra, and a more active relaxation of the smooth muscle component, remain to be determined. Urethral opening is usually seen only when performing videourodynamic testing. Conventional testing, without video or sonographic features, the kind sufficient for the majority of everyday clinical work, cannot show this initial event of the bladder cycle. Multichannel pressure transducers can be placed in such a way as to observe pressure changes at the urethra during the bladder cycle, but their accurate position requires fluoroscopy or sonography. Details of urethral opening are usually reserved for research or investigative urodynamics.
Sources of power for bladder emptying The source of power for urinary evacuation is normally a sustained contraction of detrusor smooth muscle fibers. It has been suggested that, during contraction, there is
a synchronization of spontaneous subclinical contractions leading to a sustained contraction of the whole organ with successful emptying. This may take place by coordinated release of acetylcholine released from parasympathetic postganglionic nerve terminals in the bladder. There is most likely a depolarization of smooth muscle cells with an inward flow of calcium current. Isolated electrical events in bladder muscle may spread to surrounding cells, spreading the wave of contraction. As more cells are depolarized, calcium is released from intracellular stores in individual muscle cells and made available to the actin/myosin complex in the muscle. This leads to shortening, which continues until the calcium is returned to the intracellular stores. The cellular events are dependent on energy from ATP produced by the mitochondrion. A bladder forced to contract against obstruction, or thickened by prolonged obstruction, shows decreased biochemical energy production, limiting its ability to sustain contraction. Whether abnormalities of bioenergetics are found in aging alone has not yet been determined, but the clinical findings of detrusor hyperactivity with impaired contractility in the elderly suggest this possibility.78 In some patients, gravity alone may lead to expulsion of urine when the sphincter is relaxed, as demonstrated in women by Hinman et al.22,23 In others, voluntary straining (Valsalva) or manual pressure on the bladder (Crede) can be used to enhance or replace diminished intrinsic bladder contraction. Although clinically effective, these methods of evacuation cannot be considered ‘normal’. Throughout emptying there is usually a sensation of urine passing through the urethra, as found by Barrington. During urodynamic testing it is possible to determine the relative contribution of abdominal and intrinsic forces to the expulsion of urine, and the sensation that accompanies it.
Sphincteric coordination Electromyographic activity recorded by simple external electrodes ceases during voiding and is usually associated with urethral relaxation as the first sign of normal voiding. This coordination undergoes changes in spinal cord disease/injury, most typically in quadriplegia or multiple sclerosis. Pathologic contraction of the external sphincter during bladder contraction, termed detrusor sphincter dyssynergia (DSD), may be partial or total and, unless it represents a voluntary form of extreme attempts to prevent urination (such as in the Hinman syndrome of non-neurogenic neurogenic bladder), is almost always associated with neurologic disease. The effect of DSD on the bladder is similar to that of outlet obstruction.27,79 151
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Sphincteric relaxation and initiation of voiding is subject to powerful cortical influence, so clinical urodynamic testing can often be confounded by embarrassment or unpleasant or unfamiliar testing circumstances. This is an issue with which all urodynamicists must contend.
Flow rate and pattern Urinary flow can be measured by recording the rate at which urinary volume accumulates in a receptacle on a scale, displaying the first derivative of volume with respect to time, dV/dt. Other flowmeters use different techniques to produce a similar tracing. The maximum flow rate achieved during the expulsion of urine is generally considered the most important variable. The other important aspect of the flow rate is the pattern of the tracing. When normal, it appears as an abrupt rise in flow rate during the early phase of voiding, followed by a gradual return to zero. An abnormal pattern might show a slower rise to a lower maximum value followed by a long plateau phase, suggesting obstruction or weak contraction of the bladder. An intermittent or sawtooth pattern may suggest intermittent straining to overcome limited contractility or intermittent obstruction such as would occur with DSD. Most nomograms have been compiled to assist interpreting maximum urethral flow rate values in men with infravesical obstruction.80 The Liverpool nomograms have included women.81
Pressure–flow studies Only simultaneous recording of intravesical and intraabdominal pressure during voiding with flow rate and pattern can determine whether diminished flow is due to motor failure of the bladder or high pressure voiding against an obstruction.38 Nomograms have been established relating intravesical pressure and flow rate to aid in the clinical diagnosis of obstruction.82 Much controversy regarding the correlation of predictions derived from these nomograms and clinical results from relief of obstruction still exists in urology.
Completeness of emptying The presence of residual urine at the completion of voiding is considered abnormal. Functionally, it represents intravesical dead space, similar to an increased functional residual capacity in chronic obstructive pulmonary disease. It means that the bladder cycle is already part way through its filling phase before it has even started again. Residual urine may be due to anatomic shunts such as diverticula, dilated refluxing ureters or large cystoceles.
A normal bladder contracting against high outlet resistance may fail to empty completely, but in the absence of a shunt, a more likely cause is a partially decompensated bladder that may fail to empty at all against an outlet obstruction or empty only partially after the obstruction has been relieved.
ConClusIon Further progress in neurourology will require an understanding of the basic mechanisms underlying contractility of the smooth muscle and the reflexes that coordinate and integrate the various components of the urinary tract and the central nervous system. The practitioner, however, can rely on the simple concept of the bladder cycle to incorporate all the basic elements of bladder function and continence into a single whole, creating a useful framework for everyday work.
reFerenCes 1. Abrams P, Cardozo L, Khoury S, Wein AJ (eds) Incontinence, 3rd ed. Third International Consultation on Incontinence, June 26–29, 2004. Plymouth: Health Publication, 2005. 2. Sherrington CS. Notes on the arrangement of some motor fibres in the lumbo-sacral plexus. J Physiol 1892;13:621–772. 3. Mosso A, Pellicani 1882;1:97, 291.
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4. Barrington FJF. The component reflexes of micturition in the cat. Part III. Brain 1941;64:239–43. 5. Barrington FJF. The component reflexes of micturition in the cat. Parts I & II. Brain 1931;54:177–88. 6. Barrington FJF. The nervous mechanism of micturition. Q J Exp Physiol 1915;8:33–71. 7. Jung SY, Fraser MO, Ozawa H et al. Urethral afferent nerve activity affects the micturition reflex; implication for the relationship between stress incontinence and detrusor instability. J Urol 1999;162(1):204–12. 8. Gustafson KJ, Creasey GH, Grill WM. A urethral afferent mediated excitatory bladder reflex exists in humans. Neurosci Lett 2004;360(1–2):9–12. 9. Langworthy OR, Kolb LC, Lewis LG. Physiology of Micturition. Baltimore: Williams and Wilkins, 1940. 10. Denny-Brown D, Robertson EG. On the physiology of micturition. Brain 1933;56:149–90. 11. Learmonth JR. A contribution to the neurophysiology of the urinary bladder in man. Brain 1931;54:147–76. 12. Plum F. Autonomous urinary bladder activity in man. Arch Neurol 1960;2:147–76.
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13. Plum F, Cofelt RF. The genesis of vesical rhythmicity. Arch Neurol 1960;2:487–503.
31. Cromie W, Duckett J. Urodynamics in childhood. Urol Clin North Am 1979;6:227–36.
14. Dixon JS, Gilpin SA, Gilpin CJ, Gosling JA. Intramural ganglia of the human urinary bladder. Br J Urol 1983;55(2):195–8.
32. Toguri AG, Churchill BM, Schilinger JF et al. Continence in cases of bladder exstrophy. J Urol 1978;119:538–40.
15. el-Badawi A, Schenk EA. Dual innervation of the mammalian urinary bladder. A histochemical study of the distribution of cholinergic and adrenergic nerves. Am J Anat 1966;119(3):405–27. 16. el-Badawi A, Schenk EA. The peripheral adrenergic innervation apparatus. I. Intraganglionic and extraganglionic adrenergic ganglion cells. Z Zellforsch Mikrosk Anat 1968;87(2):218–25. 17. El-Badawi A, Schenk EA. The distribution of cholinergic and adrenergic nerves in the mammalian epididymis: a comparative histochemical study. Am J Anat 1967;121(1):1–14. 18. DeGroat WC. Mechanisms underlying recurrent inhibition in the sacral parasympathetic outflow to the urinary bladder. J Physiol 1976;257:503–13. 19. DeGroat WC, Saum WR. Synaptic transmission in parasympathetic ganglia in the urinary bladder of the cat. J Physiol (Lond) 1976;256:137–58. 20. Bors E, Comarr AE. Neurological Urology. Baltimore: University Park Press, 1971. 21. Lapides J, Diokno A. Urine transport, storage and micturition. In: Lapides J (ed) Urology. Philadelphia: Saunders, 1976; 190–241. 22. Hinman F Jr, Miller GM, Nickel E. Normal micturition – certain details as shown by serial cystograms. Calif Med 1955;82:6–7. 23. Hinman F Jr, Miller GM, Nickel E. Vesical physiology demonstrated by cineradiography and serial roentgenography. Radiology 1954;62:713–9. 24. Turner-Warwick RC, Whiteside CG. Clinical urodynamics. Urol Clin North Am 1982;6:1–293. 25. Turner-Warwick RT, Whiteside CG, Arnold EP. A urodynamic view of prostatic obstruction and the results of prostatectomy. Br J Urol 1973;45:631–45. 26. Blaivas JG, Fisher DM. Combined radiographic and urodynamic monitoring: advances in techniques. J Urol 1981;125:693–4. 27. Blaivas JG, Sinha HP, Zayed AA, Labib KB. Detrusor external sphincter dyssynergia: a detailed electromyographic study. J Urol 1981;125:545–8.
33. Awad SA, Bruce AW, Cano-Ciampi G et al. Distribution of alpha and beta adrenoceptors in the human urinary bladder. Br J Pharmacol 1974;50:525–9. 34. Edvardsen P, Setekleiv J. Distribution of adrenergic receptors in the urinary bladder of cats, rabbits and guinea pigs. Acta Pharmacol Toxicol Scand 1968;26:437–45. 35. Krane R, Olssen C. Phenoxybenzamine in neurogenic bladder dysfunction. I: A theory of micturition. J Urol 1973;110:650–2. 36. Krane R, Olsson CA. Phenoxybenzamine in neurogenic bladder dysfunction. II. Clinical considerations. J Urol 1973;110:653–6. 37. Caine M, Raz S, Ziegler M. Adrenergic and cholinergic receptors in the human prostate, prostatic capsule and bladder neck. Br J Urol 1975;47:193–202. 38. Chancellor MB, Blaivas JG, Kaplan SA, Axelrod S. Bladder outlet obstruction versus impaired detrusor contractility: the role of outflow. J Urol 1991;145(4):810–2. 39. Christmas TJ, Kirby RS. Alpha-adrenoceptor blockers in the treatment of benign prostatic hyperplasia. World J Urol 1991;9:36–40. 40. Sundin T, Dahlstrom A. The sympathetic innervation of the bladder and urethra in the normal state and after parasympathetic denervation at the spinal root level. Scand J Urol Nephrol 1973;7:131–49. 41. Yoshimura N. Bladder afferent pathway and spinal cord injury: possible mechanisms inducing hyperreflexia of the urinary bladder. Prog Neurobiol 1999;57(6):583–606. 42. Chuang YC, Fraser MO, Yu Y, Chancellor MB, de Groat WC, Yoshimura N. The role of bladder afferent pathways in bladder hyperactivity induced by the intravesical administration of nerve growth factor. J Urol 2001;165(3):975–9. 43. Krenz NR, Weaver LC. Sprouting of primary afferent fibers after spinal cord transection in the rat. Neuroscience 1998;85(2):443–58. 44. Steers WD, DeGroat WC. Effect of bladder outlet obstruction on micturition reflex pathways in the rat. J Urol 1988;140:864–71. 45. Andersson KE. Bladder activation: afferent mechanisms. Urology 2002;59(5 Suppl 1):43–50.
28. Cook WS, Firlit C, Stephens FD. Techniques and results of urodynamic evaluation in children. J Urol 1977;117:346–9.
46. Wein AJ. Pharmacology of the bladder and urethra. In: Mundy AR, Stephenson T, Wein AJ (eds) Urodynamics: Principles, Practice and Applications. Edinburgh: Churchill Livingstone, 1983.
29. Allen TD. The non-neurogenic neurogenic bladder. J Urol 1977;117:232–8.
47. Milroy E. Pharmacologic management of common urodynamic problems. Urol Clin North Am 1979;6:265–72.
30. Bauer SB, Dieppa RA, Labib KK et al. The bladder in boys with posterior urethral valves. J Urol 1979;121:769–73.
48. Hald T, Bradley WF. The Urinary Bladder: Neurology and Dynamics. Baltimore: Williams and Wilkins, 1982.
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49. Bissada NK, Finkbeiner AE. Lower urinary tract function and dysfunction: diagnosis and management. New York: Appleton Century Crofts, 1978.
collagen fibrillar sheaths in empty, distended and contracted urinary bladders of the guinea pig. Arch Histol Cytol 1993;56:441–9.
50. Yalla SV, McGuire EJ, el-Badawi A et al. Neurourology and Urodynamics: Principles and Practice. New York: Macmillan, 1988.
65. Morrison J, Wen J, Kibble A. Activation of pelvic afferent nerves from the rat bladder during filling. Scand J Urol Nephrol Suppl 1999;201:73–5.
51. McGuire EJ. Clinical Evaluation and Treatment of Neurogenic Vesical Dysfunction. Baltimore: Williams and Wilkins, 1984.
66. Morrison J. The activation of bladder wall afferent nerves. Exp Physiol 1999;84(1):131–6.
52. Mundy AR. Clinical physiology of the bladder, urethra and pelvic floor. In: Mundy AR, Stephenson T, Wein AJ (eds) Urodynamics: Principles, Practice and Applications. Edinburgh: Churchill Livingstone, 1983. 53. Smith JC. The function of the bladder. In: Blandy J (ed) Urology. Oxford: Blackwell, 1976. 54. Benson T. Drug therapy for voiding disorders: why all the confusion? In: Barrett DM, Wein AJ (eds) Controversies in Neurourology. Edinburgh: Churchill Livingstone, 1981; 253–9. 55. Mundy AR. The surgical treatment of detrusor instability. Neurourol Urodyn 1986;4:357–65. 56. Lee JG, Wein AJ, Levin RM. Comparative pharmacology of the male and female rabbit bladder neck and urethra: involvement of nitric oxide. Pharmacology 1994;48:250– 9. 57. Zvara P, Folsom JB, Kliment J Jr et al. Increased expression of neuronal nitric oxide synthase in bladder afferent cells in the lumbosacral dorsal root ganglia after chronic bladder outflow obstruction. Brain Res 2004;1002(1–2):35– 42. 58. DeGroat WC, Douglas JW, Glass J, Simonds W, Weimer B, Werner P. Changes in somato-vesical reflexes during postnatal development in the kitten. Brain Res 1975;94(1):150–4. 59. Yoshimura N, de Groat WC. Increased excitability of afferent neurons innervating rat urinary bladder after chronic bladder inflammation. J Neurosci 1999;19(11):4644–53. 60. Tanagho EA. Surgical anatomy of the genitourinary tract: anatomy of the lower urinary tract. In: Walsh PC, Retik AB, Stamey TA (eds) Campbell’s Urology, 6th ed. Philadelphia: Saunders, 1992. 61. Hutch JA. Anatomy and Physiology of the Bladder, Trigone and Urethra. New York: Appleton Century Crofts, 1972.
67. Brading AF, Mostwin JL, Sibley GN et al. The role of smooth muscle and its possible involvement in diseases of the lower urinary tract. Clin Sci 1986;70:7s–13s. 68. Steers WD, Ciambotti J, Etzel B, Erdman S, de Groat WC. Alterations in afferent pathways from the urinary bladder of the rat in response to partial urethral obstruction. J Comp Neurol 1991;310(3):401–10. 69. Steers WD, Kolbeck S, Creedon D, Tuttle JB. Nerve growth factor in the urinary bladder of the adult regulates neuronal form and function. J Clin Invest 1991;88(5):1709–15. 70. Schroder A, Uvelius B, Newgreen D, Andersson KE. Bladder overactivity in mice after 1 week of outlet obstruction. Mainly afferent dysfunction? J Urol 2003;170(3):1017–21. 71. Burgard EC, Fraser MO, Thor KB. Serotonergic modulation of bladder afferent pathways. Urology 2003;62(4 Suppl 1):10–5. 72. Jackson S, Donovan J, Brookes S, Eckford S, Swithinbank L, Abrams P. The Bristol Female Lower Urinary Tract Symptoms questionnaire: development and psychometric testing. Br J Urol 1996;77(6):805–12. 73. Wan J, McGuire EJ, Bloom DA, Ritchey ML. Stress leak point pressure: a diagnostic tool for incontinent children. J Urol 1993;150(2 Pt 2):700–2. 74. Young HH, Wesson MB. The anatomy and the surgery of the trigone. Arch Surg 1921;3:1–37. 75. Jeffcoate TNA, Roberts H. Observations on stress incontinence of urine. Am J Obstet Gynecol 1952;64:721–38. 76. Bennet BC, Vizzard MA, Booth AM. Role of nitric oxide in reflex urethral sphincter relaxation during micturition. Soc Neurosci Abstr 1993;19:511. 77. Thornbury KD, Hollywood MA, McHale NG. Mediation by nitric oxide of neurogenic relaxation of the urinary bladder neck muscle in sheep. J Physiol 1992;451:133–44.
62. Hutch JA, Amar AA. Vesico-ureteral reflux and pyelonephritis. New York: Appleton Century Crofts, 1972.
78. Brading AF, Fry CH, Maggi CA et al. Cellular biology. In: Abrams P, Khoury S, Wein AJ et al (eds) Incontinence: 1st International Consultation on Incontinence of the World Health Organization. Plymouth: Health Publication, 1999; 57–104.
63. Murakumo M, Ushiki T, Abe K et al. Three-dimensional arrangement of collagen and elastin fibers in the human urinary bladder: a scanning electron microscopic study. J Urol 1995;154:251–6.
79. Bushman W, Steers WD, Meythaler JM. Voiding dysfunction in patients with spastic paraplegia: urodynamic evaluation and response to continuous intrathecal baclofen. Neurourol Urodyn 1993;12:163–70.
64. Murakumo M, Ushiki T, Koyanagi T et al. Scanning electron microscopic studies of smooth muscle cells and their
80. Siroky MB, Olsson CA, Crane RJ. The flow rate nomogram. I. Development. J Urol 1979;122:655–68.
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81. Haylen BT, Ashby D, Sutherst JR, Frazer MI, West CR. Maximum and average urine flow rates in normal male and female populations – the Liverpool nomograms. Br J Urol 1989;64(1):30–8.
82. Schafer W. Analysis of bladder-outlet function with the linearized passive urethral resistance relation, linPURR, and a disease-specific approach for grading obstruction: from complex to simple. World J Urol 1995;13(1):47–58.
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10 Pharmacology of the bladder Karl-Erik Andersson
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IntroductIon The lower urinary tract is controlled by a complex interplay between the central and peripheral nervous systems and local regulatory factors.1 Malfunction at various levels may result in micturition disorders, which can be roughly classified as disturbances of storage or emptying. Failure to store urine may lead to various forms of incontinence (mainly urge and stress incontinence). Pharmacologic treatment of urinary incontinence is a main option, and several drugs with different modes and sites of action have been tried.2–5 However, to be able to optimize treatment, knowledge about the mechanisms of micturition and of the targets for treatment is necessary. This chapter provides a brief review of the normal nervous control of the lower urinary tract and of some therapeutic principles used for treatment of urinary incontinence.
nervous mechanIsms for bladder emptyIng and urIne storage The nervous mechanisms for bladder emptying and urine storage involve a complex pattern of afferent and efferent signaling in parasympathetic, sympathetic, and somatic nerves (Fig. 10.1). These nerves constitute reflex pathways, which either maintain the bladder in a relaxed state, enabling urine storage at low intravesical pressure, or initiate micturition by relaxing the outflow region and contracting the bladder smooth muscle. Under normal conditions, there is a reciprocal relationship between the activity in the detrusor and the activity in the outlet region. During voiding, contraction of the detrusor muscle is preceded by a relaxation of the outlet region, thereby facilitating bladder emptying.6–8 On the contrary, during the storage phase, the detrusor muscle is relaxed, and the outlet region is contracted to maintain continence. Contraction of the detrusor smooth muscle and relaxation of the outflow region result from activation of parasympathetic neurons located to the sacral parasympathetic nucleus (SPN) in the spinal cord at the level of S2–S4.9 The axons pass through the pelvic nerve and synapse with the postganglionic nerves in either the pelvic plexus, in ganglia on the surface of the bladder (vesical ganglia), or within the walls of the bladder and urethra (intramural ganglia).10 The preganglionic neurotransmission is predominantly mediated by acetylcholine acting on nicotinic receptors, although the transmission can be modulated by adrenergic, muscarinic, purinergic, and peptidergic presynaptic receptors.11 The postganglionic neurons in the pelvic nerve mediate the excitatory input to the normal human detrusor smooth
Pons
Pontine micturition centre
Sympathetic chain ganglia
Hypogastric plexus Th10 –12
S2–S4
Pelvic nerve
Hypogastric nerve Pelvic plexus
Pudendal nerve
Figure 10.1. Innervation of the lower urinary tract. The bladder and urethra receive parasympathetic (pelvic nerve), sympathetic (hypogastric nerve), as well as somatic (pudendal nerve) innervation. Sensory afferents can be found in the pelvic and hypogastric nerves as well as in the pudendal nerves.
muscle by releasing acetylcholine acting on muscarinic receptors. However, an atropine-resistant (non-adrenergic, non-cholinergic, or NANC) contractile component is regularly found in the bladders of most animal species.12,13 Such a component can also be demonstrated in functionally and morphologically altered human bladder tissue,14–16 but contributes by only a few percent to normal detrusor contraction.1 Adenosine triphosphate (ATP) is one important mediator of the NANC contraction17 although the involvement of other transmitters cannot be ruled out.1,18 The pelvic nerve also conveys parasympathetic nerves to the outflow region and the urethra. These nerves exert an inhibitory effect on the
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smooth muscle by releasing nitric oxide19 and other transmitters.20,21 Most of the sympathetic innervation of the bladder and urethra originates from the intermediolateral nuclei in the thoracolumbar region (T10–L2) of the spinal cord. The axons leave the spinal cord via the splanchnic nerves and travel either through the inferior mesenteric ganglia (IMF) and the hypogastric nerve, or pass through the paravertebral chain to the lumbosacral sympathetic chain ganglia and enter the pelvic nerve. Thus, sympathetic signals are conveyed in both the hypogastric and pelvic nerves.10 The preganglionic sympathetic transmission is, like the preganglionic parasympathetic transmission, predominantly mediated by acetylcholine acting on nicotinic receptors. Some preganglionic terminals synapse with the postganglionic cells in the paravertebral ganglia or in the IMF, while others synapse closer to the pelvic organs, and short postganglionic neurons innervate the target organs. Thus, the hypogastric and pelvic nerves contain both pre- and postganglionic fibers.10 The predominant effect of the sympathetic innervation is to contract the bladder base and the urethra. In addition, the sympathetic innervation inhibits the parasympathetic pathways at spinal and ganglionic levels. In humans, noradrenaline is released in response to electrical stimulation in vitro;22 the normal response to released noradrenaline is relaxation.23,24 However, the importance of the sympathetic innervation for relaxation of the human detrusor has never been established. In contrast, in several animal species the adrenergic innervation has been demonstrated to mediate relaxation of the detrusor during filling. Most of the sensory nerves to the bladder and urethra originate in the dorsal root ganglia at the lumbosacral level of the spinal cord and travel via the pelvic nerve to the periphery. In addition, some afferents originate in dorsal root ganglia at the thoracolumbar level and travel in the hypogastric nerve. The sensory nerves to the striated muscle of the external urethral sphincter travel in the pudendal nerve to the sacral region of the spinal cord.10 The most important afferents for the micturition process are myelinated Aδ-fibers and unmyelinated Cfibers traveling in the pelvic nerve to the sacral spinal cord,25 conveying information from receptors in the bladder wall. The Aδ-fibers respond to passive distension and active contraction, thus conveying information about bladder filling.26 The activation threshold for Aδfibers is 5–15 mmH2O. This is the intravesical pressure at which humans report the first sensation of bladder filling.11 C-fibers have a high mechanical threshold and respond primarily to chemical irritation of the bladder urothelium/suburothelium27 or to cold.28 Following
chemical irritation, the C-fiber afferents exhibit spontaneous firing when the bladder is empty and increased firing during bladder distension.27 These fibers are normally inactive and are therefore termed ‘silent fibers’. The somatic innervation of the urethral rhabdosphincter and of some perineal muscles (e.g. compressor urethrae and urethrovaginal sphincter) is provided by the pudendal nerve. These fibers originate from sphincter motor neurons located in the ventral horn of the sacral spinal cord (levels S2–S4) in a region called Onuf’s (Onufrowicz’s) nucleus.29
the storage phase During the storage phase the bladder has to relax in order to maintain a low intravesical pressure. Urine storage is regulated by two separate storage reflexes: sympathetic (autonomic) and somatic.29 The sympathetic storage reflex (pelvic-to-hypogastric reflex) is initiated as the bladder distends (myelinated Aδ-fibers) and the generated afferent activity travels in the pelvic nerves to the spinal cord. Within the spinal cord, sympathetic firing from the lumbar region (L1–L3) is initiated, which, by effects at the ganglionic level, decreases excitatory parasympathetic inputs to the bladder, and, through postganglionic neurons, releases noradrenaline which facilitates urine storage by stimulating β3 adrenoceptors (ARs) in the detrusor smooth muscle (see below). As mentioned previously, there is little evidence for a functionally important sympathetic innervation of the human detrusor, in contrast to what has been found in several animal species. The sympathetic innervation of the human bladder is found mainly in the outlet region, where it mediates contraction. During micturition, this sympathetic reflex pathway is markedly inhibited via supraspinal mechanisms to allow the bladder to contract and the urethra to relax. Thus, the Aδ-afferents and the sympathetic efferent fibers constitute a vesicospinovesical storage reflex which maintains the bladder in a relaxed mode while the proximal urethra and bladder neck are contracted. In response to a sudden increase in bladder pressure, such as during a cough, laugh or sneeze, a more rapid somatic storage reflex (pelvic-to-pudendal reflex), also called the guarding or continence reflex, is initiated. The evoked afferent activity travels along myelinated Aδ-afferent fibers in the pelvic nerve to the sacral spinal cord, where efferent somatic urethral motor neurons, located in the nucleus of Onuf, are activated. Afferent information is also conveyed to the periaqueductal gray (PAG) and to the pontine storage center (the L-region). Axons from these motor neurons of the nucleus of Onuf 159
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travel in the pudendal nerve and release acetylcholine, which activates nicotinic cholinergic receptors on the rhabdosphincter, which contracts. This pathway is tonically active during urine storage. During sudden abdominal pressure increases, however, it becomes dynamically active to contract the rhabdosphincter. During micturition this reflex is strongly inhibited via spinal and supraspinal mechanisms to allow the rhabdosphincter to relax and permit urine passage through the urethra. In addition to this spinal somatic storage reflex, there is also supraspinal input from the pons, which projects directly to the nucleus of Onuf and is important for volitional control of the rhabdosphincter.30
the emptying phase Vesicobulbovesical micturition reflex Electrophysiologic experiments in cats and rats provide evidence for a voiding reflex mediated through a vesicobulbovesical pathway involving neural circuits in the pons, which constitute the pontine micturition center (PMC). Other regions in the brain important for micturition include the hypothalamus and cerebral cortex.11,31 Bladder filling leads to increased activation of tension receptors within the bladder wall and thus to increased afferent activity in Aδ-fibers. These fibers project on spinal tract neurons mediating increased sympathetic firing to maintain continence as discussed above (storage reflex). In addition, the spinal tract neurons convey the afferent activity to more rostral areas of the spinal cord and the brain. One important receiver of the afferent information from the bladder is the PAG in the rostral brainstem. The PAG receives information from both afferent neurons in the bladder and from more rostral areas in the brain, i.e. cerebral cortex and hypothalamus. This information is integrated in the PAG and the medial part of the PMC (the M-region), which also control the descending pathways in the micturition reflex. Thus, the PMC can be seen as a switch in the micturition reflex, inhibiting parasympathetic activity in the descending pathways when there is low activity in the afferent fibers, and activating the parasympathetic pathways when the afferent activity reaches a certain threshold.11 The threshold is believed to be set by the inputs from more rostral regions in the brain. In cats, lesioning of regions above the inferior colliculus usually facilitates micturition by elimination of inhibitory inputs from more rostral areas of the brain. On the other hand, transections at a lower level inhibit micturition. Thus, the PMC appears to be under tonic inhibitory control. A variation of the inhibitory input to the PMC results in a variation of bladder capacity. Experiments on rats have
shown that the micturition threshold is regulated by, for example, GABAergic inhibitory mechanisms in the PMC neurons.32
Vesicospinovesical micturition reflex Spinal lesions rostral to the lumbosacral level interrupt the vesicobulbovesical pathway and abolish the supraspinal and voluntary control of micturition. This results initially in an areflexic bladder accompanied by urinary retention.11 An automatic vesicospinovesical micturition reflex develops slowly, although voiding is generally insufficient due to bladder sphincter dyssynergia, i.e. simultaneous contraction of bladder and urethra. It has been demonstrated in chronic spinal cats that the afferent limb of this reflex is conveyed through unmyelinated C-fibers which usually do not respond to bladder distension,27 suggesting changed properties of the afferent receptors in the bladder. Accordingly, the micturition reflex in chronic spinal cats is blocked by capsaicin, a neurotoxin which is believed to block C-fiber-mediated neurotransmission.33,34
targets for pharmacologIc InterventIon cns targets Anatomically, several CNS regions may be involved in micturition control: supraspinal structures, such as the cortex and diencephalon, midbrain, and medulla, as well as spinal structures.31,35–38 Several transmitters and their receptors are involved in the reflexes and sites described above and may be targets for drugs aimed at control of micturition. Although few drugs with a CNS site of action have been developed, several agents acting on the CNS may have effects on micturition.
Opioid receptors Endogenous opioid peptides and corresponding receptors are widely distributed in many regions in the CNS of importance for micturition control, e.g. the PAG, the PMC, the spinal parasympathetic nucleus, and the nucleus of Onuf.39–41 It has been well established that morphine, given by various routes of administration to animals and humans, can increase bladder capacity and eventually cause urinary retention. Given intrathecally (i.t.) to anesthetized rats and intravenously (i.v.) to humans, the µ-opioid receptor antagonist, naloxone, has been shown to stimulate micturition,42,43 suggesting that a tonic activation of µ-opioid receptors has a depressant effect on the micturition reflex.
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Morphine given i.t. was effective in patients with detrusor overactivity due to spinal cord lesions,44 but was associated with side effects, such as nausea and pruritus. Further side effects of opioid receptor agonists comprise respiratory depression, constipation, and abuse. Attempts have been made to reduce these side effects by increasing selectivity towards one of the different opioid receptor types.45 At least three different opioid receptors – µ, δ, and κ – bind stereospecifically with morphine, and have been shown to interfere with voiding mechanisms. Theoretically, selective receptor actions, or modifications of effects mediated by specific opioid receptors, may have useful therapeutic effects for micturition control. Tramadol is a well-known analgesic drug, which, by itself, it is a very week µ receptor agonist. However, it is metabolized to several different compounds, some of them almost as effective as morphine at the µ receptor. The drug also inhibits serotonin (5-HT) and noradrenaline reuptake.46 This profile is of particular interest, since both µ-receptor agonism and amine reuptake inhibition may be useful principles for treatment of detrusor overactivity and the overactive bladder (OAB) syndrome. When tramadol is given to a normal, awake rat, the most conspicuous changes in the cystometrogram are increases in threshold pressure and bladder capacity. Naloxone can more or less completely inhibit these effects.47 There is a small difference between the doses of morphine that cause inhibition of micturition and those increasing bladder capacity and evoking urinary retention. Tramadol has effects over a much wider range of doses, which means that it could be therapeutically more useful for micturition control. It may be speculated that the difference is dependent on tramadol also inhibiting the 5-HT and noradrenaline reuptake.47 Central stimulation of δ-opioid receptors in anesthetized cats and rats inhibited micturition48,49 and parasympathetic neurotransmission in cat bladder ganglia.50 In humans, nalbuphine, a µ-receptor antagonist and κ-receptor agonist, increased bladder capacity.51 Buprenorphine (a partial µ-receptor agonist and κreceptor antagonist) decreased micturition pressure and increased bladder capacity more than morphine.51 These effects should be considered when the drugs are used in, for example, pain control. Further exploration of these non-µ-opioid receptor-mediated actions on micturition would be advantageous.
Serotonin (5-HT) mechanisms It is well established that the lumbosacral autonomic, as well as the somatic, motor nuclei (Onuf’s nuclei) receive a dense serotonergic input from the raphe nuclei, an
innervation which is not subjected to the general decline in lumbosacral spinal innervation found with increasing age.52 Multiple 5-HT receptors have been found at sites where processing of afferent and efferent impulses from and to the lower urinary tract take place.53 Although, as pointed out by de Groat,54 there is some evidence in the rat for serotonergic facilitation of voiding, the descending pathway is essentially an inhibitory circuit, with 5-HT as a key neurotransmitter. Thus, electrical stimulation of 5-HT-containing neurons in the caudal raphe nucleus causes inhibition of bladder contractions.55,56 Most experiments in rats and cats indicate that activation of the central serotonergic system by 5-HT reuptake inhibitors, as well as by 5-HT1A and 5-HT2 receptor agonists, depresses reflex bladder contractions and increases the bladder volume threshold for inducing micturition.54 5-HT1A receptors are involved in multiple inhibitory mechanisms controlling the spinobulbospinal micturition reflex pathway. The regulation of the frequency of bladder reflexes is presumably mediated by a suppression of afferent input to the micturition switching circuitry in the pons, whereas the regulation of bladder contraction amplitude may be related to an inhibition of the output from the pons to the parasympathetic nuclei in the spinal cord. There is an ongoing discussion as to whether or not there is a deficiency in serotonin behind both depression and the overactive bladder.57–59 If there is, the question then is: Are selective serotonin reuptake inhibitors (SSRIs) effective for micturition control only in depressed patients, or is selective serotonin uptake inhibition a general principle that can be used for treatment of OAB? There are no randomized controlled trials (RCTs) showing that SSRIs are useful for the treatment of OAB/detrusor overactivity.3 In contrast, there are reports suggesting that the SSRIs in patients without incontinence actually can cause incontinence, particularly in the elderly. Patients exposed to SSRIs had an increased risk (15 out of 1000 patients) for developing urinary incontinence.60 This causes doubts over the anecdotal reports that SSRIs may be used as a general treatment for OAB.
γ-Aminobutyric acid (GABA) mechanisms GABA has been identified as a main inhibitory transmitter in the brain and spinal cord. GABA functions appear to be triggered by binding of GABA to its ionotropic receptors, GABAA and GABAC, which are ligandgated chloride channels, and its metabotropic receptor, GABAB.61 Since blockade of GABAA and GABAB receptors in the spinal cord62,63 and brain63,64 stimulated rat micturition, an endogenous activation of GABAA+B receptors 161
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may be responsible for continuous inhibition of the micturition reflex within the CNS. In the spinal cord, GABAA receptors are more numerous than GABAB receptors, except for the dorsal horn where GABAB receptors predominate.65,66 Experiments using conscious and anesthetized rats demonstrated that exogenous GABA, muscimol (a GABAA receptor agonist) and baclofen (a GABAB receptor agonist) given i.v., i.t. or intracerebroventricularly (i.c.v.) inhibit micturition.63,67 Similar effects were obtained in non-anesthetized mice.68 Baclofen given i.t. attenuated oxyhemoglobin-induced detrusor overactivity in rats, suggesting that the inhibitory actions of GABAB receptor agonists in the spinal cord may be useful for controlling micturition disorders caused by C-fiber activation in the urothelium and/or suburothelium.63 In mice, where detrusor overactivity was produced by intravesical citric acid, baclofen given subcutaneously had an inhibitory effect which was blocked by the selective GABAB receptor antagonist CGP55845.68 Beneficial effects of baclofen have also been documented in humans with detrusor overactivity.69 Stimulation of the PMC results in an immediate relaxation of the external striated sphincter and a contraction of the detrusor muscle of the bladder. In cats, Blok et al.30 demonstrated a direct pathway from the PMC to the dorsal gray commissure of the sacral cord. It was suggested that the pathway produced relaxation of the external striated sphincter during micturition via inhibitory modulation by GABA neurons of the motoneurons in the sphincter of Onuf. In rats, i.t baclofen and muscimol ultimately produced dribbling urinary incontinence,62,63 and this was also found in conscious mice given muscimol and diazepam subcutaneously.68 Thus, normal relaxation of the striated urethral sphincter is probably mediated via GABAA receptors,63 GABAB receptors having a minor influence on motoneuron excitability.70 Gabapentin Gabapentin was originally designed as an anticonvulsant GABA mimetic capable of crossing the blood–brain barrier.71 However, its effects do not appear to be mediated through interaction with GABA receptors, and its mechanism of action is still controversial.71 Gabapentin is also widely used not only for seizures and neuropathic pain, but also for many other indications such as anxiety and sleep disorders due to its apparent lack of toxicity. In a pilot study, Carbone et al.72 reported on the effect of gabapentin on neurogenic detrusor activity. They found a positive effect on symptoms and a significant improvement of urodynamic parameters after treatment, and suggested that the effects of the drug should
be explored in further controlled studies in both neurogenic and non-neurogenic detrusor overactivity. Kim et al.73 found that 14 of 31 patients with OAB and nocturia, refractory to antimuscarinic treatment, improved with oral gabapentin. The drug was generally well tolerated and was considered to be an option in selected patients when conventional treatment modalities had failed.
Noradrenaline and α-adrenoceptors Noradrenergic neurons in the brainstem project to the sympathetic, parasympathetic, and somatic nuclei in the lumbosacral spinal cord. Bladder activation through these bulbospinal noradrenergic pathways may involve excitatory α1-adrenoceptors. In rats undergoing continuous cystometry, intrathecal doxazosin decreased micturition pressure, both in normal rats and in animals with postobstruction bladder hypertrophy.74 The effect was much more pronounced in the animals with hypertrophied/overactive bladders. Doxazosin given intrathecally, but not intra-arterially, to spontaneously hypertensive rats exhibiting bladder overactivity normalized bladder activity.75 It was suggested that doxazosin has a site of action at the level of the spinal cord and ganglia. However, there are no RCTs documenting positive effects of α-adrenoceptor antagonists in OAB/detrusor overactivity.2,3
Dopamine and dopamine receptors Many patients with Parkinson’s disease have neurogenic detrusor overactivity (detrusor hyperreflexia),76 possibly as a consequence of nigrostriatal dopamine depletion and failure to activate inhibitory D1 receptors.77 However, other dopaminergic systems may activate D2 receptors, facilitating the micturition reflex. Sillén et al.78 showed that apomorphine, which activates both D1 and D2 receptors, induced bladder overactivity in anesthetized rats via stimulation of central dopaminergic receptors. The effects were abolished by infracollicular transection of the brain, and by prior intraperitoneal administration of the centrally acting dopamine receptor blocker, spiroperidol. Kontani et al.79,80 suggested that the bladder overactivity induced by apomorphine in anesthetized rats resulted from synchronous stimulation of the micturition centers in the brainstem and spinal cord, and that the response was elicited by stimulation of both dopamine D1 and D2 receptors. Blockade of central dopamine receptors may be expected to influence voiding; however, the therapeutic potential of drugs having this action has not been established. On the other hand, the effects on micturition of various dopamine receptor active drugs used in, for example, different psychiatric conditions, should not be neglected.
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peripheral targets Possible peripheral targets for pharmacologic intervention may be: 1) the efferent neurotransmission; 2) the smooth muscle itself, including ion channels and intracellular second messenger systems; and 3) the afferent neurotransmission. Although many effective drugs are available for these target systems, most of them are less useful in the clinical situation due to the lack of selectivity for the lower urinary tract, which may result in intolerable side effects. Thus, a key task is to find systems or receptors, more or less specific for the lower urinary tract, which can be manipulated without disturbing other systems in the body, or, alternatively, to design drugs in a way that results in higher tissue concentrations in the lower urinary tract than elsewhere in the body.
Muscarinic receptors Muscarinic receptors comprise five subtypes, encoded by five distinct genes.81 The five gene products correspond to pharmacologically defined receptors, and M1–M5 is used to describe both the molecular and pharmacologic subtypes. In the human bladder, the mRNAs for all muscarinic receptor subtypes have been demonstrated,82 with a predominance of mRNAs encoding M2 and M3 receptors.82,83 These receptors are also functionally coupled to G-proteins, but the signal transduction systems vary.84–86 Detrusor smooth muscle contains muscarinic receptors of mainly the M2 and M3 subtypes.84–87 The M3 receptors in the human bladder are believed to be the most important for detrusor contraction. Jezior et al.88 suggested that muscarinic receptor activation of detrusor muscle includes both non-selective cation channels and activation of Rho-kinase. Supporting a role of Rhokinase in the regulation of rat detrusor contraction and tone, Wibberley et al.89 found that Rho-kinase inhibitors (Y-27632, HA 1077) inhibited contractions evoked by carbachol without affecting the contraction response to potassium chloride. They also demonstrated high levels of Rho-kinase isoforms (I and II) in the bladder. Schneider et al.87 concluded that carbachol-induced contraction of human urinary bladder is mediated via M3 receptors and largely depends on calcium entry through nifedipine-sensitive channels and activation of the Rho-kinase pathway. Thus, the main pathway for muscarinic receptor activation of the detrusor via M3 receptors may be calcium influx via L-type calcium channels, and increased sensitivity to calcium of the contractile machinery produced via inhibition of myosin light chain phosphatase through activation of Rho-kinase.90 The functional role for the M2 receptors has not been clarified, but it has been suggested that M2 receptors
may oppose sympathetically mediated smooth muscle relaxation, mediated by β-adrenoceptors.91 M2 receptor stimulation may also activate non-specific cation channels92 and inhibit KATP channels through activation of protein kinase C.93,94 In certain disease states, M2 receptors may contribute to contraction of the bladder. Thus, in the denervated rat bladder, M2 receptors, or a combination of M2 and M3, mediated contractile responses and the two types of receptor appeared to act in a facilitatory manner to mediate contraction.95–97 In obstructed, hypertrophied rat bladders, there was an increase in total and M2 receptor density, whereas there was a reduction in M3 receptor density.98 The functional significance of this change for voiding function has not been established. Pontari et al.99 analyzed bladder muscle specimens from patients with neurogenic bladder dysfunction to determine whether the muscarinic receptor subtype mediating contraction shifts from M3 to the M2 receptor subtype, as found in the denervated, hypertrophied rat bladder. They concluded that whereas normal detrusor contractions are mediated by the M3 receptor subtype, in patients with neurogenic bladder dysfunction contractions can be mediated by the M2 receptors. Muscarinic receptors may also be located on the presynaptic nerve terminals and participate in the regulation of transmitter release. In the human bladder, the prejunctional inhibitory muscarinic receptors have been classified as M4;100 prejunctional facilitatory muscarinic receptors appear to be of the M1 type.101 The muscarinic facilitatory mechanism seems to be upregulated in hyperactive bladders from chronic spinal cord transected rats. The facilitation in these preparations is primarily mediated by M3 muscarinic receptors.101,102 Muscarinic receptors have also been demonstrated on the urothelium/suburothelium, but their functional importance has not yet been clarified. It has been suggested that they may be involved in the release of an unknown inhibitory factor.86
Adrenergic receptors
α-Adrenoceptors (ARs) α-ARs may have effects on different locations in the bladder: the detrusor smooth muscle, the detrusor vasculature, the afferent and efferent nerve terminals, and intramural ganglia. For some of these possible sites only fragmentary information is available. There is ongoing discussion concerning the importance of the α1-ARs in the human detrusor in the generation of lower urinary tract symptoms (LUTS). Most investigators agree that there is a low expression of these receptors.103,104 In studies of the human bladder, Malloy et al.104 found that two-thirds of the α-AR mRNA 163
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expressed was α1D, there was no α1B, and one-third was α1A. In the rat bladder, the α1-AR distribution was different: α1A was predominant, one-third was α1D, and there was very little α1B. This was consistent in the different parts of the detrusor.105 A change of subtype distribution may be produced by outflow obstruction. Hampel et al.105 reported that there was a change in the obstructed bladder from α1A-AR to α1D-AR mRNA predominance. In humans, as mentioned previously, there is already an α1D-AR predominance in the normal bladder, which means that a change in a similar direction as in the rat would be of minor importance provided that the number of receptors did not increase. Recent work by Nomiya et al.106 suggested that this was not the case. They confirmed the low expression of αAR mRNA in normal human bladder, and further demonstrated that there was no upregulation of any of the adrenergic receptors with obstruction. In addition, in functional experiments they found a small response to phenylephrine at high drug concentrations with no difference between normal and obstructed bladders. Thus, in the obstructed human bladder, there appears to be no evidence for α-AR upregulation or change in subtype. This finding was challenged by Bouchelouche et al.107 who found an increased response to α1-AR stimulation in obstructed bladders. Whether or not this would mean that the α1D-ARs in the detrusor muscle are responsible for detrusor overactivity or OAB is unclear, and, based on available evidence, it does not seem likely that in the detrusor muscle these receptors should be an important target. This does not exclude that α1D-ARs located elsewhere in the bladder would be of importance. All subtypes of α-ARs can be found in different parts of the human vascular tree, and all mediate contraction. Expression varies with vessel bed and increases with age. In the bladder, the function of the detrusor muscle is dependent on the vasculature and the perfusion. Hypoxia induced by partial outlet obstruction is believed to play a major role in both the hypertrophic and degenerative effects of partial outlet obstruction. Das et al.108 investigated in rats whether doxazosin affected blood flow to the bladder and reduced the level of bladder dysfunction induced by partial outlet obstruction. They found that 4 weeks of treatment with doxazosin increased bladder blood flow in both control and obstructed rats. Furthermore, doxazosin treatment reduced the severity of the detrusor response to partial outlet obstruction. Thus, doxazosin could reduce the increase in bladder weight in obstructed animals which could be one of the mechanisms that contributed to a positive effect on detrusor overactivity caused by the obstruction.
β -Adrenoceptors In the human detrusor, it is now generally accepted that the most important β-AR for bladder relaxation is the β3-AR.109 This can partly explain why the clinical effects of selective β2-AR agonists in detrusor overactivity have been controversial and largely inconclusive.2 On the other hand, the β2-AR agonist, clenbuterol, inhibited electrically evoked contractions in human ‘unstable’, but not normal, bladder,110 which is in agreement with previous experiences in humans, suggesting that clenbuterol, as well as other β2-AR agonists such as terbutaline, may inhibit detrusor overactivity.111,112 The β3-AR seems to be an interesting target for drugs aimed at treatment of OAB, and selective β3-AR agonists have shown relaxant effects in vitro and in animal models of detrusor overactivity.113–115 However, no proof of concept studies, showing that this is an effective principle to treat OAB, appear to have been performed in humans.
Ion channels Ion channels are important regulators of cell function. Located within the plasma membrane, they control the permeability of different ions. The two most thoroughly investigated classes of ion channels are calcium channels and potassium channels.116 Calcium channels Calcium is a key component for function in many cells. In smooth muscle, increased intracellular calcium concentrations activate the contractile mechanisms; in nerve terminals, calcium influx in response to action potentials is an important mechanism for neurotransmitter release. Calcium channels can be divided into at least four different subtypes: L, N, P, and Q channels. The calcium channels present in smooth muscle are L-type (dihydropyridine-sensitive) and appear to be involved in contraction of the human bladder, irrespective of the mode of activation.117 A decrease of the membrane potential (depolarization) increases the open probability for calcium channels, thereby increasing the calcium influx. Thus, the channels are dependent on the membrane potential and are termed voltage-operated calcium channels (VOCC). Elevated intracellular calcium levels are also believed to initiate release of calcium from intracellular stores, a mechanism called calcium-induced calcium release.118,119 Thus, regulation of the intracellular calcium concentration in smooth muscle cells is one conceivable way to modulate bladder contraction. Dihydropyridines (e.g. nifedipine) have a potent inhibitory effect on isolated detrusor muscle. Inhibitory effects have also been demonstrated
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on experimentally induced contractions under in vivo conditions in rats, and clinically in patients with detrusor overactivity.18 Therapeutically, however, there is no evidence that calcium antagonists are of use in the treatment of OAB/detrusor overactivity.2,3 Potassium channels Potassium channels represent another mechanism to modulate the excitability of the smooth muscle cells. Under normal conditions, the resting membrane potential in smooth muscle cells is determined predominantly by the membrane conductivity for potassium ions. Increased potassium conductivity will lower the membrane potential by increasing the potassium efflux. As a consequence, this will increase the threshold for opening of VOCCs and initiation of contraction. There are several different types of potassium channels and at least two subtypes have been found in the human detrusor: ATP-sensitive potassium channels (KATP) and large conductance calcium-activated potassium channels (BKCa). Studies on isolated human detrusor muscle and on bladder tissue from several animal species have demonstrated that potassium channel openers reduce spontaneous contractions as well as contractions induced by carbachol and electrical stimulation.116 However, the lack of selectivity of presently available potassium channel blockers for the bladder versus the vasculature has thus far limited the use of these drugs. No effects of cromakalim or pinacidil on the bladder were found in studies on patients with spinal cord lesions or detrusor instability secondary to outflow obstruction.120,121 Some new potassium channel openers have been developed and are claimed to have selectivity towards the bladder.116 However, so far there is no evidence that potassium channels openers are an option for treatment of OAB/detrusor overactivity.2,3
Urothelial mechanoafferent signaling Recent evidence suggests that the urothelium may serve as a mechanosensor which – by producing nitric oxide, ATP, and other mediators – can control the activity in afferent nerves, and thereby the initiation of the micturition reflex.122 Low pH, high potassium, increased osmolality, and low temperatures can all influence afferent nerves, possibly via effects on the vanilloid receptor (capsaicin-gated ion channel TRPV1), which is expressed both in afferent nerve terminals and in the epithelial cells that line the bladder lumen.123,124 A network of interstitial cells, extensively linked by Cx43-containing gap junctions, was found to be located beneath the urothelium in human bladder by Sui et al.125,126 This interstitial cellular network was suggested to operate as a
functional syncytium, integrating signals and responses in the bladder wall. The firing of suburothelial afferent nerves and the threshold for bladder activation may be modified by both inhibitory (e.g. nitric oxide) and stimulatory (e.g. ATP, tachykinins, prostanoids) mediators. ATP, generated by the urothelium, has been suggested as an important mediator of urothelial signaling.17,122 Supporting such a view, intravesical ATP induces detrusor overactivity in conscious rats.127 Furthermore, mice lacking the P2X3 receptor were shown to have hypoactive bladders.128,129 There appear to be other, thus far unidentified, factors in the urothelium that could influence bladder function.130–136 Fovaeus et al.133 found that a previously unrecognized non-adrenergic, non-nitrergic, non-prostanoid inhibitory mediator is released from the rat urinary bladder by muscarinic receptor stimulation. However, it was not clear whether this factor came from the detrusor muscle or from both the bladder and the urothelium. Hawthorn et al.134 presented data suggesting the presence of a diffusible, urothelium-derived inhibitory factor, which could not be identified, but did not appear to be nitric oxide, a cyclooxygenase product, a catecholamine, adenosine, GABA or any substance sensitive to apamin. The identity and possible physiologic role of the unknown factor remains to be established and should offer an interesting field for further research. These mechanisms can be involved in the pathophysiology of OAB and thus would be interesting targets for pharmacologic intervention.
Sensory nerves and vanilloid receptors Appropriate bladder function is dependent on an intact afferent signaling from the bladder to the CNS. This signaling conveys information about bladder filling and the status of the tissue (e.g. presence of infectious agents etc.). The afferent nerves consist of small, slowly conducting, myelinated Aδ-fibers and slowly conducting, unmyelinated C-fibers. The former are excited by mechanoreceptors and convey information about bladder filling, whereas C-fibers mediate painful sensations recognized by chemoreceptors. By means of capsaicin, a subpopulation of primary afferent neurons innervating the bladder and urethra – the ‘capsaicin-sensitive nerves’ – has been identified. It is believed that capsaicin exerts its effects by acting on specific, ‘vanilloid’ receptors on these nerves.137 Capsaicin exerts a biphasic effect: initial excitation is followed by a long-lasting blockade, which renders sensitive primary afferents (C-fibers) resistant to activation by natural stimuli. In sufficiently high concentrations, capsaicin is believed to cause ‘desensitization’, initially by releasing and emptying the stores of 165
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neuropeptides, and then by blocking further release.138 Resiniferatoxin (RTX) is an analog of capsaicin, approximately 1000 times more potent for desensitization than capsaicin,139 but only a few hundred times more potent for excitation.140 It is possible that both capsaicin and RTX can have effects on Aδ-fibers. It is also possible that capsaicin at high concentrations (mM) has additional, non-specific effects.141 Both capsaicin and RTX have been used successfully to treat bladder function disturbances.2,3 They are known to bind to the VR1 (TRPV1) receptor, a non-selective cation channel, on the peripheral terminals of nociceptive neurons, but the role of vanilloid receptors in normal bladder function and in the pathogenesis in detrusor overactivity and autonomic dysreflexia has not been established. Birder et al.124 investigated bladder function in conscious mice lacking the VR1 receptor. VR1 receptor knockout mice appear to have an increased voiding frequency compared with wild-type mice. The VR1 knockouts also had an increased frequency of nonvoiding bladder contractions. In vitro, stretch-induced ATP release is decreased in bladders from VR1 knockout mice, and hypo-osmolality-induced ATP released from cultured urothelial cells was also reduced.124 The authors suggested that VR1 receptors participate in normal bladder function, are essential for normal mechanically evoked purinergic signaling by the urothelium, and are involved in ATP release. Experimental and clinical evidence that capsaicinsensitive afferents were involved in idiopathic detrusor overactivity was recently presented, and a case was made for intravesical RTX as a treatment in patients with this disorder.142,143 However, the difficulties with the handling of RTX (e.g. the drug may adhere to the administration device) may limit the use of this therapeutic approach.
Botulinum toxin Seven immunologically distinct antigenic subtypes of botulinum toxin have been identified: A, B, C1, D, E, F, and G. Types A and B are in clinical use in urology, but most studies have been performed with botulinum toxin A type. Botulinum toxin acts by inhibiting release of acetylcholine and other transmitters from nerve terminals interacting with the protein complex necessary for docking transmitter-containing vesicles.144,145 This results in decreased muscle contractility and muscle atrophy at the injection site, but also inactivation of afferent nerves. The produced chemical denervation is a reversible process, and axons are regenerated in approximately 3–6 months. The botulinum toxin molecule cannot cross the blood–brain barrier and therefore has no CNS effects.
This type of chemical denervation of the bladder implies an effective treatment approach. In urology, botulinum toxin injected into the external urethral sphincter was initially used to treat spinal cord injured patients with detrusor–external sphincter dyssynergia.144–146 The use of botulinum toxin has increased rapidly, and successful treatment of neurogenic detrusor overactivity by intravesical botulinum toxin injections has now been reported by several groups.147,148 However, toxin injections may also be effective in refractory idiopathic detrusor overactivity.147–149
conclusIon To effectively control bladder activity, and to treat urinary incontinence caused by detrusor overactivity, identification of suitable targets for pharmacologic intervention is necessary. Such targets may be found in the central nervous system or peripherally. Drugs specifically directed for control of bladder activity are under development and will hopefully lead to improved treatment of urinary incontinence.
acknowledgment This study was supported by the Swedish Medical Research Council (Grant No. 6837).
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41. de Groat WC, Yoshimura N. Pharmacology of the lower urinary tract. Annu Rev Pharmacol Toxicol 2001;41:691– 721. 42. Murray KH, Feneley RC. Endorphins – a role in lower urinary tract function? The effect of opioid blockade on the detrusor and urethral sphincter mechanisms. Br J Urol 1982;54(6):638–40. 43. Dray A, Nunan L, Wire W. Naloxonazine and opioidinduced inhibition of reflex urinary bladder contractions. Neuropharmacology 1987;26(1):67–74. 44. Herman RM, Wainberg MC, delGiudice PF, Willscher MK. The effect of a low dose of intrathecal morphine on impaired micturition reflexes in human subjects with spinal cord lesions. Anesthesiology 1988;69(3):313–8. 45. Kieffer BL. Opioids: first lessons from knockout mice. Trends Pharmacol Sci 1999;20(1):19–26. 46. Raffa RB, Friderichs E. The basic science aspect on tramadol hydrochloride. Pain Rev 1996;3:249–71. 47. Pandita RK, Pehrson R, Christoph T, Friderichs E, Andersson KE. Actions of tramadol on micturition in awake, freely moving rats. Br J Pharmacol 2003;139(4):741–8. 48. Hisamitsu T, de Groat WC. The inhibitory effect of opioid peptides and morphine applied intrathecally and intracerebroventricularly on the micturition reflex in the cat. Brain Res 1984;298(1):51–65. 49. Dray A, Nunan L, Wire W. Central delta-opioid receptor interactions and the inhibition of reflex urinary bladder contractions in the rat. Br J Pharmacol 1985;85(3): 717–26. 50. de Groat WC, Kawatani M. Enkephalinergic inhibition in parasympathetic ganglia of the urinary bladder of the cat. J Physiol 1989;413:13–29. 51. Malinovsky JM, Le Normand L, Lepage JY et al. The urodynamic effects of intravenous opioids and ketoprofen in humans. Anesth Analg 1998;87(2):456–61. 52. Ranson RN, Dodds AL, Smith MJ et al. Age-associated changes in the monoaminergic innervation of rat lumbosacral spinal cord. Brain Res 2003;972(1–2):149–58. 53. Thor KB, Blitz-Siebert A, Helke CJ. Autoradiographic localization of 5-hydroxytryptamine1A, 5-hydroxytryptamine1B and 5-hydroxytryptamine1C/2 binding sites in the rat spinal cord. Neuroscience 1993;55(1): 235–52.
57. Zorn BH, Montgomery H, Pieper K et al. Urinary incontinence and depression. J Urol 1999;162(1):82–4. 58. Steers WD, Lee KS. Depression and incontinence. World J Urol 2001;19(5):351–7. 59. Littlejohn JO Jr, Kaplan SA. An unexpected association between urinary incontinence, depression and sexual dysfunction. Drugs Today (Barc) 2002;38(11):777–82. 60. Movig KL, Leufkens HG, Belitser SV et al. Selective serotonin reuptake inhibitor-induced urinary incontinence. Pharmacoepidemiol Drug Saf 2002;11(4):271–9. 61. Chebib M, Johnston GAR. The ‘ABC’ of GABA receptors: a brief review. Clin Exp Pharmacol Physiol 1999;26(11):937–40. 62. Igawa Y, Mattiasson A, Andersson K-E. Effects of GABAreceptor stimulation and blockade on micturition in normal rats and rats with bladder outflow obstruction. J Urol 1993;150(2 Pt 1):537–42. 63. Pehrson R, Lehmann A, Andersson K-E. Effects of gamma-aminobutyrate B receptor modulation on normal micturition and oxyhemoglobin induced detrusor overactivity in female rats. J Urol 2002;168(6):2700–5. 64. Maggi CA, Furio M, Santicioli P et al. Spinal and supraspinal components of GABAergic inhibition of the micturition reflex in rats. J Pharm Exp Ther 1987;240(3):998– 1005. 65. Coggeshall RE, Carlton SM. Receptor localization in the mammalian dorsal horn and primary afferent neurons. Brain Res Rev 1997;24(1):28–66. 66. Malcangio M, Bowery NG. GABA and its receptors in the spinal cord. Trends Pharm Sci 1996;17(12):457–62. 67. Maggi CA, Santicioli P, Giuliani S et al. The effects of baclofen on spinal and supraspinal micturition reflexes in rats. Naunyn Schmiedebergs Arch Pharmacol 1987;336(2):197–203. 68. Zhu Q-M, Hu D-Q, Tsung S et al. Differential effects of GABAA and GABAB receptor agonists on cystometry in conscious mice. J Urol 167;4(Suppl):39–40 [abstract 157]. 69. Taylor MC, Bates CP. A double-blind crossover trial of baclofen – a new treatment for the unstable bladder syndrome. Br J Urol 1979;51(6):504–5. 70. Rekling JC, Funk GD, Bayliss DA et al. Synaptic control of
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motorneuronal excitability. Physiol Rev 2000;80(2):767– 852. 71. Maneuf YP, Gonzalez MI, Sutton KS et al. Cellular and molecular action of the putative GABA-mimetic, gabapentin. Cell Mol Life Sci 2003;60(4):742–50. 72. Carbone A, Tubaro A, Morello P et al. The effect of gabapentin on neurogenic detrusor overactivity, a pilot study. Eur Urol 2003;141(Suppl 2):3 [abstract 555]. 73. Kim YT, Kwon DD, Kim J et al. Gabapentin for overactive bladder and nocturia after anticholinergic failure. Int Braz J Urol 2004;30(4):275–8. 74. Ishizuka O, Persson K, Mattiasson A et al. Micturition in conscious rats with and without bladder outlet obstruction – role of spinal α1-adrenoceptors. Br J Pharmacol 1996;117:962–6. 75. Persson K, Pandita RK, Spitsbergen JM et al. Spinal and peripheral mechanisms contributing to hyperactive voiding in spontaneously hypertensive rats. Am J Physiol 1998;275:R1366–73. 76. Berger Y, Blaivas JG, DeLaRocha ER et al. Urodynamic findings in Parkinson’s disease. J Urol 1987;138(4):836–8. 77. Yoshimura N, Mizuta E, Kuno S et al. The dopamine D1 receptor agonist SKF 38393 suppresses detrusor hyperreflexia in the monkey with parkinsonism induced by 1-methyl-4 phenyl-1,2,3,6-tetrahydropyridine (MPTP). Neuropharmacology 1993;32:315–21. 78. Sillén U, Rubenson A, Hjalmas K. On the localization and mediation of the centrally induced hyperactive urinary bladder response to l-dopa in the rat. Acta Physiol Scand 1981;112:137–40. 79. Kontani H, Inoue T, Sakai T. Dopamine receptor subtypes that induce hyperactive urinary bladder response in anesthetized rats. Jpn J Pharmacol 1990;54:482–6. 80. Kontani H, Inoue T, Sakai T. Effects of apomorphine on urinary bladder motility in anesthetized rats. Jpn J Pharmacol 1990;52:59–67. 81. Caulfield MP, Birdsall NJM. International Union of Pharmacology: XVII. Classification of muscarinic acetylcholine receptors. Pharmacol Rev 1998;50:279–90. 82. Sigala S, Mirabella G, Peroni A, Pezzotti G, Simeone C, Spano P, Cunico SC. Differential gene expression of cholinergic muscarinic receptor subtypes in male and female normal human urinary bladder. Urology 2002;60(4):719–25. 83. Yamaguchi O, Shishido K, Tamura K et al. Evaluation of mRNAs encoding muscarinic receptor subtypes in human detrusor muscle. J Urol 1996;156:1208–13.
86. Chess-Williams R. Muscarinic receptors of the urinary bladder: detrusor, urothelial and prejunctional. Auton Autacoid Pharmacol 2002;22(3):133–45. 87. Schneider T, Fetscher C, Krege S, Michel MC. Signal transduction underlying carbachol-induced contraction of human urinary bladder. J Pharmacol Exp Ther 2004;309(3):1148–53. 88. Jezior JR, Brady JD, Rosenstein DI, McCammon KA, Miner AS, Ratz PH. Dependency of detrusor contractions on calcium sensitization and calcium entry through LOE-908-sensitive channels. Br J Pharmacol 2001;134(1):78–87. 89. Wibberley A, Chen Z, Hu E, Hieble JP, Westfall TD. Expression and functional role of Rho-kinase in rat urinary bladder smooth muscle. Br J Pharmacol 2003;138(5):757–66. 90. Andersson K-E. Detrusor contraction – focus on muscarinic receptors. Scand J Urol Nephrol Suppl 2004;(215):54–7. 91. Hegde SS, Choppin A, Bonhaus D et al. Functional role of M-2 and M-3 muscarinic receptors in the urinary bladder of rats in vitro and in vivo. Br J Pharmacol 1997;120:1409–18. 92. Kotlikoff MI, Dhulipala P, Wang YX. M2 signaling in smooth muscle cells. Life Sci 1999;64(6–7):437–42. 93. Bonev AD, Nelson MT. Muscarinic inhibition of ATP-sensitive K+ channels by protein kinase C in urinary bladder smooth muscle. Am J Physiol 1993;265(6 Pt 1):C1723–8. 94. Nakamura T, Kimura J, Yamaguchi O. Muscarinic M2 receptors inhibit Ca2+-activated K+ channels in rat bladder smooth muscle. Int J Urol 2002;9(12):689–96. 95. Braverman AS, Luthin GR, Ruggieri MR. M2 muscarinic receptor contributes to contraction of the denervated rat urinary bladder. Am J Physiol 1998;275:R1654–60. 96. Braverman AS, Legos J, Young W, Luthin G, Ruggieri MR. M2 receptors in genito-urinary smooth muscle pathology. Life Sci 1999;64:429–36. 97. Braverman AS, Tallarida RJ, Ruggieri MR Sr. Interaction between muscarinic receptor subtype signal transduction pathways mediating bladder contraction. Am J Physiol Regul Integr Comp Physiol 2002;283(3):R663–8. 98. Braverman AS, Ruggieri MR Sr. Hypertrophy changes the muscarinic receptor subtype mediating bladder contraction from M3 toward M2. Am J Physiol Regul Integr Comp Physiol 2003;285(3):R701–8.
84. Eglen RM, Hegde SS, Watson N. Muscarinic receptor subtypes and smooth muscle function. Pharmacol Rev 1996;48:531–65.
99. Pontari MA, Braverman AS, Ruggieri MR Sr. The M2 muscarinic receptor mediates in vitro bladder contractions from patients with neurogenic bladder dysfunction. Am J Physiol Regul Integr Comp Physiol 2004;286(5): R874–80.
85. Hegde SS, Eglen RM. Muscarinic receptor subtypes modulating smooth muscle contractility in the urinary bladder. Life Sci 1999;64(6–7):419–28.
100. D’Agostino G, Bolognesi ML, Lucchelli A et al. Prejunctional muscarinic inhibitory control of acetylcholine release in the human isolated detrusor: involvement of the
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M4 receptor subtype. Br J Pharmacol 2000;129(3):493– 500. 101. Somogyi GT, de Groat WC. Function, signal transduction mechanisms and plasticity of presynaptic muscarinic receptors in the urinary bladder. Life Sci 1999;64(6– 7):411–8. 102. Somogyi GT, Zernova GV, Yoshiyama M, Rocha JN, Smith CP, de Groat WC. Change in muscarinic modulation of transmitter release in the rat urinary bladder after spinal cord injury. Neurochem Int 2003;43(1):73–7. 103. Goepel M, Wittmann A, Rubben H et al. Comparison of adrenoceptor subtype expression in porcine and human bladder and prostate. Urol Res 1997;25:199–206. 104. Malloy BJ, Price DT, Price RR et al. Alpha1-adrenergic receptor subtypes in human detrusor. J Urol 1998;160:937–43. 105. Hampel C, Dolber PC, Smith MP et al. Modulation of bladder alpha1-adrenergic receptor subtype expression by bladder outlet obstruction. J Urol 2002;167:1513–21. 106. Nomiya M, Shishido K, Uchida H et al. A quantitative analysis of mRNA expression of α1- and β-adrenoceptor subtypes and their functional roles in human normal and obstructed bladders. Neurourol Urodyn 2002;21:299– 300. 107. Bouchelouche K, Andersen L, Alvarez S et al. Increased contractile response to phenylephrine in detrusor of patients with bladder outlet obstruction: effect of the alpha1A and alpha1D-adrenergic receptor antagonist tamsulosin. J Urol 2005;173(2):657–61. 108. Das AK, Leggett RE, Whitbeck C et al. Effect of doxazosin on rat urinary bladder function after partial outlet obstruction. Neurourol Urodyn 2002;21:160–6. 109. Yamaguchi O. Beta3-adrenoceptors in human detrusor muscle. Urology 2002;59(Suppl 1):25–9. 110. Hudman D, Elliott RA, Norman RI. Inhibition of the contractile response of the rat detrusor muscle by the beta(2)-adrenoceptor agonist clenbuterol. Eur J Pharmacol 2000;392:79–85. 111. Grüneberger A. Treatment of motor urge incontinence with clenbuterol and flavoxate hydrochloride. Br J Obstet Gynaecol 1984;91:275–8. 112. Lindholm P, Lose G. Terbutaline (Bricanyl) in the treatment of female urge incontinence. Urol Int 1986;41:158– 60. 113. Woods M, Carson N, Norton NW et al. Efficacy of the beta3-adrenergic receptor agonist CL-316243 on experimental bladder hyperreflexia and detrusor instability in the rat. J Urol 2001;166:1142–7. 114. Kaidoh K, Igawa Y, Takeda H et al. Effects of selective beta2 and beta3-adrenoceptor agonists on detrusor hyperreflexia in conscious cerebral infarcted rats. J Urol 2002;168:1247–52.
115. Takeda H, Yamazaki Y, Igawa Y et al. Effects of beta(3)adrenoceptor stimulation on prostaglandin E(2)-induced bladder hyperactivity and on the cardiovascular system in conscious rats. Neurourol Urodyn 2002;21:558–65. 116. Andersson KE, Arner A. Urinary bladder contraction and relaxation: physiology and pathophysiology. Physiol Rev 2004;84(3):935–86. 117. Forman A, Andersson KE, Henriksson L et al. Effects of nifedipine on the smooth muscle of the human urinary tract in vitro and in vivo. Acta Pharmacol Toxicol 1978;43:111–18. (2+) 118. Ganitkevich VY, Isenberg G. Contribution of Ca 2+ 2+ induced Ca release to the [Ca ]i transients in myocytes from guinea-pig urinary bladder. J Physiol (Lond) 1992;458:119–37.
119. Isenberg G, Wendt-Gallitelli MF, Ganitkevich V. Contribution of Ca(2+)-induced Ca2+ release to depolarizationinduced Ca2+ transients of myocytes from guinea-pig urinary bladder myocytes. Jpn J Pharmacol 1992;58:81P– 86P 120. Hedlund H, Mattiasson A, Andersson K-E. Effects of pinacidil on detrusor instability in men with bladder outlet obstruction. J Urol 1991;146(5):1345–47. 121. Komersova K, Rogerson JW, Conway EL et al. The effect of levcromakalim (BRL 38227) on bladder function in patients with high spinal cord lesions. Br J Clin Pharmacol 1995;39(2):207–9. 122. Andersson K-E. Bladder activation: afferent mechanisms. Urology 2002;59(5 Suppl 1):43–50. 123. Birder LA, Kanai AJ, de Groat WC et al. Vanilloid receptor expression suggests a sensory role for urinary bladder epithelial cells. Proc Natl Acad Sci USA 2001;98(23):13396–401. 124. Birder LA, Nakamura Y, Kiss S et al. Altered urinary bladder function in mice lacking the vanilloid receptor TRPV1. Nat Neurosci 2002;5(9):856–60. 125. Sui GP, Rothery S, Dupont E et al. Gap junctions and connexin expression in human suburothelial interstitial cells. BJU Int 2002;90(1):118–29. 126. Sui GP, Wu C, Fry CH. Electrical characteristics of suburothelial cells isolated from the human bladder. J Urol 2004;171(2 Pt 1):938–43. 127. Pandita RK, Andersson K-E. Intravesical adenosine triphosphate stimulates the micturition reflex in awake, freely moving rats. J Urol 2002;168(3):1230–4. 128. Cockayne DA, Hamilton SG, Zhu QM et al. Urinary bladder hyporeflexia and reduced pain-related behaviour in P2X3-deficient mice. Nature 2000;407(6807):1011–15. 129. Vlaskovska M, Kasakov L, Rong W et al. P2X3 knock-out mice reveal a major sensory role for urothelially released ATP. J Neurosci 2001;21(15):5670–7. 130. Pinna C, Caratozzolo O, Puglisi L. A possible role for
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urinary bladder epithelium in bradykinin-induced contraction in diabetic rats. Eur J Pharmacol 1992;214(2– 3):143–8.
effects of intravesical resiniferatoxin and capsaicin in conscious rats with and without outflow obstruction. J Urol 1995;154:611–16.
131. Pinna C, Ventura S, Puglisi L et al. A pharmacological and histochemical study of hamster urethra and the role of urothelium. Br J Pharmacol 1996;119(4):655–62.
140. Szallazi A, Blumberg PM. Vanilloid receptors: new insights enhance potential as a therapeutic target. Pain 1996;68(2–3):195–208.
132. Hypolite JA, Longhurst PA, Gong C et al. Metabolic studies on rabbit bladder smooth muscle and mucosa. Mol Cell Biochem 1993;125(1):35–42.
141. Kuo H-C. Inhibitory effect of capsaicin on detrusor contractility: further study in the presence of ganglionic blocker and neurokinin receptor antagonist in the rat urinary bladder. Urol Int 1997;59:95–101.
133. Fovaeus M, Fujiwara M, Hogestatt ED et al. A nonnitrergic smooth muscle relaxant factor released from rat urinary bladder by muscarinic receptor stimulation. J Urol 1999;161(2):649–53. 134. Hawthorn MH, Chapple CR, Cock M et al. Urotheliumderived inhibitory factor(s) influences on detrusor muscle contractility in vitro. Br J Pharmacol 2000;129(3):416–9. 135. Templeman L, Chapple CR, Chess-Williams R. Urothelium derived inhibitory factor and cross-talk among receptors in the trigone of the bladder of the pig. J Urol 2002;167(2 Pt 1):742–5. 136. Warner FJ, Shang F, Millard RJ et al. Enhancement of neurokinin A-induced smooth muscle contraction in human urinary bladder by mucosal removal and phosphoramidon: relationship to peptidase inhibition. Eur J Pharmacol 2002;438(3):171–7.
142. Cruz F. Vanilloid receptor and detrusor instability. Urology 2002;59(Suppl 1):51–60. 143. Silva C, Ribeiro MJ, Cruz F. The effect of intravesical resiniferatoxin in patients with idiopathic detrusor instability suggests that involuntary detrusor contractions are triggered by C-fiber input. J Urol 2002;168:575–9. 144. Yokoyama T, Kumon H, Smith CP et al. Botulinum toxin treatment of urethral and bladder dysfunction. Acta Med Okayama 2002;56(6):271–77. 145. Smith CP, Franks ME, McNeil BK et al. Effect of botulinum toxin A on the autonomic nervous system of the rat lower urinary tract. J Urol 2003;169(5):1896–900. 146. Smith CP, Chancellor MB. Emerging role of botulinum toxin in the management of voiding dysfunction. J Urol 2004;171(6 Pt 1):2128–37.
137. Szallasi A. The vanilloid (capsaicin) receptor: receptor types and species differences. Gen Pharmacol 1994;25:223–43.
147. Leippold T, Reitz A, Schurch B. Botulinum toxin as a new therapy option for voiding disorders: current state of the art. Eur Urol 2003;44(2):165–74.
138. Maggi CA. The dual, sensory and efferent function of the capsaicin-sensitive primary sensory neurons in the urinary bladder and urethra. In: Maggi CA (ed) Nervous Control of the Urogenital System. London: Harwood, 1993; 383–422.
148. Rackley R, Abdelmalak J. Urologic applications of botulinum toxin therapy for voiding dysfunction. Curr Urol Rep 2004;5:381–88.
139. Ishizuka O, Mattiasson A, Andersson K-E. Urodynamic
149. Rapp D, Lucioni A, Katz EE et al. Use of botulinum-A toxin for the treatment of refractory overactive bladder symptoms: an initial experience. Urology 2004;63(6):1071–5.
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11 Classification of voiding dysfunction in the female patient David Staskin, Alan J Wein
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INTRODUCTION The purpose of a classification system is communication. The value of grouping and interrelating concepts and facts into an organizational structure can be measured by the ability of the final product to provide a logical framework for introducing new theories, scientific findings, and clinical observations into the existing knowledge. In addition, the system should act as a useful clinical tool for diagnosing and treating disease. A classification system that is proposed for general use should ideally incorporate ideas and resolve conflicts rather than create new areas of contention. The attempt to devise an all-inclusive system that completely describes lower urinary tract function and dysfunction, and the decision to adopt a single classification system would certainly be ideal, but is confounded by difficulties in agreeing upon the constructs and the standardization of terminology. Complex interrelationships create difficulty in maintaining the simplicity of the system. Voiding dysfunction may be classified by symptoms and signs (patient examination), and/or by objective findings (urodynamics), and/or by structure (anatomy), and/or by function (physiology), and/or by disease states (clinical diagnosis and the expected effect on lower urinary tract function), and/or by lower urinary tract behavior (lower urinary tract dysfunction associated with a specific lesion or disease). A classification system based on function/activity of the lower urinary tract will be proposed in this chapter. The reader is specifically referred to the chapters on the Clinical Physiology of Micturition (Chapter 19), Pharmacology of the Bladder (Chapter 10), and Neurologic Disorders (Chapter 36). This chapter will conform to the definitions established by the International Continence Society1–4 (Appendix) of this textbook, but with the recognition that the current terminology continues to evolve.5
CLASSIFICATION: COMBINING SYMPTOMS AND FUNCTION The classification of voiding dysfunction purely by symptoms is simple and descriptive, but has often been demonstrated to lack both sensitivity and specificity for diagnosing the pathophysiology and lower urinary tract behavior of the underlying condition.6,7 The classification of incontinence by: 1) symptoms; 2) the alteration in bladder or outlet ‘activity’; 3) the associated clinical condition; and 4) the most common instances of ‘clinical confusion’ is presented in Table 11.1. A classification system that is specifically focused on lower urinary tract function and activity and divides the
lower urinary tract into two anatomic areas – the ‘bladder’ and the ‘bladder outlet’ – during the physiologic functions of ‘storage’ and ‘emptying’ is presented in Table 11.2.8 The bladder or outlet activity is described as ‘overactive’, ‘normal’, or ‘underactive’: an overactive bladder represents an unwanted increase in detrusor activity/pressure during urinary storage (increased contractility or decreased compliance); an underactive bladder describes insufficient detrusor activity/pressure during bladder emptying (absent or poorly sustained contraction). On the other hand, an overactive outlet describes increased resistance/obstruction during emptying (blockage or dyssynergy), and an underactive outlet describes insufficient activity/resistance during storage (intrinsic function or altered anatomic relationships). The abnormalities in function/activity can occur alone or in combination. Of note, an overactive bladder, as described, should not be confused with ‘overactive bladder syndrome’ described elsewhere in this chapter. A bladder and outlet function/activity-based classification system may be objectively demonstrated and correlated with urodynamic findings. In addition, this function/activity-based methodology can be utilized alone or in combination with the ‘symptomatic’ classification (Table 11.2). This system can be presented graphically, based on the functional areas on the vertical axis and the functions of storage and emptying on the horizontal. This graphic representation can be utilized to correlate functional anatomy, lower urinary tract function, etiology, and therapy (not illustrated) (Fig. 11.1). The classification of neurogenic voiding dysfunction can also be adapted to a system based on the nature of the lesion and the expected behavior of detrusor and sphincter, and can be correlated with symptoms (Table 11.3).8–10 The neurologic terms of hyperreflexia, normoreflexia, and areflexia, and the outlet description as dyssernergic, normal, areflexic or denervated, are utilized and correlate with the type of function/activity. The interrelationship between the lower urinary tract, the neurologic system, and the pelvic floor requires a classification system that recognizes both the individual contributions and the combined effects of the efferent systems (anatomy and function/activity) and the afferent systems from the bladder musculature and mucosa, the bladder neck and urethral mechanisms, and the pelvic floor structures. An attempt to combine the effects of the bladder musculature and mucosa, the outlet sphincter, and the levator complex on bladder activity acknowledges the complex integration and interrelationship of these areas on lower urinary tract behavior. However, combining
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Table 11.1. Symptom – Activity – Condition Stress incontinence • Symptom – the involuntary loss of urine on effort or exertion (lift, strain, cough, sneeze). • Activity – underactive outlet. • Condition – urodynamic stress incontinence (USI) – the involuntary loss of urine resulting from an increase in intra-abdominal pressure which overcomes the resistance of the bladder outlet in the absence of a true bladder contraction. The decrease in bladder outlet or urethral resistance may result from poor anatomic support of the bladder neck (urethral hypermobility) or a loss of urethral function (intrinsic sphincter deficiency) or, more commonly, a mixture. • Clinical confusion – the patient describes the symptom of urine loss with activity but the etiology of leakage is actually an uninhibited bladder contraction – USI should have urinary loss synchronous with ‘effort’; similarly, many patients will describe USI as a sensation, which is confused with ‘urge’; finally, stress and urge incontinence may coexist. Urge incontinence • Symptom – the loss of urine with the feeling of urgency, voiding before the ability to toilet. • Activity – overactive bladder. • Condition – urinary urge incontinence (urodynamic) – the involuntary loss of urine resulting from an increase in bladder pressure secondary to a true bladder contraction. An involuntary contraction may be the result of a suprasacral (spinal or intracranial) neurologic lesion that results in uncontrolled reflex contractions (detrusor hyperreflexia [ICS = overactivity]) or may be idiopathic (detrusor instability [ICS = overactivity]). Patients may demonstrate other symptoms of ‘motor urgency’ (frequency, urgency, nocturia) without urinary loss. • Clinical confusion – the patient has decreased sensation, and loses urine from motor activity of the bladder without the feeling of ‘urgency’. Overactive bladder (OAB) is a syndrome consisting of the symptoms ‘urgency, with or without urge incontinence, usually with frequency and nocturia suggestive of urodynamic bladder overactivity but inclusive of urgency and frequency without incontinence’ OAB-dry (see below). Overflow incontinence • Symptom – the involuntary loss of urine resulting from urinary retention. The retention may result from inadequate bladder contractility or outlet obstruction. • Activity – underactive bladder (retention)/overactive outlet (obstruction). • Condition – urinary loss occurs when the bladder pressure overcomes the urethral resistance owing to bladder contractility, increases in intra-abdominal pressure or urethral relaxation. • Clinical confusion – the symptoms that are described may be a mixture of stress and urge complaints. Urgency and frequency without incontinence • Symptom – urgency and frequency without urinary loss. • Activity – no detrusor contraction. • Condition – urgency is the complaint of a sudden compelling desire to pass urine which is difficult to defer, and frequency is the complaint by the patient who considers that she voids too often by day or at night (going to bed and arising), whereas nocturia equals waking at night one or more times to void preceded by and followed by sleep). ‘Sensory urgency’ describes the sensation of urinary urgency without a true contraction. • Clinical confusion – the classification of a moderate or strong ‘desire to void’ without true ‘urgency’ is unresolved. ‘Sensory urge – desire to void’ is not in the current ICS lexicon. Altered bladder sensation and pain • Symptom – frequent voiding with or without pain – conversely, loss of sensation. • Activity – no detrusor contraction/alteration in afferent input. • Condition – bladder pain, discomfort and pressure can be characterized by type, frequency, duration, location, and precipitating and relieving factors. Bladder sensation can be described as increased, normal, reduced, absent, or non-specific (neurologic). Increased or decreased voiding may be correlated with the sensation. • Clinical confusion – urinary urgency and frequency without incontinence may be a product of abnormal sensation or bladder contractile activity. The source of pelvic pain may not be the lower urinary tract. Interstitial cystitis and chronic urethritis remain diagnoses of exclusion. Functional incontinence • Symptom – the involuntary loss of urine resulting from a deficiency in the ability to perform toileting functions secondary to physical or mental limitations. • Activity – abnormal lower urinary tract function usually coexists with functional issues. • Clinical confusion – the underlying pathophysiology of stress, urge or overflow incontinence may coexist, as well as difficulty in eliciting an accurate history.
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Table 11.2. Classification by activity* Bladder
Outlet
Overactive (urge)
Overactive (retention)
Normoactive
Normoactive
Underactive (retention)
Underactive (stress incontinence)
* Symptoms in parentheses.
them into one functional area limits investigation into their individual contributions. The complex interrelationship of the bladder outlet and pelvic floor structures with voiding behavior are apparent in several common clinical conditions. For example, in ‘urodynamic stress incontinence’ (USI), the ability to maintain anatomic support through basal tone and augmented urethral sphincter and levator contraction is critical to the understanding of continence. Conversely, the initiation
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of voiding requires pelvic floor and sphincteric relaxation.11,12 An understanding of urge incontinence and overactive bladder syndrome symptomatology requires an appreciation of the relationship between afferent input from the bladder afferents,13 the bladder neck, and the pelvic floor on the detrusor, although definitive reflex arcs in the human may not have yet been identified.14 Conversely, symptoms of decreased emptying or urinary retention may result from inhibition of detrusor contractility, secondary to increased pelvic floor or sphincter afferents, decreased afferent detrusor muscular or mucosal input, or by voluntary contraction of the sphincter (pseudo-dyssynergia) during voiding. A classification system that incorporates function/activity of the lower urinary tract and incorporates afferent activity from the pelvic floor is presented in Table 11.4. The expanded classification that is presented in this table is discussed below.
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Figure 11.1. Graphic representation of the functional anatomy (bladder and outlet) and lower urinary tract function (storage and emptying) with (a) activity, (b) symptoms, and (c) etiology.
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Classification of voiding dysfunction in the female patient
Table 11.3. Neurogenic voiding dysfunction (a) Neurogenic classification* Bladder/detrusor
Outlet/sphincter
Hyperreflexic (overactive – urge)
Uncoordinated (overactive – obstruction)
Normoreflexic
Coordinated
Areflexic (underactive – retention)
Denervated (underactive – stress incontinence)
(b) Expected behavior of the bladder, internal sphincter and external sphincter based on location of the lesion Bladder
Internal sphincter
External sphincter
Infrasacral
Areflexic, underactive
Innervated
Denervated, underactive
Spinal
Hyperreflexic, overactive
Uncoordinated if T6 or above
Dyssynergic, overactive
Suprapontine
Hyperreflexic
Coordinated
Coordinated
*Underlining denotes function; italic type denotes symptoms.
EXPANDED CLASSIFICATION OF VOIDING DYSFUNCTION INCLUDING PELVIC FLOOR ACTIVITY Outlet dysfunction: bladder outlet and pelvic floor The underactive outlet The bladder outlet (sphincteric mechanism) is responsible for ‘outlet resistance’ during urinary storage. The bladder outlet remains closed at rest. Resistance to leakage is provided by the intrinsic closure pressure along the length of the urethra. The urethra can be divided into two functional areas:
• the ‘proximal’ sphincteric mechanism – a product
•
of mucosa, submucosa, smooth muscle and nonstriated skeletal muscle incorporating the bladder neck and proximal urethra; the distal mechanism or ‘external’ sphincteric mechanism located in the middle of the ‘anatomic urethra’ and intimately related anatomically and physiologically to the levator ani complex.
Anatomic support facilitates transmission of intra-abdominal pressure to both areas and is provided by both the anterior vaginal wall and its attachments to the pelvis, and by the constant tone (slow-twitch fibers). Active contraction (fast-twitch fibers) of the levator complex can increase this support, but is usually seen only after pelvic muscle training and is not a ‘normal’ reflex.15,16 USI is the involuntary loss of urine per urethram – which occurs when intravesical pressure overcomes the urethral resistance owing to an increase in intraabdominal pressure in the absence of a true bladder contraction. Urethral closure pressure is maintained
by preserving or augmenting anatomic support and by increasing the intrinsic activity of the external sphincter complex. The preservation or enhancement of the anatomic backboard facilitates pressure transmission in the proximal and distal sphincteric mechanism, and preserves the anatomic relationships of the sphincteric components to maintain or increase closure pressure. Proper anatomic support provides an obvious mechanical advantage and, just as importantly, allows efficient action of the individual structures. Type I or type II USI is classified as ‘poor anatomic support’, associated with bladder neck and urethral motion. However, an understanding of the contribution of pelvic floor activity and dysfunction allows one to appreciate that the etiology of urinary leakage is probably multifactorial. Classically, an important event in maintaining continence is the preservation of intra-abdominal pressure transmission to the bladder neck and proximal urethra with respect to the bladder during stress maneuvers. In addition, inhibiting the rotational motion of the urethra prevents a relative differential in the movement of the posterior urethra with relation to the anterior urethra, and the development of a shearing force between the anterior and posterior urethral walls which decreases urethral coaptation and compression.16,17 The most fixed point, and the area of maximal pressure transmission during increases in intra-abdominal pressure, is the external sphincter–levator complex in the mid-anatomic urethra.17 Transmission forces as well as active sphincteric contraction provide urethral resistance during stress maneuvers. The combination of defects at many levels of the sphincteric mechanism may combine to decrease urethral resistance. Type III USI, intrinsic sphincter deficiency or low urethral closure pressure describe a deficiency in any of the intrinsic urethral functions detailed above, through atrophy, denervation, devas177
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Table 11.4. Expanded functional classification of voiding dysfunction including pelvic floor activity I. OUTLET DYSFUNCTION: BLADDER OUTLET AND PELVIC FLOOR A. UNDERACTIVE OUTLET (DECREASED URETHRAL RESISTANCE) Symptomatic: USI 1. Anatomic support defects (USI-A) (types I and II USI) Pathophysiology: anatomic motion creates inequities in transmission pressures to bladder and outlet, overcoming urethral resistance, and/or and shear forces create unequal motion of anterior and posterior urethra a. anatomic defects of fascia, muscles, ligaments, and bony pelvis b. functioning support: muscular contraction – denervation or loss of identification, strength or coordination of levator musculature 2. ISD (USI-ISD) (type III) (LUCP) Pathophysiology: deficiency of urethral closure mechanism secondary to decreased innervation, vascularization or trauma to mucosa, submucosa or smooth or skeletal musculature of urethra a. proximal urethral sphincter: bladder neck and proximal urethra (USI-ISD-p) b. external sphincter: denervation or loss of voluntary or reflex control (USI-ISD-d) c. combined total proximal and external sphincter deficiency (USI-ISD-t) 3. Combined USI (USI-A-ISD) Pathophysiology: a degree of both anatomic motion and sphincter dysfunction 4. Failure to inhibit the detrusor: decreased pelvic floor activity Pathophysiology: failure to contract pelvic floor releases detrusor reflex and decreases ability to inhibit active contraction a. neurological: (infrasacral) denervation (areflexia of pelvic floor) b. behavioral: failure to contract pelvic floor (lack of identification/strength/coordination) c. mechanical: damage to pelvic floor structures with intact innervation B. OVERACTIVE OUTLET (INCREASED URETHRAL RESISTANCE) Symptomatic: overflow incontinence/retention; frequency–urgency 1. Anatomic obstruction (physical blockage) Pathophysiology: increased outlet resistance secondary to compression or narrowing a. iatrogenic: surgical (e.g. for urinary incontinence) b. other: congenital, inflammatory, neoplasm, traumatic 2. Functional obstruction (failure of relaxation) Pathophysiology: increased outlet resistance – inappropriate contraction or failure of normal relaxation a. neurogenic: detrusor sphincter dyssynergia (smooth or skeletal musculature) b. behavioral: failure to relax pelvic floor musculature or external sphincter 3. Combined anatomic and functional obstruction 4. Inhibition of detrusor activity: increased pelvic floor activity Pathophysiology: failure to relax pelvic floor inhibits initiation of detrusor activity and inhibits ability to develop or continue a sustained detrusor contraction a. neurological: (suprasacral) overactivity/hyperreflexia (dyssynergic pelvic floor activity) b. behavioral: failure to relax pelvic floor (learned, acquired, maladaptive, psychogenic) c. situational: ‘voluntary’ inhibition secondary to environment or pain II. BLADDER DYSFUNCTION A. OVERACTIVE BLADDER (INCREASED INTRAVESICAL PRESSURE) Symptomatic: urge incontinence (with or without sensation) 1. Uninhibited detrusor contractions: motor urgency Pathophysiology: increased intravesical pressure overcomes urethral resistance or causes sensation of urinary urgency a. bladder instability: primary = idiopathic, subclinical neurologic, or symptomatic phasic detrusor activity; secondary = obstruction, reflex urethral relaxation, increased detrusor/mucosal afferent activity b. detrusor hyperreflexia: suprapontine (intracranial) neurologic lesion (with or without sphincter control); spinal (suprasacral) neurologic lesion (with or without sphincteric dyssynergia) 2. Decreased compliance Pathophysiology: increased intravesical pressure secondary to decreased accommodation a. fibrosis: radiation, inflammation, immune response b. neurologic: loss/reversal of accommodation reflex – conus medullaris or peripheral 3. Combined detrusor contractions and decreased compliance 4. Pelvic floor underactivity (see I.A.4 above) B. UNDERACTIVE BLADDER (DECREASED INTRAVESICAL PRESSURE) Symptomatic: overflow incontinence/retention
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Table 11.4. Expanded functional classification of voiding dysfunction including pelvic floor activity (cont.) 1. Peripheral denervation or neuropathy Pathophysiology: decreased contractility –neural efferent or myogenic/decreased afferent stimulation a. congenital, inflammatory, neoplastic or trauma lesion to peripheral nerves b. diabetes or other metabolic cause 2. Detrusor myopathy Pathophysiology: decreased contractility secondary to smooth muscle damage a. fibrosis/collagen deposition b. inflammation/obstruction/overdistension 3. Pharmacologic inhibition Pathophysiology: decreased contractility secondary to receptor blockade of neural efferents or afferents a. anticholinergics b. smooth muscle relaxants/spasmolytics/membrane stabilizers 4. Pelvic floor overactivity (see I.B.4 above) III. COMBINED OUTLET AND BLADDER DYSFUNCTION (I and II) IV. DISORDERS OF SENSATION A. DECREASED SENSATION 1. Decreased bladder sensation Pathophysiology: denervation, myopathy, behavioral, pharmacologic a. decreased sense of fullness and normal urge response b. loss of sense of fullness/urge warning only with active contraction c. loss of sense of fullness/urge incontinence without appreciation of ‘desire to void’ d. urinary retention without appreciation of distension 1. Decreased bladder outlet and pelvic floor sensation Pathophysiology: denervation, myopathy, behavioral, pharmacologic causing decreased ability to identify/contract/ coordinate a. bladder overactivity (I.A.4): failure to inhibit? b. bladder underactivity (myogenic or mucosal) (II.B.4): failure to initiate? c. contributory to decreased bladder sensation? (IV.A.1.a–d) d. sexual dysfunction – anorgasmia B. INCREASED SENSATION 1. Increased sensation of the bladder/bladder outlet Pathophysiology: neuropathic, inflammatory, mucosal permeability defect, psychogenic, afferent amplification a. frequency–urgency symptoms b. suprapubic and pelvic pain syndromes 2. Increased sensation of the pelvic floor/bladder outlet Pathophysiology: neuromuscular myalgia, neuropathic, inflammatory, psychogenic a. levator myalgia b. frequency–urgency and pelvic pain syndromes 3. Combined deficit ISD, intrinsic sphincter deficiency; LUCP, low urethra; USI, urodynamic stress incontinence. Italic type denotes pelvic floor activity.
cularization or scarring. The degree of pudendal nerve denervation during childbirth may contribute to deficiencies in anatomic support, both by affecting levator support and by decreasing intrinsic sphincter function. It is reasonable to assume that the complex etiology of USI is a mixture of anatomic support abnormalities and intrinsic sphincter abnormalities. The pathophysiology is related to the relative loss of mechanical (ligamentous) support of functioning (innervated) intrinsic (urethral) and extrinsic musculature (slow- and fast-twitch fibers of the levator complex). Therapy may be directed at correcting the defect, or compensating for the deficiency,
by increasing the function of another component that contributes to urethral resistance.
The overactive outlet Failure to empty the bladder may be due to elevated outlet resistance or to impaired contractility of the bladder. The most commonly observed clinical etiology of elevated outlet resistance is iatrogenic obstruction following incontinence surgery. Other forms of anatomic urethral obstruction are less common. Neurogenic outlet obstruction, commonly seen following injury to the suprasacral spinal cord, is due to a loss of coordination 179
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between the bladder and sphincter (detrusor sphincter dyssynergia). The paradoxical failure of the outlet to relax during voiding may result in anatomic obstruction to flow or to inhibition of the initiation or completion of the detrusor contraction. Contraction of the pelvic floor or sphincter is a normal response for bladder inhibition, but, when pathologic, may be classified as pseudodyssynergia (voluntary or behavioral) or dyssynergia (neurogenic). The relaxation of the urethral sphincter during voiding, and dyssynergic activity in spinal cord injury, have been documented. It is not known whether the specific anatomic areas of the urethra or pelvic floor (sphincter urethrae, compressor urethrae, urethrovaginal sphincter, bulbocavernosus, anal sphincter, levator complex) act in unison, individually, or at all in detrusor inhibition in normal subjects.18,19
The overactive bladder The symptoms of overactive bladder syndrome are urgency, with or without urge incontinence, usually with frequency and nocturia. Multiple etiologies have been proposed, including reduced suprapontine inhibition, damaged axonal paths in spinal cord, increased lower urinary tract (LUT) afferent input, loss of peripheral inhibition, and enhancement of excitatory neurotransmission in the micturition reflex pathway. Therefore, the central and peripheral nervous systems mediate bladder control through complex voluntary pathways and reflex arcs. Central efferent control of the bladder smooth musculature is mediated by afferent activity from the detrusor musculature and bladder mucosa (facilitatory) and the reflex and voluntary contractions of the pelvic floor and sphincter musculature (inhibitory).
The underactive bladder During the initial phase of bladder emptying, the pelvic floor and external sphincter relax in order to decrease urethral resistance and facilitate low pressure flow. In addition, this relaxation decreases the reflex inhibition of bladder contractility. Relaxation is followed by a detrusor contraction, which continues until voiding is completed. When emptying failure is secondary to bladder dysfunction, it may be a result of either detrusor smooth muscle pathology or insufficient neural stimulation of the detrusor. Insufficient neural stimulation may occur at the neuromuscular level (pharmacologic), with nerve impairment (neuropathy), or with alterations in central control of micturition (conus medullaris, spinal column or brain). The impairment of detrusor contractility by the absence of pelvic floor relaxation is evident in spinal cord disease (failure to empty following adequate sphincterotomy in the spinal
cord patient due to incomplete detrusor contractions) and parkinsonism (failure to empty secondary to pelvic floor bradykinesia).
Combined disorders Disorders of the bladder and outlet during storage and emptying may occur alone and in combination. The most common in the female patient is underactive outlet (USI) and overactive bladder.
Sensory disorders Afferent neurons from the bladder and urethra are of major importance during both the storage and emptying phases, both initiating the voiding reflex and sustaining the voiding drive during bladder emptying. Somatic activity may inhibit the emptying reflex by voluntary contraction of the external sphincter or pelvic floor – and although not established in humans, may provide inhibitory activity during bladder filling. Traditional classification systems have focused on motor rather than sensory activity. Disorders of bladder and bladder outlet sensation may result from central or peripheral denervation, from psychological causes, or from pharmacologic agents such as pain medications. The role of decreased sensation in the function of the pelvic floor and the interaction between the pelvic floor and bladder with relation to the sensory pathway on the micturition reflexes await further investigation. The pudendal nerve is responsible for the innervation of pelvic floor structures as well as of the genital skin, urethral mucosa and anal canal. Proprioceptive information of the periurethral musculature and sensory innervation of the levator ani muscles are also mediated by the pudendal branches. Increased sensation or pain attributed to the bladder is a major clinical challenge. The symptoms of urinary frequency, urgency and suprapubic pressure often result in diagnostic evaluations and therapy for bladder disorders, even in the absence of definitive findings of mucosal or smooth muscle abnormality. Pain that may originate from fascial, muscular or neurologic etiologies within the pelvic floor should be included in the differential diagnosis of the patient with urethral or bladder syndromes.
Conclusion The classification of voiding dysfunction has been presented, with the major constructs being the division of the lower urinary tract into the bladder and the bladder outlet, and the ‘activity’ during storage and emptying. In addition to the motor functions of the bladder and bladder outlet, the modulating effects of the afferents from
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the bladder musculature and mucosa and the pelvic floor–levator complex on normal and abnormal voiding behavior deserve increased attention.
9. Hald T, Bradley WE. The Urinary Bladder: Neurology and Dynamics. Baltimore: Williams and Wilkins, 1982.
REFERENCES 1. Abrams P (Chair), Blaivas JG, Stanton S, Andersen JT. ICS standardisation of terminology of lower urinary tract function 1988. Scand J Urol Nephrol Suppl 1988;114:5–19.
11. Bo K, Stein R. Pelvic floor muscle function and urethral closure mechanism in young nullipara subjects with and without stress incontinence symptoms. Neurourol Urodyn 1993;12(4):432.
2. Abrams P, Blaivas JG, Stanton SL, Andersen J (Chair). ICS 6th report on the standardisation of terminology of lower urinary tract function. Neurourol Urodyn 1992;11:593–603.
12. Deindl F, Vodusek DB, Hesse U, Schussler B. Activity patterns of pubococcygeal muscles in nulliparous continent women. A kinesiological EMG study. Br J Urol 1994;73:413–7.
3. Stohrer M, Goepel M, Kondo A et al. ICS report on the standardisation of terminology in neurogenic lower urinary tract dysfunction. Neurourol Urodyn 1999;18:139–58.
13. Andersson K-E. Antimuscarinics for treatment of overactive bladder. Lancet Neurol 2004;3:46–53.
4. Abrams P, Cardozo L, Fall M et al. Standardisation Subcommittee of the International Continence Society. The standardisation of terminology of lower urinary tract function: report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 2002;21(2):167–78.
15. Staskin DR, Zimmern PE, Hadley HR, Raz S. The pathophysiology of stress incontinence. Urol Clin North Am 1985;12(2):271–8.
5. Sand P, Dmochowski R. Analysis of the standardisation of terminology of lower urinary tract dysfunction: report from the Standardisation Sub-Committee of the International Continence Society. Neurourol Urodyn 2002;21:167–78.
17. Petros PE, Ulmsten UI. An integral theory and its method for the diagnosis and management of female urinary incontinence. Scand J Urol Nephrol Suppl 1993;153:1–93.
6. Bergman A, Bader K. Reliability of the patient’s history in the diagnosis of urinary incontinence. Int J Obstet Gynecol 1990;32:255.
18. Chai TC, Steers WD. Neurophysiology of micturition and continence in women. Int Urogynecol J Pelvic Floor Dysfunct 1997;8:85–97.
7. Versi E, Cardozo L, Anand D, Cooper D. Symptoms analysis for the diagnosis of genuine stress incontinence. Br J Obstet Gynaecol 1991;98(8):815–9.
19. DeGroat WC, Downie JW, Levin RM et al. Basic neurophysiology and neuropharmacology. In: Abrams P, Khoury S, Wein A (eds) Incontinence: First International Consultation on Incontinence, Plymouth, UK: Health Publication, 1998; 105–54.
8. Wein AJ. Classification of neurogenic voiding dysfunction. J Urol 1981;125:605–9.
10. Krane RJ, Siroky MB. Classification of neuro-urologic disorders. In: Krane RJ, Siroky MB (eds) Clinical Neurourology. Boston: Little Brown, 1979.
14. de Groat WC. A neurologic basis for the overactive bladder. Urology 1997;50(Suppl 6A):36–52.
16. Plzak L 3rd, Staskin D. Genuine stress incontinence theories of etiology and surgical correction. Urol Clin North Am 2002;29(3):527–35.
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Section 3 Diagnostic evaluation, incontinence anD prolapse Section Editor Sender Herschorn
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12 History and examination Vikram Khullar, Lesley K Carr
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IntroductIon Symptoms are subjective observations resulting from an interaction between the disease process, the environment and the ability to modify behavior. The environment and a woman’s ability to cope with her disease can profoundly alter her quality of life. A woman who is always close to a toilet may not notice her urinary frequency but the same woman with no access to a toilet will have urinary incontinence, wear protective pads, and be severely incapacitated. Can the severity of urinary symptoms be modified by behavior? A woman can alter the volume of urine produced by changing the amount of fluid drunk.1 A change in urine production can significantly alter symptoms. Women with severe detrusor overactivity may restrict their fluid intake to less than 200 ml per day. On direct questioning the urinary problem may not appear severe, with a normal diurnal urinary frequency, and it is only with a frequency volume chart that a complete picture of the severity of the detrusor overactivity can be determined. The volume of urine excreted relies not only on fluid intake but also on the secretion of antidiuretic hormone which is impaired in diabetes insipidus. The circadian secretion of this hormone is reversed in some women2 and children suffering nocturia and nocturnal enuresis.3 All terminology should follow the most recent ICS standardization report on lower urinary tract terminology.4
History History taking must take place using the patient’s own words. This is then clarified into an easily understandable list of graded symptoms using a standard questionnaire (Fig. 12.1). When comparing the symptoms and final urodynamic diagnosis, there is a marked overlap between diagnostic groups. The diagnosis based on history and examination is only correct in about 65% of women.5,6 Mixed incontinence is found in a large proportion of women of all diagnostic categories, i.e. 55% of women with urethral sphincter incompetence and 35% of women with detrusor overactivity.7,8 Symptom complexes have been used in an attempt to improve diagnostic accuracy. Wise et al.9 evaluated the diagnostic accuracy of visual analog scores and found that these did increase discrimination between women with urodynamic stress incontinence and detrusor overactivity, but the separation on the visual analog scores was not sufficient for diagnosis. If symptoms are not of diagnostic value, why record them? Symptoms are valuable as a guide in determining treatment. In addition, symptoms should be taken into consideration during the urodynamic test as the provocative maneuvers should mimic conditions encountered
URINARY SYMPTOMS – DIRECT QUESTIONING to be completed with the doctor Daytime frequency Night-time Volume range INCONTINENCE SYMPTOMS stress incontinence
urgency
urge incontinence
wet at rest
wet on standing
wet at night
unaware of wetness
pads/pants
VOIDING CHARACTERISTICS poor stream
unable to interrupt flow
postmicturition dribble
strain to void
incomplete emptying OTHER SYMPTOMS cough
constipation
leg weakness
rectal soiling
perineal discomfort
enuresis after school age
pain on micturition
pain on intercourse leakage on intercourse
0 = no problem, 1 = occasionally, 2 = frequently Pain on micturition 0 = nil, 1 = urethral, 2 = perineal, 3 = suprapubic, 4 = loin Pain on intercourse 0 = no pain, 1 = superficial, 2 = deep
Figure 12.1.
Standard questionnaire for urinary symptoms.
by the woman in her normal daily activities and lead to her urinary symptoms. A 90-year-old woman with urgency and no stress incontinence is an inappropriate candidate for performing ‘star jumps’ with a full bladder! When questioning women complaining of urinary symptoms, all symptoms complained of should be explained in a woman’s own words. Stress incontinence is the term used to describe urinary leakage which occurs with a cough or sneeze or follows it by a few seconds, even when considerable urgency is associated with the leakage. The severity of each symptom and its effect on the woman’s quality of life are noted, as cure can be achieved through directing treatment to relieve the troublesome symptoms. The length of time that the symptoms have been present discriminates between transient and estab-
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lished incontinence and whether this has changed over time. General enquiry should be made of all urinary symptoms as the woman may not be able to describe them or may be too embarrassed to mention them. For this reason a questionnaire is a useful guide as it ensures that all symptoms are enquired about. The questionnaire should be validated in the language in which it is to be used and often the symptom questionnaire will be attached to a quality of life questionnaire.10–12 The method used to obtain the symptoms will alter the answers. Questionnaires postally administered appear to produce higher severity responses from patients than the same questions used in an interview. This is particularly the case with questions of an embarrassing nature such as those relating to sexual incontinence or to leakage,13 and the postally obtained data correlate better with urodynamic findings.14 Symptoms can be grouped into storage problems, voiding disorders, and sensory problems (Table 12.1). This classification of symptoms does not help in diagnosis as overflow incontinence can produce symptoms similar to those of detrusor overactivity: urinary frequency in overflow incontinence is caused by incomplete bladder emptying resulting in a reduced bladder capacity; detrusor overactivity causes urinary frequency due to an over active detrusor – the same symptom is produced by the different mechanisms.
urInArY SYMPtoMS Frequency
sidered to be between four to seven voids per day; in a symptomatic population the range may be greater (Fig. 12.2). Frequency is not diagnostic for detrusor overactivity15 or for urodynamic stress incontinence,16 although women with detrusor overactivity do void more frequently. Clustering of voids during the day may suggest a cause such as diuretics prescribed for congestive cardiac failure, drinking large volumes of fluid or bad habit. Urinary frequency may occur for a number of reasons (Table 12.2). Women who void infrequently are at increased risk of developing voiding difficulties.17 The diurnal frequency does not increase with age in the symptomatic population seen in our urodynamic clinic between January 1993 and September 1994 (Table 12.3). The 95% upper limit of normal for urinary frequency in an asymptomatic population has recently been stated as being 13 voids per day and this suggests a wide variation in the normal population as the median and mean values in this test–retest study was eight and seven, respectively.18
nocturia Nocturia is the number of times a woman has to wake from sleep to pass urine. It is important to discriminate between this and a woman voiding because she is awake. The normal upper limit to the number of voids alters with age (Table 12.4). If a woman passes urine more than once a night up to the age of 70 years this is abnormal; voiding at night increases on average once every decade after the age of 70 in normal women. This change is probably due to changing sleep patterns in the elderly and to postural
Frequency is the number of times a woman voids during waking hours; normal diurnal frequency is con600
Classification of symptoms into groups
Abnormal storage • Incontinence: urge, stress • Frequency/nocturia • Nocturnal enuresis Abnormal voiding • Straining to void • Hesitancy • Incomplete emptying • Poor stream • Postmicturition dribble Abnormal sensation • Urgency • Dysuria • Absent sensation • Painful bladder
500 Number of women
table 12.1.
400 300 200 100 0
3
5
7 9 11 13 15 17 19 Daytime frequency of micturition
21
23
25
Figure 12.2. Daytime frequency of micturition in a symptomatic population. 187
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table 12.2.
Causes of abnormal urinary frequency
table 12.4.
Increased fluid intake and urine output; normal bladder capacity • Osmotic diuresis (e.g. diabetes mellitus) • Abnormal antidiuretic hormone production (e.g. diabetes insipidus) • Polydipsia; often the woman enjoys drinking a favorite beverage and only rarely is the behavior psychotic
Age (years)
reduced functional bladder capacity • Inflamed bladder, increasing bladder sensation (e.g. acute bacterial cystitis, interstitial cystitis) • Detrusor overactivity • Habit or fear of urinary incontinence • Urinary residual secondary to detrusor hypotonia or outlet obstruction (rare) • Increased bladder sensation, normal bladder (e.g. anxiety) reduced structural bladder capacity • Fibrosis after infection (e.g. tuberculosis) • Non-infective cystitis (e.g. interstitial cystitis, carcinoma) • Irradiation fibrosis (e.g. for bladder or cervical carcinoma) • Postsurgery (e.g. partial cystectomy) • Detrusor hypertrophy decreased urinary frequency • Detrusor hypotonia • Impaired bladder sensation (e.g. diabetic neuropathy) • Reduced fluid intake
table 12.3. Age (years)
Diurnal frequency in a symptomatic population* Mean frequency
n
5–14
6.00
5
15–24
4.48
41
25–34
5.47
176
35–44
6.31
364
45–54
6.05
513
55–64
5.87
361
65–74
5.63
263
75–84
5.04
137
85–94
5.93
33 Total 1893
* Patients seen in the Urodynamic Clinic, King’s College Hospital, London, between January 1993 and September 1994.
effects due to daytime pooling of extracellular fluid in the lower limbs returning to the vascular compartment at night, as a result of subclinical heart failure.2 It is important to discriminate between the woman who is awake and therefore voids and the woman
Nocturnal voids and nocturia with age* Mean voids per night
% Nocturia
n
5–14
0.8
0
5
15–24
1.24
17
41
25–34
1.79
27
176
35–44
1.83
38
364
45–54
1.53
30
513
55–64
1.94
31
361
65–74
2.20
47
263
75–84
2.55
46
137
85–94
2.69
58
33
* Patients seen in the Urodynamic Clinic, King’s College Hospital, London, between January 1993 and September 1994.
who is woken by the desire to void; the first group of women often have no increase in their diurnal urinary frequency. Reduction of fluid intake in the evening does not appear to reduce nocturia even if started at 6 pm.19
urInArY IncontInence Urinary incontinence requires careful evaluation. This is involuntary urine loss, which is a social or hygienic problem and is objectively demonstrable. Loss of urine through channels other than the urethra is extraurethral incontinence.4 It is important that incontinence is regarded as a symptom or a sign and not a diagnosis. Severe urinary incontinence of any origin has overlapping symptoms associated with urethral sphincter incompetence and detrusor overactivity. The causes of urinary incontinence are many (Table 12.5). It is important to determine whether the urine loss is continuous or intermittent. Continuous urine loss is rare. It is usually seen when there is an ectopic ureter or fistula, and the woman will often complain of nocturnal incontinence as opposed to nocturnal enuresis. This occurs most often following pelvic surgery or as a result of malignancy, following surgery or radiotherapy. Obstetric fistulae are more commonly seen in developing countries. Some women complain that they are ‘never dry’, and suffer from severe intermittent urinary incontinence, rather than a continuous loss of urine. This occurs in women who have had multiple previous operations and have a fixed and fibrosed ‘drainpipe’ (type 3) urethra.20 Otherwise women who complain of urinary loss ‘all the time’ have severe detrusor overactivity.
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table 12.5.
Causes of urinary incontinence
1. Urethral sphincter incompetence • Sphincter dysfunction • Abnormal bladder neck support 2. Detrusor overactivity • Idiopathic detrusor overactivity • Neurogenic detrusor overactivity (e.g. multiple sclerosis, spinal trauma) 3. Mixed incontinence 4. Urethral diverticulae 5. Congenital abnormalities (e.g. epispadias, ectopic ureter, bladder exstrophy, spina bifida occulta) 6. Transient incontinence • Urinary tract infection • Restricted mobility • Constipation • Excessive urine production a. diuretic therapy b. diabetes mellitus c. diabetes insipidus d. cardiac failure e. hypercalcemia • Confusion (e.g. dementia, acute illness) • Atrophic urethritis and vaginitis 7. Pharmacologic causes (e.g. diuretics, tranquilizers, cholinergic agents, prazosin) 8. Fistulae (e.g. urethral, vesical, ureteral) 9. Overflow incontinence • Hypotonic detrusor • Rarely urethral obstruction 10. Urethral instability 11. Functional
The pattern of intermittent urinary incontinence should be linked with associated activity, such as physical exercise, laughing, putting the key in the front door, sexual intercourse or orgasm. The severity of the incontinence can be quantified not only by volume but also by the type and number of pads or changes of underwear required in 24 hours and the magnitude of the provoking stimulus. There is often little relationship between the findings of urodynamic tests and the symptoms described by the woman in her daily life, and this may reflect modifications in behavior and lifestyle that she has made to ameliorate the effect of lower urinary tract dysfunction. It does not, however, reduce the importance of the urinary symptoms as they may still be impairing her quality of life. Often women will not admit to urinary incontinence but state that they leak when a history is taken.
Stress urinary incontinence Stress urinary incontinence is the involuntary loss of urine with an increase in intra-abdominal pressure
such as when coughing, sneezing, running, and lifting. There is no associated urgency. The urine is lost in small discrete amounts.21,22 This must be differentiated from urge urinary incontinence. The accuracy of diagnosing urodynamic stress incontinence based on the pure symptom of stress urinary incontinence (even with a normal frequency volume chart) is poor, with 9% of incontinence in this group being due to detrusor overactivity.23
urge urinary incontinence Urge urinary incontinence occurs in association with the symptom of urgency (a strong sudden desire to void). Often women will describe getting the sensation of the desire to void and not getting to the toilet in time. The quantity of urine lost can be anything from a few drops on lowering the undergarments prior to voiding or to quite a large volume, and it is not uncommon for the patient to describe at least one occasion where the urine has poured down both legs uncontrollably. Urge urinary incontinence may be triggered by changes in temperature, opening the front door, hearing running water, and occasionally during sexual intercourse at orgasm. As the main coping strategy for this symptom is increasing voiding frequency, pad usage or incontinent episodes are not useful in assessing the severity of the condition. The symptom of urge urinary incontinence has a limited sensitivity of 78%, and a specificity of 39% in the diagnosis of detrusor overactivity.24 This contrasts with the findings of Farrar et al.25 where women with urge urinary incontinence were found to have detrusor overactivity in 80% of cases.
Mixed incontinence In the very common condition of mixed urinary incontinence, where the patient has symptoms of both stress and urge urinary incontinence, it is important to determine the balance between the two symptoms – which one troubles her more and which one has been present for longer – as this determines the outcome for surgical continence procedures.26
coital incontinence Urinary incontinence can occur during sexual intercourse, either on penetration or during orgasm. Urinary leakage on penetration is more likely to occur in women with urethral sphincter incompetence and with a cystocele.27 This type of urinary incontinence 189
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is not associated with urgency. Urinary incontinence can also occur with orgasm. The leakage is associated with urgency and is thought to be related to detrusor overactivity.28,29
Giggle incontinence This form of incontinence is found in young women. It has a clear history and is difficult to reproduce while under investigation. The problem usually resolves as the woman grows up.
nocturnal enuresis
urgency This is the complaint of a sudden compelling desire to pass urine which is difficult to defer. If this symptom is not relieved, it can result in urge urinary incontinence. If this symptom is recorded more often than once a week it may be considered abnormal.
VoIdInG dIFFIcuLtIeS Voiding difficulties may present with a variety of symptoms.
Hesitancy
Nocturnal enuresis is the complaint of loss of urine occurring during sleep. It is important to differentiate between this complaint and waking with urgency and then leaking before arriving at the toilet, which is urge urinary incontinence. Nocturnal enuresis can be primary or secondary. Primary nocturnal enuresis starts in childhood and can persist into adulthood, the woman never having consistently been dry at night.30 Secondary nocturnal enuresis is when the incontinence restarts in adulthood following a period of night-time continence, even if it resolved as a child. The causes of nocturnal enuresis can be abnormal circadian secretion of antidiuretic hormone, detrusor overactivity or abnormal control of the micturition reflex, or abnormal sleep pattern. A family history should be sought and the presence of diurnal symptoms noted.
Hesitancy is not common in women. It is the term used when an individual describes difficulty in initiating micturition resulting in a delay in the onset of voiding after the individual is ready to pass urine. The volume voided on these occasions should be noted, as small volumes (less than 100 ml) are difficult to void in normal women. However, hesitancy when voiding a full bladder may be an indication that: 1) the urethral sphincter is not relaxing when the detrusor contracts (voiding dysfunction or detrusor sphincter dyssnergia); 2) the detrusor muscle is not contracting effectively during voiding; or 3) psychological inhibition of bladder contraction, which occurs in women who can only void when alone. This symptom does not discriminate between these problems. Women with detrusor overactivity may complain of hesitancy and poor stream but this probably relates to the small volumes of urine passed by them in response to urgency.
Nocturnal urine volume
Straining to void
This is defined as the total volume of urine passed between the time the individual goes to bed with the intention of sleeping and the time of waking with the intention of rising. Therefore, it excludes the last void before going to bed but includes the first void after rising in the morning.
Nocturnal polyuria Nocturnal polyuria is present when an increased proportion of the 24-hour output occurs at night (normally during the 8 hours while the patient is in bed). The night-time urine output excludes the last void before sleep but includes the first void of the morning. The normal range of nocturnal urine production differs with age and normal ranges remain to be defined. Generally, nocturnal polyuria is present when more than 20% (young adults) to 33% (greater than 65 years) is produced at night.
Straining to void describes the muscular effort used to initiate, maintain or improve the urinary stream. The intra-abdominal pressure is increased during a Valsalva maneuver, which increases the intravesical pressure and this can improve bladder emptying. The urinary stream is impaired and may be intermittent, each transient increase in flow associated with an increase in intraabdominal pressure. In the longer term, this method of voiding can lead to the development of uterovaginal prolapse.
Incomplete emptying Feeling of incomplete emptying is a self-explanatory term for a feeling experienced by the individual after passing urine. The sensation can be due to fluid remaining in the bladder, can be secondary to an abnormality
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of sensation or due to after-contractions in women with detrusor overactivity. These women rarely have increased postmicturition urinary residual volumes. Women with prolapse can develop a functional obstruction of the urethra due to external compression and may have urinary residuals. A cystocele can act as a sump and a rectocele can press anteriorly on the urethra in women who void by straining, preventing complete emptying.
ing on passing urine’ and can be aggravated by sexual intercourse. As an isolated symptom it is associated with urinary tract infections or urethritis.
Bladder pain
Postmicturition dribble is the term used when an individual describes the involuntary loss of urine immediately after they have finished passing urine, usually after leaving the toilet in men, or after rising from the toilet in women. This symptom may be related to a urethral diverticulum, a cystourethrocele or detrusor overactivity. Where detrusor contractions occur after the completion of voiding, urgency will often accompany the urinary leakage. Postmicturition dribble should be distinguished from terminal dribble which is continuous after the main flow of urine.
Bladder pain is felt suprapubically or retropubically, and usually increases with bladder filling; it may also persist after voiding. Bladder pain is associated with inflammation of the bladder, bladder stones or tumor. The pain more commonly occurs after micturition as the bladder mucosa closes down. Some women complain of pain after voiding and have detrusor overactivity. The pain has been found to coincide with contractions. The presence of bladder pain is an indication for cystoscopy and occasionally bladder biopsy. Suprapubic pain may also be associated with pathology outside the bladder but within the pelvis and thus would be called pelvic pain. Endometriosis on the bladder may cause urethral pain which is present at certain times in the menstrual cycle. Pelvic inflammatory disease may cause urethral pain; however, the woman will have symptoms of vaginal discharge and pyrexia.
Slow stream
Loin pain
Postmicturition dribble
Slow stream is reported by the individual as a perception of reduced urine flow, usually compared to previous performance or in comparison to others. Decreased urinary stream is often described as ‘decreased force’. Urine flow rate is dependent on the volume of urine passed; if it is less than 150 ml this should be assessed with reference to a frequency/volume chart. A reduced urine flow can be due to reduced voided volumes, bladder outflow obstruction (rare in women) or decreased bladder contractility. This can be neuropathic (lower motor neuron lesion) or myopathic.
Bladder/urethral pain Pain, discomfort, and pressure are part of a spectrum of abnormal sensations felt by the individual. Pain produces the greatest impact on the patient and may be related to bladder filling or voiding, may be felt after micturition, or be continuous. Pain should also be characterized by type, frequency, duration, precipitating and relieving factors, and by location such as bladder, urethral, vulval, vaginal, and perineal pain. Dysuria, strangury, and bladder spasm are not recommended terms as these symptoms are difficult to define.
Urethral pain This is felt in the urethra and the individual indicates the urethra as the site. It is often described as ‘burn-
This pain originates in the flank and radiates to the groin of the ipsilateral side. The pain is referred from the sensory nerves innervating the kidney and ureter, for which there are many causes (Table 12.6). Acute or chronic obstruction of the urinary tract can cause pain. This becomes more acute as the pressure generated within the urinary tract is higher. Women with detrusor overactivity may complain of loin pain associated with urgency; this may indicate vesicoureteric reflux.
table 12.6.
Causes of loin pain
1. Vesicoureteric reflux 2. Renal trauma 3. Acute ureteric obstruction • Stone • Blood clot • Papillary necrosis 4. Chronic ureteric obstruction • Tumor (e.g. transitional cell carcinoma, renal cell carcinoma, Wilms' tumor) • Ureteric stricture • Retroperitoneal fibrosis • Stone • Congenital anomaly 5. Renal inflammation • Pyelonephritis • Perinephric abscess 6. Renal infarction
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Hematuria Blood in the urine should always be investigated and never be ignored.
neuroLoGIc HIStorY Women should be questioned about any alteration in sensation and motor power in the legs or perineum. The latter may be described as altered sensation during sexual intercourse or an inability to feel their urinary stream during micturition. Fecal incontinence is described as diarrhea which causes staining of underwear or urgency to defecate. Worsening symptoms of back pain with urinary and neurologic symptoms must be treated rapidly and seriously as these may indicate a worsening central intervertebral disk prolapse. Neurologic symptoms can also be a result of peripheral neuropathy associated with diabetes mellitus, cerebrovascular accidents, Parkinson’s disease or multiple sclerosis.
GYnecoLoGIc SYMPtoMS The lower urinary tract has receptors to estrogen.31 Thus it is important to enquire about changes in urinary symptoms during the menstrual cycle and note the woman’s menopausal state. The majority of women complaining of urologic symptoms have coexisting gynecologic pathology.32 As vaginal prolapse alters the range of treatments for urinary incontinence, enquiries about symptoms of vaginal prolapse and prolapse affecting micturition and defecation should be made. The feeling of a lump at or beyond the vaginal introitus, low back ache, heaviness, dragging sensation, or the need to digitally replace or support the prolapse in order to defecate or micturate, are among the symptoms that may be described. Over 40% of women with urethral sphincter incompetence will also have significant cystoceles,33 making this is an important symptom affecting management of a woman’s urinary incontinence. As vaginal prolapse can mask urethral sphincter incompetence,34 it is important to identify the prolapse before a urodynamic test, so that a vaginal ring can be inserted during the provocative phase of urodynamics to expose any underlying incompetence. Previous continence operations have an important influence on the future success of continence surgery, as the urethral sphincter may be altered by scarring and damage to sphincter innervation by previous vaginal surgery, as well as distortion and narrowing of the bladder neck. Operations on the uterus may interfere with the innervation of the bladder, particularly after radical hysterectomy for carcinoma.
PASt MedIcAL HIStorY It is important to record all past major abdominal and pelvic surgery, and urinary complications as a result of the surgery should be noted. The postoperative course can often be revealing, particularly when women have been unable to void spontaneously and required catheterization. This could indicate prolonged overdistension which can lead to voiding difficulties due to detrusor hypotonia.35 Surgery to the spine and neurologic impairment after this must be recorded, particularly in relation to any possible nerve damage. Operations on the large bowel, especially those involving dissection at the side wall of the pelvis, may result in denervation, such as abdominoperineal resection of the rectum. Conditions increasing abdominal pressure, such as chronic cough or constipation, can produce the symptom of stress incontinence and make a minor problem more severe; they are also implicated in the development of vaginal prolapse.36 Cardiac and renal failure can produce frequency and nocturia through polyuria. Endocrine disorders such as diabetes mellitus or diabetes insipidus may lead to polyuria and polydipsia. Chronic diabetes mellitus can produce frequency as a result of overflow incontinence secondary to a hypotonic detrusor and impaired bladder sensation. There does appear to be an association between schizophrenia and detrusor overactivity.37 Additionally, women suffering from dementia may not empty their bladders frequently and may not be aware of the need to void. The number of proven urinary tract infections during the past 2 years should be recorded. Childhood enuresis is particularly important as often these patients have detrusor overactivity. The obstetric history should include parity, length of labor, mode of delivery, and weight of the largest infant; however, such information has not been shown to be very useful as the details of labor are not recalled accurately. Cesarean section or epidural block during labor and the retention of urine post partum are possible progenitors of voiding difficulties.38,39
druG HIStorY Many drugs affect the lower urinary tract. Diuretics can produce urgency, frequency, and urge urinary incontinence.40 Benzodiazepines sedate and may cause confusion and secondary incontinence, particularly in elderly patients. Alcohol impairs mobility, produces a diuresis, and can impair the woman’s perception of bladder filling. Anticholinergic drugs impair detrusor contractility and may cause urinary retention with secondary overflow incontinence. These include antipsychotic drugs,
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antidepressants, opiates, antispasmodics, and antiparkinsonian drugs. Drugs that improve bladder storage are shown in Table 12.7. Sympathomimetic drugs, often found in cold remedies, can increase the urethral sphincter resistance and produce voiding difficulty. Prazosin, a postsynaptic αadrenergic blocker used to treat hypertension, has been found to cause urethral relaxation and urinary incontinence.41 Drugs that improve bladder emptying are shown in Table 12.8.
eXAMInAtIon Before examining the woman it is important to reassure her about the possibility of urinary leakage and explain table 12.7.
Drugs that improve urine storage
1. Anticholinergic drugs • Propantheline bromide • Emepronium bromide/carrageenate • Tolterodine • Darafenacin • Solifenacin 2. Musculotrophic drugs • Oxybutynin chloride • Dicycloverine chloride • Flavoxate hydrochloride 3. Calcium antagonists • Nifedipine • Flunarizine 4. Tricyclic antidepressants • Imipramine • Doxepin 5. β-Adrenoceptor agonists • Terbutaline • Salbutamol • Isoprenaline 6. α-Adrenoceptor antagonists • Phenoxybenzamine • Prazosin 7. Prostaglandin synthetase inhibitors • Flurbiprofen • Indometacin 8. Neurotoxins • Capsaicin • Resiniferatoxin 9. Drugs reducing urine production • Desmopressin 10. Drugs increasing outlet resistance • α-Adrenergic agonists a. Phenylpropanolamine hydrochloride b. Midodrine • Serotonin noradrenaline reuptake inhibitors a. Duloxetine • β-Adrenergic antagonist a. Propranolol 11. Estrogens
that she should not be embarrassed as a result of this. The woman’s mobility and mental state play a role in her ability to react to her incontinence problem and may influence management. A mini-mental state examination can be performed, as well an assessment of the woman’s motivation and manual dexterity, as these may influence her compliance with possible treatments and follow-up. It is important to perform a screening neurologic examination testing the tone, strength, and movement of the lower limbs. It is particularly useful to test the abduction and spreading of toes as the innervation for the lateral abductors comes from S3. The anal tone should be assessed and gentle tapping of the clitoris will produce a reflex contraction of the anal sphincter (bulbocavernosus reflex). Additionally, a voluntary cough should cause a reflex contraction of the anal sphincter. An intact sacral reflex can be tested by stroking the skin lateral to the anus, which should elicit a contraction of the external anal sphincter.
GYnecoLoGIc eXAMInAtIon The condition of the vulval skin is important as there may be signs of excoriation, edema or erythema due to exposure of the skin to urine on the vulva for prolonged periods of time and concomitant candidiasis. Vaginal atrophy, particularly in women more than 10 years after the menopause, may be seen. Any cystocele, rectocele, uterine or vault descent should be assessed as this can alter the patient’s urinary symptoms to a considerable extent.32 Genital prolapse table 12.8.
Drugs that improve bladder emptying
Increased detrusor contractility 1. Cholinergic agents • Carbachol • Bethanecol 2. Anticholinesterase • Distigmine 3. Prostaglandins • E2α • F2α decreased outlet resistance 1. α-Sympathetic blocking agents • Phenoxybenzamine • Phentolamine • Prazosin 2. Striated muscle relaxants • Baclofen • Dantrolene • Lisidonal • Diazepam
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can be best assessed in the Sims’ (left lateral) position on coughing and straining using a Sims’ speculum. Alternatively, examination may also be made in lithotomy using the lower blade of a Graves’ speculum to assist in assessing the opposite vaginal wall.42 Genital prolapse can now be quantified using the methods produced by the International Continence Society committee on the standardization of terminology.43 This method of quantifying prolapse has good inter- and intraobserver reliability.44,45 To demonstrate stress incontinence the woman should have a full bladder.46 Often women will empty their bladder prior to gynecologic examination, rendering the demonstration of stress incontinence impossible. Bonney described a test of bladder neck elevation47 which he claimed indicated the likelihood of curing stress incontinence with a vaginal repair. The procedure is as follows: The patient, whose bladder should not recently have been emptied, is told to cough violently and the escape of urine is noted. The index and middle finger of the examiner’s hand should be inserted into the vagina and the anterior vaginal wall pressed against the sub-pubic angle but without pressing on the urethra. The patient is now told to cough again. If the pressure of the fingers prevents the leak, the operation of anterior colporrhaphy, if properly carried out, will cure her.
The Bonney test produces occlusion of the urethra which is not reproduced surgically. Thus Bonney’s test is positive irrespective of the urodynamic diagnosis and the cause of the urinary leakage, and is of no practical use.48,49 If the woman is likely to need incontinence surgery, vaginal mobility and scarring should be assessed. The urethra should be examined for any discharge, inflammation or fixation. If a woman is complaining of a discharge, or has had a recent onset of symptoms of urgency and frequency, it may be useful to obtain swabs to culture for Chlamydia and gonococcus. The anterior vaginal wall should be examined for masses which may include a urethral diverticulum or a urethral or vaginal cyst, and a bimanual examination should be performed to exclude abnormal pelvic organs, masses or uterine impaction, and can exclude a large postmicturition urinary residual.50 Pelvic masses such as ovarian cysts and uterine enlargement greater than 12 weeks’ size can cause pressure symptoms resulting in frequency; often the symptoms resolve once the mass has been removed. Finally, rectal examination is particularly important in the elderly to exclude fecal impaction, which can aggravate urinary incontinence.
Q-tip test The mobility of the urethra and bladder neck can be evaluated by inserting a sterile, lubricated, Q-tip cotton bud into the urethra to the level of the bladder neck. The patient is then asked to strain. The rotational movement of the bladder neck around the symphysis pubis causes the Q-tip to move in a cranial direction. The angle of the Q-tip is measured relative to the horizontal using a orthopedic goniometer. The resting and straining angles are measured and the difference between the two angles is calculated. A change of greater than 30 degrees is thought to represent a hypermobile urethra. This test does not establish the diagnosis of stress incontinence51 and does not add any extra information to the history and examination.52–54 However, it is thought by some clinicians to indicate the most appropriate continence procedure when urodynamic stress incontinence has been diagnosed and may predict failure after incontinence surgery.55
concLuSIon History and examination alone cannot diagnose female urinary disorders but can guide future investigation and management. In some cases a very obvious cause can be found and dealt with, thus avoiding the need for further investigations which may be embarrassing, expensive, and invasive.
reFerenceS 1. Griffiths DJ, McCracken PN, Harrison GM, Gormley EA. Relationship of fluid intake to voluntary micturition and urinary incontinence in geriatric patients. Neurourol Urodyn 1993;12:1–7. 2. Carter PG, McConnell AA, Abrams P. The significance of atrial natriureteric peptide in nocturnal urinary symptoms in the elderly. Neurourol Urodyn 1992;11:420–1. 3. Norgaard JP. Pathophysiology of nocturnal enuresis. Scand J Urol Nephrol 1991;140(Suppl):7–31. 4. Abrams P, Cardozo L, Fall M et al. The standardisation of terminology of lower urinary tract function: report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 2002;21(2):167–78. 5. Sand PK, Ostergard DR. Incontinence history as a predictor of detrusor stability. Obstet Gynecol 1988;71:257–9. 6. Cardozo LD, Stanton SL. Genuine stress incontinence and detrusor instability – a review of 200 patients. Br J Obstet Gynaecol 1980;87:184–8. 7. Brocklehurst JC. Urinary incontinence in the community – analysis of a MORI poll. Br Med J 1993;306:832–4.
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8. Khullar V, Damiano R, Toozs-Hobson P, Cardozo LD. Prevalence of faecal incontinence among women with urinary incontinence. Br J Obstet Gynaecol 1998;105:1211–13.
24. Abrams P. The clinical contribution of urodynamics. In: Abrams P, Feneley R, Torrens M (eds) Urodynamics. Berlin: Springer-Verlag, 1983; 118–74.
9. Wise BG, Cutner A, Cardozo LD et al. Do detailed symptom questionnaires negate the need for urodynamic investigation? Neurourol Urodyn 1992;11:353–5.
25. Farrar DJ, Whiteside CG, Osborne JL, Turner-Warwick RT. A urodynamic analysis of micturition symptoms in the female. Surg Gynecol Obstet 1975;141:875–81.
10. Reese PR, Pleil AM, Okano GJ, Kelleher CJ. Multinational study of reliability and validity of the King’s Health Questionnaire in patients with overactive bladder. Qual Life Res 2003;12(4):427–42.
26. Scotti RJ, Angell G, Flora R, Greston WM. Antecedent history as a predictor of surgical cure of urgency symptoms in mixed incontinence. Obstet Gynecol 1998;91:51–4.
11. Jackson S, Donovan J, Brookes S, Eckford S, Swithinbank L, Abrams P. The Bristol Female Lower Urinary Tract Symptoms questionnaire: development and psychometric testing. Br J Urol 1996;77(6):805–12. 12. Avery K, Donovan J, Peters TJ, Shaw C, Gotoh M, Abrams P. ICIQ: a brief and robust measure for evaluating the symptoms and impact of urinary incontinence. Neurourol Urodyn 2004;23(4):322–30. 13. Khan MS, Chaliha C, Leskova L, Khullar V. A randomized crossover trial to examine administration techniques related to the Bristol female lower urinary tract symptom (BFLUTS) questionnaire. Neurourol Urodyn 2005;24(3):211–14. 14. Khan MS, Chaliha C, Leskova L, Khullar V. The relationship between urinary symptom questionnaires and urodynamic diagnoses: an analysis of two methods of questionnaire administration. BJOG 2004;111(5):468–74. 15. Larsson G, Abrams P, Victor A. The frequency/volume chart in detrusor instability. Neurourol Urodyn 1991;10:533–43. 16. Larsson G, Victor A. The frequency/volume chart in genuine stress incontinent women. Neurourol Urodyn 1992;11:23–31. 17. Swinn MJ, Lowe E, Fowler CJ. The clinical features of non-psychogenic urinary retention. Neurourol Urodyn 1998;17:383–4. 18. Fitzgerald MP, Brubaker L. Variability of 24-hour voiding diary variables among asymptomatic women. J Urol 2003;169(1):207–9. 19. Hill S, Cardozo LD, Khullar V. Does evening fluid restriction improve nocturia? Int Urogynecol J 1995;6:242. 20. Blaivas JG, Appell RA, Fantl JA et al. Definition and classification of urinary incontinence: recommendations of the Urodynamic Society. Neurourol Urodyn 1997;16:149–51. 21. James ED, Flack FC, Caldwell KPS, Martin MR. Continuous measurement of urine loss and frequency in incontinent patients. Br J Urol 1971;43:233–7.
27. Kelleher CJ, Cardozo LD, Wise BG, Cutner A. The impact of urinary incontinence on sexual function. Neurourol Urodyn 1992;11:359–60. 28. Field SM, Hilton P. The prevalence of sexual problems in women attending for urodynamic investigation. Int Urogynecol J 1993;4:212–15. 29. Sutherst JR. Sexual dysfunction and urinary incontinence. Br J Obstet Gynaecol 1979;86:387–8. 30. Foldspang A, Mommsen S. Adult female urinary incontinence and childhood bedwetting. J Urol 1994;152:85–8. 31. Iosif CS, Batra S, Ek A et al. Estrogen receptors in the human female lower urinary tract. Am J Obstet Gynecol 1981;141:817–20. 32. Benson JT. Gynecologic and urodynamic evaluation of women with urinary incontinence. Obstet Gynecol 1985;66:691–4. 33. Rosenzweig BA, Pushkin S, Blumenfeld D, Bhatia NN. Prevalence of abnormal urodynamic test results in continent women with severe genitourinary prolapse. Obstet Gynecol 1992;79:539–42. 34. Hextall A, Boos K, Cardozo L et al. Videocystourethrography with a ring pessary in situ. A clinically useful preoperative investigation for continent women with urogenital prolapse? Int Urogynecol J Pelvic Floor Dysfunct 1998;9(4):205–9. 35. Hinman F. Postoperative overdistension of the bladder. Surg Gynecol Obstet 1976;142:901–2. 36. Spence-Jones C, Kamm MA, Henry MM, Hudson CN. Bowel dysfunction: a pathogenic factor in uterovaginal prolapse and urinary stress incontinence. Br J Obstet Gynaecol 1994;101:147–52. 37. Bonney W, Gupta S, Arndt S et al. Neurobiological correlates of bladder dysfunction in schizophrenia. Neurourol Urodyn 1993;12:347–9. 38. Kerr-Wilson RHJ, Thompson SW, Orr JW et al. Effect of labor on the postpartum bladder. Obstet Gynecol 1984;64:115–18.
22. James ED. The behaviour of the bladder during physical activity. Br J Urol 1978;50:387–94.
39. Kerr-Wilson RHJ, McNally S. Bladder drainage for Caesarean section under epidural analgesia. Br J Obstet Gynaecol 1986;93:28–30.
23. James M, Jackson S, Shepherd A, Abrams P. Pure stress leakage symptomatology: is it safe to discount detrusor instability? Br J Obstet Gynaecol 1999;106(12):1255–8.
40. Fantl JA, Wyman JF, Wilson M et al. Diuretics and urinary incontinence in community-dwelling women. Neurourol Urodyn 1990;9:25–34.
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41. Hoffman BB, Lefkowitz RJ. Adrenergic receptor antagonists. In: Gilman AG, Rall TW, Nies AS, Taylor P (eds) Goodman and Gilman’s The Pharmacological Basis of Therapeutics, 8th ed. New York: Pergamon Press, 1990; 221–43.
48. Migliorini GD, Glenning PP. Bonney’s test – fact or fiction? Br J Obstet Gynaecol 1987;94:157–9.
42. Baden WF, Walker TA. Physical diagnosis in the evaluation of vaginal relaxation. Clin Obstet Gynecol 1972;15:1055–9.
50. Norton PA, Peattie AB, Stanton SL. Estimation of residual urine by palpation. Neurourol Urodyn 1989;8:330–1.
43. Bump RC, Mattiasson A, Bø K et al. The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 1996;175:10–7.
51. Bergman A, McCarthy TA, Ballard CA, Yanai J. Role of the Q-tip test in evaluating stress urinary incontinence. J Reprod Med 1987;32:273–5.
44. Hall AF, Theofrastous JP, Cundiff GW et al. Interobserver and intraobserver reliability of the proposed International Continence Society, Society of Gynecologic Surgeons, and American Urogynecologic Society pelvic organ prolapse classification system. Am J Obstet Gynecol 1996;175:1467–70.
52. Fantl JA, Hurt WG, Bump RC et al. Urethral axis and sphincteric function. Am J Obstet Gynecol 1986;155:554–8.
45. Athanasiou S, Hill S, Gleason C et al. Validation of the ICS proposed pelvic organ prolapse descriptive system [abstract]. Neurourol Urodyn 1995;14:414–15. 46. Robinson H, Stanton SL. Detection of urinary incontinence. Br J Obstet Gynaecol 1981;88:59–61. 47. Berkeley C, Bonney V. A Textbook of Gynaecological Surgery, 3rd ed. London: Cassell, 1935.
49. Bhatia NN, Bergman A. Urodynamic appraisal of the Bonney test in women with stress urinary incontinence. Obstet Gynecol 1983;62:696–9.
53. Walters MD, Diaz K. Q-tip test: a study of continent and incontinent women. Obstet Gynecol 1987;70:208–11. 54. Walters MD, Shields LE. The diagnostic value of history, physical examination and the Q-tip cotton swab test in women with urinary incontinence. Am J Obstet Gynecol 1988;159:145–9. 55. Bergman A, Koonings PP, Ballard CA. Negative Q-tip test as a risk factor for failed incontinence surgery in women. J Reprod Med 1993;34:193–7.
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Introduction The voiding diary is an important tool in the investigation of patients with lower urinary tract symptoms and voiding dysfunction.1 The chart is variously known as a frequency–volume chart (FV chart), bladder diary or voiding diary, and is completed daily by the patient over a number of days prior to the visit to the doctor. The charts may range in complexity from the simple records of intake and output to more complex diaries including symptoms and incontinence episodes, and pad use, to facilitate history taking about the degree of frequency, nocturia, and volumes voided at each episode. They are useful in the following circumstances:
• Fluid intake – compulsive or excessive fluid • • •
consumption is easily identified; metabolic disorders such as diabetes may be identified in this way. Normal fluid volumes consumed at inappropriate times (e.g. bedtime) may cause nocturia. Excessive intake of alcohol or caffeine may cause exacerbation of symptoms. Learned or habitual frequency may be semiobjectively assessed.
On the basis of findings in the FV chart, simple instruction and behavioral modification can be recommended immediately, allowing treatment to commence without recourse to more complex and expensive modalities. FV charts have developed in design and content over the last 20 years although there has been little systematic work developing the FV chart as a clinical, rather than a research tool, and it remains one of the most neglected diagnostic instruments.2
Components of the Diary Diary Most institutions use a paper diary that is easily posted out in advance or handed directly to the patient. They are easy to produce, cheap to post, and easily and safely stored. The FV chart should have space to record fluid intake, with at least a recording of the volume and time of consumption. There should also be space to record the volume and timing of urine passed, and a recording of any relevant lower urinary tract symptoms, especially incontinence (Fig. 13.1).
Figure 13.1. An example of a 3-day diary as used at King’s College Hospital, London.
Instructions Culture- and age-specific instructions should be included, explaining what information is to be collected, and the relevance for the woman attending for investigation. In a 4-week audit of completion of bladder diaries prior to attending our one-stop clinic, of the 68 women attending who received the diary, only 22 (32%) had completed it.3 Interestingly, the addition of an explanatory letter describing the importance of the diary in the overall assessment increased the compliance to 75.5%, when the audit cycle was closed. Non-Caucasian races, and pelvic organ prolapse as the primary clinical complaint, are significantly correlated with non-completion of a bladder diary,4 although this was a poor predictor of an absence of urinary symptoms. In a paper looking specifically at instruction prior to completion of a FV chart,5 278 women involved in one of three other trials completed a 7-day minimal instruction diary prior to clinical evaluation, and a 7-day intensive instruction diary afterwards. The diaries were compared for the number of episodes of voluntary diurnal and
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nocturnal voids, and incontinence episodes. Correlation coefficients ranged from 0.67 to 0.78 for each of the symptoms, although intrasubject analysis revealed a decline in reported nocturnal voids, which were not explained by urodynamic or demographic findings. This may be most likely explained by ‘diary fatigue’, which is seen to occur with longer diaries. However, the study does suggest that minimal paper instructions sent out in advance are sufficient to gain the maximum benefit from the diary for each woman.
Validity and reliability The FV chart has been shown to be a valuable, reliable tool for the assessment of micturition patterns,6 as there is poor correlation between subjective and charted estimates of diurnal and nocturnal urinary frequency.7 FV charts have been shown to be both valid and useful. In a study comprising 18 patients (mean age 63 years, range 20–80 years) completing a 3-day diary and recording fluid intake and voided volumes, a 24-hour urine collection was undertaken in addition. Median difference between recorded volume and volume collected was 100 ml/24 hours (0–1450 ml/24 hours) and 10 ml/void (0–117 ml/void),8 which was not significant. Furthermore, when 63 patients were recruited to complete two diaries of 3 days’ duration, more than a week apart, 51 managed to finish the study. There was excellent correlation for both mean voided volume (r=0.86) and 24-hour frequency (r=0.9),9 suggesting intraindividual reliability of the diary over time. Individual variation was greater for urinary frequency; this natural variation may invalidate apparently successful treatment outcomes, and the authors recommended use of mean voided volume in the assessment of treatment outcomes. Maximum voided volume has been taken to represent functional capacity. Significant positive correlation has been shown between cystometric bladder capacity and maximum voided volume on the diary (r=0.4938, p<0.01), establishing the validity of a home diary in clinical practice.10 As a tool to assess bladder sensation, the bladder diary has been assessed by comparison with sensation during filling cystometry.11 On charts, 65% of all voids were made without sensation to void; urgent desire was not noted unless voluntary delay of voiding occurred. High grades of perception of fullness were associated with higher voided volumes, and mean volumes for different sensations on the charts were not significantly different from volumes at similar sensations during cystometry. FV charts may therefore provide a reliable and non-invasive method of assessing bladder sensation.
Bladder diaries are less effective at charting quantity of urine lost during incontinence episodes.12 In a study of 51 women with mild to moderate urinary incontinence, no significant correlations existed between a pad test and a questionnaire reporting volume of urine loss. There was a weak but significant correlation between a questionnaire regarding incontinence episode frequency and a 6-day urinary diary result (r=0.33, p=0.045). The correlation between a 6-day urinary diary and a questionnaire was stronger for urinary frequency (r=0.65, p=0.000). There is therefore only a weak correlation between subjective and objective measures of urinary loss. Test–retest reliability studies show high intraclass correlation coefficients of 0.81–0.86 for symptoms of strong urge, diurnal and nocturnal micturitions, total incontinence and urge incontinence episodes.13 Moderate correlations with global questions on urge incontinence and urinary frequency supported the validity of the diary. The ability of the diary to differentiate between normal and affected individuals14 is of potential clinical importance. Larsson et al6,15,16 reported on the reliability of the voiding diary in differentiating those with detrusor overactivity (DO)15 or urodynamic stress incontinence (USI)16 from normal subjects and concluded that the overlap between normal patients and patients with DO was greater for all parameters. The same conclusion was reached regarding patients with USI. Accordingly, the diary is not a reliable test for diagnostic discrimination between either condition or normal bladder function.
Duration Optimal duration has not been standardized. Some support the use of a 7-day diary, to encompass the entire week, incorporating both work and leisure time.17 Patient compliance, however, decreases with increasing length of the diary,5 in addition to other clinical correlates. A 48-hour diary has been shown to significantly correlate with a 7-day diary,6 and, in another study, the first 3 days’ results correlated well with the results of the last 4 days.18 Test–retest reliability studies in patients with OAB symptoms showed intraclass correlations of 0.81–0.86 for a 7day diary, with similar results for a 3- and a 4-day diary.13 One might think, therefore, that a shorter diary, with appropriate counseling and instruction, might improve patient compliance without compromising validity. This was not confirmed by Robinson et al., who found that patients with at least a certain intellectual capacity were able to complete the chart with minimal instruction.5 In order for a FV chart to have value, it must be completed correctly. If the length of diary is too great, then compliance is likely to be poor. As increasing bias from 199
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day-to-day variability may compromise reduced length diaries of 1 or 2 days, a 3-day diary has been suggested as optimal.8
Paper and electronic diaries If information were readily available in the clinic setting, the consultation would most likely be facilitated. The problem with paper charts, however, is that they still need to be manually calculated, which may be time consuming in a busy clinic, and inaccuracies may occur when pressed for time. Although this is very difficult to quantify, in a trial comparing electronic and paper diaries, there were no data calculation errors in the electronic diaries, allowing rapid review in clinical and research settings.19 Hand-held computerized diaries have been developed to overcome the lack of patient compliance that has been noted in many studies.20 Matched patients and controls completed a 7-day paper diary and a 7-day computerized diary. Patients felt that their symptoms were more properly reflected by the computerized version, felt more motivated to provide the data, and found it easier to remember. The two methods were
not comparable, however, as the computerized diary prompted more data entry (urgency, urgency with leak, intake) than the written diary, where patients were only asked to mark the time of a normal void and intake, with no space for any other information. It is interesting to note that, despite the skeletal nature of the conventional diary, patients still found it easier to comply with the computerized diary. Naturally, a computer diary in a clinical setting, for completion by every patient in a reasonably sized unit, would cost considerably more than a paper diary.
Intelligent character recognition A character-recognition program with appropriate hardware might combine the cheaper cost of the paper diary with the rapid and accurate data manipulation of the computer system, and make possible more quantitative clinical measures than are currently feasible (Fig. 13.2). The urogynaecology department at King’s College Hospital is currently involved with the Bladder Diary Research Team, studying the use of intelligent character recognition diaries in normal and symptomatic women.
Figure 13.2. Intelligent character recognition form with patient instructions. (Courtesy of LifeTech Inc., Houston, Texas.) 200
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Normative Values in a Healthy Population There are very few data available about the voiding habits of asymptomatic women. Normal urinary habits have been studied in a limited sample over 24 hours but more age- and racematched data are needed.21 In a 24-hour diary study of asymptomatic women, the use of eight voids per 24 hours was questioned as defining ‘frequency’.22 Thirteen or more voids per 24 hours were found to represent the upper range in the normal distribution (Table 13.1). Race affected mean voided volume, maximum voided volume, and voids per liter intake and output; these may, in fact, represent useful clinical measures to compare populations. Additionally, a direct link between the number of voids per liter intake and the degree of bother with urinary frequency has been expressed.23 Recent independent studies by van Haarst, et al24 and Amundsen, et al25 (592 and 161 asymptomatic females Table 13.1.
respectively) found that volume per void (volume/void) decreases, and frequency increases, with age, and that both frequency and volume/void increase with increasing 24-hour volume (Figs 13.3 and 13.4). The robust relationship between 24-hour volume and volume/void runs counter to the widely held assumption that “bladder capacity” remains relatively constant, regardless of total urine output, and that an increase in voiding frequency is the primary response to increased urine production. The data show that although frequency does increase with increasing 24-hour volume, the concomitant increase in volume/void limits the frequency increase. Thus, the van Haarst and Amundsen studies24, 25 show that a 70-year-old asymptomatic woman is likely to have a higher frequency and smaller volume/void than a 20year-old asymptomatic woman. Similarly, a woman who voids 3000 ml in 24 hours is likely to have a higher frequency and larger volume/void than a woman of similar age who voids only 1000 ml in 24 hours.
Voiding parameters derived from 300 paper diaries Median
Range
95th centile
Total voids in 24 hours (no.)
8
4–18
12
Total daytime voids (no.)
8
3–16
12
Total night-time voids (no.)
0
0–4
2
Total 24-hour urine volume (ml)
1620
480–5310
3113
Total fluid intake (ml)
1927
625–4980
3480
Voids/liter intake
4
1–15
8
Voids/liter urine output
5
2–19
11
Maximum voided volume (ml)
330
90–1020
679
Mean voided volume (ml)
204
53–590
368
Daytime diuresis (ml/min)
1.1
0.3–3.2
2.4
Night-time diuresis (ml/min)
0.8
0.1–3.1
1.8
Data from ref. 21.
Table 13.2. “Normal Limits” of voiding diary measurements versus age and 24-hour volume Total 24-Hour Volume (ml) Age
1000
2000
3000
24-Hour Frequency
1000
2000
3000
1000
2000
3000
Average Voided Volume (ml)
Maximum Voided Volume (ml)
20
8.7
9.9
11.2
107
197
288
223
402
581
30
8.8
10.1
11.3
103
194
284
214
393
572
40
9.0
10.2
11.5
100
190
281
226
384
563
50
9.1
10.4
11.6
96
187
277
205
375
554
60
9.3
10.5
11.8
93
183
274
196
367
546
70
9.4
10.7
11.9
89
180
270
188
358
537
80
9.6
10.8
12.1
86
176
266
179
349
528
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13
95% C. L. Regr. Eq.
12
600
Data Points
11
Average volume (ml)
500
10
24 hour frequency
95% C. L. Regr. Eq. Data Points
9 8 7 6 5 4
400
300
200
100
r = 0.70
3 r = 0.47
2 1 0
500
0
0
500
24 hour volume
1000 1500 2000 2500 3000 3500 4000
24 hour volume (ml) Figure 13.3. Relationship between 24 hour volume and 24-hour-frequency in an asymptomatic female population. ‘95% C. L.’ = 95% confidence limits. “Regr. Eq.” = linear regression equation. ‘r’ = correlation coefficient, which is significantly (P<0.0005) different from zero.
1000 1500 2000 2500 3000 3500 4000
Figure 13.4. Relationship between 24 hour volume and 24-hour-frequency in an asymptomatic female population. Abbreviations are as in Fig 13.3. The correlation coefficient is significantly (P<0.0005) different from zero.
REFERENCES Since “normal” volume/void and frequency are influenced by age and 24-hour volume, “normal limits” of these voiding diary measurements should be adjusted for these parameters. Table 13.2, which was obtained by regression analysis, shows confidence limits of frequency and volume/void that are adjusted for age and 24-hour-volume24.
Conclusion Although there are limits as to the ability of the FV chart to differentiate between normal and abnormal voiding patterns, it remains integral in the assessment of women with lower urinary tract symptoms, and valid for the assessment of urinary frequency and functional capacity. It is easy to complete with even basic instruction to facilitate history taking. The assessment of computerized diaries has shown some promise, but data are still limited. Cost is likely to be a serious limiting issue. Intelligent character recognition may well combine the speed and accuracy of computerized analysis while limiting the cost to a single desktop PC and paper forms.
1. Abrams P, Fenely R, Torrens M. Patient assessment. In: Abrams P, Fenely R, Torrens M (eds). Urodynamics, 1st ed. New York: Springer, 1983; 6–27. 2. Fink D, Perucchini D, Schaer GN, Haller U. The role of the frequency–volume chart in the differential diagnosis of female urinary incontinence. Acta Obstet Gynecol Scand 1999;78(3):254–7. 3. Parsons M, Dixon A, Thomas M, Cardozo L. An audit of completion of a bladder diary prior to urodynamic studies. King’s College Hospital Audit Meeting, July 2004. 4. Heit M, Brubaker L. Clinical correlates in patients not completing a voiding diary. Int Urogynecol J 1996;7(5):256–9. 5. Robinson D, McClish DK, Wyman JF et al. Comparison between urinary diaries completed with and without intensive patient instructions. Neurourol Urodyn 1996;15:143–8. 6. Larsson G, Victor A. Micturition patterns in a healthy female population, studied with a frequency–volume chart. Scand J Urol Nephrol Suppl 1988;114:53–7. 7. McCormack M, Infante-Rivard C, Schick E. Agreement between clinical methods of measurement of urinary frequency and functional bladder capacity. Br J Urol 1992;9(1):17–21.
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8. Palnæs Hansen C, Klarskov P. The accuracy of the frequency–volume chart: comparison of self-reported and measured volumes. Br J Urol 1998;81:709–11.
17. Abrams P, Klevmark B. Frequency volume charts: an indispensable part of the lower urinary tract assessment. Scand J Urol Nephrol Suppl 1996;179:47–53.
9. Bryan NP, Chapple CR. Frequency volume charts in the assessment and evaluation of treatment: how should we use them? Eur Urol 2004;46:636–40.
18. Nygaard I, Holcomb R. Reproducibility of the seven-day voiding diary in women with stress urinary incontinence. Int Urogynecol J 2000;11(1):15–7.
10. Diokno AC, Wells TJ, Brink CA. Comparison of selfreported voided volume with cystometric bladder capacity. J Urol 1987;137(4):698–700.
19. Quinn P, Goka J, Richardson H. Assessment of an electronic daily diary in patients with overactive bladder. BJU Int 2003;91:647–52.
11. de Wachter S, Wyndaele J-J. Frequency–volume charts: a tool to evaluate bladder sensation. Neurourol Urodyn 2003;22:638–42.
20. Rabin JM, McNett J, Badlani GH. Computerised voiding diary. Neurourol Urodyn 1993;12:541–54.
12. Miller JM, Ashton-Miller JA, Carchidi LT, DeLancey JO. On the lack of correlation between self-report and urine loss measured with standing provocation test in older stressincontinent women. J Women’s Health 1999; 8(2):157-62 13. Brown JS, McNaughton KS, Wyman JF et al. Measurement characteristics of a voiding diary for use by men and women with overactive bladder. Urology 2003;61(4):802–9.
21. Fitzgerald MP, Brubaker L. Variability of 24-hour voiding diary variables among asymptomatic women. J Urol 2003;169:207–9. 22. Fitzgerald MP, Stablein U, Brubaker L. Urinary habits among asymptomatic women. Am J Obstet Gynecol 2002;187(5):1384–8. 23. Fitzgerald MP, Butler N, Shott S, Brubaker L. Bother arising from urinary frequency in women. Neurourol Urodyn 2002;21:36–41.
14. Kahn KS, Chien PFW, Honest MR, Norman GR. Evaluation measurement variability in clinical investigations: the case of ultrasonic estimation of urinary bladder volume. Br J Obstet Gynaecol 1997;104:1036–42.
24. Van Haarst EP, Heldeweg EA, Newling DW, Schlatmann TJ. The 24-h frequency–volume chart in adults reporting no voiding complaints: defining reference values and analysing variables. BJU Int 2004;93:1257–61.
15. Larsson G, Abrams P, Victor A. The frequency/volume chart in detrusor instability. Neurourol Urodyn 1991;10:533–43.
25. Amundsen CL, Parsons M, Tissot W, Cardozo, L, Diokno, A. Bladder diary measurements in asymnptomatic females: Functional bladder capacity, frequency, and 24-hour volume. Neurourol Urodyn, Submitted 9-Nov-2005.
16. Larsson G, Victor A. The frequency/volume chart in genuine stress incontinent women. Neurourol Urodyn 1992;11:23–31.
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14 Pad tests Marie-Andrée Harvey
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Historical aspects In 1971, James et al. first described the quantification of urine loss to determine response before and after treatment.1 This was achieved using a pair of elongated electrodes embedded within the absorbent layer of a diaper, which contained dry electrolytes. Following urine loss, the moisture between electrodes resulted in a change in electrical conductivity that could be detected and recorded. It was marketed under the name of Urilos (N.H. Eastwood & Son, Ltd, London, UK).2 However, the equipment was rather cumbersome and never caught on. The pad test as we know it today was originally simultaneously described by Sutherst et al.3 and by Walsh and Mills4 in 1981. It consists of the use of a perineal pad to document urinary incontinence and to quantify its severity, under natural conditions. The amount of loss is calculated by subtracting the weight of the pad before the test from its weight at the end of the test. A standardized 1-hour pad test (Table 14.1) was subsequently proposed in 1983,5 and endorsed by the International Continence Society (ICS) in 1988.6 Other innovative methods were developed, going from the distal urethral electrical conductance test (DUEC)7,8 to the temperature-sensitive device.9 The DUEC involves a 7 Fr catheter placed in the distal urethra, on which two rings are mounted 1 mm apart. These rings register the electric potential change occurring when fluid comes into contact with the electrodes. The temperature-sensitive device uses a diode temperature sensor embedded in the outermost layer of a pad, which records a change in voltage across the diode when urine (warmer than the table 14.1.
Standardized 1-hour pad test
0 minute Apply pre-weighed pad Drink 500 cc sodium-free liquid Sit and rest 30 minutes Walk and stairs climbing 45 minutes Activities: • Sit/stand × 10 • Cough × 10 • Run in place × 1 minute • Pick up objects from floor • Wash hands under running water × 1 minute 60 minutes Collect and weigh pad Patient voids, volume measured Adapted from ref. 6.
perineum) is lost. These were devised to detect urine leakage during ambulatory urodynamic studies, without the bulk of the Urilos, but are unable to quantify the loss. Their clinical use has never been evaluated. The accuracy of some of these methods has been disputed. Initially, the Urilos was said to be able to detect volumes from less than 1 ml to approximately 100 ml, with a variation of up to 20% when repeated. Subsequent studies have attempted to assess the reliability of the Urilos system.2,10 When measured, the difference in volume recorded between different diapers varied between 13%2 and 25%.10 When comparing diapers from different boxes, the variation between them was as much as 68%.10 Furthermore, the Urilos was noted to be uncomfortable, and did not absorb large volumes of fluid.11 Because of its lack of precision, the Urilos diaper never gained widespread popularity. The DUEC test has experienced a similar fate. In a small study comparing the ICS pad test to the DUEC, the DUEC showed no benefit over the 1-hour ICS pad test, with a greater complexity involved.12 A recent study evaluated its role in the diagnosis of women with symptoms of stress urinary incontinence (SUI) but without demonstrable leak on urodynamic or cough stress test (where leak is observed when the subjects cough with a comfortably full bladder).13 The DUEC test failed to detect stress incontinence in 33% of the women with demonstrable stress incontinence during standard urodynamic study. However, it detected SUI in 28% of symptomatic women with negative urodynamic studies, thereby possibly complementing urodynamic studies in the detection rate of SUI. Further studies are clearly needed to define the role of the DUEC test prior to its adoption for the evaluation of SUI.
indications The objective demonstration of urinary incontinence is of importance when establishing the diagnosis.6 It is of particular value during research studies for the evaluation of treatment response. Neither the patient’s perception of incontinence2 nor her perception of its severity14 is well correlated with urodynamic measures. A pad test can thus be used in two ways: as an objective means of detection of urine leakage when clinical testing is otherwise negative, or more generally to quantify urine loss prospectively. Pad tests are generally divided into short (<1 hour, 1 hour, 2 hours) or long (24 hours, 48 hours). Standardization only exists for the ICS 1-hour pad test. Staging of the severity of incontinence has been proposed for the short pad test (Table 14.2).6 Long-term protocols have, as yet, not been subject to standardization.
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table 14.2.
Interpretation of urinary incontinence from the pad test weight gain*
Category
Weight gain (g)
Dry
<2
Slight to moderate
2–10
Severe
10–50
Very severe
>50
* According to the International Continence Society classification (ref. 6).
reliability and validity Before one can obtain evidence that an instrument is measuring what is it intended, it is first necessary to gather evidence that [it] is measuring something in reproducible fashion; it says nothing about what is being measured. To determine that the test is measuring what was intended requires some evidence of ‘validity’.15 Validity expresses the relation between observed measurements and the true state of the entity being studied.16
Reliability can be defined broadly by two characteristics: internal consistency and stability.15 Internal consistency represents the average of the correlations among all items in the instrument, using different calculations (e.g. Cronbach’s alpha). This applies to instruments with multiple items, such as questionnaires. In the case of the pad test, reliability is best demonstrated through its stability, i.e. the degree of agreement between different observers (interobserver reliability), between observations made by the same observer on two different occasions (intraobserver reliability) or observation on the same patient on two distinct occasions, separated by a time interval (test– retest reliability). The second characteristic that is important in an instrument is its validity. Validity compares the performance of a test against that of a known tool, such as a ‘gold standard’. When such a standard is non-existent, validity can be ‘constructed’ by studying two or more different or similar populations in which it is expected to find a difference, or similarity, between test results. Validity of the pad test can be reflected by the accuracy of the measured volume lost and its sensitivity in detecting such a loss. If the sensitivity is poor, the test will, at times, not detect the true state of the entity, namely the presence of incontinence. However, as there is currently no means of detecting the true amount of urine leak with each incontinence episode, the validity of the pad test will be reflected in its ability to demonstrate incontinence in a patient who complains of urinary inconti-
nence, and a lack of urine loss in patients who report continence.
sHort pad tests This category includes the following tests: 1) standardized ICS 1-hour pad test; 2) modified version of the ICS 1-hour test, usually incorporating different exercise intensity; and 3) pad tests of less than 1 hour, using a fixed bladder volume, with retrograde filling.
detection limit Increased weight of the pad may be due to urine, but also to vaginal discharge, sweating or menstruation. A pad test should not be done during menstruation. In order to account for the weight resulting from discharge or sweating, it was necessary to establish a cut-off. The first report of a normal threshold in a 1-hour pad test in continent women was reported simultaneously by Sutherst et al.3 and by Walsh and Mills.4 Comparing 50 women with urinary control to 100 women referred for incontinence, a maximum weight change of the pad of 1 g was measured in all continent patients versus a mean of 12.2 g in incontinent women.3 Walsh tested six healthy continent volunteers for three consecutive days from 9 am to 9 pm, during which pads were changed every 2 hours, and reported a 1.2 g/2-hour weight gain due to perspiration (standard deviation 1.4 g). Versi and Cardozo17 compared the 1-hour pad test to videourodynamic studies (v-UDS) in continent and incontinent (urodynamic stress incontinence) patients. In 90 patients without incontinence and with normal v-UDS, the mean pad weight gain was 0.39 g, with a 99% upper confidence limit of 1.4 g. The ICS fixed the threshold for a negative pad test at <2 g. The type of exercise performed during a short pad test has been evaluated. Sutherst et al.18 published a study evaluating the type of activity leading to urine loss and the impact of voiding during the test period. They noted that, irrespective of urodynamic diagnosis, activities leading to leakage in all women included (in increasing order of urine loss) walking around/bed making (3–4 g each), climbing stairs up and down with or without a heavy pack (~5–6 g each), picking up objects from the floor (~6 g) and spending several minutes hand washing (10 g). Voiding during the test had no effect on the result, with a similar proportion being dry on the pad test whether they voided or not. Some studies have evaluated the feasibility of a home pad test, where a subject would be given pre-weighed pads and would return the used pads in a sealed plastic 207
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envelope.19,20 Mailing delays were not shown to significantly alter the measurement of pad weight.
ics 1-hour pad test The ICS 1-hour pad test set out to define a standardized objective measure to facilitate comparison between investigators. However, despite earlier favorable reports, the ICS 1-hour test has subsequently been shown to have insufficient reliability. In only one early study21 was the test–retest correlation shown to be high (r=0.91) when 16 subjects repeated the 1-hour test successively. When done on different days in 19 subjects, the correlation was similarly high (r=0.96).The reproducibility of urine loss during a single activity during the successive 1-hour tests was similarly good (r between 0.75 and 0.97). In contrast, Lose et al.22 reported a lesser test–retest (1–15 days interval) correlation of 0.68 between the two tests. However, they reported a better reproducibility when bladder volume at the start of the test was taken into account. Jørgensen et al.23 studied test–retest reproducibility in 18 women and reported a correlation of 0.68. More recently, the test–retest reliability of the ICS 1hour pad test was re-evaluated by Simons and colleagues.24 In their study, 56 women performed the 1-hour pad test twice, 3–10 days apart. Using a bladder scan, the bladder volume was ascertained to be similar both times for each patient. Reproducibility was poor, with a limit of agreement (using the Bland and Altman method25) of –43 g and +34 g, reflecting the small sample size and the great variability of measurement. They found that a pad test on the second test could be 43 g less or 34 g more than the pad weight gain on the first pad test, for a similar bladder volume and following identical provocations. Interobserver reliability was assessed by Christensen et al. in a study comparing the pad test done twice in the same patients – once in the Department of Urology and again in the Department of Obstetrics and Gynaecology.26 An abysmal correlation coefficient of 0.10 was reported for interobserver reliability. It is important to note that the statistical analysis used in the Bland and Altman’s method is better in describing agreement between two tests, whereas the correlation coefficient merely quantifies association between two test results. Since the two tests compared here are exactly the same, evidently they will be associated, but high association does not necessarily translate into high agreement. A component of the validity, i.e. the ability of the ICS 1-hour pad test to detect urinary leakage and discriminate between continent and incontinent subjects, has been evaluated. The ICS 1-hour pad test appears to have some validity as it correctly identifies conti-
nent subjects, but has a substantial false-negative rate in incontinent women (6–32%) when compared to UDS. Versi and Cardozo17 first reported on the 1-hour pad test validity. Their study included three groups of women who underwent pad testing: 17 young asymptomatic women, 73 women with urinary frequency but with normal UDS, and 99 women with urodynamic stress incontinence on v-UDS. Of those with urodynamic stress incontinence, 14 had a negative pad test (14% false-negative rate). The assessment of severity on videographic grading did not correlate with pad weight gain. In another study23 of 49 women who underwent v-UDS, 17 were confirmed as having urodynamic stress incontinence. One of them (6%), however, had a negative pad test. Versi et al. studied a further 311 additional women presenting with urinary complaints to evaluate if the test could screen for the pathology found on vUDS.27 Sixteen percent of women with no abnormality on v-UDS had a positive pad test and 32% of women with an abnormality on v-UDS had a negative pad test (68% sensitivity). The measure of agreement (Kappa’s coefficient) between the pad test and the presence of pathology on UDS was 0.43±0.07 (standard error), which denotes a moderate agreement.28 Wall et al.29 evaluated pad test results among 18 women with urodynamic stress incontinence and 23 healthy continent women, with a stronger validity reported. All women with urodynamic stress incontinence had a positive pad test, and those who were continent all had a negative pad test (maximum 0.7 g). In a subsequent smaller study (n=49) sensitivity was better (94%) but the agreement between the two tests was fair (0.31). Similar fair agreement (Kappa = 0.37) can be extrapolated from a more recent study in which 130 incontinent women were tested both urodynamically and with a pad test.30 In a study evaluating the relationship between the ICS 1-hour pad test and videourodynamic measures of urethral integrity in 274 women, Paick et al.31 reported a weak but significant negative correlation between the urine loss on pad test and the Valsalva leak point pressure (VLPP) (–0.38, p<0.05), i.e. with increasing urine loss on pad testing, the VLPP decreased. No correlation was obtained between urine loss on pad test and the maximal urethral closure profile. Assuming that UDS would represent the gold standard, the pad test seems to be able to discriminate most of the time between continent and incontinent women; a positive test will correctly identify an incontinent patient, but a negative test may be found in women demonstrated to be incontinent on UDS. The pad test is unable to discriminate among the different incontinence pathologies found on UDS, or to consistently
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determine incontinence severity.17,27 Furthermore, adding Pyridium failed to increase specificity.32 In light of its poor reliability, it may not be unexpected that, although endorsed by the ICS, the 1-hour pad test is only rarely (33%) followed in outcomes research.33 Surprisingly, despite reports of its poor reproducibility, high urine loss detected on the pad test nevertheless influences clinicians in selecting a surgical treatment option rather than conservative management.34
Modified 1-hour pad tests Some have sought to improve the reliability of the 1hour pad test through increasing exercise intensity, or controlling the bladder volume. Only the latter method appears to improve reliability consistently. Devreese et al.35 sought to assess if reliability and sensitivity would be improved using a more aggressive protocol. However, there are insufficient data to stipulate that this aggressive protocol adds any reliability or sensitivity to the current 1-hour test. Subjects were asked to drink 1 liter of water in 15 minutes. One hour after starting drinking, they were asked to drink an additional 500 ml. The pad test was started as soon as subject felt a full bladder, when 14 different vigorous exercises were performed. At the end of the test, voided volume was measured. Exercises included, but were not limited to, star jumps, sprinting, vacuuming, lifting, carrying and putting down a 10 kg box, and pulling on an elastic band, in addition to standard exercises that are included in the ICS 1-hour pad test. None of the 18 controls reported or demonstrated any leakage on pad test. Among the 25 women with symptoms of urinary incontinence tested, eight (32%) had a negative test. Test–retest was obtained in 16 of the 25 women. Correlation was 0.73. Mean micturition volume at the end of the test was 568 ml. Studies have demonstrated an improved correlation with fixed bladder volume; however, the difference in the test and retest pad weights was substantial, and thus reliability remains limited. Lose et al.22 first reported the effect of bladder volume on the reproducibility of the 1-hour pad test. They demonstrated that all subjects had significantly more urine loss with increasing bladder volume at the beginning of the exercise protocol. Test–retest reliability of a fixed bladder volume short pad test was first reported by Fantl et al.36 Correlation between the two tests done at capacity was 0.82 for those with urodynamic stress incontinence and 0.86 for those with both detrusor overactivity and urodynamic stress incontinence. However, the difference in mean pad weight was significantly different between the test and
the retest (9 g), thus limiting the test reliability. A similar result was reported when the bladder was filled at 75% capacity (r=0.74)37 and at 50% capacity.38 In the latter, the correlation was greater (0.97) and the authors reported on the limit of agreement,25 which showed considerable variability (±24 g), with the authors admitting that sensitivity was ‘hardly much better’ than the ICS 1-hour test. More recently, Hahn and Fall39 performed a slightly more provocative test on subjects with the bladder filled to 50% capacity. They had a similarly high correlation (0.94), but the test–retest differed by as much as 30%. The Committee on Imaging and Other Investigations from the Second International Consultation on Incontinence40 concluded that the 1-hour pad test was not accurate, unless done at fixed bladder volume; the sequence of exercises did not affect the result; and a positive pad test was one weighing ≥1 g. They suggested that a 20 minute to 1 hour ward test with a fixed bladder volume be used if a short pad test was undertaken.
pyridium test Phenazopyridine hydrochloride (Pyridium, Park Davis, Co, NJ) ingestion results in the dye being excreted by the kidney with consequent coloring (orange) of the urine, and this has been used by clinicians to detect incontinence. Wall et al.29 reported the sensitivity and specificity of Pyridium as a qualitative test in incontinent patients. In a study comparing this method with a standardized 1-hour pad test in asymptomatic women and those with urodynamic stress incontinence (diagnosed on subtracted cystometry), sensitivity and specificity of the Pyridium pad test were 100% and 48%, respectively. The poor specificity was due to a high false-positive rate in asymptomatic patients. This may be explained by staining of the perineum at the time of a prior void, resulting in tinting of a subsequent pad on vulvar contact, or by a minimal, non-clinically significant, loss of urine in normal women. These results were subsequently confirmed in a study testing continent (self-reported) women during exercise,32 in which Nygaard and Zmolek reported nearly 100% Pyridium staining after physical activity, with a mean pad weight of 4.59±3.55 g (outdoor exercise) or 1.33±0.97 g (indoor exercise). Pyridium staining was minimal, with a mean stained area of 2.66 mm (range 0–11 mm). No cut-off limit in the pad weight has been previously established to define a normal pad test during exercise, given that there would be a greater weight gain due to perspiration alone. In the light of these reports, the use of Pyridium in detecting urethral incontinence can be perceived as 209
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unreliable and non-specific. Nonetheless, it remains useful in the diagnosis of extraurethral urine loss (e.g. fistulae).
long pad test A long pad test is usually performed at home, during a typical day’s activities. The subject is given a number of pre-weighed pads, placed in a sealed envelope. She is instructed to wear the pads consecutively for a given period (12, 24, 48 or 72 hours) and to return the pads in their sealed envelope for weighing. A long pad test was first described by Sutherst’s group, in an abstract.41 The aim of the study was to determine if the 1-hour pad test was representative of urine loss experienced during regular activity. The 1-hour pad test has been criticized because of its artificial setting and short duration. Lose et al. suggested that performing a test during regular daily activities would be more sensitive than during a single 1-hour test.42
detection limit Lose et al. first established a detection limit by studying 23 asymptomatic female subjects.42 They noted that the median weight obtained for the 24-hour pad test was 4.0 g, with a 99% upper limit of 8 g for the 24-hour period. Ryhammer et al.43 studied 78 self-reported continent women. Their mean loss was 3.1 g (range 0–9 g) during a 24-hour pad test. Versi et al.44 studied 24 young continent women during a 48-hour pad test and reported a mean loss of 7.1 g, with a 95% upper confidence limit of 14.5 g. Mouritsen et al.45 reported a smaller detection limit in normal subjects for a 48-hour pad test: mean 2.6 g, 95% upper confidence limit of 5.5 g. The Committee on Imaging and Other Investigations from the Second International Consultation on Incontinence40 recommended that a pad gain ≥4 g during a 24-hour pad test be considered as positive.
reliability and validity The long pad tests have a good reliability as shown by the correlation obtained, bearing in mind the limitations of the ability of this measure of association in determining agreement. Victor et al. were the first to compare test– retest of the 24-hour home pad test.46 Fifteen women performed a 48-hour pad test and repeated it 1 week later. When comparing the first 24 hours of the two 48hour pad tests, correlation was significant (r=0.66). Lose et al.42 performed test–retest evaluation of the 24-hour home pad test in 31 women referred for incon-
tinence. A significant correlation (r=0.82) was noted between the two tests. The limit of agreement was approximately ±100 g, which means that the second test could yield greater or lesser results by as much as 100 g. This represents a large variability of results. Rasmussen et al.47 evaluated 14 women for test–retest reliability of the 24-hour pad test, but failed to find a linear correlation between the two tests. The second test could be anywhere between a third less to three times more than the first 24-hour period tested. Versi et al.44 looked at the reproducibility of the first 24 hours from a 48-hour pad test, compared to the first 24 hours of a second 48-hour pad test in 140 symptomatic patients. They noted a strong correlation (0.9) and a difference between the two tests of 7%. When looking at the test–retest carried out during the first 24 hours of a 72-hour pad test performed twice in 106 women, Groutz et al.48 used another statistical marker of reliability (Lin’s concordance correlation coefficient (CCC),49 in which reliability was defined as a coefficient >0.7). The coefficient obtained was 0.72. More recently, Karantanis et al.50 assessed the repeatability of seven consecutive 24hour pad tests on 108 women using repeated measure ANOVA. No difference in mean pad test among the 7 days was detected, suggesting repeatability. Similarly, the reliability of the 48-hour and 72-hour pad tests has been reported to be very good. Victor et al.46 reported a correlation coefficient of 0.9 between two tests at least 1 week apart. Versi et al.44 reported a similar correlation, with a difference in weight between the two tests of only 1.6%. Groutz et al.,48 when comparing the first 2 days of a 72-hour pad test performed on two different occasions, found a concordance correlation coefficient (Lin’s CCC) of 0.88. The test–retest correlation (using Lin’s CCC) was at the greatest for the 72-hour pad test (CCC =0.94). The latter study suggested that a 72-hour pad test was more reliable than a 24-hour pad test. The first 24 hours of a 48-hour pad test has been compared to the full 48hour test and the two tests have been shown to correlate highly (r=0.92), suggesting that the 48 hours did not add much to a 24-hour test.51 Therefore, a balance between response rate desired and accuracy of the method must be struck, as the need to perform a 24-hour pad test had been shown to deter patients’ participation in trials.52 Consequently, the Committee on Imaging and Other Investigations from the Second International Consultation on Incontinence40 concluded that the 24hour pad test was reproducible and stated that a test lasting more than 24 hours had little advantage. The validity of the home pad test, i.e. its ability to detect urine loss in patients with established urinary
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incontinence on UDS, has been reported. Most studies conclude that the 24-hour pad test is representative of UDS anomaly and is thus valid. Griffiths et al. compared the result of a supervised 24-hour pad test in 50 elderly inpatients.53 Ninety percent had a positive pad test, but vUDS detected leakage was present in only 78%, making the 24-hour pad test perhaps more sensitive than UDS. In Versi and colleagues’ study,44 149 women had both a 24-hour pad test and v-UDS. Of the 62 women who had urodynamic stress incontinence, five had a negative pad test (8% false negative). Of the 43 women who had no anomaly on UDS, 12 (28%) had a positive pad test. Eight of these 12 had a repeat UDS and were subsequently found to have detrusor overactivity. Forty-four had other UDS diagnoses, but pad test results were not described. These earlier studies suggest a reasonably low falsenegative 24-hour pad test compared to UDS, and an improved objective demonstration of urinary incontinence in symptomatic subjects with negative UDS. This is in contrast to a large recent study involving 341 women who had both a 24-hour pad test and UDS.54 Urodynamic stress incontinence, detrusor instability or both was noted in 294 women. Of these, 108 had a negative 24-hour pad test (37%), placing some doubt on the validity of this test.
sHort versus long pad tests Overall, the home pad tests (24- and 48-hour) correlate poorly with 1-hour pad tests but are more sensitive than the shorter 1-hour pad tests. Ali et al.41 first compared the 1-hour to a 12-hour pad test, and noted a ‘close correlation’. Jørgensen and co-workers42,55 studied 31 women with urinary incontinence who had a 1-hour pad test (standard volume of 200–300 ml) and a 24-hour pad test. Of these, 13 had a negative 1-hour pad test, of which 10 had a positive 24hour pad test, giving a false-negative rate of 39% for the 1-hour pad test compared to the 24-hour test. No correlation was found between the 1-hour and the 24-hour test. This report was echoed by the study of Griffiths et al.53 of 50 elderly patients who underwent a 1-hour test as well as a 24-hour pad test (supervised, while inpatients). Fortysix subjects had a positive 24-hour pad test, but only 22 (44%) had a positive 1-hour pad test. The two tests correlated weakly (r=0.42). Thind and Gerstenberg51 reported a similar poor correlation between the 1-hour and the 24-hour (r=0.35) or the 48-hour (r=0.35) pad tests, while Victor et al.46 failed to find any correlation between the 1-hour and the 48-hour pad tests in 17 patients. Of 25 women with urinary incontinence, only 12 had a positive
1-hour test, versus 21 women who had a positive 48-hour test. The data were not reported for the comparison between the 1-hour and the 24-hour test. In a recent larger study (n=341), Matharu et al.54 found a similar weak but significant correlation between the 1-hour and 24-hour tests (r=0.44). At variance with other reports, however, the 1-hour test detected more incontinent women than the 24-hour test: of the 341 women, 294 had an abnormality on UDS; of these, 52% had a positive 24hour pad test, but 70% had a positive 1-hour pad test. Both tests also lack the ability to discriminate between UDS diagnoses as there is considerable overlap between pad loss across UDS diagnoses.54
correlation with symptoms and quality of life The 1-hour, 24-hour, and 48-hour pad tests have all been shown to correlate with symptoms reported by patients, albeit that these correlations are often weak; however, the association between pad test and quality of life is weak. Elser et al. attempted to correlate the subjective report of urinary incontinence severity with a short pad (standard volume) test.56 Correlation was done only between the number of clothing changes per week by recall and the fluid loss on pad test. The correlation was significant, but weak (r=0.24). Using validated and reliable symptom and quality of life questionnaires for women with stress incontinence – the Symptom Severity Index (SSI) and the Symptom Impact Index (SII)57 – Aslan et al.58 studied the relationship between symptoms and a 1-hour pad test. A significant correlation was noted between the SSI and the pad test, but not with the SII. A poor but significant correlation between the 1-hour pad test and the King’s Health Questionnaire was noted elsewhere (r=0.48).59 Interestingly, a four-point (non-validated) subjective self-assessment was shown to have a good correlation (r=0.88). The Severity Index60 was also shown to correlate moderately with the 24-hour pad test (r=0.54) in a study of 265 women.61 In a study evaluating self-report of incontinence and a 24-hour pad test, continent women had a similar 24-hour pad test weight gain as those reporting incontinence.43 In a study using the Urinary Incontinence Severity Score, Stach-Lempinen et al.62 detected a poor but significant relationship between the quality of life tool and the 48hour pad test (r=0.25). A 10 cm visual analog scale (0 = not bothered by incontinence, 10 = severely bothered) showed a greater but fair correlation (r=0.46). When the 24-hour pad test was compared to the International Consultation on Incontinence 211
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Questionnaire – Short Form (ICIQ-SF) in a population of 59 women with urodynamic stress incontinence, Karantanis et al.63 found a significant correlation (r=0.458). Furthermore, the 24-hour pad test also correlated with the frequency of incontinence episodes as noted in the 3-day frequency volume diary (r=0.40).
paper towel test Most of the methods objectively quantifying urine loss preclude detection of small volumes, as these may overlap with perspiration and vaginal secretions. A simple non-invasive test was developed to detect such losses associated with stress incontinence.64 While a tri-fold brown paper towel is held under the perineum, the patient is asked to cough three times consecutively. The surface of the wetted area is calculated using the ellipse formula (πxy), x and y being the orthogonal axes of the area, and then converted to volume of urine lost (using a standard curve). The relationship between the measured area and a known fluid volume was found to have a very strong correlation (r=0.998). In a test–retest evaluation within the same visit and between visits the authors also showed a high correlation coefficient and concluded that the quantitative paper towel test was accurate and reliable in detecting small losses of urine due to stress incontinence. This test has not been validated against a gold standard diagnostic method such as video multichannel urodynamics and consequently the sensitivity and specificity of this diagnostic method is currently unknown.
suMMary To date, the objective urine loss test most useful in clinical practice remains the perineal pad test. A short version has been standardized to a certain degree by the ICS, rendering its use more uniform for research. However, the bladder volume at the beginning of the 1-hour test should be standardized. Although the short pad test was found to be reliable in differentiating normal from abnormal continence mechanisms, its validity is somewhat limited as it has a significant false-negative rate. The 1-hour pad test has not been found to have good reproducibility, although it is improved with standardized bladder volume. Finally, the ability of the short pad test (≤1 hour) to categorize severity of incontinence was noted to be poor. The long pad test (≥24 hours), on the other hand, was found to be valid in detecting incontinence, with good sensitivity and a lower false-negative rate. The reproducibility was similarly noted to be good for both a 48-hour
and a 24-hour test period. Hence, a 24-hour home pad test is an effective tool in detecting and quantifying incontinence. Neither test can distinguish between different urodynamic diagnoses.
acknowledgMent The contribution from Dr Eboo Versi, co-author in the first edition of this chapter, is gratefully acknowledged.
reFerences 1. James ED, Flack FC, Caldwell KP, Martin MR. Continuous measurement of urine loss and frequency in incontinent patients. Preliminary report. Br J Urol 1971;43(2):233–7. 2. Stanton SL. Urilos: the practical detection of urine loss. Am J Obstet Gynecol 1977;128(4):461–3. 3. Sutherst J, Brown M, Shawer M. Assessing the severity of urinary incontinence in women by weighing perineal pads. Lancet 1981;1(8230):1128–30. 4. Walsh JB, Mills GL. Measurement of urinary loss in elderly incontinent patients. A simple and accurate method. Lancet 1981;1(8230):1130–1. 5. Bates P, Bradley W, Glen E et al. Fifth report on the standardization of terminology of lower urinary tract function. Bristol International Society Committee on Standardisation of Terminology, 1983. 6. Abrams P, Blaivas JG, Stanton SL, Andersen JT. The standardisation of terminology of lower urinary tract function. The International Continence Society Committee on Standardisation of Terminology. Scand J Urol Nephrol Suppl 1988;114:5–19. 7. Plevnik S, Vrtacnik P, Janez J. Detection of fluid entry into the urethra by electric impedance measurement: electric fluid bridge test. Clin Physics Physiol Meas 1983;4(3):309–13. 8. Plevnik S, Brown M, Sutherst JR, Vrtacnik P. Tracking of fluid in urethra by simultaneous electric impedance measurement at three sites. Urol Int 1983;38(1):29–32. 9. Eckford SD, Finney R, Jackson SR, Abrams P. Detection of urinary incontinence during ambulatory monitoring of bladder function by a temperature-sensitive device. Br J Urol 1996;77(2):194–7. 10. Wilson PD, Al Samarrai MT, Brown AD. Quantifying female incontinence with particular reference to the Urilos system. Urol Int 1980;35(4):298–302. 11. Eadie A, Glen E, Rowan D. Assessment of urinary loss over a two-hour test period: a comparison between the Urilos recording nappy system and the weighed perineal pad method. Proceedings of the 14th Annual Scientific Meeting of the International Continence Society, Innsbruck, 1984; 94–5.
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12. Holmes D, Plevnik S, Stanton SL. Distal urethral electric conductance (DUEC) test for the detection of urinary leakage. Proceedings of the 15th Annual Meeting of the International Continence Society, London, 1985; 94–5. 13. Adekanmi OA, Freeman RM, Reed H, Bombieri L. Improving the diagnosis of genuine stress incontinence in symptomatic women with negative cough stress test: the Distal Urethral Electrical Conductance test (DUEC) revisited. Int Urogynecol J 2003;14(1):9–12. 14. Frazer MI, Haylen BT, Sutherst JR. The severity of urinary incontinence in women. Comparison of subjective and objective tests. Br J Urol 1989;63(1):14–15. 15. Streiner D, Norman G. Health measurements scales: a practical guide to their development and use, 2nd ed. Oxford: Oxford University Press, 1995. 16. Khan KS, Chien PF, Honest MR, Norman GR. Evaluating measurement variability in clinical investigations: the case of ultrasonic estimation of urinary bladder volume. Br J Obstet Gynaecol 1997;104(9):1036–42.
investigation of female urinary incontinence. J Obstet Gynaecol 1988;8(3):270–3. 28. Landis J, Kock G. The measurement of observer agreement for categorical data. Biometrics 1977;33:159–74. 29. Wall LL, Wang K, Robson I, Stanton SL. The Pyridium pad test for diagnosing urinary incontinence: a comparative study of asymptomatic and incontinent women. J Reprod Med 1990;35(7):682–4. 30. Groen J, Bosch JLHR. Agreement between cystometry and noninvasive incontinence tests in stress incontinent females. Urodinamica 2002;12(1):4–9. 31. Paick J-S, Ja HK, Jae WS et al. Significance of pad test loss for the evaluation of women with urinary incontinence. Neurourol Urodyn 2005;24(1):39–43. 32. Nygaard I, Zmolek G. Exercise pad testing in continent exercisers: reproducibility and correlation with voided volume, pyridium staining, and type of exercise. Neurourol Urodyn 1995;14(2):125–9.
17. Versi E, Cardozo LD. Perineal pad weighing versus videographic analysis in genuine stress incontinence. Br J Obstet Gynaecol 1986;93(4):364–6.
33. Soroka D, Drutz HP, Glazener CM, Hay-Smith EJ, Ross S. Perineal pad test in evaluating outcome of treatments for female incontinence: a systematic review. Int Urogynecol J 2002;13(3):165–75.
18. Sutherst JR, Brown MC, Richmond D. Analysis of the pattern of urine loss in women with incontinence as measured by weighing perineal pads. Br J Urol 1986;58(3):273–8.
34. Thomson AJ, Tincello DG. The influence of pad test loss on management of women with urodynamic stress incontinence. BJOG 2003;110(8):771–3.
19. Wilson PD, Mason MV, Herbison GP, Sutherst JR. Evaluation of the home pad test for quantifying incontinence. Br J Urol 1989;64(2):155–7.
35. Devreese AM, De Weerdt WJ, Feys HM et al. Functional assessment of urinary incontinence: the perineal pad test. Clin Rehabil 1996;10(3):210–15.
20. Flisser AJ, Figueroa J, Bleustein CB, Panagopoulos G, Blaivas JG. Pad test by mail for home evaluation of urinary incontinence. Neurourol Urodyn 2004;23(2):127–9.
36. Fantl JA, Harkins SW, Wyman JF, Choi SC, Taylor JR. Fluid loss quantitation test in women with urinary incontinence: a test–retest analysis. Obstet Gynecol 1987;70(5):739–43.
21. Klarskov P, Hald T. Reproducibility and reliability of urinary incontinence assessment with a 60 min test. Scand J Urol Nephrol 1984;18(4):293–8.
37. Kinn A-C, Larsson B. Pad test with fixed bladder volume in urinary stress incontinence. Acta Obstet Gynecol Scand 1987;66(4):369–71.
22. Lose G, Gammelgaard J, Jorgensen TJ. The one-hour padweighing test: reproducibility and the correlation between the test result, the start volume in the bladder, and the diuresis. Neurourol Urodyn 1986;5(1):17–21.
38. Lose G, Rosenkilde P, Gammelgaard J, Schroeder T. Padweighing test performed with standardized bladder volume. Urology 1988;32(1):78–80.
23. Jørgensen L, Lose G, Andersen JT. One-hour pad-weighing test for objective assessment of female urinary incontinence. Obstet Gynecol 1987;69(1):39–42. 24. Simons AM, Yoong WC, Buckland S, Moore KH. Inadequate repeatability of the one-hour pad test: the need for a new incontinence outcome measure. BJOG 2001;108(3):315–19. 25. Bland JM, Altman DG. Statistical methods for assessing agreement between two methods of clinical measurement [see comment]. Lancet 1986;1(8476):307–10. 26. Christensen SJ, Colstrup H, Hertz JB. Inter- and intradepartmental variations of the perineal pad weighing test. Neurourol Urodyn 1986;5(1):23–8. 27. Versi E, Cardozo L, Anand D. The use of pad tests in the
39. Hahn I, Fall M. Objective quantification of stress urinary incontinence: a short, reproducible, provocative pad-test. Neurourol Urodyn 1991;10(5):475–81. 40. Artibani W, Andersen JT, Gajewski JB, Ostergard DR, Raz S, Tubaro A. Imaging and other investigations. In: Abrams P, Cardozo L, Khoury S, Wein A (eds) Incontinence. Plymouth: Health Publication, 2002: 425–77. 41. Ali K, Murray A, Sutherst J et al. Perineal pad weighing test: comparison of one hour ward pad test with twelve hours home pad test. Proceedings of the 13th Annual Meeting of the International Continence Society, Aachen, 1983; 380–2. 42. Lose G, Jorgensen L, Thunedborg P. 24-hour home pad weighing test versus 1-hour ward test in the assessment of mild stress incontinence. Acta Obstet Gynecol Scand 1989;68(3):211–15.
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43. Ryhammer AM, Laurberg S, Djurhuus JC, Hermann AP. No relationship between subjective assessment of urinary incontinence and pad test weight gain in a random population sample of menopausal women. J Urol 1998;159(3):800–3. 44. Versi E, Orrego G, Hardy E, Seddon G, Smith P, Anand D. Evaluation of the home pad test in the investigation of female urinary incontinence [see comment]. Br J Obstet Gynaecol 1996;103(2):162–7. 45. Mouritsen L, Berlid G, Hertz J. Comparison of different methods for quantification of urinary leakage in incontinent women. Neurourol Urodyn 1989;8(6):579–87. 46. Victor A, Larsson G, Asbrink AS. A simple patientadministered test for objective quantitation of the symptom of urinary incontinence. Scand J Urol Nephrol 1987;21(4):277–9. 47. Rasmussen A, Mouritsen L, Dalgaard A, Frimodt-Moller C. Twenty-four hour pad weighing test: reproducibility and dependency of activity level and fluid intake. Neurourol Urodyn 1994;13(3):261–5. 48. Groutz A, Blaivas JG, Chaikin DC et al. Noninvasive outcome measures of urinary incontinence and lower urinary tract symptoms: a multicenter study of micturition diary and pad tests. J Urol 2000;164(3 Pt 1):698–701. 49. Lin LI. A concordance correlation coefficient to evaluate reproducibility. Biometrics 1989;45(1):255–68. 50. Karantanis E, Allen W, Stevermuer TL, Simons AM, O’Sullivan R, Moore KH. The repeatability of the 24-hour pad test. Int Urogynecol J 2005;16(1):63–8. 51. Thind P, Gerstenberg TC. One-hour ward test vs. 24-hour home pad weighing test in the diagnosis of urinary incontinence. Neurourol Urodyn 1991;10(3):241–5. 52. Singh M, Bushman W, Clemens JQ. Do pad tests and voiding diaries affect patient willingness to participate in studies of incontinence treatment outcomes? J Urol 2004;171(1):316–8. 53. Griffiths DJ, McCracken PN, Harrison GM. Incontinence in the elderly: objective demonstration and quantitative assessment. Br J Urol 1991;67(5):467–71. 54. Matharu GS, Assassa RP, Williams KS et al. Objective assessment of urinary incontinence in women: com-
parison of the one-hour and 24-hour pad tests. Eur Urol 2004;45(2):208–12. 55. Jørgensen L, Steen A, Bagger P et al. The one-hour padweighing test for assessment of the result of female incontinence surgery. Proceedings of the 15th Annual Meeting of the International Continence Society, London, 1985; 392–3. 56. Elser DM, Fanti JA, McClish DK. Comparison of ‘subjective’ and ‘objective’ measures of severity of urinary incontinence in women. Neurourol Urodyn 1995;14(4):311–16. 57. Black N, Griffiths J, Pope C. Development of a symptom severity index and a symptom impact index for stress incontinence in women. Neurourol Urodyn 1996;15(6):630– 40. 58. Aslan E, Beji NK, Coskun A, Yalcin O. An assessment of the importance of pad testing in stress urinary incontinence and the effects of incontinence on the life quality of women. Int Urogynecol J 2003;14(5):316–19. 59. Abdel-Fattah M, Barrington JW, Youssef M. The standard 1-hour pad test: Does it have any value in clinical practice? Eur Urol 2004;46(3):377–80. 60. Sandvik H, Hunskaar S, Seim A, Hermstad R, Vanvik A, Bratt H. Validation of a severity index in female urinary incontinence and its implementation in an epidemiological survey. J Epidemiol Community Health 1993;47(6):497–9. 61. Sandvik H, Seim A, Vanvik A, Hunskaar S. A severity index for epidemiological surveys of female urinary incontinence: comparison with 48-hour pad-weighing tests. Neurourol Urodyn 2000;19(2):137–45. 62. Stach-Lempinen B, Kirkinen P, Laippala P, Metsanoja R, Kujansuu E. Do objective urodynamic or clinical findings determine impact of urinary incontinence or its treatment on quality of life? Urology 2004;63(1):67–71. 63. Karantanis E, Fynes M, Moore KH, Stanton SL. Comparison of the ICIQ-SF and 24-hour pad test with other measures for evaluating the severity of urodynamic stress incontinence. Int Urogynecol J 2004;15(2):111–16. 64. Miller JM, Ashton-Miller JA, DeLancey JOL. Quantification of cough-related urine loss using the paper towel test. Obstet Gynecol 1998;91(5 Part 1):705–9.
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IntroductIon
uroflowmeters
The International Continence Society (ICS) has defined urodynamic observations to be observations made during urodynamic studies. In general, a urodynamic observation may have a number of possible underlying causes and does not represent a definitive diagnosis of a disease or condition, and may occur with a variety of symptoms and signs, or in the absence of any symptoms or signs.1 This statement should also be borne in mind in urodynamic testing of voiding function. This chapter will deal with the urodynamic measurement of flow. Such measurement gives a representation of the volume of urine evacuated from a patient’s bladder per time sequence during voiding. Moreover, if this equation is represented in a curve, it may also give information of how this evacuation of urine proceeds. The clinical importance of both aspects of uroflowmetry is real. In daily life, the patient is usually her own and only flow observer, and the subjective interpretation of this observation may be translated into symptoms which may often need to be objectively confirmed. It is uncertain who measured uroflow for the first time in medical history. Before electronic flowmeters became available, clinicians sometimes asked their patients to time voiding and measure the voided volume. This allowed the calculation of an average flow rate. Other clinicians may have observed the flow themselves, thus permitting a semi-objective assessment of its strength, its continuity, its start and ending. Abrams stated that a urine flow study should be regarded as a screening test, an essential preliminary to all other urodynamic testing and a routine method of preoperative and postoperative assessment of lower urinary tract (LUT) surgery.2 The report of the ICS Standardization Committee3 on good urodynamic practices confirms this: uroflowmetry is non-invasive and relatively inexpensive. Therefore, it is an indispensable, first-line screening test for most patients with suspected LUT dysfunction. Objective and quantitative data, which help in the understanding of both storage and voiding symptoms, are provided by this measurement. As with all investigations, the value will depend on the way the test is performed, the quality of the measuring equipment used, and the knowledge of the individual who does the interpretation. One thing is certain: just as all other tests, uroflowmetry does not stand alone and should be used as part of the complete diagnostic workup to find the cause of symptoms or signs related to LUT dysfunction.
Historically, many different types of uroflowmeter have been proposed. Some were based on the principle of audio,4 weight,5 variations of a constant magnetic field,6 rotating disk, measurement of size and velocity of drops,7 and air displacement.8 Susset et al.9 compared weight, rotating disk, and air displacement techniques, and found all of them to have values and limitations. The ICS Working Party on Urodynamic Equipment produced a first report10 in 1987. They described the most commonly used uroflowmeters employing one of the following methods:
• The gravimetric method: This operates by measuring
•
•
the weight of the collected fluid or by hydrostatic pressure at the base of the collecting cylinder. In either case, the output signal is proportional to the mass of fluid collected. Gravimetric meters therefore measure accumulated mass, and mass flow rate is obtained by differentiation. The electronic dip-stick method: The electrical capacitance of a dip-stick mounted in the collecting chamber changes as the urine accumulates. The output signal is proportional to the accumulated volume and the volumetric flow rate is obtained by differentiation The rotating disk method: The voided fluid is directed onto a rotating disk, increasing the inertia of the disk. The power required to keep the disk rotating at a constant rate is measured and is proportional to the mass flow rate of the fluid. The accumulated mass is obtained here by integration.
The accuracy of uroflowmeters is discussed in the Good Urodynamic Practices report.3 There are differences in the accuracy and precision of the flow rate signals that depend on the type of uroflowmeter, on internal signal processing, and on the proper use and calibration of the flowmeter. The desired and actual accuracy of uroflowmetry should be assessed in relation to the potential information that could be obtained from the urinary stream compared to the information actually abstracted for clinical and research purposes. Some relevant aspects of the physiologic and physical information contained in the urinary stream are outlined in the report. The desired clinical accuracy may differ from the technical accuracy. The ICS report10 recommends a range of 0–50 ml/s for Qmax, 0–1000 ml for voided volume, and maximum time constant of 0.75 seconds as standards. An accuracy of ±5% relative to full scale is recommended, although a calibration curve representing the percent-
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age error over the entire range of measurement should be made available but is mostly still lacking. As most flowmeters are mass flowmeters, variations in the specific gravity of the fluid will have a direct influence on the measured flow rate. For example, urine of high concentration may increase apparent flow rate by 3%. With X-ray medium, the flow rate may be overestimated by as much as 10%. Correction by calibration software is possible. Since the overall accuracy of flow rate signals is no better than ±5%, it does not seem meaningful to report a maximum flow rate to a resolution better than a full milliliter per second. A better resolution may be possible under carefully controlled research conditions, but such improvements are not required for general clinical use, especially for free flow measurements.
assumed that it is normal for the mechanical properties of a relaxed outlet to be constant, and that the properties can be defined by the dependency of the cross-sectional area of the urethral lumen on the intraurethral pressure at the flow rate controlling zone. Below the minimum urethral opening pressure, the urethral lumen is closed. The lumen then opens widely with little additional pressure increase. The interpretation of a uroflow curve can be performed by measuring several parameters and by a gross interpretation of the curve itself.
symptoms related to flow1
• Maximum flow rate (Qmax) is the maximum
Urine flow can be described either as continuous (i.e. without interruption) or as intermittent, when an individual states that the flow stops and starts during a single visit to the bathroom in order to void. Slow stream is reported by the individual as her perception of reduced urine flow, usually compared to previous performance. One should realize that women have fewer reported classic obstructive symptoms than men, probably because they void in private and have little opportunity to compare voiding patterns.11 Splitting or spraying of the urine stream may be reported. Intermittent stream (intermittency) is the term used when the individual describes urine flow that stops and starts, on one or more occasions, during micturition. Hesitancy is the term used when an individual describes difficulty in initiating micturition, resulting in a delay in the onset of voiding after the individual is ready to pass urine. Straining to void describes the muscular effort used to initiate, maintain or improve the urinary stream. Terminal dribble is the term used when an individual describes a prolonged final part of micturition, when the flow has slowed to a dribble. Postmicturition dribble is the term used when an individual describes the involuntary loss of urine immediately after she has finished passing urine, usually after rising from the toilet in women. Uroflowmetry should aim to reproduce the symptoms that bring the patient to consultation.
parameters of uroflowmetry1 (Fig. 15.1) • Flow rate is defined as the volume of fluid expelled via the urethra per unit time, expressed in ml/sec.
• Voided volume is the total volume expelled via the urethra.
•
• •
•
measured value of the flow rate after correction for artifacts. Voiding time is the total duration of micturition, including interruptions. When voiding is completed without interruption, voiding time is equal to flow time. Flow time is the time over which measurable flow actually occurs. Average flow rate (Qaverage) is voided volume divided by flow time. The average flow should be interpreted with caution if flow is interrupted or there is a terminal dribble. Time to maximum flow is the elapsed time from onset of flow to maximum flow.
parameters of uroflowmetry measurement Normal voiding occurs when the outlet relaxes to passivity and the detrusor gets into active contraction. It is
Figure 15.1. Uroflowmetry recording (International Continence Society recommended nomenclature). 217
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General aspect of the curve The Good Urodynamic Practices guidelines3 state that an easily distensible bladder outlet with a normal detrusor contraction will result in a smooth arc-shaped curve with high amplitude. The shape of the curve is determined by the kinetics of the detrusor contraction, which – arising as it does from smooth muscle – does not show rapid variations. The continuous flow curve is defined either as a smooth arc-shaped curve or as fluctuating when there are multiple peaks during a period of continuous urine flow (Fig. 15.2). It is a widespread assumption that normal micturition behavior is reflected in a normal flow pattern. This would also mean that a normal flow curve would correspond with normal voiding and would even permit the exclusion of voiding difficulties. Pauwels et al.12 investigated the value of a normal flow pattern in four different groups: stress incontinent women, women with bladder overactivity, healthy
middle-aged volunteers, and healthy students. These women voided with a bell-shaped flow curve on pressure flow in 50, 65, 57, and 50%, respectively. Women who strained to void (a major component of dysfunctional voiding) managed to void a bell-shaped flow curve in 46, 60, 70, and 100%, respectively. This study demonstrates that a ‘normal’ bell-shaped flow curve does not exclude voiding dysfunction in women. Other shapes – such as flat, asymmetric, or with multiple interruptions – are indicative of abnormal voiding but are not specific as to cause. A decreased detrusor power and/or constant increased urethral pressure will both result in a lower flow rate and a smooth flat curve. A constrictive obstruction, such as urethral stricture with reduced lumen size, results in a plateau-like curve. The same pattern may also originate from a weak detrusor in aging females. Fluctuations in detrusor contractility or abdominal straining, as well as intermittent sphincter activity, may lead to complex flow rate patterns. Rapid changes in flow rate may be due to sphincter/pelvic floor contraction or relaxation, mechanical compression of the urethral lumen or interference at the meatus, or to changes in the driving energy as with straining. Rapid changes may, however, also be due to artifacts caused by interference between the stream and the collecting funnel, movement of the stream across the surface of the funnel or patient movements.
problems In uroflowmetry3 As already indicated, the shape of the flow curve may suggest specific types of abnormality, but reliable, specific, and detailed information about the cause for abnormal voiding cannot be derived from a flow curve alone. Therefore, measurement of the pressure–flow relationship is necessary. Urine flow rate measurement is influenced by several factors:
• Patients’ behavior and nervousness. • Age: Increased flow time and decreased flow rate
• Figure 15.2. Different types of uroflow curve: (a) normal; (b) undulating continuous; (c) intermittent flow rate; (d) prolonged flow rate.
were found in postmenopausal women by Sorensen et al.13 This might indicate that these women have reduced bladder contractility or a less compliant urethra. Madersbacher et al. also found flow rates to decrease with age.14 Detrusor contractility: For steady outflow conditions, all variations in flow rate are related to changes in detrusor activity alone. The detrusor contraction strength can vary with neurogenic, myogenic, and combined causes.
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• Bladder outflow resistance: With changes in outflow •
• •
•
•
•
•
resistance, flow rate will change if detrusor contractility is constant. Bladder volume: Qmax is physiologically dependent on bladder volume. A positive relation has been shown between initial bladder volume, voided volume, and Qmax.15 As the bladder volume increases and the detrusor muscle becomes more stretched, the potential bladder power and work associated with a contraction will also increase. This is most pronounced in the range from empty up to 150– 250 ml. At volumes higher than 400–500 ml, the detrusor may become overstretched and contractility may decrease again. There are large individual differences. The flow–bladder volume dependency will also vary with type and degree of pathology as, for example, in constrictive obstruction, where Qmax will be almost independent of volume. It is not uncommon for patients to void an insufficient volume. Most flowmeters require at least 100 ml for accurate measurement. Nomograms: These have been developed relating voided volume to Qmax and Qaverage.16,17 Technical considerations: The flow rate measurement is influenced by the technique and by the signal processing. Any part of a uroflowmeter (e.g. funnel or collecting device) will introduce modifications to the recording. Physically, the external urinary stream breaks into drops, not far from the meatus, with a high frequency that should be eliminated by signal processing for standard uroflowmetry. For free uroflowmetry, all intracorporeal modulations of the flow rate are physiologic artifacts and should be minimized (e.g. by asking the patient to relax and not to strain). Again, however, for precise interpretation of variations in the flow rate signal, simultaneously recorded pressure-flow recordings are needed. Influence of posture: Sitting in anteversion, retroversion, and forward bending (all without straining) showed no differences for peak flow, total flow time, and mean flow in healthy women.18 Irregularities of the curve were seen less frequently in the forward-bending position, suggesting that this position permits optimal relaxation of the pelvic floor muscles. Influence of straining: independent of the position on the toilet, straining was shown to increase the peak flow and mean flow rates but reduced the total voiding time.18 As discussed previously, straining can produce a bell-shaped flow curve.12 Influence of catheterization: One study showed no difference between pre- and post-instrumentation
•
•
flow rates.19 However, catheterization to fill the bladder in order to perform uroflowmetry can alter the flow parameters: Qmax and Qaverage can become lower, and time to maximum flow and duration of flow longer.20–22 In particular, the use of a catheter (7 Fr or above) can produce such a result.13 The effect of flexible cystoscopy was evaluated by Issa et al., although it is not clear if the study was in patients of both sexes or only in men. After instrumentation, the Qmax became significantly lower.23 Intra- and interobserver variability: This proved sizeable when done by four physicians with a minimum of 6 months’ experience in urogynecology and with an 8-week interval between both evaluations.24 This difference was not so large in the study by Jorgensen et al.25 when the evaluation showed that visually read values were significantly lower than the mechanically determined ones, especially for Qmax in abnormal curves. These authors conclude that automatic computerized evaluation of uroflow curves may be misleading and should not replace a visual evaluation. Valentini et al.26 developed a mathematical computer micturition model and used it to analyze uroflowmetry curves in healthy women and female patients. Curve-fitting led to the determination of critical events during flow, such as break point and plateau phase, providing additional information on detrusor function. The group developed the technique further into analyzing detrusor activity and motor neuron firing during micturition by means of modeling of urodynamic traces.27 Home uroflowmetry: By means of a portable device, this proved a more accurate technique because it facilitates multiple measurements in men.28 Home uroflowmetry is also applicable in women.29
recommendatIons for uroflowmetry3 • Provide a separate room, with clean material and • •
•
as few factors as possible that can interfere with the voiding (noise, disturbance, smell, insufficient light). For graphical scaling, 1 mm should equal 1 second on the x-axis and 1 ml/sec and 10 ml voided volume on the y-axis. A sliding average over 2 seconds should be used to remove positive and negative spike artifacts in order to make electronically read Qmax values more reliable, comparable, and clinically useful. Only flow rate values smoothed either electronically or manually should be reported: when reading Qmax graphically, the line should be smoothed by eye 219
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•
• • • • • •
into a continuous curve so that in each period of 2 seconds there are no rapid changes. The interpretation of any dynamic variation in free flow will rely on personal experience, can only be descriptive and, more generally, will remain speculative. Maximum urine flow rate should be rounded to the nearest whole number (e.g. 10.25 ml/sec recorded as 10 ml/sec). Voided volume and post-void residual volume should be rounded to the nearest 10 ml (e.g. 322 ml recorded as 320 ml). Maximum flow rate should always be documented, together with voided volume and post-void residual volume. If a flow/volume nomogram is used, this should be stated and referenced. Do more than one test, especially if the first one does not permit a clear interpretation. Measurement or estimation of the residual urine will improve interpretation of the test.
More recommendations were made by the Second International Consultation on Incontinence:30
• Flowmeter calibration should be checked regularly. • Patients should void with a ‘comfortably full bladder’.
• •
Since this may be difficult to arrange, the concept of a flow clinic, where patients may drink fluids and void a number of times, may be considered. After voiding, patients should be asked whether the void was representative of their usual pattern. Flow traces and the computer output-derived form should be carefully scrutinized for artifacts and corrected if necessary.
uroflowmetry data In healthy volunteers It is important to have data on an age-matched healthy population for the proper interpretation of urodynamic tests. Although selecting groups of healthy, symptomfree, and history-free volunteers is difficult, some authors have been successful, and the data from their studies are given in Table 15.1. Normal Qmax ranges between 12 and 30 ml/s32 depending on the voided volume. Average flow rates vary from 6 to 25 ml/s with a substantial overlap between normal and abnormal individuals. Voiding time varies from 10– 20 seconds at a volume of 100 ml to 25–35 seconds for a volume of 400 ml.33 Arbitrary criteria have been set by a number of authors to diagnose voiding difficulty: peak flow <15 ml/s and/
table 15.1.
Data from literature on parameters from free uroflowmetry in healthy, symptom-free and history-free women Wyndaele*
Pauwels et al.†
Population
10 healthy women
32 healthy women
Age (years)
24 (19–28)
49 ± 6 (38–60)
Voided volume (ml)
337.5 ± 234.2
340 ± 165
Qmax (ml/s)
30.5 ± 10.8
29 ± 12
Qaverage (ml/s)
21.5 ± 13.7
17.5 ± 8
Time to Qmax (s)
8.3 ± 8.1
7±3
Voiding time (s)
27.6 ± 22
23 ± 12
Flow time (s)
26 ± 20
20 ± 9
* Data from ref. 31. † Unpublished data. Qaverage, mean flow rate; Qmax, maximum flow rate.
or residual urine >50 ml, with a minimum total bladder volume of 150 ml before the void (volume voided + residual).34,35 Costantini et al.35 showed that these criteria accorded well with an evaluation with the Liverpool nomogram excluding voided volumes <15 and >600 ml, and accepting values below the 10th centile to be abnormal. Wyndaele31 compared the pattern of the uroflow curve in 10 young female volunteers and found seven to have a bell-shaped curve on free flow, one voiding in two separate curves, and two presenting a continuous but undulating curve during the entire flow. If compared to the curve pattern obtained during a subsequent pressure flow study, seven had the same pattern but three, with bell-shaped flow during free flow, had an irregular or interrupted flow pattern. Pauwels et al.12 found that on free uroflowmetry only 83% of middle-aged healthy women had a normal voiding pattern. In a young healthy group, this number was even less (75%). On pressure flowmetry, only half of the healthy women voided with a normal flow pattern. The flow patterns in free flow and in pressure flow corresponded in 47% to 75%, respectively, depending on patients’ symptoms. Free and pressure flow patterns matched better in healthy women than in patients. Miyata et al.36 analyzed voiding parameters in 36 healthy adult females and found voiding time a useful parameter. Voiding time was independent of the voided volume from 100 to 400 ml and never exceeded 21 seconds in all micturitions. Voiding time was shorter in healthy than in 84% of neurogenic patients and 67% of patients with chronic cystitis.
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uroflowmetry In clInIcal practIce • Uroflowmetry and menstrual cycle: No difference was
•
•
•
•
• •
seen in any measured uroflowmetry parameter when comparing similar voids between phases of the menstrual cycle. Therefore, when evaluating premenopausal patients, uroflowmetry may be scheduled and performed during either phase of the menstrual cycle.20 Uroflowmetry in pregnancy and puerperium: Significant increase in flow rate was seen in the second trimester only.37 Major opposite effects were seen from βadrenergics only in intravenous tocolysis. Flow rates were worse after forceps delivery but better after spontaneous delivery than in controls. However, all rates remained within normal range. Uroflowmetry in stress urinary incontinence (SUI). Bottaccini et al.38 contended that stress incontinent women void with a lower flow rate than healthy women because the distal urethral cross-sectional area appears to be incapable of opening as widely as the distal urethra of normal women. Other studies have demonstrated the opposite: SUI women void with a higher flow rate because of the reduced outlet resistance.39 Free flow appears to have a low predictive value for abnormal pressure/flow study in SUI with or without previous surgery.40 Uroflowmetry in genital prolapse: Peak flow rate, average flow rate, and voided volume have been described to be significantly lower than in healthy controls.29 Cystocele is significantly more frequent in patients with voiding difficulties, and the frequency of cystocele and voiding dysfunctions was shown to be significantly higher in women with abnormal uroflowmetry.35 Valentini et al.26 demonstrated a constrictive effect on outflow in women with various degrees of cystocele. A poor flow rate and elevated residual urine may be associated with a pronounced cystocele.41 Uroflowmetry in patients with large uterine fibroids: Peak flow rate, average flow rate, and voided volume were found to be significantly lower than in healthy controls in one study.29 Uroflowmetry in female voiding disturbances: Voiding difficulty, defined as abnormally slow and incomplete voiding, is often not suspected. Uroflowmetry in preoperative evaluation in incontinent women: Peak flow rate does not appear to be associated with postoperative retention in women following pubovaginal sling surgery.42 There is, however, some evidence that poor bladder emptying, as shown by an abnormally low flow rate and/or
•
•
residual urine, may predict voiding difficulties after surgery for stress incontinence.43,44 Uroflowmetry in women operated for SUI: Urodynamics at 1-year follow-up compared to preoperative data showed a statistically significant decrease in Qmax and an increase in post-void residual.45 By applying modeling of free uroflow, Fritel et al.46 showed compressive obstruction in 34/50 patients after tension-free vaginal tape (TVT) and due to the TVT. This counter-pressure results in continence. During voiding, this effect can be unmasked if the woman strains, resulting in lower flow rate and/or dysuria. The hypothesis of a constrictive obstruction with reduction of the cross-section of the urethra of about 60% was proposed for 27 patients. Uroflowmetry before and after radical hysterectomy for cervical cancer: Increased residual urine volumes and decreased uroflow rates were detected in one series.47 This was attributed to a significant reduction in detrusor contractility with concomitant abdominal straining due to impaired parasympathetic motor innervation.48 However, the values improved from baseline at 6 months after surgery.
conclusIon Uroflowmetry is a valuable, inexpensive, and fairly reliable screening tool in women suspected of LUT dysfunction. Practical application and interpretation have to follow strict rules. Uroflow does not stand alone, and the workup to establish a diagnosis needs to be completed with more extended urodynamic studies, when appropriate, as before surgery.
references 1. Abrams P, Cardozo L, Fall M et al. The standardisation of terminology of lower urinary tract function: report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 2002;21:167–78. 2. Abrams P. The practice of urodynamics. In: Mundy AR, Stephenson TP, Wein AJ (eds) Urodynamics. Principles, Practice and Application. Edinburgh: Churchill Livingstone, 1984; 76–92. 3. Schafer W, Abrams P, Liao L et al. Good urodynamic practices: uroflowmetry, filling cystometry, and pressure-flow studies. Neurourol Urodyn 2002;21:261–74. 4. Keitzer WA, Huffman GC. The voiding audiograph: a new voiding test. J Urol 1966;96:404–10. 5. Drake WM Jr. The uroflowmeter in the study of bladder neck obstructions. J Am Med Assoc 1954;156:1079–80.
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6. Cardus D, Quesada EM, Scott FB. Use of an electromagnetic flowmeter for urine flow measurements. J Appl Physiol 1963;18:845–7.
24. Chou TP, Gorton E, Stanton SL et al. Can uroflowmetry patterns in women be reliably interpreted? Int Urogynecol J Pelvic Floor Dysfunct 2000;11:142–7.
7. Zinner NR, Ritter RC, Sterling AM et al. Drop spectrometer: a non-obstructive, non-interfering instrument for analyzing hydrodynamic properties of human urination. J Urol 1969;101:914–8.
25. Jorgensen JB, Mortensen T, Hummelmose T et al. Mechanical versus visual evaluation of urinary flow curves and patterns. Urol Int 1993;51:15–8.
8. Palm L, Nielsen OH. Evaluation of bladder function in children. J Pediatr Surg 1967;2:529–35. 9. Susset JG, Picker P, Kretz M et al. Critical evaluation of uroflowmeters and analysis of normal curves. J Urol 1973;109:874–8. 10. Rowan D, James ED, Kramer AE et al. Urodynamic equipment: technical aspects. Produced by the International Continence Society Working Party on Urodynamic Equipment. J Med Eng Technol 1987;11:57–64. 11. Nitti VW, Tu LM, Gitlin J. Diagnosing bladder outlet obstruction in women. J Urol 1999;161:1535–40. 12. Pauwels E, De Wachter S, Wyndaele JJ. A normal flow pattern in women does not exclude voiding pathology. Int Urogynecol J Pelvic Floor Dysfunct 2005;16:104–8; discussion 108. 13. Sorensen S, Jonler M, Knudsen UB et al. The influence of a urethral catheter and age on recorded urinary flow rates in healthy women. Scand J Urol Nephrol 1989;23:261–6. 14. Madersbacher S, Pycha A, Schatzl G et al. The aging lower urinary tract: a comparative urodynamic study of men and women. Urology 1998;51:206–12. 15. Rollema HJ, Griffiths DJ, van Duyl WA et al. Flow rate versus bladder volume. An alternative way of presenting some features of the micturition of healthy males. Urol Int 1977;32:401–12. 16. Siroky MB, Olsson CA, Krane RJ. The flow rate nomogram: I. Development. J Urol 1979;122:665–8. 17. Haylen BT, Ashby D, Sutherst JR. Maximum and average urine flow rates in normal male and female populations – the Liverpool nomograms. Br J Urol 1989;64:30–8. 18. Devreese AM, Nuyens G, Staes F et al. Do posture and straining influence urinary-flow parameters in normal women? Neurourol Urodyn 2000;19:3–8. 19. Bergman A, Bhatia NN. Uroflowmetry: spontaneous versus instrumented. Am J Obstet Gynecol 1984;150:788–90. 20. Visco AG, Cholhan HJ, O’Toole L et al. Effects of menstrual cycle and urinary tract instrumentation on uroflowmetry. Neurourol Urodyn 2000;19:147–52. 21. Tessier J, Schick E. Does urethral instrumentation affect uroflowmetry measurements? Br J Urol 1990;65:261–3.
26. Valentini FA, Besson GR, Nelson PP et al. A mathematical micturition model to restore simple flow recordings in healthy and symptomatic individuals and enhance uroflow interpretation. Neurourol Urodyn 2000;19:153–76. 27. Valentini FA, Nelson PP, Besson GR. [Detrusor activity and motor neuron firing during micturition: analysis by means of modeling of urodynamic tracings.] Ann Readapt Med Phys 2003;46:594–600. 28. Boci R, Fall M, Walden M et al. Home uroflowmetry: improved accuracy in outflow assessment. Neurourol Urodyn 1999;18:25–32. 29. Porru D, Scarpa RM, Onnis P et al. Urinary symptoms in women with gynecological disorders: the role of symptom evaluation and home uroflowmetry. Arch Esp Urol 1998;51:843–8. 30. Homma Y, Batista J, Bauer S et al. Urodynamics. In: Abrams P, Cardozo L, Khoury S, Wein A (eds) Incontinence. Plymouth: Health Publication, 2002; 318–72. 31. Wyndaele JJ. Normality in urodynamics studied in healthy adults. J Urol 1999;161:899–902. 32. Blaivas JG. Techniques of evaluation. In: Yalla SV, McGuire EJ, Elbadawi A, Blaivas JG (eds) Neurourology and Urodynamics. Principles and Practice. New York: Macmillan, 1988; 155–98. 33. Kondo A, Mitsuya H, Torii H. Computer analysis of micturition parameters and accuracy of uroflowmeter. Urol Int 1978;33:337–44. 34. Romanzi LJ, Chaikin DC, Blaivas JG. The effect of genital prolapse on voiding. J Urol 1999;161:581–6. 35. Costantini E, Mearini E, Pajoncini C et al. Uroflowmetry in female voiding disturbances. Neurourol Urodyn 2003;22:569–73. 36. Miyata M, Mizunaga M, Saga Y et al. Micturition and uroflowmetric analysis of adult females. Nippon Hinyokika Gakkai Zasshi 1990;81:1071–8. 37. Fischer W, Kittel K. Urine flow measurement in pregnancy and the puerperium. Zentralbl Gynakol 1990;112:593–9. 38. Bottaccini MR, Gleason DM. Urodynamic norms in women. I. Normals versus stress incontinents. J Urol 1980;124:659–62.
22. Groutz A, Blaivas JG, Sassone AM. Detrusor pressure uroflowmetry studies in women: effect of a 7Fr transurethral catheter. J Urol 2000;164:109–14.
39. Lemack GE, Baseman AG, Zimmern PE. Voiding dynamics in women: a comparison of pressure-flow studies between asymptomatic and incontinent women. Urology 2002;59:42–6.
23. Issa MM, Chun T, Thwaites D et al. The effect of urethral instrumentation on uroflowmetry. BJU Int 2003;92:426–8.
40. Defreitas GA, Lemack GE, Zimmern PE. Nonintubated uroflowmetry as a predictor of normal pressure flow
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study in women with stress urinary incontinence. Urology 2003;62:905–8.
cal outcome? Int Urogynecol J Pelvic Floor Dysfunct 2000;11:285–9.
41. Coates KW, Harris RL, Cundiff GW et al. Uroflowmetry in women with urinary incontinence and pelvic organ prolapse. Br J Urol 1997;80:217–21.
45. Al-Badr A, Ross S, Soroka D et al. Voiding patterns and urodynamics after a tension-free vaginal tape procedure. J Obstet Gynaecol Can 2003;25:725–30.
42. Miller EA, Amundsen CL, Toh KL et al. Preoperative urodynamic evaluation may predict voiding dysfunction in women undergoing pubovaginal sling. J Urol 2003;169:2234–7.
46. Fritel X, Valentini F, Nelson P et al. Contribution of modeling to the analysis of mictional modifications caused by TVT: study of free uroflows. Prog Urol 2004;14:197–202.
43. McLennan MT, Melick CF, Bent AE. Clinical and urodynamic predictors of delayed voiding after fascia lata suburethral sling. Obstet Gynecol 1998;92:608–12. 44. Thompson PK, Duff DS, Thayer PS. Stress incontinence in women under 50: does urodynamics improve surgi-
47. Chuang TY, Yu KJ, Penn IW et al. Neurourological changes before and after radical hysterectomy in patients with cervical cancer. Acta Obstet Gynecol Scand 2003;82:954–9. 48. Scotti RJ, Bergman A, Bhatia NN et al. Urodynamic changes in urethrovesical function after radical hysterectomy. Obstet Gynecol 1986;68:111–20.
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16 Cystometry Hashim Hashim, Paul Abrams
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Definition Cystometry, part of urodynamic studies, is the measurement of relevant physiologic parameters taken during the filling and voiding phases of micturition, allowing direct assessment of lower urinary tract function.1 It is divided into two parts: 1. Filling cystometry: the method by which the relationship of pressure and volume in the bladder is measured during filling. 2. Pressure-flow studies of voiding: the method by which the relationship of pressure in the bladder and urine flow rate is measured during bladder emptying.
that will be answered by the investigation.6 Cystometry should be preceded by the completion of a voiding diary (e.g. frequency/volume chart) and multiple free uroflowmetry. Urodynamic tests should be considered in women:
• with mixed LUTS in whom surgery is contemplated • • • • •
Aims Cystometry is performed clinically as part of urodynamic investigations in patients complaining of lower urinary tract symptoms (LUTS) to help make a diagnosis and hence plan a suitable treatment or further appropriate investigations. Cystometry aims to evaluate detrusor and urethral function during the storage (filling) and voiding phases of micturition. It is essential that diagnoses made at the time of cystometry are related to the patient’s signs and symptoms and the physical findings at the time of examination. The aim is to reproduce the patient’s symptoms and to quantify the pathophysiologic processes, thus providing an explanation of the patient’s problems and an understanding of their implications. Cystometry can also be used for research purposes or to provide objective measurements following particular treatments.
inDicAtions Ideally, all patients with LUTS suggesting a bladder or urethral disorder should undergo urodynamic studies. The bladder is known as the ‘unreliable witness’: urinary symptoms alone do not always allow the correct diagnosis to be made and inappropriate treatment may be given.2–5 However, with limited resources and access to such a service, patients with ‘clear-cut’ symptoms can initially be managed empirically, for example, with pelvic floor exercises and now with duloxetine (serotonin norepinephrine reuptake inhibitor), available in some parts of the world for suspected stress urinary incontinence, and bladder training and antimuscarinic medication for overactive bladder syndrome and suspected detrusor overactivity (DO). Urodynamics should not be performed without clear indications and a proposed ‘urodynamics question’
(e.g. urgency/urgency incontinence and stress urinary incontinence); with a suspected voiding disorder; being considered for bladder neck surgery; with previous unsuccessful incontinence surgery; with neurogenic bladder disorders; in whom conservative and pharmacologic measures have failed; for example, physiotherapy for symptoms of stress incontinence, and antimuscarinic drug treatment and bladder training for symptoms of urgency.
PrePAring for cystometry Quality control during cystometry Quality control is vital to allow accurate, reproducible, and interpretable pressure readings and to allow identification of artifacts. The International Continence Society (ICS) has defined these steps in the 2002 Good Urodynamics Practices report:6
• Flushing: The manometer tubing connecting the
•
•
transducers must be flushed before setting zero to remove any air bubbles that could give low false pressure readings.7 Setting zero at atmospheric pressure: This can be done either prior to inserting the catheters into the patient or after insertion as long as the transducers are open only to atmosphere. Zero pressure is the value recorded when an external transducer is open only to the environment (the other two sides of a 3-way tap are closed) or when the open end of a connected, fluid-filled tube is at the same vertical level as the transducer before insertion into the patient. Calibrating the transducers: They should be calibrated at 0 and +100 cmH2O; the bladder intravesical pressure (pves) and rectal intra-abdominal pressure (pabd) lines should be in the positive range +5 to +50 cmH2O (depending on body position); the detrusor pressure (pdet) should be between 0 and +10 cmH2O; however, in clinical practice it can usually range from –5 to +10 cmH2O.8
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• Establishing a reference level for pressure: The superior border of the symphysis pubis is the fixed reference level for external and fluid-filled catheter systems; the transducers should be leveled to this horizontal plane so that all measurements have the same hydrostatic component. During the investigation, quality control is ensured by asking the patient to cough at regular (e.g. 1 minute) intervals (Fig. 16.1). Before recording is started, the patient is asked to cough and the pves and pabd traces are observed. An equal rise in the two pressure lines must be observed and a complete subtraction of these two pressures should result in no change of the pdet line. Sometimes a small artifactual biphasic blip (Fig. 16.1) is seen on pdet, but this also indicates acceptable subtraction. The biphasic blip occurs due to different speeds of transmission of impulses between the bladder and rectal lines, mainly in older urodynamic systems. The two blips of the biphasic wave should be equal in size; if they are not equal in height then this indicates poor quality control. The patient should cough before and after voiding to reconfirm quality control and that no displacement of catheters has occurred. During filling, the pves and pabd lines should not decline.
Patient position For convenience, the catheters are put in position with the patient supine after the physical examination (Fig. 16.2). Cystometry should then be done in the upright position: 1) because this is the physiologic position; and
Pump artifact
2) because the majority of women complain of symptoms when upright and active. It is expedient to ask the patient to sit on a commode with a flowmeter situated below it to measure any leakage of urine during the test, and also because most women void when sitting down. Some women complain of leakage when changing position (e.g. on bending over or getting up from the sitting position); these changes in posture can be mimicked during the test to try to reflect everyday stresses on the bladder and to provoke leakage. Whenever the patient’s position is altered, the position of the transducer must be readjusted to the pressure reference level of the upper border of the symphysis pubis. With the catheters in position, the filling catheter is connected to a suitable filling medium (see below). The rest of the equipment should be close to the patient for convenience and, if a computer screen is available, this should be in a position viewable by the patient so that explanations can be given during the test. If there is severe detrusor overactivity that prevents proper filling, even at a reduced rate (10–20 ml/min), then filling in the supine position may be required in order for any useful information to be gathered from cystometry. Reduced mobility or severe disablement of patients (e.g. by neurologic disease) may necessitate cystometry in the supine position.
filling medium Water and 0.9% (normal) saline are the fluids most frequently used as they are cheap, convenient, and mimic
Filling stopped
Figure 16.1. Normal cystometrogram with coughs showing equal rises on intravesical pressure (pves) and intra-abdominal pressure (pabd). Pump artifact can be seen on pves and detrusor pressure (pdet). Slower filling rate can be used to eliminate the artifact and often disappears if filling is paused. (Qura, flow rate in ml/s; Vinfus, volume infused.) 227
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2. Medium-fill cystometry between 10 and 100 ml/min; 3. Fast-fill cystometry when the rate is greater than 100 ml/min.
Peristaltic pump
Intravesical pressure (pves ) Computer Pressure transducers
Intra-abdominal pressure (pabd )
Tilting table
Figure 16.2. Catheter positions. Patient is supine only for catheter insertion.
urine in consistency. The fluid is commonly used at room temperature (22°C); however, body temperature (37°C) may be more physiologic. Cystometry has been performed with the filling medium warmed to body temperature with no observable difference in results;9 however, this has not yet been scientifically investigated and standardization is required. It is known that ice-cold infusion fluid can stimulate bladder contraction at low bladder volumes10 and therefore should not be used in routine cystometry. In the past, carbon dioxide has been used in gas cystometry11 but is no longer recommended as it is not a physiologic medium for the bladder, it dissolves in urine to form irritant carbonic acid, and it can cause pain in ‘hypersensitive’ bladders; furthermore, capacity measurement is inaccurate as the gas is both compressible and soluble in urine.12 In addition, it is not possible to obtain a pressure–flow analysis of the voiding phase of micturition after gas cystometry.
In the latest standardization report, the ICS no longer divides filling rates into slow, medium or fast. Currently, the term ‘non-physiologic filling rate’ is being used, and the precise filling rate should be stated. We recommend a filling rate of 50 ml/min, which, although convenient in the setting of a busy urodynamic unit, is not so fast as to be grossly unphysiologic; it also allows time to discuss symptoms with the patient and to assess whether those symptoms have been successfully reproduced. In a patient with very marked detrusor overactivity, the rate can be reduced to 30 ml/min or lower. Slower filling rates are indicated in patients with neurogenic bladders. Rapid filling is rarely used but can be a further provocative test for detrusor overactivity.
equipment Multichannel cystometry requires a urine flowmeter, two (or three) transducers, an electronic subtraction unit to derive pdet (pves – pabd), a recorder with a printout, and an amplifying unit (Fig. 16.3). All measurements are made in centimeters of water (cmH2O). The bladder pressure is measured using either:
• a fluid-filled line (a double-lumen or single-lumen
•
epidural catheter is inserted into the bladder and connected to an external pressure transducer; Fig. 16.4), or a solid micro-tip pressure transducer (a transducer is mounted on the tip of this solid 7 Fr catheter and
filling rates Previously, three filling rates were defined by the ICS:13 1. Slow-fill cystometry up to 10 ml/min;
Figure 16.3. Equipment: couch/cystometry unit/patient unit and flowmeter.
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Figure 16.4. From top to bottom: epidural catheter, rectal line, filling catheter.
Figure 16.5.
Solid catheter-tip transducer (Gaeltec).
of making rectal catheters; however, some companies make their own, more expensive, rectal catheters. It is important to remember that these commercial rectal catheters do not have a hole and thus if you keep on flushing, the balloon continues to expand, resulting in false rectal pressures. It is therefore advisable to make a small cut in the rectal balloon even if you are using a commercial rectal catheter. The reference height for all measurements is taken as being level with the upper edge of the symphysis pubis and the transducers are zeroed to atmospheric pressure. A double-lumen filling catheter (6 Fr) is inserted into the bladder via the urethra (or, occasionally, by the suprapubic route). Sometimes a single-lumen (8 Fr) filling catheter with a 16 G epidural catheter inserted alongside it can be used instead of the double-lumen. Double-lumen catheters are expensive and thus the twocatheter combination is a cheaper alternative that gives similar results. The single-lumen filling catheter is pulled out just before voiding and the epidural catheter is left in the bladder and used to measure pressure. The advantage of the double-lumen catheter is that the patient’s bladder can be filled and refilled multiple times should the test require it, and the post-void residual (if any) can easily be drained and measured through it; however, it is more expensive to use. The catheters are fixed in place by tape close to the external urethral meatus on the medial aspect of the thigh.
meAsurements The following measurements are made (Fig. 16.1):
hence is an internal pressure transducer system; Fig. 16.5). This catheter-mounted transducer eliminates artifacts arising from the fluid-filled system, which needs to be connected to an external transducer. Abdominal pressure is measured with a rectal (or occasionally vaginal)14 catheter (6 Fr manometer tubing covered with a fingerstall obtained from a non-sterile surgical rubber glove to prevent blockage by feces) which is inserted into the rectum to a distance approximately 10–15 cm above the anal margin. It is important to make sure that a small cut is made in the fingerstall to allow expulsion of fluid during flushing. If a hole is not made in the glove, then the pressure measured will be that of the water-filled balloon and not true rectal pressure. This line is taped to the patient’s buttock close to the anal verge to prevent any slippage during the test. The tubing must be flushed from the transducer end before recording is commenced. This is a very economical way
1. pves is measured with the bladder transducer via a urethral or suprapubic catheter; 2. pabd is taken as the pressure outside and around the bladder and measured with the rectal (or occasionally a vaginal) line; 3. pdet is obtained by subtracting the abdominal from the intravesical pressure (pdet = pves – pabd) and represents the pressure generated by the bladder wall, usually as detrusor contractions; 4. The volume infused into the bladder is recorded; 5. The urine flow rate, as leakage during filling and flow during voiding, is recorded. Measuring bladder and intra-abdominal pressure simultaneously ensures that any pressure changes observed can be interpreted correctly. A rise in the bladder pressure line could be due to either detrusor overactivity or abdominal straining being transmitted to the 229
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bladder. The electronic subtraction allows detrusor pressure to be measured and any change in pressure seen on the traces to be attributed appropriately. Detrusor function is assessed directly from observation of the pressure changes. Urethral function must be inferred from the pressure changes within the bladder, and by measuring any leakage during filling and urine flow during voiding.
methoD The test and all side effects (e.g. risk of urinary tract infection) should be fully explained to the patient and, in particular, the importance of indicating any bladder sensations during the test, as they happen, should be emphasized. The symptoms can then be used to annotate the cystometry trace and help with interpretation. Before cystometry is performed, the patient undergoes free uroflowmetry. Any residual urine on subsequent catheterization is then measured.
filling cystometry The filling phase starts when filling commences and ends when the patient is given permission to void by the urodynamicist. Bladder sensation, detrusor activity, bladder compliance, bladder capacity, and urethral function can all be assessed during this procedure.
Bladder sensation During the filling phase the patient is asked to indicate the following:
• first desire to void (FDV) – this sensation may not • •
be truly representative, owing to the interfering presence of the catheter; strong desire to void (SDV); urgency (sudden compelling desire to void).
These volumes should be noted. The above terminology has been defined by the ICS.10 Other terms that are also used during filling cystometry and related to bladder sensation include first sensation of bladder filling, and bladder pain and bladder sensation which can be categorized as increased, normal, reduced, absent or non-specific (seen mainly in neurologic patients). Bladder hypersensitivity is a term that has been used in the past and found to be helpful.9 It was defined as a condition where there is an early FDV at less than 100 ml and this persists and worsens, limiting the bladder cystometric capacity to 250 ml. This term has now
been replaced with the term ‘increased bladder sensation’, which is an early first sensation of bladder filling (or an early desire to void) and/or an early strong desire to void, which occurs at low bladder volume and which persists. The new term is subjective and thus it is not possible to quantify volumes.
Detrusor activity Detrusor activity is described as either ‘normal’ or ‘overactive’. A normal detrusor allows bladder filling with little or no change in pressure, with no involuntary phasic contractions occurring during cystometry, despite provocation.1 The presence of involuntary phasic detrusor contractions, occurring throughout filling, is diagnosed by detecting a rise in the detrusor pressure line (there is no lower limit for the amplitude of an involuntary detrusor contraction) and a similar rise in the vesical line with no rise in the abdominal line during filling cystometry (Fig. 16.6). The patient should be asked whether there is any associated urgency and if the sensation mimics the one that is normally experienced and causes problems. Precipitating factors such as coughing or running water, used to provoke symptoms, may also induce detrusor overactivity and should be noted. If the detrusor is shown during cystometry to contract spontaneously or with provocation, then it is said to have phasic detrusor overactivity. Some women will not experience any symptoms at the time of these contractions, in which case the significance of detrusor overactivity is unknown. If a single involuntary detrusor contraction occurs at the end of filling, resulting in incontinence, with no overactivity during filling, then this is known as terminal detrusor overactivity. When there is a known neurologic condition (e.g. multiple sclerosis), any detrusor overactivity observed is termed neurogenic detrusor overactivity (this replaces the older term of detrusor hyperreflexia). Detrusor overactivity is idiopathic if there is no identified cause.
Bladder compliance The term bladder compliance describes the relationship between change in bladder volume and detrusor pressure (∆V/∆pdet) and is measured in ml/cmH2O. As a normal bladder fills there is very little or no change in the pressure (i.e. the bladder is a low-compliance system). As filling rates can alter bladder compliance, the filling rate of cystometry must always be documented. In neurologically normal women, reduced compliance is usually artifactual owing to the bladder being filled excessively fast. Should compliance start to rise during filling, the filling should be stopped for approximately 1 minute to see if
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a detrusor contraction (Fig. 16.7). When filling volume reaches 200 ml, the patient is asked to strain and then to cough to observe any leakage during these two maneuvers which tend to increase intra-abdominal pressure above urethral closure pressure.
Voiding cystometry
Leak
Figure 16.6. Cystometrogram showing detrusor overactivity and detrusor overactivity incontinence (leak). (pabd, intraabdominal pressure; pdet, detrusor pressure; pves, intravesical pressure; Qura, flow rate in ml/s; Vinfus, volume infused.) the compliance returns to normal: if compliance returns to normal, the increase is artifactual and secondary to fast filling; if compliance does not return to normal, then it is secondary to a pathologic condition.
Urethral function During the filling phase, in normal women, the urethral closure pressure remains positive (i.e. it is greater than the intravesical pressure), even at times of increased intra-abdominal pressure; hence, continence is maintained. To allow voiding, closure pressure falls as the urethra relaxes. If involuntary loss of urine is observed without detrusor activity, then the urethral closure mechanism is said to be incompetent. A diagnosis of urodynamic stress incontinence can be made if leakage is associated with an increase in intraabdominal pressure that causes the intravesical pressure to exceed the intra-urethral pressure in the absence of
At the end of filling, the bladder-filling catheter is removed (only if filling and epidural catheters are used instead of a double-lumen catheter) to avoid any artifacts during voiding as a result of urethral obstruction. If leakage has not been noted during the filling phase, the patient is asked to cough a few times. If leakage is still not noted at this time, the patient is asked to stand and is given provocative instructions (stand with legs apart and cough, star jumps, squatting, hand washing) to try to induce leakage. The patient, now back on the commode with the intravesical and rectal pressure catheters still in situ, is instructed to void and the detrusor pressure and urine flow rate are recorded simultaneously. Detrusor pressure at maximum flow (pdetQmax) and flow rate are recorded. Voluntary initiation of a detrusor contraction is required for normal micturition and this is normally sustained until the bladder is empty. The pressure rise is dependent on the outlet resistance and on the contraction of the detrusor itself (Table 16.1): if the detrusor pressure is low with low flow rates, the detrusor is defined as underactive; if the pressure is high with low or normal flow rates, this may be indicative of an obstructive problem. If the detrusor muscle is functioning normally, then abdominal straining should not be required. Many nomograms have been suggested as being able to diagnose bladder outlet obstruction and detrusor underactivity in women; however, neither the ICS nor the International Consultation on Incontinence (ICI) has yet adopted a nomogram for women and none has been widely used or universally accepted. A further rise in detrusor pressure after the completion of voiding or an ‘after-contraction’ is sometimes seen at the end of a completed void, especially in patients with detrusor overactivity; however, the significance of this finding is unknown. The patient is asked to cough at the end of voiding to check for quality control, and to ensure that the pves measuring catheter has not moved out of the bladder during voiding. If it has, then the pves data for voiding should be regarded as unreliable.
PitfAlls of cystometry To ensure accurate measurements, the bladder line, rectal line and all tubing should be flushed to ensure that all 231
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Leak
table 16.1.
Figure 16.7. Cystometrogram showing urodynamic stress incontinence with coughing. Although the downspikes during coughing are bigger, the fine details subtract out completely, demonstrating that this is a good quality trace. (pabd, intra-abdominal pressure; pdet, detrusor pressure; pves, intravesical pressure; Qura, flow rate in ml/s; Vinf, volume infused.)
Leak
Lower urinary tract function according to clinical diagnosis, detrusor and urethral action during the filling and voiding cycles of micturition with possible urodynamic diagnosis Urodynamics
Clinical diagnosis
Detrusor
Urethra
Diagnosis
Normal
Stable
Competent
Normal
SUI
Stable
Incompetent
USI
OAB
Overactive
Competent
DO
OAB + SUI
Overactive
Incompetent
DO + USI
Neurogenic
Underactive
Relaxed
Underactive
Normal
Normal
Relaxed
Normal
POP
High/normal pressure
Obstructed
BOO
Filling phase
Voiding phase
BOO, bladder outlet obstruction; DO, detrusor overactivity; OAB, overactive bladder; POP, pelvic organ prolapse; SUI, stress urinary incontinence; USI, urodynamic stress incontinence.
air bubbles have been removed before recording begins. In addition, all connections should be tight, as any leak will cause errors in the pressure measurements recorded. Pressure values will tend to be lower, and recorded with a delay, if there are bubbles or leaks in the pressure system.
Rectal contractions can sometimes be seen on the recording trace (Fig. 16.8) and may be misinterpreted as detrusor overactivity; it is, therefore, important to be aware of rectal activity. If possible, the patient should have an empty rectum. If the rectal line slips slowly dur-
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Rectal contractions
100 80 pabd cmH20
pves cmH20 pdet cmH20
Flow ml/s
60 40 20 0 60 40 20 0 60 40 20 0 60 40 20 0 00:40
01:20
02:00
02:40
ing the recording, the pabd line will be seen to drift downwards, which could be incorrectly interpreted as a rise in the detrusor pressure and reduced compliance. Careful examination of the intravesical line shows the bladder pressure to be constant and should allow this false reading to be noticed. Quality control at the start of each cystometry is vital, and should be repeated at regular intervals during the test and again at the end of the test to ensure that good pressure transmission is continuing. This is done by asking the patient to cough and seeing an equal rise in the abdominal and vesical line with no rise (or a small biphasic deflection in a fluid-filled system) on the detrusor line.
normAl cystometry Cystometry of a normal bladder shows the following: 1. Residual urine of less than 50 ml; 2. First desire to void between 150 and 200 ml; 3. Capacity (taken as strong desire to void) between 300 and 600 ml; 4. Little or no detrusor pressure rise on filling (Fig. 16.9); 5. Absence of detrusor contractions during the filling phase; 6. No leakage on coughing; 7. No detrusor contraction provoked by coughing or running water (precipitating factors); 8. A maximum voiding detrusor pressure of less than 50 cmH2O, with a maximum flow rate greater than 15 ml/s for a volume greater than 150 ml. If cystometry has been performed for storage symptoms, then at the end of the test the question that
03:20
04:00
has to be answered is: ‘Did the cystometry succeed, partially succeed or fail to reproduce the patient’s symptoms?’
conclusions Cystometry is a component of urodynamic studies to investigate lower urinary tract dysfunction. It is vital that women are assessed with a proper history and examination, and the results of the cystometric findings evaluated in light of the signs and symptoms with the aid of voiding diaries. The majority of women will have their symptoms explained, and/or further management decisions can be made from conventional cystometry. Further cystometry can be performed using ambulatory monitoring over a longer period of time and in more natural circumstances, together with video cystourethrography for simultaneous assessment of the anatomy.
80 pdet(cmH2O)
00:00
Figure 16.8. Cystometrogram showing rectal contractions. (pabd, intra-abdominal pressure; pdet, detrusor pressure; pves, intravesical pressure.)
60 40 20 0
200
400 Volume (ml)
600
800
Figure 16.9. Normal filling cystometrogram showing minimal increase in detrusor pressure (pdet). The filling speed is 50 ml/min, the patient is seated, the bladder capacity is 403 ml, and the first desire to void is at 160 ml. 233
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references 1. Abrams P, Cardozo L, Fall M et al. The standardisation of terminology of lower urinary tract function: report from the Standardisation Subcommittee of the International Continence Society. Neurourol Urodyn 2002;21(2):167–78. 2. Cardozo LD, Stanton SL. Genuine stress incontinence and detrusor instability – a review of 200 patients. Br J Obstet Gynaecol 1980;87(3):184–90. 3. Shepherd AM, Powell PH, Ball AJ. The place of urodynamic studies in the investigation and treatment of female urinary tract symptoms. J Obstet Gynecol 1982;3:123–5. 4. Largo-Janssen AL, Debruyne FM, van Weel C. Value of the patient’s case history in diagnosing urinary incontinence in general practice. Br J Urol 1991;67(6):569–72. 5. Jarvis GJ, Hall S, Stamp S et al. An assessment of urodynamic examination in incontinent women. Br J Obstet Gynaecol 1980;87(10):893–6. 6. Schäfer W, Abrams P, Liao L et al. Good urodynamic practices: uroflowmetry, filling cystometry and pressure flow studies. Neurourol Urodyn 2002;21(3):261–74. 7. Byrne DJ, Stewart PA, Gray BK. The role of urodynamics in female urinary stress incontinence. Br J Urol 1987;59(3):228–9.
8. Sullivan J, Lewis P, Howell S et al. Quality control in urodynamics: a review of urodynamic traces from one centre. BJU Int 2003;91(3):201–7. 9. Abrams P. Urodynamic techniques – cystometry. Urodynamics, 2nd ed. London: Springer-Verlag, 1997; 17–117. 10. Åslund K, Rentzhog L, Sundström G. Effects of ice-cold saline and acid solution in urodynamics. Proceedings of the International Continence Society 18th annual meeting. Oslo, Norway, 1988; 1–2. 11. Torrens MJ. A comparative evaluation of carbon dioxide and water cystometry and sphincterometry. Proceedings of the International Continence Society 7th Annual Meeting. Portoroz, Slovenia, 1977; 103–104 [abstract 46]. 12. Wein AJ, Hanno PM, Dixon DO et al. The reproducibility and interpretation of carbon dioxide cystometry. J Urol 1978;120(2):205–6. 13. Abrams P, Blaivas JG, Stanton SL et al. The standardisation of terminology of lower urinary tract function. The International Continence Society Committee on Standardisation of Terminology. Scand J Urol Nephrol Suppl 1988;114:5–19. 14. James ED, Niblett PG, MacNaughton JA et al. The vagina as an alternative to the rectum in measuring abdominal pressure during urodynamic investigations. Br J Urol 1987;60(3):212–6.
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17 Pressure–flow plot in the evaluation of female incontinence and postoperative obstruction Philippe Zimmern, Jason P Gilleran
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INTRODUCTION The definition of bladder outlet obstruction (BOO) in women remains controversial since it is a much less frequent condition than in men, and the leading etiologies resulting in BOO are more complex and not just limited to prostatic conditions. For men with lower urinary tract symptoms (LUTS) secondary to benign prostatic enlargement, several nomograms are available but it is now accepted that these cannot be applied to obstruction in women. Because the definition is uncertain, the prevalence of BOO is unknown and has been estimated to be between 2.7 and 8% of women in large urodynamic database studies.1,2 In its purest form, the only means of defining BOO is by the pressure–flow study (PFS) portion of the urodynamic study (UDS). After briefly exploring limitations of the PFS, this chapter will focus on PFS interpretation and its role in the evaluation of female incontinence and in patients with voiding complaints in whom obstruction is clinically suspected.
BIOMECHANICS OF THE LOWER URINARY TRACT Voiding is governed by the bladder (which facilitates storage of urine and, in most cases, provides the driving force behind emptying) and by the urethra (which acts not only as a major continence mechanism but also as a point of outlet resistance in a variety of pathologic states). To aid understanding of the clinical aspects of the pressure–flow study, we will review the physiology of the ‘pump’ (bladder) and the ‘pipe’ (urethra) and attempt to understand their relationship.
The bladder The mechanical properties of smooth muscle, such as the detrusor, have not been explored as thoroughly as those of striated muscle, but the general principles relevant to striated muscle provide a valid approximation.3 In addition, these tissue properties appear to be organspecific and not gender-specific. Muscle contraction is dependent upon the tension and the speed at which the muscle can shorten. The maximum isometric force (when there is no shortening allowed) is dependent primarily upon the velocity of shortening of the muscle in a manner similar to that described by Hill4 for striated muscle. The equation that describes this relationship is: (F/Fiso + a/Fiso)(u + b) = (1 + a/Fiso) b
where b and a/Fiso are constants independent of the degree of extension, Fiso is the isometric force of the
bladder, F/Fiso is the ratio of observed force of contraction to isometric force and u is the speed of shortening. Griffiths adapted the Hill equation to the bladder and described the bladder output relation (BOR) relating detrusor pressure to urinary flow.5 This adaptation was achieved by mathematically relating the changes in a single strip of bladder to the changes occurring in the whole bladder. If the bladder is treated as a simple sphere of radius R, then the detrusor pressure (pdet) is given by: pdet = T/πR2
where T is the total tension across the bladder circumference and R is the radius of the sphere. This relates detrusor pressure, measured clinically, to the tension measured in muscle strips in laboratory experiments.6 Likewise, a relationship between linear speed of shortening of a bladder strip and flow rate from the bladder may be derived: (pdet/pdet,iso + a/Fiso)(Q + Q*) = (1 + a/Fiso) Q*
where Q is the flow rate from the bladder and Q* is a volume-dependent measure of the speed of shortening of the bladder muscle.7 The detrusor pressure is dependent upon both the volume of urine within the bladder and the outlet resistance, with an optimal pressure–flow relationship obtained during the plateau phase of voiding. The isovolumetric detrusor pressure is largely volume independent and may be used to assess the contractile function of the bladder. The stop test – voluntary cessation of voiding – may be performed to determine a value for isometric pressure (pdet.iso). Using the values on the pressure–flow plot just before and just after the stop test, a straight line may be plotted to give an approximate value for Q*, which is reasonably accurate provided that the detrusor pressure during flow is more than half of the pdet.iso. Because of the volume dependence of Q*, the bladder volume should be above 200 ml. In practice, assessment of detrusor contractile function is difficult: the shape of the relationship, the dependence on bladder volume, and variations during voiding all complicate the process. ‘Watts factor’, which represents the power of the bladder during contraction, may be calculated from pdet, flow rate, and bladder volume at any point during a void, but has not yet found much clinical relevance.8 The hydrodynamic findings thus far described reflect ‘normal’ bladder function. Prolonged obstruction has been shown to impair detrusor contractile function that may persist even after the relief of obstruction. Based on studies in the male rabbit, the initial stages of
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obstruction (approximately 2 weeks) are characterized by focal hypoxia, increased bladder mass secondary to increased vascularization (angiogenesis) and blood flow.9 The point at which the bladder enters a ‘decompensation’ stage – which features decreased blood flow, altered compliance, and contractile responses to electrical stimulation, as well as increased deposition of connective tissue elements – depends on the severity and duration of obstruction. Bladder wall ischemia is at least partially contributory to these changes.9 Age at which obstruction occurs also appears to have an impact. Although the physiologic alterations as a response to partial outlet obstruction are similar, more extensive histologic damage has been observed in younger rabbits compared to adult counterparts.10 How much of these findings in male animal models apply to BOO in women is unknown. Additionally, obstruction in the animal model is created acutely whereas the clinical setting of obstruction in women can be both acute (obstruction from a sling) or chronic (large cystocele or urethral pathology).
The urethra The properties of the urethra interact with the contracting detrusor throughout voiding. Thus, the urethral outlet resistance modulates the performance of the bladder and influences what may be measured clinically. A prior edition of this book covered urethral properties influencing flow in men, treating the urethra as an elastic, distensible tube, the properties of which change throughout voiding.11 In women, much less is known regarding urethral resistance and the flow-controlling zone, other than what has been measured by urodynamic testing in controls. Note that patients with stress incontinence cannot serve as controls since it was found that they have a lower urethral resistance compared to age-matched controls.12,13 Certainly, urethral resistance in neurologically intact women plays a lesser role than in men. A good example of a unique voiding mechanism in women is urethral relaxation with no demonstrable rise in detrusor pressure and a normal flow.
RECORDING THE PRESSURE–FLOW PLOT The PFS represents a graphic record of the relationship between the detrusor contraction and the flow rate over time. As described in Chapter 16, detrusor pressure is measured by subtraction cystometry using vesical and rectal catheters which read the intravesical and intraabdominal pressures, respectively, and is expressed in centimeters of water (cmH2O). The flow is measured by
a number of methods – rotating disc, air displacement, etc.14 – and expressed in milliliters per second (ml/s). These two measurements, alone or combined, provide some information on the voiding function; however, these findings can be affected by several factors (Table 17.1). After briefly reviewing the parameters affecting the PFS, we will discuss its interpretation and its role in female incontinence and postoperative obstruction.
Factors affecting the pressure–flow study Catheter effects As in men,15 the presence of a catheter alone can affect flow rates. In one study that examined flow rates in 20 healthy female volunteers with and without a 6 Fr double-lumen urethral catheter in place, a significant difference in mean maximum flow rate (Qmax) values (22.65 ml/s vs 16.25 ml/s, p=0.0006) was observed.16 Similar findings were noted in another study which compared the free-flow Qmax values in 100 women to PFS with a 7 Fr catheter in place, excluding those in whom the non-intubated flow (NIF) voided volumes differed by >20% from the PFS voided volume.17 The mean Qmax was significantly higher in free compared to intubated flow (26.9 vs 13.9 ml/sec, p<0.001) and a higher percentage of patients had an intermittent, interrupted flow curve during PFS. Placing two catheters during filling cystometrogram, with removal of the larger filling catheter prior to voiding, is another option that has been studied. A study of 33 women with a variety of LUTS used a 12 Fr catheter for filling.18 This large catheter was then removed, leaving only a 4 Fr urethral pressure catheter for pressure–flow recording. No significant difference was observed between free Qmax and intubated Qmax across different categories of voided volumes (101–250, 251–500, and >500 ml). More recently, the effect of catheter diameter during PFS was investigated. A prospective study randomized 239 women to a 7 or 9 Fr catheter for PFS. Regardless of catheter size, a significantly lower level of Qmax was noted compared to free flow in each subset of volume voided from 150 to 400 ml and over.19 Catheter size was not shown to have an impact on diagnosing BOO when using the criteria Qmax ≤15 ml/s and pdetQmax ≥20 cmH2O.
Prolapse reduction Significant pelvic organ prolapse, particularly cystocele, can mechanically obstruct the bladder neck by creating an angulation at the urethrovesical junction. This finding may be more pronounced after a prior anti-incontinence procedure if this particular procedure also added an element of outlet obstruction. Reducing the cystocele 237
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Table 17.1. ‘Troubleshooting’ the pressure–flow study in women ‘Action’
Effect on PFS
‘Reaction’
Change in pressure readings in relation to position of transducers
Adjust transducers to upper edge of symphysis pubis. Annotate tracing ‘sit’, then ‘transducers adjusted’
Inability to detect changes in pabd or pves makes the pdet measurement invalid
Confirm recording with pre-void cough and verify pressure agreement between pves and pabd
Loss of tracing for either pabd or pves renders pdet uninterpretable
Reinsert catheter, secure properly. Refill to capacity, and repeat PFS
Drop in pabd secondary to pelvic floor relaxation
Decrease in pabd artificially raises the pdet (by subtraction)
Measure ∆pves (change from pves at baseline to pves at Qmax) to determine true detrusor contraction
Patient unable to void
No flow generated; difficult to interpret true obstruction vs catheter effect
Give patient privacy and time to relax. May stimulate patient with sound of running water. Otherwise, may need to rely on NIF only
Straining during voiding (Valsalva voiding)
Elevation of pabd may artificially lower the pdet, or no pdet is recorded when pabd = pves (both pressure lines mirror each other)
Possible catheter artifact. Repeat PFS and/ or NIF to confirm same voiding pattern
Inability to detect changes in pabd or pves makes the pdet measurement invalid
Confirm recording with cough at end of void to verify pressure agreement between pves and pabd. (Note: vesical recording may be blunted or absent if bladder is empty)
Pre-void Positional change: standing to sitting
Poor recording from one or both catheters prior to voiding study During void Expulsion of bladder or rectal catheter
Post-void Poor recording from one or both catheters during voiding study
NIF, non-intubated flow; pabd, intra-abdominal pressure; pdet, detrusor pressure; PFS, pressure–flow study, pves, intravesical pressure.
may relieve obstruction (Fig. 17.1). Urinary retention, defined as post-void residual (PVR) ≥100 ml, was eliminated in 18/24 (75%) of women who underwent reduction of stage 3 and 4 anterior vaginal wall prolapse with a pessary prior to repair.20 This ‘pessary test’ involved an outpatient trial of pessary reduction followed by preoperative UDS and PVR by in–out catheterization, and was predictive of a low PVR after prolapse repair. Using alternative methods of reduction (speculum, swab, or physician’s fingers), another study also demonstrated normalization of PVR after surgical correction and found these methods predicted postoperative voiding function if the preoperative study was normal.21 Among the cystocele reduction methods, a vaginal pack has been recommended as a less operator-dependent and interfering method during UDS. However, conceivably such a pack could be too tight and artificially obstruct the bladder neck. A recent study noted a low incidence of pack-induced obstruction and a high frequency of BOO resolution during PFS with the pack in place.22
Patient position during voiding The effect of position on voiding is very important for obstructed patients. Maneuvers such as bending forward, tilting sideways, half-standing, or leaning back are often reported by these patients and can favorably influence the test results. Most published data are on non-invasive flow23 and sometimes relate to cultural differences (squatting versus sitting).24 Reporting on patient positioning during PFS is critical to a proper interpretation of the study, and should be clearly annotated on the PFS tracing.
Filling medium Saline, sterile water, or iodinated contrast can be used as the filling fluid depending on whether conventional or videourodynamics is being performed. The higher specific gravity of contrast may falsely elevate the Qmax by as much as 10% (as compared to water, saline, or urine of normal concentration) when the flow is measured by weight transduction.25
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Figure 17.1. Standing lateral voiding cystourethrogram demonstrating normal bladder and urethral position in a woman with a large cystocele on physical examination reduced by a tampon in place (arrow) which is visible due to absorption of voided contrast. The bladder neck and urethra, as well as the symphysis pubis, are outlined in this voiding view (dashed lines).
Pressure–flow Study INTERPRETATION Firstly, a brief review of how an ideal PFS tracing should look in order to be considered valid and interpretable is warranted. A representative tracing is depicted in Figure 17.2. Before the study, the transducers are opened to air and ‘zeroed’ to atmosphere according to good urodynamic practices.25 The bladder is filled to maximum cystometric capacity (MCC). In some studies, the patient remains sitting throughout; in others the patient may be standing for the filling cystometry. It is important, in this situation, to annotate when the patient sits to void and when the transducers are readjusted to the upper edge of the symphysis pubis. A cough confirms agreement of pressure transmission from both catheters and a PFS baseline is established as a reference point before the start of voiding. During voiding, a parallel rise in intravesical pressure (pves) and pdet , with minimal or no change in intra-abdominal pressure (pabd), is observed, indicating a detrusor contraction of normal amplitude and duration accompanied by a normal, ‘bell-shaped’ flow curve. At completion of the detrusor contraction, a post-void cough is performed to confirm that both catheters functioned adequately during voiding. Alterations in the pdet curve can be due to artifact (Fig. 17.3) or variable voiding pat-
terns that may be considered ‘normal’ in some women (Fig. 17.4). Following these guidelines is expected but not always realized in real-life practice. A recent ‘quality control’ review of 100 male PFS tracings at one center focused on frequency of cough annotations before and after voiding and on pressure concordance between pabd and pves during each cough. A grading system was recommended, with the best cough having a 70–100% concordance (grade A) which occurred in 86% of cases.26 Furthermore, an ideal tracing, even in a normal subject, is not always easily obtainable due to several artifacts, which must be recognized and corrected during the test. Simple adjustments to obtain a valid and interpretable PFS tracing are suggested in Table 17.1. In cases where the tracing is severely altered and cannot be interpreted, the test should be repeated until a valid and plausible tracing is obtained.
Electromyography (EMG) One simple method to document pelvic floor relaxation during voiding employs surface patch EMG. Needle electrodes have also been recommended to document urethral relaxation.27 EMG amplitude at rest with an empty bladder is usually 20–100 microvolts, and activity will typically increase as the bladder is filled and with coughing or straining.28 During normal voiding, pelvic floor relaxation is reflected in the silencing or minimal activity on the EMG tracing. Inability of the pelvic floor to relax may be seen in conditions such as dysfunctional voiding and detrusor–sphincter dyssynergia (DSD), but may also appear as an artifact from straining to initiate the void or towards its end.
URODYNAMIC DEFINITION OF BLADDER OUTLET OBSTRUCTION In men, a number of nomograms exist to define and quantify BOO secondary to benign prostatic enlargement, including the Abrams–Griffith, Schäfer, and the linear passive urethral resistance, all of which are readily available and used in clinical practice. Not only is BOO less prevalent in women than in men, but anatomic differences, aging changes, duration of obstruction, and the various etiologies for BOO render the extension of male BOO nomograms to women somewhat irrelevant. Historically, the first attempts at defining obstruction were based on arbitrary values and observations in women who had a history suggestive of obstruction. Parameters included free flow rate, detrusor pressure at 239
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Figure 17.2. An ideal pressure–flow study (PFS) with key components highlighted. All these steps need to be clearly annotated on the tracing. (1) At end of filling, maximum cystometric capacity is reached. (2) There is a normal drop in vesical and abdominal pressures with change from standing to sitting position. (3) This is followed by an adjustment of transducers to the upper edge of the symphysis pubis. (4) Pre-void cough test confirms agreement in pressure recording from both catheters. (5) Before the void starts, and just after the cough, it is important to have a short section of tracing to determine the PFS baseline. Ideally, detrusor pressure (pdet) at baseline should be between 0 and +5 cmH2O. (6) A parallel rise in (a) intravesical pressure (pves) and (b) pdet with no change in intra-abdominal pressure (pabd) is indicative of a normal detrusor contraction (amplitude and duration), accompanied by (c) a normal, ‘bell-shaped’ flow curve. (7) At completion of the detrusor contraction, a post-void cough test is performed to confirm that both catheters functioned properly during voiding.
Figure 17.3. Representative examples of abnormalities in the pressure–flow study tracing that artificially elevate the detrusor pressure (pdet). Tracing A: A mild drop in abdominal pressure (1) is common due to pelvic floor relaxation (2), resulting in an artificially elevated pdet. Tracing B: Expulsion of the rectal catheter is reflected in the sharp drop in intraabdominal pressure (pabd) to a zero level (4), which also results in an artificially elevated pdet (5) which remains elevated. Note that the rise in intravesical pressure (pves) during each void is identical, but does not correlate with the corresponding rise in pdet (arrows).
Figure 17.4. Representative examples of voiding patterns in which no rise in detrusor pressure (pdet) is observed. Tracing A: Straining pattern as demonstrated by irregular, fluctuating pressure curve similar for intra-abdominal pressure (pabd) and intravesical pressure (pves) (1), resulting in minimal or no change in pdet (2) and a corresponding irregular flow curve (3). Tracing B: No discernible change in pves, pabd or pdet (4), with a normal flow curve (5) due to voiding by urethral relaxation, as reflected by the silent EMG during voiding (6). 240
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peak flow (PFP or pdetQmax), PVR, and urethral resistance, the last defined as pressure/flow2 (P/F2) with an abnormal value <0.2.1 However, limitations recognized early included the facts that only 40% of these ‘obstructed’ women complained of the classic obstructive symptoms (hesitancy, poor flow, and incomplete emptying), and that a number of normal women void by urethral relaxation or with a low-pressure detrusor contraction.29 Once it became clear that such arbitrary values for diagnosing obstruction were not particularly accurate, receiver operator characteristics (ROC) were used to determine cut-off values for BOO in women and attain the optimal sensitivity and specificity for combining Qmax and pdetQmax values. One study reported using cut-off values of Qmax ≤15 ml/s and pdetQmax ≥20 cmH2O to define obstruction, and found a sensitivity and specificity of 74.3 and 91.1%, respectively.30 These values were then applied to an expanded group of 87 women with clinical obstruction (women in urinary retention and those who strained during voiding were not included in the analysis), and referenced to 124 stress-incontinent controls.31 Optimal values to define BOO in this study were Qmax ≤11 ml/s and pdetQmax ≥21 cmH2O. Several years later,
the same group of researchers published details of their growing experience with 169 women with clinical BOO compared to PFS data in 20 healthy volunteers with no urologic complaints by Urogenital Distress Inventory (UDI-6) questionnaire.12 Using a minimum specificity of 60% with the highest sensitivity, the authors determined that a Qmax ≤12 ml/s and pdetQmax ≥25 cmH2O was the most accurate cut-off criteria in defining BOO (Fig. 17.5). Another approach to the diagnosis of BOO sought to combine PFS data with bladder neck and urethral imaging by fluoroscopy (videourodynamics) or voiding cystourethrogram (VCUG). In one study, women with radiographic evidence of obstruction on videourodynamics and a sustained detrusor contraction during PFS were compared to those with no obstruction on imaging and were found to have a lower Qmax (9 vs 20.2 ml/s), a higher pdetQmax (42.8 vs 22.1 cmH2O), and a higher PVR (157 vs 33 ml).32 Contrary to videourodynamics, VCUG is a readily available tool that carries a low radiation risk.33 In addition, it can provide high-resolution lateral views of the urethra during voiding,34 which may help in determining the site of obstruction, as detailed in Figure 17.6.
Figure 17.5. (a, b) Receiver–operator characteristics for defining bladder outlet obstruction (BOO) in women using the Qmax and corresponding pdetQmax. The dashed vertical line in each graph represents the best sensitivity, specificity, and accuracy. Optimal cut-off values in 169 women with clinical BOO compared to 20 controls were found at Qmax ≤12 ml/sec and pdetQmax ≥25 cmH2O. (Reproduced from ref. 12 with permission.) 241
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Figure 17.6. Representative examples of urethral obstruction on lateral voiding views from differing etiologies. All patients were obstructed clinically with abnormal pressure–flow studies. Periurethral fibrosis causes obstruction throughout the entire length of the urethra (a) or distally with proximal dilation (b). (c) Extrinsic compression is seen underneath the urethra in a woman with an unsuspected urethral diverticulum (oval with arrow). Mid-urethral obstruction with proximal dilation (d) in a woman after transvaginal tape placement requiring urethrolysis. To reduce the effect of a urethral catheter during PFS, one study defined BOO by plotting the non-intubated Qmax on one hand, and the maximum detrusor pressure (pdet-max) generated during a separate PFS on the other.2 Their definition – free flow Qmax ≤12 ml/s and a pdet-max ≥20 cmH2O – did not rely solely on PFS parameters; it was further expanded to include those who were unable to generate a flow by using radiographic evidence of obstruction during videourodynamics with a sustained detrusor contraction ≥20 cmH2O. Of 50 women who met these obstruction criteria, two were in retention, and five were unable to void with the catheter in place. The NIF-Qmax was plotted against the pdet-max and a four-zone nomogram (zones 0, I, II, and III) was constructed, similar to the Abrams–Griffith nomogram in men. However, since the free Qmax and pdet-max were obtained during different voids, this nomogram failed to account for differences in voided volume and the presence of straining during the PFS or NIF. In addition, 10/50 (20%) clinically unobstructed women had plotted values consistent with mild or borderline
mild obstruction. A recent prospective study applied this nomogram to 109 women with urinary incontinence and found 68.7% were obstructed (57.8% mild, 11% moderate, 0.9% severe),35 a much higher percentage than the reported prevalence of 6.5% on the initial application of these criteria to a urodynamic database of 587 consecutive women.36 In search for a better definition of BOO, a method to calculate the area under the detrusor pressure curve (AUCdet) for a given Qmax and voided volume was recently reported.37 The AUCdet is a product of detrusor pressure × time (dt) and reflects the whole bladder contraction during voiding, using the formula 0∫t(pdet × dt), and is expressed as cmH2O/s/ml (Fig. 17.7). In the initial report, these calculated values were applied to 85 women categorized as obstructed, unobstructed, or equivocal by two urologists blinded to each other’s findings. Criteria traditionally used to diagnose obstruction – obstructive symptoms within 3 months after anti-incontinence surgery, conditions associated with obstruction (urethral stenosis, stage III–IV prolapse, and primary bladder neck
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Figure 17.7. Pressure–flow plot in an obstructed patient with the calculated area under detrusor pressure curve (AUCdet) in shading. Note that changes in the intra-abdominal pressure (pabd) occurring throughout the voiding study may have an effect on the detrusor pressure (pdet) curve and in turn on this method’s accuracy. (pves, intravesical pressure; Qura, flow rate in ml/s; Vuro, voided volume.) (Reproduced from ref. 37 with permission.) obstruction), Qmax <12 ml/s on NIF, and PVR >150 ml – were compared to the AUCdet data. Linear discriminant analysis classified an AUCdet value >5.83 cmH2O/s/ml as obstructed, 2.56–5.83 as equivocal, and <2.56 as unobstructed. These AUCdet values have not yet been applied to unobstructed controls, and have not been tested by other investigators. Computerized mathematical micturition models have been introduced for men. One of them, the VBN, which derives pressure within the urethra and counter-pressure outside the urethra, as well as detrusor function during voiding,13 has been applied to women. The effect of prolapse reduction of a grade IV cystocele was studied with the VBN model and demonstrated an improvement in urethral parameters in 10/14 patients, but no change in detrusor function.38 The same model was applied to 50 continent women after a tension-free vaginal tape (TVT) procedure and determined that a compressive obstruction could explain the continence mechanism in 34 (68%) of the women.39 Each of the aforementioned series, summarized in Table 17.2, has contributed valuable insights into the urodynamic criteria necessary to define BOO in women. However, none of them can be applied rigidly to all women, but rather should take into consideration clinical data (from history, physical examination, cystourethroscopy, and imaging methods) and act as an adjunct in confirming a diagnosis of obstruction.
Therefore, reflecting on the challenges posed by a urodynamic definition of obstruction, it is apparent that a number of obstacles must be overcome to create a valid obstruction nomogram for women. First and foremost is defining ‘a normal PFS’ in age-matched controls. Even when asymptomatic candidates are willing to undergo an invasive test such as a PFS, not all are truly asymptomatic. Of 59 community-dwelling adult women recruited to undergo PFS, 39 were excluded due to abnormal UDI questionnaire answers, prior bladder surgery, or withdrawal from the study.40 Clinically obstructed women for the most part tend to be older, and normative data for PFS have not been published in this age group in whom a high prevalence of mild irritative urinary symptoms (frequency and urgency) exists at baseline.41–44 Moreover, the voiding pattern and PFS parameters of normal volunteers are not necessarily consistent over time. In a study investigating PFS findings in 10 young, asymptomatic nulliparous women, a disparity of normative values was observed, many of which would really be considered pathologic, including a low Qmax.45 The use of non-neurogenic women with pure stress urinary incontinence (SUI) as controls was common in earlier studies.31,32,34,46 These women have since been found to void with relatively low detrusor pressures, thought in part to be due to decreased urethral resistance.47 Comparing 20 asymptomatic volunteers with 40 stress-incontinent women, a significantly higher Qmax and lower pdetQmax was observed in the stress-incontinent population stratified for age, menopausal status, and parity.40 Furthermore, the presence of SUI does not necessarily exclude concomitant obstruction.48 These findings strongly argue that women with SUI should not serve as controls to establish PFS criteria for obstruction. Beyond establishing normative age-matched values for the pressure–flow plot, study technique should be uniform to eliminate inconsistencies and artifacts. Minimizing catheter interference by using the smallest size catheter – preferably 7 Fr or less – is recommended; a smaller size catheter (e.g. 4 Fr) would be optimal but filling the bladder with smaller catheters is time-consuming and the filled volume is not reliable. To compare patients, voided volume categories may be necessary since volume and flow are interrelated.49 A number of other technical issues have been raised earlier in this chapter (voiding position, prolapse reduction, documentation of pelvic floor relaxation by EMG, etc.) and will require further study before the PFS procedure can be better standardized. Assuming a valid and plausible PFS tracing with clear annotations, the interpretation of the tracing must follow guidelines that should be validated both between 243
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Table 17.2. Published series on definitions of female obstruction n (mean age in years) Author (year)
BOO
Controls
Etiology of BOO
Control population
Catheter size
Definition of obstruction
Massey & Abrams (1988)1
163 (NR)
None
Extramural (39), intramural (120) , intraluminal (4)
N/A
NR
Qmax <12 ml/s, pdetQmax >50 cmH2O, urethral resistance >0.2, PVR >100 ml
Chassagne et al. 35 (NR) (1998)30
124 (NR)
Prior BNS (13), prolapse (11), other (6)a
SUI, no prior pelvic surgery, no cystocele or urethral pathology on VCUG
6 Fr
Qmax <15 ml/s, pdetQmax >20 cmH2O ROC curve (sensitivity 74.3%, specificity 91.1%)
Nitti et al. (1999)32
76 (57.5)
184 (55)
DV (25), POP (24), PBNO (12), AIS (11), US (3), UD(1)
Women with LUTS who did not meet the specified criteria
7 Fr
Radiographic evidence of BOO with a sustained detrusor contraction of any magnitude on videourodynamics
Blaivas & Groutz 50 (64.4) (2000)2
50 (64.8)
AIS (10), POP (8), US (9), PBNO (3), UD (3), DV (2), DSD (2), idiopathic (11)
20 with LUTS and ‘normal’ UDS, 30 with sphincteric incontinence
7 Fr
Free Qmax <12 ml/s and pdet-max >20 cmH2O; or evidence of obstruction on fluoroscopy with detrusor contraction >20 cmH2O
Lemack & Zimmern (2000)31
87 (NR)
124 (NR)
Cystocele (33), prior BNS (25), othera (29)
SUI, no prior pelvic surgery, no obstructive complaints, no cystocele or urethral pathology on VCUG
6 Fr
Qmax <11 ml/s, pdetQmax >21 cmH2O ROC curve (sensitivity 73.6%, specificity 91.5%)
Cormier et al. (2002)37
85 (55)
None
Prior BNS (7), US (5), PBNO (1), POP (1), idiopathic (7)
‘Traditional’ diagnosis of BOO
6 Fr
Area under detrusor pressure curve (AUCdet)/voided volume >5.83 cmH2O per ml/s
Defreitas et al. (2004)12
169 (60)
20 (42)
Cystocele (53), AIS (48), distal urethral fibrosis (68)
Normal UDI-6, no history of prior pelvic surgery
6 Fr
Qmax <12 ml/s, pdetQmax >25 cmH2O ROC curve (accuracy 68%)
Di Grazia et al. (2004)46
43 (55*)
136 (55*)
Advanced POP (20), prior BNS (6), DV (6), PBNO (2), US (1), idiopathic (8)
UI, no prior AIS, POP
12 Fr + 4 Fr (filling) 4 Fr only (voiding)
Qmax <13 ml/s, pdet-max >22 cmH2O ROC curve (sensitivity 55.8%, specificity 96.3%)
AIS, anti-incontinence surgery; BNS, bladder neck suspension; BOO, bladder outlet obstruction; B-W, Baden–Walker halfway classification system; DSD, detrusor–sphincter dyssynergia; DV, dysfunctional voiding; LUTS, lower urinary tract symptoms; N/A, not applicable; NR, not reported; PBNO, primary bladder neck obstruction; POP, pelvic organ prolapse; PVR, post-void residual; ROC, receiver operator characteristics; SUI, stress urinary incontinence; UD, urethral diverticulum; UDI-6, Urogenital Distress Inventory; UDS, urodynamic study; UI, urinary incontinence; US, urethral stricture/stenosis; VCUG, voiding cystourethrogram. a
Periurethral fibrosis (21), retroverted uterus (4), excessive collagen (1), UD (1).
* Mean age reported only for all patients in study.
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observers (interobserver) and by the same observer at different times (intraobserver). In a single-center study on PFS tracings in 621 women, good intra- and interobserver agreement was noted for all parameters, with the exception of intraobserver agreement on pde50 In the Stress Incontinence Surgical Treatment tQmax. Efficacy Randomized (SISTER) trial run by the Urinary Incontinence Treatment Network (UITN), interpretation guidelines had to be developed to enhance the interrater reliability between local and central reviewers.51 Overall, there is a recognized need to further our understanding of voiding mechanisms in women. As discussed in the next section, several procedures to correct incontinence may result in various degrees of outlet obstruction. Some believe it is a necessary result to achieve continence,52 whereas others worry about the long-term effect of raising urethral outlet resistance on detrusor function.53 This debate can only be solved if a consensus can be reached on the urodynamic definition of BOO.
INCONTINENCE SURGERY AND THE PRESSURE– FLOW PLOT When UDS is performed before deciding on an antiincontinence procedure, its first aim is to document the presence of SUI and assess its severity by determining the leak point pressure. Possibly more important, its second aim should be to gain some baseline knowledge on voiding detrusor function. Altered voiding dynamics is often reflected by changes in PFS parameters following anti-incontinence surgery. In this final section, we will review the PFS data following anti-incontinence procedures in the recent literature.
Anti-incontinence surgery Bladder neck suspension (BNS), pubovaginal sling (PVS), and mid-urethral sling procedures all aim to correct SUI by restoring support to the bladder neck and urethra with minimal tension. Nevertheless, the risk of inadvertently creating obstruction exists with each procedure. Postoperative voiding changes can occur across a broad spectrum, ranging from minor changes with no significant clinical relevance to frank obstruction and/ or urinary retention requiring surgical intervention.
Bladder neck suspension Whether or not the mechanism by which various transvaginal and retropubic BNS techniques restore continence is based on creating obstruction has long been debated. Obstruction following a retropubic Marshall–
Marchetti–Kranz (MMK) procedure has been reported as being between 7 and 21%. This has been attributed to suture placement in the urethral wall itself, or more commonly to periurethral scarring,54 but little is known about PFS parameters in asymptomatic continent women after MMK. Pre- and postoperative urodynamic parameters (maximum voiding pressures, urethral resistance) were compared in 20 continent women after a modified Pereyra BNS and no significant changes were observed, suggesting that this procedure did not cause outflow obstruction.55 On the contrary, changes in urethral resistance at 1 year postoperatively52 and long term,56 and significant differences in pressure–flow parameters, have been reported after retropubic colposuspension.57 These studies differed in concluding that a retropubic suspension returns voiding parameters to a ‘normal’ level versus an ‘obstructive’ state. Interestingly, some have suggested that the superior outcome of the retropubic suspensions over needle suspensions58 is due to the more ‘obstructive’ nature of the former procedures.
Pubovaginal sling The incidence of urethral obstruction after placement of a pubovaginal sling (PVS), regardless of the material used, has been reported in approximately 8% of cases,58 and is thought to be due to excessive tensioning. In one study comparing preoperative videourodynamic findings to those 3 months after rectus fascia PVS in 85 women, a statistically significant increase in the mean pdetQmax and a decrease in Qmax was noted.59 Conversely, a comparative videourodynamic study examined 50 women who underwent PVS – 24 using rectus fascia, 26 using polypropylene mesh – and noted a non-significant decrease in Qmax at 7–14 days postoperatively which returned to baseline upon reassessment at 3–6 months.60 Similarly, a recent study examined PFS findings at 3–6 months in 48 women with successful outcomes after a modified vaginal wall sling procedure, and reported no significant difference in any pressure–flow or urethral pressure profile parameter.61
Mid-urethral sling procedures Although the TVT and transobturator tape (TOT) procedures have success rates comparable to more established anti-incontinence procedures, voiding dysfunction and urinary retention occur in 1.4–9% of patients postoperatively.62 Preoperative and 1-year postoperative PFS data were reported in 65 patients who underwent TVT sling placement with a 25% decrease in flow rate and a 21% increase in pdetQmax (p<0.001 and 0.02, respectively).63 Other pressure–flow parameters as well as the nonintubated Qmax were also negatively affected; short-term 245
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(median duration 4 days) urinary retention occurred in 36% of patients, with 8% ultimately requiring sling release. In two other studies that investigated postoperative UDS at 1 year after TVT,62,64 a similar trend was noted, with a statistically significant decrease in Qmax and an increase in PVR compared to preoperative baseline values. In a randomized trial comparing the suprapubic arc (SPARC) sling to TVT, no significant difference in flow rates during PFS was noted,65 whereas a case-control series reported contrasting results, observing a significantly lower free Qmax at a mean follow-up of 7 months in 69 and 37 women who underwent TVT or SPARC, respectively.66 Preoperative and 1-year postoperative pressure–flow studies were performed in a multicenter randomized trial comparing TVT (n=30) to TOT (n=31) and reported no significant difference in the rate of BOO between the two procedures.67 All these data suggest that altered voiding dynamics following each of the above anti-incontinence procedures can occur to varying degrees. Long-term data on these procedures with pressure–flow information will be needed to test their long-term effect on detrusor function.
PREDICTIVE VALUE OF THE PRESSURE–FLOW PLOT Thus far we have discussed the PFS as a means of documenting pre- and postoperative changes after antiincontinence surgery. The predictive merit of PFS in the preoperative evaluation of incontinence has also been investigated. Impaired detrusor function on preoperative PFS appears to have some value in predicting voiding dysfunction after anti-incontinence procedures. One report examining preoperative voiding patterns in 30 women undergoing Burch colposuspension revealed that women who voided by Valsalva maneuver and urethral relaxation were 12 times more likely to require postoperative catheterization >7 days.68 Using time to resume normal voiding postoperatively, findings in two studies differed with regard to the predictive value of abdominal straining on preoperative PFS prior to Burch colposuspension.69,70 Accelerated flow rate (AFR) – which reflects the speed of detrusor contraction and opening of the bladder neck and is defined as the maximum flow rate divided by the time to reach maximum flow during PFS – was investigated in 209 women with stress incontinence who underwent a Burch colposuspension.71 The AFR, which is independent of voided volume, was useful in predicting the outcome of continence surgery and the occurrence of de novo detrusor overactivity in 18% of women at 1 year.
Pubovaginal sling Clinical obstruction may occur more frequently after PVS in those patients with an abnormal preoperative PFS. The presence of a Valsalva-only voiding mechanism on preoperative PFS was associated with a longer duration of postoperative catheterization and objective failure after rectus fascia sling placement in 50 women.72 Although Valsalva voiding did not correlate with urinary retention in 73 women followed after allograft fascia lata sling placement, another study found that no woman with a detrusor contraction >12 cmH2O on preoperative PFS developed urinary retention, while 23% of those who voided without a detrusor contraction developed urinary retention.73 Conversely, preoperative urodynamic investigation poorly predicted the necessity of long-term catheterization after rectus fascia sling in 58 non-neurogenic women using the contraction parameters power factor WF and bladder contractility index (BCI).74
Mid-urethral slings Data regarding the predictive role of the preoperative pressure–flow plot on voiding function after TVT or other mid-urethral slings is limited. Attempts to do so using linear regression analysis have been unable to find a correlation between PFS and outcomes such as postoperative voiding dysfunction,64 time to voiding, or urinary retention.63,75 Although the existing literature has focused on short-term changes, these often do not reflect the voiding status at intermediate and long-term follow-up.
URETHROLYSIS AND THE PRESSURE–FLOW PLOT Conservative measures for relieving iatrogenic bladder outlet obstruction have been described – including pharmacotherapy, urethral dilation, sling stretching and/or incision – but the definitive intervention has been urethrolysis. Originally described by Richardson and Stonington in 1969 to treat ‘urethral syndrome’ in a young woman,76 the technique was later reported by Leach and Raz in 1984 to manage obstruction after anti-incontinence surgery.77 The procedure is most commonly performed transvaginally, but has been described using a suprameatal or a retropubic approach. Pressure–flow studies may assist in documenting obstruction prior to transvaginal urethrolysis (TVU), especially when there is no clear temporal relationship between the anti-incontinence procedure and onset of BOO symptoms. The ‘classic’ findings of high detrusor pressure with low flow suggestive of obstruction are not always observed, and have been reported as being between 33 and 61%, even when clinical obstruction is
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suspected.78,79 The predictive role of PFS with regard to outcome after urethrolysis has been somewhat disappointing. A study involving 41 patients who underwent TVU found that the strength of detrusor contraction and the pressure–flow study did not predict the clinical outcome.79 Similar findings were described in a series of 32 women who underwent suprameatal TVU.80 Obstruction was defined as pdetQmax >20 ml/s with a Qmax <12 ml/s, but the success rate after urethrolysis in patients who met these criteria was no different from those who underwent TVU based on physical examination and clinical judgment.
CONCLUSION The pressure–flow study is a valuable tool in the evaluation of incontinence and obstruction in women. It remains the most challenging step in a urodynamic study, not only because of numerous technical issues, but also because of current limitations in defining normative values and the lack of universally agreed-upon interpretation guidelines. These shortcomings currently limit its clinical usefulness as a stand-alone test, thus forcing the clinician to use the PFS information judiciously in combination with other clinical elements.
REFERENCES 1. Massey JA, Abrams PH. Obstructed voiding in the female. Br J Urol 1988;61:36–9. 2. Blaivas J, Groutz A. Bladder outlet obstruction nomogram for women with lower urinary tract symptomatology. Neurourol Urodyn 2000;19:553–64. 3. Vowles JE, Wagg AS. The pressure–flow plot in the evaluation of female incontinence. BJU Int 1999;84:948–52. 4. Hill AV. The heat of shortening and the dynamic constants of muscle. Proc R Soc Lond (Biol) 1938;126:136–95. 5. Griffiths DJ. Urodynamics: The Mechanics and Hydrodynamics of the Lower Urinary Tract. Medical Physics Handbooks 4. Bristol: Adam Hilger, 1980. 6. Griffiths DJ. Urethral resistance to flow: the urethral resistance relation. Urol Int 1975;30:28–32. 7. Van Mastrigt R, Griffiths DJ. Clinical comparison of bladder contractility parameters calculated from isometric contractions and pressure–flow studies. Urology 1987;29:102–6. 8. Schäfer W. The contribution of the bladder outlet to the relation between pressure and flow rate during micturition. In: Hinman F Jr (ed) Benign Prostatic Hypertrophy. New York: Springer-Verlag, 1983; 470–96. 9. Buttyan R, Chen M, Levin R. Animal models of bladder outlet obstruction and molecular insights into the basis
for the development of bladder dysfunction. Eur Urol Suppl 1997;32:32–9. 10. Agartan CA, Whitbeck C, Chichester P et al. Effect of age on rabbit bladder function and structure following partial outlet obstruction. J Urol 2005;173:1400–5. 11. Wagg A, Malone-Lee J. The pressure-flow plot in the evaluation of female incontinence. In: Cardozo L, Staskin D (eds) Textbook of Female Urology and Urogynecology. London: Taylor and Francis, 2001. 12. Defreitas G, Zimmern P, Lemack G et al. Refining diagnosis of anatomic female bladder outlet obstruction: comparison of pressure–flow study parameters in clinically obstructed women with those of normal controls. Urology 2004;64:675–81. 13. Valentini FA, Besson GR, Nelson PP et al. A mathematical micturition model to restore simple flow recordings in healthy and symptomatic individuals and enhance uroflow interpretation. Neurourol Urodyn 2000;19:153–76. 14. Susset JG, Picker P, Kretz M et al. Critical evaluation of uroflowmeters and analysis of normal curves. J Urol 1973;109:874–8. 15. Ryall R, Marshall V. The effect of a urethral catheter on the measurement of maximum urinary flow rate. J Urol 1982;128(2):429–32. 16. Baseman AG, Baseman J, Zimmern P et al. Effect of 6F urethral catheterization on urinary flow rates during repeated pressure–flow studies in healthy female volunteers. Urology 2002;59:843–6. 17. Groutz A, Blaivas J, Sassone M. Detrusor pressure uroflowmetry studies in women: effect of a 7 Fr transurethral catheter. J Urol 2000;164:109–14. 18. Di Grazia E, Bartolotta S, Nicolisi F et al. Detrusor pressure uroflowmetry studies in women: effect of 4 Fr transurethral. Arch Ital Urol Androl 2002;74:134–7. 19. Costantini E, Mearini L, Biscotto S et al. Impact of different sized catheters on pressure–flow studies in women with lower urinary tract symptoms. Neurourol Urodyn 2005;24:106–10. 20. Lazarou G, Scotti R, Mikhail M et al. Pessary reduction and postoperative cure of retention in women with anterior vaginal wall prolapse. Int Urogyn J 2004;15:175–8. 21. FitzGerald MP, Kulkarni N, Fenner D. Postoperative resolution of urinary retention in patients with advanced pelvic organ prolapse. Am J Obstet Gynecol 2000;183:1361–4. 22. Gilleran JP, Lemack G, Zimmern PE. Impact of a vaginal pack in reducing cystocele during preoperative urodynamic studies. International Continence Society (ICS) Annual Meeting, August 2005, Montreal, Canada. ICS, 2005; abstract 683. 23. Devreese AM, Nuyens G, Staes F et al. Do posture and straining influence urinary-flow parameters in normal women? Neurourol Urodyn 2000;19(1):3–8.
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24. Moore KH, Richmond DH, Sutherest JR et al. Crouching over the toilet seat: prevalence among British gynaecological outpatients and its effect upon micturition. Br J Obstet Gynaecol 1991;98:569–72. 25. Schafer W, Abrams P, Liao L et al. Good urodynamic practices: uroflowmetry, filling cystometry, and pressure–flow studies. Neurourol Urodyn 2002;21:261–74.
between asymptomatic and incontinent women. Urology 2002;59:42–6. 41. Madersbacher S, Pycha A, Schatzl G et al. The aging lower urinary tract: a comparative urodynamic study of men and women. Urology 1998;51:206–12. 42. Desgrandchamps F, Cortesse A, Rousseau T et al. Normal voiding behaviour in women. Eur Urol 1996;30:18–23.
26. Sullivan J, Lewis P, Howell S et al. Quality control in urodynamics: a review of urodynamic traces from one centre. BJU Int 2003;91:201–7.
43. Terai A, Matsui Y, Ichioka K, Ohara H, Terada N, Yoshimura K. Comparative analysis of lower urinary tract symptoms and bother in both sexes. Urology 2004;63(3):487–91.
27. FitzGerald MP, Brubaker L. The etiology of urinary retention after surgery for genuine stress incontinence. Neurourol Urodyn 2001;20:13–21. 28. O’Donnell P. Electromyography. In: Nitti V (ed) Practical Urodynamics. Philadelphia: WB Saunders, 1998; 65–71.
44. Svatek R, Roche V, Thornberg J et al. Normative values for the American Urological Association symptom index (AUA-7) and short form urogenital distress inventory (UDI6) in patients 65 and older presenting for non-urological care. Neurourol Urodyn 2005; Oct 5; [Epub ahead of print]
29. Tanagho EA. Vesico-urethral dynamics. In: Lutzyer W, Melchior H (eds) Urodynamics. Berlin: Springer-Verlag, 215.
45. Wyndaele JJ. Normality in urodynamics studied in healthy adults. J Urol 1999;161:899–902.
30. Chassagne S, Bernier P, Haab F et al. Proposed cutoff values to define bladder outlet obstruction in women. Urology 1998;51:408–11.
46. Di Grazia E, Sanroman RT, Aceves JG. Proposed urodynamic pressure–flow nomogram to diagnose female bladder outlet obstruction. Arch Ital Urol Androl 2004;76:59–65.
31. Lemack GE, Zimmern PE. Pressure flow analysis may aid in identifying outflow obstruction. J Urol 2000;163:1823–8.
47. Karram MM, Partoll L, Bilotta V et al. Factors affecting detrusor contraction strength during voiding in women. Obstet Gynecol 1997;90:73–6.
32. Nitti V, Tu LM, Gitlin J. Diagnosing bladder outlet obstruction in women. J Urol 1999;161:1535–40. 33. Arbique G, Gilleran J, Guild J et al. Radiation exposure during a voiding cystourethrogram (VCUG) in women. Urology 2005, Submitted. 34. Lemack G, Zimmern P. Voiding cystourethrography and magnetic resonance imaging of the lower urinary tract. In: Corcos J, Schick E (eds) The Urinary Sphincter. New York: Marcel Dekker, 2001; 407–21. 35. Massolt E, Groen J, Vierhout M. Application of the Blaivas–Groutz bladder outlet obstruction nomogram in women with urinary incontinence. Neurourol Urodyn 2005;24:1–6. 36. Groutz A, Blaivas J, Chaikin D. Bladder outlet obstruction in women: definition and characteristics. Neurourol Urodyn 2000;19:213–20. 37. Cormier L, Ferchaud J, Galas JM et al. Diagnosis of female bladder outlet obstruction and relevance of the parameter area under the curve of detrusor pressure during voiding: preliminary results. J Urol 2002;167:2083–7. 38. Valentini F, Zimmern PE, Besson G et al. [Modeled analysis of the effect of cystocele reduction with vaginal pack on micturition in women with grade IV cystocele.] Prog Urol 2000;10(3):432–7. 39. Fritel X, Valentini F, Nelson P et al. [Contribution of modeling to the analysis of micturitional modifications caused by the TVT: study of free uroflows.] Prog Urol 2004;14(2):197–202. 40. Lemack G, Baseman A, Zimmern P. Voiding dynamics in women: a comparison of pressure–flow studies
48. Bradley CS, Rovner ES. Urodynamically defined stress urinary incontinence and bladder outlet obstruction coexist in women. J Urol 2004;171:757–60. 49. Haylen BT, Ashby D, Sutherest JR et al. Maximum and average urine flow rates in normal male and female populations – the Liverpool nomograms. Br J Urol 1989;64:30–8. 50. Digesu GA, Hutchings A, Salvatore S et al. Reproducibility and reliability of pressure flow parameters in women. BJOG 2003;110:774–6. 51. Nager CW, Albo ME, FitzGerald MP et al for the Urinary Incontinence Treatment Network. Quality control of multicenter urodynamic studies. Neurourol Urodyn 2005, In press. 52. Klutke JJ, Klutke CG, Bergman J et al. Bladder neck suspension for stress urinary incontinence: how does it work? Neurourol Urodyn 1999;18:623–7. 53. Zimmern PE. Vaginal surgery for stress urinary incontinence: beyond horizon 2000. In: Stanton SL, Zimmern PE (eds) Female Pelvic Reconstructive Surgery. Berlin: Springer-Verlag, 2002; 360–3. 54. Zimmern PE, Hadley HR, Leach GE et al. Female urethral obstruction after Marshall–Marchetti–Kranz operation. J Urol 1987;138;517–20. 55. Leach GE, Yip CM, Donovan BJ. Mechanism of continence after modified Pereyra bladder neck suspension. Prospective urodynamic study. Urology 1987;29(3):328–31. 56. Herbertsson G, Iosif CS. Surgical results and urodynamic studies 10 years after retropubic colpourethrocystopexy. Acta Obstet Gynecol Scand 1993;72:298–301.
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57. Belair G, Tessier J, Bertrand P et al. Retropubic cystourethropexy: is it an obstructive procedure? J Urol 1997;158:533–8. 58. Leach GE, Dmochowski RR, Appell RA et al. Female stress urinary incontinence clinical guidelines panel summary report on surgical management of female stress urinary incontinence. J Urol 1997;158:857–80. 59. Fulford S, Flynn R, Barrington J et al. An assessment of the surgical outcome and urodynamic effects of the pubovaginal sling for stress incontinence and the associated urge syndrome. J Urol 1999;162:135–7. 60. Kuo H-C. Comparison of video urodynamic results after the pubovaginal sling procedure using rectus fascia and polypropylene mesh for stress urinary incontinence. J Urol 2001;165:163–8. 61. Mikhail MS, Rosa H, Palan P et al. Comparison of preoperative and postoperative pressure transmission ratio and urethral pressure profilometry in patients with successful outcome following the vaginal wall patch sling technique. Neurourol Urodyn 2005;24:31–4. 62. Sander P, Moller L, Rudnick P et al. Does the tension-free vaginal tape procedure affect the voiding phase? Pressure–flow studies before and 1 year after surgery. BJU Int 2002;89:694–8.
voiding following incontinence surgery. Obstet Gynecol 1984;63:85–91. 69. Sze E, Miklos J, Karram M. Voiding after Burch colposuspension and effects of concomitant pelvic surgery; correlation with preoperative voiding mechanism. Obstet Gynecol 1996;88:564–7. 70. Kobak WH, Walters MD, Piedmonte MR. Determinants of voiding after three types of incontinence surgery: a multivariable analysis. Obstet Gynecol 2001;97:86–91. 71. Digesu GA, Khullar V, Cardozo L et al. Preoperative pressure-flow studies: useful variables to predict the outcome of continence surgery. BJU Int 2004;94:1296–9. 72. Iglesia C, Shott S, Fenner D et al. Effect of preoperative voiding mechanism on success rate of autologous rectus fascia suburethral sling procedure. Obstet Gynecol 1998;91:577–81. 73. Miller E, Amundsen C, Toh KL et al. Preoperative urodynamic evaluation may predict voiding dysfunction in women undergoing pubovaginal sling. J Urol 2003;169:2234–7. 74. Groen J, Bosch JL. Bladder contraction strength parameters poorly predict the necessity of long-term catheterization after a pubovaginal rectus fascial sling procedure. J Urol 2004;172:1006–9.
63. Lukacz E, Luber K, Nager C. The effects of tension-free vaginal tape on voiding function: a prospective evaluation. Int Urogyn J 2004;15:32–8.
75. Sokol AI, Jelovsek JE, Walters MD et al. Incidence and predictors of prolonged urinary retention after TVT with and without concurrent prolapse surgery. Am J Obstet Gynecol 2005;192:1537–43.
64. Al-Badr A, Ross S, Soroka D et al. Voiding patterns and urodynamics after a tension-free vaginal tape procedure. Obstet Gynecol Can 2003;25(9):725–30.
76. Richardson F, Stonington O. Urethrolysis and external urethroplasty in the female. Surg Clin North Am 1969;49:1201–8.
65. Tseng L-H, Wang AC, Llin Y-H et al. Randomized comparison of the suprapubic arc sling procedure vs tension-free vaginal taping for stress incontinent women. Int Urogyn J 2005;16(3):230–5.
77. Leach GE, Raz S. Modified Pereyra bladder neck suspension after previously failed anti-incontinence surgery. Surgical technique and results with long-term follow-up. Urology 1984;23:359–62.
66. Dietz HP, Foote AJ, Mak H et al. TVT and Sparc suburethral slings: a case-control series. Int Urogyn J 2004;15:129–31.
78. Webster GD, Kreder KJ. Voiding dysfunction following cystourethropexy: its evaluation and management. J Urol 1990;144:670–73.
67. de Tayrac R, Deffieux X, Droupy S et al. A prospective randomized trial comparing tension-free vaginal tape and transobturator suburethral tape for surgical treatment of stress urinary incontinence. Am J Obstet Gynecol 2004;190:602–8. 68. Bhatia NN, Bergman A. Urodynamic predictability of
79. Nitti V, Raz S. Obstruction following anti-incontinence procedures: diagnosis and treatment with transvaginal urethrolysis. J Urol 1994;152:93–8. 80. Petrou SP, Brown JA, Blaivas JG. Suprameatal transvaginal urethrolysis. J Urol 1999;161:1268–71.
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INTRODUCTION Urethral pressure measurements have been used for nearly a century to assess urethral closure function.1 Urethral pressure and urethral closure pressure are idealized concepts which aim to represent the ability of the urethra to prevent leakage. As long as the intraurethral pressure exceeds the proximal fluid pressure, urine cannot leak and so the subject should be continent. The lack of general agreement on an explicit definition of urethral pressure and standardization of the methodology for measurement have limited the utility of urethral pressure measurements.
DEFINITION OF URETHRAL PRESSURE Urethral pressure is defined as ‘the fluid pressure needed to just open a closed (collapsed) urethra’. This definition suggests that urethral pressure is similar to ordinary fluid pressure, i.e. is a scalar (does not have a direction) quantity with a single value at each point along the length of the urethra. The concept of urethral pressure is only useful if the urethra collapses easily at attainable pressures to zero cross-sectional area, as is normally the case. The use of a catheter introduces a non-zero cross-sectional area (given by the probe) and changes the natural shape of the lumen. The effect on the measured urethral pressure is small for highly distensible/collapsible tubes.2
CIRCUMSTANCES AND TYPES OF MEASUREMENT Intraluminal urethral pressure may be measured:2
• with the subject at rest, with the bladder at any given volume;
• during coughing or straining; • during the process of voiding. Measurements can be made at one point in the urethra over a period of time (continuous urethral pressure recording) (Fig. 18.1) or as a urethral pressure profile (UPP) (Fig. 18.2). Urethral pressure profilometry is the measurement of intraluminal pressure along the length of the urethra. A mechanical retracting puller (Fig. 18.3) that is synchronized with the chart or digital recorder allows measurement of anatomic distances in the profile. Two types of UPP may be measured: 1. Resting UPP (Figs 18.2 and 18.3), with the bladder and subject at rest;
Urethral pressure (cmH2O)
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EMG 110 100 90 80 30 0 20 10 0
MTT1
MTT2
0
10 Time (min)
20
Figure 18.1. Pressure variations recorded from a healthy female volunteer. The registration was done with a microtip transducer catheter (MTT) (5 Fr). The orientation of the transducer was in an anterior position. MTT1 is the pressure variation recorded at maximum urethral closure pressure, MTT2 1 cm distally. (Reproduced from ref. 23 with permission. Copyright ©1986 John Wiley & Sons). 2. Stress UPP (Fig. 18.2), with a defined applied stress (e.g. cough, strain or Valsalva maneuver). The simultaneous recording of both intraurethral (pura) and intravesical (pves) pressure enables calculation of urethral closure pressure, i.e. pura – pves (Fig. 18.2).
TECHNIQUES Urethral pressure recording requires a catheter to be placed in the urethra, inevitably distending the urethra to the catheter’s diameter. Therefore, the catheter should be as thin as possible. As any catheter will have some stiffness and weight that will deform the curved, soft urethra, the catheter should be as flexible and as light as possible. As the urethra has significant pressure gradients along its length, the location of the recorded pressure must be known. The three main methods for UPP measurement are: 1. perfused catheters with side holes (Fig. 18.4a); 2. catheter-tip transducer catheters (Fig. 18.4b) 3. balloon catheters (Fig. 18.4c).
Perfused catheters with side holes The technique is mainly based on the description by Brown and Wickham.3 The perfusion technique appears to mimic best the condition for which urethral pressure is defined: a fluid pressure just opening the urethra. For such measurements, it is possible to use small-diameter flexible catheters and low perfusion rates (about 1 ml/ min under resting conditions). The technique is relatively simple. It has been documented that water-filled perfusion catheters fulfill the demands for recording cough-produced variations.4 The catheters are relatively cheap and are disposable.
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Urethral pressure measurements
100
0
100
$ pura
0
Bladder pressure (pves)
PTR =
$ pura $ pves
s 100%
100
Figure 18.2. Urethral pressure profiles at rest (a) and during coughs (b) in a continent woman: 7 Fr dual sensor tip transducer catheter, supine position, 200 ml bladder volume. PTR, pressure transmission ratio (= [∆pura/∆pves] × 100%).
$ pves
0 0
a
5 Distance (cm)
0 b
5
10 Distance (cm)
a
Pressure (cmH2O)
b
10 0 1s
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Figure 18.3. Urethral pressure profilometry (a) technique for urethral pressure measurement; (b) puller device for retraction of catheter during profilometry (Medtronic, Dantec, Urology); (c) urethral pressure profile trace at rest.
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Figure 18.4. (a) Two-lumen catheters (10 Fr) for urethral pressure profilometry (Medtronic, Dantec, Urology). (b) A single (6 Fr) and a dual (8 Fr) sensor tip transducer catheter (Medtronic, Dantec, Urology). (c) Balloon catheter, mounted on a double micro-tip transducer catheter. The proximal pressure sensor is placed inside the balloon.
Catheter-tip transducer catheters This technique was popularized by Asmussen and Ulmsten.5 In fact, the transducer measures not the hydrostatic pressure but the normal stress component on its surface. Because of the rapid-frequency response of around 2000 Hz, the technique is suitable for recording very rapid changes in intraurethral pressure, such as those occurring during coughing. The technique is also ideal for long-term measurements. The stiffness of the catheters may lead to an interaction between the transducer and the urethral wall, resulting in a directional artifact.6–8 This means that conventional UPP parameters at rest and during coughing give different results, depending on the orientation of the transducer. The directional differences exist only with the catheter in the urethra. The results obtained with the transducer in the lateral orientation (9 or 3 o’clock), compared with the anterior position, appear to be most in accor-
dance with the clinical situation in women with stress incontinence.6 The sensing surface area of the transducer is small and only a minimal force is needed to yield a significant apparent pressure (1 g weight acting on 1 mm2 results in an apparent pressure of 100 cmH2O). Obviously, the ‘pressure’ measured in a small area in a given direction may not always be indicative of the pressure in an adjacent location and hence may not be representative of the state of the entire urethra. Culligan and co-workers compared an 8 Fr micro-tip catheter with a 10 Fr fiber-optic catheter and found that the urethral pressures measured with the larger catheter were significantly greater, on average by 14 cmH2O.9 In combined bladder and urethral pressure measurements, micro-tip transducers may record pressures that differ from those of liquid-perfused catheters because of the difference in the height of the bladder. Additionally, urethral transducers are not cancelled out
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Balloon catheters Balloon catheters – either water or air filled (T-doc) – may be connected to external pressure transducers10 or may be modified micro-tip transducer catheters11,12 (Fig. 18.4c). A true hydrostatic pressure is measured. The technique averages out the variations over the length equivalent to the length of the balloon. The resolution appears, however, to be better than 5 mm for T-docs. Urethral planimetry enables a more point-specific measurement (e.g. of a 2 mm long segment of the urethra).12 By placing a balloon around the micro-tip pressure transducer, the directional artifact is eliminated and the sensitivityto-movement artifact is reduced. Furthermore, since the balloon measures the pressure over 0.5 or 1.5 cm length of the urethra, it may more accurately represent the state of the entire urethra.
RELIABILITY OF MEASUREMENTS Reliability of measurements depends on accuracy (validity) and reproducibility (precision) of the test results. The available information shows that UPP parameters are subject to a certain amount of inter- and intraindividual variation.13–16 This variation is due to methodologic and biologic factors. The variation because of pure intrinsic instrumental factors is generally low, of the order of a few per cent.14,17 Measurements in vivo, however, are subject to significant variation because of methodologic differences in terms of size, type of catheter (perfusion, micro-tip, balloon or optic), rate of perfusion, retraction, posture of the patient, and content of the bladder. Furthermore, the urethral pressure at a given point in the urethra is not constant: it is subject to significant normal physiologic fluctuations of the order of 40 cmH2O (Fig. 18.1) due to changes in the activity of smooth muscle18 and/or striated muscle.19 In this context it is important to be aware that the patient is often unable to relax her pelvic floor during urethral pressure measurement, especially during the first profile. The reliability of measurements also depends on the quality of the urodynamic practice, routine, and expertise.
Finally, all techniques imply the introduction of a probe and hence opening of the urethral lumen, which introduces a systematic artifact for all measurements. Consequently, the accuracy (validity) of urethral pressure data is difficult to establish since the true urethral pressure is unknown. The test–retest variation is significant (i.e. low reproducibility) because of the influence of so many different factors. Currently, there is no consensus on how to standardize the technique of urethral profilometry. It is recommended that authors specify their technique according to the International Continence Society (ICS)2 and provide reproducibility data (or indicate their absence).
CLINICAL MEASUREMENTS AND PARAMETERS The Standardization Committee of the ICS has defined the parameters in common use20 (Fig. 18.5). Recordings of profile parameters must be repeated several times to verify reproducibility.
Static measurements in the resting urethra The static parameters relate to the permanently acting closure forces along the urethra.21 One specific aspect of the UPP is the maximum urethral closure pressure (MUCP) (Fig. 18.5), which is the highest pressure (relative to bladder pressure) generated along the functional length of the urethra. It usually corresponds to the striated sphincter in the mid-urethra. The maximum urethral closure pressure alone does not provide any information about the integrity of the bladder neck or proximal urethra (i.e. the proximal continence mechanism), and it can be highly variable as a result of involuntary contractions of the smooth and
120 Intra-urethral pressure (cmH2O)
by the siphon effect in saline-filled catheters with external pressure transducers. Thus, the vertical distance between two transducers during measurement should be taken into account when data are analyzed. The micro-tip transducer catheters are fragile and relatively costly.
100 80
Maximum urethral pressure
Maximum urethral closure pressure
60 40 20 0
Bladder pressure 0
Figure 18.5. profilometry.
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striated muscles of the urethral sphincter, perhaps provoked by the irritative nature of the catheter itself. The size, stiffness, and type of catheter, the rate of perfusion, patient position, and bladder volume all have an effect on the pressure readings.
Interobserver variability
Normative and comparative data for maximum urethral closure pressure
Reproducibility
A variety of values of MUCP has been obtained by different authors in normal (or, at least, without urodynamic stress incontinence) and abnormal female populations.22 It has several striking features: 1. the between-centre variability in the values reported, with mean MUCP varying from 36 to 101 cmH2O in non-stress-incontinent subjects; 2. the large between-subject standard deviation reported in most studies (from 10 to 52 cmH2O); 3. in spite of this variability, in every study the mean MUCP was smaller in stress-incontinent patients than in non-stress-incontinent women, sometimes significantly so and sometimes not. Although some of the variations are clearly the result of different patient populations, and others are the result of technical errors, a weighted averaging of the mean values suggests that a normal MUCP is approximately 54 ± 25 cmH2O (SD). In stress-incontinent women the corresponding figures are 39 ± 24 cmH2O. There is clearly so much overlap that it has been impossible to define a cut-off level that allows differentiation between women with and without stress incontinence.22 Maximum urethral pressure (MUP), like maximum urethral closure pressure (MUCP), declines as a function of age.22
Reliability of urethral pressure variables Within-patient reproducibility of maximum urethral closure pressure In clinical practice, use of a fluid-perfusion technique to measure resting UPP parameters (e.g. MUCP) yields a standard deviation varying from 3.3 to 8.1 cmH2O. On average, the standard deviation is approximately 5 cmH2O (95% confidence limits ±10 cmH2O) or ±5%. With a micro-tip transducer technique, the standard deviation varies between 3.3 and 16.5 cmH2O, which means that the 95% confidence limits may be as high as ±33cm H2O. The coefficient of variation when using the micro-tip transducer technique has been reported to be 17% (95% confidence limits ±34%).22
Investigations into interobserver variability are scarce. In one study using fluid perfusion, the coefficient of variation of MUCP varied from 3 to 11% (95% confidence limits 6–23%).22
Reproducibility depends on the position of the patient (sitting position appears to have a higher SD compared with the supine position) and also whether other maneuvers are performed during testing, such as straining or coughing. Since the results of urethral pressure measurements are so highly dependent on the technique used and the circumstances of measurement, it is recommended that each laboratory draw up its own frame of reference. In long-duration measurements, the urethral pressure shows considerable variation in patients and healthy women.19 Sørensen et al.23 found urethral pressure variations from 3 to 66 cmH2O during 1-hour’s continuous recording in healthy women. These pressure variations appear to be genuine;24 however, during ambulatory urodynamic monitoring the urethral pressure may decrease to zero without leakage, because of artifacts and methodologic problems attendant on the use of micro-tip transducer catheters.25 Consequently, it has been recommended that ambulatory monitoring of urethral pressure should involve the use of a leak detector.25 The correlation between severity of stress incontinence and standard static profile parameters varies considerably between investigators.26,27 This may relate to the lack of a consistent grading system for severity of incontinence. Conventional static urethral parameters provide very limited pathophysiologic information.26,27 MUCP has been reported to correlate with the degree of urethral incompetence.28 Successful surgical treatment of stress incontinence is not associated with significant changes in the resting parameters.29,30 To summarize, urethral pressure recording in a resting patient is possible but quite difficult. Even with standardized methodology, there is a variety of potential artifacts that should be considered critically when interpreting the results.
Pressure/Cross-sectional area measurement Conventional urethral pressure measurement yields a single pressure at a given site in the urethra. This pressure depends on the cross-sectional area (CA) of the probe used.21 If the CA of the urethra is changed consecutively,
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c
pura (cmH2O)
120 }=Elastance 80 pmin p0 40
Urethral pressure (pura) (cmH2O)
150 125 100
20
40 CA (mm2)
60
Figure 18.6. Related values of urethral pressure (pura) and cross-sectional area (CA) in a healthy volunteer. Measurement is performed 0.75 cm from the bladder neck with the subject in the supine position with an empty bladder. The solid line is the regression line (pura = dpura/dCA) CA + p0, where p0 is the theoretical uninstrumented urethral pressure. The slope of the curve dpura/dCA is the elastance, where elastance is the reciprocal of compliance (a measure of the increase in [e.g. airway] pressure for a given increase in volume of [e.g.] gas or air).
b
75 50 25 0
0
a
0
10
20 30 40 50 60 70 Urethral cross-sectional area (CA) (mm2)
80
Figure 18.7. The urethral pressure (pura) and cross-sectional area (CA) relationship in (a) a normal woman, (b) a stressincontinent woman with urethral hyperlaxity, and (c) a stressincontinent woman with intrinsic sphincter deficiency. The figure shows that the pressure measured with a probe with a CA of 11 mm2 (~12 Fr) (indicated by arrows) would yield the same pressure in patients b and c.
and hyperlaxity. This can be done by estimation of elastance and p0.20
Dynamic measurements in the resting urethra a pressure–CA relationship is outlined (Fig. 18.6). This relationship, given by the equation pura = E × CA + p0, characterizes the urethral sphincter function, since p0 describes the pressure at which the urethra opens and elastance (E = dpura/dCA) is the resistance against dilation. The maintenance of continence depends on the ability of the closure mechanism to produce a p0 that is higher than pves and/or a high elastance in order to prevent opening and subsequent dilation of the urethra, both at rest and during stress episodes. Reference values have been reported by several authors.21,31–33 Elastance and p0 can be estimated by conventional techniques if measurements are performed with different sized catheters.34 The usability of these parameters remains to be documented. A MUCP value <20 cmH2O (‘low-pressure urethra’) has been considered predictive of poor outcome of conventional bladder neck suspension operations,35 and has been the most popular single predictor of intrinsic sphincter deficiency (ISD). As can be seen from Figure 18.7, urethral pressure depends on the CA of the measuring probe; for instance, if a probe with a CA of 11 mm2 (=12 Fr) is used, the same pressure will be obtained in the patient with hyperlaxity and the patient with ISD. Measurement of MUCP does not allow for the differentiation between a rigid malfunctioning urethra
Conventional methods measure the urethral pressure at a fixed CA given by the dimensions of the probe. Urinary stress incontinence, however, is a dynamic event with forced opening of the urethra. The dynamic urethral pressure response to a simulated urine ingression has been studied by several authors (Fig. 18.8a).31,32,36–38 The pressure response represents an integrated stress response from the surrounding tissues, which may reflect the viscoelastic properties of the involved structures (Fig. 18.8b). Bagi et al.37 have found that striated muscle fibers are of dominating significance for the pressure response. Pudendal nerve blockade affects urethral stress relaxation significantly by a reduction in the fast time constant, tb.39 Data show that the stress relaxation response is significantly changed at the bladder neck and mid-urethrally in patients with stress incontinence (Fig. 18.8b), indicating that the resistance against dilation of the urethra by ingression of urine is decreased.21,31,36,40 Thind38 has estimated that urethral viscoelasticity may account for 25% of the urethral resistance to dilation.
Measurements during coughing and voluntary contraction of the pelvic floor Stress incontinence normally occurs in relation to an 257
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stress incontinence (GSI) (Fig. 18.1). Thus, the concept is defined as an ‘all-or-nothing’ phenomenon. However, the test may be ‘negative’ in patients with GSI and ‘positive’ in situations where urine loss does not occur.6,25,42 The test result may vary within the individual woman, according to the size of the cough.43 Cough profile parameters correlate poorly with the severity of GSI.27 Reproducibility of the test has not been established. Richardson42 has reported the predictive value of a positive test to be 82–86% and the predictive value of a normal test to be 57–58% in the diagnosis of GSI in women with lower urinary tract symptoms. The reliability (and hence the usefulness) of cough profilometry using conventional micro-tip transducer catheters is dubious.
40 0
50 0
p0.5 p0.1
pequ 1s
a
Urethral pressure (cmH2O)
250 200
Pressure transmission ratio (PTR) p0.1
150 100
p0.5
50 0
pequ 0 0.1
b
0.5
1.0 Time (s)
2.0
Figure 18.8. (a) Simultaneous measurement of urethral pressure and cross-sectional area during forced dilation; measurement at the bladder neck in a healthy 28-year-old female volunteer. The pressures 0.1 s and 0.5 s after dilation and at equilibrium were used for calculation. (b) Illustration of urethral stress relaxation in a continent –●– and a stress incontinent –– woman. increase in abdominal pressure such as during coughing. Consequently, it seems relevant to test the urethral closure function during coughing. Furthermore, it has been shown that changes in static pressure profile parameters measured in the resting urethra do not necessarily reflect changes in cough-produced profile data.41 Therefore, it seems relevant to supplement resting profile results with measurements during stress episodes to assess urethral competence. The parameters commonly in use are the cough profile, pressure transmission ratio (PTR), leak point pressure, and time separation during coughing.
Cough profile If every cough along the urethral closure pressure profile generates a negative spike that reaches the zero zone (i.e. pressure equalization), the test is considered ‘positive’ and hence suggests the diagnosis of genuine
The concept of the PTR, defined as the increment in urethral pressure during coughing as a percentage of the simultaneously recorded increment in bladder pressure, has received considerable attention. However, it remains unclear what is really recorded. It has been suggested that the urethral pressure spike represents the sum of passively and actively generated closure forces, which may explain why the PTR can exceed 100%. Data indicate that differences in PTR between continent and stress-incontinent women are due to differences in the actively created forces.44 Pressure studies have shown that the pressure created inside the urethral lumen is higher than the pressure outside the urethra during coughing.43,45 Thus, the term ‘pressure transmission’ is misleading, as there appears to be a pressure gradient from inside to outside the urethra. Clinically, Bump et al.46 found that a PTR value of less than 90% in the proximal urethra had a positive predictive value of 53% and a negative predictive value of 97%. As previously stated, test results may vary within the individual woman, according to the intensity of the cough.47 Studies have shown that PTR measurement is subject to marked variation and that the overlap between normal and stress-incontinent values is so great that PTR is of limited value in predicting whether the urethral mechanism is competent or incompetent.48–50 The within-subject standard deviation for the pressure transmission ratio varies between 13 and 18.5% (95% confidence limits up to ±37%). The coefficient of variation has been estimated to be 20% (95% confidence limits ±39%).22 In practice, it seems to be impossible to identify the origin of a higher or lower transmission ratio, and sophisticated interpretations are therefore questionable. Dynamic urethral pressure parameters are generally affected by surgery.29,51 However, the association between
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the result and the change in the parameter used is not straightforward.51
Leak point pressure Valsalva or cough leak point pressure has been introduced as a quantifiable dynamic measure of urethral sphincter function.52 According to some authors, the test is remarkably reproducible;53 however, others have found significant test–retest variation.54 The cough leak point pressure has been found to show a moderate degree of inverse correlation with pad test data.55,56 At the moment the test is not standardized. The test result depends on the size of the catheter, vesical volumes, and patient position.57 Although leak point pressure measurement appears to be useful in quantifying urethral sphincter competence,58 the test cannot disclose the underlying pathophysiology, and thus cannot differentiate between stress incontinence due to hypermobility and that due to ISD.58 There are no compelling data to suggest that knowledge of abdominal leak point pressure aids in either improving surgical outcome by altering surgical technique or by improving patient selection.
to
$t o
te
$t e
Figure 18.9. Normal pressure variations in bladder (top line) and urethra (bottom line) during a stress episode: to, time of onset of pressure increase in the bladder; te, time at the end of pressure increase in the bladder; ∆to, time difference between the onset of pressure increase in the urethra and that in the bladder; ∆te, time difference between the end of pressure increase in the urethra and that in the bladder.
Time separation during coughing Several authors have studied the time separation between changes in bladder and urethral pressure during coughing.11,59,60 In continent women, urethral pressure has been found to rise approximately 200 ms before pressure in the bladder begins to rise during coughing (Fig. 18.9), whereas this preceding increase in urethral pressure is lacking in stress-incontinent women.11,60 A recent study showed that successful anti-incontinence surgery restored this preceding urethral pressure rise, whereas unsuccessful surgery did not.61 The cough urethral pressure profile is highly susceptible to artifacts and pitfalls. The main problem is that micro-tip transducer catheters measure a unidirectional force instead of a true pressure. Artifacts occur because of catheter stiffness, weight, and movement.7,8,62
Contraction of the pelvic floor Urethral pressure measurement has been used to assess the effect of pelvic floor contraction.10,16,31,63 Significant differences have been found between stress-incontinent and healthy women.10,62,64 Advanced techniques enable measurement of the effect of the urethral closure function in terms of power generation during coughing and voluntary contraction of the pelvic floor.62 In women with GSI, the mean power generation during such contraction is reduced by
approximately 50% all along the urethra, while the mean power generation during coughing is reduced by 25% in the mid-urethra.63 Urethral pressure measurement during contraction may have potential in the investigation of pelvic floor function and in the assessment of the effect of intervention.
Detrusor overactivity and urethral relaxation Urethral pressure measurement may have a role in the identification of the chronologic sequence of bladder and urethral pressure changes in order to differentiate between different pathophysiologic entities. Incontinence may occur because of a urethral pressure decrease without a detrusor contraction;25 this appears to be a rare entity, which has been termed urethral relaxation incontinence. The simultaneous measurement of urethral and bladder pressures in patients with detrusor overactivity reveals two different patterns: one type is characterized by an uninhibited bladder contraction followed by urethral relaxation; the other comprises a detrusor contraction preceded by urethral relaxation.65 This differentiation may have therapeutic relevance. 259
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Local pathology in the urethra
Research tool
Urethral pressure measurements may be useful to disclose local pathology in the urethra, such as diverticula and strictures.66–68 New techniques can localize the exact site of an obstructive area in the urethra.21
Although all parameters show a certain degree of interindividual variability, they may still be useful when large series of women are studied for the understanding of normal physiologic and pathophysiologic mechanisms. In the individual subject, some parameters are fairly reproducible, which implies that they may be especially useful in sequential measurements (e.g. before and after intervention in the individual patient). There is no doubt that the ‘urethral pressure’ is of significant importance for the continence mechanism. However, urethral pressure is a complex measure.74 It is important to improve the quality of our techniques of measurement and our concepts of interpretation instead of merely increasing the quantities of data based on standard questionable urodynamic measurements.
Impaired bladder emptying Impaired bladder emptying may be suspected in women with low flow rate or significant postmicturition residual urine. A pressure–flow study can differentiate between infravesical obstruction and detrusor hypoactivity. In obstructed and equivocal cases, urethral investigation may add important diagnostic information. Conventional urethral pressure profilometry during rest may reveal a stricture. More advanced techniques – such as urethral pressure profilometry during urination,69 or measurement of related values of pressure and cross-sectional area along the urethra21,70,71 – may be useful to assess the mechanical properties of the urethra and detect local areas of obstruction. Thus, urethral investigation may be helpful in planning the correct treatment in women with impaired bladder emptying, and may prevent inappropriate urethrotomy in cases of poor detrusor function, which potentially may damage the closure apparatus and lead to stress incontinence.
AMBULATORY URODYNAMICS Ambulatory urodynamics may be performed in an effort to capture more realistic or more physiologic observations, especially of incontinence episodes. Monitoring is usually continued for a period of approximately 3–4 hours.72 Urethral pressure measurements may be performed to identify a poorly functioning urethral sphincter (intrinsic sphincter deficiency), a possible contributor to both urodynamic stress incontinence and urethral relaxation incontinence. If urethral pressure is recorded, the transducer should be maintained at the maximum urethral pressure point. This may be achieved by a single stitch to the female urethral opening25 or taping of the catheter to the vulva, penis or thigh. However, movement artifacts and catheter displacement, as well as damage to the catheter, remain a problem.73 Conduction rings on the urethral catheter outside the maximum urethral pressure point can act as a simple, cheap, and sensitive leak detector.25 The Urilos electronic diaper and a temperature-sensitive device are other methods of detecting leakage.
NEW ‘CATHETER-FREE’ METHODS The urethral retroresistance pressure (URP) is a retrograde urethral pressure measured by a new urodynamic system.75 URP is the pressure required to achieve and maintain an open urethra by retrograde infusion of fluid at a controlled rate of 1 ml/s. Although the concept is not new,1 it is still unclear what aspect of urethral function (physiology) the technique precisely discloses. URP appears to decrease with increasing severity of incontinence,76 and there seems to be a positive linear relationship of URP to MUCP and leak point pressure.76 The utility of the concept remains to be defined. One new and promising technique is urethral reflectometry, a modification of acoustic rhinometry, which enables simultaneous measurements of pressure and cross-sectional area.77 The technique provides a new parameter for characterization of urethral sphincter function. Significant differences between continent and stress-incontinent women have been reported in terms of opening pressure, closing pressure, elastance, and hysteresis.33
CONCLUSIONS • Urethral pressure measurement with conventional techniques is of limited value in assessment of urethral sphincter function. The ‘standard’ parameters do not: 1) discriminate between stress incontinence and other disorders; 2) provide a precise measure of the severity of the condition; or 3) return to normal after successful incontinence surgery.
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• Urethral pressure measurements may be useful
•
•
in disclosing local pathology such as strictures or diverticula, and in targeting the intervention of specific conditions. Urethral pressure measurements may be useful as a research tool to study normal physiologic and pathophysiologic mechanisms and changes after intervention (e.g. pharmacologic treatment) in the individual patient. Urethral pressure measurements should not be performed automatically with the current equipment but should be based on good urodynamic practice in terms of: 1) careful indication and selection of test parameters and procedures; 2) precise measurement with data quality control and complete documentation; and 3) accurate analysis and critical reporting of results.
REFERENCES
mal and stress incontinent women. Acta Chir Scand Suppl 1961;276:1–68. 11. Van der Kooi JB, Van Wanroy PJA, De Jonge MC, Kornelis JA. Time separation between cough pulses in bladder, rectum and urethra in women. J Urol 1984;132:1275–8. 12. Lose G, Colstrup H, Saksager K, Kristensen JK. New probe for measurement of related values of cross-sectional area and pressure in a biological tube. Med Biol Eng Comput 1986;24:488–92. 13. Hilton P. The urethral pressure profile at rest: an analysis of variance. Neurourol Urodyn 1982;1:303–11. 14. Lose G, Schroeder T. Pressure/cross-sectional area probe in the assessment of urethral closure function. Urol Res 1990;18:143–7. 15. Meyhoff HH, Nordling J, Walter S. Short and long term reproducibility of urethral closure pressure profile parameters. Urol Res 1979;7:269–71. 16. Plante P, Susset J. Studies of female urethral pressure profile. Part I. The normal urethral pressure profile. J Urol 1980;123:64–9.
1. Bonney V. On diurnal incontinence of urine in women. J Obstet Gynaecol Br Emp 1923;30:358–65.
17. Ghoneim MA, Rottenbourg JL, Fretin J, Susset JG. Urethral pressure profile. Urology 1975;5:632–7.
2. Lose G, Griffiths D, Hosker G et al. Standardisation of urethral pressure measurement: Report from the Standardisation Sub-Committee of the International Continence Society. Neurourol Urodyn 2002;21:258–60.
18. Sørensen S. Urethral pressure variations in healthy and incontinent women. Neurourol Urodyn 1992;11:549–91.
3. Brown M, Wickham JEA. The urethral pressure profile. Br J Urol 1969;41:211–17.
20. Abrams P, Cardozo L, Fall M et al. The standardisation of terminology of lower urinary tract function. Report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 2002;21:167–78.
4. Thind P, Bagi P, Lose G, Mortensen S. Characterization of pressure changes in the lower urinary tract during coughing with special reference to the demands of the pressure recording equipment. Neurourol Urodyn 1994;13:219–25. 5. Asmussen M, Ulmsten U. Simultaneous urethrocystometry and urethral pressure profile measurement with a new technique. Acta Obstet Gynecol Scand 1975;54:385–6. 6. Anderson RS, Shepherd AM, Feneley RCL. Microtransducer urethral profile methodology in variations caused by transducer orientation. J Urol 1983;130:727–8. 7. Plevnik S, Janez J, Vratcnik P, Brown M. Directional differences in urethral pressure recording: contributions from the stiffness and weight of recording catheter. Neurourol Urodyn 1985;4:117–28. 8. Schäfer W. Regarding ‘directional differences in urethral pressure recording: contributions from the stiffness and weight of recording catheter’. Neurourol Urodyn 1986;5:119–20. 9. Culligan PJ, Goldberg RP, Blackhurst DW et al. Comparison of microtransducer and fiberoptic catheters for urodynamic studies. Obstet Gynecol 2001;98:253–7. 10. Enhörning G. Simultaneous recording of intravesical and intra-urethral pressure: a study of urethral closure in nor-
19. Kulseng-Hanssen S. Urethral pressure variation. Int Urogynecol J 1993;4:366–72.
21. Lose G. Simultaneous recording of pressure and crosssectional area in the female urethra: a study of urethral closure function in healthy and stress incontinent women. Neurourol Urodyn 1992;11:55–89. 22. Griffiths D, Kondo A, Bauer S et al. Dynamic testing: In: Abrams L, Cardozo L, Khoury S et al (eds) Incontinence: 3rd International Consultation on Incontinence. Plymouth, UK: Health Publication, 2005; 23. Sørensen S, Kirkeby HJ, Stødkilde-Jørgensen H, Djurhuus JC. Continuous recording of urethral activity in healthy female volunteers. Neurourol Urodyn 1986;5:5–16. 24. Colstrup H, Lose G, Jørgensen L. Pressure variation in the female urethra measured by the infusion technique: is it an artefact? Neurourol Urodyn 1988;7:457–60. 25. Kulseng-Hanssen S. Ambulatory urodynamic monitoring of women. Scand J Urol Nephrol Suppl 1996;30:27–37. 26. Homma Y. The clinical significance of the urodynamic investigation in incontinence. BJU Int 2002;90:489–97. 27. Weber AM. Is urethral pressure profilometry a useful diagnostic test for stress urinary incontinence? Obstet Gynecol Surv 2001;56:720–35.
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28. Schick E, Bertrand PE, Jolivet-Tremblay M et al. Observations on the function of the female urethra: II: Relation between maximum urethral closure pressure at rest and the degree of urethral incompetence. Neurourol Urodyn 2004;23:16–21. 29. Henriksson L, Ulmsten U. A urodynamic evaluation of the effect of abdominal urethrocystopexy and vaginal sling urethroplasty in women with stress incontinence. Am J Obstet Gynecol 1987;131:77–82. 30. Bergman A, McCarthy TA. Urodynamic changes after successful operation for stress urinary incontinence. Am J Obstet Gynecol 1983;147:325–7.
A comparison between stress incontinent and continent women. Urol Res 1978;6:127–34. 44. Lose G. Urethral pressure and power generation during coughing and voluntary contraction of the pelvic floor in females with genuine stress incontinence. Br J Urol 1991;67:580–5. 45. Papa Petros PE, Ulmsten U. Urethral pressure increase on effort originates from within the urethra and continence from musculovaginal closure. Neurourol Urodyn 1995;14:337–50.
31. Colstrup H. Closure mechanism of the female urethra. Neurourol Urodyn 1987;6:271–98.
46. Bump RD, Copeland WE, Hurt WG, Fantl JA. Dynamic urethral pressure/profilometry pressure transmission ratio determinations in stress-incontinent and stress-continent subjects. Am J Obstet Gynecol 1988;159:749–55.
32. Thind P. The significance of smooth and striated muscles in the sphincter function of the urethra in healthy women. Neurourol Urodyn 1995;14:585–618.
47. Swift SE, Rust PF, Ostergard DR. Intrasubject variability of pressure-transmission ratio in patients with genuine stress incontinence. Int Urogynecol J 1996;7:312–16.
33. Klarskov N, Lose G. Urethral sphincter properties measured using reflectometry in healthy and stress incontinent women. In: 34th Annual Meeting of International Continence Society. Paris, 2004; Abstract 326.
48. Richardson DA, Ramahi A. Reproducibility of pressure transmission ratios in stress incontinent women. Neurourol Urodyn 1993;12:123–30.
34. Thind P, Lose G, Colstrup H. How to measure urethral elastance in a simple way. Elastance: definition, determination and complications. Urol Res 1991;19:241–4.
49. Lose G, Thind P, Colstrup H. The value of pressure transmission ratio in the diagnosis of stress incontinence. Neurourol Urodyn 1990;9:323–4.
35. Sand PK, Bowen LW, Panganiban R, Ostergard DR. The low pressure urethra as a factor in failed retropubic urethropexy. Obstet Gynecol 1987;68:399–402.
50. Rosenzweig BA, Bhatia NN, Nelson AL. Dynamic urethral pressure profilometry pressure transmission ratio: what do the numbers really mean? Obstet Gynecol 1991;77(4):586–90.
36. Lose G, Colstrup H. Mechanical properties of the urethra in healthy and stress incontinent females: dynamic measurements in the resting urethra. J Urol 1990;144:1258–62.
51. Sayer TR, Hosker GL, Warrell DW. Does successful bladder neck surgery alter urethral closure? Neurourol Urodyn 1991;10:448–9.
37. Bagi P, Thind P, Norsten M. Passive urethral resistance to dilatation in healthy women: an experimental simulation of urine ingression in the resting urethra. Neurourol Urodyn 1995;14:115–23.
52. McGuire ES, Fitzpatrick CC, Wan J et al. Clinical assessment of urethral sphincter function. J Urol 1993;150:1452–4.
38. Thind P. An analysis of urethral viscoelasticity with particular reference to the sphincter function in healthy women. Int Urogynecol J 1995;6:209–28.
53. Bump RC, Elser DM, McClish DK. Valsalva leak point pressures in adult women with genuine stress incontinence: reproducibility effect of catheter caliber and correlations with passive urethral pressure profilometry. Neurourol Urodyn 1993;12:307–8.
39. Thind P, Bagi P, Mieszczak C, Lose G. Influence of pudendal nerve blockade on stress relaxation in the female urethra. Neurourol Urodyn 1996;15:31–6.
54. Siltberg H, Larsson G. Victor A. The reproducibility of a new method to measure leak point pressure in patients with GSI. Neurourol Urodyn 1994;13:456–8.
40. Thind P, Lose G. Urethral stress relaxation phenomenon in healthy and stress incontinent women. Br J Urol 1992;69:75–8.
55. Theofrastous JP, Bump RC, Elser DM et al. Correlation of urodynamic measures of urethral resistance with clinical measures of incontinence severity in women with pure genuine stress incontinence. The Continence Program for Women Research Group. Am J Obstet Gynecol 1995;173:407–12.
41. Thind P, Lose G, Colstrup H, Andersson K-E. The effect of pharmacological stimulation and blockade of autonomic receptors on the urethral pressure and power generation during coughing and squeezing of the pelvic floor in healthy females. Scand J Urol Nephrol 1993;27:519–25. 42. Richardson DA. Value of the cough pressure profile in the evaluation of patients with stress incontinence. Am J Obstet Gynecol 1986;155:808–11. 43. Bunne G, Öbrink A. Urethral closure pressure with stress.
56. Siltberg H, Larsson G, Victor A. Reproducibility of a new method to determine cough-induced leak-point pressure in women with stress urinary incontinence. Int Urogynecol J 1996;7:13–19. 57. Bump RC, Elser DM, Theofrastous JP, McClish DK. Valsalva leak point pressures in women with genuine stress
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incontinence: reproducibility, effect of catheter caliber and correlations with other measures of urethral resistance. Am J Obstet Gynecol 1995;173:551–7. 58. Weber AM. Leak point pressure measurement and stress urinary incontinence. Current Women’s Health Reports 2001;1:45–59. 59. Faysal MH, Constantinou CE, Rother LF, Govan DA. The impact of bladder neck suspension on the resting and stress urethral pressure profile: a prospective study comparing controls with incontinent patients preoperatively and postoperatively. J Urol 1981;125:55–60. 60. Thind P, Lose G, Jørgensen L, Colstrup H. Urethral pressure increment preceding and following bladder pressure elevation during stress episode in healthy and stress incontinent women. Neurourol Urodyn 1991;10:177–83. 61. Pieber D, Zivkovic F, Tamussino K. Timing of urethral pressure pulses before and after continence surgery. Neurourol Urodyn 1998;17:19–23. 62. Richardson DA. Reduction of urethral pressure response to stress: relationship to urethral mobility. Am J Obstet Gynecol 1986;155:20–5. 63. Lose G, Golstrup H. Urethral pressure and power generation during coughing and voluntary contraction of the pelvic floor in healthy females. Br J Urol 1991;67:573–9. 64. Susset J, Plante P. Studies of female urethral pressure profile. Part II: Urethral pressure profile in female incontinence. J Urol 1980;123:70–4. 65. Elia G, Bergman A. Urethral pressure changes in women with detrusor instability. Int Urogynecol J 1994;5:98–101. 66. Højsgaard A. The urethral pressure profile in female patients with meatal stenosis. Scand J Urol Nephrol 1976;10:97–9. 67. Summitt RH, Stovall TG. Urethral diverticula: evaluation
by urethral pressure profilometry, cystourethroscopy and voiding cystourethrogram. Obstet Gynecol 1992;80:695–9. 68. Bhatia NN, McCarthy TA, Ostergard DR. Urethral pressure profiles in women with diverticula. Obstet Gynecol 1981;58:375–8. 69. Sullivan MP, Yalla SV. Micturition profilometry. In: Raz S (ed) Female Urology. Philadelphia: Saunders, 1996; 132–42. 70. Regnier CH. Direct static measurement of obstruction. Neurourol Urodyn 1986;5:251–7. 71. Susset IG, Ghoniem GM, Regnier CH. Abnormal urethral compliance in females: diagnosis, results and treatment. J Urol 1983;129:1063–5. 72. van Waalwijk van Doorn E, Anders K, Kullar V et al. Standardisation of ambulatory urodynamic monitoring: Report of the Standardisation Sub-committee of the International Continence Society for ambulatory urodynamic studies. Neurourol Urodyn 2000;19:113–25. 73. Helsington K, Hilton P. Ambulatory urodynamics. Br J Urol 1996;103:393–6. 74. Golstrup H, Lose G, Thind P. Urethral pressure – which one? Urol Res 1992;20:169–72. 75. Slack M, Tracey M, Hunsicker K et al. Urethral retro-resistance pressure: a new clinical measure of urethral function. Neurourol Urodyn 2004;23:656–61. 76. Slack M, Culligan P, Tracey M et al. Relationship of urethral retro-resistance pressure to urodynamic measurements of incontinence severity. Neurourol Urodyn 2004;23:109–14. 77. Klarskov N, Rasmussen SB, Lose G. Pressure reflectometry: in vitro recordings with a new technique for simultaneous measurement for cross-sectional area and pressure in a collapsible tube. Physiol Meas 2005;26:1–12.
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Background Detrusor pressure during urine flow in the urethra reflects outlet resistance and not the strength or power of the bladder muscle. Measurement of the pressure in the bladder at the instant of urinary leakage evolved as an indirect measure of urethral resistance. Both Griffiths and Schaeffer noted that detrusor pressure (pdet) during urine flow was not related to detrusor contractility but rather was a direct reflection of moment by moment urethral resistance.1–3 Pressure/flow (P/Q) studies showed that very high flow rates could be recorded during a low pressure detrusor contraction. Obviously, that could happen only if the outlet resistance were also very low. Direct measurement of urethral resistance during flow proved difficult and thus P/Q data were used to determine urethral resistance by calculation. Gleason and co-workers used a different technique that involved measurement of residual stream energy as a reflection of outlet resistance.4 From these and other data it is clear that at every point of urine flow pdet reflects outlet resistance at that instant. This means that a very poor detrusor muscle can develop a very high instantaneous pressure if outlet resistance is very high. This situation occurs in obstructive uropathy related to prostatism and in neurogenic conditions where detrusor sphincter dyssynergia is present. In both cases, high pressures do not reflect the strength of the detrusor contraction but the level of outlet resistance.
bladder contraction. In addition to a low compliance bladder, nearly all of these children could be shown to have true stress incontinence on an upright video study, a finding we attributed to the lack of internal sphincter function. Further study in this patient population showed that patients with high outlet resistance and high detrusor leak point pressures always had a low compliance bladder. A pressure-based management system was then developed where very young children were evaluated by leak point pressure testing and treatment initiated on that basis alone. Initial treatment was intermittent catheterization and anticholinergic therapy; if that failed, urethral dilation was employed to decrease outlet resistance. The objective was control of detrusor pressure, either by frequent emptying and drug therapy or by an achieved reduction in outlet resistance.6 Most pediatric urologists attained a low pressure bladder by creating a cutaneous vesicostomy which obviated urethral resistance. We achieved the same effect with a urethral dilation aimed at the distal sphincter mechanism. Re-study of those children who had a urethral dilation showed, to our surprise, that low compliance bladder dysfunction resolved with evolution of much lower pressure storage behavior. In other words, a reduction in outlet resistance resolved the problem of the low compliance bladder, reinforcing the hypothesis that the outlet was the basis of the problem in the first place.
detrusor leak point pressures
urethral function and continence
These were first described in children with myelodysplasia. In these cases a decentralized, areflexic bladder coexists with a non-functional proximal sphincter mechanism. Some sphincteric function is present in the distal sphincter area, but this is fixed, and not reflexly active, or linked to phases of detrusor activity, as no neural mechanism to drive such activity exists. Given the nature of the neurogenic bladder and urethra present in these children, it is not surprising that very severe incontinence is almost always present. A longitudinal database consisting of repetitive urodynamic studies and serial upper tract imaging was assembled at two institutions caring for populations of these children. From a study of the data, it became obvious that upper tract changes and vesicoureteral reflux were linked to high detrusor pressures at the time of leakage driven by volume. That is: a supine cystometrogram, which demonstrated a detrusor pressure greater than 40 cm at the instant of leakage, was invariably associated with upper tract damage if untreated.5 In most cases detrusor pressure was a product of poor bladder compliance and not a reflex
Control of bladder pressure by one means or another prevented upper tract damage but did little for urinary continence which remained a problem in most of these children. This appeared to be related to poor urethral function and to the lack of proximal urethral closure in particular.7 In an effort to achieve continence in patients with myelodysplasia, urologists used the artificial urinary sphincter and other measures to close the open proximal urethra. The artificial sphincter, while effective in control of stress incontinence, unfortunately increased outlet resistance to a level which sharply raised the detrusor leak point pressure, which in turn led to dramatic upper tract changes. As a result, the artificial urinary sphincter was largely abandoned in these children, and slings, or bladder neck wraps, using autologous fascia were used instead. Unlike the artificial sphincter, slings and wraps placed around the proximal urethra in girls, or prostatic urethra in boys, effectively raise the abdominal pressure required to cause urine leakage, but change the detrusor leak point pressure very slightly or not at all.8,9 Upper
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tract changes do not occur in patients treated with slings. These findings suggested that, as far as the urethra is concerned, abdominal pressure and detrusor pressure are very different expulsive forces. Indeed, when a group of myelodysplastic children were studied with videourodynamics we found that the pdet to induce leakage was very different from the intra-abdominal pressure (pabd) required to do the same thing.10 Since both pabd and pdet are measured in the bladder, it was initially a little difficult to imagine that for the urethra these are different forces. The best evidence for that concept was the ability to close the urethra gently with a sling and in so doing elevate the abdominal pressure required to induce leakage dramatically but at the same time not changing the detrusor pressures required to induce flow. There are some rare but specific instances where urethral pressure profile data have a relationship to the detrusor leak point pressure. In lower motor neuron lesions characterized by absent proximal sphincter function, the pdet at leakage will be very close to the maximum urethral closing pressure measured at the start of filling. This is related to the fact that fixed outlet resistance at any level of the urethra requires an equivalent detrusor pressure to overcome it. The abdominal leak point pressure in this circumstance will not be identical to the resting urethral pressure profile (UPP) but will be higher than that value. It is a peculiarity of urethral function that the proximal urethra appears to be the primary site of resistance to abdominal pressure as an expulsive force. When proximal sphincter function is absent, or lost, even a normal reflexly and volitionally active distal sphincter mechanism manifesting a normal closure pressure will not prevent stress incontinence. That brings us back to the central problem with urethral pressures and outlet resistance. It is difficult, or impossible, to use intraluminal urethral pressures determined at rest or during flow as a measure of urethral continence function. Normal urethral profile values, especially maximum urethral closing pressures, do not rule out stress incontinence nor is every low pressure urethra incompetent. To determine the resistance of the urethra to detrusor pressure, one measures the force (pdet) required to cause flow. To determine the ability of the urethra to resist abdominal pressure, pabd is measured at the instant leakage occurs. As in P/Q testing, if no leakage or flow occurs in the urethra the measurement is not quantitative. On the other hand, a detrusor pressure over 100, with a closed sphincter on videourodynamics and no flow, indicates very high urethral resistance. A measured abdominal pressure in excess of 150 cm, with no leakage, defines a reasonable sphincter mechanism against that expulsive force.
stress incontinence The International Continence Society defines stress incontinence as involuntary leakage induced by abdominal pressure where there is no evidence of a detrusor pressure component. That is, of course, a correct definition, but sometimes the determination that there is no detrusor pressure component to a given patient’s incontinence is not easy. Using twin channel, subtracted cystometry, one can determine that there is no detrusor activity when the patient is asked to cough or strain and leakage occurs at that time. If leakage does occur, stress incontinence is certainly present. On the other hand, a cystometrogram which shows no detrusor activity does not rule out motor urge incontinence; indeed, standard cystometry grossly underestimates the existence of conditions where reflex bladder contractility is the cause of incontinence. That is the reason why epidemiologic data suggesting a high prevalence of motor urge incontinence are not reflected in the diagnosis of motor urge incontinence when patients with overactive bladder (OAB) symptoms are subjected to a rigorous urodynamic evaluation. The problem is not the OAB symptoms but the test we use to determine if motor urge incontinence is present, i.e. the cystometrogram. Using cystometry to rule out motor urge incontinence is not possible. However, if a videourodynamic study shows no stress incontinence at moderate bladder volumes and high abdominal pressures, one can reasonably conclude that stress incontinence is probably not present and that a bladder cause for a given person’s incontinence is likely.
leak point pressure testing in patients with incontinence A urethra that leaks with an increase in abdominal pressure identifies the condition of stress incontinence. The pressure required to drive urine out of the urethra is inversely proportional to the strength of the continence mechanism. Leak point pressures are best done in the nearly upright position under fluoroscopic monitoring. We use a triple lumen 7 Fr urodynamic catheter. The urethral and bladder pressure channels are zeroed with flow on, outside the patient, at the level of the symphysis.10 The urethral pressure channel aperture is positioned, via the radio-opaque marker, in the area of the distal sphincter, while the bladder pressure channel aperture is in the bladder. The patient is placed in the upright position or nearly so. The bladder is filled to 250 ml with 20% iodinated contrast material. Bladder compliance is carefully monitored. At 250–300 ml the patient is asked to strain several times in an effort to induce leakage. 267
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If that does occur, the event marker is triggered and a fluoroscopic image captured. Patients have a tendency to strain until they leak and then stop. During this part of the study we look for urethral mobility and for any bladder prolapse. If several separate straining efforts do not induce leakage we ask the patient to cough several times in a row as vigorously as possible. If coughing produces leakage we set the event marker and capture rapid sequence images. This makes possible a detailed analysis of the degree of urethral mobility, if any, and freezes and records the digitized pressure at the instant of the leak captured on the image(s). We normally do not use subtracted cystometric data, since the video study provides clear detail of a phasic reflex bladder contraction. Detrusor compliance is very important here. A poorly compliant bladder gains pressure with volume. That pressure gain tends to open the proximal urethra and makes the leak point pressure look lower than it actually is. Part of the expulsive force here is detrusor pressure and thus the leakage is not really true stress incontinence, even if it looks very much like it. This is one of the reasons to avoid leak point pressure testing with a single pressure sensing device in the vagina or rectum as this obviates part of the expulsive force, i.e. detrusor pressure. Although normally this is relatively low, it is not always so. In addition, patient position is vital. Even patients with serious stress incontinence may not leak in the supine position, thus the nearly upright position is best for this test. Vaginal prolapse also interferes with the test, as does bladder prolapse. In these cases the urethra may not leak, even if stress incontinence is present. This may occur because the urethra is supported by the prolapse or because the pabd is dissipated in the cystocele. There are other problems with the leak point pressure test, though the most frequent comment about leak point pressure testing is that the technique is ‘nonstandardized’.11,12 The technique is standardized to the extent that we have always done it exactly this way, and find the data consistent. On the other hand, the data are not precise enough to be absolutely quantitative. Leak point pressure values taken together with the physical findings, the video images, and the patient history provide an almost complete picture of the function of the urethral continence mechanism in a given patient. A ‘low’ leak point pressure ranges from 0 to approximately 60–70. Very low values, where the leak point pressure is less than 40, suggest urethral compression will be required to achieve stress competence. The upper range for lower leak point pressures (~50–70) has to be considered together with data on urethral mobility. If there is urethral mobility, and the leak point pressure is greater
than 50, urethral compression is probably not required. However, if there is no urethral mobility, some compression may be required to achieve stress competence.13
abdominal leak point pressures and the urethral pressure profile Urethral pressure profile (UPP) data by necessity concentrates on maximal pressure areas within the urethra. Closing pressure is a calculated value where pdet is subtracted from maximum profile pressure, based on an assumption that a pressure anywhere in the urethra reflects continence function against pabd as the expulsive force. That is an error. As Lose noted, UPP data do not permit the diagnosis of stress incontinence, do not correlate with the severity of the condition, and do not change with successful therapy.14 Most studies of these measures of urethral function – leak point pressures and urethral pressure profilometry – find poor correlation between the two.15–17 This would appear understandable, as they measure different things.
conditions within stress incontinence Although grading stress incontinence severity in relation to certain activities is useful, independent variables – including prolapse, bladder dysfunction, and the patient’s activity level – make it less than quantitative. Some more precise method would be helpful, especially where multiple operations have failed or reconstruction of a damaged urethra is contemplated, or neurogenic conditions exist.
Worst cases Stress incontinence associated with lack of function of the internal sphincter, regardless of function of the distal sphincter, is severe. Treatment is specifically designed to close the open urethra, not to support it, as the latter does not reliably cure urethral incontinence associated with this kind of urethral dysfunction.18 For this reason it is important to identify the condition. Upright cystography, at very low bladder volumes, shows an open non-functional bladder outlet. The bladder and proximal urethra are isobaric. This occurs in neurogenic conditions such as myelodysplasia and T12 spinal cord injury, after radical pelvic surgery with bilateral pelvic neural plexus injury, occasionally after pelvic trauma and urethral diverticulectomy, and sometimes after labor and delivery; it also occurs spontaneously (Figs 19.1–19.3). Patients with absent proximal sphincter function have low to very low abdominal leak point pressures and are incontinent in the upright position
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Figure 19.1. Leak point pressure image from a 22-year-old man with a T12 spinal cord injury. The proximal sphincter is non-functional as a result of the spinal injury which involves the sympathetic supply to the urethral smooth sphincter. The distal sphincter does function but leakage occurs at an intraabdominal pressure (pabd) of 55.
Figure 19.3. Leak point pressure image from a 32-year-old woman with multiple sclerosis treated with a Foley catheter for 5 years. The urethra is non-functional. The leak point pressure is not measurable. with very little effort and may be more or less continuously incontinent (Fig. 19.4).
Failure of prior operative procedures for stress incontinence
Figure 19.2. Leak point pressure image at the instant of leakage from a 74-year-old woman with continuous leakage of urine without regard to activity. She has had a radical hysterectomy and adjuvant radiation therapy. The urethra is non-functional. The leak point pressure is 14.
Basically, operative procedures for stress incontinence support the urethra, compress it, or do a little of both. Failure of an operation (or operations) to eliminate stress incontinence does not suggest that proximal urethral function is impaired, although that may be the case. Recurrent urethral hypermobility and stress incontinence can occur after retropubic suspensions and other procedures for stress incontinence. Recurrent hypermobility and higher leak point pressures suggest that the stress incontinence can be resolved with another suspension procedure (Fig. 19.5). Hypermobility alone is rarely the cause of persistent or recurrent incontinence after one of the newer synthetic sling procedures which support the urethra very well indeed. Inadequate compression of the urethra is associated with failure to cure stress incontinence, either immediately or over time. This can occur with any procedure but it can be a problem with bone anchor slings and the newer synthetic sling procedures. When this occurs, leak point pressures are low and videourodynamics that includes leak point pressure testing shows an open or partly open urethra (Figs 19.6–19.8). Another important cause of recurrent stress incontinence after any stress incontinence operation, including 269
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Figure 19.4. Leak point pressure image after 3 years’ treatment with a catheter for ‘inoperable incontinence’. The urethra is non-functional and there is extensive urethral erosion. The leak point pressure is not measurable.
Figure 19.7. Recurrent stress incontinence after a donor fascia, bone anchored, sling. The sling fixes the urethral position but there is persistent leakage at a pressure of 51.
Figure 19.5. Leak point pressure image from a 55-year-old woman with urethral hypermobility. The leak point pressure is 130.
Figure 19.6. Leak point pressure image from a 74-year-old woman who had synthetic sling erosion into the urethra with resultant severe stress incontinence after the sling was removed. The leak point pressure is 6.
Figure 19.8. Persistent stress incontinence after a tensionfree vaginal tape (TVT) procedure. The bladder neck is slightly open. The leak point pressure is 34.
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autologous fascial slings, is vaginal prolapse, especially cystocele formation which appears to place a traction force on the urethra, ultimately causing failure with recurrent stress incontinence (Fig. 19.9). An open urethra at low to moderate bladder volumes usually indicates the presence of type III stress incontinence. This varies from the totally incompetent urethra
Figure 19.9. There is a very large cystocele, which is both central and lateral. Despite the prolapse, the urethra is very mobile. The marker in the mid-urethra can be seen well below the normal urethral position. The axis of the urethra is horizontal, and the internal meatus is lower than the external meatus. This degree of urethra mobility indicates that stress incontinence is present even if there are no symptoms to suggest it.
Figure 19.10. Leak point image from a 44-year-old woman with stress incontinence symptoms after a synthetic sling. There is no mobility of the urethra. The leak point pressure is 51.
associated with prolonged catheter drainage (Fig. 19.10) to a partly open urethra with persistent stress incontinence after a tension-free vaginal tape (TVT) procedure (Fig. 19.11). Mobility of the urethra is another variable. It is best assessed on video study, but a Q-tip test or careful vaginal examination gives more or less the same information. A non-mobile urethra may leak at relatively low abdominal pressures (Fig. 19.12) or higher pressures (Fig. 19.13), or a previously mobile urethra may be well supported and immobile as a result of an operative procedure and still leak at relatively low pressures (Fig. 19.14), or high to very high pressures (Fig. 19.15). Urethral mobility suggests that a no tension support procedure will be effective but leak point pressures appear to be an independent variable, even when mobility is fairly gross (Figs 19.16, 19.17). Vaginal prolapse is also a factor in at least 30% of patients with stress incontinence, and pelvic examination tends to underestimate the degree of prolapse of the anterior vaginal wall and bladder when compared to videourodynamics. If prolapse is present, leak point pressures are suspect, and urethral function may actually be worse than the leak point pressure data suggest (Fig. 19.18). On the other hand, there are times when there is vaginal prolapse but the urethra is non-mobile and appears to resist high to very high abdominal pressures well (Fig. 19.19). In this circumstance we would try to reduce the cystocele and repeat the leak point pressure test. If that did not reveal urethral leakage, or any mobility with coughing or straining, we would not ordinarily suspend the urethra at the time of isolated cystocele repair. There are other conditions diagnosed during videourodynamics that have a bearing on treatment (Figs 19.20, 19.21). The most important of these is altered bladder compliance because this produces a symptom complex that suggests stress incontinence is present when in fact the expulsive force is detrusor pressure. These patients do extremely poorly with any treatment that increases outlet resistance. While a detrusor contraction that cannot be inhibited does occur from time to time during videourodynamic testing, this is not a dangerous condition as is altered compliance, nor does it have much effect on treatment outcome if stress incontinence is objectively demonstrated during the study. If stress incontinence is not present by rigorous upright videourodynamic testing, one may assume that there is a detrusor-related cause for the incontinence.
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Figure 19.11. Primary stress incontinence in a 65-year-old woman with overactive bladder symptoms. The urethra is non-mobile but the leak point pressure is 30.
Figure 19.12. Primary stress incontinence in a 72-year-old woman. The urethra is non-mobile and the leak point pressure is 85. 272
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Figure 19.13. Leak point image from a 44-year-old woman wet despite two prior cadaveric fascia slings with bone anchors. The leak point pressure is 38.
Figure 19.14. Recurrent stress incontinence after a Burch colposuspension. There is urethral mobility and the leak point pressure is 121.
Figure 19.15. Leak point image from a 55-yearold woman with primary stress incontinence. There is urethral mobility. The leak point pressure is 65. 273
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Figure 19.16. Severe stress incontinence, with more or less continuous leakage in a 32-year-old woman after multiple pelvic fractures. Three prior operations for stress incontinence did not help. Note the low position of the bladder neck and the open urethra. There is gross hypermobility of the urethra but the leak point pressure is only 24.
Figure 19.17. Leakage occurs at a pressure of 72, but there is a central cystocele, and considerable mobility of the urethra. The leak point pressure may be inaccurate because of the prolapse.
Figure 19.18. A central cystocele with uncomfortable bladder pressure symptoms, overactive bladder symptoms, with incomplete bladder emptying as demonstrated by residual urine volumes on multiple occasions of 150 ml. The urethra is not mobile, and appears well suspended by a prior sling procedure. The tracings show no leakage at abdominal pressures in excess of 160. We would not re-suspend this urethra were a cystocele repair to be done. 274
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Figure 19.19. A very low compliance bladder associated with chronic catheterization. There is gross leakage but the expulsive force here is detrusor pressure associated with volume.
Figure 19.20. A reflex uninhibited contraction elicited during videourodynamics testing. The expulsive force here is detrusor pressure. pclo, closure pressure; pura, urethral pressure; pves, intravesical pressure.
Figure 19.21. Continuous leakage without sensation in a young woman with a neurogenic bladder. The expulsive force here is detrusor pressure. The low compliance bladder causes reflux into the ureters and gross continuous urinary leakage. pclo, closure pressure; pura, urethral pressure; pves, intravesical pressure. 275
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references 1. Griffiths D. Basis of pressure–flow studies. World J Urol 1995;13:30–3. 2. Schafer W. Analysis of bladder outlet function with linearized passive urethral resistance relation (linPURR) and a disease specific approach to grading obstruction: from complex to simple. World J Urol 1995;13:47–51. 3. Schafer W, Abrams P, Liao L et al. Good urodynamics practice: uroflometry, filling cystometry, and pressure– flow studies. Neurourol Urodyn 2002;21:261–74. 4. Gleason D, Bottaccini M, Reilly B. Office urodynamics. Urol Clin North Am 1979;6:154–60. 5. McGuire E, Woodside J, Bordon T et al. Prognostic value of urodynamic testing in myelodysplastic patients. J Urol 2002;167:1049–53. 6. Wang S, McGuire E, Bloom D. A bladder pressure management system for myelodysplasia – clinical outcome. J Urol 1988;140:1499–1502. 7. Bloom D, McGuire E. Practical management of children with myelodysplasia. Dialogues Pediatr Urol 1989;12:3–4. 8. McGuire E, Wang S, Usitalo H et al. Modified pubovaginal sling in female children with myelodysplasia. J Urol 1989;135:94–6. 9. Raz S, McGuire E, Ehrlich R et al. Fascial sling to correct male neurogenic incontinence. Neurourol Urodyn 1983;7:563–7.
10. McGuire E, Fitzpatrick C, Wan J et al. Clinical assessment of urethral sphincter function. J Urol 1993;150:1463–6. 11. Daneshgari F. Valsalva leak point pressure: steps toward standardization. Curr Urol Res 2001;5:388–91. 12. Weber A. Leak point pressure measurement and stress urinary incontinence. Curr Womans Health Rep 2001;1:45–52. 13. Ghoneim G, Elgamasy A, Elsergany R et al. Grades of intrinsic sphincter deficiency associated with female stress incontinence. Int Urogynecol J Pelvic Floor Dysfunct 2002;13:99–105. 14. Lose G. Urethral pressure measurement – problems and clinical utility. Scan J Urol Nephrol Suppl 2001;207:61–6. 15. Sultana C. Urethral closure pressure and leak point pressure in the incontinent woman. Obstet Gynecol 1995;86:839–42. 16. Pajoncini C, Costantini E, Guercini F et al. Intrinsic sphincter deficiency: do maximum urethral closure pressure and Valsalva leak point pressure identify different pathogenic mechanisms? Int Urogynecol J Pelvic Floor Dysfunct 2002;13:30–5. 17. Nager C, Schulz J, Stanton S et al. Correlation of urethral closure pressure, leak point pressure and incontinence severity measures. Int Urogynecol J Pelvic Floor Dysfunct 2001;12:395–400. 18. Woodside J, McGuire E. Urethral hypotonicity after suprasacral spinal cord injury. J Urol 1979;121:283–5.
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20 Electromyography ˇ David B Vodusek, Clare J Fowler
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IntroductIon Modern electromyography (EMG) started with the introduction of the concentric needle electrode in 1929,1 the design of which has endured ever since, almost unchanged (Fig. 20.1).2 Clinical EMG studies of the pelvic floor were initially sparse,3,4 but in the 1970s several important papers were published;5–8 since then EMG has been used increasingly in urogynecology, neurourology, and proctology research. Nowadays it is used – at least in some centers – as a routine diagnostic investigation. EMG may be performed for two quite distinct although complementary purposes. On the one hand, it can reveal the ‘behavior’ (i.e. patterns of activity) of a particular muscle; on the other, it can be used to demonstrate whether a muscle is normal, myopathic or denervated/reinnervated. The former can be called ‘kinesiologic EMG’ and the latter ‘motor unit’ EMG, but usually this division is not specified and both types of examination are just called ‘EMG’, which can confuse the uninitiated.
the motor unIt EMG is the extracellular recording of bioelectrical activity generated by muscle fibers. Bioelectrical activity – action potentials – are generated by depolarization of single muscle fibers, but the innervation of muscle is such that a single muscle fiber does not contract on its own but rather in concert with other muscle fibers which are part of the same motor unit, i.e. innervated by the same motor neuron. Knowledge of the structure and function of the motor unit is fundamental to understanding the application of these methods.
Needle recording electrode
Needle tip and recording surface
Motor neurons that innervate striated muscle lie in the anterior horn of the spinal cord. Their cell bodies are relatively large and their axonal processes correspondingly of large diameter and myelinated to allow rapid conduction of impulses, although the neurons which innervate the sphincters are relatively smaller than those innervating skeletal limb and trunk muscles. Within the muscle, the motor axon tapers and then branches to innervate muscle fibers which are scattered throughout the muscle (Fig. 20.2). The innervation of muscle is such that it is unlikely that fibers that are part of the same motor unit will be adjacent to one another. This dispersion of muscle fibers is said to be non-random although the stage of development at which it occurs and the factors determining the arrangement are not yet known. The number of muscle fibers innervated by an axon is known as the ‘innervation ratio’. There is no simple neurophysiologic method for estimating this parameter and the number of motor units per muscle is also difficult to estimate by clinical neurophysiologic means. The contraction properties of a motor unit depend on the nature of its constituent muscle fibers. Muscle fibers can be classified according to their twitch tension, speed of contraction, and histochemical staining properties. In the pelvic floor and sphincters the majority of muscle fibers are type 1 although there is some regional variation.9,10 The fatigue-resistant type 1 fibers constitute motor units which fire for prolonged periods of time at lower firing frequencies, i.e. ‘tonically’ (see below). Type 2 fibers make up motor units which fire briefly and rapidly in bursts, i.e. ‘phasically’. Unfortunately, there is no clinical electrophysiologic method which can estimate the proportion of motor units of different muscle fiber types.
Pick-up
Needle diameter
Filter settings
Activity recorded
Concentric needle electrode: central insulated platinum wire inside a steel cannula
Hemisphere radius 0.5 mm
0.3–0.65 mm
5 Hz–10 kHz
Motor units
Single-fiber needle electrode: fine platinum wire (25 Mm diameter) inside steel cannula which records from a side aperture
Hemisphere radius 250–300 Mm
0.5–0.6 mm
500 Hz–10 kHz
Individual muscle fibers of motor units. In health the potentials are either singles or pairs: after reinnervation the potentials have multiple components
Figure 20.1. The concentric needle electrode and the single fiber needle electrode, their physical characteristics, the filter settings required for use, and the nature of the activity that each records. (Modified from ref. 2 with permission.) 278
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Figure 20.2. Diagram of a motor unit showing the motor neuron which is located in the anterior horn of the spinal cord, Onuf’s nucleus in the case of the sphincters, the motor axon which travels in the peripheral nerve to the muscle. Here it divides, innervating a number of muscle fibers, most of which are not adjacent. (Modified from ref. 2 with permission.)
KInesIologIc emg method By prolonged recording of bioelectrical activity of a muscle, a qualitative and quantitative description of its activity over time is obtained. Such techniques are frequently used in rehabilitation and sports medicine to study movement. Meaningful kinesiologic EMG can, of course, only be performed from an innervated muscle. If the lower motor neuron integrity of a particular muscle is questioned, ‘motor unit’ EMG analysis (see below) has to be performed first. The choice of muscle for EMG examination depends on the aims of the investigation. Routine EMG as part of urodynamic studies usually employs a single channel for recording from the urethral or anal sphincter muscle. The sphincters being small circular muscles, it is assumed that the two sides react in a similar fashion, although this may not always be the case, as was shown for the levator ani.11 When we are interested in the pattern of activity of an individual muscle, the technique should ideally provide a selective recording, uncontaminated by neighboring muscles on one hand, and a faithful detection of any activity within the source muscle on the other hand. Unfortunately, both objectives are difficult to achieve simultaneously and the purpose of the investigation will suggest an acceptable compromise. Overall detection from the bulk of a muscle can only be achieved with non-selective electrodes; selective recordings from small muscles can only be made with intramuscular electrodes with small detection surfaces. Non-selective recordings carry the risk of contamination with activity from other muscles; selective recordings may fail to detect activity
in all parts of the source muscle. Meaningful recordings from deep muscles can only be accomplished by invasive techniques. Considering the above, truly selective recording from sphincter muscles can probably only be obtained by intramuscular electrodes; in clinical routine, often the concentric needle electrode is used. This electrode has the advantage of being widely available, sturdy, easy to introduce and adjust in position, and has a standardized active surface. It is, however, painful to have inserted and subsequent movement of the source muscle can be uncomfortable and the needle then easily dislodged. Instead, two thin isolated/bare tip wires (with a hook at the end) can be introduced into the muscle with a cannula; the latter is then withdrawn, and the wires stay in place. The advantage of this type of recording is good positional stability and painlessness once the wires are inserted, although their position cannot be much adjusted. To make EMG recording less invasive, various types of surface electrode have been devised:
• small skin-surface electrodes can be applied to the •
•
perineal skin; for intravaginal placement, a disposable electrode set on a vinyl foam pad is available,12 and other special intravaginal recording devices have been described;13 anal plugs can be used for recording from the anal sphincter, and catheter-mounted ring electrodes14 to record from the urethral sphincter (Fig. 20.3).
Recordings with surface electrodes are more artifact prone and, furthermore, the artifacts may be less easily
Figure 20.3. Electrodes used to record sphincter activity. (Reproduced from ref. 2 with permission from Elsevier.) 279
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identified. Critical on-line assessment of the ‘quality of the EMG signal’ is mandatory in kinesiologic EMG, and this requires either auditory or oscilloscope monitoring of the raw signal. Integration of high quality EMG signals may help in quantification of results, as can automatic analysis of the interference pattern.15
Findings in normal and abnormal conditions The normal kinesiologic sphincter EMG shows some continuous activity at rest (which may be increased voluntarily or reflexly) (Fig. 20.4); such activity could be recorded for up to 2 hours,7 and even after a subject has fallen asleep during the examination.6,16 This physiologic spontaneous activity may be called ‘tonic’. It consists of prolonged firing of tonic motor units, not rapidly interchanging activation and inactivation of different motor units.16 The ‘amount’ of recorded activity depends on the uptake area of the electrode (Fig. 20.1). Using a concentric needle electrode (CNE), activity from 1 to 5 motor units is usually recorded per detection site at rest. ‘Tonic’ activity is encountered in many but not all detection sites of the levator ani muscle.17 Typically, it consists of low amplitude motor unit potentials (MUPs) that fire fairly regularly at low frequencies. In a study of 39 such motor
Figure 20.4. Kinesiologic EMG recordings from the pubococcygeus muscles (recording with intramuscular wires: right, upper traces; left, lower traces). (a) Recordings from a 33-year-old nulliparous woman. Continuous firing of motor unit potentials is seen on the right with a gradual recruitment on voluntary contraction. On the left, no ongoing activity is present. Symmetrical recruitment on voluntary contraction is present. (b) Recordings from a 52-year-old stress urinary incontinent woman. Some ongoing muscle activity can be seen in both pubococcygeal muscles. On voluntary contraction, recruitment can only be seen on the left. On the right, there is actually a decrease in firing of motor units on ‘voluntary contraction’.
units from the anal sphincter in 17 subjects (inclusion criterion was rhythmic spontaneous firing for 2 minutes before onset of measurement), the range of discharge rates was found to be 2.5–9.4 Hz (mean ± SD 5.3 ± 1.8 Hz).18 Any reflex or voluntary activation procedure is mirrored first by an increase in the firing frequency of the motor units; then, with any stronger activation or increase in abdominal pressure, new so-called ‘phasic’ motor units are recruited (Fig. 20.4). These are usually of higher amplitude and their discharge rates are higher and irregular. A small percentage of motor units with an ‘intermediate’ activation pattern can also be encountered.18 Apart from differences in amplitude, the different types of MUP may also differ in duration, as evidenced by EMG frequency analysis.19 Both the urethral and anal sphincter show short-lasting voluntary activation times (typically below 1 minute20), which is also the case for pubococcygeus muscles.17 On voiding, all EMG activity in the urethral sphincter ceases prior to a detrusor contraction. Coordinated detrusor/sphincter activity is lost with lesions between the lower sacral segments and the upper pons; detrusor contractions are then accompanied by an increase in sphincter EMG activity.21 This pattern of activity is called ‘detrusor sphincter dyssynergia’. On the basis of the temporal relationship between urethral sphincter and detrusor contractions, three types of dyssynergia have been described.22 This neurogenic uncoordinated sphincter behavior has to be differentiated from ‘voluntary’ contractions that may occur in the so-called ‘nonneuropathic voiding disorders’ that may be a learned abnormality of behavior,23 and may be encountered in women with dysfunctional voiding.24 Urethral sphincter contraction, or at least failure of relaxation during involuntary detrusor contractions, have also been reported in patients with Parkinson’s disease.25 Normal physiologic behavior of the striated anal sphincter is characterized by its relaxation with defecation;26 a paradoxical sphincter activation during defecation has been described in Parkinson’s disease, so-called ‘anismus’.27 The pubococcygeus in the healthy female reveals patterns of activity similar to those found in the urethral and anal sphincters at most detection sites, i.e. continuous activity at rest, some increase in activity during bladder filling, and a reflex increase in activity during any activation maneuver such as talking, deep breathing, and coughing. It relaxes during voiding and in health the muscles on both sides act in concert.17 In stress-incontinent women, the physiologic patterns of activation, as well as the coordination between the two sides, may be lost11 (Fig. 20.4).
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Little is known about the normal complexity of activity patterns of different pelvic floor muscles (i.e. urethral sphincter, urethrovaginal sphincter, anal sphincter muscle, different parts of the levator ani) but it is generally assumed that they act as one, in a coordinated fashion. Differences have, however, been demonstrated even between the intra- and periurethral sphincter28 and in activation of the levator ani and the urethral sphincter in normal females. Coordinated behavior is often lost in disease states, as has been shown, for example, for the levator ani and the urethral and anal sphincters.5,29 Disturbances of pelvic floor muscles activity have been modified by using the kinesiologic EMG recording as a biofeedback signal.30 Kinesiologic needle EMG analysis of the urethral sphincter with the patient both at rest and while coughing may predict the outcome after certain types of incontinence surgery.
diagnostic usefulness of kinesiologic emg The demonstration of voluntary and reflex activation of pelvic floor muscles is indirect proof of the integrity of respective neural pathways. Kinesiologic EMG recordings of sphincter muscles, either urethral or anal, are obtained in selected patients in urodynamic laboratories to ascertain sphincter behavior during bladder filling and voiding. Such simultaneous studies of detrusor and sphincter activity are, as a rule, obtained only in patients with suspected detrusor–sphincter dyssynergia. External anal sphincter EMG is recorded in some laboratories in the assessment of anorectal dysfunction.26 Other than the polygraphic urodynamic recordings to diagnose detrusor–sphincter dyssynergia, the diagnostic contribution of kinesiologic EMG is yet to be established.
emg methods to dIFFerentIate normal From pathologIc muscle Needle EMG may help to differentiate between normal, denervated, reinnervated, and possibly myopathic muscle. Such EMG has also been called ‘motor unit’ EMG to distinguish it from ‘kinesiologic’ EMG. The needle electrode needs to be placed appropriately in the target muscle. The levator ani muscle can be located by transrectal or transvaginal palpation and reached transcutaneously. The urethral sphincter is anatomically separate from the pelvic floor musculature31 and can be approached either perineally with a needle insertion 0.5 cm laterally to the urethral orifice (the authors suggest one single skin insertion per side) or it can be reached transvaginally using a Sims speculum to
retract the posterior vaginal wall. The latter approach is less uncomfortable,32 although a paraurethral injection of local anesthetic lessens the discomfort of that approach and does not appear to alter the EMG signal. The position of the needle should be adjusted in a systematic way so that the same motor unit is not repeatedly analyzed.
normal findings using a concentric needle emg electrode The needle electrode most commonly used in EMG is the single use disposable concentric needle electrode (CNE); it consists of a central insulated platinum wire encased within a steel cannula and the tip ground to give an elliptical area of 580 × 150 µm (Fig. 20.1). This type of electrode has the recording characteristics necessary to record spike or near activity from about 20 muscle fibers. The number of motor units recorded therefore depends both upon the local arrangement of muscle fibers within the motor unit and the level of contraction of the muscle. The long-established method of CNE EMG4,33 can provide information on insertion activity, abnormal spontaneous activity, MUPs, and interference pattern. In healthy skeletal muscle, initial placement of the needle elicits a short burst of ‘insertion activity’ which is due to mechanical stimulation of excitable membranes. This phenomenon may also be seen in the sphincters; however, because of the reflex, pain-induced burst of motor units which occurs, insertion activity may be difficult to discern. Insertion activity is recorded at a sensitivity setting of 50 µV per division, which is also the gain used to record spontaneous activity. Absence of insertion activity with an appropriately placed needle electrode usually indicates a complete denervation atrophy of the examined muscle. At rest, tonic MUPs are the only normal activity recorded. In partially denervated sphincter muscle there is – by definition – a loss of motor units (MUs). The number of continuously active MUPs during relaxation can be estimated by counting the number of continuously firing low-threshold MUPs. In patients with cauda equina or conus medullaris lesions, fewer MUPs fire continuously during relaxation, probably due to partial axonal loss. In addition to continuously firing lowthreshold (‘tonic’) motor units, new MUPs are recruited voluntarily and reflexly in the sphincters. It has been shown that the two MUP populations differ in their characteristics, reflexly or voluntarily activated highthreshold MUPs being larger than continuously active ‘low-threshold MUPs’. As a consequence, a standardized 281
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level of activity at which a template-based multi-MUP analysis obtains between three and five MUPs on a single muscle site was suggested. The main obstacle to qualified assessment of a reduced number of activated MUs, and activation of MUs at increased firing rates (as occurs in limb muscles), is a lack of concomitant measurement of the level of contraction of the examined muscle (this can be readily assessed when studying limb muscles). Phasic (high threshold) MUPs can be activated reflexly or voluntarily. Normally, MUPs should intermingle to produce an ‘interference’ pattern on the oscilloscope during muscle contraction, and during a strong cough. MUPs should be analyzed at a sensitivity setting which allows their full display. The commonly used time scale is 5 or 10 ms per division, with an amplitude gain of 50–500 µV per division (Fig. 20.5). The commonly used amplifier filter settings for concentric needle EMG (CN EMG) are 10–10,000 Hz. The amplitude of a MUP is largely determined by the activity of those muscle fibers closest to the recording electrode. Other fibers within
2
3
a 0.5 mm radius of the recording electrode contribute little to the amplitude but in a normal motor unit there are unlikely to be more than two or three fibers belonging to the same motor unit.2 Amplitude is highly sensitive to needle position and very minor adjustments of the electrode will result in major changes, i.e. a change in position by 0.5 mm alters the amplitude 10- to 100-fold. The duration of a motor unit is the time between the first deflection and the point when the waveform finally returns to the baseline. This will depend on the number of muscle fibers within the motor unit and is little affected by the proximity of the recording electrode to the nearest fiber. The difficulty with this measurement is defining the exact point of return to the baseline. The phases of a motor unit potential are defined by the number of times the potential crosses the baseline. A unit that has four phases or more is said to be polyphasic. A related parameter is a ‘turn’ which is defined as a shift in direction of a potential of greater than a specified amplitude. Using the standard recording facilities available on all modern EMG machines, individual MUPs can be captured and their amplitude and duration measured. To allow identification of MUPs, and to be certain the late components of complex potentials are not due to superimposition of several MUPs, it is necessary to capture the same potential repeatedly (Fig. 20.6). MUPs are mostly below 1 mV and certainly below 2 mV in the
1
5 ms 100 mV
Figure 20.5. Concentric needle EMG recording of motor unit potentials from the urethral sphincter of a 35-year-old stress incontinent female, several years after second vaginal delivery. At this detection site three motor unit potentials are firing continuously, and can be analyzed. It can be seen that the motor unit potential (MUP) with the asterisk is different from the others of similar overall shape. Further analysis of such a signal is needed to ascertain whether it is a superimposition of two individual MUPs or an instability within a complex of MUPs. The use of trigger and delay facility is advantageous to solve such questions (see Fig. 20.6).
5 ms 200 mV
Figure 20.6. A concentric needle EMG recording from the urethral sphincter of an 18-year-old nulliparous female 4 years after a partial cauda equina injury. A trigger and delay facility is used. A complex motor unit potential (MUP) with prolonged duration is shown. Superimposition of another individual MUP (asterisk) may be falsely interpreted as instability of the potential.
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normal urethral and anal sphincter. Most are less than 7 ms in duration, and few (less than 15%) are above 10 ms. Additionally, most are bi- and triphasic, but up to 15–33% may be polyphasic. Normal MUPs are stable – their shape on repetitive recording does not change.20,28,34–38 There are two approaches to analyzing the bioelectrical activity of motor units quantitatively: either individual MUPs are analyzed, or the overall activity of intermingled MUPs (the ‘interference pattern’, or IP) is analyzed. Generally, three techniques of MUP analysis (‘manual-MUP’, ‘single-MUP’ and ‘multi-MUP’) and one technique of IP analysis (turn/amplitude, or T/A) are available on advanced EMG systems. By either method a relevant sample of EMG activity needs to be analyzed for the test to be valid. In the small half of the sphincter muscle collecting ten different MUPs has been accepted as the minimal requirement for using single-MUP analysis. Using manual-MUP and multiMUP techniques, sampling of 20 MUPs (standard number in limb muscles) from each external anal sphincter (EAS) presents no difficulty in healthy controls and most patients. Normative data obtained from the EAS muscle by standardized EMG technique using all three MUP analysis techniques (manual-MUP, single-MUP, multi-MUP) have been published. The technical differences in the methods are many and no in-depth description is attempted here. MUPs are identified either using a trigger and delay line (‘single-MUP’) or appearing repeatedly in a prolonged recording of EMG activity (‘manual-MUP’). Both approaches favor identification of relatively larger MUPs and become less reliable on stronger activation of muscle. Both methods are relatively slow and subject to examiner bias. The template-based multi-MUP analysis and the T/A analysis of IP (both run by automated computer analysis) are fast (5–10 and 2–3 minutes per muscle, respectively), easy to apply, and allow little opportunity for examiner bias. Use of quantitative MUP and IP analyses of the EAS is further facilitated by the availability of normative values that can be introduced into the EMG system’s software. It has been shown that normative data are not significantly affected by age, gender, number of uncomplicated vaginal deliveries, mild chronic constipation, and the part of the EAS muscle (i.e. subcutaneous or deeper) examined. This makes quantitative analysis much simpler and results from different laboratories easily comparable. Similar in-depth analyzed normative data from standardized techniques for other pelvic floor and perineal muscles are not yet available, but individual laboratories use their own normative data.
single fiber electromyography: method and normal findings The single fiber electromyography (SFEMG) electrode has similar external proportions to a concentric needle electrode, being made of a steel cannula 0.5–0.6 mm in diameter with a beveled tip. However, instead of having the recording surface at the end, a fine insulated platinum or silver wire embedded in epoxy resin is exposed through an aperture on the side, 1–5 mm behind the tip (Fig. 20.1). The platinum wire which forms the recording surface has a diameter of 25 µm and will pick up activity from within a hemispherical volume 300 µm in diameter. This is very much smaller than the volume of muscle tissue from which a concentric needle electrode records, which has an uptake area of 1 mm diameter. Because of the arrangement of muscle fibers in a normal motor unit, a SFEMG needle will record only between one and three single muscle fibers from the same motor unit. When recording with a SFEMG needle, the amplifier filters are set so that low frequency activity is eliminated (500 Hz to 10 kHz). Thus the contribution of each muscle fiber appears as a biphasic positive–negative action potential. The SFEMG parameter that reflects motor unit morphology is ‘fiber density’ (FD), which is the mean number of muscle fibers belonging to an individual motor unit per detection site. To measure FD, recordings from 20 different detection sites are necessary (Fig. 20.7) and the number of component potentials to each motor unit recorded and averaged. The normal fiber density for the anal sphincter is below 2.0.39–41 Small changes with age
1 ms 200 mV
Figure 20.7. Single fiber EMG recording from the anal sphincter of a 51-year-old nulliparous female with an extrapyramidal syndrome and recent development of poor bladder emptying accompanied by stress incontinence. The fiber density in the anal sphincter was found to be 3.7 and a diagnosis of possible multiple system atrophy was suggested. Further development of the clinical picture supported the diagnosis. 283
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have been reported; women have significantly greater fiber density than men (1.52 ± 0.5 vs. 1.43 ± 0.14).41 Due to its technical characteristics, a SFEMG electrode is able to record even small changes that occur in motor units due to reinnervation, but is less suitable to detect changes due to denervation itself, i.e. abnormal insertion and spontaneous activity. The SFEMG electrode is also suitable for recording instability of motor unit potentials, the ‘jitter’.42 SFEMG is not widely used in general clinical neurophysiologic laboratories. The recording needles are very expensive, and disposable needles are not available.
emg findings due to denervation and reinnervation After complete denervation, all motor unit activity ceases and there may be electrical silence for several days. Between 10 and 20 days after a denervating injury, ‘insertion activity’ becomes more prolonged and abnormal spontaneous activity in the form of short biphasic spikes (‘fibrillation potentials’) and biphasic potentials with prominent positive deflections (‘positive sharp waves’) appear. With axonal reinnervation MUPs appear again; first short bi- and triphasic, soon becoming polyphasic, serrated and of prolonged duration.43 In perineal muscles, complete denervation can be observed after traumatic lesions to the lumbosacral spine and damage to the cauda equina. Most lesions will, however, cause only partial denervation. In partially denervated muscle, some MUPs remain and mingle eventually with abnormal spontaneous activity. As the MUPs in sphincter muscles are also short and mostly bior triphasic, it requires considerable EMG experience to recognize abnormal spontaneous activity in the presence of a few surviving motor units. Abnormal spontaneous activity has been described as a specific marker for degeneration of Onuf’s nucleus occurring in patients with multiple system atrophy.44 In longstanding partially denervated muscle a peculiar abnormal insertion activity appears, so-called ‘repetitive discharges’. These are made up of repetitively firing groups of potentials with so little jitter between the potentials that it is assumed the activity must be due to ephaptic or direct transmission of impulses between muscle fibers.45,46 However, this activity may be found in the striated muscle of the urethral sphincter without any other evidence of neuromuscular disease and it has been hypothesized that it causes impaired relaxation of the muscle when spontaneous and profuse.47 In partially denervated muscle there is, by definition, a loss of the number of motor units; however, the
amount is difficult to estimate48 as the amount of motor unit activity recorded depends on needle position and voluntary activation. In partially denervated muscle, collateral reinnervation takes place and – provided there are still some intact motor units within the muscle – surviving motor nerves will sprout and grow out to reinnervate those muscle fibers which have lost their nerve supply, resulting in a change in the arrangement of muscle fibers within the unit. Whereas in healthy muscle it is unusual for two adjacent muscle fibers to be part of the same motor unit, following reinnervation several muscle fibers all belonging to the same motor unit come to be adjacent to one another. Early in the process of reinnervation the newly outgrown motor sprouts are thin and therefore conduct slowly so that the time taken for excitatory impulses to spread through the axonal tree is abnormally prolonged. This is reflected by prolongation of the waveform of the MUP which may have small, late components (Fig. 20.6). Neuromuscular transmission in these newly grown sprouts may also be insecure so that the motor unit may show ‘instability’. In skeletal muscle, with time and provided there is no further deterioration in innervation, the reinnervating axonal sprouts increase in diameter and thus increase their conduction velocity so that activation of all parts of the reinnervated motor unit become more synchronous. This has the effect of increasing the amplitude and reducing towards normal the duration of the MUPs measured with a CNE. This phenomenon may be different in the sphincter muscles where long duration motor units seem to remain a prominent feature of reinnervated motor units.49 There are several conditions in which gross changes of reinnervation may be detected in motor units of the pelvic floor. Following a cauda equina lesion the MUPs are likely to be prolonged and polyphasic,36 and similar marked changes are seen in patients with lumbosacral myelomeningoceles. Neuropathic changes can be recorded in sphincter muscles of patients with multiple system atrophy (MSA).49 MSA is a progressive neurodegenerative disease which often, particularly in its early stages, is mistaken for Parkinson’s disease but is poorly responsive to antiparkinsonian treatment. Autonomic failure causing postural hypotension, and cerebellar ataxia causing unsteadiness and clumsiness, may be additional features. Urinary incontinence in both women and men occurs early in this condition, often some years before the onset of obvious neurologic features.50 As part of the neurodegenerative process, loss of motor units occurs in Onuf’s nucleus so that partial but progressive denervation of the sphincter occurs and recorded motor units show changes of reinnervation, becoming markedly prolonged. Sphincter
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EMG has been demonstrated to be of value in distinguishing between idiopathic Parkinson’s disease and MSA,49,51 but may not be obvious in the early phase of disease.52 Similar changes of chronic reinnervation may be found in other parkinsonian syndromes such as progressive supranuclear palsy (PSP).53 These changes can also be demonstrated as a increase in fiber density on SFEMG.38
emg changes in genuine stress incontinence Pelvic floor muscle denervation has been implicated in the pathophysiology of genuine stress incontinence (GSI). EMG techniques have been used to identify sphincter injury after childbirth and to evaluate women with GSI. Fiber density in the EAS measured by SFEMG was increased in women with urinary stress incontinence. Not only stress incontinence but also genitourinary prolapse was associated with partial denervation of the pelvic floor. CNE EMG revealed a significant increase in duration of individual motor units in the pubococcygeus labor and vaginal delivery. The changes were most marked in women who had urinary incontinence 8 weeks after delivery, who had a prolonged second stage of labor, and had given birth to heavier babies. Myogenic histologic changes in pelvic floor muscles after vaginal delivery were also reported, with some EMG support by another group. Myopathic EMG changes (i.e. short, small MUPs) may, however, be a consequence of deficient reinnervation. Although CNE EMG of the urethral sphincter appears to be the logical choice in patients with urinary incontinence of possibly neurogenic origin, only a small amount of pathologic muscle tissue remains in many incontinent parous women. CNE EMG findings generally will not affect therapeutic considerations, but there have been claims that urethral sphincter EMG can assist in selecting the type of surgery for patients with intrinsic sphincter deficiency. The practical value of the urethral sphincter CNE EMG in women after vaginal delivery and/or with urinary incontinence is not defined, but seems to be restricted in practice to the rare cases of severe sacral plexus involvement.
emg changes in women with urinary retention and obstructed voiding For many years it was said that isolated urinary retention in young women was due either to psychogenic factors or was the first symptom of onset of multiple sclerosis.54 However, CNE EMG in this group has demonstrated that many such patients have profuse complex repetitive
discharges (CRDs) and decelerating burst (DB) activity in the urethral sphincter muscle.55 It was proposed that this pathologic spontaneous activity leads to sphincter contraction, which endures during micturition and causes obstruction to flow. Positive proof of this has only recently been demonstrated by combined CNE EMG and kinesiologic EMG analysis of a group of females with dysfunctional voiding.24 The CRDs have a very characteristic sound quality over the loudspeaker on the EMG machine, similar to a helicopter or motorcycle engine. It is the DBs which produce the myotonic-like sound which has been likened to underwater recordings of whales. CRDs may be difficult to distinguish from chronically reinnervated motor units except that the jitter of the potentials is very much less.47 Why this activity should occur is not known but in the syndrome described by one of the authors it was associated with polycystic ovaries (Fowler’s syndrome).55 The explanation probably lies in some (as yet unidentified) hormonal susceptibility of the female striated urethral sphincter which causes a loss of stability of the muscle membrane and permits ephaptic transmission to develop, manifest as complex repetitive discharges. The current hypothesis is that it is the sustained contraction of the urethral sphincter that has an inhibitory effect on the detrusor. When recording from the striated urethral sphincter in this condition, sometimes only complex repetitive discharges may be heard and then it is difficult to be certain whether or not the activity is that of reinnervated motor units; however, if decelerating bursts are also present it is easier to be certain that the EMG is abnormal. Although EMG may indicate the presence of an abnormality, it is inevitably only a sample and it is difficult to know whether the abnormality is sufficient to account for the clinical finding of complete or partial urinary retention. The investigations that have proved to be useful as adjuncts to the EMG are measurement of the urethral pressure profile (UPP) and volume of the sphincter muscle estimated with ultrasound.56 Young women with urinary retention due to the sphincter abnormality regularly have UPPs in excess of 100 cmH2O. The typical clinical presentation of this syndrome is of a young woman with either spontaneous onset of urinary retention or retention following some sort of operative intervention. The mean age of a series of women with this problem was 27 years; spontaneous onset appears to be more common in women under 30.56 Characteristically, the women present with a bladder capacity in excess of 1 liter and, although this may cause painful distension, they lack any expected sensations of urinary urgency. There may or may not be a history of infrequent voiding 285
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prior to the onset of urinary retention. These women are taught to do clean intermittent self-catheterization and commonly experience difficulties with this technique, in particular pain and difficulty in removing the catheter. Patients with Fowler’s syndrome seem to respond particularly well to sacral neuromodulation.57 Although the mechanism of its effect is still the subject of research using functional brain imaging methods, the stimulation does not appear to lower the UPP or cause a cessation of the abnormal EMG activity.58 It seems likely that the same type of EMG abnormality affecting the striated urethral sphincter can also produce obstructed voiding in women. Presumably in this group of patients the overactive sphincter, although it produces obstruction, does not have the same inhibitory effect on the detrusor muscle as it does in those women who develop urinary retention. Because CNE EMG will detect changes of both denervation and reinnervation as occur with a cauda equina lesion, as well as abnormal spontaneous activity, it has been argued that this test is mandatory in women with urinary retention.59 It should certainly be carried out before stigmatizing a woman as having ‘psychogenic urinary retention’.
emg changes in primary muscle disease As is evident from the foregoing sections, EMG changes reflect pathologic changes in the structure of the motor unit. Changes in EMG due to disease of the muscle fibers are much more subtle, and although in skeletal muscle the ‘typical’ features of myopathy are said to be showers of small, low amplitude polyphasic units recruited at mild effort, such changes have not been reported in the pelvic floor, even in patients known to have generalized myopathy.60 Pelvic floor muscle involvement in limb-girdle muscular dystrophy in a nulliparous female has been reported, but concentric needle EMG of her urethral sphincter was reported as normal.61 Myopathic changes were observed in the puborectalis and the EAS in patients with myotonic dystrophy. Little is currently known about what might be expected of an EMG recording from muscle which has been subject to a severe stretch injury – as occurs during childbirth – but there may well be changes reflecting rupture of individual muscle fibers and injury to small intramuscular nerves.
diagnostic usefulness of emg methods Both CNE EMG and SFEMG have been employed in neurourologic, urogynecologic, and proctologic
research. Although SFEMG determination of fiber density has been introduced as a relatively easily learned technique, providing a quantifiable parameter to measure the reinnervation changes in sphincter muscle, little else of clinical relevance can be learnt. Using CNE EMG however, an experienced examiner can quickly come to a conclusion regarding normality or abnormality of the muscle examined simply by ‘observing’ the motor unit activity on the oscilloscope screen. This may be one reason why quantified determination of MUP parameters by CNE EMG is not as widely used as would be expected, although quantified CNE EMG does provide the same information on reinnervation changes in muscle as the SFEMG parameter of ‘fiber density’.16,38 In the authors’ experience, the concentric needle is preferable for routine diagnostics in neurourology as the whole spectrum of changes in the course of denervation/reinnervation and spontaneous activity can be observed. CNE EMG is the electrophysiologic method of choice in routine examination of skeletal muscle. It should be logical to extend an ‘EMG examination’ from, for example, lumbar and upper sacral myotomes to the lower sacral myotomes in, say, a child with myelomeningocele or an adult after a cauda equina lesion. Furthermore, the concentric electrode can be employed at the same diagnostic session for recording motor evoked responses and/or reflex responses.62
conclusIon Both ‘kinesiologic’ and ‘motor unit’ EMG have contributed significantly to our understanding of pelvic floor, lower urinary tract, and bowel function in health and disease, but there is still much research to be done. For wider application of diagnostic EMG in patients with suspected neurogenic dysfunction, better-defined agestratified control values will have to be obtained.
reFerences 1. Adrian ED, Bronck DW. The discharge of impulses in motor nerve fibres. Part II. The frequency of discharge in reflex and voluntary contractions. J Physiol (Lond) 1929;67:119–51. 2. Fowler CJ, Tedman BM. Electromyography: normal and pathological findings. In: Binnie CD, Cooper R, Mauguiere F, Osselton J, Prior P, Tedman B (eds) Clinical Neurophysiology: EMG, Nerve Conduction and Evoked Potentials, vol. 1 (revised and enlarged edition). Amsterdam: Elsevier, 2004; 77–105. 3. Franksson C, Petersen I. Electromyographic recording from the normal human urinary bladder, inter-
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nal urethral sphincter and ureter. Acta Physiol Scand 1953;106:150. 4. Chantraine A, Leval J, Onkelinx A. Electromyographie des sphincters striés urétal et anal humains. Etude descriptive et analytique. Rev Neurol (Paris, 1973;115:396–403. 5. Vereecken RL, Verduyn H. The electrical activity of the paraurethral and perineal muscles in normal and pathological conditions. Br J Urol 1970;42(4):457–63. 6. Jesel M, Isch-Treussard C, Isch F. Electromyography of striated muscle of anal and urethral sphincters. In: Desmedt JE (ed) New Developments in Electromyography and Clinical Neurophysiology. Basel: Karger, 1973; 406. 7. Chantraine A, Leval J, Onkelinx A. Motor conduction velocity in the internal pudendal nerves. In: Desmedt JE (ed) New Developments in Electromyography and Clinical Neurophysiology. Basel: Karger, 1973; 433–8. 8. Blaivas JG, Labib KL, Bauer SB, Retik AB. A new approach to electromyography of the external urethral sphincter. J Urol 1977;117(6):773–7. 9. Gilpin SA, Gosling JA, Smith AR, Warrell DW. The pathogenesis of genitourinary prolapse and stress incontinence of urine. A histological and histochemical study. Br J Obstet Gynaecol 1989;96(1):15–23. 10. Heit M, Benson JT, Russel B, Brubaker L. Levator ani muscle in women with genitourinary prolapse. Neurourol Urodyn 1996;15:17–29.
18. Vodusek DB. Neurophysiological study of bulbocavernosus reflex in man [in Slovene]. Ljubljana: University of Ljubljana, 1988; 1–129. 19. Vereecken RL, Ketelaer P, Joossens J, Leruitte A. Frequency analysis of the electromyographic activity in striated pelvic floor muscles: a preliminary report. Eur Urol 1977;3(6):333–6. 20. Vereecken RL, Derluyn J, Verduyn H. Electromyography of the perineal striated muscles during cystometry. Urol Int 1975;30(1):92–8. 21. Blaivas JG, Sinha HP, Zayed AA, Labib KB. Detrusor–external sphincter dyssynergia. J Urol 1981;125(4):542–4. 22. Chancellor MB, Kaplan SA, Blaivas JG. Detrusor–external sphincter dyssynergia. Ciba Found Symp 1990;151:195– 206; discussion 207–13. 23. Rudy DC, Woodside JR. Non-neurogenic neurogenic bladder: the relationship between intravesical pressure and the external sphincter electromyogram. Neurourol Urodyn 1991;10:169–76. 24. Deindl FM, Vodusek DB, Bischoff C, Hartung R. Zwei verschiedene Formen von Miktionsstorungen bei jungen Frauen: Dyssynerges Verhalten im Beckenboden oder Pseudomyotonie im externen urethralen sphinkter? Akt Urol 1997;28:88–94. 25. Pavlakis AJ, Siroky MB, Goldstein I et al. Neurourologic findings in Parkinson’s disease. J Urol 1983;129(1):80–3.
11. Deindl FM, Vodusek DB, Hesse U, Schüssler B. Pelvic floor activity patterns: comparison of nulliparous continent and parous urinary stress incontinent women. A kinesiological EMG study. Br J Urol 1994;73(4):413–17.
26. Read NW. Functional assessment of the anorectum in faecal incontinence. In: Bock G, Wheelan J (eds) Neurobiology of Incontinence (Ciba Foundation Symposium 151). Chichester: Wiley, 1990; 119.
12. Lose G, Tanko A, Colstrup H, Andersen JT. Urethral sphincter electromyography with vaginal surface electrodes: a comparison with sphincter electromyography recorded via periurethral coaxial, anal sphincter needle and perianal surface electrodes. J Urol 1985;133(5):815–18.
27. Mathers SE, Kempster PA, Law PJ et al. Anal sphincter dysfunction in Parkinson’s disease. Arch Neurol 1989;46(10):1061–4.
13. Smith AR, Hosker GL, Warrell DW. The role of pudendal nerve damage in the aetiology of genuine stress incontinence in women. Br J Obstet Gynaecol 1989;96(1):29–32.
29. Nordling J, Meyhoff HH. Dissociation of urethral and anal sphincter activity in neurogenic bladder dysfunction. J Urol 1979;122(3):352–6.
14. Nordling J, Meyhoff HH, Walter S, Andersen JT. Urethral electromyography using a new ring electrode. J Urol 1978;120:571–3.
30. O’Donnell PD, Doyle R. Biofeedback therapy technique for treatment of urinary incontinence. Urology 1991;37(5):432–6.
15. Aanestad O, Flink R, Stalberg E. Interference pattern in perineal muscles: I. A quantitative electromyographic study in normal subjects. Neurourol Urodyn 1989;8:1–9.
31. Gosling JA, Dixon JS, Humperson JR. Functional Anatomy of the Urinary Tract, vol. 1. London: Churchill Livingstone, 1983; Ch. 5.
16. Vodusek DB. Electrophysiology. In: Schuessler B, Laycock J, Norton P, Stanton S (eds) Pelvic Floor Re-education: Principles and Practice. London: Springer-Verlag, 1994; 83–97.
32. Lowe EM, Fowler, CJ, Osborne, JL et al. Improved method for needle electromyography of the urethral sphincter in women. Neurourol Urodyn 1994;13(1):29–33.
17. Deindl FM, Vodusek DB, Hesse U, Schussler B. Activity patterns of pubococcygeal muscles in nulliparous continent women. Br J Urol 1993;72(1):46–51.
28. Chantraine A, de Leval J, Depireux P. Adult female intraand periurethral sphincter–electromyographic study. Neurourol Urodyn 1990;9:139–44.
33. Petersen I, Franksson C, Danielson CO. Electromyographic study of the muscles of the pelvic floor and urethra in normal females. Acta Obstet Gynecol Scand 1955;34(3):273–85.
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34. Bartolo DC, Jarratt JA, Read NW. The cutaneoanal reflex: a useful index of neuropathy? Br J Surg 1983;70(11):660–3. 35. Vodusek DB, Light JK. The motor nerve supply of the external urethral sphincter muscles. Neurourol Urodyn 1983;2:193–200. 36. Fowler CJ, Kirby, RS, Harrison, MJG et al. Individual motor unit analysis in the diagnosis of disorders of urethral sphincter innervation. J Neurol Neurosurg Psychiatry 1984;47(6):637–41. 37. Varma JS, Smith AN, McInnes A. Electrophysiological observations on the human pudendo-anal reflex. J Neurol Neurosurg Psychiatry 1986;49(12):1411–16. 38. Rodi Z, Vodusek DB, Denislic M. Clinical uro-neurophysiological investigation in multiple sclerosis. Eur J Neurol 1996;3:574–80. 39. Neill ME, Swash M. Increased motor unit fibre density in the external anal sphincter muscle in ano-rectal incontinence: a single fibre EMG study. J Neurol Neurosurg Psychiatry 1980;43(4):343–7. 40. Vodusek DB, Janko M. SFEMG in striated sphincter muscles [abstract]. Muscle Nerve 1981;4:252. 41. Jameson JS, Chia YW, Kamm MA et al. Effect of age, sex and parity on anorectal function. Br J Surg 1994;81(11):1689– 92. 42. Stalberg E, Trontelj JV. Single Fiber Electromyography: Studies in Healthy and Diseased Muscle, 2nd ed. New York: Raven Press, 1994. 43. Brown WF. The physiological and technical basis of electromyography. London: Butterworth, 1984. 44. Schwarz J, Kornhuber M, Bischoff C, Straube A. Electromyography of the external anal sphincter in patients with Parkinson’s disease and multiple system atrophy: frequency of abnormal spontaneous activity and polyphasic motor unit potentials. Muscle Nerve 1997;20(9):1167–72. 45. Trontelj J, Stalberg E. Bizarre repetitive discharges recorded with single fibre EMG. J Neurol Neurosurg Psychiatry 1983;46(4):310–16. 46. Fowler CJ. Pelvic floor neurophysiology. In: Binnie CD, Cooper R, Mauguiere F, Osselton J, Prior P, Tedman B (eds) Clinical Neurophysiology. Oxford: ButterworthHeinemann; 1995; 233–52. 47. Fowler CJ, Kirby RS, Harrison MJ. Decelerating burst and complex repetitive discharges in the striated muscle of the urethral sphincter, associated with urinary retention in women. J Neurol Neurosurg Psychiatry 1985;48(10):1004–9.
48. Siroky MB. Electromyography of the perineal floor. Urol Clin North Am 1996;23(2):299–307. 49. Palace J, Chandiramani VA, Fowler CJ. Value of sphincter electromyography in the diagnosis of multiple system atrophy. Muscle Nerve 1997;20(11):1396–403. 50. Beck RO, Betts CD, Fowler CJ. Genitourinary dysfunction in multiple system atrophy: clinical features and treatment in 62 cases. J Urol 1994;151(5):1336–41. 51. Eardley I, Quinn NP, Fowler CJ et al. The value of urethral sphincter electromyography in the differential diagnosis of parkinsonism. Br J Urol 1989;64(4):360–2. 52. Stocchi F, Carbone A, Inghilleri M et al. Urodynamic and neurophysiological evaluation in Parkinson’s disease and multiple system atrophy. J Neurol Neurosurg Psychiatry 1997;62(5):507–11. 53. Valldeoriola F, Valls Sole J, Tolosa ES et al. Striated anal sphincter denervation in patients with progressive supranuclear palsy. Mov Disord 1995;10(5):550–5. 54. Siroky MB, Krane RJ. Functional voiding disorders in women. In: Krane RJ, Siroky MB (eds) Clinical Neurourology. Boston: Little, Brown, 1991; 445–57. 55. Fowler CJ, Christmas TJ, Chapple CR et al. Abnormal electromyographic activity of the urethral sphincter, voiding dysfunction, and polycystic ovaries: a new syndrome? Br Med J 1988;297(6661):1436–8. 56. Swinn MJ, Wiseman OJ, Lowe E et al. The cause and natural history of isolated urinary retention in young women. J Urol 2002;167(1):151–6. 57. Swinn MJ, Kitchen ND, Goodwin RJ et al. Sacral neuromodulation for women with Fowler’s syndrome. Eur Urol 2000;38(4):439–43. 58. DasGupta R, Fowler CJ. Urodynamic study of women in urinary retention treated with sacral neuromodulation. J Urol 2004;171(3):1161–4. 59. Fowler CJ, Kirby RS. Electromyography of urethral sphincter in women with urinary retention. Lancet 1986;1(8496):1455–7. 60. Caress JB, Kothari MJ, Bauer SB, Shefner JM. Urinary dysfunction in Duchenne muscular dystrophy. Muscle Nerve 1996;19(7):819–22. 61. Dixon PJ, Christmas TJ, Chapple CR. Stress incontinence due to pelvic floor muscle involvement in limb-girdle muscular dystrophy. Br J Urol 1990;65(6):653–4. 62. Podnar S, Voduˇsek JB, Stilberg E. Standardisation of anal sphincter electromyography: normative data. Clin Neurophysiol 2000;11:2200–2007.
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IntroductIon Clinical neurophysiologic tests consist of electrical recordings from muscles and the nervous system (i.e. electromyography) and conduction studies. Conduction studies examine the capacity of a nerve (or nervous pathway) to transmit along its length a test volley of depolarization elicited by a stimulus. If the nerve being tested has a motor function, its responsiveness can be measured by stimulating at a proximal point and recording an elicited muscle response (Fig. 21.1). Both the time taken to muscle contraction as well as the amplitude of the muscle response (known as the compound muscle action potential or ‘M’ response1) can be measured. The latter depends on the number of intact individual motor fibers, whereas measures of latency (i.e. time to onset of response) and conduction velocity reflect the conduction speed of the single fastest motor fiber. For this reason, measures of latency are a poor guide to integrity or level of innervation. The amplitude of the evoked muscle response gives a somewhat better guide, but because this measurement depends so heavily on the configuration of the electrodes employed, amplitude is not as valuable as might have been expected on a theoretical basis. Ideally, to measure compound muscle action potential amplitude, the reference electrode should be placed over an insertion tendon and the active recording reference over the motor end plate (i.e. point of entry of nerve into muscle). For a strap-shaped muscle this can be identified as midway along its anatomic length, but in more anatomically complex muscles such as exist in the pelvis, the motor end plate region has not been identified and recording well-formed compound muscle action potentials is difficult.
CD (mm)
DML (ms) PML (ms) R CT (ms)
Figure 21.1. Measurements to be made in calculating motor conduction velocity (CV). (CD, conduction distance; CT, conduction time; DML, distal motor latency; PML, proximal motor latency; R, recording electrodes. CV = CD/CT.)
If the nerve being tested contains sensory fibers and is accessible over sufficient length to be stimulated at one point and electrodes placed some distance away (at least 10 cm to lessen stimulus artifact), it may be possible to record nerve activity directly. This response is called a ‘compound nerve action potential’. The amplitude of a compound nerve action potential is related to the number of nerve fibers being depolarized by the stimulating impulse and, when measured in limb muscles, is a good measure of the number of active nerve fibers. If a nerve is purely sensory, as may be the case for some peripheral cutaneous branches, electrical stimulation (perhaps by ring electrodes around a finger) excites sensory nerves. By recording over the median or ulnar nerve at the wrist and using the technique of ‘averaging’, this results in a discernible response known as a sensory action potential. Unfortunately, the recording of sensory action potentials (with the exception of recording from the dorsal nerve of the penis) is not possible in the pelvis for anatomic reasons. The nerve conduction studies carried out in the sacral region have been developed based on principles which are suited to the stimulating and recording conditions of the limbs, but adapt less well to the neuroanatomic arrangements of the pelvis.
nEuroPHYSIoLoGY oF tHE SAcrAL Motor SYStEM Measurement of motor conduction velocity is routinely carried out to evaluate limb motor nerves. However, the technique requires access to stimulation of the nerve at two separated points and measurement of the distance between them (Fig. 21.1) – a requirement which cannot be met in the pelvis. An electrophysiologic parameter that requires a shorter length of motor nerve to be accessible is measurement of the terminal motor latency of a muscle response.1 Terminal motor latency of the pudendal nerve can be measured by recording with a concentric needle electrode from the bulbocavernosus, anal or urethral sphincter muscles in response to bipolar stimulation placed on the perianal or perineal surface. The latencies of muscle-evoked potentials (MEPs) from the perineal muscles obtained by this means are between 4.7 and 5.1 ms;2 similar latencies have been obtained for the same method of stimulation and recording from the anal sphincter.3,4 The more widely employed technique of obtaining the pudendal terminal motor latency relies on stimulation with a special ‘surface electrode assembly’ fixed on a gloved index finger. Developed at the St Mark’s Hospital,
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London,5 this is often referred to as the ‘St Mark’s stimulator’. It consists of a bipolar stimulating electrode fixed to the tip of the gloved finger with the recording electrode pair placed 5 cm proximally on the base of the finger. The finger is inserted into the rectum or vagina and stimulation is performed close to the ischial spine. Using this stimulator, the terminal motor latency for the anal sphincter ‘M wave’ is typically around 2 ms. If a cathetermounted electrode is used, responses from the urethral sphincter can also be obtained. Unfortunately, despite a special focus of attention to this point, amplitudes of the ‘M wave’ response have not proved contributory. The difference in latencies obtained by the ‘perineal’ and ‘transrectal’ methods has not yet been explained. Cadaveric studies have shown that the levator ani or pubococcygeus muscle receives innervation direct from sacral nerve roots S2–S4 before the formation of the pudendal nerve trunk,6 so that theoretically these muscles should not contract with stimulation of the pudendal nerve at the level of the ischial spine. However, Smith and colleagues7 and subsequently Allen et al.8 were able to record the latency of pelvic floor responses stimulating at this point. The pudendal terminal motor latency has been found to increase with age in some studies,9,10 but not on others.11 The initial studies by the group from St Mark’s showed the perineal latency was abnormally prolonged in patients with urinary stress incontinence12 – a finding that was confirmed by the Manchester group.7 Working on the hypothesis that the pudendal nerve was stretched and injured during childbirth, several studies looked at the pudendal or perineal latency immediately postpartum. Although Allen et a1.8 using concentric needle electromyography (CNE) were able to demonstrate that there had been damage to the innervation of pubococcygeus in some women postpartum, they did not find a prolongation of the latency to stimulation of that muscle when women were examined 2 months postpartum. Snooks et al.13 found a significant increase in the mean pudendal nerve terminal motor latency 48–72 hours after vaginal delivery but in 60% this had returned to normal 2 months later. A followup study of 14 multiparous women from this group was made 5 years later,14 when the mean pudendal motor latency was found to be prolonged on both sides, fiber density of the anal sphincter was increased, and anal manometry showed there had been a reduction in anal canal pressure during maximal squeeze contraction. From this it was concluded that occult damage to the pudendal innervation of the external anal sphincter had persisted and worsened over the 5-year period; the authors hypothesized this to be exacerbated by abnormal straining patterns of defecation.
Sultan et al.15 also demonstrated a small (0.1 ms) but statistically significant increase in pudendal nerve latency following vaginal delivery, but, more importantly, they demonstrated a defect of either the internal or external anal sphincter, or both, in 35% of women after vaginal delivery using anal endosonography, and a strong association between these defects and the development of bowel symptoms. The prolonged latency and the muscle defect were thought to reflect a common traumatic cause. Prolongation of pudendal terminal latency has also been found in women with pelvic floor prolapse,16,17 with a further lengthening of the latency following vaginal dissection for repair or suspension procedures.17 Although no correlation of pudendal nerve terminal latency to parity was found in another study,9 the term ‘pudendal neuropathy’ has become established in the literature and authors less familiar with clinical neurophysiology theory tended to equate a prolongation of pudendal motor latency with pelvic floor denervation. This however, as explained in the introduction, is mistaken, as prolongation of latency is a poor measure of denervation. In fact, experts differ in their estimation of validity of the pudendal latency test. A lack of correlation to sphincter pressure measurements has been demonstrated: in one study, approximately 50% of patients with prolonged pudendal nerve terminal motor latency (PNTML) had normal anal canal squeeze pressures.18 In contrast to earlier studies, more recent work suggests the test does not predict improvement, or the lack of improvement, after surgical repair of anal sphincter defects.19 A prospective evaluation of anorectal physiologic tests in 90 patients with fecal incontinence did not find that pudendal terminal latency test results changed treatment decisions.20 Indeed, the American Gastroenterological Association statement indicated that ‘pudendal terminal latency cannot be recommended for evaluation of patients with fecal incontinence’.21 Currently, the utility of measuring pudendal nerve latencies in urinary incontinence is dubious. In the authors’ laboratories this test is only used in conjunction with a needle EMG examination if a proximal block of conduction in the motor axons is suspected, or when a motor versus sensory lesion of the sacral reflex has to be differentiated in a patient with an absent sacral reflex response.
Anterior sacral root (cauda equina) stimulation Transcutaneous stimulation of deeply situated nervous tissue became possible with the development of special electrical22 and magnetic23 stimulators. When applied over the spine these stimulators stimulate mainly the 291
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roots at the exit from the vertebral canal,24 although there have been various reports of these techniques applied to the sacral roots.25,26 Whether or not parasympathetic efferents can be stimulated using magnetic stimulation remains controversial. While it has been claimed that motor evoked potentials from detrusor can be produced following magnetic stimulation of the cauda equina,27 others have demonstrated inhibition of detrusor hyperreflexia following sacral root stimulation,28 which is expected after depolarization of perineal afferents. Needle EMG rather than non-selective surface electrodes should be used to record MEPs to electrical or magnetic stimulation because both depolarize underlying neural structures in a non-selective fashion and there may be activation of several muscles innervated by lumbosacral segments. It has been shown that responses from gluteal muscles may contaminate attempts to record from the sphincters and lead to error.29 Recording of MEPs with magnetic stimulation has been less successful, at least with standard coils,30,31 than with electrical stimulation, and there is often large stimulus artifact. Positioning of the ground electrode between the recording electrodes and the stimulating coil should decrease the artifact32 (Fig. 21.2). Stimulation of the roots may be used to obtain a peripheral conduction time so that a central conduction time (see next section) can be calculated.30 Demonstrating the presence of a perineal MEP on stimulation over the lumbosacral spine and recording this with a concentric needle (CN) EMG electrode may
occasionally be helpful; however, an absent response has to be evaluated with caution and the clinical value of the test has yet to be established.
Assessment of central motor pathways Using the same magnetic or electrical stimulation, it is possible to stimulate the motor cortex and record a response from the pelvic floor. Magnetic stimulation is less unpleasant, and cortical electrical stimulation is no longer used in awake subjects. By electrical stimulation over the motor cortex of healthy subjects, MEPs in anal29 and urethral33 sphincters, and in the bulbocavernosus29 muscles were reported. The mean latencies were between 30 and 35 ms if no ‘facilitatory maneuver’ was used. If, however, stimulation was performed during a period of slight voluntary contraction of the muscle, the latencies of MEPs shortened significantly (for up to 8 ms) (Fig. 21.3). By applying stimulation both over the scalp and in the back (at level L1), and subtracting the latency of the respective MEPs, a ‘central conduction time’ can be obtained. Central conduction times of approximately 22 ms without, and about 15 ms with, the facilitation (i.e. slight voluntary contraction) have been reported.30 Substantially longer central conduction time in patients with multiple sclerosis and spinal cord lesions as compared to healthy controls have been found,34 but as all those patients had clinically recognizable cord disease, the diagnostic contribution of the method remains doubtful.
2 ms 200 mV
Figure 21.2. Concentric needle EMG recording from the anal sphincter showing responses on ‘strong’ electrical stimulation with surface electrodes over the back (upper trace at level L1; lower trace at level S3). Digitimer stimulator: stimulus duration 50 µs, stimulus amplitude 50%. Three and two consecutive responses are superimposed, respectively.
Figure 21.3. Recording from the urethral sphincter with a concentric needle electrode in response to magnetic stimulation of the lower lumbar spine (lower trace; latency 6.5 ms) and the motor cortex (upper trace; latency 25.4 ms). The effect of ‘facilitation’ (i.e. a slight voluntary contraction) on shortening the latency of the response following cortical stimulation is evident.
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Recently, carefully collected normative values for the urethral sphincter and the puborectal muscle in adult women have been reported for transcranial magnetic stimulation.35,36 The necessity to use concentric needle EMG for recording37 has been reconfirmed.38 Because of the significant influence of voluntary contraction, the variability of both total conduction times and central conduction times makes the method somewhat clinically undependable. A well-formed sphincter MEP with a normal latency in a patient with a functional disorder or a medicolegal case may on occasion be helpful, but there is no established clinical use for this type of testing.
nEuroPHYSIoLoGY oF tHE SAcrAL SEnSorY SYStEM cerebral somatosensory evoked potentials (SEPs) The pudendal evoked response is easily recorded following electrical stimulation of the clitoral nerve.30,39–43 This SEP is of highest amplitudes at the central recording site ([Cz –2 cm: Fz] of the International 10–20 EEG System)44 and is highly reproducible. Amplitudes of the P40 measure between 0.5 and 12 µV.40 The first positive peak at 41 ± 2.3 ms40 (called P1 or P40) is usually clearly defined in healthy subjects using a stimulus two to four times the sensory threshold current strength40,43 (Fig. 21.4). Later negative (at around 55 ms) and then further positive waves are interindividually quite variable in amplitude and expression, and furthermore have little known clinical relevance. Pudendal SEP recordings have been widely employed in patients with neurogenic bladder dysfunction due to multiple sclerosis,34 but it has since been shown that the tibial cerebral SEPs are more often abnormal than the pudendal SEP45 and only in exceptional cases is the pudendal SEP abnormal but the tibials normal, pointing to an isolated conus involvement.45 Cerebral SEPs on clitoral stimulation were reported as a possibly valuable intraoperative monitoring method in patients with cauda equina or conus at risk of a surgical procedure.46,47 A study which looked at the value of the pudendal evoked potential when investigating urogenital symptoms for detecting relevant neurologic disease found it to be of lesser value than a clinical examination looking for signs of spinal cord disease in the lower limbs, i.e. lower limb hyperreflexia and extensor plantar responses.48 There may, however, be circumstances such
Figure 21.4. Cerebral somatosensory evoked potential (SEP) (above) and bulbocavernosus reflex (below) on dorsal clitoral nerve stimulation (rectangular pulses, 0.2 ms long at 1 Hz) in a 37-year-old woman with a compressive fracture of L1, complaining of difficulties in initiation of micturition. SEP is recorded with surface electrodes (Cz –2 cm: Fz); the bulbocavernosus reflex is recorded from the anal sphincter with surface electrodes. Two consecutive averages of 128 responses are superimposed. The P40 of the SEP and the first component of the bulbocavernosus reflex are indicated. The first reflex component is spurious at the applied stimulation strength, which was two-times sensory threshold; the second (late) reflex component is obvious. as when a patient is complaining of loss of bladder or vaginal sensation that it is reassuring to be able to record a normal pudendal evoked response. Newer techniques of stimulation isolate each dorsal clitoral nerve and may be more sensitive at locating the precise site of pathology.49 Following spinal cord injury, tibial and pudendal SEPs have been claimed to predict recovery in bladder control.50 Pudendal SEPs were used to study the mechanism of sacral neuromodulation.51
Electrical stimulation of urethra, bladder, and anal canal Cerebral SEPs can also be obtained on stimulation of the bladder urothelium.52 When making such measurements, it is of utmost importance to use bipolar stimulation in the bladder or proximal urethra, otherwise somatic afferents will be depolarized.33,53,54 These cerebral SEPs have been shown to have a maximum amplitude over the mid-line (Cz –2 cm: Fz);54 even so, the potential is of low amplitude (1 µV or less) and of variable configuration, and may be difficult to identify in some control subjects.54,55 The typical latency of the most prominent negative potential (N 1) is approximately 100 ms.54,55 The responses are of more relevance to neurogenic bladder dysfunction than the pudendal SEP, as the Aδ delta sensory afferents from bladder and proximal urethra accompany the autonomic fibers in the pelvic nerves.54 293
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Another stimulation site in the perineal region is the anal canal, following which cerebral SEPs with a slightly longer latency than those obtained following stimulation of the clitoris have been reported,31 but it is not possible to record this response from all control subjects. The rectum and sigmoid colon have also been stimulated, and cerebral SEPs of two types recorded. One was similar in shape and latency to pudendal SEP, and the other to SEP recorded on stimulation of bladder/posterior urethra.56
SAcrAL rEFLEXES Physiologic background, methods, and terminology ‘Sacral reflexes’ refer to electrophysiologically recordable responses of perineal/pelvic floor muscles to (electrical) stimulation in the urogenitoanal region. There are two reflexes – the anal and the bulbocavernosus – which are commonly clinically elicited in the lower sacral segments; both have the afferent and efferent limb of their reflex arc in the pudendal nerve, and are centrally integrated at the S2–S4 cord levels (Fig. 21.4). Electrophysiologic correlates of these reflexes have been described. It is possible to use electrical,2,57–60 mechanical,61 or magnetic31 stimulation. Whereas the last two modalities have been applied only to the clitoris, electrical stimulation can be applied at various sites: to the dorsal clitoral nerve2,43,62,63 or perianally.46,64 The pudendal nerve itself may be stimulated by applying needle electrodes transperineally61 or by using ‘St Mark’s electrode’.65 As a rule, reflex responses are recorded as EMG activation of target muscles, but responses of the external urethral sphincter have also been recorded with a micro-tip transducer catheter as pressure rises, with latencies between 27 and 41 ms.66 Bladder neck/proximal urethra can be stimulated using a catheter-mounted ring electrode53,67 and reflex responses obtained from perineal muscles. Bradley, one of the pioneers of uroneurophysiology, called this ‘electromyelography’,67 but fortunately this term did not persist. These reflexes are often referred to as ‘vesicourethral’ and ‘vesicoanal’,68 depending from which muscle the reflex response is recorded. With visceral denervation (e.g. following radical hysterectomy) the viscerosomatic reflexes (from both bladder and urethral stimulation) may be lost while the bulbocavernosus reflex is preserved. Loss of bladder–urethral reflex with preservation of bladder–anal reflex has been described
with urethral afferent injury after recurrent urethral surgeries.69 Reports of sacral reflexes obtained following electrical stimulation of clitoral nerve give consistent mean latencies of between 31 and 38.5 ms.2,43,57–60,62,63,70 Sacral reflex responses obtained on perianal or bladder neck/proximal urethra stimulation have latencies between 50 and 65 ms.2,63,65 This more prolonged response is thought to be due to the afferent limb of the reflex being conveyed by thinner myelinated nerves with slower conduction velocities than the thicker myelinated pudendal afferents. The longer latency ‘anal reflex’ – the contraction of the anal sphincter on stimulation of the perianal region – may also have thinner myelinated fibers in its afferent limb as it is produced by a nociceptive stimulus. On stimulation perianally, a short latency potential can also be recorded as a result of depolarization of motor branches to the anal sphincter;2,3 this ‘M wave’ has been mistaken for a reflex response.
Sacral reflex on electrical stimulation of clitoris The sacral reflex evoked on dorsal penile or clitoral nerve stimulation (the ‘bulbocavernosus reflex’) was shown to be a complex response, often formed by two components.2,60,71 The first component (with typical latency of about 33 ms) is the response that has been most often called the bulbocavernosus reflex. It is stable, does not habituate, and is thought to be an oligosynaptic reflex response, as the variability of single motor neuron discharges within this reflex is similar to that of the first component of the blink reflex.71 The second component has a similar latency to the sacral reflexes evoked by stimulation perianally or from the proximal urethra. The variability of single motor neuron responses within this component is much larger, as is typical for a polysynaptic reflex.71 The second component is not always demonstrable as a discreet response.61 The two components of the reflex may behave somewhat differently in control subjects and in patients: whereas in normal subjects it is usually the first component that has a lower threshold, in patients with partially denervated pelvic floor muscles the first reflex component cannot be obtained with single stimuli, but on strong stimulation the later reflex component does occur.60 This can cause confusion, and very ‘delayed’ reflex responses may be recorded in patients without recognizing the possibility that it is not a delayed first component but an isolated second component of the reflex. The situation can be clarified by using double stimuli that facilitate the reflex response61 and may reveal the first component, which was not obvious on stimulation with single stimuli.72
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Sacral reflex responses recorded with needle or wire electrodes can be analyzed separately for each side of the anal sphincter;60 this is important because unilateral or asymmetrical lesions are common. Newer techniques of stimulation isolate each dorsal clitoral nerve and may be more sensitive for identifying pathology.49 Using unilateral dorsal penile nerve blocks, the existence of two unilateral bulbocavernosus reflex arcs has been demonstrated.73,74 Thus, by detection from the left and right bulbocavernosus (and probably also the EAS) muscles, separate testing of right and left reflex arcs can be performed. In cases of unilateral (sacral plexopathy, pudendal neuropathy) or asymmetrical lesions (cauda equina), a healthy reflex arc may obscure a pathologic one. Sacral reflex responses on stimulation of the clitoral nerve have been proposed as being valuable in patients with cauda equina and lower motor neuron lesions;58 however, a reflex with a normal latency does not exclude the possibility of an axonal lesion in its reflex arc. Although most reports deal with abnormally prolonged sacral reflex latencies, it was suggested that a very short reflex latency may indicate the possibility of a tethered cord,75 the shorter latency being attributed particularly to the low location of conus. Shorter latencies of sacral reflexes in patients with suprasacral cord lesions were also reported.63 Continuous intraoperative recording of sacral reflex responses on clitoris stimulation is feasible if double pulses76,77 or a train of stimuli are used. Sacral reflex testing should be a part of the ‘diagnostic battery’ of which concentric needle EMG exploration of the pelvic floor muscles is the most important part. Measurement of sacral reflexes is established and carried out in laboratories worldwide and is – apart from EMG – the most time-honored uroneurophysiologic diagnostic procedure. However, the expectation of some authors that, with measurement of sacral reflexes, a single, easily learned test could distinguish between neurogenic and non-neurogenic sacral dysfunction was unrealistic. Although testing reflex responses is a valid and useful method to assess integrity of reflex arcs, and electrophysiologic assessment of sacral reflexes is a more quantitative, sensitive, and reproducible way of assessing the S2–S4 reflex arcs than any of the clinical methods, uncritical interpretation of results should be discouraged.
Sacral reflex on mechanical stimulation Mechanical stimulation has been used to elicit the bulbocavernosus reflex in both sexes,78 but there is as yet little experience with female patients. Either a standard
commercially available reflex hammer or a customized electromechanical hammer can be used.79 Such stimulation is painless and can be used in children or patients with pacemakers in whom electrical stimulation is contraindicated.
AutonoMIc nErVouS SYStEM The uroneurophysiologic methods discussed so far assess only the myelinated fibers, whereas it is the autonomic nervous system, and the parasympathetic component in particular, that is most relevant for sacral organ function. It has been argued that local involvement of the sacral nervous system (such as trauma, compression, etc.) will usually involve somatic and autonomic fibers simultaneously. However, as there are some local pathologic conditions (such as mesorectal excision of carcinoma or radical hysterectomy) which can cause a pure autonomic lesion, methods by which the parasympathetic and sympathetic nervous systems innervating the pelvic viscera could be assessed directly would be very helpful. Information on parasympathetic bladder innervation can, to some extent, be obtained by cystometry, but from a clinical neurophysiologic point of view, direct electrophysiologic testing would be desirable. In cases where a general involvement of thin fibers is expected, an indirect way to examine autonomic fibers is to assess thin sensory fiber function. As unmyelinated afferent fibers transmit temperature sensation and pain, unmyelinated fiber neuropathy can be identified by testing thermal sensitivity. Thin (visceral sensory) fibers are tested by stimulating the proximal urethra or bladder, and recording sacral reflex responses or cerebral SEPs.
Sympathetic skin response The sympathetic nervous system mediates sweat gland activity in the skin, and changes in this activity lead to changes in skin resistance. On ‘stressful stimulation’, a potential shift can be recorded with surface electrodes from the skin of palms and soles, and has been reported to be a useful parameter in assessment of neuropathy involving unmyelinated nerve fibers.80 The response (sympathetic skin response, or SSR) can also be recorded from perineal skin.81,82 The SSR is a reflex which consists of myelinated sensory fibers, a complex central integrative mechanism, and a sympathetic efferent limb (with postganglionic non-myelinated C-fibers). The stimulus used in clinical practice is usually an electric pulse delivered to the upper or lower limb (to mixed nerves), but the genital organs can also be stimulated.81 The latencies of SSR on the penis following stimu295
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lation of a median nerve at the wrist have been reported as being between 1.581 and 2.3 seconds,82 and could be obtained in all normal subjects with a large variability (Fig. 21.5); however, no equivalent control data exist in women as yet. The responses are easily habituated, and depend on a number of endogenous and exogenous factors including skin temperature, which should be at least above 28°C. Only an absent SSR can be taken as abnormal. Limited literature exists regarding the relationship between SSR results and bladder dysfunction. One study reports that diabetic cystopathy was associated with autonomic neuropathy as detected by SSR.83 A correlation has been shown between the absence of the SSR response in foot and bladder neck dyssynergia following spinal cord injury.84 Recording from the perineal region increases the diagnostic sensitivity for assessing sympathetic nerve function within the thoracolumbar cord.85 The test is not sensitive for partial lesions as only complete absence of response can be regarded as abnormal. Its utility in evaluating bladder and urethral dysfunction is not yet established.
concLuSIonS Uroneurophysiologic techniques have been used most often in research. Neurophysiology was valuable in substantiating the hypothesis that a proportion of patients with sacral dysfunctions had involvement of the nervous system, such as patients with stress urinary and idiopathic fecal incontinence.5,13 The tests also helped to establish 500 uV/D
1 s/D 20 000 ms
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the function of the sacral nervous system in patients with suprasacral spinal cord injury,86 to reveal the consequences of particular surgeries,87 and to elucidate innervation of pelvic floor muscles.88,89 Recently introduced has been the technique of intraoperative monitoring, where evoked potential studies have long since become established to help prevent lesions of the neural structures at risk from the surgical procedure.46,76,90 Further research applications of uroneurophysiologic methods are expected, as many of the neurologic aspects of urologic, gynecologic, and proctologic problems have yet to be elucidated.
rEFErEncES 1. Fowler CJ, Tedman BM. Clinical measurements of nerve conduction. In: Binnie CD, Cooper R, Mauguiere F, Osselton J, Prior P, Tedman B (eds) Clinical Neurophysiology: EMG, Nerve Conduction and Evoked Potentials, vol. 1 (revised and enlarged edition). Amsterdam: Elsevier, 2004; 59–75. 2. Vodusek DB, Janko M, Lokar J. Direct and reflex responses in perineal muscles on electrical stimulation. J Neurol Neurosurg Psychiatry 1983;46(1):67–71. 3. Bartolo DC, Jarratt JA, Read NW. The cutaneoanal reflex: a useful index of neuropathy? Br J Surg 1983;70(11):660–3. 4. Pedersen E, Klemar B, Schroder J et al. Anal sphincter responses after perianal electrical stimulation. J Neurol Neurosurg Psychiatry 1982;45(9):770–3. 5. Kiff ES, Swash M. Normal proximal and delayed distal conduction in the pudendal nerves of patients with idiopathic (neurogenic) faecal incontinence. J Neurol Neurosurg Psychiatry 1984;47(8):820–3. 6. Juenemann KP, Lue TF, Schmidt RA, Tanagho EA. Clinical significance of sacral and pudendal nerve anatomy. J Urol 1988;139:74–80. 7. Smith AR, Hosker GL, Warrell DW. The role of pudendal nerve damage in the aetiology of genuine stress incontinence in women. Br J Obstet Gynaecol 1989;96(1):29–32. 8. Allen RE, Hosker GL, Smith AR, Warrell DW. Pelvic floor damage and childbirth: a neurophysiological study. Br J Obstet Gynaecol 1990;97(9):770–9. 9. Jameson JS, Chia YW, Kamm MA et al. Effect of age, sex and parity on anorectal function. Br J Surg 1994;81(11):1689–92.
Figure 21.5. Sympathetic skin responses recorded from the foot at 2.3 s (upper trace), from the penis at 1.52 s (middle trace), and from the hand (lower trace) with silver/silverchloride electrodes in response to a sudden noise. The possible value of the equivalent potentials recorded in women has not yet been examined.
10. Laurberg S, Swash M. Effects of aging on the anorectal sphincters and their innervation. Dis Colon Rectum 1989;32(9):737–42. 11. Barrett JA, Brocklehurst JC, Kiff ES et al. Anal function in geriatric patients with faecal incontinence. Gut 1989;30(9):1244–51.
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12. Snooks SJ, Badenoch DF, Tiptaft RC, Swash M. Perineal nerve damage in genuine stress urinary incontinence. An electrophysiological study. Br J Urol 1985;57(4):422–6. 13. Snooks SJ, Setchell M, Swash M et al. Injury to innervation of pelvic floor sphincter musculature in childbirth. Lancet 1984;2(8402):546–55. 14. Snooks SJ, Swash M, Mathers SE, Henry MM. Effect of vaginal delivery on the pelvic floor: a 5-year follow-up. Br J Surg 1990;77(12):1358–60. 15. Sultan AH, Kamm MA, Hudson CN et al. Anal-sphincter disruption during vaginal delivery. N Engl J Med 1993;329(26):1905–11. 16. Smith AR, Hosker GL, Warrell DW. The role of partial denervation of the pelvic floor in the aetiology of genitourinary prolapse and stress incontinence of urine. A neurophysiological study. Br J Obstet Gynaecol 1989;96(1):24–8. 17. Benson JT, McClellan E. The effect of vaginal dissection on the pudendal nerve. Obstet Gynecol 1993;82(3):387–9. 18. Wexner SD, Marchetti F, Salanga VD et al. Neurophysiologic assessment of the anal sphincters. Dis Colon Rectum 1991;34(7):606–12. 19. Malouf AJ, Morton CS, Engel AF et al. Long-term results of overlapping anterior anal-sphincter repair for obstetric trauma. Lancet 2000;355(9200):260–5. 20. Liberman H, Faria J, Ternent CA et al. A prospective evaluation of the value of anorectal physiology in the management of fecal incontinence. Dis Colon Rectum 2001;44(11):1567–74. 21. AGA, American Gastroenterological Association medical position statement on anorectal testing techniques. Gastroenterology 1999;116:732–60.
Motor bladder responses after magnetic stimulation of the cauda equina. Neurourol Urodyn 1991;10(4):380–1. 28. Sheriff MK, Shah PJ, Fowler C et al. Neuromodulation of detrusor hyper-reflexia by functional magnetic stimulation of the sacral roots. Br J Urol 1996;78(1):39–46. 29. Vodusek DB, Zidar J. Perineal motor evoked responses. Neurourol Urodyn 1988;7:236–7. 30. Opsomer RJ, Caramia MD, Zarola F, Pesce F, Rossini PM. Neurophysiological evaluation of central–peripheral sensory and motor pudendal fibres. Electroencephalogr Clin Neurophysiol 1989;74(4):260–70. 31. Loening-Baucke V, Read NW, Yamada T, Barker AT. Evaluation of the motor and sensory components of the pudendal nerve. Electroencephalogr Clin Neurophysiol 1994;93(1):35–41. 32. Jost WH, Schimrigk K. A new method to determine pudendal nerve motor latency and central motor conduction time to the external anal sphincter. Electroencephalogr Clin Neurophysiol 1994;93(3):237–9. 33. Thiry AJ, Deltenre PF. Neurophysiological assessment of the central motor pathway to the external urethral sphincter in man. Br J Urol 1989;63(5):515–19. 34. Eardley I, Nagendran K, Lecky B et al. Neurophysiology of the striated urethral sphincter in multiple sclerosis. Br J Urol 1991;68(1):81–8. 35. Brostrom S, Jennum P, Lose G. Motor evoked potentials from the striated urethral sphincter and puborectal muscle: normative values. Neurourol Urodyn 2003;22(4):306–13. 36. Brostrom S. Motor evoked potentials from the pelvic floor. Neurourol Urodyn 2003;22(7):620–37. 37. Vodusek DB, Zidar J. Perineal motor evoked responses. Neurourol Urodyn 1988;7:236–7.
22. Merton PA, Morton HB. Stimulation of the cerebral cortex in the intact human subject. Nature 1980;285(5762):227.
38. Brostrom S, Jennum P, Lose G. Motor evoked potentials from the striated urethral sphincter: a comparison of concentric needle and surface electrodes. Neurourol Urodyn 2003;22(2):123–9.
23. Barker AT, Jalinous R, Freeston IL. Non-invasive magnetic stimulation of human motor cortex. Lancet 1985;1(8437):1106–7.
39. Haldeman S, Bradley WE, Bhatia N. Evoked responses from the pudendal nerve. J Urol 1982;128(5):974–80.
24. Mills KR, Murray NM. Electrical stimulation over the human vertebral column: which neural elements are excited? Electroencephalogr Clin Neurophysiol 1986;63(6):582–9. 25. Swash M, Snooks SJ. Slowed motor conduction in lumbosacral nerve roots in cauda equina lesions: a new diagnostic technique. J Neurol Neurosurg Psychiatry 1986;49(7):808–16. 26. Vodusek DB. Electrophysiology. In: Schuessler B, Laycock J, Norton P, Stanton S (eds) Pelvic Floor Re-education: Principles and Practice. London: Springer-Verlag, 1994; 83–97. 27. Bemelmans BLH, van Kerrebroeck EV, Debruyne FMJ.
40. Vodusek DB. Pudendal SEP and bulbocavernosus reflex in women. Electroencephalogr Clin Neurophysiol 1990;77(2):134–6. 41. Haldeman S, Bradley W, Bhatia, N et al. Cortical evoked potentials on stimulation of pudendal nerve in women. Urology 1983;21(6):590–3. 42. Tackmann W, Vogel P, Porst H. Somatosensory evoked potentials after stimulation of the dorsal penile nerve: normative data and results from 145 patients with erectile dysfunction. Eur Neurol 1987;27:245–50. 43. Vodusek DB. Pudendal somatosensory evoked potentials. Neurologija 1990;39(Suppl 1):149–55. 44. Guerit J, Opsomer R. Bit-mapped imagine of somatosensory evoked potentials after stimulation of the posterior
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tibial nerves and dorsal nerve of the penis/clitoris. Electroencephalogr Clin Neurophysiol 1991;80:228–37.
60. Krane RJ, Siroky MB. Studies on sacral evoked potentials. J Urol 1980;124(6):872–6.
45. Rodi Z, Vodusek DB, Denislic M. Clinical uro-neurophysiological investigation in multiple sclerosis. Eur J Neurol 1996;3:574–80.
61. Vodusek DB. Neurophysiological study of bulbocavernosus reflex in man [in Slovene]. Ljubljana: University of Ljubljana, 1988; 1–129.
46. Vodusek DB, Deletis V, Abbott, R et al. Prevention of iatrogenic micturition disorders through intraoperative monitoring. Neurourol Urodyn 1990;9:444–5.
62. Varma JS, Smith AN, McInnes A. Electrophysiological observations on the human pudendo-anal reflex. J Neurol Neurosurg Psychiatry 1986;49(12):1411–6.
47. Cohen BA, Major MR, Huizenga BA. Pudendal nerve evoked potential monitoring in procedures involving low sacral fixation. Spine 1991;16(8 Suppl):S375–S378.
63. Bilkey WJ, Awad EA, Smith AD. Clinical application of sacral reflex latency. J Urol 1983;129(6):1187–9.
48. Delodovici ML, Fowler CJ. Clinical value of the pudendal somatosensory evoked potential. Electroencephalogr Clin Neurophysiol 1995;96(6):509–15. 49. Yang CC, Bowen JR, Kraft GH. Cortical evoked potentials of the dorsal nerve of the clitoris and female sexual dysfunction in multiple sclerosis. J Urol 2000;164:2010–13. 50. Curt A, Rodic B, Schurch B, Dietz V. Recovery of bladder function in patients with acute spinal cord injury: significance of ASIA scores and somatosensory evoked potentials. Spinal Cord 1997;35(6):368–73. 51. Malaguti S, Spinelli M, Giardiello G et al. Neurophysiological evidence may predict the outcome of sacral neuromodulation. J Urol 2003;170(6 Pt 1):2323–6. 52. Badr G, Fall M, Carlsson CA et al. Cortical evoked potentials following stimulation of the urinary bladder in man. Electroencephalogr Clin Neurophysiol 1982;54(5):494–8.
64. Contreras Ortiz O, Bertotti AC, Rodriguez Nunez JD. Pudendal reflexes in women with pelvic floor disorders. Zentralbl Gynaekol 1994;116(10):561–5. 65. Pedersen E, Harving H, Klemar B, Torring J. Human anal reflexes. J Neurol Neurosurg Psychiatry 1978;41(9):813–8. 66. Reitz A, Schmid DM, Curt A, Knapp PA, Schurch B. Afferent fibers of the pudendal nerve modulate sympathetic neurons controlling the bladder neck. Neurourol Urodyn 2003;22(6):597–601. 67. Bradley WE. Urethral electromyelography. J Urol 1972;108(4):563–4. 68. Fowler CJ, Betts CD. Clinical value of electrophysiological investigations of patients with urinary symptoms. In: Mundy AR, Stephenson TP, Wein AJ (eds) Urodynamics: Principles, Practice and Application, 2nd ed. Edinburgh: Churchill Livingstone, 1994; 165–81.
53. Sarica Y, Karacan I. Bulbocavernosus reflex to somatic and visceral nerve stimulation in normal subjects and in diabetics with erectile impotence. J Urol 1987;138(1):55–8.
69. Benson JT. Clinical neurophysiologic techniques in urinary and fecal incontinence. In: Bent AE (ed) Ostergaard’s Urogynecology and Pelvic Floor Dysfunction. Philadelphia: Lippincott Williams and Wilkins, 2003; p155–184.
54. Hansen MV, Ertekin C, Larsson LE. Cerebral evoked potentials after stimulation of the posterior urethra in man. Electroencephalogr Clin Neurophysiol 1990;77(1):52–8.
70. Vereecken RL, De Meirsman J, Puers B, Van Mulders J. Electrophysiological exploration of the sacral conus. J Neurol 1982;227(3):135–44.
55. Gaenzer H, Madersbacher H, Rumpl E. Cortical evoked potentials by stimulation of the vesicourethral junction: clinical value and neurophysiological considerations. J Urol 1991;146(1):118–23.
71. Vodusek DB, Janko M. The bulbocavernosus reflex. A single motor neuron study. Brain 1990;113(Pt 3):813–20.
56. Loening-Baucke V, Read NW, Yamada T. Further evaluation of the afferent nervous pathways from the rectum. Am J Physiol 1992;262(5 Pt 1):G927–G933. 57. Rushworth G. Diagnostic value of the electromyographic study of reflex activity in man. Electroencephalogr Clin Neurophysiol 1967;Suppl 25:65–73. 58. Ertekin C, Reel F. Bulbocavernosus reflex in normal men and in patients with neurogenic bladder and/or impotence. J Neurol Sci 1976;28(1):1–15. 59. Vacek J, Lachman M. [The bulbocavernosus reflex in diabetics with erectile dysfunction: a clinical and EMG study. (In Czech)] Cas Lek Cesk 1977;33:1014–7.
72. Rodi Z, Vodusek DB. The sacral reflex studies: single versus double pulse stimulation. Neurourol Urodyn 1995;14:496–7. 73. Rechthand E. Bilateral bulbocavernosus reflexes: crossing of nerve pathways or artifact? Muscle Nerve 1997;20(5):616–18. 74. Amarenco G, Kerdraon J. Clinical value of ipsi- and contralateral sacral reflex latency measurement: a normative data study in man. Neurourol Urodyn 2000;19(5):565–76. 75. Hanson P, Rigaux P, Gillard C, Biset E. Sacral reflex latencies in tethered cord syndrome. Am J Phys Med Rehabil 1993;72(1):39–43. 76. Vodusek DB et al. Intraoperative monitoring of pudendal nerve function. In: Rother M, Zwiener U (eds) Quanti-
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tative EEG Analysis – Clinical Utility and New Methods. Jena: Universitatsverlag Jena, 1993; 309–12. 77. Deletis V, Vodusek DB. Intraoperative recording of the bulbocavernosus reflex. Neurosurgery 1997;40(1):88–92; discussion 92–3. 78. Dykstra D, Sidi A, Cameron J et al. The use of mechanical stimulation to obtain the sacral reflex latency: a new technique. J Urol 1987;137(1):77–9. 79. Podnar S, Vodusek DB, Trsinar B, Rodi Z. A method of uroneurophysiological investigation in children. Electroencephalogr Clin Neurophysiol 1997;104(5):389–92. 80. Shahani BT, Halperin JJ, Boulu P, Cohen J. Sympathetic skin response – a method of assessing unmyelinated axon dysfunction in peripheral neuropathies. J Neurol Neurosurg Psychiatry 1984;47(5):536–42. 81. Opsomer RJ et al. Electrophysiologic testing of motor sympathetic pathways: normative data and clinical contribution in neurourological disorders. Neurourol Urodyn 1993;12:336–8. 82. Daffertshofer M, Linden D, Syren M, Junemann KP, Berlit P. Assessment of local sympathetic function in patients with erectile dysfunction. Int J Impot Res 1994;6(4):213–25. 83. Ueda T, Yoshimura N, Yoshida O. Diabetic cystopathy: relationship to autonomic neuropathy detected by sympathetic skin response. J Urol 1997;157(2):580–4.
84. Schurch B, Curt A. Rossier AB. The value of sympathetic skin response recordings in the assessment of the vesicourethral autonomic nervous dysfunction in spinal cord injured patients. J Urol 1997;157(6):2230–3. 85. Rodic B, Curt A, Dietz V, Schurch B. Bladder neck incompetence in patients with spinal cord injury: significance of sympathetic skin response. J Urol 2000;163(4):1223–7. 86. Koldewijn EL, Van Kerrebroeck PE, Bemelmans BL et al. Use of sacral reflex latency measurements in the evaluation of neural function of spinal cord injury patients: a comparison of neuro-urophysiological testing and urodynamic investigations. J Urol 1994;152(2 Pt 1):463–7. 87. Liu S, Christmas TJ, Nagendran K et al. Sphincter electromyography in patients after radical prostatectomy and cystoprostatectomy. Br J Urol 1992;69(4):397–403. 88. Vodusek DB, Light JK. The motor nerve supply of the external urethral sphincter muscles. Neurourol Urodyn 1983;2:193–200. 89. Percy JP, Neill ME, Swash M, Parks AG. Electrophysiological study of motor nerve supply of pelvic floor. Lancet 1981;1(8210):16–17. 90. Gearhart JP, Burnett A, Owen JH. Measurement of pudendal evoked potentials during feminizing genitoplasty: technique and applications. J Urol 1995;153(2):486–7.
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22 Videourodynamics Sender Herschorn, Jerome Green, Dudley Robinson
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IntroductIon Videourodynamics is a diagnostic tool that incorporates urodynamics with simultaneous imaging of the lower urinary tract. The incorporation of radiologic visualization of the lower urinary tract during bladder filling and voiding is useful for determining the site of bladder outlet obstruction, the integrity of the sphincter mechanism, and the presence of vesicoureteral reflux, bladder diverticula, fistulae, and trabeculation.1 Urodynamics was first synchronized with cineradiography in the early 1950s through the pioneering efforts of E.R. Miller.2,3 The initial goal was to minimize the radiation exposure to the patient during cystourethrography. Originally, patient exposure to radiation was high when ‘movies’ were taken, but with the advent of image intensifiers, video transduction, and later videotape recording, patient exposure was reduced. This permitted bursts of continuous activity to be recorded during critical phases of lower urinary tract activity without overexposing the patient. Today most studies can be done with less than 1 minute of fluoroscopy time.4 These developments have contributed to the wealth of information about lower urinary tract function and dysfunction. Modern videourodynamic techniques incorporate fluoroscopy with the evolution of the urodynamic machine from a strip chart recorder to a microcomputer. Videourodynamic studies are not necessary in every patient and simpler studies frequently provide enough information to adequately delineate and treat the dysfunction. Videourodynamic studies are beneficial when simultaneous evaluation of function and anatomy is needed to provide detailed information about the whole or parts of the storage and emptying phases. Common indications well suited for videourodynamic evaluation include complex incontinence, where the history does not fit with the findings on preliminary investigations; incontinence when there has been previous anti-incontinence surgery; and incontinence in the face of a neurologic abnormality. Aside from the minimal radiation exposure to the patient, the only disadvantage of videourodynamics is its cost. This is a result of the time and effort of the personnel required and the expense of the equipment which may limit its utility to larger centers with larger patient populations. The cost can, however, be justified by its utility in solving complicated problems. In this chapter the procedures are outlined, examples of the applications are provided, and the limitations are discussed.
components of VIdeourodynamIcs A typical arrangement for videourodynamic studies includes a multichannel recorder, a fluoroscopy unit with
a table that can be positioned in the supine and upright position, and a flowmeter (Fig. 22.1). A commode seat attachment facilitates fluoroscopic screening of voiding in the seated position, which is ideal for women. Most modern systems are computer based, which permits complex analysis to be performed. A schematic diagram of the setup is shown in Figure 22.2.
multichannel recorder As the procedure involves measuring simultaneous pressures during both phases of lower urinary tract function and flow during the voiding phase, a multichannel recorder is necessary (Fig. 22.3). Many systems are available,5 most of which have dispensed with a strip chart
a
b
Figure 22.1. A videourodynamic suite: (a) the patient has been catheterized and her bladder is being filled in the supine position; (b) the patient is in the upright position after the filling catheter has been removed. She will be asked to cough and strain to demonstrate stress incontinence and then to void. The study will be stored on the multichannel recorder.
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Figure 22.2.
Diagram of videourodynamic setup.
tial, as these can be measured manually. The sphincter electromyography (EMG) channel is not necessary for routine clinical practice but can be helpful in patients with neurologic disease; its inclusion introduces another level of complexity and sophistication. Controversy exists regarding the use of subtracted detrusor pressure versus intravesical pressure, although most reports at present use the subtracted pressures (intravesical pressure minus the intra-abdominal pressure). Bladder pressures can only be recorded using a pressure line in the bladder. This pressure is affected by intra-abdominal pressure, which can be measured separately by a rectal catheter. Increases in intra-abdominal pressure can result from straining, the upright position, and other provocative activities such as coughing, jumping, and heel bouncing. In order to get an accurate recording of bladder pressure and to eliminate the effect of intra-abdominal pressure, Bates et al.6 emphasized the value of electronically subtracting the intra-abdominal pressure from the intravesical pressure. However, even with the patient quiescent and totally cooperative, artifacts may be produced by intrinsic rectal contractions4 since the bladder pressure is derived from the electronic subtraction. On the other hand, McGuire et al.7 do not measure rectal or abdominal pressure with a separate catheter. They monitor urethral pressure along with bladder pressure via two lumens of the same catheter. They state that urethral pressure reflects rectal or abdominal pressure, allowing them to differentiate bladder contractions from abdominal straining. In our unit, we use subtracted detrusor pressures.
urine flowmeters Flowmeters are commonly of one of three types: weight, electronic dip-stick, or rotating disk.8 The first measures the weight of the collected urine, the second measures the changes in electrical capacitance of a dip-stick mounted in the collecting chamber, and the third measures the power required to keep a disk rotating at a constant speed while the urine, which tends to slow it down, is directed towards it. All three can provide high sensitivity and reproducibility of data. A commode chair with uroflow is illustrated in Figure 22.4. Figure 22.3.
Multichannel urodynamic recorder.
output in favor of a television monitor display of the procedure. The choice of components of the study is up to the individual clinician. Figure 22.2 illustrates possible inclusions. The channels demonstrating volume of fluid instilled and volume voided are helpful but not essen-
fluoroscopy A good quality fluoroscopy unit with a high resolution image intensifier and a table that can function in both the supine and erect positions are required. Fluoroscopic images are obtained selectively during the filling and voiding study and are either superimposed on the pres303
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Figure 22.4.
A commode chair with uroflowmeter.
sure–flow tracing or displayed on a separate screen. The fluoroscopic images can be stored and reproduced individually or as continuous clips during key parts of the study. A recording of the procedure can be made for subsequent review. Since the contrast medium instilled into the bladder is unlikely to be absorbed, we generally use the less expensive high-osmolality contrast media. A dilute solution of one liter of Hypaque is prepared by the pharmacy and supplied in sterile intravenous bags.
VIdeourodynamIc technIque The patient reports for the study with a full bladder and a flow rate is obtained. The equipment is zeroed and the transducer is placed at a height adjacent to the upper edge of the patient’s symphysis pubis. Either a double lumen catheter or two 8 Fr feeding tubes (one for filling which is removed prior to the voiding study and one for pressure measurements) are inserted into the bladder. Residual urine is measured. The rectal catheter is a 42 cm 14 Fr with a balloon over the tip. If desired, EMG recording devices may be attached to the patient. The study is conducted by an urodynamics specialist who is present in the room, communicates with the patient throughout the procedure, and records the findings manually and electronically. A supine or semioblique filling study is carried out, with various measure-
ments being taken throughout this study; responses to actions such as Credé, cough, and Valsalva are recorded. The filling rate is no longer divided into slow, medium or fast, but rather is described as physiologic or non-physiologic.9 In practice, most clinicians use a medium fill rate of 50–75 cc per minute.10 The bladder is filled, emptied and then refilled in the patient’s usual voiding position (lying, sitting or standing). Two bladder fillings are usually done since decreased compliance may be a result of the medium filling11 and a second test verifies it. The upright position of the second filling is also a provocative test for overactivity (instability).10 Additional responses to Credé, cough, and Valsalva are again recorded. A commonly used method is to fill the bladder supine and stand the patient up for provocative maneuvers. During the study, recordings are made of bladder images in the filling phase in the supine and/or in the upright positions (Fig. 22.3). Anteroposterior (AP) and oblique views are obtained. The AP position permits documentation of reflux and its extent, and in the oblique position the course of the urethra can be seen separate from a cystocele. Note is made of the bladder outline, the appearance of the bladder neck at rest, and its position relative to the inferior margin of the symphysis at rest and with straining and coughing. Leakage of urine with overactivity, decreased compliance, or with various stress maneuvers is recorded. In the upright position, the presence of a cystocele and its relationship to the urethra are also noted. If the patient is able to void in front of the camera, the voiding phase (or parts of it) is recorded, along with the pressures and flow tracings. If the patient is unable to void with the catheters in place, these are removed and a flow rate and a voided volume are measured. Total fluoroscopy time is usually less than 1 minute. The recorded study provides an opportunity for the case to be reviewed and discussed. All of the events of the study are recorded and displayed on the monitor during the study. The urodynamic machine is usually equipped with the capability of compressing the study so that it can be viewed on an ordinary letter-size sheet of paper.
tests performed urinary flow rate A urinary flow rate is a simple urodynamic test that can provide objective and quantitative measures on both storage and voiding symptoms.12 An abnormal pattern is generated in the presence of a weak detrusor, abdomi-
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nal straining, or bladder outlet obstruction. Although the urodynamic catheters have less effect on voiding patterns in females than in males, it is still useful to obtain a urinary flow rate on arrival that may be compared with the flow data generated during the urodynamic study. After the initial flow is completed, a post void residual can be determined on introduction of the urodynamic catheters.
cystometry The first part of the filling study is cystometry, the method by which the pressure–volume relationship of the bladder is measured.9 It is used to assess detrusor activity, sensation, compliance, and capacity. The detrusor pressure (pdet) is calculated by subtraction of the abdominal pressure (pabd), as measured by a balloon in the rectum, vagina, or bowel stoma, from the total intravesical pressure (pves), as measured by the intravesical catheter. The subtracted detrusor pressure reflects the activity and pressures generated by the detrusor muscle alone. Artifacts in the pdet may be produced by intrinsic rectal contractions.10 The terminology to describe detrusor activity has been standardized by the International Continence Society.9 Detrusor overactivity is characterized by spontaneous or provoked involuntary detrusor contractions during filling. Although an involuntary contraction was originally defined as a minimum pressure rise of 15 cmH2O,13 there is presently no lower limit for the amplitude of an involuntary contraction.9 When leakage is detected in association with an involuntary detrusor contraction, is it termed detrusor overactivity incontinence. Detrusor overactivity can be further characterized into idiopathic and neurogenic detrusor overactivity: idiopathic detrusor overactivity describes involuntary detrusor contractions of unknown etiology and has replaced the term detrusor instability; an involuntary detrusor contraction secondary to an underlying neurologic condition is neurogenic detrusor overactivity, which has replaced the term detrusor hyperreflexia.9 Another type of overactive bladder dysfunction is reduced compliance. Bladder compliance is defined as the change in pressure for a given change in volume. It is calculated by dividing the volume change by the change in detrusor pressure during that change in bladder volume, and is expressed as ml/cmH2O.9 Normal bladder compliance is high and in the laboratory the normal pressure rise is less than 6–10 cmH2O.4 Low bladder compliance implies a poorly distensible bladder. The actual numeric values to indicate normal, high or low compliance have yet to be defined.9
The finding of detrusor overactivity on cystometry is important if it correlates with the clinical condition of the patient. Idiopathic detrusor overactivity has been reported in 30–35% of patients with stress incontinence undergoing surgery. It resolves in the majority following repairs and does not have a significant impact on outcomes.14,15 Alternatively, if the patient’s symptoms are primarily from bladder overactivity, or other factors predisposing to abnormal bladder behavior are present, the cystometric findings will influence treatment. These include a history of radiation, chronic bladder inflammation, indwelling catheter, chronic infection, chemotherapy, voiding dysfunction following pelvic surgery or other neurologic conditions.
Leak point pressures The Valsalva or abdominal leak point pressure (VLPP or ALPP) is the intravesical pressure that exceeds the continence mechanism resulting in a leakage of urine in the absence of a detrusor contraction.9 This is performed by a progressive Valsalva maneuver or cough.16 VLPP tests the strength of the urethra. The study is performed in the sitting or standing position with at least 150–200 ml of fluid in the bladder. Historically, a VLPP of less than 60 cmH2O was evidence of significant intrinsic sphincter deficiency (ISD), between 60 and 90 cmH2O suggested a component of ISD, and greater than 90 cmH2O suggested minimal ISD with leakage mainly due to hypermobility.4 Currently, no prospective studies have shown that VLPP less than 60 can accurately diagnose ISD. The VLPP has been shown to be reproducible17 but has not yet been standardized. There are limitations to a VLPP. If the patient’s Valsalva effort is inadequate, urinary leakage may not be seen and thus a VLPP cannot be determined. A cystocele may produce inferior pressure on an incompetent urethra that will prevent incontinence or falsely elevate the VLPP. When a cystocele is present, the VLPP should be repeated with the prolapse reduced by insertion of a vaginal pack or pessary. The detrusor or bladder leak point pressure (DLPP) is the detrusor pressure (pdet) at which urinary leakage occurs during bladder filling on cystometry. This parameter is used to investigate and follow patients with neurogenic and low compliant bladders. In general, patients with a DLPP greater than approximately 25–30 cmH2O are at risk for upper tract deterioration from reflux or obstruction.18,19 In these patients it is also necessary to assess compliance. A high DLPP indicates poor compliance with urethral obstruction whereas a low DLPP is seen in patients with an incompetent urethra. In order 305
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to demonstrate poor compliance in these patients, filling may be done with a Foley catheter to obstruct the outlet.20
pressure–flow studies Pressure–flow studies are designed to provide dynamic information on the emptying phase of lower urinary tract function. Obstruction is not common in females21 but may be found after surgical correction of stress urinary incontinence and less commonly with detrusor sphincter dyssynergia, pseudodyssynergia,22 and rarely stricture disease. Interference with voiding may also be associated with pelvic organ prolapse. Although there are no established nomograms to depict pressure/flow in women as there are in men, the pattern of high detrusor pressure and low urinary flow indicates obstruction (Fig. 22.5). Simultaneous cystography can demonstrate the level of obstruction. Detrusor pressure during voiding is characteristically low in females. A preoperative study that demonstrates a low detrusor pressure with a low flow rate may aid in counseling the patient about postoperative urinary retention after stress incontinence surgery.
Figure 22.5. Videourodynamic study of a 62-year-old woman with urgency, frequency, and slow stream following multiple urethral dilations. The study shows a stable bladder on filling. Her voiding pressure exceeds 170 cmH2O and her flow rate is low. There is a urethral stricture visible (arrow in b) with proximal urethral dilation. (IH2O, infusion rate of water; pabd, abdominal pressure; pdet, detrusor pressure; pves, intravesical pressure; VH2O, volume of water.)
electromyography Sphincter electromyography (EMG) during videourodynamics is used to examine striated sphincter activity during filling and voiding. These kinesiologic studies can be performed with surface electrodes, vaginal or anal probes, and needles. Normal sphincter EMG activity has characteristic audio quality that may be monitored simultaneously. Its most important role is the identification of abnormal sphincter activity in patients with neurogenic bladder dysfunction and in those with behavioral voiding dysfunction.23 The fluoroscopy component, however, can demonstrate detrusor external sphincter dyssynergia in patients with suprasacral lesions and can show urethral obstruction in patients with dysfunctional voiding. EMG recordings are not usually necessary in routine videourodynamics for incontinence in females who have no neurologic abnormalities. Artifacts can be secondary to room appliances, fluorescent lights, defective insulation, and patient movement.4
IndIcatIons wIth exampLes urinary incontinence The main advantage of fluoroscopic imaging during the urodynamic study is to obtain an anatomic view of the function or dysfunction. The technique is ideally suited to evaluation of incontinence. A useful anatomic/radiologic classification of female incontinence, devised by Blaivas and colleagues,24 is described in Table 22.1 and illustrated in Figure 22.6. We use this classification to determine the radiologic abnormality and add to it the information from the VLPP and the position of the urethra in relation to the cystocele to describe the functional problem. Each of the following urodynamic tracings in the figures is shown in full with annotations made during the study. The video recordings depicting parts of the studies were obtained from a video printer connected to the fluoroscopy. A type I abnormality is illustrated in Figure 22.7 where the patient has a VLPP of 62 cmH2O and minimal hypermobility. The patient in Figure 22.8 has a VLPP of >120 cmH2O on straining during upright filling. At the end of filling a cough caused a large leak without much hypermobility and appeared to be accompanied by a small bladder contraction. This indicates that she has stress incontinence as well as cough-induced overactivity. Figures 22.9–22.11 demonstrate type IIa abnormalities. The patient in Figure 22.9 has a high VLPP indi-
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table 22.1.
Radiologic type of stress incontinence
Type
Features
0
Vesical neck and proximal urethra closed at rest and situated at or above the lower end of the symphysis pubis. They descend during stress but incontinence is not seen.
I
Vesical neck closed at rest and is well above the inferior margin of the symphysis. During stress the vesical neck and proximal urethra open and descend <2 cm. Incontinence is seen.
IIa
Vesical neck closed at rest and is above the inferior margin of the symphysis. During stress the vesical neck and proximal urethra open and descend >2 cm. Incontinence is seen.
IIb
Vesical neck closed at rest and is at or below the inferior margin of the symphysis. During stress there may or may not be further descent but as the proximal urethra opens incontinence is seen.
III
Vesical neck and proximal urethra are open at rest. The proximal urethra no longer functions as a sphincter. There is obvious urinary leakage with minimal increases in intravesical pressure.
From ref. 23.
cating primarily a hypermobile urethra without any appreciable cystocele. In Figure 22.10, the patient has an involuntary detrusor contraction with incontinence in the upright position and a high VLPP. The patient shown in Figure 22.11 has a grade II cystocele that appears with straining. She probably has mainly a lateral defect.25 Type IIb abnormalities are shown in Figures 22.12– 22.14. The bladder neck in Figure 22.12 is seen well below the lower margin of the symphysis and is associated with a grade II cystocele. Since the bladder neck is above the base of the cystocele, but below the lower margin of the symphysis, the patient most likely has a combined central and lateral defect. In Figure 22.13, the large cystocele is not associated with demonstrable stress incontinence, despite coughing and straining pressures of >100 cmH2O. It appears primarily to be a central defect. Clinical examination must include reducing the cystocele and checking for stress incontinence. The patient in Figure 22.14 has a combined central and lateral defect. She has marked detrusor overactivity with leakage but stress incontinence is not demonstrated, most likely because of the compressive effect of the cystocele. Type III incontinence or pure ISD is demonstrated by the patient in Figure 22.15. Her bladder neck is open at rest, no appreciable descensus is seen with coughing or straining, and her VLPP is low at 59 cmH2O.
Figure 22.6. The various types of female stress urinary incontinence. (a) Type I: The bladder neck is closed at rest and is well above the inferior margin of the symphysis. During stress, the bladder neck and proximal urethra open and descend <2 cm. Incontinence is seen. (b) Type IIa: The bladder neck is closed at rest and is above the inferior margin of the symphysis. During stress the bladder neck and proximal urethra open and descend >2 cm. Incontinence is seen. (c) Type IIb: The bladder neck is closed at rest and is at or below the inferior margin of the symphysis. During stress there may or may not be further descent but as the proximal urethra opens, incontinence is seen. (d) Type III: The bladder neck and proximal urethra are open at rest. The proximal urethra no longer functions as a sphincter. There is obvious urinary leakage with minimal increases in intravesical pressure.
neurogenic bladder dysfunction Videourodynamics can be helpful in assessing bladder dysfunction patients with neurologic disorders. Since incontinence and upper tract dilation can be prevented and treated by achieving low-pressure bladder storage and emptying,19,26 the urodynamic study provides a framework for treatment. Anatomic abnormalities can also be correlated with pressure changes. Examples of neurogenic problems are shown in Figures 22.16–22.18. Since the flow rate is not measured in Figures 22.16 and 22.17, fewer channels are used during the study. The patient in Figure 22.16 has a small capacity, overactive but compliant bladder with grade I left vesicoureteral reflux. Her main problem was incontinence between catheterizations and she was treated with anticholinergics and upper tract monitoring. The patient 307
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Figure 22.7. Videourodynamic study of a 64-year-old G4P4 woman with type I stress incontinence. She has a bladder capacity of more than 300 cc. The bladder neck is slightly open at rest (a). With coughing there is a small amount of descent and her Valsalva leak point pressure is 62 cmH2O. She has no apparent cystocele and her voiding phase is normal. Abbreviations as in Figure 22.5.
Figure 22.8. Videourodynamic study of a 74-year-old G2P2 woman with type I stress incontinence. Her bladder neck is slightly open at rest (a). In the upright position (b) she leaks with straining and a Valsalva leak point pressure of 122 cmH2O. She also leaks with coughing (c) that is followed by a detrusor contraction (arrow). Her voiding is normal (d). Abbreviations as in Figure 22.5. in Figure 22.17 has a markedly trabeculated overactive bladder with filling pressures of >100 cmH2O. The study demonstrates detrusor external sphincter dyssynergia with an open bladder neck and tight sphincter. She also had bilateral hydronephrosis on upper tract
Figure 22.9. Videourodynamic study of a 47-year-old G1P1 woman with type IIa stress incontinence. Her bladder neck is open at rest (a). Leakage and hypermobility are seen with coughing (b). Abbreviations as in Figure 22.5.
Figure 22.10. Videourodynamic study of a 52-year-old G2P2 woman with a type IIa abnormality who complains of both stress and urgency incontinence. The bladder neck is slightly open at rest (a). She has an uninhibited contraction (arrow) on upright filling that results in incontinence (b). With straining she leaks with a Valsalva leak point pressure of >140 cmH2O (c). Abbreviations as in Figure 22.5.
imaging and required an augmentation cystoplasty for management. Since she was quadriplegic, a continent abdominal stoma was brought from the augmentation to the umbilicus to permit self-intermittent catheterization. The patient in Figure 22.18 developed increasing hydronephrosis and elevated creatinine after insertion of an artificial sphincter for urinary incontinence. She had previously undergone multiple bilateral ureteral
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Figure 22.11. Videourodynamic study of a 64-year-old G2P2 woman with type IIa stress incontinence. Her bladder neck is well supported on upright filling (a) and with straining (b) she leaks with a Valsalva leak point pressure of 144 cmH2O and a cystocele is demonstrated. She most likely has mainly a lateral defect. Abbreviations as in Figure 22.5.
Figure 22.12. Videourodynamic study of a 62-year-old G5P5 woman with type IIb stress incontinence. Her bladder neck (arrow) on filling (a) is below the lower margin of the inferior symphysis and a cystocele is seen. She most likely has a combined central and lateral defect. She has leakage with coughing (b) and a Valsalva leak point pressure of 62 cmH2O on straining. Abbreviations as in Figure 22.5.
reimplants for reflux. The study shows a bladder with poor compliance and gross bilateral reflux. The refluxing ureters probably dampen the bladder pressure, thus improving the appearance of the compliance curve. She was treated with an augmentation cystoplasty.
Figure 22.13. Videourodynamic study of a 75-year-old G1P1 woman with a large cystocele. Although she complains of stress incontinence it is not visible on this study. Her bladder neck (arrow) is at the lower margin of the symphysis. The cystocele appears primarily to be a central defect. Clinical evaluation must include reducing the cystocele and testing for stress incontinence. Abbreviations as in Figure 22.5.
Figure 22.14. Videourodynamic study of an 81-year-old G1P1 woman with a central and lateral defect. The bladder neck is below the symphysis (arrow). She has marked detrusor overactivity on supine and upright filling (arrows). Although she complains of stress, in addition to urge incontinence, it is not demonstrated on this study. Abbreviations as in Figure 22.5.
obstruction Although outflow obstruction is uncommon in females,22 it is occasionally seen. The patient in Figure 22.4 had an 309
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Figure 22.15. Videourodynamic study of a 69-year-old G3P3 woman with type III abnormality after two previous stress incontinence repairs. Her bladder neck is open at rest (arrow in a). There is almost no urethral movement on straining (b) and her Valsalva leak point pressure is 59 cmH2O. Abbreviations as in Figure 22.5.
Figure 22.16. Videourodynamic study of a 64-year-old woman 5 years after a T8–T9 spinal cord injury following a motor vehicle accident. She has left vesicoureteral reflux (arrow) seen during an involuntary detrusor contraction (arrows). Abbreviations as in Figure 22.5.
iatrogenic and functionally significant urethral obstruction that was treated with a visual internal urethrotomy and subsequent long-term self-dilation.
complex problems Videourodynamics allows for the identification and characterization of a pathologic process that can be associated with complex voiding dysfunction, including
Figure 22.17. Videourodynamic study of a 25-year-old woman with C7–C8 lesion 16 months after spinal cord injury following a motor vehicle accident. She needed an indwelling catheter for repeated attacks of autonomic dysreflexia and her upper tracts showed marked bilateral hydronephrosis. Her bladder is markedly trabeculated and during contractions of >75–100 cmH2O her external sphincter remains tight, consistent with detrusor sphincter dyssynergia. She was subsequently treated with an ileal augmentation cystoplasty and a continent abdominal stoma. Abbreviations as in Figure 22.5. reflux, diverticula, fistulae, and stones.4 The patient in Figure 22.19 had a fistula at the anastomosis between an ileal neobladder and the urethra after a cystectomy for bladder cancer. The study was done with a catheter obstructing the bladder neck to test the compliance. The neobladder itself was compliant and stable and was not contributing to the incontinence. No urethral leakage was seen with stress. All of the contrast emanated through the vagina. She was successfully treated with a transvaginal fistula repair with an interposition labial fat pad flap.
pItfaLLs of VIdeourodynamIcs Patient cooperation, comfort and compliance are necessary in order to obtain a meaningful and relevant study. Occasionally, apprehensive patients will have a vasovagal reflex and faint when the table is moved from the supine to the upright position and the study cannot be completed. In addition, stress incontinence may not be demonstrated in an anxious patient. Of 2259 studies reviewed in our laboratory for neurologically normal women whose chief complaint was stress incontinence, we were unable to demonstrate
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Figure 22.18. Videourodynamic study of a 25-yearold woman with sacral dysgenesis. She had an artificial sphincter inserted for urinary incontinence at age 14 and then developed bilateral vesicoureteral reflux unresponsive to multiple ureteral reimplantations. The study shows decreased bladder compliance on filling (arrows). She has gross bilateral reflux and a small capacity bladder. The reflux most likely dampens the poor compliance measurement. She subsequently underwent augmentation ileal cystoplasty and bilateral reimplants. Abbreviations as in Figure 22.5. stress incontinence on fluoroscopy in 630 (28%). It is also difficult for many patients to void in front of the camera with catheters in the bladder and rectum and observers watching them. In our series, only 1348 patients (59.7%) were able to void and some of these did so with abdominal straining. The others were unable to void during the procedure and the voiding data were obtained from the uroflow. To optimize visibility of the lower urinary tract on fluoroscopy, patient positioning must be correct. However, visibility may be poor or absent with very obese patients. The clinician must also maintain a dialogue with the patient to image crucial events as the patient must relay changes in sensation during filling and may be the first to sense incontinence. The radiation equipment must be well maintained and undergo regular maintenance and safety inspections. The failure to maintain equipment may lead to inaccurate results. Since fluoroscopy time is short, radiation exposure to the patient is inconsequential; however, the clinician should use radiation protection including aprons and thyroid shields. Other pitfalls relate to the urodynamic aspects and are similar to those previously outlined by O’Donnell.27 Standardized terminology to communicate results and concepts should always be used.9 The testing procedures
Figure 22.19. Videourodynamic study of a 60-year-old G2P2 woman who underwent an ileal neobladder to her urethra after cystectomy for muscle invasive carcinoma of the bladder. The study was done with a Foley catheter blocking the urethra to test compliance (a) which is normal. All of the leakage was demonstrated to exit the fistula at the anastomosis (arrow in a). She underwent a transvaginal fistula repair with a Martius labial fat pad flap. Abbreviations as in Figure 22.5. and equipment should be compatible with commonly accepted methodologies. The value and limitations of each measurement must be realized, i.e. the VLPP may not be useful in the presence of a large prolapsing cystocele. To confirm reliability within a particular laboratory, it is necessary to have a high test–retest correlation of studies. The validity of a test refers to its ability to measure what it is supposed to measure. The clinician must always be aware of the how it compares to a ‘gold standard’ test, which in urodynamics may be difficult to establish. The urodynamic studies should correlate with other clinical data. The voiding history, physical examination, endoscopic examination, and videourodynamic evaluation should serve to validate one another and strengthen the clinical assessment.
future deVeLopments Videourodynamic techniques have evolved over the years with improvements in technology and refinements in the concepts of lower urinary tract structure, function, and treatment. There are exciting developments in other newer imaging technologies. Ultrasound can be used during urodynamic studies but the vaginal probe may alter bladder neck position and perineal probes are undergoing investigation.28 Although magnetic reso311
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nance imaging (MRI) has provided significant advances in knowledge about the pelvic floor,29 it is carried out in the supine position and interventional MRI has not yet been adapted to the technique. Videourodynamic testing, when indicated, is still as applicable today as when it was first developed more than 50 years ago.
references 1. Blaivas JG. Techniques of evaluation. In: Yalla SV, McGuire EJ, Elbadawi A, Blaivas JG (eds) Neurourology and Urodynamics: Principles and Practice. New York; Macmillan, 1988. 2. Miller E. The beginnings. Urol Clin North Am 1979;6:7–9. 3. Enhörning G, Miller ER, Hinman F Jr. Urethral closure studied cine-roentgenography and simultaneous bladder–urethra pressure recording. Surg Gynecol Obstet 1964;118:507–16. 4. Webster GD, Guralnick ML. The neurourologic evaluation. In: Walsh PC, Retik AB, Vaughan ED Jr, Wein AJ (eds) Campbell’s Urology, 8th ed. Philadelphia: WB Saunders, 2002; 900–30. 5. Blaivas JG. Deciding on the right urodynamic equipment. In: Blaivas JG (ed) Atlas of Urodynamics. Baltimore: Williams and Wilkins, 1996; 19–28. 6. Bates CP, Whiteside G, Turner-Warwick R. Synchronous cine/pressure/flow cysto-urethrography with special reference to stress and urge incontinence. Br J Urol 1970;42:714–23. 7. McGuire EJ, Cespedes RD, Cross CA, O’Connell HE. Videourodynamic studies. Urol Clin North Am 1996;23:309–21. 8. Massey A, Abrams P. Urodynamics of the female lower urinary tract studies. Urol Clin North Am 1985;12:231–46. 9. Abrams P, Cardozo L, Fall M et al. The standardization of terminology of lower urinary tract function: Report from the Standardization Sub-committee of the International Continence Society. Neurourol Urodyn 2002;21:167–78. 10. Abrams P, Blaivas JG, Stanton SL, Andersen JT. Standardisation of terminology of lower urinary tract function. Neurourol Urodyn 1988;7:403–27. 11. Webb RJ, Styles RA, Griffiths CJ, Ramsden PD, Neal DE. Ambulatory monitoring of patients with low compliance as a result of neurogenic bladder dysfunction. Br J Urol 1989;64:150–4. 12. Schafer W, Abrams P, Liao L et al. Good urodynamic practice: uroflowmetry, filling, cystometry, pressure–flow studies. Neurourol Urodyn 2002;21:261–74.
13. Bates P, Bradley WE, Glen E et al. First report on the standardization of terminology of lower urinary tract function. Br J Urol 1976;48:39–42. 14. Awad SA, Flood HD, Acker KL. The significance of prior anti-incontinence surgery in women who present with urinary incontinence. J Urol 1988;140:514–7. 15. McGuire EJ. Bladder instability in stress incontinence. Neurourol Urodyn 1988;7:563–7. 16. McGuire EJ, Fitzpatrick CC, Wan J et al. Clinical assessment of urethral sphincter function. J Urol 1993;150:1452–4. 17. Heritz DM, Blaivas JG. Reliability and specificity of the leak point pressure. J Urol 1995;153:492A. 18. Blaivas JG. Cystometry. In: Blaivas JG (ed) Atlas of Urodynamics. Baltimore: Williams and Wilkins, 1996; 31–47. 19. McGuire EJ, Woodside JR, Borden TA, Weiss RM. Prognostic value of urodynamic studies in myelodysplastic children. J Urol 1981;126:205–9. 20. Woodside JR, McGuire EJ. Technique for detection of detrusor hypertonia in the presence of urethral sphincteric incompetence. J Urol 1982;127:740–3. 21. Farrar D, Turner-Warwick R. Outflow obstruction in female studies. Urol Clin North Am 1979;6:217–25. 22. Wein AJ, Barrett DM. Other voiding dysfunctions and related topics. In: Wein AJ, Barrett DM (eds) Voiding Function and Dysfunction. Chicago: Year Book, 1988; 274–301. 23. Fowler C. Electromyography. In: Blaivas JG (ed) Atlas of Urodynamics. Baltimore: Williams and Wilkins, 1996; 60–76. 24. Blaivas JG, Olsson CA. Stress incontinence: classification and surgical approach. J Urol 1988;139:727–31. 25. Herschorn S, Carr LK. Vaginal reconstructive surgery for sphincteric incontinence and prolapse. In: Walsh PC, Retik AB, Vaughan ED Jr, Wein AJ (eds) Campbell’s Urology, 8th ed. Philadelphia: WB Saunders, 2002; 1092–139. 26. Barkin M, Dolfin D, Herschorn S. The urologic care of the spinal cord injured patient. J Urol 1983;129:335–9. 27. O’Donnell PD. Pitfalls of urodynamic testing. Urol Clin North Am 1991;18:257–68. 28. Virtanen HS, Kiilhoma PJA. Ultrasound urodynamics. In: Blaivas JG (ed) Atlas of Urodynamics. Baltimore: Williams and Wilkins, 1996; 117–25. 29. Yang A, Mostwin JL, Rosenshein N, Zerhouni EA. Pelvic floor descent in women: dynamic evaluation with fast MR imaging and cinematic display. Radiology 1991;179:25–33.
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INTRODUCTION Laboratory urodynamics is currently the ‘gold standard’ in the objective assessment of urinary symptoms. However, it is necessarily unphysiologic because it measures pressures during retrograde bladder filling using a fast filling rate and during voiding. In the past, attempts were made to monitor lower urinary tract function on a long-term basis and in an ambulant patient, with the aim of overcoming some of the problems encountered in standard urodynamics. The first problem is physiologic: when monitoring detrusor function using standard urodynamics, fast retrograde bladder filling is employed, which is necessarily provocative. The second is environmental: incontinence is a benign condition, and reliance is placed on the person’s symptoms as evidence of disease; many of these symptoms are related to acts of everyday life, all of which are removed in a laboratory atmosphere. Thirdly, throughout the period of time during which the standard urodynamic tests are being conducted, the individual is the focus of attention and is asked to respond to certain commands; this may lead to cortical suppression of detrusor activity. The first description of a bladder pressure measurement in an ambulant patient was reported by Mackay1 using radiotelemetry, followed by many other methods. To allow an individual to be mobile, the system must employ telemetry, long cables or portable recording units. In the first systems, telemetry was used.2–5 A pressure-sensitive radio pill was inserted into the bladder, allowing intravesical pressure to be monitored without the presence of a foreign body in the urethra. However, the cost, limited range of transmission, and occasional difficulty in retrieval prevented its widespread use. In standard urodynamics the lines used are fluid filled. A study of natural filling in spinal injury patients6 demonstrated increased phasic activity. However, in general, fluid-filled lines are not recommended as they are prone to movement artifact and the pressures measured are dependent on the relative position of the pressure transducer to the tip of the fluid-filled line; thus the baseline measurement alters as the woman changes position. Air is not subject to the same movement artifact, and air-filled tubes have been used in ambulatory urodynamics.2 In this system, one end of the tube is filled by a meniscus of urine and the other is covered by a compliant balloon to prevent fluid traveling down the tube and thus producing artifact. In this set-up, the position of the catheter relative to the transducer is unimportant; unfortunately, however, changes in the temperature can alter pressure measurement.
As time has progressed, tape-recording systems have been used. Initially, these systems had a limited capacity which enabled pressures to be recorded only above a certain pre-set threshold.7 If the patient became symptomatic during the test, but the threshold had not been met, then the pressure was unrecorded, and therefore no substantive diagnosis was provided. Subsequently, Griffiths et al.8 developed an ambulatory system using micro-tip pressure transducers and a digital solid-state recorder. In this system the information is recorded digitally, transferred, and then reviewed at the end of the test. The trace can then be compressed or expanded without loss of information.
EQUIPMENT There are three main components to an ambulatory system (Figs 23.1–23.3): 1) the transducers; 2) the recording unit; and 3) the analyzing system. The transducers are solid state and are mounted on a 5 Fr to 7 Fr bladder and rectal catheter, to measure the pressure impinging on it. Most transducers have the
Figure 23.1. Bladder pressure catheter.
Figure 23.2. Rectal pressure catheter. 314
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Figure 23.3. Ambulatory urodynamic equipment.
pressure-sensitive membrane a few millimeters beyond the tip of the catheter and therefore pressure changes are recorded when the tip touches the side of the bladder. This can be overcome by inserting two catheters, and the intravesical pressure change is deemed significant only if it is recorded on both transducers. The rectal catheter is covered with silicone in order to protect it from deformation.9 There can be problems with drift of the transducers, but this is usually less than 3 cmH2O within the 4-hour test.8 The recording system must be portable and, ideally, battery powered to allow freedom of movement. Sampling of the pressures should be at 4 Hz and the memory should be digital, allowing the trace to be compressed and expanded. A trace should not be interpreted in isolation: a recording unit should have some means of marking events during the test – the simpler the better, as patients often find multiple buttons confusing and pressing the wrong button can confuse the interpretation. More sophisticated systems, however, are available,10 providing the subject with separate switches on a single remote unit which sends a coded signal to the recorder depending on the button pressed. As well as marking the event, it is helpful if there is some mechanism of timing, either by having an in-built timer in the unit or by asking the patient to record the time. The recorder should have an option to be connected to an electronic ‘diaper’ (nappy), allowing accurate information about urine loss. In addition, there should be a connector to a gravimetric flowmeter that will calculate pressure–flow curves and check when detrusor overactivity has occurred.
The pressure traces are downloaded onto a computer, which can then analyze detrusor and urethral function. There is a variety of different formats. The software available today enables the trace to be expanded or compressed, the scales to be changed, a pressure–flow study to be analyzed, and a computerized archive of the tests performed to be maintained. It is important to choose the appropriate scale for the pressure and time measurements; the patient’s diary and trace should be reviewed with the patient. This allows further information to be gleaned, which a simple system of pushing buttons might have missed. For some new ambulatory urodynamic equipment the Wireless Bluetooth techniques allow data to be viewed while recording. The urine loss itself needs to be evaluated. Using a weighed perineal pad for the length of the test gives some idea of the severity of the incontinence, but gives little information about when the loss occurred. If the timing of the loss can be calculated, then the manometric changes leading to incontinence can be interpreted and may be helpful in determining the cause of urinary leakage. There are three ways of achieving this. The first is the Urilos (Exeter) (Fig. 23.4) electronic diaper, which has already been alluded to. It has elongated, interleaved electrodes embedded in absorbent material. A 50 mV (low voltage) alternating current is passed between the two electrodes; as the urine loss increases, so does this current. Obviously this depends on the electrodes being within the urine, which is definitely not guaranteed, and so the pad has to be preloaded with a known volume of electrolyte solution. This method is suitable only for volumes between 1 and 100 ml and is reproducible within 20%. The second method is to measure perineal temperature, which is usually 30–40°C. Urine has a higher temperature than that of the body surface, 37°C. When there is leakage of urine there is a transient rise in temperature
Figure 23.4. Urilos pad connected to the recording unit. 315
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which then falls rapidly, allowing effective detection of distinct episodes of urine loss. The rate of the temperature increase may correlate well with the quantity of leaked urine. A single temperature detector is ineffective, as the position of the detector in relation to the leaked urine changes; hence, a parallel array of diodes has been used with a separate reference diode. Problems of interpretation can occur if the patient has her legs together when seated, as the perineal temperature may then rise. The third method relies on a catheter placed within the urethra. Two electrodes are mounted on the catheter and an electrical current is passed between them. If urine is passed, either voluntarily or involuntarily, there is increased conduction and a larger current passes across the electrodes. It is vital that the electrodes are placed correctly: for instance, with the electrode in the proximal urethra, a change in the electrical current would indicate the presence of urine; however, this may not have originated from urinary leakage, as this can occur with urethral instability. Conversely, if the electrodes are not in the urethra, then no leakage would be detected. Distal urethral electrical conductance is not used clinically in ambulatory urodynamics, but is mainly a research tool.
STANDARDIZATION OF AMBULATORY URODYNAMIC MONITORING
Definitions An ambulatory urodynamic investigation is defined as any functional test of the lower urinary tract predominantly utilizing natural filling of the urinary tract and reproducing the subject’s normal activity. The terms intro-duced by this definition are further explained below.
• Ambulatory: This refers to the nature of monitoring
•
•
rather than the mobility of the subject. Monitoring will usually take place outside a urodynamic laboratory. Natural: This refers to the natural production of urine rather than an artificial medium. Stimulation by forced drinking or pharmacologic manipulation must be stated in the methodology. (Remark: The bladder may be pre-filled with an artificial medium but this is not comparable with natural bladder filling. This method of investigation needs further evaluation.) Normal activity: This refers to the activities of the subject during which symptoms are likely to occur. These may include maneuvers designed specifically to identify the presence of involuntary detrusor or urethral behavior or to provoke incontinence.
Methodology
11
A standardization report on ambulatory urodynamic monitoring (AUM) was published by a specific International Continence Society (ICS) Committee in 2000. In this document the authors cover different aspects such as indications, technical suggestions, and both clinical and scientific reports for ambulatory urodynamics. In this chapter we will include the most relevant parts of the report for clinical purposes:
Indications for AUM • Lower urinary tract symptoms which conventional • • •
urodynamic investigation fails to reproduce or explain; Situations in which conventional urodynamics may be unsuitable; Neurogenic lower urinary tract dysfunction; Evaluation of therapies for lower urinary tract dysfunction.
Terminology The terminology applied to observations during AUM should, wherever possible, be consistent with terminology used during conventional urodynamic investigation.12
Signals The following signals have been recorded by AUM:
• Pressure: intravesical, abdominal, urethral, • • • • • •
intrapelvic (renal); Flow rate; Micturition volume; Urinary leakage; Leakage volume; Urethral electrical conductance; Perineal integrated surface electromyography.
Additional information that should be recorded during any AUM investigation as event markers include the following phenomena:
• • • • • • • •
initiation of voluntary voids; cessation of voluntary voids; episodes of urgency; episodes of discomfort or pain; provocative maneuvers; time and volume of fluid intake; time and volume of urinary leakage; time of pad change.
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Signal quality AUM is more versatile than equivalent conventional urodynamic investigation, but for the same reasons AUM is associated with a greater risk of losing signal quality. Therefore, although all signals should be recorded as outlined in the ICS recommendations on ‘Good Urodynamic Practices’,13 there are a number of cautions which apply specifically to AUM, as described below. Intravesical and abdominal pressure measurement Although it is possible to measure intravesical and abdominal pressures using fluid-filled lines (water or air), the use of catheter-mounted micro-tip transducers allows greater mobility during AUM. In the absence of continuous supervision, stringent checks on signal quality should be incorporated in the measurement protocol. At the start of monitoring, these should include testing of recorded pressure on-line by coughing and abdominal straining in the supine, sitting, and erect positions. The investigator must be convinced that signal quality is adequate before proceeding with the ambulatory phase of the investigation. Prior to termination of the investigation and at regular intervals during monitoring similar checks of signal quality such as cough tests should be carried out. Such tests will serve as a useful retrospective quality check during the interpretation of traces. The following considerations must be taken into account when using micro-tip transducers:
• Transducers should be calibrated prior to every investigation.
• The ‘zero point’ is atmospheric pressure (there is
•
•
•
no fixed reference point). All transducers must be ‘zeroed’ at atmospheric pressure prior to insertion of the catheters. Water-filled pressure catheters have a fixed reference point at the upper edge of symphysis pubis whereas catheter-mounted micro-tip pressure transducers have no fixed reference point. Micro-tip transducers will record direct contact with solid material (the wall of a viscus or fecal material) as a change in pressure. The use of multiple transducers may eliminate this source of artifact. Under some circumstances, the pressure measured at the transducer surface will result in a discrepancy equal to the difference in vertical height between the two transducers. This can result in the estimated detrusor pressure being less than zero (i.e. negative) with, for instance, the patient in the supine position.
Urethral pressure and conductance The recording of urethral pressure is a qualitative measurement with emphasis on changes in pressure rather than absolute values. The use of urethral electrical conductance to identify leakage in association with pressure monitoring facilitates interpretation of urethral pressure traces. Precise positioning and secure fixation are essential to maintain signal quality. The orientation of the transducer should be documented. (Remark: The use of multiple pressure transducers facilitates identification of movement artifact but increases catheter stiffness and thereby deformation of the urethra during recording.) Catheter fixation As indicated earlier, secure catheter fixation is essential to maintain signal quality. Methods that have been used include adhesive tape, suture fixation, and purposedesigned silicone-fixation devices.
Recording of urinary leakage The method of urine leakage determination should be recorded. It should be stated whether the urinary leakage is recorded as a signal with the pressure measurements, or is dependent on the subject pressing an event marker button or completing a urinary diary.
Instructions to the patient Detailed instructions as to recording of symptoms, identification of catheter displacement, and hardware failure should be given to the patient. It is the recommendation of this group that such verbal instructions should be reinforced by written instructions and, in addition to the hardware built into the system, the patient is provided with a simple diary to record events. This facilitates the common primary aim of all urodynamics, i.e. to correlate the test outcome with symptoms.
Analysis Quality assessment The first step in the analysis of an AUM trace is the assessment of the quality of data recorded. The specific points that should be addressed with regard to pressure measurement are:
• Is the trace ‘active’, i.e. fine second to second variation in pressure rather than a fine line?
• Is the baseline static or highly variable? • Are the cough tests or other activities causing abdominal pressure changes that can be used for signal plausibility check, regularly present? 317
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• Is the subtraction adequate, e.g. minimal change in subtracted detrusor pressure with coughing? If the technical quality of the trace is less than perfect, then, although the investigation may yield valuable clinical information, in the context of accurate measurement the pressure recordings must be viewed only as qualitative; further quantitative analysis may well be flawed.
Phase identification Depending on the purpose of the investigation, markers must be placed to identify voluntary voids and allow differentiation of such events from involuntary events, which may be associated with changes in recorded pressure. The protocol of the investigation should state specifically the point at which the markers identifying commencement and cessation of a voluntary void are placed. Analysis of the voiding phase follows the same principles and terminology used during conventional pressure–flow investigation.
Events
• Results of provocative maneuvers employed during the test;
• Reasons for termination of recording if prematurely terminated.
COMMENTS Although the ICS standardization report is accurate and precise, some additional tips are recommended to ensure quality control during ambulatory urodynamics, as follows.
Patient preparation • The reasons for the test and all the procedures should be explained in full; patient compliance is essential.
• Urinary tract infection should be excluded before the test.
• All patients should be informed about the duration of the procedure prior to starting it.
• They should be asked to wear loose comfortable separate clothing (e.g. tracksuit).
The use of a patient diary considerably improves the detailed analysis of events occurring during AUM and is strongly recommended. Typical events occurring during the filling phase are detrusor contractions, urethral relaxations, and episodes of urgency and incontinence. (Remark: At least for research purposes, it is strongly advised that variables for quantitative interpretation are defined and validated. Validation means to establish data on healthy volunteers and specific patient groups, test–retest reproducibility, interrater validity, and sensitivity to treatment modalities.)
• Catheters are inserted using an aseptic technique.
CLINICAL REPORT
Procedure
The report should be tailored to the urodynamic investigations and can include the following indication(s) and/or urodynamic question(s) (obligatory):
• The patient is instructed in the use of the diary
•
• Duration of recording; • Fill rate, timing, method and volume of any • • • • • • •
retrograde filling prior to commencing AUM; Dose and timing of diuretics if administered; Volume of fluid drunk during the test; Number of voids; Total and range of voided volumes and postmicturition urinary residual; Episodes of urgency, urinary incontinence, and pain; Detrusor activity during the filling phase (frequency, time, duration, amplitude, area, form); Pressure/flow analysis;
• •
Both bladder transducers are placed in the bladder in order to exclude artifacts during analysis (Fig. 23.5). The rectal catheter is inserted into the rectum inside a non-lubricated condom to prevent contamination of the silicone coating. Once inserted, the catheters are taped to the inner thigh close to the labia (as close to the urethra as possible) using several pieces of 5 cm micropore tape. The lines are then brought forward, over the abdomen, and arranged to be accessible through the clothing.
(Fig. 23.6). This will provide information of activity during the test. It is essential that the woman understands the diary as this is very important in the final analysis. The diary should be checked frequently to ensure compliance. The patient should use the timer on the ambulatory box, not her own watch. The patient is instructed on how to use the flow-rate machine and the event button, if unable to return to the flowmeter. If this is required, the button is pressed once on entry to a toilet, and once again when void starts. The event button should not be used at any other time. Instructions for the event button should be included on the diary sheet, as
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Figure 23.5. Ambulatory urodynamic trace showing abnormal detrusor activity with pressure rise on the detrusor line and on both ‘intravesical’ transducers in the presence of urgency.
• •
are the names and telephone numbers of the test coordinators. Contact with the test coordinator should be easy for the patient. The patient needs to be checked on-line at least once an hour (or more if deemed necessary); for example,
•
•
• Figure 23.6. Ambulatory urodynamic diary.
if the lines have come out, if there is an ambulatory box failure (such as low batteries), if the patient is uncomfortable, or if the test becomes unacceptable. At the end of the test period, the patient is asked to carry out a series of activities, with a full bladder (if possible). The use of provocative maneuvers such as 10 coughs, 10 star jumps, hand washing or heel bouncing, can improve diagnostic yield.14,15 The patient is then asked to void. Once the test is complete, the traces are then reviewed by the test coordinator, interpreting the diary with the patient present. If possible, another observer should also be present. In our opinion, it is mandatory to interpret the trace and the diary with the patient present at the end of the study. The use of a diary emphasizes the importance of linking urinary symptoms with the investigation; this is as valid for laboratory urodynamics as it is for ambulatory urodynamics. Urinary symptoms are important, as abnormal detrusor activity cannot be diagnosed unless it is associated with symptoms such as urgency or urge incontinence. In fact, we found16 that both the symptom diary and the placement of two transducers in the bladder can decrease, by almost two-thirds, the diagnosis of pathologic detrusor activity on ambulatory urodynamics by minimizing possible artifacts. After the test the patient is warned that she may have a stinging sensation in her urethra and bladder for up to 24 hours. For this reason, fluid intake should be maintained and, if symptoms of cystitis are present or 319
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the urine becomes offensive, she should seek advice from her doctor. Routine antibiotic prophylaxis is not indicated. In fact, in 91 women who completed a 4hour test, Anders et al.17 reported an infection rate of 1.1% (1 patient) whereas 17 women reported mild to moderate de novo dysuria without a positive urinary culture. Women who are known to have residuals, reflux, recurrent urinary tract infection or diabetes should be given antibiotic cover.
CLINICAL STUDIES Asymptomatic volunteers The clinical use of ambulatory urodynamics is limited by the high prevalence (38–69%) of abnormal detrusor contractions detected with this method in asymptomatic volunteers.5,18–20 These results call ambulatory urodynamics and its validity into question, suggesting that it is oversensitive in the diagnosis of detrusor overactivity (instability). Van Waalwijik van Doorn et al.19 proposed an equation, the detrusor activity index, to distinguish ‘abnormal’ from ‘physiologic’ detrusor contractions. The mean detrusor activity index is calculated as the sum of the number of uninhibited contractions per hour multiplied by 10, the mean amplitude and the mean duration of these contractions. In a prospective study21 of 26 asymptomatic women, we showed that the diagnosis of ‘detrusor overactivity (instability)’ is highly dependent on trace interpretation and the technique used to conduct the test. In our population of asymptomatic volunteers, the prevalence of abnormal detrusor contractions varied from 76.9 to 11.5%, according to the definition used of an abnormal event, the use of the diary with the woman present during interpretation, and the placement of two transducers in the bladder. We defined abnormal detrusor contraction as the point at which a simultaneous detrusor pressure rise on both bladder lines occurred, but only if associated with symptoms (urgency or leakage), in line with the ICS definition of detrusor instability. According to our definition of abnormal detrusor contraction, ambulatory urodynamics findings are normal in almost 90% of asymptomatic women, which is similar to the rate of normal findings in laboratory urodynamic studies. This definition is also applied during our laboratory urodynamic tests, indicating that ambulatory urodynamics does not need new diagnostic standards or methods. Laboratory urodynamics involves the careful observation of urinary symptoms correlated with the cystometric trace. Ambulatory urodynamics does not differ in this respect, and the process becomes even
more important in the correct diagnosis of abnormal detrusor contraction.
Variables recorded on ambulatory urodynamics Voided volume Many authors have reported that the volume voided during ambulatory urodynamic studies is less than during laboratory urodynamics.18,22–24 There may be various reasons for this: • The irritation of the catheter in an ambulant patient may exacerbate the desire to void. • During conventional urodynamics we usually try to reach the maximum functional bladder capacity; presumably, this does not happen in ambulatory urodynamics, with a patient voiding at comfortable bladder fullness. However, Groen et al.25 compared the voidings from 47 patients at their modal volume (the volume most often voided by the patient as derived from frequency/volume charts) with voidings at maximum cystometric capacity during a routine videourodynamic examination. The authors concluded that the differences between ambulatory and conventional urodynamics could not be explained from possible differences in the voided volume. In fact, they found that although the maximum flow rate depended significantly on the voided volume, the associated detrusor pressure, urethral resistance, and bladder contraction did not.
Detrusor pressure It is not possible to detect low bladder compliance using ambulatory urodynamics.26 Both abnormal detrusor contractions at the maximum detrusor pressure during the voiding phase are greater in ambulatory urodynamic than in conventional urodynamic studies. Schmidt et al.27 showed that the detrusor pressure at maximum flow is dependent on the fluid intake during the test, being higher in a fluid-loaded group.
Flow rate The flow rate is higher in ambulatory urodynamic than in laboratory urodynamic studies.28
CLINICAL APPLICATIONS Inconclusive urodynamics A proportion of women complaining of urinary symptoms can have an inconclusive laboratory urodynamic evaluation. Vereecken and Van Nuland24 showed abnor-
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malities on ambulatory urodynamics in 20 of 28 subjects with urinary symptoms but with an inconclusive laboratory urodynamics result.
Poor correlation between symptoms and conventional urodynamics One hundred patients29 complaining of urinary symptoms underwent ambulatory urodynamics after having a laboratory urodynamics result that did not correlate with their symptoms or after unsuccessful incontinence surgery. The ambulatory urodynamic studies diagnosed detrusor overactivity twice as often as laboratory urodynamics. The test was described as normal in 32 patients undergoing laboratory urodynamics, but in only 5 undergoing ambulatory urodynamics. The latter test diagnosed only 8 patients as having urethral sphincter incompetence, compared with 13 on laboratory urodynamics. In another study,14 52 patients underwent a laboratory urodynamic study, with poor symptom correlation. All of these patients also underwent ambulatory urodynamics, which showed detrusor instability in 31 patients with a conventional urodynamic diagnosis of a stable bladder. Of these 31 patients, 11 had detrusor overactivity only after provocative maneuvers, emphasizing the need to carry out this part of the test. This study also showed that incontinence was detected more frequently on ambulatory urodynamics using a Urilos diaper. Anders et al.30 compared the diagnosis obtained via ambulatory urodynamics with that obtained by conventional urodynamics in 475 symptomatic women. Ambulatory urodynamics proved to be more sensitive than laboratory urodynamics in the diagnosis of detrusor overactivity, but less sensitive to urodynamic stress incontinence. Radley et al.31 compared ambulatory urodynamics and conventional videocystometry findings in 106 women with symptoms of bladder overactivity. Detrusor overactivity was detected in 32 and 70 cases on videourodynamics and ambulatory monitoring, respectively (p<0.001). Stress incontinence was diagnosed in 42 women on videocystometry and in 34 on ambulatory urodynamics (p=0.629). Robinson et al.,32 in a blinded prospective study, assessed whether the ultrasound measurement of bladder wall thickness could replace ambulatory urodynamics in a group of 128 women with a conventional urodynamic diagnosis which did not explain their urinary symptoms. The authors concluded that in women with urodynamic stress incontinence ambulatory urodynamics remains the investigation of choice.
Swithinbank et al.33 analyzed ambulatory urodynamics results in 111 women and 11 men with a conventional urodynamic diagnosis which failed to explain their symptoms. They found that ambulatory urodynamics influenced the management of all but 8.7% patients. It still has to be demonstrated that changes in patient management after the procedure led to an improvement in outcome, since Gorton and Stanton34 raised doubts after analyzing 71 ambulatory urodynamic notes of women with inconclusive conventional urodynamics.
Low compliance Low bladder compliance does not have a standardized definition and it is characterized by a steep detrusor pressure rise during the filling phase on laboratory urodynamics. The significance of this is debated: some feel that this is a passive phenomenon related to the reduced elasticity of the bladder wall, others that increase in pressure is associated with a tonic detrusor contraction. In the former, the pressure rise should not decrease at the end of filling; in the latter, the detrusor pressure should decay exponentially as the contracting detrusor relaxes. In a series of patients with neuropathic bladders,26 who developed an increase in detrusor pressure of more than 25 cmH2O at a filling rate of 100 ml/min, during ambulatory urodynamics there was a much smaller increase in detrusor pressure on orthograde filling than when these patients underwent cystometry using faster filling rates; however, the frequencies of phasic detrusor instability correlated well with the magnitude of the pressure increase during conventional cystometry. It was also found that the greater number of phasic detrusor contractions during ambulatory monitoring correlated well with the presence of a dilated upper renal tract. However, the diagnosis of low compliance on filling during laboratory urodynamics did not correlate with upper tract dilation.
Preoperative evaluation Incontinence surgery is indicated in cases of urodynamic stress incontinence. Detrusor overactivity should be excluded prior to surgery, as it is an important cause of operative failure. However, detrusor overactivity can appear after an incontinence operation (such as Burch colposuspension or tension-free vaginal tape (TVT)like procedures) and is referred to as de novo. It is still debated whether this could be due to an excessive dissection during the operation, or that detrusor overactivity was not diagnosed prior to surgery. Ambulatory urodynamics has been used to predict the appearance of 321
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de novo detrusor overactivity after incontinence surgery in two studies,35,36 with conflicting results.
Pressure–flow study Ambulatory urodynamics can be useful to assess the voiding phase in patients who are unable to void during conventional urodynamic studies because of embarrassment or in those who experience suprapubic pain after voiding. The latter can be associated with the post-void uninhibited detrusor contraction, which should be treated as detrusor overactivity; however, these patients may also require cystoscopy and possibly bladder biopsy.
Increased bladder sensation A conventional urodynamic diagnosis of increased bladder sensation may require cystoscopy and biopsies. Where histology is inconclusive it may be appropriate to perform ambulatory urodynamics.
Figure 23.7. The Gaeltec NanoLogger ambulatory urodynamic system.
Pharmacologic treatment monitoring Ambulatory urodynamics can be used in the assessment of pharmacologic treatment for overactive bladder. The optimal duration of monitoring in this context appears to be 6 hours.37 Compared to conventional urodynamics, ambulatory monitoring allows the effects of drugs for the treatment of detrusor overactivity to be assessed and appears to be more sensitive, thus allowing smaller groups of patients to be studied.
CONCLUSIONS
lead for on-line assessment at any stage of the investigation. The patient simply presses a convenient event marking button in communication with the recorder’s built-in clock to keep a reliable and accurate diary. Fast data downloading to the PC allows rapid record processing.
MMS The Luna (Fig. 23.8) is an easy to use ambulatory urodynamic recorder. Using a Bluetooth technique the Luna offers an on-line view of recordings. The Luna weighs
Ambulatory urodynamics is a useful tool in the assessment of lower urinary tract disorders, particularly when conventional urodynamics fail to explain the urinary symptoms. Interesting developments of some research applications of ambulatory urodynamics, such as monitoring pharmacologic treatment efficacy, need to be confirmed.
AMBULATORY SYSTEMS Gaeltec The Gaeltec NanoLogger™ (Fig. 23.7) has between one and seven input channels and an event marker. There can be up to eight axes on the screen to display the input channels and signals derived from them. Optical isolation allows easy connection to the PC with a serial
Figure 23.8. The MMS Luna ambulatory urodynamic system.
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less than 200 g. It has three pressure channels (bladder, urethra and abdominal), flow, EMG, and automated leak point pressures through conductivity. More than 24 hours of investigation data can be downloaded. A complete range of micro-tip catheters is available for use with the Luna, even small sizes such as 3 or 4 Fr for children.
Neomedics Acquilog (Fig. 23.9) is a multichannel ambulatory urodynamic system that can record for up to 12 or 24 hours. It has two pressures with a third (pdet) also displayed when in analysis mode with an optional urine loss detector channel. It employs straightforward patient event commenting and it downloads data into the Acquidata Uromac urodynamics system with a simple, prompted, step-by-step set-up and download procedure. A range of active microtransducer catheters is available, including miniscule 3 Fr single sensor and 5 Fr dual sensor devices.
Figure 23.10. The Menfis Blu Runner ambulatory urodynamic system.
Menfis
1. Mackay RS. Radiotelemetering from within the human body. Institute of Radio Engineers Transactions on Medical Electronics (ME6) 1959;11:100–5.
Blu Runner (Fig. 23.10) is an ambulatory recorder with up to eight channels and a plug-and-play system. It can record pressures, pHmetric, EMG, flow, volume, and conductance signals. It has a large graphic LCD display with a touch-screen type. It is also possible to have a real-time/on-line display of up to four measurement curves.
REFERENCES
2. Warrell DW, Watson BW, Shelley T. Intravesical pressure measurements in women during movement using a radiopill and an air-probe. J Obstet Gynaecol Br Commonw 1963;70:959–67. 3. Miyagawa I, Nakamura I, Ueda M et al. Telemetric cystometry. Urol Int 1993;41:263–5. 4. Vereecken RL, Puers B, Das J. Continuous telemetric monitoring of bladder function. Urol Res 1983;11:15–18. 5. Thuroff JW, Jonas V, Frohneberg D et al. Telemetric urodynamic investigation in normal males. Urol Int 1980;35:427–34. 6. Tsuji I, Kuroda K, Nakajima F. Excretory cystometry in paraplegic patients. J Urol 1960;83:839–44. 7. Bhatia NN, Bradley WE, Haldeman S, Johnson BK. Continuous monitoring of bladder and urethral pressure: new technique. Urology 1981;18:207–10. 8. Griffiths CJ, Assi MS, Styles RA et al. Ambulatory monitoring of bladder and detrusor pressure during natural filling. J Urol 1989;142:780–4. 9. German K, MacLachlan D, Johnson S et al. Improvements in the design of equipment used for ambulatory urodynamics. Br J Urol 1994;74:377–8. 10. Chu AC. Improved remote event marker for use in ambulatory monitoring. Med Biol Eng Comput 1998;36(2):238– 40.
Figure 23.9. The Neomedics Acquilog ambulatory urodynamic system.
11. Van Waalwijk van Doorn E, Anders K, Khullar V et al. Standardisation of ambulatory urodynamic monitoring: Report of the Standardisation Sub-Committee of the
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International Continence Society for Ambulatory Urodynamic Studies. Neurourol Urodyn 2000;19(2):113–25. 12. Abrams P, Cardozo L, Fall M et al. The standardisation of terminology of lower urinary tract function: report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 2002;21:167–78. 13. Schaefer W, Abrams P, Liao L et al. Good urodynamic practices: uroflowmetry, filling cystometry, and pressure– flow studies. Neurourol Urodyn 2002;21:261–74. 14. Webb RJ, Ramsden PD, Neal DE. Ambulatory monitoring and electronic measurement of urinary leakage in the diagnosis of detrusor instability and incontinence. Br J Urol 1991;68:148–52. 15. Athanasiou S, Anders K, Salvatore S et al. Short term provocative ambulatory urodynamics. Neurourol Urodyn 1996;4:276–8.
25. Groen J, van Mastrigt R, Bosch R. Factors causing differences in voiding parameters between conventional and ambulatory urodynamics. Urol Res 2000;28(2):128– 31. 26. Webb RJ, Styles RA, Griffiths CJ et al. Ambulatory monitoring of bladder pressures in patients with low compliance as a result of neurogenic bladder dysfunction. Br J Urol 1989;64:150–4. 27. Schmidt F, Jorgensen TM, Djurhuus JC. Twenty-four-hour ambulatory urodynamics in healthy men. Scand J Urol Nephrol Suppl 2004;215:75–83. 28. Webb RG, Griffiths CJ, Zacharin KK, Neal DE. Filling and voiding pressures measured by ambulatory monitoring and conventional studies during natural and artificial bladder filling. J Urol 1991;91:815–8.
16. Salvatore S, Khullar V, Anders K, Cardozo LD. Reducing artefacts in ambulatory urodynamics. Br J Urol 1998;81:211–4.
29. Van Waalwijk Van Doorn ESC, Remmers A, Janknegt RA. Extramural ambulatory urodynamic monitoring during natural filling and normal daily activities: evaluation of 100 patients. J Urol 1992;146:124–31.
17. Anders K, Cardozo L, Ashman O, Khullar V. Morbidity after ambulatory urodynamics. Neurourol Urodyn 2002;21(5):461–3.
30. Anders K, Khullar V, Cardozo L et al. Ambulatory urodynamic monitoring in clinical urogynaecological practice. Neurourol Urodyn 1997;5:510–12.
18. Robertson AS, Griffiths CJ, Ramsden PD, Neal DE. Bladder function in healthy volunteers: ambulatory monitoring and conventional urodynamic studies. Br J Urol 1994;73:242–9.
31. Radley SC, Rosario DJ, Chapple CR, Farkas AG. Conventional and ambulatory urodynamic findings in women with symptoms suggestive of bladder overactivity. J Urol 2001;166(6):2253–8.
19. Van Waalwijk Van Doorn ESC, Remmers A, Janknegt RA. Conventional and extramural ambulatory urodynamic testing of the lower urinary tract in female volunteers. J Urol 1992;47:1319–26.
32. Robinson D, Anders K, Cardozo L, Bidmead J, ToozsHobson P, Khullar V. Can ultrasound replace ambulatory urodynamics when investigating women with irritative urinary symptoms? BJOG 2002;109(2):145–8.
20. Heslington K, Hilton P. Ambulatory monitoring and conventional cystometry in asymptomatic female volunteers. Br J Obstet Gynaecol 1996;103:434–41.
33. Swithinbank LV, James M, Shepherd A, Abrams P. Role of ambulatory urodynamic monitoring in clinical urological practice. Neurourol Urodyn 1999;18(3):215–22.
21. Salvatore S, Khullar V, Cardozo L, Anders K, Zocchi G, Soligo M. Evaluating ambulatory urodynamics: a prospective study in asymptomatic women. Br J Obstet Gynaecol 2001;108:107–11.
34. Gorton E, Stanton S. Ambulatory urodynamics: do they help clinical management? BJOG 2000;107(3):316–19.
22. Styles RA, Neal DE, Ramsden PD. Comparison of longterm monitoring and standard cystometry in chronic retention of urine. Br J Urol 1986;58:652–6. 23. Yeung CK, Godley ML, Duffy PG, Ransley PG. Natural filling cystometry in infants and children. Br J Urol 1995;75:531–7. 24. Vereecken RL, Van Nutland T. Detrusor pressure in ambulatory versus standard urodynamics. Neurourol Urodyn 1998;17:129–33.
35. Khullar V, Salvatore S, Cardozo L et al. Ambulatory urodynamics: a predictor of de-novo detrusor instability after colposuspension. Neurourol Urodyn 1994;13:443–4. 36. Brown K, Hilton P. The incidence of detrusor instability before and after colposuspension: a study using conventional and ambulatory urodynamic monitoring. BJU Int 1999;84(9):961–5. 37. Rosario DJ, Smith DJ, Radley SC, Chapple CR. Pharmacodynamics of anticholinergic agents measured by ambulatory urodynamic monitoring: a study of methodology. Neurourol Urodyn 1999;18:223–33.
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INTRODUCTION This chapter provides an updated review on the use of radiologic imaging in female patients with storage symptoms, urinary incontinence, fecal incontinence, and voiding dysfunction. Recommendations for the proper use of imaging studies in the field of urinary and fecal incontinence are now available, and this chapter will provide indications for optimal use of intravenous urography, voiding cystourethrography, and other studies.
IMAGING OF THE UPPER URINARY TRACT The rationale for imaging the upper urinary tract (UUT) is two-fold: to identify significant congenital or acquired abnormalities in the UUT which may be related to lower urinary tract (LUT) dysfunction and to observe the possible consequences on the kidney. Nonneurogenic patients rarely benefit from imaging of the UUT although radiologic studies are currently indicated in the presence or suspicion of:
• ectopic ureter or ureterovaginal fistula; • bladder dysfunction with high storage pressure;1 • severe uterine prolapse.2 Bilateral hydronephrosis can be rarely observed in patients with grade IV genital prolapse (Fig. 24.1). In severe uterine prolapse, angulation of the pelvic ureter by uterine arteries is thought to play a role.3 Intravenous pyelography (IVP) was the foundation of UUT imaging until ultrasonography, computed tomography (CT), magnetic resonance (MR) and isotope scanning techniques developed. The choice among the different techniques depends on availability, expertise, and management policies. IVP depends on adequate renal function, as concentration of the contrast is necessary for satisfactory imaging of the renal cortex, medulla, and collecting system. Beyond the diagnosis of possible co-morbidities such as tumors and stones, IVP can identify congenital or acquired anomalies of the UUT, delayed nephrographic effect, reduced cortex to medulla ratio, small overall renal size, and dilation of the renal collecting system (hydronephrosis) and of the ureter. When ureteral ectopia is suspected, IVP is performed to identify the associated renal moiety, which may be small, malfunctioning, and ectopic, so that delayed films may be required. Whenever an IVP is performed, voiding pictures are recommended in patients with voiding dysfunction or urinary incontinence. Unless the radiologic pictures are diagnostic, CT or MR scan may be required to confirm the suspected diagnosis (Fig. 24.2).
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Figure 24.1. Intravenous pyelography. Bilateral hydronephrosis in a 54-year-old patient with grade IV genital prolapse: (a) anteroposterior; (b) oblique. (Courtesy of Professor G. Tomiselli.)
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c
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In the case of ureterovaginal fistula, mild to moderate dilation of the UUT proximal to the fistula level and extravasation of the contrast medium can be observed.4,5 Diagnosis of the fistula size and location is better achieved with retrograde ureteropyelography. CT scan is independent of renal function, although the use of contrast medium can help in identifying accessory, small or malfunctioning renal moieties and in delineating the collecting system and ureter. Renal contrast CT is still limited to those patients with normal
Figure 24.2. Intravenous pyelography in a 16-year-old patient with urinary incontinence. The intravenous pyelogram shows a complete duplex system on the left side. On a lateral projection, the ureter of the upper renal moiety travels below the bladder base, reaching the most distal part of the urethra (a); the anatomic condition is confirmed on uro-MR (b, c). (Courtesy of Professor G. Tomiselli.)
renal function. Modern multi-slice equipment (dynamic CT scanning) allows a fast acquisition of a certain volume which can then be analyzed in axial, coronal, sagittal or oblique planes and also rendered in three-dimensional views. In conclusion, radiologic imaging of the UUT is not indicated in non-neurogenic incontinence. It is, however, recommended in neurogenic incontinence or voiding dysfunction with high bladder storage pressures which may damage renal function, in patients with 327
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severe uterine prolapse, and with incontinence-associated malformation of the UUT. The choice of imaging technique depends on the clinical problem, availability of equipment, expertise, and cost.
IMAGING OF THE LOWER URINARY TRACT Radiologic imaging of the lower urinary tract has frequently been used in women with urinary incontinence and/or voiding dysfunction. It helps to define the morphology of the urinary bladder and urethra and their function during voiding or stress conditions. In addition to the evaluation of hypermobility, bladder imaging can reveal vesicoureteral reflux, trabeculation, diverticula, and fistulae. It also helps to identify the level of outlet obstruction, to image urethral diverticula, and to diagnose possible co-morbidities such as stones, tumors, foreign bodies, etc. (Figs 24.3–24.5).
a
Cystourethrography Although this technique has been around for over 70 years and has been widely used in the diagnostic workup of female urinary incontinence, the indications for cystourethrography are currently fairly limited. The imaging technique has evolved over the years. In 1931, Mikulicz-Radecki proposed the use of true lateral projection.6 In 1937, a metallic bead chain for delineating the urethra was introduced.7 The cinematographic technique with concurrent contrast opacification of the vagina and rectum was pioneered by Ardran and co-workers in 1956. It was combined with simultaneous recording of bladder and urethral pressures in the following two decades.8–12 The technique of cystourethrography is important. Patients are best imaged while sitting rather than lying or standing. Following plain X-ray films, the bladder is filled with contrast and anteroposterior films are taken at rest and during straining. Although displacement of the bladder base can be observed at rest and during stress, an anteroposterior projection does not allow discrimination of the type of displacement during voiding. The use of oblique projections is not accurate for the same reason. True lateral projections are recommended as they allow observation of the relationship between the bladder base, urethra, and pubic bones, both at rest and during voiding (Figs 24.5, 24.6). The need for high-energy radiation to overcome the superimposing of the trochanteric region over the urethra and of the urethrovesical junction with the lateral parts of the bladder has sometimes prevented the use of true lateral projections. Some of these technical prob-
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Figure 24.3. Digital fluoroscopy picture obtained during videourodynamics in a 63-year-old female with voiding dysfunction. Dilation of proximal urethra and a bladder diverticulum is evident on a voiding picture (a); vesicoureteral reflux is apparent on the post-voiding image (b). (Courtesy of Professor G. Tomiselli.) lems have now been resolved by the availability of digital subtraction techniques. The clinical benefit of opacifying both the vagina and the rectum is unclear and the technique is now rarely used (Fig. 24.7). Radiologic diagnosis of vaginal vault prolapse can be difficult (Fig. 24.8). Patients are currently imaged at rest and during provocative maneuvers such as straining, coughing, squeezing, and during micturition. Coughing is known to result in a reflex contraction of the pelvic floor but the speed of such reflex makes the contraction
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Videourodynamics
a
The combined use of imaging and pressure–flow measurement has been considered the gold standard technique in the management of lower urinary tract dysfunction15 although the evidence of its superior clinical benefit is missing. The advantages of videourodynamics include easy documentation of opacified urine leakage, the ability to standardize provocative maneuvers such as straining, to relate the degree of bladder displacement with the abdominal pressure values produced by the individual patient, and the urine leakage observed during the Valsalva maneuver with the produced pressure values.16 The combined use of urodynamics and imaging increases the diagnostic complexity because of the need to repeat urodynamic measurements which are known to have limited reproducibility17,18 and to limit radiation exposure (although the use of digital fluoroscopy has significantly reduced the exposure).19 No data as to the reproducibility of the pressure–flow study are available. The introduction of digital fluoroscopy has greatly improved the quality of radiologic imaging during videourodynamic studies (Figs 24.3, 24.4), although currently available urodynamic equipment rarely accepts high-resolution inputs from modern treatment equipment.
The evaluation of bladder support
b
Figure 24.4. Digital fluoroscopy in a 72-year-old patient with voiding dysfunction. A decompensated bladder is observed during voiding (a) and severe dilation of proximal urethra is seen during videourodynamics (b). (Courtesy of Professor G. Tomiselli.)
difficult to catch on spot films. Squeezing is used to test the awareness of the pelvic floor and results in a contraction of the pelvic floor with elevation of the bladder base.13 The effect of straining on the pelvic floor is variable and depends upon proper muscle coordination. The evaluation of bladder suspension defects during cystourethrography has been evaluated in several studies. In one study, a suspension defect was diagnosed at rest in 49% of patients, and during coughing and voiding in an additional 20% and 4% of patients, respectively.14
The urinary bladder has a smooth surface at rest, which is maintained during voiding. Irregular bladder shapes are observed in neurogenic patients and in the presence of diverticula or hernias. The bladder trigone is situated immediately behind the urethrovesical junction. The ureterovesical junctions are positioned on the posterior margins of the trigone in the anterior third of the bladder base on a true lateral projection. The trigone and the ureteric orifices lie along a horizontal plane passing through the lowermost part of the symphysis pubis. The bladder base is basically flat although it slides upwards and backwards. The urethra lies on a relatively straight vertical line with a little forward inclination. In a sagittal plane, the urethra forms a slightly acute anterior and a slightly obtuse posterior angle with the bladder base. The vagina lies posterior to the urethra and trigone in a parallel plane. No significant changes should occur during straining or coughing, although minor downward movement has been described. Squeezing can cause a slightly opposite displacement. During voiding, the bladder base lowers slightly (Fig. 24.9) and the posterior urethrovesical angle opens (Fig. 24.10), resulting in bladder neck funneling. Evaluation of residual urine at the end of the voiding phase can be misleading because of the possible interference of the 329
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Figure 24.5. Voiding cystourethrogram in a 29-year-old patient with urinary incontinence. During the voiding phase, reflux of contrast medium into an ectopic ureter draining the upper moiety of a complete duplicated left renal system can be seen. In the last phase of the voiding study, the refluxing medium drains into the urethra. (Courtesy of Professor G. Tomiselli.) 330
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Figure 24.6. Cystourethrography in a 68-year-old patient without urinary incontinence. A symmetrically distended bladder is evident on the anteroposterior image (a), with the bladder base above the lower margin of the symphysis pubis; in the true lateral projection (b), the anterior and posterior urethrovesical angles are easily observed in the picture taken just before micturition. (Courtesy of Professor G. Tomiselli.)
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Figure 24.7. Grade IV genital prolapse can be observed in a 63-year-old patient during intravenous pyelography in anteroposterior (a) and true lateral projection (b); the relationship between pubic bone, bladder trigone and urethra is best appreciated during voiding cystourethrogram in a true lateral projection (c). (Courtesy of Professor G. Tomiselli.) 331
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a
c
environment on the patient’s ability to empty the bladder during the test. A number of studies have addressed the reproducibility and validity of quantitative parameters of cystourethrography in patients with and without urinary incontinence. The diagnosis of bladder suspension defects was proposed in the early 1960s as it was considered to be related to specific fascial and muscle defects. Anterior defects (Table 24.1) (corresponding to Green type I descent) were diagnosed by a symphysis orifice distance <20 mm with a normally positioned vagina at rest, during coughing or micturition and/or funneling of the bladder base at rest or during coughing. Posterior bladder suspension defects, corresponding to Green type II descent were diagnosed by a posterior–inferior bladder displacement
b
Figure 24.8. Voiding cystourethrogram in a patient with contrast medium both in the bladder and in the rectum. Pictures taken (a) at rest, (b) during Valsalva, and (c) voiding show a gradual distension of the rectocele pouch. (Courtesy of Professor G. Tomiselli.) with a urethropelvic angle of less than 70°. The clinical benefit of such a classification of suspension defects has been questioned and it is no longer applied. The reproducibility of cystourethrography was found to be in the range of other radiologic examinations, with an intraobserver variability of 53–99% and an interobserver variability of 43–79%.13,21,23,24 The accuracy of cystourethrography for the diagnosis of urinary incontinence is low and a consensus has been reached that the imaging study cannot discriminate stress incontinent versus continent patients. The specificity of the different parameters of cystourethrography for the diagnosis of stress incontinence ranges between 44 and 76% with a sensitivity of 53–100%.25,26 The severity of stress urinary incontinence was found to be unrelated to the type or degree of suspension defect.13,23,27
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Figure 24.10. Voiding cystourethrogram with digital subtraction. There is normal funneling of the bladder neck with mild downward displacement during micturition. (Courtesy of Professor G. Tomiselli.) optional test in patients with recurrent or complicated incontinence.
Residual urine measurement
b
Figure 24.9. Cystourethrography with simultaneous administration of small bowel contrast allows the diagnosis of enterocele in a 61-year-old patient suffering from vaginal vault prolapse. Small bowel protruding down to the perineum level can be observed both at rest (a) and during voiding cystourethrogram (b), with a significant increase of the enterocele mass when abdominal pressure increases. (Courtesy of Professor G. Tomiselli.) Cystourethrography has been used extensively to evaluate the results of incontinence surgery but no parameter has been identified which could distinguish successes from failures.13,14,26–33 In conclusion, cystourethrography is not recommended for the evaluation of patients suffering primary, uncomplicated urinary incontinence. It remains an
Measurement of residual urine (the volume of fluid remaining in the bladder immediately after the completion of micturition) is of importance because it is a proxy for bladder decompensation. It also has some relation to the risk of adverse events such as urinary tract infection. Measurement of residual urine can be performed using invasive and non-invasive techniques such as in-and-out catheterization or ultrasonography. Radiologic studies are not usually performed solely to measure residual urine, although the information is often available from postmicturition films. No studies have investigated the reliability of post-voiding residual volume obtained at the end of cystourethrography versus flowmetry. The residual urine volumes observed at the end of invasive diagnostic tests should always be interpreted with caution. The results can be inaccurate because of difficulty voiding after instrumentation of the lower urinary tract. Furthermore, voiding may not be normal while sitting or standing in a radiologic suite, with the patient being observed, or because the bladder has been distended beyond cystometric capacity. Consequently, abnormal post-voiding residual urine observed during radiologic studies may be inaccurate and residual urine should be measured after voiding in a more patient-friendly environment. 333
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Table 24.1.
Measurements of angles on cystourethrography Cut-off values
Posterior urethrovesical angle (PUV)
115° or more*
Urethropelvic angle (UP)
95°; values of 70° or lower define bladder descent†
Urethral inclination
45°; discriminates between Green type I and II descent‡
Symphysis orifice distance (SO)
Normal values are 31 ± 6 mm; 20 mm is the cut-off for descent†
* From refs 20 and 21; † from ref. 14; ‡ from ref. 22.
Open bladder neck and proximal urethra at rest The observation of an open bladder neck and proximal urethra at rest is not unusual during urethrocystography and videourodynamics, and is not necessarily diagnostic of an underlying neurologic disorder. In patients with a low spinal cord injury, the presence of an open bladder neck and proximal urethra has been considered to be dependent upon sympathetic or parasympathetic damage, although no consensus has yet been reached.34 The reduced α-adrenergic innervation resulting from a peripheral sympathetic injury can reduce the tone of smooth muscle fibers at the bladder neck and in the proximal urethra. Partial denervation
a
of the detrusor and normal EMG activity of the external sphincter are usually observed.35 In one report, 21 of 54 patients with spinal stenosis were found to have a relatively incompetent bladder neck and proximal urethra; this was considered to be dependent upon the interruption of the peripheral reflex arc, similar to patients with low spinal cord injury.36 In a large study of 550 patients, 29 of 33 patients with open bladder neck and proximal urethra at rest were found to be suffering from some form of neurologic disease. No significant relation between the site of the lesion and the condition was found, although the open bladder neck was more frequently seen in patients with thoracic, lumbar or sacral defects compared to cervical and supraspinal
b
Figure 24.11. Voiding cystourethrogram: anteroposterior picture with a fully distended bladder (a); the acute anterior urethrovesical angle and the obtuse posterior angle are evident on true lateral projection when the bladder neck is filled with contrast medium, at the beginning of the voiding phase (b). (Courtesy of Professor G. Tomiselli.) 334
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lesions. Furthermore, myelodysplasia would appear to be associated with a higher incidence of open bladder neck compared to any other neurologic disease (10 out of 19 patients versus 19 of 290). The condition of an open bladder neck and proximal urethra at rest has also been described in non-neurogenic girls with diurnal and nocturnal incontinence37 and in asymptomatic women.38,39 The diagnosis of an open bladder neck and proximal urethra at rest in the absence of detrusor contraction was a key factor for defining type III non-neurogenic stress incontinence in the classification of Blaivas and Olsson, although the classification is no longer used.40 In conclusion, the observation of an open bladder neck and proximal urethra at rest on radiologic imag-
a
c
ing should raise the question of a possible underlying autonomic neural deficit.
Female urethral diverticula The introduction of positive pressure urethrography in 1956 significantly improved the diagnosis of female diverticula (first described in 1805).41,42 Urinary incontinence is frequently associated with urethral diverticula although the condition classically presents with dysuria, post-void dribbling, and dyspareunia.43 The radiologic diagnosis of urethral diverticula may be confirmed by voiding cystourethrography (Figs 24.11, 24.12) or positive pressure urethrography, although both can give false-negative results if inflammation of
b
Figure 24.12. Urethral diverticulum of the posterior urethral wall is evident on voiding cystourethrogram in oblique (a) and in anteroposterior projections (b, c). (Courtesy of Professor G. Tomiselli.) 335
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the diverticulum neck prevents reflux of the contrast medium into the diverticular cavity. Two different catheter types are available for positive pressure urethrography: the Davis-Telinde and the Trattner. The accuracy of urethrography for the diagnosis of urethral diverticula has been estimated at 69% versus MRI and in 55% versus surgery.44 In conclusion, imaging is recommended in the clinical suspicion of urethral diverticula. Positive pressure urethrography is a valuable diagnostic test although MRI is now considered the gold standard technique (Fig. 24.13); ultrasonography is a valuable alternative.
IMAGING OF THE NERVOUS SYSTEM Lumbosacral spine X-rays Radiologic imaging of the lumbosacral spine may be required in patients with urinary incontinence when an underlying spinal abnormality such as spina bifida occulta is suspected.45 Lumbosacral spine X-rays with anterior and lateral projections are recommended when there is a suspicion of congenital neurogenic inconti-
a
nence, even if no neurologic abnormalities are demonstrated on physical examination.
CT and SPECT Imaging of the central nervous system (CNS) is of importance to diagnose a number of CNS conditions which may be responsible for urinary incontinence, particularly in the elderly population. CT and single photon emission tomography (SPECT) are often used to investigate the CNS in patients with urinary incontinence when this is one of the many symptoms caused by a CNS lesion. A correlation between CT pictures and urodynamic parameters has been shown after cerebrovascular accidents.46,47 In the absence of any neurologic sign, significant CNS lesions can be observed on CT and SPECT in patients suffering from urge incontinence.48 A significant association between depressed perfusion of the cerebral cortex and midbrain was also found in an elderly cohort of patients with urge incontinence.49 In conclusion, CNS imaging is recommended in patients with urinary incontinence when a CNS disorder is suspected based on clinical and/or neurophysiologic test findings.
b
Figure 24.13. Magnetic resonance (MR) and voiding cystourethrogram in a 69-year-old patient with urinary incontinence. A urethral diverticulum was suspected on a pelvic floor MR (a) and confirmed on voiding cystourethrogram (b). (Courtesy of Professor G. Tomiselli.) 336
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REFERENCES 1. McGuire EJ, Woodside JR, Borden TA et al. Prognostic value of urodynamic testing in myelodysplastic patients. J Urol 1981;126:205–9. 2. Kontogeorgos L, Vassilopoulos P, Tentes A. Bilateral severe hydroureteronephrosis due to uterine prolapse. Br J Urol 1985;57:360–1. 3. Gemer O, Bergman M, Segal S. Prevalence of hydronephrosis in patients with genital prolapse. Eur J Obstet Gynecol Reprod Biol 1999;86:11–3. 4. Mandal AK, Sharma SK, Vaidyanathan S et al. Ureterovaginal fistula: summary of 18 years’ experience. Br J Urol 1990;65:453–6. 5. Murphy DM, Grace PA, O’Flynn JD. Ureterovaginal fistula: a report of 12 cases and review of the literature. J Urol 1982;128:924–5. 6. Mikulicz-Radecki F. Rontgenologische studien zur atiologie der urethralen inkontinenz. Zbl Gynak 1931;55:795. 7. Stevens WE, Smith SP. Roentgenological examination of the female urethra. J Urol 1937;37:194–201. 8. Ardran GM, Simmon CA, Stewart JH. The closure of the female urethra. J Obst Gynaec Brit Emp 1956;63:26–35. 9. Bates CP, Whiteside CG, Turner-Warwick R. Synchronous cine/pressure/flow/cysto-urethrography with special reference to stress and urge incontinence. Br J Urol 1970;42:714–23. 10. Enhorning G, Miller ER, Hinman FJ. Urethral closure studied with cineroentgenography and simultaneous bladder–urethra pressure recording. Surg Gynec Obstet 1964;118:507. 11. Palm L. Bladder function in women with disease of lower urinary tract. Thesis. Mungsgaard, Copenhagen, 1971; 1–226. 12. Shopfner CE. Cystourethrography. J Urol 1970;103:92– 103. 13. Klarskov P, Vedel Jepsen P, Dorph S. Reliability of voiding colpo-cysto-urethrography in female urinary stress incontinence before and after treatment. Acta Radiol 1988;29:685–8. 14. Olesen KP. Descent of the female urinary bladder. A radiological classification based on colpo-cysto-urethrography. Dan Med Bull 1983;30:66–84. 15. Barnick CG, Cardozo LD, Beuness C. Use of routine videocystourethrography in the evaluation of female lower urinary tract dysfunction. Neurourol Urodyn 1989;8:447–9. 16. Rud T, Ulmsten U, Asmussen M. Initiation of micturition: a study of a combined urethrocystometry and urethrocystography in healthy and stress incontinent females. Scand J Urol Nephrol 1979;13:259–64. 17. Hansen F, Olsen L, Atan A et al. Pressure-flow studies: an evaluation of within-testing reproducibility-validity of the measured parameters. Neurourol Urodyn 1997;16:521–32.
18. Sorensen S, Knudsen VB, Kirkeby HJ et al. Urodynamic investigations in healthy fertile females during the menstrual cycle. Scand J Urol Nephrol 1988;114:28–34. 19. Pick EJ, Davis R, Stacey AJ. Radiation dose in cinecystourethrography of the female. Br J Radiol 1960;33:451–4. 20. Drutz HP, Shapiro BJ, Mandel F. Do static cystourethrograms have a role in the investigation of female incontinence? Am J Obstet Gynecol 1978;130:516–20. 21. Fantl JA, Hurt G, Beachley MC et al. Bead-chain cystourethrogram: an evaluation. Obstet Gynecol 1981;58:237–40. 22. Green TH Jr. Development of a plan for the diagnosis and treatment of urinary stress incontinence. Am J Obstet Gynecol 1962;83:632–48. 23. Mouritsen L, Strandberg C, Jensen AR et al. Inter- and intra-observer variation of colpo-cysto-urethrography diagnoses. Acta Obstet Gynecol Scand Suppl 1993;72:200–4. 24. Thind PO, Lose G, Falkenlove P et al. Assessment of micturition cystourethrography. Intra- and inter-observer variation. Ugeskr Laeger 1991;153:338. 25. Bergman A, McKenzie C, Ballard CA et al. Role of cystourethrography in the preoperative evaluation of stress urinary incontinence in women. J Reprod Med 1988;33:372–6. 26. Bergman A, McKenzie CJ, Richmond J et al. Transrectal ultrasound versus cystography in the evaluation of anatomical stress urinary incontinence. Br J Urol 1988;62:228–34. 27. Christ F, Meyer-Delpho W. The radiological diagnosis of urinary incontinence in a female. Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 1981;134:551–6. 28. Ala-Ketola L, Kauppila A, Jouppila P et al. Pre- and postoperative bead chain urethrocystography in female stress urinary incontinence. Acta Obstet Gynecol Scand 1981;60:369–74. 29. Greenwald SW, Thornbury JR, Dunn LJ. Cystourethrography as a diagnostic aid in stress incontinence. An evaluation. Obstet Gynecol 1967;29:324–7. 30. Kitzmiller JL, Manzer GA, Nebel WA et al. Chain cystourethrogram and stress incontinence. Obstet Gynecol 1972;39:333–40. 31. Meyhoff HH, de Nully MB, Olesen KP et al. The effects of vaginal repair on anterior bladder suspension defects. A radiological and clinical evaluation. Acta Obstet Gynecol Scand 1985;64:433–5. 32. Stage P, Fischer-Rasmussen W, Hansen RI. The value of colpo-cysto-urethrography in female stress- and urge incontinence and following operation. Acta Obstet Gynecol Scand 1986;65:401–4. 33. Thuneborg P, Fischer-Rasmussen W, Jensen SB. Stress urinary incontinence and posterior bladder suspension defects. Acta Obstet Gynecol Scand 1990;69:369–74. 34. Nordling J, Meyhoff HH, Olesen KP. Cysto-urethrographic appearance of the bladder and posterior urethra in neu-
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romuscular disorders of the lower urinary tract. Scand J Urol Nephrol 1982;16:115–24. 35. Blaivas JG, Barbalias GA. Characteristics of neural injury after abdominoperineal resection. J Urol 1983;129:84–7. 36. Wein AJ. Neuromuscular dysfunction of the lower urinary tract. In: Walsh PC, Retik AB, Stamey TA et al. (eds) Campbell’s Urology, 6th ed. Philadelphia: Saunders, 1992; 573.
urethrovaginal fistula and urethral diverticulum. In: Walsh PC, Retik AB, Stamey TA et al. (eds) Campbell’s Urology, 7th ed. Philadelphia: Saunders, 1998; 1135. 44. Kim B, Hricak H, Tanagho EA. Diagnosis of urethral diverticula in women: value of MR imaging. Am J Roentgenol 1993;161:809–15.
37. Stanton L, Williams DI. The wide bladder neck in children. Br J Urol 1973;45:60–4.
45. Kondo A, Kato A, Kanai S et al. Bladder dysfunction secondary to tethered cord syndrome in adults. It is curable? J Urol 1986;135:313–6.
38. Chapple CR, Helm CW, Blease S et al. Asymptomatic bladder neck incompetence in nulliparous females. Br J Urol 1989;64:357–9.
46. Khan Z, Starer P, Yang WC et al. Analysis of voiding disorders in patients with cerebrovascular accidents. Urology 1990;35:265–70.
39. Versi E. The significance of an open bladder neck in women. Br J Urol 1988;68:42–3.
47. Tsuchida S, Noto H, Yamaguchi O et al. Urodynamic studies in hemiplegic patients after cerebrovascular accidents. Urology 1983;21:315–8.
40. Blaivas JG, Olsson CA. Stress incontinence: classification and surgical approach. J Urol 1988;139:727–31. 41. Davis HJ, Cian LG. Positive pressure urethrography: a new diagnostic method. J Urol 1956;75:753–7. 42. Hey W. Practical observations in surgery. J Humphreis 1805. 43. Leach GE, Trockmann BA. Surgery for vesicovaginal and
48. Andrew J, Nathan PW. Lesions of the anterior frontal lobes and disturbances of micturition and defecation. Brain 1964;87:233–62. 49. Griffiths DJ, McCracken PN, Harrison GM et al. Geriatric urge incontinence: basic dysfunction and contributory factors. Neurourol Urodyn 1990;9:406.
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25 Magnetic resonance imaging (MRI) and the female pelvic floor Lennox Hoyte
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IntroductIon Female pelvic floor dysfunction (PFD) includes pelvic organ prolapse, and urinary and fecal incontinence. Appropriate therapy for PFD depends on a proper understanding of the female pelvic anatomy, in both asymptomatic and symptomatic women. In the past, cadaveric dissections have been used to aid understanding of the pelvic anatomy but these have been limited by artifacts of fixation and other changes which occur when living tissues become non-viable. A more realistic understanding of the anatomic relationships in symptomatic and asymptomatic living women is possible if the subjects can be imaged. Over the past decade, magnetic resonance imaging (MRI) has evolved as a useful tool for evaluating the living anatomy in the female pelvis, both in the upright and supine positions, and under differing physiologic conditions, such as rest, squeeze, and strain. The results from such imaging studies are beginning to shed new light on our understanding of the behavior of the asymptomatic and symptomatic female pelvic floor, and may yet pave the way to help triage those with PFD for appropriate therapy, and possibly aid in predicting which women may be at risk for pelvic floor dysfunction. At present, however, there is no currently agreed-upon role for MRI in the diagnostic evaluation of female pelvic floor dysfunction. With the above reality in mind, the aims of this chapter are manifold:
• To review the development of MRI as a tool for understanding female pelvic floor anatomy;
• To show the range and variability of the female pelvic anatomy;
• To show how pelvic anatomic changes may relate to various forms of PFD;
• To study the possible effects of childbirth on the pelvic floor;
• To introduce MR-based methods for advanced
• •
study of the female pelvic floor – for example, MR-based three-dimensional (3D) reconstruction and computer-based pelvic floor simulation models (which may be used to gain a better understanding of the parameters of childbirth-related female pelvic floor injury); To describe the basic MRI techniques, their interpretation, and pitfalls in application; To briefly present current public domain tools for visualization, analysis, and management of the MR images.
MrI for understandIng feMale pelvIc floor anatoMy MRI has been used to assess the normal anatomy of the female pelvic floor, as well as to study the anatomic determinants of pelvic organ dysfunction. When Strohbehn et al. compared MRI findings with anatomy at dissection in two cadavers1 (Fig. 25.1), they found that sagittal and axial MRI demonstrated the levator ani muscle from its fascial origination at the pubic bone, along its course passing alongside the urethra, distal vagina, and posterior to the rectum, noting its insertion between the internal and external anal sphincters (Fig. 25.2). Furthermore, MRI showed the iliococcygeus muscle attachment to the arcus tendineus laterally, as well as the relative thickness of the medial aspect of the levators when compared to the thinner, more lateral aspect. Their work demonstrated that MRI findings reflected actual anatomy; however, they did have the benefit of long MRI scan times which increased resolution without introducing the motion artifact that would limit scan times in living subjects.
Basic female pelvic Mr anatomy Magnetic resonance images are routinely obtained in the axial, coronal, and sagittal planes. By convention, coronal slices are presented with the subject facing the observer, axial images are presented with the subject’s feet closest to the observer, and sagittal images are presented with the subject facing to the left of the observer. Examples of these three slice orientations are illustrated in Figure 25.3. Axial slices are obtained for best visualization of the puborectalis, the urethra, and the distal vagina; coronal slices best demonstrate the iliococcygeus portion of levator ani and also the external anal sphincter; midsagittal images are usually obtained in order to evaluate descent of the pelvic floor structures with straining versus rest or squeeze maneuvers. Oblique slices may also be collected, depending on the specific question to be answered. Typical MRI findings in the nullipara include a urethra and bladder neck that are close to the symphysis, puborectalis muscle arms which come into close proximity with the superior pubic rami, and a downwardly convex distal vagina with upwardly curving edges bilaterally. The general shape of the puborectalis muscle is that of a ‘V’. These findings are shown in Figure 25.4. Findings in the vaginal multipara are much more variable. They can range from closely resembling the nullipara, all the way to having a lower urethra and bladder
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Uterus
Rectum
Bladder
Anococc. raphe Pubovis. m. EAS
Urethra Vagina
a
EAS Int. anal sphincter m.
b
c
Figure 25.1. Comparison of cadaveric anatomy from MRI and dissection. Midline sagittal view of the pelvis. (a) Cross-sectional anatomy. (b) Corresponding diagram. EAS, external anal sphincter muscle. (c) Fast spin-echo T2-weighted 1.5-tesla magnetic resonance imaging (MRI) of a 26-year-old living patient (repetition time 3600 milliseconds, echo delay time 85 milliseconds, field of view 24 cm, scan time 11:44 minutes). Incidental ovarian cyst (black arrow) is seen anterior to the uterus. BL, bladder; UT, uterus; R, rectum. (d) T2-weighted MRI of cadaver specimen at the same level. (*Note: The asterisk posterior to the symphysis on the cadaver MRI represents fixation artifact from a fluid collection in the space of Retius in this and subsequent figures.) The fibers of the pubovisceralis muscle (puborectalis) that decussate behind the rectum are seen in relationship to the internal and external anal sphincter muscles. The image clarity is less in the patient MRI compared with the cadaver MRI because of motion artifact and shorter scan time, but the external anal sphincter muscle (arrowhead) and the pubovisceralis muscle (open arrow) are seen. (Reproduced from ref. 1 with permission.)
d
Urethra Vagina Pubovisc. m. Obturator int. m. Illiococcygeus m.
Rectum a
b
c
d
Figure 25.2. Cadaveric and MRI anatomy, demonstrating the relationship of levator with pubic bone, rectum, and vagina. Axial views of the pelvis near the level of the symphysis pubis. (a) Proton density magnetic resonance imaging (MRI) of 28-year-old living patient, using a pelvic phased-array coil (repetition time 3800 milliseconds, echo delay time 18 milliseconds, field of view 20 cm, scan time 8:59 minutes). Note a small group of distinct fibers of the left iliococcygeus muscle (white arrow) originating laterally at the oburator internus muscle, and fibers from the pubovisceralis musccle (black arrow) originating at the symphysis pubis. (b) Cross-sectional anatomy of the right hemipelvis. (c) Corresponding diagram of the left hemipelvis. (d) T2-weighted MRI at the same level. This plane demonstrates the relationship of the modline viscera to the pubovisceralis muscle. The patient MRI also demonstrates the difference in origin of the pubovisceralis muscle and the iliococcygeus muscle. (Reproduced from ref. 1 with permission.) 341
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a b
c
d
Figure 25.3. Examples of MR slice orientations from a young nullipara. (a) Axial slice at the level of the bladder neck (B, bones). (b) Coronal slice at the level of the distal rectum: note the left to right asymmetry of the slice; the femoral head (F) is seen on the left, but not on the right. (c) Sagittal slice: Midsagittal view (B, bladder). (d) Left parasagittal slice: note the left simple ovarian cyst (C) anterior to the uterus. Levator ani (LA) is seen running posterior to anterior. The superior pubic ramus (SR) is seen as well as the obturator internus (OI). (Other abbreviations: A, anus; IC, iliococcygeus; PR, puborectalis; R, rectum; S, symphysis; U, urethra; UT, uterus; V, vagina.)
neck, loss of puborectalis approximation to the superior rami, loss of the downward concavity of the distal vagina, and a ‘bowing’ of the puborectalis muscle, causing it to resemble a ‘U’ instead of the nulliparous ‘V’. The range of multiparous variation is shown in Figure 25.5. Findings in symptomatic women are also quite variable, as can be seen from the following discussion.
symptomatic pelvic MrI findings
Figure 25.4. Typical MRI findings in the nullipara include a urethra and bladder neck which are close to the symphysis, puborectalis muscle arms which come into close proximity with the superior pubic rami, and a downwardly convex distal vagina with upwardly curving edges bilaterally. The general shape of the puborectalis muscle is that of a ‘V’.
Huddleston et al.2 demonstrated MRI findings of three alterations in vaginal shape that were associated with clinical pelvic organ prolapse, demonstrating a relationship between pathologic MR and clinical findings (Fig. 25.6). Kirshner-Hermanns et al. reported increased T1 signal intensity as evidence of muscle atrophy in 66% of their subjects with stress incontinence,3 suggesting a relationship between levator weakness and stress urinary incontinence (SUI). Their conclusions were supported by Fielding et al.4 who found a trend towards levator muscle laxity and thinning in women with SUI. However, it is possible that their results were a reflection of the wide normal range of levator variation. This idea was demonstrated by Tunn et al. who used pelvic MRI to show two- to three-fold differences in distance, area, and
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a b
c
Figure 25.5. MRI Findings in the vaginal multipara. (a) A V-shaped puborectalis, with loss of upward vaginal curve bilaterally. (b) Loss of puborectalis approximation to the pubic rami, with flattened vagina. (c) Bilateral bowing of the puborectalis, and sagging of the vagina on the left.
Figure 25.6. Alterations in vaginal shape associated with pelvic organ prolapse. Upper panel: MRI of normal support. Lower panel: MRI of abnormal support, both at DeLancey’s levels I, II, and III. (Reproduced from ref. 2 with permission.)
volume of pelvic floor structures among a group of 20 asymptomatic nulliparas.5 Klutke et al. studied bladder neck MRI findings taken in the supine position in normals compared to those with a urodynamic diagnosis of stress incontinence.6 They found that, when compared to patients with stress incontinence, normal subjects were characterized by MR findings of a bladder neck positioned close to the symphysis, a vaginal lumen with a widened ‘H’ shape, and nearly horizontal ‘urethropelvic’ ligaments. It should be noted that they considered the urethropelvic ligaments to attach the lateral aspect of the urethra to the medial aspect of the levator sling (Fig. 25.7). This point was also emphasized by Tunn et al. who identified these lateral attachments on MR scans in 20 continent nulliparas.7 Looking retrospectively at women with PFD, Handa et al. compared pelvic MRI findings of the bony pelvis in 59 women with PFD with 39 controls.8 They found that women with PFD tended to have a wider transverse inlet, intertuberous and interspinous diameter, a longer
sacrum with a deeper curve, and a narrower anteroposterior outlet, when compared to those without PFD. Their findings were independent of race. These results echoed the findings of Sze et al. who previously used CT pelvimetry to correlate the bony pelvic shape with the risk of female PFD. They found wider transverse pelvic inlet diameters in 34 multiparous white women with prolapse, compared to 34 matched controls with normal pelvic support.9 These findings also suggest a relationship between the wide, deep bony pelvis and the presence of PFD among parous women. In seeking a better understanding of the specific anatomic defects that might correlate to female pelvic floor dysfunction, our group evaluated the morphology, volume, and integrity of the levator ani and the bladder neck, using reconstructed 3D MR-based models in living women. Fielding and colleagues demonstrated the feasibility of the 3D technique and yielded early estimates of the normal range of levator volume in a group of 10 asymptomatic women aged 22–33 years.10 Our 343
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Pubic symphysis Urethra UPL Obturator Vagina Rectum Levator sling
a
b
subsequent study used MR-based 3D reconstruction techniques to evaluate a group of 30 women, divided into three groups:11 10 were asymptomatic (ASY), 10 had urodynamic stress incontinence (USI), and 10 had symptomatic pelvic organ prolapse (POP). The data showed significant differences in levator volume, integrity, and shape across the range of ASY to USI to POP, suggestive of a continuum of disease. In that study, we identified a marker for anterior puborectalis attachment disruption – the levator–symphysis gap (LSG) – which is measured as the distance from the inferior symphysis to the nearest occurrence of the puborectalis muscle on each side. Shorter distances suggest closer approximation of levator to pubis, and longer distances suggest disruption of the puborectalis attachment. Our findings of LSG indicated greater disruption in POP and USI subjects, compared to asymptomatics. As will be discussed in the next section, DeLancey’s group showed that these levator disruptions appear to occur only in parous women. Magnetic resonance imaging has also been used to study the anatomy of the urethra. Aronson’s group looked at MRI anatomy of the female urethra using an endoanal coil, placed vaginally.12 They compared MR images from four continent nulliparas with four incontinent women. They found that they were able to effectively image the periurethral and paravaginal connective tissues, and found that the MR images correlated well with each subject’s assessed clinical defects. They measured the volume of the space of Retzius, and observed that the volume was twice as high in the incontinent versus the continent, but this was not statistically
Figure 25.7. MRI findings in asymptomatics and those with stress incontinence. (a) Axial magnetic resonance image at level of bladder neck in wellsupported continent woman shows urethropelvic ligaments (UPL, arrows) supporting the bladder neck. (b) Corresponding step-section at the same level shows urethropelvic ligaments attaching to levator (arrows) at level of arcus tendineus. (Reproduced from ref. 6 with permission.)
significant. DeLancey’s group looked at the position of the striated urethral sphincter in a cohort of 78, young, healthy nulliparas using MRI.13 They observed the urethra to start between 0.5 and 2.5 cm distal to the bladder base, extending to the perineal membrane, which was located 2–3 cm distal to the bladder base. Examples of urethral MR images are given in Figure 25.8. These two studies demonstrated the ability of MRI to identify the urethral and periurethral structures.
chIldBIrth-related changes as seen on MrI Childbirth-related damage to the levator muscle, as well as to nerves and connective tissues in the pelvis, is believed to be a major contributor to female PFD.14–18 Notably, approximately 75% of the 4 million annual US births are delivered vaginally.19,20 There is epidemiologic evidence of a relationship between childbirth and pelvic floor dysfunction.21,22 However, not all women who undergo vaginal childbirth develop PFD.23 Furthermore, not all nulliparous women are free of PFD.24 This apparently variable response of the pelvic floor to childbirth has prompted investigators to use MRI to look more closely at the possible effects of birth on the pelvic floor. When DeLancey examined MRI scans of 80 nulliparas, he found intact puborectalis muscle arms in 100%. Among 160 primiparas, however, 20% demonstrated disruptions in one or both puborectalis arms. These findings suggested that childbirth may have caused injury to the puborectalis attachment at the superior pubic
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Figure 25.8. The female striated urethra as seen on MRI. Variations of normal urethral anatomy. Each column shows three examples of typical urethral anatomy, each from a different woman. Rows do not represent individual urethrae. (B, bladder; CU/CVS, region of the compressor urethrae and urethrovaginal sphincter muscles; PM, region of the perineal membrane; PS, pubic symphysis; SUS, region of the striated muscle sphincter; V, vagina. *Arcuate pubic ligament below the symphysis pubis.) (Reproduced from ref. 13 with permission; © DeLancey, 2003.) ramus. Of the primiparas with these disruptions, 71% were found to have SUI.17 This suggests that SUI is correlated with puborectalis disruptions, probably caused by vaginal childbirth. Furthermore, Miller compared maximum urethral closure pressures (MUCPs) in 17 women with MRI-proven puborectalis disruptions to MUCPs in 28 women without such disruptions. Those women with disruptions in the puborectalis muscles were seen to generate lower MUCPs with voluntary pelvic muscle contractions when compared to those without the disruptions.25 Taken together, these findings would suggest that vaginal childbirth may weaken the urethral closure mechanism, thereby disposing the patient to urinary incontinence. Our group looked at the impact of childbirth on the levator ani and bladder neck in 10 nulliparas and 9 parous women, all of whom were asymptomatic with respect to pelvic floor dysfunction.26 We found that the nulliparas had a narrower levator hiatus, a higher bladder neck, and closer approximation of the puborectalis to the superior rami when compared to the parous women. In addition, all of the nulliparas had a V-shaped puborectalis (see Fig. 25.4), but 33% of the parous women had U-shaped puborectalis muscles (see Fig. 25.5b). Despite the study limitations, these results point to demonstrable anatomic changes in key pelvic floor structures, associated with childbirth.
race and pelvIc MrI fIndIngs Previous investigators have reported striking differences in the prevalence and incidence of PFD among different races.27–33 There is, however, no consensus in the medical literature on exactly how race affects the development of PFD. Anecdotally, urinary incontinence and pelvic organ prolapse may occur less often in women of African descent, when compared to Caucasians.27,34,35 Work by Handa et al.8 and Sze et al.9 suggested that bony pelvic shape, rather than race, may be a factor in the development of PFD among parous women. Our group attempted to ascertain if there were bony and soft tissue differences in pelvic geometry between well-characterized, asymptomatic nulliparous Caucasian and African– American women. In this prospective observational cohort study, we examined MRI data from two groups of nulliparous women: 12 African–American and 10 Caucasian–American.36 All were premenopausal, and had stage 0 or 1 pelvic support as defined by the POPQ system37 by examination in the supine straining position. To be eligible for inclusion, each subject had to deny pelvic floor symptoms of chronic pain, urinary incontinence, prolapse, or defecatory dysfunction. Our study data showed statistically significant increased levator ani muscle bulk among African–American nulliparas when compared to age-matched Caucasian 345
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nulliparas. In addition, the arms of the puborectalis muscle were carried closer to the superior pubic rami bilaterally, suggestive of closer, more extensive attachments between muscle and bone. The bladder neck is held higher and closer to the symphysis in the AfricanAmericans than in the Caucasians, and the pubic arch is slightly wider among the African–Americans. All levators were V-shaped. Taken collectively, these differences suggest a levator ani complex in African–American subjects that is bulkier and more intimately associated with its bony attachments. DeLancey’s group also looked at racial differences in the female continence mechanism using MRI and other techniques.38 Their study groups consisted of 18 black women and 17 white women, all young, asymptomatic nulliparas. Their data showed that the African–American women had a higher urethral volume and demonstrated higher resting and squeezing maximum urethral closure pressures, when compared to the Caucasians in the study. Whether these differences are sufficient to explain any possible differences in the rates of PFD between racial groups remains to be answered.
Furthermore, for similar appearing axial slices rotated slightly with respect to each other, identical measurements varied by up to 16%.42 These findings are illustrated in Figure 25.9. These findings suggest that in order to evaluate linear measurements on 2D images accurately, a consistent method for standardizing the slice acquisition angle must be adopted. This could be accomplished in a number of ways:
a
pItfalls In Mr-Based analysIs Magnetic resonance analysis affords excellent visualization of soft tissue relationships in the female pelvis. However, it is possible to encounter pitfalls in the interpretation of MRI studies. The attentive observer will be alert to these, and will have methods available to account for the artifacts which can occur in the acquisition of MR data. Two important pitfalls in MR-based analysis relate to the slice acquisition angle and the chemical shift artifact.
b
slice acquisition angle Magnetic resonance images are acquired in multiple parallel ‘slices’, oriented in some way with respect to the subject being scanned. This ‘angle of orientation’, or ‘slice angle’, can introduce errors in linear and angular measurements made on the acquired images. These ‘slice angle errors’ are unrelated to the actual anatomy being studied. Using data from the Visible Human project,39,40 and specialized image reslicing tools,41 our group demonstrated that identical linear measurements made on twodimensional (2D) source images can vary based solely upon the slice acquisition angle. From our simple experiments, we demonstrated measurement variations of up to 15% for slice angle variations as low as 20 degrees.
c
Figure 25.9. The relationship between slice acquisition angle and linear measurement. (a) The reference (zero degree) axial image is presented and marked to show the parameter levator hiatus. For reference (line A) and resliced (lines B, C) axes. (b) Resliced images at +10 degrees, with levator hiatus measurements marked. (c) Resliced images at –10 degrees, with levator hiatus measurements marked. (Reproduced from ref. 42 with permission.)
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• The MR slice acquisition angle could be rigorously
•
standardized with respect to a known landmark (e.g. ischial tuberosities, femoral heads). This would result in consistent slice angles across multiple scans, but would require agreement between centers regarding the standardization protocol. Examples of properly and poorly aligned axial slices are given in Figure 25.10a and 25.10b, respectively. Another method would involve reorienting (mathematically transforming) the MRI data into standardized planes after it has been acquired. This approach has the advantage of eliminating the need for exact slice alignment prior to scanning; however, it is likely that the reorienting would result in a degradation of the image quality, which might be unacceptable in some cases.
Additionally, optimal slice angle standardization would depend upon the measurement goals. For evaluating puborectalis integrity, levator hiatus width and height, a plane parallel to the puborectalis sling is optimal. An example of such a plane is shown in Figure 25.5, defined by the line running from the inferior-most point of the symphysis to the external sphincter. A sound definition of a plane that could become an accepted standard will require further assessment. To evaluate the bladder neck descent, levator plate angle, and posterior urethrovesical angle, the wellknown midsagittal plane is appropriate. However, it is important that this plane be rigorously specified in order to avoid measurement artifacts. To date, we have not been successful in using the coronal plane for making measurements. The slice angle artifact can also be overcome by converting the 2D stack into a 3D image, which can then be
a1
a2
directly measured. This option is discussed in the next section.
chemical shift artifact The second important potential MR pitfall is the socalled ‘chemical shift’ artifact. This effect can result in changes to the width of anatomic structures, depending on certain MRI scan parameters. For example, a structure on the right side of an axial slice (e.g. puborectalis) can appear to be thinner or thicker than its contralateral counterpart. For this reason, left to right thickness comparisons should not be attempted on axial or coronal scans. Furthermore, if data from multiple MR datasets are to be compared, all of the MRI scanning parameters should be established and consistent across all of the acquisitions. In order to avoid these and other potential pitfalls, it will be important to consult a trained radiologic expert, in order to define and standardize appropriate MRI scanning protocols, well before beginning any investigation involving multiple MRI datasets.
Mr IMagIng protocols While many protocols for MR image acquisition exist, we have had good success with the particular sequence publicized by Fielding,10,11 and summarized here. Prior to imaging, the patient is asked to void so that a distended bladder will not distort the adjacent anatomy. A pelvic or torso multicoil array is wrapped around the lower aspect of the pelvis, low enough to capture data from prolapsing structures. In the absence of a multicoil array, the body coil can be used. A standard axial fast spin echo sequence with the following imaging parameters is typi-
b
Figure 25.10. Variations in slice angle alignment. (a1) Well-aligned axial slice: note structural symmetry to the left and right of the symphysis at the bladder neck. (a2) Another slice taken from the femoral heads: note symmetry about the midline. (b) A misaligned MR slice: note the femoral head is seen on the right, but not on the left. This MR series was misaligned by about 12 degrees. Such misalignments can account for discrepancies in linear measurements made on MR images. 347
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cally employed: TR = 4200 ms, TE(eff) = 108 ms, 128 phase encoding steps, 24 cm field of view, 3 mm slice thickness, no gap. This sequence obtains high-resolution axial images of the puborectalis, vagina, urethra, anus and rectum, along with pubocervical fascia and fascial condensations supporting the urethra. The axial scan should encompass points 5–10 mm inferior to the ischial tuberosities, up to points 10 mm superior to the femoral heads. This scan should also include all pelvic anatomy medial to the femoral necks. To obtain rest and strain images, a midline slice 10 mm thick should include the symphysis, bladder neck, vagina, rectum, and coccyx. If all the relevant structures cannot be imaged on a single slice, two contiguous locations may be specified. The patient is then asked to Valsalva at maximum effort. Using a fast, T2-weighted imaging technique, sagittal midline images are then obtained at rest and at maximal strain. Typical imaging parameters are: TR = 10,000 ms, TE1/TE2 = 90 ms, ETL = 8, one acquisition, 10 mm section thickness, 256 phase encoding steps, 24–30 cm field of view. Using these parameters, each image is obtained in less than 3 seconds. The strain images can be repeated with additional verbal coaching if necessary. If a perineal hernia or ballooning of the puborectalis is suspected, this same series of images should be repeated in the coronal plane. T1-weighted and contrast-enhanced images are usually not required.
advanced Mr-Based technIques 3D female pelvic floor reconstruction As noted earlier, MR data are acquired and presented as ‘stacks’ of 2D images. While these stacks contain all of the information required to analyze the study, many surgeons prefer to think of pelvic anatomy in three dimensions. For this reason, Fielding and colleagues43 built MR-based 3D reconstructions of the female pelvic floor structures, as follows. Acquired MRI data were electronically transferred to a Sun UltraSparc-30 graphics computer workstation. The axial image data were segmented into anatomically significant components, including bladder, urethra, vagina, levator ani, symphysis, and coccyx, and then labeled using a combination of semi-automated and manual editing using the 3DSlicer, a computer tool developed by our group.44 A gynecologist experienced in pelvic radiologic anatomy performed the manual segmentation, which required approximately 2 hours per subject. Threedimensional surface models were generated using a pipeline consisting of dividing cubes, triangle reduction, triangle smoothing, and a surface-rendering method.45–47
The computer processing time for 3D model generation was less than 10 minutes per subject. The resulting reconstructions permitted outstanding 3D visualization of the intimate anatomic relationships in the living female pelvis for the first time. Examples of the 3D reconstructions are given in Figure 25.11a (dorsal lithotomy view) and 25.11b (left sagittal view). The reconstructed 3D models also permitted linear, angular, and volumetric measurements to be made, allowing parametric comparison between groups of MR datasets.10,11,48 The 3D reconstructions have also proven useful in planning surgical interventions for gynecologic49,50 and obstetric51 applications. Public domain tutorials (including videos) of MR-based female pelvic reconstruction may be found at http://splweb.bwh.harvard.edu:8000/ pages/ppl/lennox/tutorial/img0.html. Cornella et al.52 also used the 3DSlicer to reconstruct 3D models of the external anal sphincter in 10 healthy nulliparous women who also underwent anal manometry. They were able to visualize the external sphincter as a funnel-shaped structure, with the internal sphincter appearing more cylindrical. Both sphincters appeared somewhat elongated in the anteroposterior dimension. They also found that the volume of the internal anal sphincter was correlated with the length of the highpressure zone at squeeze. This group also noted very high interrater reliability of the sphincter volume measurements, with a 95% confidence interval of 94–98% for external and internal sphincter volume assessment. In these and other applications, the 3D reconstructions permitted improved visualization of the pelvic floor structures, leading to a better appreciation of the pelvic anatomy. It also afforded straightforward evaluation of the volumes and complex linear measurements on the reconstructured structures when compared to the 2D MR source images.
color thickness mapping MR-based segmentations have also been used to generate color maps of the levator ani, with the color varying according to the muscle thickness at each point. This color thickness mapping technique consists of a computer algorithm which was first used by Fielding et al. to detect bladder tumors, based on wall thickness variations.53 When this technique was adapted to study the levator ani muscles,54 it demonstrated thinning of the puborectalis muscle in female stress incontinent and prolapse subjects when compared to asymptomatics. The technique can be used to evaluate thickness variations among large groups of levator muscles. An example of a color-mapped levator is illustrated in Figure 25.12.
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a
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Figure 25.12. An example of an MRI-based color-mapped levator. (a) A reconstructed levator is shown in brown, with the symphysis (S). Views of the front, left, and right sides are shown. In the front view, the inner layer faces the label I, and the outer layer faces the label O. (b) Three views of a colormapped levator are shown. The color bar on the left shows the thickness (in millimeters) corresponding to the colors seen. (Reproduced from ref. 54 with permission.)
pelvic floor childbirth simulation
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Figure 25.11. Representative 3D reconstructions from a young nullipara. (a) Viewed in the dorsal lithotomy position. (b) Left sagittal view, with bones and obturator removed. (c) Posterior view, with bladder removed. (Color legend: Pubic bones, white; Obturator internus, rose; Urethra and bladder, yellow; Vagina, pink; Levator, brown; Symphysis and coccyx, gray.)
MR imaging has also been used to generate pelvic floor models for childbirth simulation. DeLancey’s group used MR-based information from a 32-year old nulliparous woman in order to build a simulation model of the bony pelvis and levator ani, through which they simulated passage of a fetal head as in vaginal childbirth.55 Their results showed stretching of all portions of the levator muscle, with maximum stretch of 300% occurring in a band of the muscle corresponding to the pubococcygeus portion. This was the same portion of levator found on other studies to be intact in nulliparas, but disrupted in 20% of their primiparous subjects. Ongoing work in this area will likely yield improved insights into the mechanisms of childbirthrelated pelvic floor injury. An example of the childbirth 349
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simulation at the point of cranial delivery is illustrated in Figure 25.13.
tools for processing and evaluating MrI data The analysis of MRI and other imaging data was previously limited by the need to use expensive, specialized hardware to view the acquired MR images. With the advent of ever more powerful personal computers, software tools for viewing MR images on personal computers have become available. With inexpensive, standardized storage afforded by CD-ROMs, and flash memory disks, the MR data can be moved easily from the MR scanner to most personal computers for viewing and analysis. For research purposes, our group has developed and evolved a comprehensive, public domain, PC-based software tool (3DSlicer) to support all aspects of MR and CT image analysis.44 The 3DSlicer can be used for visualization, measurement, segmentation, 3D reconstruction, animation, and recording of images based on MR or CT data. It is available for download at no charge at www.slicer.org for Windows™, Macintosh™, and other computing platforms. The 3DSlicer is user friendly, and reads many commercial MR image data formats from standard media (e.g. CD-ROM). Examples of 3DSlicer interactive windows are shown in Figure 25.14. This tool has proven instrumental in permitting analysis of large groups of MR datasets.
conclusIon Magnetic resonance imaging has afforded a closer view into the anatomy and interactions of the female pelvic structures in living women. Advanced processing techniques have further improved visualization and enabled simulation models to be built and tested. This work will continue to be built upon. Most of the work in pelvic MRI to date has been performed with MR images acquired in the supine position. Images may also be acquired with the subject in the sitting position, at some cost in image resolution. Such upright imaging may better capture the effects of gravity. In addition, more powerful MR scanners are becoming available, and will undoubtedly offer higher resolution images, and perhaps better views of the pelvic connective tissues, to further elucidate their role in supporting the pelvic viscera.
Figure 25.13. An MRI-based childbirth simulation at the point of cranial delivery. Simulated effect of fetal head descent on the levator ani muscles in the second stage of labor. At top left, a left lateral view shows the fetal head (blue) located posteriorly and inferioly to the public symphysis (PS) in front of the sacrum (S). The sequence of five images at left show the fetal head as it descends 1.1, 2.9, 4.7, 7.9, and 9.9 cm below the ischial spines as the head passes along the curve of Carus (indicated by the transparent, light blue, curved tube). The sequence of five images at right are front -left, three-quarter views corresponding to those shown at left. (Reproduced from ref. 55 with permission; © Biomechanics Research Lab, University of Michigan, Ann Arbor.)
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Figure 25.14. Interactive windows from the 3DSlicer (www.slicer.org). (a) The 3D window (top), and the axial, sagittal, and coronal 2D windows (bottom). (b) The 2D windows (bottom), with selected anatomic structures outlined.
references 1. Strohbehn K, Ellis J, Strohbehn JA, DeLancey JOL. Magnetic resonance imaging of the levator ani with anatomic correlation. Obstet Gynecol 1996;87:277–85. 2. Huddleston HT, Dunnihoo DT, Huddleston PM III, Meyers PC. Magnetic resonance imaging of defects in DeLancey’s support levels I, II, and III. Am J Obstet Gynecol 1995;172:1778–84. 3. Kirshner-Hermanns R, Wein B, Niehaus S, Schaeffer W, Jakse G. The contribution of magnetic resonance imaging of the pelvic floor to the understanding of urinary incontinence. Br J Urol 1993;72:715–18. 4. Fielding JR, Griffiths DJ, Versi E, Mulkern RV, Lee MLT, Jolesz FA. MR imaging of pelvic floor continence mechanisms in the supine and upright positions. Am J Radiol 1998;171:1607–10. 5. Tunn R, DeLancey JOL, Howard D, Ashton-Miller J, Quint LE. Anatomic variations in the levator ani muscle, endopelvic fascia, and urethra in nulliparas evaluated by magnetic resonance imaging. Am J Obstet Gynecol 2003;188:116–21. 6. Klutke C, Golomb J, Barbaric Z, Raz S. The anatomy of stress incontinence: magnetic resonance imaging of the female bladder neck and urethra. J Urol 1990;143:563–6. 7. Tunn R, DeLancey JOL, Quint LE. Visibility of pelvic organ support system structures in magnetic resonance images without an endovaginal coil. Am J Obstet Gynecol 2001;184:1156–63. 8. Handa VL, Pannu HK, Siddique S, Gutman R, Vanrooyen J, Cundiff G. Architectural differences in the bony pelvis of women with and without pelvic floor disorders. Obstet Gynecol 2003;102:1283–90. 9. Sze EHM, Kohli N, Miklos JR, Roat T, Karram MM. Computed tomography comparison of bony pelvis dimensions
between women with and without genital prolapse. Obstet Gynecol 1999;93:229–32. 10. Fielding JR, Dumanli H, Schreyer A et al. MR-based three dimensional modeling of the normal pelvic floor in women: quantification of muscle mass. Am J Radiol 2000;174:657–60. 11. Hoyte L, Schierlitz L, Zou K, Flesh G, Fielding JR. Two and 3 dimensional MRI comparison of levator ani structure, volume and integrity in women with stress incontinence and prolapse. Am J Obstet Gynecol 2001;185:11–19. 12. Aronson MP, Bates SM, Jacoby AF, Chelmow D, Sant GR. Periurethral and paravaginal anatomy: an endovaginal magnetic resonance imaging study. Am J Obstet Gynecol 1995;173:1702–8; discussion 1708–10. 13. Umek WH, Kearney R, Morgan DM, Ashton-Miller JA, DeLancey JO. The axial location of structural regions in the urethra: a magnetic resonance study in nulliparous women. Obstet Gynecol 2003;102:1039–45. 14. Gregory WT, Lou J, Stuyvesant A, Clark AL. Quantitative electromyography of the anal sphincter after uncomplicated vaginal delivery. Obstet Gynecol 2004;104:327–35. 15. Snooks SJ, Swash M, Mathers SE, Henry MM. Effect of vaginal delivery on the pelvic floor: a 5-year follow-up. Br J Surg 1990;77:1358–60. 16. Dietz HP, Bennett MJ. The effect of childbirth on pelvic organ mobility. Obstet Gynecol 2003;102:223–8. 17. DeLancey JOL, Kearney R, Chou Q, Speights S, Binno S. The appearance of levator ani muscle abnormalities in magnetic resonance images after vaginal delivery. Obstet Gynecol 2003;101:46–53. 18. Allen RE, Hosker GL, Smith ARB, Warrel DW. Pelvic floor damage and childbirth: a neurophysiological study. Br J Obstet Gynaecol 1990;97:770–9.
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19. Menacker F, Curtin SC. Trends in cesarean birth and vaginal birth after previous cesarean. Natl Vital Stat Rep 2001;49:1–16. 20. Martin JA, Park MM, Sutton PD. Births: preliminary data for 2001. Natl Vital Stat Rep 2002;50:1–20. 21. Hendrix SL, Clark AM, Nygaard I, Aragaki A, Barnabei V, McTiernan A. Pelvic organ prolapse in the Women’s Health Initiative: gravity and gravidity. Am J Obstet Gynecol 2002;186:1160–6. 22. Madoff RD, Williams JG, Caushaj PF. Fecal incontinence. N Engl J Med 1992;326:1002–7. 23. Rortveit G, Daltveit AK, Hannestad YS, Hunskaar S. Urinary incontinence after vaginal delivery or cesarean section. N Engl J Med 2003;348:900–7. 24. Buchsbaum GM, Chin M, Glantz C, Guzick D. Prevalence of urinary incontinence and associated risk factors in a cohort of nuns. Obstet Gynecol 2002;100:226–9. 25. Miller JM, Umek WH, DeLancey JO, Ashton-Miller JA. Can women without visible pubococcygeal muscle in MR images still increase urethral closure pressures? Am J Obstet Gynecol 2004;191:171–5. 26. Hoyte L, Jakab M, Shott S, Brubaker L. Does your bony pelvic shape determine your soft tissue destiny? Results from a 3D MRI study. International Continence Society Meeting August 2004; Paris, France. 27. Bump RC. Racial comparisons and contrasts in urinary incontinence and pelvic organ prolapse. Obstet Gynecol 1993;81:421–5. 28. Duong TH, Korn AP. A comparison of urinary incontinence among African–American, Asian, Hispanic, and white women. Am J Obstet Gynecol 2001;184:1083–6. 29. Grodstein F, Fretts R, Lifford K, Resnick N, Curhan G. Association of age, race, and obstetric history with urinary symptoms among women in the nurses’ health study. Am J Obstet Gynecol 2003;189:428–34. 30. Hendrix SL, Clark A, Nygaard I, Aragaki A, Barnabei V, McTiernan A. Pelvic organ prolapse in the women’s health initiative: gravity and gravidity. Am J Obstet Gynecol 2002;186:1160–6. 31. Klingele CJ, Carley ME, Hill RF. Patient characteristics that are associated with urodynamically diagnosed detrusor instability and genuine stress incontinence. Am J Obstet Gynecol 2002;186:866–8.
35. Howard D, DeLancey JOL, Tunn R, Ashton-Miller JA. Racial differences in the structure and function of the stress urinary continence mechanism. Obstet Gynecol 2000;95:713–17. 36. Hoyte L, Thomas J, Foster RT, Shott S, Jakab M, Weidner AC. Racial differences in pelvic geometry among asymptomatic nulliparas as seen on three-dimensional MR images. Am J Obstet Gynecol 2005; 2005 Annual Meeting, Society of Gynecologic Surgeons. 37. Bump RC, Mattiasson ABK, Brubaker LP et al. The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 1996;175:10–17. 38. Howard D, DeLancey JO, Tunn R, Ashton-Miller JA. Racial differences in the structure and function of the stress urinary continence mechanism. Obstet Gynecol 2000;95:713–7. 39. Hersch RD, Gennart B, Figueiredo O et al. The visible human slice web server: a first assessment. Proceedings IS&T/SPIE Conference on Internet Imaging. San Jose, CA, 2000 (vol 3964). 40. Spitzer V, Whitlock DG. The visible human dataset: the anatomical platform for human simulation. Anat Rec (New Anatomist) 1998;253:49–57. 41. Messerli V, Figueiredo O, Gennart B, Hersch RD. Parallelizing I/O intensive image access and processing applications. IEEE Concurrency 1999;7:28–37. 42. Hoyte L, Ratiu P. Linear measurements in 2-dimensional pelvic floor imaging: the impact of slice tilt angles on measurement reproducibility. Am J Obstet Gynecol 2001;185:537–44. 43. Fielding J, Ratiu P, Hoyte L, Versi E, Mamisch C, Kikinis R. Three-dimensional MR-based imaging of the female pelvic floor in vivo. Annual meeting, Radiologic Society of North America, Chicago, 1997. 44. Gering DT, Nabavi A, Kikinis R et al. An integrated visualization system for surgical planning and guidance using image fusion and interventional imaging. Second International Conference on Medical Image Computing and Computer-assisted Interventions (MICCAI). Cambridge, U.K, 1999. 45. Lorensen W, Cline H. Marching cubes: a high resolution 3D surface construction algorithm. Comput Graph 1987;21:163–89.
32. Knobel J. Stress incontinence in the black female. S Afr Med J 1975;49:430–2.
46. Schroeder WZJ, Lorenson W. Decimation of triangle meshes. Comput Graph 1992;26:65–70.
33. Vandongen L. The anatomy of genital prolapse. S Afr Med J 1981;60:657–9.
47. Taubin G. Curve and surface smoothing without shrinkage. IBM Research Report 1994; RC-19536.
34. Sampselle CM, Harlow SD, Skurnick J, Brubaker L, Bondarenko I. Urinary incontinence predictors and life impact in ethnically diverse perimenopausal women. Obstet Gynecol 2002;100:1230–8.
48. Singh K, Jakab M, Reid WM, Berger LA, Hoyte L. Threedimensional magnetic resonance imaging assessment of levator ani morphologic features in different grades of prolapse. Am J Obstet Gynecol 2003;188:910–5.
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49. Hoyte L, Lu K, Muto M, Nucci M, Versi E, Kikinis R, Fielding JR. Magnetic resonance imaging based three dimensional modeling of a complex vulvar tumor as a component of presurgical planning. J Women’s Imaging 2000;2:138–40. 50. Hundley AF, Fielding JR, Hoyte L. Double cervix and vagina with septate uterus: an uncommon mullerian. Obstet Gynecol 2001;98:982–5. 51. Norwitz ER, Hoyte LPJ, Jenkins K et al. Conjoined twins with twin reversed arterial perfusion sequence: a novel technique for antenatal surgical planning. N Engl J Med 2000;343(6):399–402. 52. Cornella JL, Hibner M, Fenner DE, Kriegshauser JS, Hentz J, Magrina JF. Three-dimensional reconstruction
of magnetic resonance images of the anal sphincter and correlation between sphincter volume and pressure. Am J Obstet Gynecol 2003;189:130–5. 53. Fielding JR, Hoyte L, Okon S et al. Tumor detection by virtual cystoscopy with color mapping of bladder wall thickness. J Urol 2002;167:559–62. 54. Hoyte L, Jakab M, Warfield SK, Shott S, Flesh G, Fielding JR. Levator ani thickness variations in symptomatic and asymptomatic women using magnetic resonance-based 3-dimensional color mapping. Am J Obstet Gynecol 2004;191:856–61. 55. Lien K-C, Mooney B, DeLancey JOL, Ashton-Miller JA. Levator ani muscle stretch induced by simulated vaginal birth. Obstet Gynecol 2004;103:31–40.
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IntroductIon The increasing availability of ultrasound and magnetic resonance imaging equipment has, over the last decade in particular, triggered a renewed interest in diagnostic imaging in urogynecology and female urology. Largely as a result of cost and access problems, MRI has been of limited clinical use in the evaluation of pelvic floor disorders, and slow acquisition speeds have until very recently precluded dynamic imaging. Ultrasound, on the other hand, is almost universally available and provides for real-time observation of maneuvers. This chapter will consider pelvic floor ultrasound, i.e. the use of this imaging modality for the investigation of women with symptoms of lower urinary tract dysfunction and prolapse. While ultrasound is also useful for transabdominal bladder imaging (e.g. for determining residual urine) and for the investigation of upper tract disorders, these indications are covered elsewhere. For general information on ultrasound imaging the reader is referred to current textbooks.1
2d PelvIc Floor ultrasound Basic methodology Translabial or transperineal ultrasound, first described in the mid to late 1980s,2–4 is the most commonly used modality at present and will be the focus of this text. Most statements about this technique also apply to introital ultrasound, which implies the use of an endocavitary transducer held in the introitus. A midsagittal view is obtained by placing a transducer (usually a 3.5–7 MHz curved array) on the perineum (Fig. 26.1) after covering the transducer with a glove or Gladwrap or similar. Powdered gloves can markedly impair imaging quality and should be avoided. Imaging can be performed in dorsal lithotomy, with the hips flexed and slightly abducted, or in the standing position. Bladder filling should be specified; for some applications prior voiding is preferable. The presence of a full rectum may impair diagnostic accuracy and sometimes necessitates a repeat assessment after defecation. Parting of the labia often improves image quality, especially in very obese women, labial hypertrophy or in the presence of hair. The transducer can generally be placed quite firmly against the symphysis pubis without causing significant discomfort. The resulting image includes the symphysis anteriorly, the urethra and bladder neck, the vagina, cervix, rectum, and anal canal (Fig. 26.1). Posterior to the anorectal junction a hyperechogenic area indicates the central portion of the levator plate, i.e. the puborectalis
Figure 26.1. Field of vision for translabial/perineal ultrasound, midsagittal plane. Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: Part 1: 2D aspects. Ultrasound Obstet Gynecol 2004;23:80–92 with permission of John Wiley & Sons, Ltd, New York (Publishers). muscle. The cul de sac may also be seen, filled with a small amount of fluid, echogenic fat or peristalsing small bowel. Imaging quality seems to depend on hydration of tissues, with best resolutions achieved in late pregnancy. Imaging quality is lowest in very elderly women with marked urogenital atrophy. There has been disagreement regarding image orientation in the midsagittal plane. Some prefer image orientation as in the standing patient facing right5 which requires image inversion on the ultrasound system, an option that is not universally available. Others (including the author) prefer an orientation showing cranioventral aspects to the left and dorsocaudal aspects to the right. This disagreement is reminiscent of the situation regarding transvaginal ultrasound where practitioners in North America and Australasia use a different orientation compared to their colleagues in Europe. A minimal consensus may be to limit oneself to orientations that can be converted to the other by simply rotating the image by 180 degrees, without requiring mirroring. Perineal ultrasound of the lower urinary tract yields information equivalent or superior to the lateral urethrocystogram (Fig. 26.2) or fluoroscopic imaging. Comparative studies have mostly shown good correlations between radiologic and ultrasound data.4,6–10 One remaining advantage of X-ray fluoroscopy may be the ease with which the voiding phase can be observed, although some investigators have used specially
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constructed equipment to document voiding with ultrasound.11
Bladder neck position and mobility
Figure 26.2. Lateral urethrocystogram with bead chain outlining the urethra. The images are rotated by 180 degrees to allow comparison with standard translabial ultrasound views. Image on left is at rest, on right during Valsalva. Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: Part 1: 2D aspects. Ultrasound Obstet Gynecol 2004;23:80–92 with permission of John Wiley & Sons, Ltd, New York (Publishers).
Bladder neck position and mobility can be assessed with a high degree of reliability. Points of reference are the central axis of the symphysis pubis12 or its inferoposterior margin.10 The latter is the simpler and more practical technique, especially in older women in whom the interpubic disk is not sonolucent, making determination of the central axis more difficult. However, use of the inferoposterior margin for reference risks the introduction of an angle error unless care is taken to avoid angling the transducer during Valsalva. In practice, one should make sure the appearance of the symphysis pubis does not vary markedly between images taken at rest and on Valsalva. Imaging can be undertaken supine or erect, and with a full or empty bladder. The full bladder is less mobile than the empty organ13 and may prevent complete development of pelvic organ prolapse. In the standing posi-
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Figure 26.3. Perineal ultrasound image (a) and line drawing (b) illustrating some of the measured parameters (distances between bladder neck and symphysis pubis: craniocaudal coordinates x-r, x-s; dorsoventral coordinates y-r, y-s; bladder neck descent [BND] equals x-r – x-s, urethral rotation and retrovesical angle [RVA]). Reproduced from Dietz HP, Hansell N, Grace M, Eldridge A, Clarke B, Martin N. Bladder neck mobility is a heritable trait. Br J Obstet Gynaecol 2005;112:334–339 with permission of Blackwell Publishing. 357
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tion, the bladder is situated lower at rest but descends about as far as in the supine patient on Valsalva.14 In either patient position, it is essential not to exert undue pressure on the perineum so as to allow full development of pelvic organ descent. Measurements are generally performed at rest and on Valsalva maneuver. The difference between these two measurements yields a numerical value for bladder neck descent (Fig. 26.3). On Valsalva, the proximal urethra may be seen to rotate in a posteroinferior direction. The extent of rotation can be measured by comparing the angle of inclination between the proximal urethra and any other fixed axis, or by measuring the angle between the urethral axis at rest and its equivalent on Valsalva (Fig. 26.3). Some investigators measure the retrovesical (or posterior urethrovesical) angle between the proximal urethra and the trigone;15 others determine the angle between the central axis of the symphysis pubis and a line from the inferior symphyseal margin to the bladder neck.8,16 The reproducibility of bladder neck descent as illustrated in Figure 26.3 has recently been assessed,17 with a coefficient of variation (% CV) of 0.16 between multiple effective Valsalva maneuvers, a % CV of 0.21 for interobserver variability, and a % CV of 0.219 for a test–retest series at an average interval of 46 days. Intraclass correlation coefficients were between 0.75 and 0.98, indicating ‘excellent’ agreement.17 There is no definition of ‘normal’ for bladder neck descent. A number of factors – such as bladder and bowel filling, position, and patient cooperation – can influence measurements. It is occasionally quite difficult to obtain an effective Valsalva maneuver, especially in nulliparous women with high levator tone. If a prolapse is suspected in a symptomatic woman, assessment in the
standing position may be necessary. Perhaps not surprisingly, publications to date have presented widely differing reference measurements in nulliparous women.18–20 The author has obtained bladder neck descent measurements of 1.2–40.2 mm (mean 17.3 mm) in a group of 106 stress continent nulligravid young women of 18–23 years of age.21 It is likely that methodologic differences such as patient position, bladder filling, and quality of Valsalva maneuver (i.e. controlling for confounders such as concomitant levator activation) account for the above-mentioned discrepancies. Attempts at standardizing Valsalva maneuvers have not found widespread application since this requires intra-abdominal pressure measurement, i.e. a rectal balloon catheter.22,23 Other methods, such as the use of a spirometer, are likely to lead to suboptimal Valsalva maneuvers; the pressures used in the one study describing the use of such a device were clearly insufficient to achieve even near-maximal descent.22 The etiology of increased bladder neck descent is likely to be multifactorial. The wide range of values obtained in young nulliparous women suggests a congenital component, and a recently published twin study has confirmed a high degree of heritability for anterior vaginal wall mobility.24 Vaginal childbirth25–27 is probably the most significant environmental factor, with a long second stage of labor and vaginal operative delivery being associated with increased postpartum descent.27 Figure 26.4 shows a primiparous woman with markedly increased bladder neck descent (from 6 to 38 mm) after a vacuum delivery for failure to progress in the second stage. This association between increased bladder descent and vaginal parity is also evident in older women with symptoms of pelvic floor dysfunction.28 In another interesting development, the hypothesis that progress in
Figure 26.4. The effect of a vacuum delivery for failure to progress in second stage (136 min) in a primiparous woman. The first pair of images demonstrates excellent bladder neck support (BND = 6 mm), the second pair shows marked rotation and descent of the bladder neck (BND = 38 mm). Reproduced from Dietz HP, Bennett, MJ. The effect of childbirth on pelvic organ mobility. Obstet Gynecol 2003;102:223–228 with permission of Lippincott, Williams & Wikins. 358
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Figure 26.5. A typical finding in a patient with stress incontinence and anterior vaginal wall descent (cystourethrocele Grade I–II): posteroinferior rotation of the urethra, opening of the retrovesical angle to 180 degrees, funneling of the proximal urethra (arrowhead) and bladder neck descent of over 40 mm. Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: Part 1: 2D aspects. Ultrasound Obstet Gynecol 2004;23:80–92 with permission of John Wiley & Sons, Ltd, New York (Publishers). labor is not independent of pelvic floor biomechanics29 has been confirmed: anterior vaginal wall mobility on Valsalva was found to be a potential predictor of progress in labor in two independent studies.30,31
Funneling In patients with stress incontinence, but also in asymptomatic women,32 funneling of the internal urethral meatus may be observed on Valsalva (Fig. 26.5) and sometimes even at rest. Funneling is often associated with the sensation of impending or actual leakage. Other indirect signs of urine leakage on B-mode real-time imaging are weak grayscale echoes (‘streaming’) and the appearance of two linear (‘specular’) echoes defining the lumen of a fluid-filled urethra. However, funneling may also be observed in urge incontinence and cannot be used to prove urodynamic stress incontinence. Marked funneling has been shown to be associated with poor urethral closure pressures.33,34 Funneling is a finding that may occur with or without significant anterior vaginal wall descent or cystocele. If it is seen without descent we assume that stress incontinence is likely to be due to intrinsic sphincter deficiency. On the other hand, significant anterior compartment descent often occurs without funneling (Fig. 26.6). Women with a large cystocele and absent funneling often have an intact retrovesical angle and urethral kinking, resulting in voiding dysfunction
Figure 26.6. A large cystocele with intact retrovesical angle. Note the absence of funneling. There is very marked urethral rotation of about 140 degrees on Valsalva, as well as urethral kinking. rather than incontinence. This is not surprising when one considers the marked urethral distortion documented in Figure 26.6.
color doppler Color Doppler ultrasound has been used to demonstrate urine leakage through the urethra on Valsalva maneuver or coughing.35 This method yielded satisfactory results with or without an indwelling catheter. Agreement between color Doppler and fluoroscopy was very high in a controlled group with indwelling catheters and identical bladder volumes.36 Both velocity (CDV, Fig. 26.7) and energy mapping (CDE, Fig. 26.8) were able to document leakage. As a result, routine sonographic documentation of stress incontinence during urodynamic testing has become feasible. Color Doppler imaging may also facilitate the documentation of leak point pressures.37 Whether this is in fact desired will depend on the clinician and their preferences.
Bladder wall thickness There has recently been renewed interest in the quantification of detrusor wall thickness (DWT) by transvaginal and/or translabial ultrasound almost a decade after the original description of the technique.38 Measurements are obtained after bladder emptying and perpendicular to the mucosa (see Fig. 26.9 for a case of marked bladder wall thickening). Usually three sites are assessed: anterior wall, trigone, and dome of the bladder, and the mean of all three is calculated. Another option is to mea359
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Figure 26.7. Color Doppler ultrasound (CDV) demonstrating urine leakage (arrowhead) through the urethra on Valsalva maneuver. Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: Part 1: 2D aspects. Ultrasound Obstet Gynecol 2004;23:80–92 with permission of John Wiley & Sons, Ltd, New York (Publishers).
Figure 26.9. Measurement of bladder wall thickness in a patient with symptoms of an overactive bladder and detrusor instability on urodynamic testing, parasagittal view. Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: Part 1: 2D aspects. Ultrasound Obstet Gynecol 2004;23:80–92 with permission of John Wiley & Sons, Ltd, New York (Publishers). Detrusor hypertrophy as described by detrusor wall thickness seems to be acquired, as a study on young nulliparous women showed no measurement over the cut-off of 5 mm.43 It remains to be seen whether determination of this parameter can add any useful clinical information to the workup of a patient with pelvic floor and bladder dysfunction. Nonetheless, it appears obvious that detrusor hypertrophy as a pathophysiologic factor deserves more attention.
Figure 26.8. CD energy (CDE) imaging in genuine stress incontinence. The Doppler signal outlines most of the proximal urethra. Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: Part 1: 2D aspects. Ultrasound Obstet Gynecol 2004;23:80–92 with permission of John Wiley & Sons, Ltd, New York (Publishers). sure the dome in three locations and use the mean. A bladder wall thickness of over 5 mm appears to be associated with symptoms and signs of the overactive bladder,38–40 although the association may not be as strong as originally claimed.41 Increased bladder wall thickness probably signifies hypertrophy of the detrusor muscle;42 this may be the cause of symptoms or simply the effect of an underlying abnormality. While bladder wall thickness on its own seems only moderately predictive of detrusor overactivity, the method may be clinically useful when combined with symptoms of the irritable bladder.42
levator activity Perineal ultrasound has been used for the quantification of pelvic floor muscle activity, both in women with stress incontinence and in continent controls,44 as well as before and after childbirth.45,46 A cranioventral shift of pelvic organs imaged in a sagittal midline orientation is taken as evidence of a levator contraction (Fig. 26.10). The resulting displacement of the internal urethral meatus is measured relative to the inferoposterior symphyseal margin, as for bladder neck descent. The method can also be utilized for pelvic floor muscle exercise teaching by providing visual biofeedback.47 The technique has helped validate the concept of ‘the knack’, i.e. of a reflex levator contraction immediately prior to increases in intra-abdominal pressure such as those resulting from coughing.48 Correlations between a cranioventral shift of the bladder neck on the one hand
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Figure 26.10. Quantification of levator contraction: cranioventral displacement of the bladder neck is measured relative to the inferoposterior symphyseal margin. The measurements indicate 5 (33.8–28.8) mm of cranial displacement and 8.9 (7.5– -1.4) mm of ventral displacement of the bladder neck. and palpation/perineometry on the other, have been shown to be good.49
Prolapse quantification Translabial ultrasound can demonstrate uterovaginal prolapse.50,51 The inferior margin of the symphysis pubis serves as a line of reference against which the maximal descent of bladder, uterus, cul de sac, and rectal ampulla on Valsalva maneuver can be measured (Fig. 26.11). When ultrasound findings were compared to clinical staging and a standardized prolapse assessment according to criteria developed by the International Continence Society,52 good correlations were obtained for the anterior and central compartments.53 Different degrees of cystocele are shown in Figures 26.3–26.6. Figure 26.12 shows first degree uterine descent after Burch colposuspension. While correlations between posterior compartment clinical assessment and ultrasound are weaker, it is possible to distinguish between a ‘true’ and a ‘false’ rectocele, i.e. a fascial defect of the rectovaginal septum (Fig. 26.13) and perineal hypermobility without fascial defects.54 True rectoceles may be present in young nulliparous women55 but are more common in the parous. From imaging experience to date, fascial defects almost always appear to arise in the same area, i.e. very close to the anorectal junction, and most commonly are transverse and symmetrical. Many are asymptomatic. Hopefully the identification of such posterior compartment fascial defects will allow better
Figure 26.11. Ultrasound quantification of uterovaginal prolapse. The inferior margin of the symphysis pubis serves as a line of reference against which the maximal descent of bladder, uterus, cul de sac and rectal ampulla on Valsalva maneuver can be measured. Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: Part 1: 2D aspects. Ultrasound Obstet Gynecol 2004;23:80–92 with permission of John Wiley & Sons, Ltd, New York (Publishers).
Figure 26.12. First degree uterine descent in a patient after Burch colposuspension. The latter is evident as a ridge-like deformation of the trigone (arrow), posterior to the internal urethral meatus. Image on left is at rest, right on Valsalva. Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: Part 1: 2D aspects. Ultrasound Obstet Gynecol 2004;23:80–92. With permission of John Wiley & Sons, Ltd, New York (Publishers). surgical management in the future, since enterocele can easily be distinguished from rectocele (see Fig. 26.14 for a patient showing both an enterocele and a rectocele). 361
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Figure 26.13. First degree rectocele in a 23-year-old nulliparous asymptomatic volunteer. The anal canal is seen to the right of both images, with a small rectocele clearly visible on Valsalva (right). The width and depth of the rectocele is measured relative to the anal canal.
Figure 26.15. Urethral diverticulum (arrow), herniating downwards and clinically simulating a cystourethrocele on Valsalva maneuver. The neck of the diverticulum is seen close to the bladder neck. Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: Part 1: 2D aspects. Ultrasound Obstet Gynecol 2004;23:80–92 with permission of John Wiley & Sons, Ltd, New York (Publishers). success of the procedure, and may also predict complications such as voiding dysfunction.16,58 Postoperative irritative symptoms may be due to overelevation or trigonal distortion, although there is no agreement on this issue.59–61 Some authors advocate the use of ultrasound to help with intraoperative adjustment of elevation.62
Figure 26.14. Rectoenterocele after Burch colposuspension, at rest (left) and on Valsalva maneuver (right). Usually, enteroceles (filled by peristalsing small bowel, epiploic fat or omentum) appear more homogeneous and nearly isoechoic, whereas the rectocele is filled by a stool bolus, resulting in hyperechogenicity with distal shadowing. Reproduced from Dietz HP, Steensma AB. Posterior compartment prolapse on 2D and 3D pelvic floor ultrasound: the distinction between true rectocele, perineal hypermobility and enterocele. Ultrasound Obstet Gynaecol 2005;26(1):73–77 with permission of John Wiley & Sons, Ltd, New York (Publishers). Occasionally, other conditions may mimic prolapse, such as a urethral diverticulum that may clinically appear as a cystocele (Fig. 26.15).
Findings after anti-incontinence surgery Abdominal Burch colposuspension almost always results in the typical findings of permanent bladder neck elevation and trigonal distortion (Fig. 26.12).56,57 The degree of elevation or overelevation appears important for the
Laparoscopic colposuspension results in sonoanatomic changes that are generally indistinguishable from open colposuspension.63 Elevation may be less permanent, possibly due to less effective scar formation.64 Urethropexies, on the other hand, do not cause trigonal distortion as sutures are more distally placed, and cystocele recurrence is more likely.65 Bladder neck needle suspensions and bone anchor procedures appear to result in less elevation of the bladder neck and faster recurrence of hypermobility. Traditional anterior repairs are even less effective in this regard, and while immediate postoperative results often look encouraging, recurrence of hypermobility is very common. Traditional fascial slings such as the Aldridge-type slings usually result in effective immobilization of the bladder neck, and the fascial implant remains visible for many years. The same is true for synthetic slings such as the Silastic implants. Conversely, the ‘sling-on-a-string’ – a fascial patch on Prolene sutures – often becomes invisible over time. This is frequently associated with recurrent hypermobility, probably as a result of suture pull-through.
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Ultrasound has contributed significantly to the investigation of new surgical procedures such as the recently developed loose-weave suburethral Prolene slings. It is superior to MRI for this indication as the currently available synthetic slings are easily visualized posterior to the urethra66–70 (Fig. 26.16). Ultrasound has helped clarify the mode of action of these procedures, i.e. urethral kinking or ‘dynamic compression’ against the posterior surface of the symphysis pubis.66 Loose-weave monofilament meshes such as tension-free vaginal tape (TVT) or suprapubic arc sling (SPARC) are more echogenic than more tightly woven multifilament implants such as the intravaginal slingplasty (IVS), but all can be identified and followed in their course from the pubic rami laterally to the urethra centrally71 (Fig. 26.17).
Ultrasound has demonstrated the wide margin of safety and efficacy of such tapes as regards placement which explains their extraordinary success72 and allayed concerns regarding tape shrinkage and tightening due to scar formation.73 Some authors have hypothesized that a midurethral location is preferable to distal or proximal tape placement. The assessment of bladder neck mobility before implantation of a suburethral sling may predict success or failure,74 an observation that makes perfect sense when one considers that dynamic compression relies on relative movement of implant and native tissues. Ultrasound can also detect paraurethral implants although the correlation between sonographic appearance and success is poor (Fig. 26.18). Finally, sonographic imaging seems similarly useful in evaluating the effect of pessaries and/or bladder neck support prostheses, and may be of help in optimizing the design of such devices.75
other findings
Figure 26.16. Synthetic implants such as the tension-free vaginal tape (TVT) or suprapubic arc sling (SPARC) are easily visualized as highly echogenic structures posterior to the urethra. The images illustrate tape position relative to the symphysis pubis and urethra at rest (left) and on Valsalva (right). Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: Part 1: 2D aspects. Ultrasound Obstet Gynecol 2004;23:80–92 with permission of John Wiley & Sons, Ltd, New York (Publishers).
A range of other abnormalities, incidental or expected, may at times be detected on translabial ultrasound although a full pelvic ultrasound assessment does of course require a transvaginal approach. Urethral diverticula76,77 (Fig. 26.15), strictures,78 fistulae,79 Gartner duct cysts (Fig. 26.19) or bladder tumors (Fig. 26.20) may be identified, and intravesical stents and bladder diverticula can also be visualized.5 Hyperechoic foci are a common finding within the hypoechoic area representing the urethral mucosa and rhabdosphincter, but do not seem to be associated with any particular symptoms or problems.80 Postoperative hematomata (Fig. 26.21) may be visible after vaginal surgery or TVT, and may at times explain clinical symptoms such as voiding dysfunction or persistent pain.
Figure 26.17. A comparison of tension-free vaginal tape (TVT), suprapubic arc sling (SPARC) and intravaginal slingplasty (IVS) (left to right) on midsagittal imaging. Reproduced from Dietz HP, Barry C, Lim Y, Rane A. 2D and 3D Ultrasound Imaging of suburethral slings. Ultrasound Obstetrics and Gynaecology 2005;26:175–179 with permission of John Wiley & Sons, Ltd, New York (Publishers). 363
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Figure 26.18. Macroplastique silicone macroparticles used in incontinence surgery are very echogenic and are located surrounding the urethra both anteriorly and posteriorly. Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: Part 1: 2D aspects. Ultrasound Obstet Gynecol 2004;23:80–92 with permission of John Wiley & Sons, Ltd, New York (Publishers).
Figure 26.20. Transitional cell carcinoma of the bladder as seen on parasagittal translabial ultrasound (arrow). Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: Part 1: 2D aspects. Ultrasound Obstet Gynecol 2004;23:80–92 with permission of John Wiley & Sons, Ltd, New York (Publishers).
Figure 26.19. Gartner duct cyst close to bladder neck (arrow). (CX, cervix; U, uterus; V, vagina.) Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: Part 1: 2D aspects. Ultrasound Obstet Gynecol 2004;23:80-92 with permission of John Wiley & Sons, Ltd, New York (Publishers).
Figure 26.21. Retroperitoneal hematoma and subcutaneous vaginal hematoma after mesh sacrocolpopexy and posterior repair. Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: Part 1: 2D aspects. Ultrasound Obstet Gynecol 2004;23:80–92 with permission of John Wiley & Sons, Ltd, New York (Publishers).
3d/4d PelvIc Floor ultrasound technical overview Two engineering solutions have been developed to allow integration of two-dimensional (2D) sectional images
into three-dimensional (3D) volume data: motorized acquisition and external electromagnetic position sensors. The latter has not achieved widespread popularity, largely due to technical problems with implementation. Motorized acquisition may take the shape of automatic withdrawal of an endocavitary probe or motor action within the transducer itself, the mechanical characteristics of which will determine data coordinates. The
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first such probe was described in 1974, and by 1987 transducers for clinical use had been developed.81 The first commercially available system platform, the Kretz Voluson, used such a ‘fan scan’ probe. Further development resulted in the abdominal and endovaginal probes used in systems such as the GE Kretz Voluson 730 series. The widespread acceptance of 3D ultrasound in obstetrics and gynecology was helped considerably by the characteristics of such transducers since they do not require any movement relative to the investigated tissue during image acquisition. Most of the major suppliers of US equipment have now developed their own transducers along similar lines, although it is expected that this technology will be replaced by matrix array transducers within the next 2–5 years.82 These are already available for use in echocardiography.83 With current 3D transducers, automatic image acquisition is achieved by rapid oscillation of a group of elements within the transducer head. This allows the acquisition of multiple sectional planes that can be integrated into a volume. Fortuitously, transducer characteristics on currently available systems for use in obstetrics and gynecology are highly suitable for pelvic floor imaging. A single volume obtained at rest, using a transabdominal 7-4 MHz probe with an acquisition angle of 70 degrees or higher will include the entire levator hiatus with symphysis pubis, urethra, paravaginal tissues, the vagina, anorectum, and puborectalis muscle from the pelvic sidewall in the area of the arcus tendineus of the levator ani (ATLA) to the posterior aspect of the anorectal junction (Fig. 26.22). This also holds true for volumes acquired on levator contraction. A Valsalva maneuver, however, may result in parts of the puborectalis being displaced outside the field of vision, especially in women with significant prolapse.
display modes Figure 26.22 demonstrates the two basic display modes currently in use on 3D ultrasound systems. The multiplanar or orthogonal display mode shows cross-sectional planes through the volume in question. For pelvic floor imaging, this most conveniently means the midsagittal (top left), the coronal (top right) and the axial plane (bottom left). One of the main advantages of volume ultrasound for pelvic floor imaging is that the method gives access to the axial plane which, until recently, was only visible on MRI (see Fig. 26.23 for an axial view of the levator hiatus on MRI and 3D ultrasound). Imaging planes on 3D ultrasound can be varied arbitrarily to enhance the visibility of a given anatomic structure, either at acqui-
Figure 26.22. The usual acquisition/evaluation screen on Voluson-type systems shows the three orthogonal planes: sagittal (top left), coronal (top right) and axial (bottom left), as well as a rendered volume (bottom right) which is a semitransparent representation of all grayscale data in the rendered box volume. Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: 3D aspects. Ultrasound Obstet Gynecol 2004;23(6):615–625 with permission of John Wiley & Sons, Ltd, New York (Publishers).
Figure 26.23. The axial plane on MRI and US (freehand 3D). While these images were obtained in different patients, all significant structures can be identified by both methods. (MR image courtesy of Dr B. Adekamni, Plymouth, UK.) sition or at a later time. For optimal visualization, the levator ani, for example, usually requires an axial plane that is tilted in a ventrocaudal to dorsocranial direction. The three orthogonal images are complemented by a ‘rendered image’, usually a semi-transparent representation of all voxels (i.e. volume pixels) in an arbitrarily defined volume. The bottom right hand image in Figure 26.22 shows a standard rendered image of the puborectalis muscle and levator hiatus, with the rendering direction set from caudally to cranially. This rendering direction seems most convenient for pelvic floor imaging and has been used for all rendered volumes shown here. The default setting on Voluson 365
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systems then results in structures being shown as if the examiner is looking at the patient’s pelvis from below, i.e. the patient’s right is represented on the image’s left. The possibilities for postprocessing are restricted only by the software used for this purpose; programs such as GE Kretz 4D view allow extensive postprocessing as well as different rendering modes, and include a measurement package.
would be the solution but currently appears anything but imminent. Consequently, more and more clinicians and researchers are frustrated by the inability to exchange volume data. Users will have to exert significant pressure on manufacturers who may not necessarily be inclined to cooperate with competitors on this issue.
4d imaging
Until now, most publications on 3D ultrasound in obstetrics and gynecology focus on obstetric applications.82 While 3D data may enhance the understanding of certain conditions or abnormalities for both patients and caregivers,82 some critics contend that 3D ultrasound has been a technology searching for an application. Pelvic floor imaging is a minor niche within the field of ultrasound in obstetrics and gynecology, but it may provide a true indication for the new technique. To date, 3D pelvic floor ultrasound has been used to evaluate the urethra and paraurethral structures, for imaging of the inferior aspects of the levator ani complex, for the visualization of paravaginal supports, as well as for prolapse and implant imaging.
4D imaging implies the real-time acquisition of multiple successive volume datasets which can be represented in orthogonal planes or rendered volumes virtually without delay. This recent development is of particular usefulness in pelvic floor imaging, allowing evaluation of maneuvers such as a levator contraction and Valsalva in all dimensions. This makes the technology potentially superior to MRI. Prolapse assessment by MRI requires ultrafast acquisition84,85 which is of limited availability and will not allow optimal resolution. Alternatively, some systems allow imaging of the sitting or erect patient,85 but again accessibility will be limited for the foreseeable future. The sheer physical characteristics of MRI systems make it much harder for the operator to ensure efficient maneuvers, as over 50% of all women will not perform a proper pelvic floor contraction when asked,86 and a Valsalva maneuver is often confounded by concomitant levator activation. Without real-time imaging, these confounders are impossible to control. Therefore, ultrasound has major potential advantages when it comes to depicting prolapse, especially when associated with fascial or muscular defects, and in defining functional anatomy. It is now feasible to acquire a dataset of dozens of successive volumes that, if timed properly, can document both levator contraction and maximal Valsalva. It allows a complete assessment of pelvic floor structures on one single dataset of about 130 MB. Handling and storage require up-to-date processing capabilities and adequate hard disk space. Such amounts of data will tax even the most modern network, and DVD burners or external hard disks are indispensable for portability. Once volumes are stored, however, the effect for the clinician is akin to having the patient available for re-examination at any given time. Unfortunately, the de-facto software standard of 3D image files provided by licensing of the original technology to other manufacturers has now been lost, with at least six companies developing their own proprietary standard. A DICOM standard for 3D/4D ultrasound data
Practical applications
3D imaging of the urethra The first publication on 3D ultrasound in urogynecology dates from 199487 when Linda Cardozo’s group at King’s College, London, demonstrated that this technique could be used to assess the urethra. It was shown that urethral volumetry correlated with urethral pressure profilometry,87 and that urethral volume decreased with parity. More recently, this technique has been used to assess delivery-related changes,88 and 3D ultrasound with intravaginal systems may also aid in identifying paraurethral support structures. In the male, probes designed for prostatic imaging have also been employed for the assessment of the urethra and paraurethral structures by the transrectal route.89
3D imaging of the levator ani complex To date, the levator ani has not been comprehensively investigated by 3D volume ultrasound. While it was identified on early studies using transvaginal techniques90 and translabial freehand volume acquisition,91 as well as on translabial ultrasound using a Voluson system,92 the focus of these reports was on the urethra and paraurethral tissues. With translabial acquisition, the whole levator hiatus and surrounding muscle can be visualized as a highly echogenic structure (see Fig. 26.23 for a comparison of MRI and ultrasound of the levator hiatus). Hiatal dimensions vary markedly, even in young nulliparous women (Figs 26.24, 26.25).
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Similar to MR imaging, it is currently impossible to distinguish the different components of the pubovisceral or puborectalis/pubococcygeus complex.93 Observation of the muscle during contraction and on Valsalva seems to increase the likelihood of detecting abnormalities of levator morphology which are not uncommon in parous women (see Fig. 26.26 for a comparison of ultrasound and MR imaging of levator avulsion). In a series of 52 young, nulligravid women no significant asymmetry of the levator was observed,
supporting the hypothesis that significant morphologic abnormalities of the levator are likely to be evidence of delivery-related trauma,94 and our own data have recently confirmed this (Fig. 26.27). Of 38 women delivered vaginally, 13 (34%) showed evidence of avulsion of the levator ani from the pelvic sidewall,95 an observation which concurs with an MRI study demonstrating a high
Figure 26.24. The effect of a Valsalva maneuver on the levator hiatus (left, at rest; right, on Valsalva) in a young nulliparous woman without significant pelvic organ descent. The dimensions of the levator hiatus are measured in the sagittal (1) and coronal (2) planes. Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: 3D aspects. Ultrasound Obstet Gynecol 2004;23(6):615–625 with permission of John Wiley & Sons, Ltd, New York (Publishers).
Figure 26.26. Levator avulsion (lower arrows) on MRI (left) and 3D ultrasound (right). While these images were obtained in different patients, the appearances are typical in that a levator avulsion (arrows) appears to occur more often on the patient’s right (left side of the images). In both cases paravaginal tenting is also absent on the patient’s right side (top arrows). (MR image courtesy of Dr B. Adekamni, Plymouth, UK.) Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: 3D aspects. Ultrasound Obstet Gynecol 2004;23(6):615–625 with permission of John Wiley & Sons, Ltd, New York (Publishers).
Figure 26.25. The levator hiatus at rest (left) and on Valsalva (right) in a young woman with significant pelvic organ descent. On Valsalva the levator is situated partly outside the acquisition volume. Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: 3D aspects. Ultrasound Obstet Gynecol 2004;23(6):615–625 with permission of John Wiley & Sons, Ltd, New York (Publishers).
Figure 26.27. Large right-sided levator avulsion in a 32year-old woman after normal vaginal delivery (arrow). The image on the left shows an intact pubovisceral muscle 4 weeks before childbirth, the one on the right was obtained 3 months postpartum. Reproduced from Dietz HP, Lanzarone V. Levator trauma after vaginal delivery. Obstetrics and Gynecology, 2005;106:707–712 with permission of Lippincott, Williams & Wilkins. 367
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prevalence of morphologic abnormalities of the pubovisceral muscle in parous women.96 Hiatal depth and area measurements seem highly reproducible (ICC 0.70–0.82) and correlate strongly with pelvic organ descent, both at rest and on Valsalva.94 These data constitute the first hard evidence for the hypothesis that the state of the levator ani is important for pelvic organ support,97 even in the absence of levator trauma. Further work will have to focus on the observation of levator anatomy and function before and after childbirth (to determine the etiology of – and risk factors for – morphologic abnormalities) and on cross-sectional studies of levator anatomy in asymptomatic and symptomatic older women to determine whether such abnormalities are associated with clinical symptoms, conditions or surgical outcome. The opportunity to observe the hiatus ‘live’ may well lead to a paradigm shift in pelvic floor surgery, away from a focus on fascial suspension and towards a focus on muscular support. Many of us are familiar with the phenomenon of a postnatal prolapse which is undetectable a few weeks later. While the hiatus has to stretch to 70–90 cm2 to allow passage of the fetal head, it does return to less than 20 cm2 in many parous women. Clearly, prolapse that was present while the hiatus was massively stretched may well become completely inapparent once the levator has regained its previous tone. This also implies that we ignore the dimensions of the hiatus at our (and the patient’s) peril. A wide hiatus may predispose to recurrent prolapse, in the original compartment or at another site. Every practicing pelvic floor surgeon is familiar with the phenomenon of a de novo rectoenterocele after colposuspension, or a newly developed cystocele after successful vault suspension, and one may speculate that hiatal dimensions are likely to be an important factor in such recurrence.
3D imaging of paravaginal supports It has long been speculated that anterior vaginal wall prolapse and stress urinary incontinence are at least partly due to disruption of paravaginal and/or paraurethral support structures, i.e. the endopelvic fascia and pubourethral ligaments, at the time of vaginal delivery.98 In a pilot study in a group of women before and after their first delivery, the author attempted to define the integrity of paravaginal supports using a freehand acquisition technique.99 Alterations in paravaginal supports were observed in 5 out of 21 women seen both ante- and postpartum (Fig. 26.28). Somewhat counterintuitively, there was no significant correlation between a loss of paravaginal support and increased bladder neck or urethral mobility on Valsalva in this study. Increased mobil-
Figure 26.28. Loss of tenting postpartum (arrow) in a primipara after a full-term, normal vaginal delivery. Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: 3D aspects. Ultrasound Obstet Gynecol 2004;23(6):615–625 with permission of John Wiley & Sons, Ltd, New York (Publishers). ity might not necessarily mean disruption or avulsion of structures, but rather stretching or distension, although the freehand technique might have limited the power of this study. In another pilot study, paravaginal tissues have also been assessed by transrectal or transvaginal 3D ultrasound using probes designed for pelvic or prostatic imaging.14 It remains to be shown whether loss of paravaginal tenting is in fact equivalent to what is clinically described as a ‘paravaginal defect’, a concept that is controversial in clinical urogynecology.100,101 In a study of 62 women presenting with pelvic floor disorders, only weak correlations were found between a blinded clinical assessment for paravaginal defects and the presence or absence of tenting in single planes or rendered volumes obtained by 3D ultrasound, and even this weak correlation was seen only on Valsalva.102 As the clinical assessment of anterior vaginal wall supports is notoriously unreliable,103 this may have been due to limitations of the clinical technique rather than insufficiently sensitive imaging. However, another explanation may be that true paravaginal defects are either not common or not that relevant for anterior vaginal wall support.
3D imaging of prolapse The downward displacement of pelvic organs on Valsalva maneuver in and of itself does not require 3D imaging technology, whether MRI- or ultrasound-based. Descent of the urethra, bladder, cervix, cul de sac, and rectum is easily documented in the midsagittal plane.53 However, 3D ultrasound may become useful for the localization of fascial defects (e.g. transverse or lateral tears in the rectovaginal septum). Rendered volumes allow a com-
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plete 3D visualization of a cystocele or rectocele (Figs 26.29, 26.30). When processed into rotational volumes, hyperechoic structures such as a rectocele become particularly evident. Figure 26.31 demonstrates the extent of a rectocele within the levator hiatus in a rendered volume obtained in the axial plane. The ease with which pre- and postoperative data can be compared with the help of stored volumes will be especially useful in audit activities.
3D imaging of synthetic implant materials Suburethral slings such as the TVT, SPARC or IVS have become very popular during the last 10 years and are
now the primary anti-incontinence procedures in many developed countries. These slings are not without their problems, even if biocompatibility is markedly better than that of previously used synthetic slings. Imaging of such slings may be indicated in research, in order to determine location and function, and possibly even for assessing in vivo biomechanical characteristics. Clinically, patients with complications such as sling failure, voiding dysfunction, erosion and symptoms of the irritable bladder are likely to benefit from imaging assessment. 3D ultrasound has been used to locate the implant over its whole course,104 from above the pubic rami to behind the urethra, and back up on the contralateral
Figure 26.29. Large cystocele in the three standard planes (sagittal top left, coronal top right, axial bottom left) and rendered image (axial, caudocranial rendering), showing a view through the cystocele onto the bladder roof. The coronal view demonstrates both ureteric orifices as papillary excrescences 1–2 cm from the internal urethral meatus. The urethra has rotated by about 140 degrees on Valsalva and now runs from caudal to cranial for about 2 cm before describing a marked kink.
Figure 26.30. Large rectocele in the three standard planes (sagittal top left, coronal top right, axial bottom left) plus rendered volume (bottom right), showing a large symmetrical rectocele filling most of the levator hiatus (arrow). There also is a suburethral tape. Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: 3D aspects. Ultrasound Obstet Gynecol 2004;23(6):615– 625 with permission of John Wiley & Sons, Ltd, New York (Publishers). 369
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Figure 26.31. Rectocele as imaged by rendered volume in the axial plane. It is evident that the rectocele develops symmetrically and occupies a large part of the levator hiatus. side (Fig. 26.32). The best visualization is achieved in caudocranially rendered volumes of approximately 2–4 cm thickness after rotation of the reference plane to follow the dorsocaudal to cranioventral course of the implant. Variations in placement such as asymmetry, varying width, the effect of tape division and tape twisting can be visualized.71 While denser tapes such as the
IVS are often difficult to identify on 2D imaging, they are much more readily visualized in the axial plane.105 The difference between transobturator tapes and the TVT-type implants, impossible to distinguish on 2D imaging, is readily apparent on rendered volumes, with the transobturator tapes assuming the appearance of a yoke rather than a U-shaped loop (Fig. 26.33). It is quite likely therefore that 3D imaging will prove to be helpful in the assessment of suburethral slings. The same holds true for mesh implants used in prolapse surgery. There is a worldwide trend towards mesh implantation, especially for recurrent prolapse, and complications such as suspension failure, infection, and erosion are not uncommon.106 While there are no publications on the imaging of mesh by 3D ultrasound at present, the new method will likely be useful in determining functional outcome and location of such implants. Figure 26.34 shows a recurrent cystocele due to unilateral mesh detachment. Finally, most of the injectables used in anti-incontinence surgery (such as silicone macroparticles) are highly echogenic and can be visualized as a hyperechoic ‘donut’ surrounding the urethra (Fig. 26.35).
conclusIons Ultrasound imaging, and in particular translabial or transperineal ultrasound, is in the process of becoming a new diagnostic standard in urogynecology. Several factors are contributing to its increasing acceptance, the
Figure 26.32. The tension-free transvaginal tape (TVT) as imaged on an oblique rendered volume of the levator hiatus. The mesh structure of the tape is clearly visible. There also is a local abnormality of uncertain significance visible in the levator on the patient’s right (left side of the image, arrow). Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: 3D aspects. Ultrasound Obstet Gynecol 2004;23(6):615–625 with permission of John Wiley & Sons, Ltd, New York (Publishers).
Figure 26.33. Monarc sling (left) versus tension-free transvaginal tape (TVT) sling in rendered volumes of the levator hiatus. The difference in placement is obvious: the Monarc sling is inserted through the obturator foramen, the TVT through the space of Retzius. As a result, the latter is situated much more medially. Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: 3D aspects. Ultrasound Obstet Gynecol 2004;23(6):615–625 with permission of John Wiley & Sons, Ltd, New York (Publishers).
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Figure 26.34. Recurrent cystocele after mesh detachment on the left. Rendered volume, seen from below (caudocranial rendering). The edge of the mesh is clearly apparent close to the midline (arrow). Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: 3D aspects. Ultrasound Obstet Gynecol 2004;23(6):615–625 with permission of John Wiley & Sons, Ltd, New York (Publishers).
Figure 26.35. Macroplastique injectable in optimal position around the urethra as demonstrated in a rendered axial volume. Reproduced from Dietz HP. Ultrasound Imaging of the Pelvic Floor: 3D aspects. Ultrasound Obstet Gynecol 2004;23(6):615–625 with permission of John Wiley & Sons, Ltd, New York (Publishers).
most important being the availability of suitable equipment. Recent developments such as the assessment of levator activity and prolapse, and the use of color Doppler to document urine leakage, enhance the clinical usefulness of the method. The convenience with which pre- and post-treatment imaging data can now be obtained will simplify outcome studies after prolapse and incontinence surgery. Ultrasound imaging may be able to significantly enhance our understanding of the different mechanisms by which conservative methods, colposuspension or urethropexy procedures, slings and (most recently) suburethral tapes restore continence. It may even be possible to identify distinct fascial defects (such as defects of the rectovaginal septum in true rectoceles) which should open up new surgical possibilities. Regardless of which methodology is used to determine descent of pelvic organs, it is evident that there is a wide variation in pelvic organ mobility, even in young nulliparous women. This variation is likely to be at least partly genetic in origin. Ultrasound imaging now allows quantification of the phenotype of pelvic organ prolapse which will facilitate molecular and population genetic approaches to evaluating the etiology of pelvic floor and bladder dysfunction. On the other hand, there is little doubt that childbirth can affect pelvic organ support and levator function, and that the prior state of pelvic floor tissues may influence the course of labor. It is likely that pelvic floor ultrasound will help us identify women at high risk of operative delivery and/or significant pelvic floor damage. It remains to be seen, however, whether such information can have a positive effect on clinical outcomes. 3D volume ultrasound adds not one, but several dimensions to pelvic floor imaging, in particular in its most recent incarnation using automatic real-time volume acquisition. The technology opens up new possibilities for observing functional anatomy and examining muscular and fascial structures of the pelvic floor. Access to the axial plane may in fact completely alter our approach to pelvic floor surgery, leading to a new appraisal of the role of levator plasty and facilitating the development of new forms of surgical and non-surgical means of improving hiatal anatomy and biomechanics. There is little doubt that it will be many years before the potential for true progess inherent in this new technology is fully realized. There is currently no evidence to prove that the use of modern imaging techniques improves patient outcomes in urogynecology and pelvic reconstructive surgery. However, this is true for many diagnostic modalities in clinical medicine. Due to methodologic problems, this 371
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situation is unlikely to improve soon. In the meantime, it has to be recognized that any diagnostic method is only as good as the operator behind the machine, and diagnostic ultrasound is well known for its operatordependent nature. Teaching is therefore of paramount importance to ensure that imaging techniques are used appropriately and effectively.
12. Schaer GN, Koechli OR, Schuessler B, Haller U. Perineal ultrasound for evaluating the bladder neck in urinary stress incontinence. Obstet Gynecol 1995;85(2):220–4.
reFerences
15. Alper T, Cetinkaya M, Okutgen S, Kokcu A, Lu E. Evaluation of urethrovesical angle by ultrasound in women with and without urinary stress incontinence. Int Urogynecol J 2001;12(5):308–11.
1. Sanders R, James A, Fleischer A. Sonography in Obstetrics and Gynecology: Principles and Practice, 6th ed. New York: McGraw Hill, 2001. 2. Kohorn EI, Scioscia AL, Jeanty P, Hobbins JC. Ultrasound cystourethrography by perineal scanning for the assessment of female stress urinary incontinence. Obstet Gynecol 1986;68(2):269–72. 3. Grischke EM, Dietz HP, Jeanty P, Schmidt W. [A new study method: the perineal scan in obstetrics and gynecology.] Ultraschall Med 1986;7(4):154–61. 4. Koelbl H, Bernaschek G, Wolf G. A comparative study of perineal ultrasound scanning and urethrocystography in patients with genuine stress incontinence. Arch Gynecol Obstet 1988;244(1):39–45. 5. Tunn R, Petri E. Introital and transvaginal ultrasound as the main tool in the assessment of urogenital and pelvic floor dysfunction: an imaging panel and practical approach. Ultrasound Obstet Gynecol 2003;22:205–13. 6. Grischke EM, Anton HW, Dietz P, Schmidt W. [Perineal sonography and roentgenologic procedures within the scope of diagnosis of female urinary incontinence.] Geburtshilfe Frauenheilkd 1989;49(8):733–6. 7. Gordon D, Pearce M, Norton P, Stanton SL. Comparison of ultrasound and lateral chain urethrocystography in the determination of bladder neck descent. Am J Obstet Gynecol 1989;160(1):182–5. 8. Voigt R, Halaska M, Michels W, Martan A, Starker K, Voigt P. Examination of the urethrovesical junction using perineal sonography compared to urethrocystography using a bead chain. Int Urogynecol J 1994;5:212–4. 9. Ammann ME, Winkelbauer F, Fitzal P. [The urethrocystogram and perineal sonography compared.] Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 1992;156(4):309–12. 10. Dietz HP, Wilson PD. Anatomical assessment of the bladder outlet and proximal urethra using ultrasound and videocystourethrography. Neurourol Urodyn 1996;15:363–4. 11. Schaer GN, Siegwart R, Perucchini D, DeLancey JO. Examination of voiding in seated women using a remote-controlled ultrasound probe. Obstet Gynecol 1998;91(2):297–301.
13. Dietz HP, Wilson PD. The influence of bladder volume on the position and mobility of the urethrovesical junction. Int Urogynecol J 1999;10(1):3–6. 14. Dietz HP, Clarke B. The influence of posture on perineal ultrasound imaging parameters. Int Urogynecol J 2001;12(2):104–6.
16. Martan A, Masata J, Halaska M, Voigt R. Ultrasound imaging of the lower urinary system in women after Burch colposuspension. Ultrasound Obstet Gynecol 2001;17(1):58–64. 17. Dietz HP, Eldridge A, Grace M, Clarke B. Test–retest reliability of the ultrasound assessment of bladder neck mobility. Int Urogynecol J 2003;14(S1):S57–S58. 18. Reed H, Waterfield A, Freeman RM, Adekanmi OA. Bladder neck mobility in continent nulliparous women: normal references. Int Urogynecol J 2002;13(Suppl 1): S4. 19. Brandt FT, Albuquerque CD, Lorenzato FR, Amaral FJ. Perineal assessment of urethrovesical junction mobility in young continent females. Int Urogynecol J 2000;11(1):18–22. 20. Peschers UM, Fanger G, Schaer GN, Vodusek DB, DeLancey JO, Schuessler B. Bladder neck mobility in continent nulliparous women. Br J Obstet Gynaecol 2001;108(3):320–4. 21. Dietz H, Eldridge A, Grace M, Clarke B. Pelvic organ descent in young nulliparous women. Am J Obstet Gynecol 2004;191:95–9. 22. King J, Freeman R. Can we predict antenatally those patients at risk of postpartum stress incontinence? Neurourol Urodyn 1997;15:330–1. 23. Martan A, Masata J, Halaska M, Kasikova E, Otcenasek M, Voigt R. The effect of increasing of intraabdominal pressure on the position of the bladder neck in ultrasound imaging. Annual Meeting, International Continence Society 2001, Seoul, South Korea. 24. Dietz HP, Hansell N, Grace M, Eldridge A, Clarke B, Martin N. Bladder neck mobility is a heritable trait. Br J Obstet Gynaecol 2005;112:334–339. 25. Peschers U, Schaer G, Anthuber C, DeLancey JO, Schuessler B. Changes in vesical neck mobility following vaginal delivery. Obstet Gynecol 1996;88(6):1001–6. 26. Meyer S, Schreyer A, De Grandi P, Hohlfeld P. The effects of birth on urinary continence mechanisms and other pelvic-floor characteristics. Obstet Gynecol 1998;92(4 Pt 1):613–8.
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27. Dietz HP, Bennett MJ. The effect of childbirth on pelvic organ mobility. Obstet Gynecol 2003;102(2):223–8. 28. Dietz HP, Clarke B, Vancaillie TG. Vaginal childbirth and bladder neck mobility. Aust N Z J Obstet Gynaecol 2002;42(5):522–5. 29. Digesu GA, Toosz-Hobson P, Bidmead J, Cardozo LD, Robinson D. Pregnancy, childbirth and urinary incontinence: Caesarean for all? Neurourol Urodyn 2000;19(4):508–9. 30. Dietz HP, Moore KH, Steensma AB. Antenatal pelvic organ mobility is associated with delivery mode. Aust N Z J Obstet Gynaecol 2003;43(1):70–4.
43. Lekskulchai O, Dietz HP. Normal values for detrusor wall thickness in young Caucasian women. Abstract, ICS 2005 Montreal. 44. Wijma J, Tinga DJ, Visser GH. Perineal ultrasonography in women with stress incontinence and controls: the role of the pelvic floor muscles. Gynecol Obstet Invest 1991;32(3):176–9. 45. Peschers UM, Schaer GN, DeLancey JO, Schuessler B. Levator ani function before and after childbirth. Br J Obstet Gynaecol 1997;104(9):1004–8. 46. Dietz H. Levator function before and after childbirth. Aust N Z J Obstet Gynaecol 2004;44(1):19–23.
31. Balmforth J, Toosz-Hobson P, Cardozo L. Ask not what childbirth can do to your pelvic floor but what your pelvic floor can do in childbirth. Neurourol Urodyn 2003;22(5):540–2.
47. Dietz HP, Wilson PD, Clarke B. The use of perineal ultrasound to quantify levator activity and teach pelvic floor muscle exercises. Int Urogynecol J 2001;12(3):166–8; discussion 168–9.
32. Schaer GN, Perucchini D, Munz E, Peschers U, Koechli OR, DeLancey JO. Sonographic evaluation of the bladder neck in continent and stress-incontinent women. Obstet Gynecol 1999;93(3):412–6.
48. Miller JM, Perucchini D, Carchidi LT, DeLancey JO, Ashton-Miller J. Pelvic floor muscle contraction during a cough and decreased vesical neck mobility. Obstet Gynecol 2001;97(2):255–60.
33. Dietz HP, Clarke B. The urethral pressure profile and ultrasound imaging of the lower urinary tract. Int Urogynecol J 2001;12(1):38–41. 34. Huang WC, Yang JM. Bladder neck funneling on ultrasound cystourethrography in primary stress urinary incontinence: a sign associated with urethral hypermobility and intrinsic sphincter deficiency. Urology 2003;61(5):936–41. 35. Dietz HP, McKnoulty L, Clarke B. Translabial color Doppler for imaging in urogynecology: a preliminary report. Ultrasound Obstet Gynecol 1999;14:144–7. 36. Dietz HP, Clarke B. Translabial color Doppler urodynamics. Int Urogynecol J 2001;12(5):304–7. 37. Masata J, Martan A, Halaska M, Kasikova E, Otcenasek M, Voigt R. Detection of Valsalva leak point pressure with colour Doppler – new method for routine use. Neurourol Urodyn 2001;20(4):494–6. 38. Khullar V, Cardozo LD, Salvatore S, Hill S. Ultrasound: a noninvasive screening test for detrusor instability. Br J Obstet Gynaecol 1996;103(9):904–8. 39. Khullar V, Cardozo LD. Imaging in urogynaecology. Br J Obstet Gynaecol 1996;103(11):1061–7. 40. Robinson D, Anders K, Cardozo LD, Bidmead J, Toozs-Hobson P, Khullar V. Can ultrasound replace ambulatory urodynamics when investigating women with irritative urinary symptoms? Br J Obstet Gynaecol 2002;109(2):145–8. 41. Yang JM, Huang WC. Bladder wall thickness on ultrasound cystourethrography. J Ultrasound Med 2003;22:777–82. 42. Soligo M, Khullar V, Salvatore S, Luppino G, Arcari V, Milani R. Overactive bladder definition and ultrasound measurement of bladder wall thickness: the right way without urodynamics. Neurourol Urodyn 2002;21(4):284–5.
49. Dietz HP, Jarvis SK, Vancaillie TG. The assessment of levator muscle strength: a validation of three ultrasound techniques. Int Urogynecol J 2002;13(3):156–9. 50. Creighton SM, Pearce JM, Stanton SL. Perineal video-ultrasonography in the assessment of vaginal prolapse: early observations. Br J Obstet Gynaecol 1992;99(4):310–3. 51. Petri E, Koelbl H, Schaer G. What is the place of ultrasound in urogynecology? A written panel. Int Urogynecol J 1999;10(4):262–73. 52. Bump RC, Mattiasson A, Bá K et al. The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 1996;175(1):10–7. 53. Dietz HP, Haylen BT, Broome J. Ultrasound in the quantification of female pelvic organ prolapse. Ultrasound Obstet Gynecol 2001;18(5):511–4. 54. Dietz HP, Steensma AB. Posterior compartment prolapse on 2D and 3D pelvic floor ultrasound: the distinction between true rectocele, perineal hypermobility and enterocele. Ultrasound Obstet Gynaecol 2005;26(1):73–77. 55. Dietz H, Eldridge A, Grace M, Clarke B. The prevalence of rectovaginal fascial defects in young nulliparae: can rectocele be a congenital condition? Neurourol Urodyn 2004;23:440–1. 56. Bombieri L, Freeman RM. What happens to the bladder neck a year after colposuspension? Does it affect outcome? Int Urogynecol J 2000;11(Suppl 1):S7. 57. Dietz HP, Wilson PD. Colposuspension success and failure: a long-term objective follow-up study. Int Urogynecol J 2000;11(6):346–51. 58. Bombieri L, Freeman RM. Do bladder neck position and
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amount of elevation influence the surgical outcome of colposuspension? Neurourol Urodyn 1999;18(4):316–7. 59. Bombier L, Freeman RM, Perkins EP, Williams MP, Shaw SR. Why do women have voiding dysfunction and de novo detrusor instability after colposuspension? BJOG 2002;109(4):402–12. 60. Viereck V, Pauer HU, Bader W et al. Introital ultrasound of the lower genital tract before and after colposuspension: a 4-year objective follow-up. Ultrasound Obstet Gynecol 2004;23(3):277–83. 61. Dietz HP, Wilson PD, Clarke B, Haylen BT. Irritative symptoms after colposuspension: are they due to distortion or overelevation of the anterior vaginal wall and trigone? Int Urogynecol J 2001;12(4):232–5. 62. Viereck V, Bader W, Skala C et al. Determination of bladder neck position by intraoperative introital ultrasound in colposuspension: outcome at 6-month follow-up. Ultrasound Obstet Gynecol 2004;24(2):186–91. 63. Huang WC, Yang JM. Anatomic comparison between laparoscopic and open Burch colposuspension for primary stress urinary incontinence. Urology 2004;63(4):676–81. 64. Dietz H, Wilson P. Long-term success after open and laparoscopic colposuspension: a case control study. Gynecol Endoscopy 2002;11:81–4. 65. Dietz H, Wilson P. Laparoscopic colposuspension vs. urethropexy: a case-control series. Int Urogynecol J 2005;16:15–8. 66. Dietz HP, Wilson PD, Gillies K, Vancaillie TG. How does the TVT achieve continence? Neurourol Urodyn 2000;19(4):393–4. 67. Geiss I, Dungl A, Riss PA. Position of the prolene tape after TVT: a sonographic and urodynamic study. Int Urogynecol J 2000;11(S1):S30.
74. Fritel X, Zabak K, Pigne A, Demaria F, Benifla JL. Predictive value of urethral mobility before suburethral tape procedure for urinary stress incontinence in women. J Urol 2002;168(6):2472–5. 75. Mouritsen L. Effect of vaginal continence products evaluated by ultrasonography of bladder neck mobility. Int Urogynecol J 1999;10(S1):S110. 76. Mouritsen L, Bernstein I. Vaginal ultrasonography: a diagnostic tool for urethral diverticulum. Acta Obstet Gynecol Scand 1996;75(2):188–90. 77. Fortunato P, Schettini M, Gallucci M. Diagnosis and therapy of the female urethral diverticula. Int Urogynecol J 2001;12(1):51–7. 78. Huang WC, Yang JM. Transvaginal sonographic findings in diagnosis and treatment of urethral stricture. J Ultrasound Med 2003;22(12):1405–8. 79. Huang WC, Yang JM. Transvaginal sonography in the treatment of a rare case of total urethral stenosis with a vesicovaginal fistula. J Ultrasound Med 2002;21(4):463–7. 80. Yang JM, Huang WC. The significance of urethral hyperechogenicity in female lower urinary tract symptoms. Ultrasound Obstet Gynecol 2004;24(1):67–71. 81. Gritzky A, Brandl H. The Voluson (Kretz) technique. In: Merz E (ed) 3-D Ultrasound in Obstetrics and Gynecology. Philadelphia: Lippincott Williams and Wilkins Healthcare, 1998; 9–15. 82. Timor-Tritsch IE, Platt LD. Three-dimensional ultrasound experience in obstetrics. Curr Opin Obstet Gynecol 2002;14(6):569–75. 83. Stetten G, Tamburo R. Real-time three-dimensional ultrasound methods for shape analysis and visualization. Methods 2001;25(2):221–30.
68. Dungl A, Geiss I, Riss PA. Postoperative voiding problems according to the position of the prolene tape after TVT procedure. Int Urogynecol J 2002;13(S1):S30.
84. Dohke M, Mitchell DG, Vasavada SP. Fast magnetic resonance imaging of pelvic organ prolapse. Tech Urol 2001;7(2):133–8.
69. Martan A, Masata J, Svabik K, Halaska M, Voigt P. The ultrasound imaging of the tape after TVT procedure. Neurourol Urodyn 2002;21(4):322–4.
85. Law PA, Danin JC, Lamb GM, Regan L, Darzi A, Gedroyc WM. Dynamic imaging of the pelvic floor using an openconfiguration magnetic resonance scanner. J Magnetic Reson Imaging 2001;13(6):923–9.
70. Lo TS, Wang AC, Horng SG, Liang CC, Soong YK. Ultrasonographic and urodynamic evaluation after tension free vaginal tape procedure (TVT). Acta Obstet Gynecol Scand 2001;80(1):65–70. 71. Dietz HP, Wilson PD. The ‘iris effect’: how two-dimensional and three-dimensional ultrasound can help us understand anti-incontinence procedures. Ultrasound Obstet Gynecol 2004;23(3):267–71. 72. Dietz HP, Mouritsen L, Ellis G, Wilson PD. How important is TVT location? Acta Obstet Gynecol Scand 2004;83(10):904–8. 73. Dietz HP, Mouritsen L, Ellis G, Wilson PD. Does the tension-free vaginal tape stay where you put it? Am J Obstet Gynecol 2003;188(4):950–3.
86. Bo K, Larson S, Oseid S, Kvarstein B, Hagen R, Jorgensen J. Knowledge about and ability to do correct pelvic floor muscle exercises in women with urinary stress incontinence. Neurourol Urodyn 1988;7:261–2. 87. Khullar V, Salvatore S, Cardozo LD. Three dimensional ultrasound of the urethra and urethral pressure profiles. Int Urogynecol J 1994;5(S1):319. 88. Toozs-Hobson P, Khullar V, Cardozo L. Three-dimensional ultrasound: a novel technique for investigating the urethral sphincter in the third trimester of pregnancy. Ultrasound Obstet Gynecol 2001;17(5):421–4. 89. Umek W, Kratochwil A, Obermair A, Stutterecker D, Hanzal E. 3-Dimensional ultrasound of the female ure-
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thra comparing transvaginal and transrectal scanning. Int Urogynecol J 1999;10(S1):S109.
98. DeLancey JO. The anatomy of the pelvic floor. Curr Opin Obstet Gynecol 1994;6(4):313–6.
90. Wisser J, Schaer G, Kurmanavicius J, Huch R, Huch A. Use of 3D ultrasound as a new approach to assess obstetrical trauma to the pelvic floor. Ultraschall Med 1999;20(1):15–8.
99. Dietz HP, Steensma AB, Hastings R. Three-dimensional ultrasound imaging of the pelvic floor: the effect of parturition on paravaginal support structures. Ultrasound Obstet Gynecol 2003;21(6):589–95.
91. Dietz H, Steensma A. Three-dimensional ultrasound imaging of the pelvic floor: the effect of parturition on paravaginal support structures. Ultrasound Obstet Gynecol 2003;21:589–95.
100. Ostrzenski A, Osborne NG. Ultrasonography as a screening tool for paravaginal defects in women with stress incontinence: a pilot study. Int Urogynecol J 1998;9(4):195–9.
92. Khullar V, Cardozo L. Three-dimensional ultrasound in urogynecology. In: Merz E (ed) 3-D Ultrasound in Obstetrics and Gynecology. Philadelphia: Lippincott, Williams and Wilkins Healthcare, 1998; 65–71.
101. Nguyen JK. Current concepts in the diagnosis and surgical repair of anterior vaginal prolapse due to paravaginal defects. Obstet Gynecol Survey 2001;56(4):239–46.
93. Fielding JR, Dumanli H, Schreyer AG et al. MR-based three-dimensional modeling of the normal pelvic floor in women: quantification of muscle mass. Am J Radiol 2000;174(3):657–60. 94. Dietz HP, Shek C, Clarke B. Biometry of the pubovisceral muscle and levator hiatus by 3D pelvic floor ultrasound. Ultrasound Obstet Gynaecol 2005;25(6):580–585. 95. Dietz HP, Lanzarone V. Levator trauma after vaginal delivery. Obstetrics and Gynecology 2005;106:707–712. 96. DeLancey JO, Kearney R, Chou Q, Speights S, Binno S. The appearance of levator ani muscle abnormalities in magnetic resonance images after vaginal delivery. Obstet Gynecol 2003;101(1):46–53. 97. DeLancey JO. Functional anatomy of the pelvic floor and urinary continence mechanism. In: Schuessler B, Laycock J, Norton P, Stanton SL (eds) Pelvic Floor Reeducation: Principles and Practice. London: Springer, 1994; 9–21.
102. Dietz HP, Pang S, Korda A, Benness C. Paravaginal defects: A comparison of clinical examination and 2D/ 3D ultrasound imaging. Aust NZ J Obstet Gynaecol 2005; 45:187–190. 103. Whiteside JL, Barber MHS, Paraiso MF, Hugney CM, Walters MD. Clinical evaluation of anterior vaginal wall support defects: interexaminer and intraexaminer reliability. Am J Obstet Gynecol 2004;191(1):100–4. 104. Dietz H, Wilson P. The iris effect: how two-dimensional and three-dimensional volume ultrasound can help us understand anti-incontinence procedures. Ultrasound Obstet Gynecol 2004;23(3):267–71. 105. Dietz H, Barry C, Lim Y, Rane A. 2D and 3D pelvic floor ultrasound in the evaluation of suburethral sling implants. Ultrasound Obstet Gynecol 2004;24:253. 106. Iglesia CB, Fenner DE, Brubaker L. The use of mesh in gynecologic surgery. Int Urogynecol J 1997;8(2):105–115.
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Evaluation of Urinary Incontinence Urinary incontinence is a non-specific symptom resulting from a variety of different conditions, and the differential diagnosis of urinary incontinence in women is broad, including urodynamic stress incontinence (USI), overactive bladder disorders, overflow incontinence, urinary tract fistulae, and urethral diverticula. Distinguishing these different etiologies is imperative as each condition warrants a different therapeutic approach. Prior to the advent of sophisticated diagnostic modalities, most physicians depended on historical information related to inciting events and associated symptoms combined with physical findings to determine the etiology of incontinence. There is now a substantial body of literature addressing the inaccuracy of historical and physical findings.1–3 Although physiologic subtypes of urinary incontinence demonstrate significant population differences in the distribution of symptoms, the considerable overlap in symptoms limits predictive value in the individual patient. Attempts to improve this sensitivity by using pure symptoms or symptom complexes have proven equally inaccurate.4 Consequently, while historical and physical examination findings are valuable to correlate findings with patient complaints, they are no more than a guide to lower urinary tract diagnosis. Recognition of the inaccuracy of symptomatology as the sole basis for diagnosing urinary incontinence fostered the development of new diagnostic modalities to better evaluate the condition. Dynamic urethroscopy was initially proposed as a complete method of evaluating lower urinary tract dysfunction and has been used in this capacity for more than 30 years.5 The subsequent refinement of urodynamic evaluation has demonstrated its superiority for diagnosing the common etiologies of urinary incontinence. In comparing urodynamics directly to urethrocystoscopy, several authors have concluded that it is a more sensitive method of diagnosing USI and detrusor overactivity (DO).6,7 While these comparisons illustrate the superiority of urodynamics in evaluating abnormalities of lower urinary tract physiology, they fail to recognize the unique anatomic information provided by urethrocystoscopy combined with urodynamics. Urethrocystoscopy contributes an anatomic assessment of the urethra and bladder, enabling the diagnosis of benign and malignant mucosal lesions that would remain undiagnosed by urodynamics alone. Cundiff and Bent illustrate the value of urethrocystoscopy as an adjunct to urodynamics in a study of women undergoing combined urodynamics and urethrocystoscopy.8 Urethrocystoscopy was considered important to 19% of the final diagnoses. Specifically, it provided new information in patients with anatomic abnormalities
including intravesical lesions, intravesical foreign bodies, and urethral diverticulum. While not present in this series, urogenital fistula should be included in this category of anatomic lesions amenable to diagnosis by endoscopy.
Indications The modern era of cost containment in medicine challenges physicians to determine a cost-effective approach to diagnosis that does not compromise the accuracy of the evaluation. In this context, it is important to define those women presenting with urinary incontinence who need the anatomic assessment provided by cystourethroscopy. There are several clear indications that will be addressed individually.
Suspected anatomic lesions Anatomic abnormalities, such as urogenital fistulae and urethral diverticula, might be suspected based on history or urodynamics but require an anatomic assessment for confirmation. For example, a diverticulum can be suspected based on a history of recurrent urinary tract infections, post-void dribbling, or pelvic pain. In such a patient, a biphasic urethral pressure profile is supportive of the diagnosis of a urethral diverticulum; however, Leach and Bavendam found that only 72% of patients with a urethral diverticulum demonstrated a biphasic pattern.9 This contrasts with the reported diagnostic accuracy for urethrocystoscopy of 84–90%.10,11 Beyond diagnosis, urethrocystoscopy also provides important information about the size and location of the ostia, as well as the presence of multiple diverticula. The ability of cystourethroscopy to define the location, size, and surrounding anatomic relationships also pertains for urogenital fistulae, and both Massee et al.12 and Symmonds13 consider it the simplest method of evaluating urinary tract fistulae.
Recurrent incontinence Women with recurrent urinary incontinence following a prior therapeutic intervention are a complex group of patients that may suffer from preoperative misdiagnosis, failed intervention, or a complication of the intervention. The fallibility of symptoms in determining the etiology of incontinence is even greater in this group of patients, and they all deserve a thorough evaluation, including multichannel urodynamics as well as the anatomic assessment provided by cystourethroscopy. When recurrent incontinence is associated with a urodynamic diagnosis of DO, the differential diagnosis
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includes new onset DO, persistent but previously undiagnosed DO, DO related to obstruction, and mucosal irritation leading to DO. Mucosal irritation may be due to foreign bodies, such as urolithiasis or an intravesical suture, which are easily diagnosed at cystourethroscopy. Outflow obstruction due to overzealous elevation of the urethrovesical junction (UVJ) at the time of surgery has also been shown to be a cause of DO in recurrent incontinence.14 Cystourethroscopy is useful in these patients to achieve a visual evaluation of UVJ elevation and eliminate other possible etiologies in the differential diagnosis. Recurrent USI after continence surgery may result from persistent urethral hypermobility or poor coaptation. Persistent urethral hypermobility occurs from inadequate elevation of the UVJ or failed UVJ stabilization secondary to suture failure, poor tissue quality, or excessive stress on the repair.15 Poor coaptation, whether due to a damaged sphincter muscle, poor compressibility due to urethral fibrosis, or a lack of compressibility by surrounding organs, results in intrinsic sphincteric deficiency. This is another group of women that clearly benefit from an anatomic assessment such as that provided by cystourethroscopy.
Intrinsic sphincteric deficiency The Agency for Health Care Policy and Research coined the term ‘intrinsic sphincteric deficiency’ (ISD), defining it as a condition in which ‘the urethral sphincter is unable to coapt and generate enough resistance to retain urine in the bladder’.16 ISD is generally contrasted with the more common form of USI caused by bladder neck hypermobility, although most women with USI have varying degrees of both. Unfortunately, clinical criteria for ISD have not been standardized. In the absence of validated standard criteria for diagnosing ISD, an approach that combines historical risk factors with measures of incontinence severity, urodynamic evidence of poor urethral resistance, and an anatomic evaluation of urethral coaptation appears to be warranted. Cystourethroscopy is perhaps the simplest approach to the anatomic evaluation of the UVJ. The anatomic evaluation provided by cystourethroscopy can also be achieved using radiologic techniques, discussed in the preceding chapters. Transrectal and perineal ultrasound have been used to evaluate women with urinary incontinence, and while most investigators have utilized ultrasound to assess UVJ mobility,17–19 others have advocated it as a means of differentiating between USI and ISD.20 This might be an alternative to urethroscopy for evaluating the UVJ but does not pro-
vide the mucosal evaluation of the lower urinary tract achieved with urethrocystoscopy. The same is true of fluoroscopy, although some authors feel that it is superior to cystourethroscopy for diagnosing ISD. Moreover, while videourodynamics can provide an equivalent anatomic evaluation of the UVJ, the cost for providing such a service is considerably higher than the cost of basic urethrocystoscopy.
Universal evaluation There is general agreement that cystoscopy is indicated for patients complaining of irritative symptoms, persistent incontinence or voiding dysfunction following incontinence surgery. There is less agreement about the role of cystoscopy in the baseline evaluation of all women with urinary incontinence and there are relatively few analyses to define its role in this capacity. However, one series suggests that at the time of cystourethroscopy, up to 5% of patients presenting with urinary incontinence may have unsuspected neoplastic lesions, including bladder malignancies and potentially premalignant lesions such as cystitis glandularis.8 Ideally, historical factors or urodynamic parameters could be used to distinguish those patients that merit urethrocystoscopy based on risks for neoplastic lesions; however, in this relatively limited population, age over 60, symptoms of urgency, and a urodynamic diagnosis of DI were not predictive of these mucosal lesions. Moreover, common symptoms associated with mucosal lesions, such as pain and hematuria, were not present in these patients. The annual age-adjusted incidence rate per 100,000 population for bladder cancer in women is reported as 6.2. It rises with increasing age, approaching 20 for age 55 years, and there are also regional variations.21,22 Whether women presenting with urinary incontinence have a higher incidence of bladder cancer has not been determined. Individual clinicians, therefore, must determine the benefits of combining cystourethroscopy with urodynamic evaluation for women presenting with urinary incontinence.
Instrumentation Rigid cystoscopy There are three components to the rigid cystoscope: the telescope, the sheath, and the bridge (Fig. 27.1). Each component performs a different function and is available with various options to facilitate its role under different circumstances. 379
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diameter sheath is useful for diagnostic procedures, those of larger caliber provide space for the placement of instruments into the irrigation-working channel. The proximal end of the sheath has two irrigating ports: one for introduction of the distending media and another for its exit. The distal end of the cystoscope sheath is fenestrated to permit use of instrumentation in the angled field of view. It is also beveled, opposite the fenestration, to increase the comfort of introduction of the cystoscope into the urethra. Bevels increase with the diameter of the cystoscope and larger diameter sheaths may require an obturator for placement. Figure 27.1. Components of a rigid cystoscope (from top to bottom): telescope, diagnostic (17 Fr) sheath, bridge and assembled cystoscope.
Telescopes The telescope transmits light to the bladder cavity as well as an image to the viewer. Today, virtually all rigid telescopes use a rod lens system. Telescopes designed for cystoscopy are available with several viewing angles, including 0 degrees (straight), 30 degrees (forwardoblique), 70 degrees (lateral), and 120 degrees (retroview). The angled telescopes have a field marker that helps maintain orientation. It is visible as a blackened notch at the outside of the visual field and opposite the angle of deflection. The different angles facilitate the inspection of the entire bladder wall. Although the 0-degree lens is essential to adequate urethroscopy, it is insufficient for cystoscopy. The 30-degree lens provides the best view of the bladder base and posterior wall, while the 70-degree lens permits inspection of the anterolateral walls. The retroview of the 120-degree lens is not usually necessary for cystoscopy of the female bladder but can be useful for evaluating the urethral opening into the bladder. For many applications, a single telescope is preferable. In diagnostic cystoscopy, the 30-degree telescope is usually sufficient, although a 70-degree telescope may be required in the presence of fixation of the UVJ. For operative cystoscopy, the 70-degree telescope is preferable.
Sheaths The cystoscope sheath provides a vehicle for introducing the telescope and distending media into the vesicle cavity. Sheaths are available in various calibers, ranging from 17 to 28 Fr. When placed within the sheath, the telescope, which is 15 Fr, only partially fills the lumen, leaving an irrigation-working channel. The smallest
Bridges The bridge serves as a connector between the telescope and sheath, and forms a watertight seal with both. It may also have one or two ports for introduction of instruments into the irrigation-working channel. The Albarran bridge is a variation of the bridge that has a deflector mechanism at the end of an inner sheath. When placed within the cystoscope sheath, the deflector mechanism is located at the distal end of the inner sheath within the fenestra of the outer sheath. In this location, elevation of the deflector mechanism assists the manipulation of instruments within the field of view.
Urethroscopes versus cystoscopes The architectural differences between the urethra and bladder place unique demands on the endoscopes used to evaluate these two structures. The narrow caliber, straight lumen of the urethra is not adequately assessed by the angled cystoscope. The rigid urethroscope is a modification of the cystoscope designed exclusively for evaluation of the female urethra (Fig. 27.2). The urethroscope uses a telescope that is shorter and has a 0-degree viewing angle that provides a circumferential view of the urethral lumen as the mucosa in front of the urethroscope is distended by the distension media. The 0-degree lens is essential for adequate urethroscopy. The urethroscope sheath is designed to maximize distension of the urethral lumen. The proximal end of the sheath has a single irrigating port and the telescope only partially fills the sheath, leaving space for the irrigant to flow around it. Sheaths are available in 15 and 24 Fr calibers. The larger diameter sheath is useful, if tolerated, as it provides the best view of the urethral lumen by providing more rapid fluid flow for maximal distension. As the rigid urethroscope is primarily a diagnostic instrument, it does not have a bridge. Just as the cystoscope is inadequate for evaluation of the urethra, the urethroscope is inadequate for a complete assessment of the bladder.
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Figure 27.2. Urethroscope.
Figure 27.3. Flexible cystourethroscope.
There are other urethroscopes with lenses angled up to 30 degrees from the horizontal, thus permitting a more panoramic view of the urethra.
In spite of these restrictions, several studies have compared rigid to flexible cystoscopy and found no compromise of diagnostic capabilities.23,24 Many urologists prefer the flexible cystoscope because of improved patient comfort, although the improvement in patient comfort primarily applies to male patients. The absence of a prostate and the short length of the female urethra make rigid cystoscopy well tolerated by women. This may offset any perceived advantage of flexible cystoscopy in female patients.
Flexible endoscopes Unlike the rigid cystoscope, the flexible cystoscope combines the optical systems and irrigation-working channel in a single unit. The optical system consists of a single image-bearing fiberoptic bundle and two lightbearing fiberoptic bundles. The fibers of these bundles are coated parallel coherent optical fibers that transmit light even when bent. This permits incorporation of a distal tip-deflecting mechanism that will deflect the tip 290 degrees in a single plane. A lever at the eyepiece controls the deflection. The optical fibers are fitted to a lens system that magnifies and focuses the image. A focusing knob is located just distal to the eyepiece. The irrigation-working port enters the instrument at the eyepiece opposite the deflecting mechanism. The coated tip is 15–18 Fr in diameter and 6–7 cm in length, with the working unit comprising half the length (Fig. 27.3). Because of the individual coating of the fibers, there is a small space between each fiber in the image guide. Consequently, the image appears somewhat granular. The delicate 5–10 µm diameter of the fibers makes them susceptible to damage that will further compromise the image or light transmission. Gentle handling is, therefore, essential not only to good visualization but also to the longevity of the instrument. The flow rate of the irrigation-working channel is approximately one-quarter that of a similar size rigid cystoscope and is further curtailed by passage of instruments down this channel. Some tip deflection is also lost with use of the instrument channel.
Endoscopic Techniques Since a complete endoscopic evaluation for urinary incontinence demands evaluation of both the bladder and the urethra, diagnostic urethroscopy and cystoscopy are usually combined. Diagnostic cystourethroscopy in women is well tolerated as an office procedure without anesthesia. Urethroscopy usually precedes the cystoscopic examination to prevent sheath-associated trauma from compromising the urethroscopic evaluation. Both rigid and flexible endoscopes will provide adequate visualization of the lower urinary tract, but only rigid endoscopy is described. The approach using a flexible cystoscope is similar to the technique described for rigid cystoscopy.
Dynamic urethroscopy Sterile water and saline at room temperature are the most commonly used distending media. Instillation is by gravity through a standard intravenous infusion set with the bag at a height of 100 cm above the patient’s pubic symphysis. The urethroscope has a 0-degree viewing angle (straight), ideal for viewing the urethral lumen directly in front of the urethroscope. The urethral 381
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meatus is cleansed with a disinfectant and, with the distension medium flowing, the urethroscope is introduced into the urethral meatus. The center of the urethral lumen is maintained in the center of the operator’s visual field and the urethral lumen, distended by the infusing medium, is followed to the UVJ. The urethral mucosa is examined for redness, pallor, exudate, and polyps as the urethroscope is advanced. Dynamic urethroscopy, as originally described by Robertson,25 provides a subjective evaluation of urethral function. With a bladder volume of at least 300 ml, the urethroscope is withdrawn until the UVJ closes onethird of the way, and the response of the UVJ to ‘hold your urine’ and ‘squeeze your rectum’ commands, as well as Valsalva maneuver and cough, is observed. The UVJ should close with all of these commands. The urethroscope is then withdrawn while a finger in the vagina obstructs the urethral lumen proximal to the urethroscope. This maximizes distension of the urethral lumen, providing the best possible view of the urethral mucosa. Gentle massage of the urethra against the scope milks exudate from glands and diverticular openings, which helps to localize the ostia.
Diagnostic cystoscopy Cystoscopy is performed using a 30- or 70-degree angled telescope in a 17 Fr sheath. Topical anesthetics should be avoided during urethroscopy since they can affect the color of the urethral mucosa. Following urethroscopy, however, 1% lidocaine jelly may be used as a lubricant and topical anesthetic. The cystoscope is placed into the urethral meatus with the blunt beak of the sheath directed posteriorly and advanced to the bladder under direct visualization. An obturator is not usually necessary since downward pressure on the posterior urethral lumen with the blunt bleak of a 17 Fr sheath fully opens the urethral lumen and is well tolerated by the majority of women. The infusion of water is maintained at a slow rate until a volume of 300–400 ml is reached or until the patient reports fullness. At this volume, the flow may be stopped unless it is required to improve the endoscopic view, in which case a small volume can be removed for patient comfort. Orientation is easily established by identifying an air bubble at the anterior dome of the bladder. This serves as a landmark during the remainder of the examination of the bladder mucosa. Beginning at the superior dome to the UVJ, the survey progresses in 12 sweeps, mimicking the points of a clock. Orientation is maintained by placing the field marker directly opposite that portion of the bladder to be inspected. Visualization of the bladder base can be difficult in patients with a
large cystocele although reduction of the prolapse with a finger in the vagina easily circumvents this problem. The mucosa is examined for color, vascularity, trabeculation, and abnormal lesions such as plaques or masses.
‘Flat tire’ test Endoscopic evaluation for urinary vaginal fistulae requires several modifications from the usual diagnostic technique. The ‘flat tire’ technique permits differentiation of a vesicovaginal from a ureterovaginal fistula, while also identifying the vaginal fistula opening. Prior to cystoscopy, the vaginal vault is filled with 10% dextrose solution, and CO2 gas is used in place of sterile water as a distending medium through the cystoscope. The CO2 distends the bladder and, if a vesicovaginal fistula is present, CO2 bubbles into the water-filled vaginal vault, identifying the diverticular opening. Simultaneous administration of intravenous indigo carmine will identify a ureterovaginal fistula, as the dye seeps into the hypertonic fluid in the vagina. A vesicovaginal fistula following hysterectomy is most commonly identified in the supratrigonal area of the bladder.
Endoscopic Findings Normal endoscopic findings Normally, the urethral mucosa is pink and smooth with a posterior longitudinal ridge, called the urethral crest (Fig. 27.4). The UVJ is typically round or an inverted horseshoe shape and is completely coapted until the
Figure 27.4. Urethral lumen showing urethral crest and normal coaptation.
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lumen is opened by the irrigant. The UVJ normally closes briskly and has minimal mobility on Valsalva maneuver. In its normal state, the bladder mucosa has a smooth surface with a pale pink to glistening white hue. The translucent mucosa affords easy visualization of the branched submucosal vasculature. As the mucosa of the dome gives way to the trigone, it thickens and develops a granular texture. The trigone is triangular in shape, with the inferior apex directed toward the UVJ and the ureteral orifices forming the superior apices. As the cystoscope is advanced past the UVJ, the trigone is apparent at the bottom of the field. The interureteric ridge is a visible elevation that forms the superior boundary of the trigone, running between the ureteral orifices. The intramural portion of the ureters can often be seen as they course from the lateral aspect of the bladder towards the trigone and ureteral orifices. Although there is marked variation in the ureteral orifices, they are generally circular or slit-like openings at the apex of a small mound (Fig. 27.5). With efflux of urine, the slit opens and the mound retracts in the direction of the intramural ureter. When distended, the bladder is roughly spherical in shape, but numerous folds of mucosa are evident in the empty or partially filled bladder. The uterus and cervix can usually be seen indenting the posterior wall of the bladder, which creates posterolateral pouches where the bladder drapes over the uterus into the paravaginal spaces. At times, visualization of the anterior bladder dome requires manual pressure on the lower abdomen.
cally the most anterior lumen drains the true bladder (Fig. 27.6). Due to the blind ending and the possibility of urine deposition and entrapment in the false urethra, resection of the duplicate urethra may be required.
Polyps and fronds Fibroepithelial polyps of the bladder and ureter (which can extend into the bladder) have also been identified and usually appear as smooth lesions, commonly on a long stalk. Diagnosis is made by endoscopic resection. Bladder neck and/or urethral pseudopolyps appear as pink frondular lesions within the urethra proper or extending into the bladder. They are non-malignant lesions that do not require histologic confirmation, and have been associated with irritative symptoms. It has not been clearly demonstrated that fulguration is associated with long-lasting symptom resolution.
Urodynamic stress incontinence The urethral hypermobility typical of USI causes the UVJ to open and descend in response to cough and Valsalva maneuver, and the patient may not be able to close the UVJ to the ‘hold’ and ‘squeeze’ commands. Urethroscopic findings typical of the patient with ISD include a rigid, immobile urethra with poor coaptation (Fig. 27.7). In severe cases, the UVJ is unresponsive to commands and the lumen is visualized in its entirety from meatus to UVJ. DO should be suspected if there is uncontrollable urethral opening during filling.
Urethral findings While congenital urethral anomalies are quite uncommon, urethral duplication has been reported, and typi-
Figure 27.5. Left urethral orifice with squamous metaplasia overlying trigone. The interureteric ridge is also visible.
Figure 27.6. Cystogram of urethral duplication. Note blind ending posterior urethral lumen. (Courtesy of Dr P. Zimmern, University of Texas Southwestern Medical Center, Dallas, Texas.) 383
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Figure 27.7. Intrinsic sphincteric deficiency.
Diverticula Urethral diverticula occur in 1–3% of women, and are located along the posterolateral wall of the urethra as single or multiple outpouchings. Over half of the diverticular openings are at the mid-urethra, with a number more proximal, and some more distal (Fig. 27.8). The urethroscopic diagnosis is most accurate when the bladder is filled, and a finger in the vagina occludes the bladder neck or proximal urethra. A steady flow of fluid into the urethra is maintained as the scope is withdrawn and the urethra massaged by the finger pressing upward from below.
Abnormal Bladder Findings Non-malignant bladder lesions
cobblestoning appearance of the trigone found exclusively in women. A benign lesion that may represent ectopic vaginal epithelium, it does not require bladder biopsy. Cystitis cystica and cystitis glandularis are histologic diagnoses of bladder lesions that typically appear as reddened, inflamed areas, often indistinguishable from carcinoma in situ, and are associated with recurrent and chronic infections. They appear to result from Brunn’s nests (subepithelial islands of transitional cells that form cystic lesions). Though both are benign lesions, adenocarcinoma of the bladder occurring in conjunction with cystitis glandularis has been reported.26 Eosinophilic cystitis may appear as a red–brown patch cystoscopically, and the diagnosis can only be made by histologic evaluation. Steroid treatment has been employed in patients with this form of cystitis. Malakoplakia of the bladder results from some form of chronic irritation, often as a result of recurrent infection. The cystoscopic appearance is non-diagnostic, often appearing as yellow or brown flat plaques, although the pathologic finding of Michaelis–Gutmann bodies (partially digested cell wall fragments) is confirmatory. Long-term antibiotic treatment may be required in symptomatic patients. Bladder trabeculations have been most commonly described in association with bladder outlet obstruction (Fig. 27.9), though this is a non-specific finding. Grades of trabeculation have been proposed, though none is universally accepted. In general, more severe trabeculation has been associated with detrusor compromise. Histologic analysis of trabeculations has demonstrated a mixture of smooth muscle bundles with an abundance
One of the more common findings on initial cystoscopic evaluation is squamous metaplasia, seen as a whitish,
Figure 27.8. Urethral diverticula.
Figure 27.9. Bladder trabeculations.
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of interfascicular collagen deposition. Diverticula are urothelial-lined pockets without smooth muscle backing that can either be congenital (i.e. Hutch diverticula located adjacent to a ureteral orifice) or acquired (commonly in the setting of outlet obstruction). They may have either a large or a narrow neck, and if poorly draining can be a source of recurrent infection. As noted above, each must be carefully examined at the time of cystoscopy to evaluate for mucosal tumors.
Foreign bodies Intravesical foreign bodies may present with hematuria or as urge incontinence due to mucosal irritation. Bladder calculi may result from urinary stasis or the presence of a foreign body, or an inflammatory exudate may coalesce and serve as a nidus for stone formation (Figs 27.10, 27.11). Stones have an extremely variable cystoscopic appearance in terms of color, size, and shape, but generally have an irregular surface. Foreign bodies and stones are usually accompanied by varying degrees of general or localized inflammatory reaction. Cystourethroscopy can provide valuable information in making these diagnoses.
Fistulae Diagnosis is made in three steps after a fistula is suspected. Step one is to confirm that watery drainage is urine; Pyridium may be used for this purpose. The next step is to exclude urinary incontinence occurring from the urethra by filling the bladder and observing for loss from the urethra or vagina. Finally, the source of the fistula needs to be determined. This commences with a thorough speculum inspection, which may reveal a fistula site to the vagina. The double-contrast test is
Figure 27.11. Bladder stones in setting of poorly draining bladder secondary to severe anterior vaginal wall prolapse. also useful, although cystoscopy and the flat tire test are the best ways to visualize the fistula site in the bladder. A posthysterectomy vesicovaginal fistula on the bladder side appears above the trigone medial to the ureters (Fig. 27.12); at vaginoscopy it is at the vaginal vault. Cystoscopy may show edema and congestion, or even mucosal papillomatous hyperplasia in enterovesical fistulae. Sometimes a ureteral catheter can be passed into a visible fistula opening to outline its path. Enterovesical fistulae are not uncommon, particularly among patients with a history of diverticulitis (colovesical fistulae). Often noted as a ‘herald’ patch on diagnostic cystoscopy (reddened appearance typically at the dome or on the left lateral wall), the diagnosis can be confirmed by cystography or pelvic computed tomography (CT) scanning. Occasionally, oral administration of charcoal will help confirm the diagnosis (apparent in urinary sediment) when radiologic studies are equivocal.
Interstitial cystitis
Figure 27.10. Intravesical suture with adherent calculi.
While interstitial cystitis (IC) remains largely a diagnosis made by symptom assessment, the inclusion of typical cystoscopic findings in the original National Institute of Arthritis, Diabetes, Digestive and Kidney Disease (NIDDK) criteria27 highlights the importance of cystoscopy in the evaluation of patients with IC, though more recent studies have suggested the absence of cystoscopic findings does not preclude the diagnosis.28 Office cystoscopy in patients with IC will typically reveal a small capacity bladder (less than 200 cc) that is readily inflamed 385
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are certainly uncommon in other conditions, they may be present in only 5–20% of patients with IC.29,30
Malignant bladder lesions
Figure 27.12. Supratrigonal fistula. with the slightest provocation. Petechial hemorrhages at sites of mucosal glomerulations are common with slight distension (Fig. 27.13); discrete areas of mucosal breaks can also be seen with more aggressive distension. Therapeutic hydrodistension under anesthesia will usually lead to significant petechial hemorrhaging, which is common in patients with IC, though certainly nondiagnostic, as patients with altered compliance (e.g. secondary to radiation cystitis) may have a similar response to distension. Hunner’s ulcers, which appear as discrete areas of ulcerated mucosa, are thought to be characteristic (and perhaps diagnostic) of IC. Overall, there are few data to suggest that the presence of petechial hemorrhaging is specific for IC, and although Hunner’s ulcers
Figure 27.13. Glomerulations secondary to minimal hydrodistension in presumed case of interstitial cystitis. (Courtesy of Dr P. Zimmern, University of Texas Southwestern Medical Center, Dallas, Texas.)
Transitional cell carcinoma (TCC) of the bladder typically has a papillary appearance (Fig. 27.14) and may be multifocal. Patients found to have a bladder mass should undergo careful cystoscopy with both 30- and 70-degree lenses or a flexible cystoscope to evaluate the complete mucosal surface, including the bladder neck circumferentially. With a flexible cystoscope, this is best achieved by advancing the cystoscope and retroflexing the scope on itself to view the bladder neck. If diverticula are noted in the bladder, each diverticulum must be carefully inspected to rule out the presence of TCC, which can be difficult to detect in these poorly draining areas. Other TCC lesions may have a more sessile appearance (Fig. 27.15). Generally, this type of appearance portends a more aggressive, potentially invasive tumor. Carcinoma in situ typically has a flat, red, velvety appearance that may be multifocal (Fig. 27.16). Other malignant bladder lesions include squamous cell tumors, sometimes associated with chronic infections or chronic indwelling catheters,31 and metastatic lesions. Melanoma (Fig. 27.17), breast adenocarcinoma, as well as several other tumors, have been noted to metastasize to the bladder,
Figure 27.14. Papillary transitional cell carcinoma. (Courtesy of Dr A. Sagalowsky, University of Texas Southwestern Medical Center, Dallas, Texas.)
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Figure 27.15. Sessile transitional cell carcinoma. (Courtesy of Dr Y. Lotan, University of Texas Southwestern Medical Center, Dallas, Texas.) Figure 27.17. Metastatic melanoma to the bladder. (Courtesy of Dr Y. Lotan, University of Texas Southwestern Medical Center, Dallas, Texas.) in determining if malignant cells are present in bladder washings, none at this point is sensitive enough to preclude the need for tissue diagnosis, particularly when the lesion is not a typical papillary mass. Bladder masses of likely malignant nature require complete transurethral endoscopic removal, and may require adjuvant intravesical chemotherapy or further surgical endeavors, depending on the depth of invasion and grade of tumor present.
Ureteral and urethral anomalies
Figure 27.16. Carcinoma in situ. (Courtesy of Dr Y. Lotan, University of Texas Southwestern Medical Center, Dallas, Texas.) often resulting in repeated bouts of gross hematuria. Locally advanced malignancies, typically of the colon, can also directly invade the bladder wall and eventually disrupt the bladder mucosa, resulting in an abnormal cystoscopic appearance and hematuria. Bladder lesions of uncertain etiology on initial evaluation must be investigated under anesthesia, as often cold cup biopsies and fulguration will be required to determine their malignant potential. Although both urinary cytologies and other urinary markers are helpful
Ureteral anomalies are not uncommonly found in patients undergoing diagnostic cystoscopy. Duplicated systems can occur bilaterally or unilaterally, with two orifices from the same renal unit typically being adjacent to one another. The medial and caudal-most of the ureteral orifices normally serve the upper pole system. Vesicoureteral reflux is often present in the ureter serving the lower pole system (a finding confirmed on cystography). In women, ectopic ureters may also be found to drain into the urethra and vaginal vestibule, though most of these abnormalities will be found in childhood secondary to ongoing incontinence. Asymptomatic, single system ureteroceles are also not uncommon in adults, with the typical appearance being a thin layer of urothelium covering a bulging orifice in a normal location. Often, a pinpoint opening is noted on 387
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the membrane, and, due to urinary stasis, ureteral stone formation can occur proximal to this opening, particularly in children. Upper tract imaging may be required to evaluate the collecting system in these instances. Occasionally, ureteroceles will be ectopic in location, at times presenting as far distally as the mid and distal urethra. In contrast, urethral anomalies are quite uncommon. Urethral duplication has been reported, and typically the most anterior lumen drains the true bladder (Figs 27.6, 27.18). Due to the blind ending and the possibility of urine deposition and entrapment in the false urethra, resection of the duplicate urethra may be required.
Conclusion Endoscopy of the lower urinary tract is an invaluable tool to the physician treating women for urinary incontinence. While it is not the best method for diagnosing USI and DI, it does provide unique anatomic information with a simple, minimally invasive approach. Endoscopy is a useful adjunct to multichannel urodynamics in women with possible ISD, urethral diverticula, urogenital fistulae, foreign bodies or urothelial lesions.
3. Korda A, Krieger M, Hunter P, Parkin G. The value of clinical symptoms in the diagnosis of urinary incontinence in the female. Aust N Z Obstet Gynaecol 1987;27:149–51. 4. Cundiff GW, Harris RL, Coates KW, Bump RC. Clinical predictors of urinary incontinence in women. Am J Obstet Gynecol 1997;177:262–7. 5. Robertson JR. Air cystoscopy. Obstet Gynecol 1968;32:328– 30. 6. Sand PK, Hill RC, Ostergard DR. Supine urethroscopic and standing cystometry as screening methods for detection of detrusor instability. Obstet Gynecol 1987;70:57– 60. 7. Scotti RJ, Ostergard DR, Guillaume AA, Kohatsu KE. Predictive value of urethroscopy as compared to urodynamics in the diagnosis of genuine stress incontinence. J Repro Med 1990;35:772–6. 8. Cundiff GW, Bent AE. The contribution of urethrocystoscopy to a combined urodynamic and urethrocystoscopic evaluation of urinary incontinence in women. Int J Urogynecol 1996;7:307–11. 9. Leach GE, Bavendam TG. Female urethral diverticula. Urology 1987;30:407–15. 10. Robertson JR. Urethral diverticula. In: Ostergard DR, Bent AE (eds) Urogynecology and Urodynamics: Theory and Practice, 3rd ed. Baltimore: Williams and Wilkins, 1991; 283–91. 11. Drutz HP. Urethral diverticula. Obstet Gynecol Clin North Am 1989;16:923–9. 12. Massee JS, Welch JS, Pratt JH, Symmonds RE. Management of urinary–vaginal fistula. JAMA 1964;190:124–8. 13. Symmonds RE. Incontinence: vesical and urethral fistulas. Clin Obstet Gynecol 1984;27:499–514. 14. Bump RC, Hurt WG, Theofrastous JP, Addison WA, Fantl JA, Wyman JF, McClish DK. Continence Program for Women Research Group. Randomized prospective comparison of needle colposuspension versus endopelvic fascia plication for potential stress incontinence prophylaxis in women undergoing vaginal reconstruction for stage II or IV pelvic organ prolapse. Am J Obstet Gynecol 1996;175:326–35.
Figure 27.18. Urethral duplication. Note ectopic urethral orifice. (Courtesy of Dr P. Zimmern, University of Texas Southwestern Medical Center, Dallas, Texas.)
REFERENCES 1. Largo-Janssen ALM, Debruyne FMJ, Van Weel C. Value of the patient’s case history in diagnosing urinary incontinence in general practice. Br J Urol 1991;67:569–72. 2. Sand PK, Hill RC, Ostergard DR. Incontinence history as a predictor of detrusor stability. Obstet Gynecol 1988;71:257–9.
15. Bruskewitz R, Nielsen K, Graversen P et al. Bladder neck suspension material investigated in a rabbit model. J Urol 1989;142:1361–3. 16. Urinary Incontinence Guideline Panel. Urinary incontinence in adults: clinical practical guidelines. AHCPR Pub. No. 92-0038. Rockville, MD: Agency for Health Care Policy and Research, Public Health Service, U.S. Department of Health and Human Services. 1992. 17. Bergman A, McKenzie CJ, Richmond J, Ballard CA, Platt LD. Transrectal ultrasound versus cystography in the evaluation of anatomical stress urinary incontinence. Br J Urol 1988;62:228–34.
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18. Chang HC, Chang SC, Kuo HC, Tsai TC. Transrectal sonographic cystourethrography: studies in stress urinary incontinence. Urology 1990;36:488–92. 19. Gordon D, Pearce M, Norton P, Stanton S. Comparison of ultrasound and lateral chain urethrocystography in the determination of bladder neck descent. Am J Obstet Gynecol 1989;160:182–5. 20. Weil EHK, van Waalaijk van Doorn ESC, Heesakkers JPFA, Meguid T, Janknegt RA. Transvaginal ultrasonography: a study with healthy volunteers and women with genuine stress incontinence. Eur Urol 1993;24:226–30. 21. Young JL Jr, Percy CL, Asire AJ (eds) Surveillance, epidemiology, end results: incidence and mortality data, 1973–77. Natl Cancer Inst Monogr 1981;57:1–1082.
25. Robertson JR. Endoscopic examination of the urethra and bladder. Clin Obstet Gynecol 1983;26:347–8. 26. Sozen S, Gurocak S, Uzum N, Biri H, Memis L, Bozkirli I. The importance of re-evaluation in patients with cystitis glandularis associated with pelvic lipomatosis: a case report. Urol Oncol 2004;22:428–30. 27. Gillenwater JY, Wein AJ. Summary of the National Institute of Arthritis, Diabetes, Digestive and Kidney Diseases Workshop on Interstitial Cystitis. J Urol 1988;140:203–6. 28. Awad SA, MacDiarmid S, Gajewski JB, Gupta R. Idiopathic reduced bladder storage versus interstitial cystitis. J Urol 1992;148:1409–12. 29. Sant GR. Interstitial cystitis. Monograms in Urology 1991;12:37–63.
22. Anton-Culver H, Lee-Feldstein A, Taylor TH. Occupation and bladder cancer risk. Am J Epidemiol 1992;136:89–94.
30. Koziol JA. Epidemiology of interstitial cystitis. Urol Clin North Am 1994;21:7–20.
23. Figueroa TE, Thomas R, Moon TD. Taking the pain out of cystoscopy: a comparison of rigid with flexible instruments. J La State Med Soc 1987;139:26–8.
31. Delnay KM, Stonehill WH, Goldman H, Jukkola AF, Dmochowski RR. Bladder histological changes associated with chronic indwelling urinary catheter. J Urol 1999;161:1106–9.
24. Clayman RV, Reddy P, Lange PH. Flexible fiberoptic and rigid-rod lens endoscopy of the lower urinary tract: a prospective controlled comparison. J Urol 1984;131:715–6.
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28 Natural history and prevention of incontinence and prolapse Robert M Freeman
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INTRODUCTION There are few studies which have prospectively evaluated the natural history of urinary incontinence and pelvic organ prolapse (POP) in women who have not undergone treatment. One, on urinary incontinence after pregnancy, is reported below.1 Epidemiologic studies are described in Chapters 2a–e. An hypothesis for the natural history is presented.
NATURAL HISTORY OF STRESS URINARY INCONTINENCE The association between stress urinary incontinence (SUI) and parity is well known and, based on the available evidence, the following hypothesis regarding the genesis and natural history can be made (Fig. 28.1).2 This might also be relevant for POP.
Hypothesis for the genesis of SUI During pregnancy the endopelvic fascial attachments of the bladder neck and distal sphincter are weakened, possibly due to hormonal influences.3 This might be a progesterone effect resulting in reduced urethral closure pressure4 and connective tissue weakness.5 Along with the increasing intra-abdominal pressure from the pregnant uterus, this might increase the risk of SUI antenatally. In fact, incidences of up to 40% have been reported,2 with approximately 20% having severe symptoms.6 In most cases incontinence improves after delivery, with an incidence of postpartum SUI of approximately 15%.2 In these cases SUI is rarely ‘new onset’; it has usually been present during the pregnancy. Why SUI should persist postpartum is unclear, but vaginal delivery is implicated. If the endopelvic fascial attachments and sphincter function are not damaged at delivery, then the changes seen antenatally are likely to revert to the ‘non-pregnant’ state with the return of normal urethral function and continence. However, if these structures are damaged at delivery or are inherently weak in the non-pregnant state, then recovery might not arise. Support for this hypothesis comes from studies suggesting the presence of a constitutional factor (e.g. weak connective tissue/fascia in women) with SUI.7,8 For example, there is a known association between connective tissue disorders and urinary incontinence and POP (e.g. in Marfan’s and Ehlers–Danlos syndromes).9 In addition, an association with joint hypermobility has been demonstrated in women with POP, suggesting connective tissue weakness.10 Should such individuals
suffer pelvic floor trauma at delivery, then recovery might not be complete, resulting in postpartum SUI. This – along with further deliveries, aging, menopause, and muscle weakness – seems to increase the risk of long-term incontinence11 (see Fig. 28.1). Further support for the hypothesis comes from the growing volume of evidence suggesting that antenatal SUI, and in particular incontinence before a first pregnancy, are high risk factors for the development of incontinence in later years.1,12,13
Natural history As mentioned above, there are few published data. In an unpublished study of women reassessed 6 years after childbirth,1 there was a rate of new onset incontinence of approximately 30% in women who had been continent at 3 months postpartum. However, in 27% who were incontinent at 3 months, there was spontaneous remission at 6 years. Antenatal Hormonal effects
Fascial support
Pressure effects
Sphincter weakness
BN mobility
Reduced urethral resistance
+
Increased abdominal pressure
Antenatal stress incontinence
+ +
DELIVERY Trauma
Congenital weakness
No trauma
De novo stress incontinence
Fascial weakness
Recovery
Failure to recover
Continence
Postnatal stress incontinence (mild) Deliveries Age Menopause
+
Levator weakness
‘Bothersome’ stress incontinence
Figure 28.1. Hypothesis for the genesis of stress urinary incontinence and natural history. (BN mobility, bladder neck mobility.) (Reproduced from Incontinence in Women (Maclean AB, Cardozo L, eds), RCOG Press, 2002, with the permission of the Royal College of Obstetricians and Gynaecologists.)
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Of particular interest were those women who were incontinent prior to pregnancy; there was a markedly increased risk for leakage at 6 years (odds ratio =12). Identification of such individuals might help in prevention of SUI (and POP) if they can be identified at an early stage (see ‘Childbirth’, below).
NATURAL HISTORY OF PROLAPSE The natural history of untreated POP has been assessed in menopausal women as part of the estrogen, progestin trial of the Women’s Health Initiative (University of California).14 Annual pelvic examinations for POP were performed on 412 women (mean 5.7 years) using a (non-validated) classification system. At baseline, 31.8% had POP. The annual incidences of new-onset POP were 9, 5, and 7 per 100 woman years for cystocele, rectocele, and uterine POP, respectively. Of interest were the rates of progression and regression:
• For progression, the rates were 9.5, 13.5 and 1.9 per 100 woman years, respectively;
• Corresponding figures for spontaneous regression, especially Grade 1 POP, were 23.5, 22 and 48, suggesting that spontaneous regression is common. Only three women (0.7%) required surgery. These data suggest that the clinical sign of POP is common and that spontaneous regression occurs in many cases. Treatment might be unnecessary unless the symptoms are bothersome. Previously, prevalence studies which might help in identifying the natural history of POP have been hampered by selection bias (e.g. hospital-based populations in developed countries). In such groups, 30–50% of women seen for other gynecologic problems have signs of POP,15,16 but most will be asymptomatic. In older age groups (>70 years), many are symptomatic, and approximately 11% will undergo surgery, but there are few data on the numbers treated conservatively (e.g. with pessaries).17 In developing countries, untreated POP might be more prevalent. For example, in rural Gambia an epidemiologic study showed a prevalence of 46%. Only 8 of 152 women with ‘severe POP’ (i.e. subjective and objective) accepted the offer of treatment.18 There are no data on the outcome for these untreated women. If severe and left untreated, POP can sometimes result in obstructed voiding and recurrent urinary infection. This could progress to obstruction of the
upper tracts and renal failure. In a small case series of women with untreated severe POP (i.e. beyond the introitus), all had evidence of bilateral upper tract dilatation and three had obstructive renal failure. Treatment of POP resolved the renal failure in all but one patient.19 These findings highlight the need for prevention of upper tract changes by early treatment of advanced POP. Trauma to the cervix and vaginal skin might increase the risk of neoplasia in patients with severe POP. However, there are few prospective studies to assess the risk.
PREVENTION Ideally, the aim of healthcare is prevention rather than cure. Prevention can be classified as primary (interventions in asymptomatic individuals to reduce known risk factors for the development of a disease) or secondary (to detect symptoms at an early stage and to intervene to stop further development or to improve the prognosis of the condition). To stop recurrence of an illness or to prevent it from becoming chronic is tertiary prevention. In urogynecology there is a paucity of large prospective trials to assess the impact of prevention on incontinence and POP. There are known predisposing factors such as age, obesity, family history, parity/vaginal childbirth, and surgery. Identification of individuals at risk might help with implementing preventive measures.
AGE Although the prevalence of incontinence is increased in the elderly,20 the two do not necessarily have a causeand-effect relationship; other pathologic processes associated with aging might be responsible. Resnick21 has created the mnemonic DIAPPERS to describe these: Delirium, Infection, Atrophic change, Pharmacologic, Psychological, Excess urine output, Restricted mobility, and Stool impaction. There is a known association between constipation and POP,22 and attention to regular bowel habit, avoiding straining, a high-fiber diet and, if necessary, laxatives might have a positive effect on prevention. Likewise, management of other risk factors (e.g. chronic cough, smoking) and adjusting medication that has an adverse effect on the bladder could help incontinence – for example, diuretics, calcium channel antagonists (that can produce polyuria), non-steroidal anti-inflammatory drugs (that can lead to fluid retention), angiotensin-converting enzyme (ACE) inhibitors (leading to chronic cough), and sedatives. 395
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Regular toileting, easy access to toilets, restricting fluids (especially caffeine), and prevention of urinary tract infection (UTI) (e.g. with cranberry juice or vitamin C), might be effective in prevention of incontinence in the elderly although evidence is lacking.
Hormone replacement therapy There is a definite aging process in the lower urinary tract,23 resulting in atrophic change and poor urethral function. Hormone replacement therapy (HRT) should in theory prevent lower urinary tract symptoms. While this has not been proven objectively in patients with urodynamic stress incontinence (USI) or detrusor overactivity (DO),24 in postmenopausal women low dose vaginal estradiol appears to improve the symptom of urgency;25 this could be important in prevention although it is not clear if the mechanism of action is on the bladder or the atrophic change. A Cochrane Review suggests that estrogens might help 50% of women with all types of urinary incontinence compared with 25% on placebo, the effect being most marked in those with urge incontinence.26 However, in the 4-year randomised controlled trial heart and estrogen/progestin replacement study (HERS)27 combined HRT was associated with worsening stress and urge incontinence. The odds ratios are not high which might question the clinical significance of the findings. The data on HRT are conflicting and the effects on prevention of incontinence and prolapse unknown.
Urgency Urgency is a distressing symptom for the older patient with restricted mobility, causing panic and anxiety on the sensation of bladder fullness. Often patients void more frequently to prevent urge incontinence, which can have the opposite effect, by reducing bladder capacity and worsening the symptoms.28 Strategies such as explanation, bladder retraining, pelvic floor exercises, easy access to toilets, and the use of bedside commodes might prevent urgency developing into urge incontinence. There is evidence that patients with urge incontinence (more than once a week) are at increased risk of falls and bone fracture than in those without.29 These might be preventable by employing the above strategies.
age weight for height and age’, obesity has been shown to be more common in patients with USI and DO than in the asymptomatic population.30 In pregnancy, an increased body mass index (BMI) has been shown to be an important risk factor for persistent urinary incontinence post partum.31,32 In theory, weight loss should be preventive. However, studies are often hampered by the failure of subjects to lose weight. One, in morbidly obese women undergoing surgically induced weight loss, showed subjective and urodynamic improvement in incontinence 1 year after surgery.33 In another (randomised controlled trial of 40 women, using diet and behavioral modification), patients losing >5% body weight had a greater reduction in incontinence episodes compared with those who failed to lose weight.34 In a larger case series of women (BMI >30) with urinary incontinence undergoing weight loss by diet, exercise, and drug therapy, reduced incontinence loss (pad test) and improved quality of life were demonstrated in 46/50 women losing more than 5% body weight.35 All studies involving weight loss are difficult as few patients lose sufficient weight to assess the effect on incontinence. However, it has been recommended by the International Consultation on Incontinence36 that such studies be given research priority to answer the question whether or not weight loss helps and prevents urinary incontinence. The two studies which have used incontinence as the primary outcome34,35 suggest that weight loss can result in improvement both subjectively and objectively. Weight loss should be recommended as part of the treatment ‘package’ and might also be useful in secondary prevention.
FAMILIAL RISK FACTORS Identification of risk groups is important and family history might be relevant. It has been shown that daughters of women with urinary incontinence are more likely to develop incontinence themselves.8,37 In addition, a history of childhood symptoms (e.g. nocturnal enuresis and overactive bladder) might predispose to incontinence in adulthood.38–40 Identifying and treating these children (e.g. by behavioral modifications and pelvic floor muscle training) might help to prevent symptoms in adulthood.
OBESITY
CHILDBIRTH
Obesity is common in women with urinary incontinence and POP. When defined as ‘more than 20% above aver-
There is good evidence that vaginal delivery is associated with pudendal nerve injury.41,42 As such nerve damage is
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also seen in patients with USI,43 it has been assumed that vaginal delivery is responsible for subsequent USI and POP. However, this assumption might not be correct; pregnancy itself might be responsible.44 For example, nulliparous women with USI appear to have weak pelvic floor collagen7 and vaginal delivery in these women might increase the risk of SUI and POP if/ when they become pregnant. Identifying them before, or early in a first pregnancy, might enable preventive measures to be introduced. For example, primigravidae with excessive bladder neck mobility antenatally (a possible marker for weak pelvic floor collagen) appear to be at higher risk of post-partum stress incontinence,45 itself a risk factor for long-term incontinence.11 Antenatal and pre-pregnancy incontinence,1,12 family history of incontinence in pregnancy,37 obesity,32 and persistent postnatal incontinence46 also appear to be important risk factors. Intervention in such groups might help with prevention but what this should be is a matter of debate.47 While elective cesarean section might prevent neuromuscular damage41 and post-partum SUI,48 this latter finding is not consistent with incidences of SUI in up to 16% of patients undergoing cesarean section being reported.6,49 Pelvic floor muscle training (PFMT) might be a less invasive and more appropriate form of prevention. For example, in primigravidae with antenatal bladder neck mobility,45 antenatal PFMT has shown a reduced incidence of post-partum SUI compared with untreated controls.31 Similar results have been seen in ‘unselected’ primigravidae.50 While supervised post-partum PFMT seems to be preventive in the short term,51,52 long-term results show a high relapse by six years.53 Nonetheless PFMT antenatally and postnatally should be considered in the short-term. Cesarean section might not be necessary except for those women with severe incontinence and/or POP before and during the first pregnancy. However, further prospective studies are required to confirm if this will prevent SUI and POP in the long term.
Can changing the management of labor help in the prevention of SUI? This is unlikely as the role of obstetric factors in the genesis of post-partum SUI is unclear. For example, there is conflicting evidence regarding prolonged second stage of labor, birth weight, epidural, episiotomy, and mode of delivery.
Although forceps delivery has been implicated,41 this is not a consistent finding.55 The vacuum/ventouse is arguably less traumatic to the pelvic floor. While one study has suggested that the incidence and severity of SUI 1 year after forceps delivery was greater than that after spontaneous delivery or vacuum/ventouse,56 this is not a consistent finding.42 The role of episiotomy is also unclear. A Cochrane Review has failed to show evidence that this prevents urinary incontinence or prolapse.57 It would appear that prevention by changing obstetric practice is not possible with the current state of knowledge.
Overactive bladder symptoms in pregnancy Frequency and nocturia are common in pregnancy and probably ‘physiologic’, due to the effects of hormonal changes and pressure effects of the pregnant uterus. For overactive bladder (OAB) and urge incontinence in pregnancy, incidences of 8–18% have been quoted.6,58 However, the diagnostic accuracy of urodynamics in pregnancy (for DO) is poor.6 A detailed history should identify women with OAB antenatally and bladder retraining might help in secondary prevention. However, few studies have follow-up beyond 3 months and long-term assessment is necessary to ascertain if symptoms persist. Prevention might not be necessary if symptoms are shown to subside with time.
Prevention of obstetric anal sphincter injury (OASI) and fecal incontinence Incidence Fecal incontinence, of either liquid or solid stool, has been reported in 4% of women for the first time postnatally.59 If incontinence of flatus and urgency are added, this figure is increased.60 Although pudendal nerve injury in labor might be responsible,41,42 occult anal sphincter defects have been identified in 35% of primiparae and 44% of multiparae on endo-anal ultrasonography.61 In 13 and 23%, respectively, there were defecatory symptoms (urgency and/or fecal incontinence). The main obstetric factor associated with symptoms was forceps delivery; cesarean section was protective.61
Detection of OASI In women with recognized OASI/third-degree tears, 85% have been shown to have residual sphincter damage despite repair at delivery, with 50% being symptomatic.61 However, many remain unrecognized, 397
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with one-third of women having an undetected OASI after their first delivery.60 It is important that obstetricians and midwives are adequately trained in the identification and treatment of OASI as this might help in the prevention of fecal incontinence. Endo-anal ultrasound might improve the detection rate and help with prevention. In a randomised controlled trial of 752 primiparous women without clinically obvious OASI, ultrasound performed immediately after delivery followed by sphincter repair resulted in a reduced incidence of severe incontinence at 3 months compared with controls (who underwent standard clinical examination and repair).62 Evidence suggests that OASI is associated with long-term risk of fecal incontinence following trauma at first delivery.63 Appropriate methods of defect repair are also important. For example, the ‘overlap repair’ seems to be associated with a lower incidence of long-term incontinence compared with ‘end-to-end’ repair.64 Training is therefore recommended. Identification and repair of OASI might be important in prevention of long-term fecal incontinence. However, prospective follow-up studies are required.
Obstetric management Episiotomy might prevent OASI. However, the evidence is conflicting. Some studies have suggested that fewer third- and fourth-degree tears are seen following mediolateral episiotomy,65,66 whereas the risk is increased by midline episiotomy.67 However, mediolateral episiotomy is not always preventative possibly because they might not be mediolateral, i.e. at 45° to the midline. In one study of doctors and midwives who performed episiotomy none of the midwives performed a true 45° mediolateral episiotomy compared with 22% of those performed by doctors.68
These factors are outside the obstetrician’s control. Nonetheless, awareness might help in prevention – for example, by performing elective mediolateral episiotomy or, if there are other obstetric indications, cesarean section.
Subsequent deliveries In primiparous women with persistent fecal incontinence, the risk of deterioration appears to increase after the second vaginal delivery.72 For these women, secondary prevention might be achieved by elective cesarean section. However, further studies are required to test this hypothesis.
Pelvic floor muscle training For women without incontinence, PFMT might be preventive. For example, in one study treating women with persistent SUI 3 months after delivery, lower rates of fecal incontinence were seen compared with controls.46 It is recommended that women with OASI receive supervised PFMT as a form of secondary prevention. However the protective effects have been shown to disappear at 6 years.53 It is possible that bio-feedback using EMG might have more effect and one study has shown good results in the short term.73 These research findings should focus the attention of obstetricians and midwives to the potential risk of anal sphincter injury and the possible association with longterm fecal incontinence. This should result in improved awareness, training, and prevention.
PREVENTION OF INCONTINENCE AND PROLAPSE FOLLOWING GYNECOLOGIC SURGERY Hysterectomy and incontinence
Forceps and ventouse Use of the ventouse rather than forceps might help in prevention. While it has been claimed that both are risk factors for OASI,59 other data suggest that ventouse is associated with fewer OASIs compared with forceps.69 In a randomized controlled trial of ventouse versus forceps delivery, there was a significant reduction in the incidence of third- and fourth-degree tears in the ventouse group.70 However, it might not be the particular instrument which is important but the indication for the assisted delivery – for example, prolonged labor, large baby,41 and occiput posterior position71 (known risk factors for pelvic floor trauma and OASI).
Urinary tract fistulae are (fortunately) rare, but are not always preventable. Between 0.5 and 3% of lower urinary tract injuries have been reported at hysterectomy. Many of these are due to congenital abnormalities and distortion of structures caused by disease.74 Preoperative intravenous urography and the use of ureteric catheters in potentially difficult cases might help prevent trauma to the urinary tract. An increased risk of urinary incontinence after hysterectomy has been reported. In a systematic review, women over the age of 60 years who had undergone hysterectomy had a higher odds ratio for incontinence compared to women under 60 years.75
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Overall, the estimates suggest a 60% increased risk of developing incontinence after hysterectomy. How this can be prevented is unclear, but with a reduction in the number of hysterectomies for menorrhagia, by the use of progesterone-containing intrauterine devices and endometrial ablation, posthysterectomy incontinence might become less prevalent. For those patients with pre-existing urodynamic stress incontinence requiring hysterectomy, consideration might be given to concomitant continence surgery, as secondary prevention. This has been shown to improve the chances of continence at 1 year postoperatively.76 However, there is no evidence that this is indicated for primary prevention. It has been suggested that subtotal hysterectomy might reduce the incidence of urinary incontinence,77 as the cervix might act as a posterior support for the sphincteric mechanism. It is also thought that division of the cardinal ligaments can result in denervation.78 However, randomized controlled trials have failed to show any benefit of subtotal over total hysterectomy with regards to the onset of urinary incontinence.79–81 On the basis of current evidence, urinary incontinence does not seem to be adversely affected in the short term following hysterectomy. However, as there is an association with incontinence long term,75 preventive measures need to be considered (e.g. PFMT).
Hysterectomy and POP The risk of vaginal vault prolapse and enterocele following hysterectomy has been reported as 3.6/1000 person-years. The risk increases from 1% (at 3 years) to 5% (at 15 years).17 After colposuspension, the incidence of new onset enterocele has a reported incidence of 18–30%.82,83 Possible causes of postsurgical POP include reduced and weakened collagen,10,84 failure to support the vault at hysterectomy or ‘anteversion’ of the anterior vaginal wall following colposuspension. Similarly, ‘retroversion’ of the vaginal vault at sacrospinous ligament fixation can result in a high incidence of cystocele (see Chapter 73). Prevention will depend on the surgical procedure, the technique, and the strength of the supporting structures. Attempts to prevent enterocele, by performing a Moschowitz procedure, or vault prolapse by attaching the round ligaments to the vaginal vault, or cystocele by prophylactic anterior repair at sacrospinous fixation, have been tried but with few data on effectiveness. Long-term follow-up studies are required.
Prevention of urge incontinence after surgery for SUI Colposuspension Following colposuspension, OAB (± DO) with urge incontinence can arise in 15–18.5% of cases.83–85 Longterm follow-up suggests that this persists.86 The causes are unclear, but neuropathy and outlet obstruction as a result of bladder neck over-elevation are possible factors. Of these, bladder neck elevation (>2.6 cm on magnetic resonance imaging, MRI) and a history of previous incontinence surgery have been shown to correlate with the development of postoperative DO and urge incontinence.87 Preoperative urodynamic studies do not appear to help to identify those at risk because of the low specificity and sensitivity of cystometry for DO. It is possible that some patients with urgency, but a stable bladder, might have ‘undetected’ DO. It is therefore important not to ignore the symptoms. Improving the detection of DO preoperatively using bladder wall thickness (on threedimensional ultrasound)88 or ambulatory monitoring89 might prevent unnecessary surgery in these patients. Some patients with preoperative OAB are helped by colposuspension,90 but identifying them is difficult. The history might help. For example, it has been suggested that where the symptom of stress incontinence has preceded the urge, both are helped by colposuspension; when the urge has preceded the stress, the outcome is worse.91 It is usually recommended that, if USI is the main component symptomatically and urodynamically, then colposuspension can be performed. However, the patient should be warned of the risk of postoperative urge incontinence. Changes in surgical technique – for example, avoiding excessive bladder neck elevation (i.e. >2.6 cm)87 – could be preventive. At present, however, no reliable intraoperative method has been found to reproduce the measurement of elevation on MRI; it can only be done subjectively. Excessive elevation should be avoided. Despite the history, urodynamics, and surgical technique, there will be some patients who develop de novo urge incontinence without any obvious preoperative risk factors. Further research is required to determine how this can be prevented. In the meantime, identifying those at risk and avoiding outlet obstruction is all that can be recommended.
Mid-urethral tapes There are few data on whether tension-free vaginal tape (TVT) has a better effect in prevention of de novo urge 399
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symptoms/DO than colposuspension. In the only large randomized controlled trial comparing the two procedures there were no data regarding new-onset urgency or urge incontinence at 2 years. However, there was a significant reduction in the numbers still reporting preexisting OAB symptoms in both groups, but not between the groups.92 In a follow-up of patients 7 years after TVT, 22.5% had ‘urge symptoms’. In a further 6.3% this was ‘de novo’,93 similar to the 9.1% incidence reported by other authors.94 In those with preoperative OAB symptoms, 57% resolved after surgery.94 From these case series it would appear that the incidence of urge incontinence and OAB is similar to that reported after colposuspension.
Prevention of ‘occult or potential’ incontinence Incontinence is a particularly worrying complication following surgery for POP. It has been shown that 7–22% of patients can develop incontinence de novo following POP surgery.95,96 A trial of ring pessary has been used to identify those at risk. In an uncontrolled series, 67 patients undergoing anterior repair for large cystocele (without urinary incontinence) had a preoperative ring pessary test and urodynamic studies.97 There was a drop in pressure transmission ratio in 24 patients and demonstrable stress incontinence in 17. All 24 patients underwent a ‘prophylactic’ needle suspension procedure together with the anterior repair. This resulted in an increase in the pressure transmission ratio, with all patients being dry postoperatively. It is possible that these patients would have been rendered incontinent by the anterior repair alone. However, as the patients were not randomized to ‘no anti-incontinence procedure’, it is not clear if incontinence would have occurred or not. One small randomized trial failed to confirm that a concomitant anti-incontinence procedure is preventive.96 It is generally acknowledged that the incidence of ‘potential’ stress incontinence (i.e. that seen preoperatively following a pessary test) exceeds that actually seen after the procedure.98 However, more data are required. While there are case series using prophylactic TVT at the time of prolapse surgery, and a large ongoing randomized controlled trial assessing the effects of prophylactic colposuspension at the time of sacrocolpopexy for vaginal vault prolapse (CARE study), at present there is no clear evidence that anti-incontinence surgery performed prophylactically at the time of POP surgery will prevent incontinence. In the meantime, it is advisable to
warn patients of the potential risk of incontinence and the possible need for treatment in the future.
Recurrence of stress incontinence after vault suspension: prevention A rare but potentially distressing scenario is recurrence of stress incontinence following vault prolapse surgery in patients who have had a previously successful colposuspension. A case study has highlighted the potential risk and suggested methods of prevention.99 For example, measuring the amount of vault elevation preoperatively which does not result in incontinence and reproducing it at, for example, sacrocolpopexy, might prevent this complication. In addition, performing sacrospinous fixation under spinal anesthesia allows the patient to perform a cough stress test, thus enabling alterations in the placement of the sutures to prevent incontinence.99 How often this complication arises is unclear. However, these reports highlight the need for ‘vigilance’ and to be aware of the possible risk of rendering a patient incontinent again despite previously successful incontinence surgery.
PREVENTION OF FAILED SURGERY FOR INCONTINENCE AND PROLAPSE Stress incontinence surgery The usually quoted success rates for USI surgery are 80– 90%.83 However, this figure has been called into question.90 The difference might be due to the definition of ‘success’ or diagnostic, patient or technical factors. Previous incontinence surgery100 and intrinsic sphincter deficiency (ISD) might be important. For example, a 54% failure rate has been reported in patients with ISD,101 although this is not a consistent finding.102 Studies are required to compare the various surgical procedures for ISD, such as slings, colposuspension, injectables, and mid-urethral tapes so that failure can be prevented. The surgical ‘gold standard’ for USI due to bladder neck ‘hypermobility’ has been the Burch colposuspension,103,104 although the mid-urethral tapes (e.g. TVT) have become popular, with comparable short- and medium-term outcomes.92,93 Prevention of failed surgery might be achieved by avoiding procedures with a poor success rate (e.g. anterior repair) or those which have not been fully evaluated or failed to show benefit over colposuspension.
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Attention to the above should lead to reduced failure rates with surgery. The old adages are still apt: ‘The first operation must be the best one’ and ‘We should choose the right operation for the right patient and the right patient for the right operation’. The latter will depend on factors such as obesity, age, previous surgery, concomitant prolapse, and detrusor overactivity.
Cystocele/anterior repair The anterior repair has long been known to have a high failure rate,105,106 with quoted incidences as high as 40%.107 The reasons for failure are unclear and might be related to surgical technique, patient selection, etc. It is also possible that the anatomic defects associated with cystocele have not been corrected. For example, in many cases the anatomic defect is a detachment of the paravaginal fascia from the arcus tendineus fasciae pelvis (ATFP) or ‘white line’. It is unlikely that an anterior repair which is a midline fascial plication will correct this defect; paravaginal repair might be more appropriate. While success rates of 76–97% have been quoted,108 a randomized controlled trial is required to see if paravaginal repair produces a better outcome than anterior repair in cases of paravaginal defect. At present there are no validated tests that will identify these defects, either pre- or intraoperatively, and whether prevention is possible.
PREVENTION OF DETRUSOR OVERACTIVITY As the etiology and natural history of DO are unclear, prevention is difficult. There are few studies assessing long-term outcomes. Those that exist suggest that overactive bladder (OAB) is a chronic condition that persists urodynamically and symptomatically.109 For prevention of postoperative urge incontinence, accurate diagnosis by urodynamic studies might help avoid unnecessary surgery in patients who have DO and not USI. It is possible that DO might have its origins in childhood (see ‘Familial risk factors’ above). For example, patients with persistent primary nocturnal enuresis have a high incidence of DO.110 In an attempt to prevent symptoms in their children, some mothers who themselves have OAB often ‘toilet’ the children more frequently.111,112 This might be counterproductive as frequent voiding might develop into urgency and urge incontinence.28 Although none of the studies cited here is large or the findings conclusive, nonetheless they highlight the need for further investigation in this area. Should symptoms in childhood be relevant to the eti-
ology of DO, then education of parents regarding toileting and bladder drill might be preventive. Psychological factors have been implicated in the etiology of DO.113,114 Identification, together with appropriate psychotherapy, has shown encouraging results.114 This might also prove valuable in prevention. Anecdotal evidence suggests that a high fluid intake is associated with symptoms of frequency and urgency. Restricting bladder stimulants (e.g. caffeine and alcohol) should be considered. Finally, the ‘integral theory’ suggests that bladder neck opening (due to a weak anterior vaginal wall) might lead to the development of DO.115 PFMT might therefore have a role in prevention. However, long-term studies are needed to test this hypothesis. Further research is needed into the etiology of DO, which might be multifactorial. In the meantime, prevention can only be speculative.
CONCLUSIONS The natural history of incontinence and POP requires more study but there is evidence that spontaneous remission occurs. Effective prevention will only be achieved by long-term prospective studies of appropriate interventions in ‘atrisk’ groups. For example:
• Treatment of coexisting problems, such as obesity, •
• •
•
•
chronic cough or constipation, might help in primary and secondary prevention. Studies of interventions in children with symptoms, and asymptomatic individuals with a strong family history of incontinence and/or POP, should prove informative. Further research is required to assess the preventive effects of hormone replacement therapy in menopausal women. Long-term follow-up of patients with incontinence as a result of pregnancy and vaginal delivery is required before cesarean section can be recommended for prevention. In the short term PFMT seems to have a beneficial effect in ‘at-risk’ groups. Attention to the potential risk of incontinence following hysterectomy or POP surgery is suggested. For a patient to be rendered incontinent following unrelated surgery is distressing; measures to identify the risk and prevent this outcome should be considered. Further research is required to identify the reasons for poor treatment outcomes (e.g. POP surgery) and measures taken to improve success. 401
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With attention to the above and the natural history, appropriate preventive measures should be found to ‘protect’ women from incontinence and pelvic organ prolapse.
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37. Iosif S. Stress incontinence during pregnancy and the puerperium. Int J Gynecol Obstet 1981;19:13–20.
52. Wilson P, Herbison GP. A randomized controlled trial of pelvic floor muscle exercises to treat postnatal urinary incontinence. Int Urogynaecol J Pelvic Floor Dysfunct 1998;9:257–64.
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39. Kuh D, Cardozo L, Hardy R. Urinary incontinence in middle aged women: Childhood enuresis and other life time risk factors in a British Cohort Study. J Epidemiol Community Health 1999;53:453–458.
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55. Allen RE, Hosker GL, Smith ARB, Warrell DW. Pelvic floor damage and childbirth: a neurophysiological study. BJOG 1990;97:770–9.
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56. Arya LA, Jackson ND, Myers DL, Verma AV. Risk of new-onset urinary incontinence 1 year after forceps and vacuum delivery in primiparous women. Am J Obstet Gynecol 2001;185:1318–24.
42. Sultan AH, Kamm A, Hudson CN. Pudendal nerve damage during labour: a prospective study before and after childbirth. BJOG 1994;101:22–8.
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58. Cutner A, Cardozo LD, Benness CJ. Assessment of urinary symptoms in early pregnancy. BJOG 1991;98:1283–6.
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59. MacArthur C, Bick DE, Keighley MR. Faecal incontinence after childbirth. BJOG 1997;104:46–50. 60. Sultan AH, Kamm MA, Hudson CN. Anal sphincter disruption during vaginal delivery. N Engl J Med 1993;329:1905–11. 61. Sultan AH, Kamm MA, Bartram I, Hudson CN. Third
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62. Faltin DL, Boulvain M, Floris LA, Irion O. Diagnosis of anal sphincter tears to prevent fecal incontinence: A randomised controlled trial. Obstet Gynecol 2005;106:6–13.
76. Kjeiulff KH, Langenberg PW, Greenaway L et al. Urinary incontinence and hysterectomy in a large prospective cohort study in American women. J Urol 2002;167:2088–92.
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77. Kikku P. Supravaginal uterine amputation v hysterectomy with reference to subjective bladder symptoms and incontinence. Acta Obstet Gynecol Scand 1985;64:375–9.
64. Fernado R, Sultan A, Kettle C et al. A randomized trial of overlap versus end-to-end primary repair of the anal sphincter [abstract]. Neurourol Urodyn 2004;23:411–412. 65. Poen AC, Felt-Bersma RJF, Dekker GA et al. Third degree obstetric perineal tears: risk factors and the preventative role of mediolateral episiotomy. BJOG 1997;104:563–6.
78. Parys BT, Haylen BT, Hutton JL, Parsons KF. The effects of simple hysterectomy on vesicourethral function. Br J Urol 1989;64:594–9. 79. Thakar R, Ayes S, Clarkson P et al. Outcomes after total and subtotal hysterectomy. N Engl J Med 2002;347:1318–29.
66. De Leeuw JW, Struijk PC, Vierhout ME, Wallenburg HCS. Risk factors for third degree perineal ruptures during pregnancy. BJOG 2001;108:383–7.
80. Lerman LA, Summitt RL, Varner RE et al. A randomized comparison of total or supracervical hysterectomy: surgical complications and clinical outcomes. Obstet Gynecol 2003;102:453–62.
67. Helwig JT, Thorp JM, Bowes WA. Does midline episiotomy increase the risk of third and fourth-degree lacerations in operative vaginal deliveries? Obstet Gynecol 1993;82:276–9.
81. Gimbel H, Zobbe V, Anderson BM et al. A randomized controlled trial of total compared with subtotal hysterectomy with one year follow-up results. BJOG 2003;110:1088–98.
68. Andrews V, Thakar R, Sultan AH, Jones PW. Are mediolateral episiotomies actually mediolateral? BJOG 2005;112:1156–8.
82. Wiskind AK, Crighton SM, Stanton SL. The incidence of genital prolapse after the Burch colposuspension. Am J Obstet Gynecol 1992;167:399–405.
69 Sultan AH, Johanson RB, Carter JE. Occult anal sphincter trauma following forceps and vacuum delivery. Int J Gynecol Obstet 1998;61:113–9.
83. Jarvis GJ. Surgery for genuine stress incontinence. BJOG 1994;101:371–4.
70. Bofill JA, Rust OA, Schorr SJ et al. A randomised prospective trial of the obstetric forceps versus the M-cup vacuum extractor. Am J Obstet Gynecol 1996;175:1325–30. 71. Combs CA, Robertson PA, Laros RK. Risk factors for third degree and fourth degree perineal lacerations in forceps and vacuum deliveries. Am J Obstet Gynecol 1990;163:100–4. 72. Fynes M, Donnelly V, Behan M et al. Effect of second vaginal delivery on anorectal physiology and faecal continence: a prospective study. Lancet 1999;354:983–6. 73. Mahony RT, Malone PA, Nalty J et al. Randomised clinical trial of intra-anal electromyographic biofeedback physiotherapy with intra-anal electromyographic biofeedback augmented with electrical stimulation of the anal sphincter in the early treatment of postpartum fecal incontinence. Am J Obstetc Gynecol 2004;191:885–90. 74. Hendry WF. Urinary tract injuries during gynaecological surgery. In: Studd J (ed) Progress in Obstetrics and Gynaecology, vol. 5. Edinburgh: Churchill Livingstone, 1985; 362–77. 75. Brown JS, Sawayer G, Tom DH, Grady D. Hysterectomy
84. Jackson SR, Avery NC, Tarlton JF et al. Changes in the metabolism of collagen in genitourinary prolapse. Lancet 1996;347:1658–61. 85. Cardozo LD, Stanton SL, Williams JE. Detrusor instability following surgery for genuine stress incontinence. Br J Urol 1979;51:205–7. 86. Steel SA, Cox C, Stanton SL. Long term follow-up of detrusor instability following the colposuspension operation. Br J Urol 1985;58:138–42. 87. Bombieri L, Freeman RM, Perkins EP. Why do women have voiding dysfunction and de novo detrusor instability after colposuspension? BJOG 2002;109:402–12. 88. Khullar V, Salvatore S, Cardozo LD et al. Prediction of the development of detrusor instability after colposuspension [abstract]. Neurourol Urodyn 1995;14:486. 89. Eckford ESD, Bailey RA, Jackson SR et al. Occult preoperative detrusor instability – an adverse prognostic feature in genuine stress incontinence surgery [abstract]. Neurourol Urodyn 1995;14:487. 90. Black N, Griffiths J, Pope C et al. Impact of surgery for stress incontinence: cohort study. BMJ 1997;315: 1493–8. 91. Scotti RJ, Angell G, Flora R, Greston WM. Antecedent his-
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tory as a predictor of surgical cure of urgency symptoms in mixed incontinence. Obstet Gynecol 1998;91:51–4.
ment of stress incontinence in patients with low urethral pressures. Gynecol Obstet Invest 1991;31:106–9.
92. Ward K, Hilton P. A prospective multi-centre randomized trial of tension-free vaginal tape and colposuspension for primary urodynamic stress incontinence: two-year followup. Am J Obstet Gynecol 2004;109:324–31.
103. Burch JC. Urethrovaginal fixation to Cooper’s ligament for correction of stress incontinence, cystocele and prolapse. Am J Obstet Gynecol 1961;81:281–290.
93. Nilsson CG, Falconer C, Rezapour M. Seven-year follow-up of the tension-free vaginal tape procedure for treatment of urinary incontinence. Obstet Gynecol 2004;104:1259–62. 94. Segal JL, Vassallo B, Kleeman S et al. Prevalence of persistent and de novo overactive bladder symptoms after tension-free vaginal tape. Obstet Gynecol 2004;104:1263–9. 95. Borstad E, Rud T. The risk of developing urinary stress incontinence after vaginal repair in continent women: a clinical and urodynamic follow-up study. Acta Obstet Gynecol Scand 1989;68:545–54. 96. Bump RC, Hurt WG, Theofrastous JP et al. Randomised prospective comparison of needle colposuspension v endopelvic fascia plication for potential stress incontinence, prophylaxis in women undergoing vaginal reconstruction for Stage III or IV pelvic organ prolapse. Am J Obstet Gynecol 1996;175:326–35. 97. Bergman A, Koonings PP, Ballard CA. Predicting postoperative urinary incontinence development in women undergoing operations for genito-urinary prolapse. Am J Obstet Gynecol 1988;158:1171–75. 98. Karram MM. What is the optimal anti-incontinence procedure in women with advance prolapse in ‘potential’ stress incontinence? [editorial] Int Urogynaecol J 1999;10:1–2. 99. Bombieri LB, Freeman RM. Recurrence of stress incontinence after vault suspension: can it be prevented? Int Urogynaecol J 1998;9:58–60. 100. Francis LN, Sand PK, Hamrang K, Ostergard DR. Urodynamic appraisal of success and failure after retropubic urethropexy. J Reprod Med 1987;32:693–6. 101. Sand PK, Bowen LW, Panganiban R, Ostergard DR. The low pressure urethra as a factor in failed retropubic urethropexy. Obstet Gynecol 1987;69:399–402. 102. Richardson DA, Ramahi A, Chalas E. Surgical manage-
104. Stanton SL, Cardozo LD. Results of the colposuspension operation for incontinence and prolapse. BJOG 1979;86:693–9. 105. White GR. Cystocoele, a radical cure by suturing lateral sulci of vagina to white line of pelvic fascia. JAMA 1909;21;1707–10. 106. Olsen AL, Smith VJ, Bergstrom JO et al. Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Am J Obstet Gynecol 1997;89;501–5. 107. Weber AM, Walters M, Piedmonte M et al. Anterior colporrhaphy. A randomised trial of three surgical techniques. Am J Obstet Gynecol 2001;185:1299–306. 108. Monga A. Fascia: defects and repair. Curr Opin Obstet Gynaecol 1996;8:366–71. 109. Garnett S, Abrams P. The natural history of the overactive bladder and detrusor overactivity. A review of the evidence regarding the long-term outcome of the overactive bladder. J Urol 2003;169:843–8. 110. Whiteside CG, Arnold EP. Persistent primary enuresis: a urodynamic assessment. BMJ 1975;1:364–7. 111. De Jonge JA. The urge syndrome. In: Kolvin I, MacKeith RC, Meadow R (eds) Bladder control and enuresis. Clin Dev Med 1973;48/49:66–9. 112. Foote AJ, Moore KH. Bladder training: should you listen to what your mother says? [abstract]. Neurourol Urodyn 1996;15:137–8. 113. Freeman RM, McPherson FM, Baxby K. Psychological features of women with idiopathic detrusor instability. Urol Int 1985;40:257–9. 114. Macauley AJ, Stanton SL, Stern RS, Holmes DM. Micturition and the mind: psychological factors in the aetiology and treatment of urinary disorders in women. BMJ 1987;294:540–3. 115. Petros PEP, Ulmsten U. Role of the pelvic floor in bladder neck opening and closure II: vagina. Int Urogynecol J 1997;8:69–73.
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29 Outcomes of conservative treatment Don Wilson
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IntroductIon Conservative treatment is any therapy that does not involve pharmacologic or surgical intervention. In urinary incontinence, conservative treatment includes, principally, lifestyle interventions, physical therapies, scheduled voiding regimes, complementary therapies (e.g. not considered part of the traditional biomedical model), anti-incontinence devices, supportive rings/pessaries for pelvic organ prolapse, and pads/catheters. To date, however, only a relatively small number of objective clinical comparative studies with adequate patient numbers have been carried out to assess the effectiveness of conservative treatment of urinary incontinence and pelvic organ prolapse. This chapter will review the outcomes of research investigating the principal types of conservative treatment in urinary incontinence (excluding anti-incontinence devices, supportive rings/pessaries, and pads/catheters; see Chapters 34 and 35) and make recommendations based on their effectiveness to assist with the counseling of women with incontinence and prolapse regarding these treatment options. The recommendations are based on the best level of evidence currently available. At present this is provided by randomized controlled trials (RCTs) and, in particular, a meta-analysis (quantitative synthesis) of all available RCTs identified after a systematic review of the literature.1 Where this is not available, then lesser levels of evidence will be considered2 (Table 29.1).
LIfestyLe InterventIons Various lifestyle factors may play a role in either the pathogenesis or, later, the resolution of incontinence. While published literature about lifestyle factors and incontinence is sparse, alterations in lifestyle are frequently recommended by healthcare professionals and lay people alike. However, to date, most studies about lifestyle have reported associations only and have not assessed the actual effect of applying or removing the behavior in question. Currently, only a relatively small number of randomized trials have been carried out to assess the effect of a specific lifestyle on incontinence. Principal forms of lifestyle intervention include weight loss, reduction of physical forces (exercise, work), cessation of smoking, alteration of dietary factors (caffeine reduction and fluid management), relieving constipation, and postural changes.
Weight loss Obesity has been shown to be an independent risk factor for incontinence, with several studies reporting
table 29.1.
Levels of evidence and grades of recommendation for conservative treatment of incontinence and prolapse
Level Levels of evidence 1
Evidence obtained from a meta-analysis of randomized controlled trials (RCTs) or a ‘good quality’ RCT
2
Evidence obtained from a ‘low quality’ RCT or a meta-analysis of good quality prospective cohort studies
3
Evidence obtained from ‘good quality’ retrospective case control studies or ‘good quality’ case series
4
Evidence obtained from expert opinion where the opinion is based not on evidence but on ‘first principles’ (e.g. physiologic or anatomic) or bench research Grades of recommendation
A
Recommendation usually depends on consistent Level 1 evidence and often means that the recommendation is effectively mandatory and placed within a clinical care pathway
B
Recommendation usually depends on consistent Level 2 and/or 3 studies or ‘majority evidence’ from RCTs
C
Recommendation usually depends on Level 4 evidence or ‘majority evidence’ from Level 2/3 studies
D
‘No recommendation possible’ would be used where the evidence is inadequate or conflicting
Adapted from ref. 2.
an association between increased weight and urinary incontinence.3–9 Brown et al.,9 in their large multivariate analysis involving almost 8000 people, reported that the prevalence of daily incontinence increased by an odds ratio of 1.6 per 5 BMI. Two intervention studies, looking at incontinence after weight loss in morbidly obese women,10,11 showed a reduction in incontinence after massive weight loss (mean 44 kg). In a relatively small RCT of 47 moderately obese women (mean baseline weight 93 ± 13 kg),12 women in the weight loss group lost 15 ± 7 kg, compared to 0 (± 4 kg in the control group) and experienced a 51% reduction in weekly incontinent episodes compared to 5% in the control group. Maintaining normal weight through adulthood may be an important factor in the prevention of incontinence; however, published data to substantiate this hypothesis are lacking. Given the high prevalence of both incontinence and obesity in women, the dual issues of weight
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loss and prevention of weight gain and their effect on incontinence should receive high research priority. Obesity is an independent risk factor for urinary incontinence. There is Level 2 evidence that weight loss in morbidly obese women decreases incontinence and scant Level 1 evidence that moderately obese women who lose weight have less incontinence than those who do not.
Physical forces (exercise, work) Minimal stress incontinence is common in young exercising women,13–15 and it is believed that strenuous exercise is likely to unmask the symptom of stress incontinence in otherwise asymptomatic women. There is little available information on whether strenuous exercise or activity causes the condition of incontinence later in life. In a study of former female Olympians, competitors in gymnastics or track and field were no more likely to currently report daily or weekly incontinence than competitive swimmers.16 Traumatic exercise may cause incontinence; a recent report described nine nulliparous infantry trainees who developed stress incontinence and pelvic floor defects for the first time during airborne training, which included parachute jumping.17 Surprisingly little information is available on workplace stressors. Danish nursing assistants, who were exposed to frequent heavy lifting, were 1.6 fold more likely to undergo surgery for genital prolapse and/or incontinence than women in the general population; however, the study did not control for parity.18 Although healthcare professionals commonly advise restricting exercise and heavy lifting following incontinence or prolapse surgery, there is no published evidence that this improves surgical outcome. Given the large proportion of women employed in occupations that require heavy lifting and the paucity of scientific data about the association between exertion and incontinence, this should be investigated further. Specifically, research must establish whether heavy exertion is an etiologic factor in the pathogenesis of incontinence, and whether changing exertions can alleviate established incontinence or influence the outcome of surgery for either incontinence or prolapse.
smoking The data regarding the association of smoking and incontinence are conflicting. Smokers are more likely to report incontinence than non-smokers in some studies,19–22 but not in others.9,23 After adjusting for age, parity, type of delivery, and pre-pregnancy BMI, smokers had a
1.3-fold higher risk (95% CI 1.0–1.8) of reporting incontinence at 16 weeks gestation than non-smokers.21 The adjusted odds ratio (OR) for moderate or severe incontinence among women reporting incontinence was 1.38 (95% CI 1.04–1.82) in current smokers, after adjusting for perimenopausal status, BMI, diabetes, and ethnicity.22 In the large population-based study by Hannestad et al.,19 smoking increased the risk of severe incontinence (OR 1.4, 95% CI 1.2–1.6) but not of mild incontinence. Incontinent smokers were found to have stronger urethral sphincters and lower overall risk profiles than incontinent non-smokers,24 and therefore it was proposed that more violent coughing promotes anatomic defects which allow incontinence. In potential support of nicotine as a risk factor for incontinence, Hisayama et al.25 and Koley et al.26 found that nicotine produces phasic contraction of isolated bladder muscle probes in vitro. However, Milsom and colleagues27 reported an apparent paradoxical local estrogenic effect of nicotine on the vagina, resulting in a decrease in vaginal pH and an increase in lactobacilli. Current data suggest that smoking increases the risk of more severe urinary incontinence. Smokers may have a different mechanism causing their incontinence than non-smokers (Level of evidence 2/3/4). No data have been reported examining whether smoking cessation resolves incontinence.
dietary factors Caffeine The data on caffeine intake and incontinence are conflicting. While large cross-sectional surveys indicate no association,9,19 small clinical trials do suggest that decreasing caffeine intake improves continence.28,29 Caffeine consumption is pervasive in many societies and may play a role in exacerbating urinary incontinence. Larger randomized trials to assess the effect of caffeine and other dietary factors are feasible and important.
Decreased fluid intake In incontinent women over the age of 55 years, there was a modest positive relationship between fluid intake and severity of incontinence in women with stress incontinence; fluid intake accounted for 14% of the explained variability in the number of incontinent episodes.30 No such correlation was found in women with detrusor overactivity. In a randomized trial,31 32 women were assigned to one of three groups: increase fluid intake by 500 cc over baseline, decrease by the same amount, or maintain baseline level. While non-adherence to the protocol 409
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made results difficult to interpret, the authors reported that 20 women who had fewer incontinent episodes at the end of the trial attributed this to drinking more fluids. Given the fact that decreasing fluids may lead to urinary tract infections, constipation, or dehydration, this intervention should be reserved for patients with abnormally high fluid intakes.
Alcohol After adjusting for age and gender, no association was found between urinary incontinence and consumption of alcohol.32 After adjusting for age and fluid intake, consumption of wine, beer or spirits did not increase the incidence of either stress incontinence or overactive bladder (there was a trend towards less stress incontinence in beer drinkers; OR 0.75 (95% CI 0.56–1.01) for weekly drinkers versus those that drank beer less than monthly).33
Diet After adjusting for age, physical functioning, stress incontinence at baseline, obesity, smoking and certain dietary factors, the incidence of overactive bladder was increased with the consumption of carbonated drinks, and decreased with high consumption of vegetables, bread, and chicken.33 After similar adjustment, the incidence of stress incontinence was increased with carbonated drinks and decreased with bread consumption. Anecdotal evidence suggests that eliminating dietary factors such as artificial sweeteners and certain foods may play a role in continence; however, no treatment trials have tested this hypothesis.
relieving constipation There are some data to suggest that chronic straining may be a risk factor for the development of incontinence. This is based on studies which found a positive association of straining at stool as a young adult34 and constipation35 with subsequent incontinence34,35 and uterovaginal prolapse.34 There also appears to be an association between straining and pudendal nerve function; the mean pudendal nerve terminal motor latency increased after straining, correlated with the amount of descent, and returned to resting by 4 minutes after a strain.36 However, evidence of pudendal neuropathy was found in only 25% of women with abnormal perineal descent; in this large group of patients with defecating dysfunction no relationship was seen between neuropathy and pelvic descent, leading to the conclusion that pelvic descent and neuropathy may be two independent findings.37
There have been no intervention trials that address the effect of regulating bowel function on incontinence and research is needed to determine whether eliminating straining by treating constipation improves incontinence. Further research is also needed to delineate the role of straining in the pathogenesis of incontinence. If this association holds, public education, particularly of parents and pediatricians, is needed to make an impact on the common problem of straining in children.
Postural changes and other lifestyle interventions Urine loss during provocation can be significantly decreased by crossing the legs while coughing or by crossing the legs and bending forward.38 However, no study has evaluated whether postural changes are a satisfactory form of treatment outside the laboratory setting and they will be of limited value for women who are incontinent during exercise. Many other lifestyle interventions are suggested by either healthcare professionals or lay press for the treatment of urinary incontinence but have not been evaluated in the non-geriatric population. These include reducing emotional stress, wearing non-restrictive clothing, utilizing a bedside commode, decreasing lower extremity edema, treating allergies and coughs, wearing cotton underwear, and increasing sexual activity. Evidence concerning these interventions remains anecdotal and studies evaluating their effects are warranted. While some lifestyle changes may prove beneficial for individuals, it is unlikely that manipulating these factors will have a major effect on the overall incontinence problem.
conclusions Most lifestyle intervention studies to date have reported associations only and have not assessed the actual effect of applying or removing the behavior in question.
• Obesity seems to be an independent risk factor for
• •
the development of urinary incontinence and weight loss may be an appropriate treatment option for morbidly and moderately obese women. There is scant Level 1 evidence that decreasing caffeine improves continence. Chronic straining may also be a risk factor for the development of urinary incontinence; however there have been no intervention trials that have examined the effect of resolving constipation on incontinence.
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• Further research is needed to evaluate the effect of heavy exertion/exercise, smoking, caffeine and fluid intake on incontinence and whether their cessation can alleviate or prevent this condition.
PHysIcAL tHerAPIes Physical therapies include pelvic floor muscle training, biofeedback, intravaginal resistance devices, vaginal cones, and electrical and magnetic stimulation. These are used either singly or in combination. In order to represent the best possible evidence and in an attempt to differentiate specific treatment effects from a host of other variables, this section has looked at mainly Level 1 evidence from existing systematic reviews and in particular the available Cochrane Reviews; if these were not available then the evidence was taken from randomized controlled trials.
Pelvic floor muscle training (PfMt) PFMT programs In the trials reviewed there was a lack of consistency in PFMT programs, which implies an underlying lack of understanding of the physiologic principles of rehabilitating (pelvic floor) muscle dysfunction, or differences in muscle training philosophies. In general, many PFMT programs were poorly reported, and other advice/education given concurrently rarely detailed. Success of PFMT will partly depend on ability to perform a correct voluntary pelvic floor muscle contraction (VPFMC) initially. Bump et al.39 reported that 50% of women were unable to perform a correct VPFMC following brief verbal instruction, and as many as a quarter were mistakenly performing a Valsalva maneuver. Therefore, it seems appropriate that all women should be examined and taught how to perform a correct VPFMC by a person with specialist training in this area before PFMT is undertaken. Effective strength training relies on specificity (i.e. training reflects the functional activity of the muscle) and overload (i.e. increasing resistance to, frequency or duration of, muscle contraction). Effective overload strategies are likely to include maximal VPFMC, increased length of contraction, increased number of contractions, and reduced rest periods. Strength training theory suggests that near maximal contractions are the most significant factor in increasing strength40 and ideally contractions need to be sustained for 6–8 seconds to recruit an increasing number of motor units and fast twitch fibers.41
It is not clear what the most effective PFMT parameters are; clinicians and researchers should refer to exercise physiology literature to provide a biologic rationale for their choice of training parameters. PFMT parameters can be selected based on the aim(s) of treatment (e.g. muscle strength, endurance, coordination, and function). Therefore programs might comprise small numbers of maximal or near maximal contractions held for short periods, repeated once or more daily, at least 3 days a week (suggests strength training), and/or a moderate number of daily submaximal contractions held for long periods (suggests endurance training), and/or voluntary contractions timed with activities, in different body positions, and with varying levels of task difficulty (suggests coordination and functional training). Prior to PFMT, a person with skills in the assessment and training of pelvic floor muscles should assess each woman to ensure that a correct voluntary pelvic floor muscle contraction is being performed and to determine what facilitation, techniques or adaptations, if any, are required to the recommended training program to ensure an appropriate training intensity. Clinicians should provide the most intensive PFMT supervision that is possible within service constraints. Supervision could be provided in individual or group settings as there appears to be no significant difference in the proportion of women who reported they were ‘dry’ posttreatment or in the number of leakage episodes per day after treatment between those receiving individual or group supervision.42
PFMT versus no treatment, placebo or control treatments Seven RCTs comparing PMFT alone with no treatment for women with urinary incontinence have been published.43–48 Both self-reported cure (relative risk [RR] 16.80, 95% CI 2.37–119.04) and self-reported cure/ improvement (RR 27.60, 95% CI 4.00–190.24) are much more likely after PFMT than no treatment in women with urodynamic stress incontinence (USI).45 Five RCTs49–53 and two quasi-randomized controlled trials (qRCTs)54,55 compared PFMT with a sham, placebo or control treatment. Based on pooled data from five trials, it seems women who train are more likely to report cure/ improvement; this effect was seen in women with USI, detrusor overactivity (DO), and mixed urinary incontinence. Women who trained also reported approximately two fewer incontinent episodes per 3 days than controls. Based on this evidence of efficacy and the apparent lack of adverse events, PMFT should be offered as a first line therapy to all women with stress, urge or mixed urinary incontinence (Grade of recommendation: A). 411
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PFMT in combination with other physical therapy adjuncts PFMT is commonly used in combination with other adjuncts such as biofeedback (BF), intravaginal resistance devices (IVRD), electrical stimulation (ES), and vaginal cones (VC). Electrical stimulation and vaginal cones are discussed later (p. 413). PFMT with biofeedback versus PFMT alone Four RCTs compared PFMT with BF versus PFMT alone. All four trials46,56–58 reported significant improvement in both treatment groups; however, only Glavind et al.58 reported PFMT with BF to be superior to PFMT alone. There is therefore Level 1 evidence to suggest that PFMT with BF is no more effective than PFMT alone in women with (urodynamic) stress incontinence. It is important to emphasize, however, that this evidence should be viewed with caution in view of the small group sizes and the chance of type II error. There was also some variation in the types of BF used – all four studies used vaginal probes, with three studies using electromyography BF,57,58 and the other using pressure BF.56 Anecdotal evidence suggests BF is used to particular effect in some subgroups (e.g. those women unable to perform a VPFMC on initial assessment). However, the role of BF in any subgroup is unclear due to a lack of published evidence to date. Clinicians may find occasions when biofeedback would be a useful adjunct to treatment for the purposes of teaching, motivation and compliance. PFMT with IVRD versus PFMT alone To date there have been two RCTs59,60 that found significant improvement in both groups but with no differences between the groups. Thus, the same conclusions regarding biofeedback apply also to IVRD with PFMT.
PFMT versus other treatments PFMT versus vaginal cones or balls Five trials45,61–64 compared PFMT with vaginal cones/balls in women with stress urinary incontinence (SUI). Pooled data demonstrated no statistically significant differences between the groups for self-reported cure, cure/ improvement or leakage episodes per day, but some trials favored PFMT45 and others cones.62 The direction of effect appeared to relate to supervisory intensity. Four of the five trials reported that some women dropped out because they could not or chose not to use cones. Where supervisory intensity is similar, PFMT and vaginal cones/ balls might have similar effects for SUI women. However, the use of vaginal cones/balls is limited by contraindications to use and/or dislike of cones by some women.
PFMT versus electrical stimulation Eight trials compared PFMT with ES.45,47,52,65–69 Pooled data demonstrated self-reported cure and cure/improvement were statistically significantly more likely in PFMT than ES groups for SUI women, although only one trial individually demonstrated a statistically significant difference.45 Supervisory intensity was greater in the PFMT group in this trial. There were no statistically significant differences between PFMT and ES groups for leakage episodes or quality of life in SUI women, based on a single trial. Self-reported cure/improvement rates were not statistically significantly different in a trial in women with SUI, urge urinary incontinence (UUI) or mixed incontinence. Self-reported cure and cure/improvement rates were not statistically significantly different in a trial in women with UUI,65 although PFMT women had fewer leakage episodes per day, and women in the ES group had better quality of life in three of nine domains measured. Some women reported adverse events attributable to ES. In conclusion, PFMT might be better than ES for SUI women, particularly if PFMT is intensive. However, there is so much variation in the PFMT and ES protocols investigated in the available trials, it is difficult to be sure about the relative effects of these treatments. It is not clear if PFMT or ES is better in a sample of women with a variety of incontinence symptoms, or in UUI women. The use of ES might be limited by contraindications to use and/or side effects of treatment. PFMT versus bladder training Two trials compared PFMT and bladder training in samples of women with SUI, UUI or mixed incontinence.70,71 While more women reported they were much or somewhat better in PFMT groups than bladder training groups, in the trial by Wyman and colleagues,71 the difference did not reach statistical significance after treatment (RR 1.73, 95% CI 0.83–3.60) or 3 months later (RR 1.96, 95% CI 0.97–3.94). Similarly, while PFMT women had fewer leakage episodes per day than bladder training women, the difference was not statistically significant at post-treatment (weighted mean differences [WMD] –0.14, 95% CI –0.83 to 0.55) or at 6 months (WMD –0.09, 95% CI –0.73 to 0.55). PFMT versus medication Burgio et al.50 compared PFMT with oxybutynin in a sample of women with DO or DO with USI. There was no statistically significant difference for the number of women who were dry (cured) (RR 1.31, 95% CI 0.73– 2.34), but PFMT women were more likely to report that they were much better than women receiving the drug
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(RR 1.46, 95% CI 1.08–1.97). PFMT women also had fewer leakage episodes per day post-treatment (WMD –0.41, 95% CI –0.80 to –0.02). Some women taking oxybutynin reported side effects (dry mouth and inability to void in particular). Henalla and colleagues compared PFMT and vaginal estrogens for 6 weeks48 and 12 weeks47 in women with USI. In the 12-week study, PFMT was superior to the vaginal estrogen cream, with those women reporting cure improvement at 3 months of 65% versus 12% of the women taking the local estrogens. Two trials compared adrenergic agonists and PFMT in women with stress or mixed incontinence.72,73 While women who took the drug had fewer leakage episodes per day post-treatment, the proportion of women reporting cure or cure/improvement was no different. One trial reported drug side effects, sufficient to discontinue treatment, associated with the adrenergic agonist.72 PFMT versus surgery One published RCT74 compared PFMT with surgery for women with USI with significantly greater reduction in symptoms within the surgery group. One abstract of an RCT compared 3 months of PFMT with Burch colposuspension for women with USI.75 The authors reported 2 of 21 women from the PFMT group objectively cured on urodynamic testing at 6 months, compared with 18 of 24 women following colposuspension.
the pelvic floor muscle (PFM).80 Theoretically, the sensation of ‘losing the cone’ from the vagina might provide strong sensory feedback and prompt a PFM contraction in order to retain the cone. Since their introduction, a variety of cones have been developed (i.e. different sizes, shapes and weights). They have been in widespread use in the past, and directly marketed to women through mail order companies. A review that questions the theoretical framework and effects of vaginal cones on PFM strength has been published.81 There have been two fully published RCTs comparing VC with control treatment (i.e. offered use of incontinence device) in women with USI,45 and also comparing VC with standard care in women 3 months post partum with urinary incontinence.82 While there was some evidence that training with VC might be better than control treatments (for self-reported outcome), the data are not consistent. Some women who were training with VC reported adverse events. It is therefore not clear if training with VC is better than control treatments for postnatal women with urinary incontinence or women with USI. VC are not suitable for some women due to adverse events. More research is needed to be sure about the effect of VC versus no treatment, placebo or control treatment.
One approach to cones versus another No studies have been found addressing this question.
The addition of PFMT to other treatments
VC versus other treatments and the addition of VC to other treatments
To be included, trials needed to investigate the effects of therapy A versus therapy A plus PFMT, to address the additive benefit of PFMT over therapy A. Seven RCTs were found, addressing the additive effect of PFMT over vaginal cones,76 electrical stimulation,52,77 bladder training,71 drugs72,78 or urethral occlusive devices.79 While the findings of Wyman and colleagues71 suggested benefit of adding PFMT to bladder training for women with USI, or DO with USI, in the short term (3 months), there was no statistically significant difference between single and combination therapy groups for leakage episodes per day, or condition-specific quality of life after 6 months. However, more women in the bladder training/PFMT group felt they were much better at 6 months. Because there were no useable data, it is not clear if there is any benefit in adding PFMT to vaginal cones, electrical stimulation or drug therapy.
Pooled data from two trials comparing VC and electrical stimulation45,83 found no statistically significant difference between the groups for self-reported cure (RR 1.13, 95% CI 0.39–3.25), self-reported cure/improvement (RR 0.95, 95% CI 0.75–1.19) or leakage episodes in 24 hours (WMD 0.25, 95% CI –0.59 to 1.08). Both VC and electrical stimulation groups, however, reported adverse events in the trial by Bø and colleagues.45 In conclusion, either VC or ES appear to be equally effective for SUI women (Grade A recommendation), but either treatment may be precluded by side effects. Based on a single outcome from one trial addressing the additive effect of VC over PFMT,84 there may be no further benefit from adding VC to PFMT for SUI women. However, more research is needed to determine if there is any further benefit from adding VC to PFMT.
Weighted vaginal cones
electrical stimulation
Weighted vaginal cones (VC) were developed as a method of strengthening and testing the function of
ES protocols There was a wide variation in ES protocols used with 413
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no consistent pattern emerging. Women with urinary incontinence have received a range of types of stimulation including faradism (low frequency current with pulse duration of 1 millisecond or less), interferential therapy (two interfering medium frequency currents), and specifically programmed neuromuscular electrical stimulation. In the included trials there was a lack of consistency in ES types and parameters that implies a lack of understanding of the physiologic principles of rehabilitating pelvic floor muscle through electrical stimulation, and this inconsistency means direct comparison between studies is inadvisable. In addition, the small group sizes mean that results may be affected by type II error.
ES versus no/control treatment or placebo/sham treatment There are only single trials of good quality investigating the effect of ES versus no treatment (or control treatment) in women with USI47 or women with DO.85 Consequently, there is insufficient evidence to judge whether ES is better than no treatment for women with these conditions. Due to the variation in stimulation protocols it is difficult to interpret the findings of trials comparing ES with placebo/sham stimulation. For women with USI the findings of two good quality trials using similar stimulation protocols are contradictory.86,87 For women with DO there is a trend in favor of active stimulation over placebo stimulation.88–91 For women with mixed incontinence, no conclusions can yet be made. More research of high quality using adequate sample sizes and consistent protocols is needed to be confident about the effectiveness of ES versus placebo/sham treatment.
ES versus other treatments ES versus magnetic stimulation With only one single small trial (involving both men and women) comparing electrical stimulation with magnetic stimulation,92 there is insufficient evidence to determine if electrical stimulation is better than magnetic stimulation in women with DO. ES versus PFMT See PFMT section (p. 411). ES versus vaginal cones See Weighted vaginal cones section (p. 411). ES versus medication With only a few small trials comparing ES with medica-
tion, there is insufficient evidence to determine if ES is better than vaginal estrogens in women with USI,93 or ES is better than anticholinergic or antimuscarinic therapy in women with DO.69,94
The addition of other treatments to ES/addition of ES to other treatments ES with biofeedback-assisted PFMT versus biofeedback-assisted PFMT alone versus self-administered PFMT (control group) For comparisons of ES with biofeedback-assisted PFMT versus biofeedback-assisted PFMT alone versus a control condition, reporting was limited to a single trial. Goode et al.51 concluded that treatment with additional ES did not increase effectiveness of a comprehensive PFMT program for women with stress urinary incontinence.
ES with PFMT versus PFMT alone Women with stress incontinence Four trials compared ES in combination with PFMT versus PFMT alone in women with stress incontinence.52,75,95,96 The two small trials of Tapp and colleagues using faradic stimulation were reported only as abstracts,75,96 and another small trial gave minimal detail of participants, methods and stimulation parameters.52 In a three-arm RCT, Knight et al.95 compared PFMT versus PFMT with home-based low intensity ES versus PFMT with clinic-based maximal intensity stimulation. Overall, Knight et al. did not find any clear benefits of ES in addition to PFMT. This finding is similar to that of the three small poorly reported trials,52,75,96 which found no significant differences between the groups receiving combined ES/PFMT and PFMT alone. Women with detrusor overactivity In a four-arm RCT in women with DO, Berghmans et al.85 investigated the effect of no treatment, PFMT alone, ES alone, and ES in combination with PFMT. The main outcome measure was change in the Detrusor Overactivity Index (DAI). The combination therapy group did not demonstrate any significant changes pre- to post-treatment. There was a positive (but not significant) trend towards improvement in the PFMT group for the DAI. These findings do not suggest added benefit from electrical stimulation to PFMT.
Magnetic stimulation Magnetic stimulation has been developed for stimulating both central and peripheral nervous systems non-invasively.97
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Magnetic stimulation versus no treatment, placebo or control treatment Four RCTs comparing magnetic stimulation with placebo/sham treatments for women with urinary incontinence were found.98–101 The trial by But98 compared magnetic stimulation using a home device (Pulsegen) with sham magnetic stimulation in a group of women with stress, urge and mixed incontinence. Fujishiro and colleagues compared magnetic stimulation with sham stimulation in one RCT involving women with stress urinary incontinence99 and in another involving women with urinary frequency and urge incontinence.101 Gilling et al.100 recruited women with stress urinary incontinence, and compared active magnetic stimulation of the pelvic floor to sham treatment, using the Neocontrol system. All patients also underwent low-intensity home-based PFMT supervised by a urotherapist.
Women with stress, urge and mixed incontinence The trial by But98 of 52 women with stress, urge and mixed incontinence showed a 56.3% improvement for urinary incontinence symptoms in the active group compared to 26.3% in the sham group (p=0.00012). There was also a significant reduction in the number of pads (p=0.0017) and also pad weight (p=0.038).
Women with stress urinary incontinence Results of two trials were contradictory with Fujishiro’s study99 of 62 women showing a 74% improvement rate in the active group versus 32% in the sham group (p=0.0009). There was also a significant decrease in the number of leaks and the amount of urine lost on a pad test in the active compared with the sham group (0.0023 and 0.0377, respectively). However Gilling et al.,100 in their study of 70 women with stress urinary incontinence, did not show any significant difference between the active and sham groups at 8 weeks for any parameter. However, in a subgroup with poor pelvic floor tone at baseline, Gilling et al. did find a significant difference between groups in the number of grams of urinary leakage on the 24-hour pad test and mean abdominal leak point pressure, measured pre- and post-treatment after 6 weeks. The authors reported that follow-up was ongoing, but provided no data on this.
Women with urge urinary incontinence In the study of Fujishiro et al.101 in women with urinary frequency and urge incontinence, mean urine volume per void, mean number of leaks and mean quality of life score improved more significantly in the active than in
the sham stimulation group (23.5 ± 25.6 ml versus 6.2 ± 22.5, p=0.04; 3.6 ± 4.1 versus 0.4 ± 1.4, p=0.04; and 1.4 ± 1.3 versus 0.4 ± 0.8, p=0.01, respectively). No adverse effects were noted in any patients. In conclusion, magnetic stimulation might be effective in the treatment of women with urinary incontinence (Grade C recommendation). There were no reported adverse events using this treatment modality. Further high quality studies with adequate sample sizes and long-term follow up are needed.
One approach to magnetic stimulation versus another No studies were found addressing this question.
Magnetic stimulation versus other treatments This comparison is described and evaluated in the section on electrical stimulation in women.
factors affecting outcomes of physical therapy interventions Many of the factors traditionally supposed to affect outcomes of physical therapy interventions (e.g. age, severity of incontinence, previous pelvic surgery, prolapse, and parity) may be less crucial than previously thought.46,47,52,87 The single factor that appeared to be most associated with positive outcome was greater motivation and/or compliance with physical therapy interventions.54,58,73 It should be noted, however, that the association between compliance with physical therapy interventions and improvement may not be due to the effect of the intervention alone but to some other unknown factor. For example, trial participants who were compliant with active or placebo drug did better than those who were not compliant with either active or placebo medication.102 Further investigation of all the above factors is required in subsequent high quality RCTs before any real conclusions may be drawn. DeLancey57 makes a compelling argument for intervention for stress urinary incontinence to be based on accurate diagnosis of the underlying pathology, whether it be neurologic, ligamentous/fascial, or muscular. For example, he suggests that PFMT may be inappropriate where innervation of the muscles is not intact or where the muscles have been detached from their fascial connections. These hypotheses remain to be tested, and will rely in part on improving diagnostic accuracy. Interestingly, an abstract of an RCT103 investigating the use of urodynamics prior to conservative treatment found this did not improve outcome in comparison to treatment based on symptom reporting only. 415
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conclusions PFMT
• There is Level 1 evidence to suggest that for women
•
•
•
•
with the range of urinary incontinence symptoms (stress, mixed, urge), pelvic floor muscle training (PFMT) is better than no treatment. For those women with mixed and urge incontinence, it may be beneficial to offer PFMT in combination with bladder training. It is not clear what the most effective PFMT parameters are; clinicians and researchers should refer to exercise physiology literature to provide a biologic rationale for their choice of training parameters. PFMT parameters can be selected based on the aim(s) of treatment (e.g. muscle strength, endurance, coordination, and function). Therefore programs might comprise small numbers of maximal or near maximal contractions held for short periods, repeated once or more daily, at least 3 days a week (suggests strength training), and/or a moderate number of daily submaximal contractions held for long periods (suggests endurance training), and/or voluntary contractions timed with activities, in different body positions, and with varying levels of task difficulty (suggests coordination and functional training). Prior to PFMT, a person with skills in the assessment and training of pelvic floor muscles should assess each woman to ensure that a correct voluntary pelvic floor muscle contraction is being performed and to determine what facilitation, techniques or adaptations, if any, are required to the recommended training program to ensure an appropriate training intensity. Clinicians should provide the most intensive PFMT supervision that is possible within service constraints. Supervision could be provided in individual or group settings. On the basis of the limited evidence currently available, there is no apparent difference in the effectiveness of PFMT with or without biofeedback (home or clinic) or intravaginal resistant devices over PFMT alone. Clinicians may have or find occasions when these would be useful adjuncts to treatment for the purposes of teaching, motivation, and compliance. Regarding PFMT versus other treatment, the following statements should be viewed with caution, in view of the limitations of current evidence (i.e. few trials, poor quality trials, contradictory trial findings): 1. PFMT and vaginal cones might have similar effectiveness for SUI women (Grade B);
•
2. PFMT might be better than ES for SUI women (Grade B); 3. PFMT and bladder training might be similarly effective for women with SUI, UUI or mixed urinary incontinence (Grade B); 4. PFMT might be better than oxybutynin for women with DO, or DO with USI (Grade B); 5. PFMT and adrenergic agonists might be similarly effective for women with SUI or mixed incontinence (Grade B); 6. PFMT might be less effective than surgery for women with USI (Grade B). However, when recommending treatment, clinicians should consider that adverse events are more common and more severe with cones, electrical stimulation, drugs and surgery than with PFMT. It is possible that the addition of PFMT to bladder training for women with USI, or DO with USI, is more effective in the short term, but it is not clear if the benefit is sustained. Otherwise, because there are so few trials, it is not possible to make recommendations about the possible benefits of adding PFMT to other therapies. If clinicians/ researchers are interested in the additive effects of PFMT, further large good quality trials are needed.
Weighted vaginal cones
• It is not clear if training with VC is better than
•
control treatments for postnatal women with urinary incontinence or women with USI. VC are not suitable for some women due to adverse events. More research is needed to be sure about the effects of VC versus no treatment, placebo or control treatments. No trials comparing approaches to training with VC were found. Research is needed if this is a comparison of interest for women and clinicians. VC and ES appear to be equally effective for SUI women (Grade A), but either treatment may be precluded by side effects. Based on a single outcome, from one trial, there may be no further benefit from adding VC to PFMT for SUI women.
Electrical stimulation
• There is a marked lack of consistency in the
•
electrical stimulation protocols that implies a lack of understanding of the physiologic principles of rehabilitating urinary incontinence through electrical stimulation used in clinical practice to treat women with stress, urge and mixed incontinence. There is no apparent difference in either electrical stimulation or placebo treatment in women with
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•
urodynamic stress incontinence. For women with detrusor overactivity there is a trend in favor of active stimulation over placebo stimulation. There is insufficient evidence to determine if electrical stimulation is better than magnetic stimulation or anticholinergic or antimuscarinic therapy in women with detrusor overactivity. There is also insufficient evidence to determine if electrical stimulation is better than vaginal estrogens in women with urodynamic stress incontinence. At present it seems that there is no extra benefit in adding electrical stimulation to PFMT.
Magnetic stimulation
• There is considerable variation in the regime, protocols, intensity, and duration of magnetic stimulation. Magnetic stimulation might be effective in the treatment of women with urinary incontinence. Women did not report adverse events using this treatment. Further high quality studies with long-term follow-up and adequate sample sizes are needed to further investigate magnetic stimulation.
scHeduLed voIdInG reGIMes Scheduled voiding regimes include bladder training, timed voiding, habit training, and prompted voiding104 (see Chapter 31). Although these regimes share a common feature of a toileting schedule, they differ on the basis of adjustments to the voiding schedule, the active or passive involvement of the patient, the nature of patient education including the teaching of strategies to control urgency and prevent stress leakage, the use of reinforcement techniques, and the nature of the interactions between clinicians and patients. In practice, however, scheduled voiding regimes may share aspects of one or more of these features.
• Bladder training (also referred to as bladder drill,
•
•
bladder discipline, bladder re-education, and bladder retraining) involves a program of patient education along with a scheduled voiding regime with gradually progressive voiding intervals. Timed voiding is a fixed voiding schedule that remains unchanged over the course of treatment.104 The goal of timed voiding is to prevent incontinence by providing regular opportunities for bladder emptying prior to exceeding bladder capacity. Habit training is a toileting schedule that is matched to the patient’s voiding pattern. Using the patient’s voiding chart, a toileting schedule is assigned to
•
fit a time interval that is shorter than the patient’s normal voiding pattern and to precede the time period when incontinent episodes are expected. Prompted voiding refers to a caregiver education program in combination with a scheduled voiding regime, typically every 2 hours. It is used to teach people with or without cognitive impairment to initiate their own toileting through requests for help and positive reinforcement from caregivers when they do so.105 Prompted voiding has been used primarily in institutionalized settings with cognitively and physically impaired older adults.
This section will examine the evidence for the use of timed voiding and habit training for the treatment of urinary incontinence in non-institutionalized women of all ages without cognitive or mobility impairments. Because of scant evidence with the use of timed voiding and none on habit training in this population, the majority of this review will focus on bladder training.
timed voiding There are no high quality trials providing evidence on the effect of timed voiding on urinary incontinence in women. Based upon the data from one small uncontrolled study of 20 women,106 there is some suggestion that a 2-hour timed voiding schedule may be beneficial in treating women with mild urinary incontinence, infrequent voiding patterns, and stable bladder function (15 patients became totally dry, one patient had less leakage, three patients with neurogenic diseases remained unchanged and one patient was lost to follow up). A 3-hour voiding interval appears to be too long to be beneficial.107 RCTs are needed that include standardized outcome assessment.
Habit training There are anecdotal reports that habit training may be beneficial for women who have a consistent pattern of urinary incontinence such as diuretic-induced incontinence. However, there is insufficient evidence to come to any conclusion regarding the role of habit training in women. Research is needed in this regard in women with a consistent pattern of urinary incontinence who are cognitively intact. In summary, there is no evidence regarding the benefit of habit training in women. It may be useful as sole or adjunct to other treatments when there is a consistent pattern of urinary incontinence. Further research is recommended (Grade D). 417
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Bladder training Bladder training protocols Four systematic reviews have been published, including two Cochrane Reviews.107–110 There is a lack of consistency in bladder training protocols with no clear evidence available indicating which is the most effective bladder training protocol to use. On the basis of extrapolation from the bladder training literature, an outpatient training protocol should include an initial voiding interval, typically beginning at 1 hour during waking hours, which is increased by 15–30 minutes per week depending on tolerance of the schedule (i.e. fewer incontinent episodes than the previous week, minimal interruptions to the schedule, and the woman’s feeling of control over urgency), until a 2–3 hour voiding interval is achieved. A shorter initial voiding interval, i.e. 30 minutes or less, may be necessary for women whose baseline micturition patterns reveal an average daytime voiding interval of less than 1 hour. Education should be provided about normal bladder control and methods to control urgency such as distraction and relaxation techniques and pelvic floor muscle contraction. Self-monitoring of voiding behavior using diaries or logs should be included in order to determine adherence to the schedule, evaluate progress, and determine whether the voiding interval should be changed. Clinicians should monitor progress, determine adjustments to the voiding interval, and provide positive reinforcement to women undergoing bladder training at least weekly during the training period. If there is no improvement after 3 weeks of bladder training, the patient should be re-evaluated and other treatment options considered. Inpatient bladder training programs may follow a more rigid scheduling regime with progression of the voiding interval on a daily basis (Grade C recommendation).
Bladder training versus no treatment, placebo or control treatments Bladder training as the sole therapy has been used in the treatment of DO, USI, mixed incontinence, urge incontinence, urge incontinence with a stable bladder, and urgency–frequency syndrome. Five RCTs involving 515 women compared the effect of bladder training to no treatment.54,70,111–113 However, in two trials, it was not possible to identify the effect of bladder training alone54,112 and, in the three trials with analyzable data, two of the three RCTs reported significant improvements in the bladder training group as compared to an untreated control group with respect
to incontinent episodes.111,113 The third RCT70 did not report data on incontinent episodes. Jarvis and Millar113 reported that 90% of the participants in the treatment group were continent and 83.3% were symptom-free at 6 months (method for determination of continence and symptom status was not specified but probably self-report) as compared to 23.3% of the control group who were both continent and symptomfree. All women who were symptom-free after treatment reverted to a normal cystometrogram. Fantl et al.111 reported that 12% of participants in their treatment group were continent and 75% had reduced their incontinent episodes at least 50% or more at 6 weeks as measured by a 7-day voiding diary, as compared to 3% with no incontinent episodes and 24% with at least 50% reduction in their incontinent episodes in the control group. These results were maintained at 6 months. Women with DO and those with USI with and without DO had similar improvement rates. Participants in the treatment group also significantly decreased the grams of fluid lost on a retrograde pad filling test by 54% with results maintained 6 months later; this was more pronounced in those who had DO with or without USI. While some women did revert back to normal bladder function following bladder training, no relationship was found between changes in urodynamic variables and the number of incontinent episodes.114 Yoon et al.70 reported that there was no difference between the bladder training and control groups in the amount of leaked urine at an immediate followup; however, it was not clear if this referred to pad test weights solely or a urinary incontinence severity score. Conclusions from this trial are uninterpretable because of insufficient power. The Cochrane Review110 found that although point estimates of effect favored bladder training, confidence intervals were wide with no statistically significant differences observed for any of the prespecified outcome variables. In conclusion therefore, from the few trials available, there is scant Level 1 evidence that bladder training compared to no treatment may be an effective treatment for women with urge, stress and mixed urinary incontinence. However, bladder training is recommended as a first line treatment of urinary incontinence in women (Grade A). Additional high quality studies are needed that examine the effect of bladder training in treatment of women with urge, stress and mixed incontinence.
Bladder training versus other treatments Bladder training versus PFMT See Physical therapies section (p. 411).
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Bladder training versus drug therapy Two RCTs conducted with drugs available prior to 1995 suggest that bladder training may be superior to drug therapy in women with DO.115,116 Jarvis115 found that inpatient bladder training was superior to an outpatient program of combined drug therapy of flavoxate hydrochloride and imipramine. Cure/improvement rates in the bladder training group were 84% subjectively continent and 76% symptom-free versus 56% continent and 48% symptom-free in the drug therapy group. Patients who were symptom-free at 4 weeks were able to maintain the effects at 12 weeks. Cystometric changes in both groups were related to the clinical changes. Columbo and associates116 reported that a 6-week course of oxybutynin had a similar clinical cure rate as bladder training (74% versus 73%, respectively). However, a higher cure rate was noted in women with detrusor overactivity alone (74% versus 42%). Conversely, the relapse rate at 6-months was higher for the oxybutynin group, whereas those in the bladder training group maintained their results better. Changes in bladder stability corresponded to symptom improvement in both groups. In a more recent RCT (abstract only), Park and colleagues117 compared a 12-week bladder training program to 2 mg tolterodine twice daily in women (ages unknown) with overactive bladders (unclear if incontinence was present), and concluded that both treatments were effective as a first line therapy in treating women with overactive bladders. In conclusion, there is scant Level 1 evidence indicating that bladder training is more effective than drug therapy available prior to 1995 for women with DO. There is insufficient evidence regarding the comparative effectiveness of bladder training and newer drug therapies (Level of evidence 3). Since there is insufficient evidence regarding the comparative effectiveness of bladder training and current drug therapies, bladder training – which has few if any adverse effects as compared to drug therapy – should be considered as a first line of treatment of detrusor overactivity (Grade B recommendation). Bladder training versus bladder training and drug therapy Three trials comparing different drug therapies available before 1995 with bladder training to bladder training with placebo118–120 were inconsistent with respect to the additive benefit when combining bladder training with drug therapy in the treatment of DO in women and a small number of men. However, Park and colleagues117 concluded that bladder training and combined therapy (bladder training and tolterodine 2 mg twice daily) were effective first line treatments but that combined therapy had some better effects than bladder training alone.
However, significant improvement rates were higher in the combined therapy group (69.3%) as compared to the bladder training group (50%). Based on the limited reporting (abstract only), it was impossible to discern the treatment effects on incontinence separately. In conclusion, in small placebo-controlled trials using drugs available before 1995 for treatment of DO, outcomes varied based on the medication used. In a more recent trial of a newer drug, it was impossible to discern the treatment’s effects on incontinence. Thus, there was insufficient evidence to derive a conclusion related to the effectiveness of augmenting bladder training with drug therapy (Level of evidence 2/3). Drug therapy versus bladder training and drug therapy Mattiason and colleagues121 reported no difference between participants (combined female and male) with overactive bladders with and without urge incontinence who were given brief written bladder training instructions plus tolterodine 2 mg twice daily versus tolterodine alone with respect to reducing incontinent episodes (median reduction 87% versus 81%, respectively). Park et al.117 concluded that tolterodine and combined therapy (tolterodine plus a nurse-supervised bladder training program) are effective first line therapies but that combined therapy had some better effects than tolterodine alone. At the end of treatment, subjective perception of bladder symptom scores was 1.4 in the drug therapy group and 1.3 in the combined therapy group. However, significant improvement rates were higher in the combined therapy group (69.3%) as compared to the drug therapy group (58.3%). In conclusion, there is conflicting Level 1 evidence as to whether there is an added benefit of combining bladder training with drug therapy (tolterodine 2 mg twice daily) as compared to drug therapy alone. Results might be attributed to differences in study populations, the intensity of the bladder training protocols, and outcome measures. More research is needed using other antimuscarinic drug therapies and incorporating traditional bladder training protocols.
factors affecting outcome of bladder training Few bladder training trials have examined predictors of treatment response. In conducting analyses of factors predicting outcomes of bladder training alone, two trials reported that age was not a factor in treatment outcome.70,71 Several trials discussed the effect of diagnosis on treatment outcome. Two trials reported that urodynamic diagnosis did not have an effect on the treatment outcome as measured by incontinent epi419
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sodes and the Incontinence Impact Questionnaire.71,111 Further research is needed to determine the subgroup of patients who will derive the greatest benefit from bladder training.
• There is insufficient evidence regarding the comparative effectiveness of bladder training and current drug therapy. However, bladder training, which has no adverse effects as compared to drug therapy, should be considered as first line treatment for detrusor overactivity. The additional benefit of combining drug therapy with bladder training and vice versa was not consistently noted and further investigation is warranted.
conclusions • Timed voiding with a 2-hour voiding interval may be
•
•
beneficial as a sole intervention for women with mild incontinence and infrequent voiding patterns. It may also be helpful as an adjunct to other treatment. However, there is no evidence regarding the benefit of habit training in women. There is scant Level 1 evidence to suggest that for women with urge, stress and mixed urinary incontinence, bladder training is more effective than no treatment. Evidence is inconsistent about expected cure rates, which may be dependent on when and how the outcome was measured or reflect differences in the bladder training protocol. There is a lack of consistency in bladder training protocols. On the basis of extrapolation from the bladder training literature, an outpatient training protocol should include an initial voiding interval typically beginning at 1 hour during waking hours, which is increased by 15–30 minutes per week depending on tolerance of the schedule (i.e. fewer incontinent episodes than the previous week, minimal interruptions to the schedule, and the woman’s feeling of control over urgency), until a 2–3 hour voiding interval is achieved. A shorter initial voiding interval (e.g. 30 minutes or less) may be necessary for women whose baseline micturition patterns reveal an average daytime voiding interval of less than 1 hour. Education should be provided about normal bladder control and methods to control urgency such as distraction and relaxation techniques and pelvic floor muscle contraction. Selfmonitoring of voiding behavior using diaries or logs should be included in order to determine adherence to the schedule, evaluate progress, and determine whether the voiding interval should be changed. Clinicians should monitor progress, determine adjustments to the voiding interval, and provide positive reinforcement to women undergoing bladder training at least weekly during the training period. If there is no improvement after 2–3 weeks of bladder training, the patient should be reevaluated and other treatment options considered. Inpatient bladder training programs may follow a more rigid scheduling regimen with progression of the voiding interval on a daily basis.
coMPLeMentAry tHerAPIes In WoMen Complementary therapies include those not part of the traditional biomedical model, such as relaxation, meditation, imagery, hypnosis, acupuncture and naturopathic and herbal remedies. Uncontrolled data suggest that acupuncture and hypnosis improve overactive bladder symptoms:
• After 12 weeks of treatment, 77% of patients
• • •
with ‘idiopathic detrusor overactivity’ were symptomatically improved, though urodynamic assessment showed resolution of detrusor activity in only 1 of 20 subjects.122 Three months after completing 12 acupuncture sessions, 12 of 15 women considered themselves improved.123 In spinal cord injured patients, after four acupuncture treatments, incontinence resolved in 2 and improved in 6 of 13 patients.124 A total of 50 patients took part in 12 hypnosis sessions over 1 month, after which subjects continued at home with a pre-recorded cassette. After 12 sessions, 29 patients were symptom free, 14 improved and 7 were unchanged. Seven patients subsequently relapsed by 6 months.125
However, the current studies are limited by the lack of a placebo group and by very short follow-up. Given the high placebo response rate in most studies that address overactive bladder symptoms, it is crucial that future studies on complementary therapies have a control group. When placebo treatment is not possible due to the nature of the intervention, a standard treatment control group (e.g. bladder training) should be used (Grade C/D recommendation).
PeLvIc orGAn ProLAPse Pelvic organ prolapse is common and is seen in 50% of parous women.126 Women with prolapse can experience a variety of pelvic floor symptoms. Treatments include
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surgery and conservative treatment. Choice of treatment depends on the severity of the prolapse and its symptoms, and the woman’s general health. Conservative treatment is generally considered for women with a mild degree of prolapse, those who wish to have more children, the frail, or those unwilling to undergo surgery. Conservative treatment is defined here as lifestyle interventions, physical therapies, complementary therapies, rings and pessaries. This section will examine the evidence for the use of conservative treatments (excluding rings and pessaries – see Chapter 34) in the management of pelvic organ prolapse, utilizing information from two recent Cochrane Systematic Reviews.127,128
Lifestyle interventions Lifestyle interventions include weight loss, reducing exacerbating activities (e.g. lifting, coughing) and treating constipation. These interventions seek to avoid exacerbation of the prolapse by decreasing intraabdominal pressure. The extent to which any of these lifestyle interventions is effective in managing prolapse is unknown.129 There is some evidence that occupations involving heavy lifting/hard physical labor or being overweight may play a role in the development of pelvic organ prolapse. Existing studies, however, are hampered by their cross-sectional nature, inconsistent definitions of pelvic organ prolapse, failure to adjust for potentially important variables (such as parity and socioeconomic status), failure to account for past occupational history, and use of broad occupational codes to determine level of activity. Currently there is no evidence regarding the effectiveness of lifestyle interventions in the treatment of women with pelvic organ prolapse.
Physical therapies While pelvic floor muscle training appears to be effective in the treatment of urinary stress and mixed incontinence (see p. 411), its role in managing prolapse is not established.130 Two RCTs were found that evaluated the effects of PFMT131,132 for treating pelvic organ prolapse. Piya-Anant et al.131 reported that PFMT was effective in elderly women who had a severe degree of genital prolapse. After 24 months of PFMT, the rate of worsening of genital prolapse was 72.2% in the control group and 27.3% in the intervention group (p=0.005). However, in women with a mild degree of genital prolapse, while the rate of worsening at 12 months was significantly less in
the PFMT compared with the control group (p=0.02), there was no significant difference at 2 years (p=0.13). Jarvis et al.132 reported a significant improvement in both quality of life (p=0.004) and symptom-specific problems (p=0.02) when preoperative physiotherapy was given to women undergoing surgery for urinary incontinence and/or prolapse compared with women who received no physiotherapy. One other small cohort study assessed the effectiveness of biofeedback therapy in 32 women with a rectocele of 2 cm or more who were complaining of impaired rectal evacuation.133 At follow-up (median 10 months), 18 patients (72%) felt that their constipation had improved, with complete resolution of symptoms reported by three of these patients. Frequency of bowel movements normalized after biofeedback and this improvement was maintained at follow-up. Current research evidence regarding the effectiveness of physical therapies for the treatment of pelvic organ prolapse is particularly weak. Although PFMT may prevent deterioration of anterior prolapse, the one existing RCT in this area is limited by its failure to utilize a recognized objective measurement of degree of prolapse and its application to an elderly population only.131 Preoperative PFMT may help to improve quality of life and symptom-specific problems in women undergoing surgery for prolapse; however, the evidence available is based on a study sample that includes women undergoing surgery for urinary incontinence and/or prolapse (Level of evidence 2/3). Given the prevalence of pelvic organ prolapse in women and the fact that physical therapies may already be part of the treatment offered to women in many centers,127 the lack of evidence of effectiveness is disconcerting. There is a need therefore for further research regarding the effectiveness of PFMT, which is costly in terms of therapist time. It is crucial that such studies have a control group, are randomized and use recognized objective measurements of prolapse severity. At least two such studies are now underway, one of which is a feasibility study that may lead to a multicentered randomized controlled trial.134 The other study may lead to evidence regarding the effectiveness of PFMT used in conjunction with surgery.135 Future studies should also aim to reach a consensus on the optimal physical therapy intervention program prescribed in terms of the number of repetitions, type and duration of exercises, and should also consider outcome measures that compare individualized training with group training. Finally, there is a need for studies of the effectiveness of physical therapies in comparison with surgery and rings and pessaries (Grade C/D recommendation). 421
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complementary therapies No studies have been found that evaluate the role of complementary therapies in the prevention and treatment of pelvic organ prolapse.
GenerAL concLusIons Conservative treatment (lifestyle interventions, physical therapies, scheduled voiding regimes, complementary therapies, anti-incontinence devices, supportive rings/pessaries for pelvic organ prolapse, and pads/ catheters) should be included in the counseling of women with urinary incontinence and/or pelvic organ prolapse, regarding treatment options. The evidence for their effectiveness is summarized in Table 29.2 (excluding anti-incontinence devices, rings/pessatable 29.2.
ries, and pads/catheters – discussed in Chapters 34 and 35). Further research on the effectiveness of conservative treatment is necessary, and investigators should use wellestablished methodologic criteria when planning and implementing trials. These trials need to include the use of valid and reliable outcome measures (measures of cost, patient satisfaction, clinical morbidity, function, and quality of life) that are lacking from much of the existing research. Investigation of factors affecting outcomes (e.g. severity, age, previous surgery, and parity) is also urgently needed.
AcKnoWLedGeMents This chapter has been based largely on the work of the Adult Conservative Management group of the Third
Summary of evidence for effectiveness of conservative treatments for women with urinary incontinence and/or pelvic organ prolapse
1. Level 1 evidence • PFMT is better than no treatment for women with stress, urge or mixed incontinence • Bladder training is better than no treatment for women with stress, urge or mixed incontinence 2. Level 2 evidence • Weight loss in morbidly and moderately obese women decreases incontinence • Decreasing caffeine improves continence • More intensively supervised PFMT is more effective than less intensely supervised PFMT • PFMT with biofeedback or intravaginal resistance is no more effective than PFMT alone • PFMT and vaginal cones might have similar effectiveness for SUI women • PFMT might be better than ES for SUI women • PFMT and bladder training might be similarly effective for women with SUI, UUI or mixed urinary incontinence • PFMT might be better than oxybutynin for women with DO, or DO with USI • PFMT and adrenergic agonists might be similarly effective for women with SUI or mixed incontinence • PFMT might be less effective than surgery for women with USI • For women with stress or mixed incontinence, a combination of PFMT/bladder training may be more effective than PFMT alone in the short term (3 months), but any additional benefit may not be maintained longer term (6 months) • PFMT may be as effective as PFMT plus VC for SUI women • VC and ES appear to be equally effective for SUI women • There may be no difference in ES or placebo treatment for women with USI • For women with detrusor overactivity there is a trend in favor of ES over placebo stimulation • PFMT appears to be as effective as PFMT plus ES • Bladder training may be more effective than drug therapy available prior to 1995 for women with detrusor overactivity • PFMT may prevent deterioration of anterior prolapse 3. Level 3 evidence • Older women with urinary incontinence benefit as much from PFMT as younger women • Magnetic stimulation might be effective in the treatment of women with urinary incontinence • Timed voiding with a 2-hour voiding interval may be beneficial as a sole intervention for women with mild incontinence and infrequent voiding patterns • Acupuncture and hypnosis improve overactive bladder symptoms • Preoperative PFMT may improve quality of life and symptom-specific problems in women undergoing surgery for prolapse 4. Level 4 or insufficient evidence There is insufficient evidence regarding the comparative effectiveness of: • ES with magnetic stimulation, anticholinergic/antimuscarinic therapy in women with detrusor overactivity • electrical stimulation and vaginal estrogens in women with USI • bladder training and current drug therapies • combining drug therapy with bladder training and vice versa
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International Consultation on Incontinence. Particular thanks are due to Jean Hay-Smith (principal author of Physical Therapies – Pelvic Floor Muscle Training and Weighted Vaginal Cones), Ingrid Nygaard (principal author for Lifestyle Interventions and Complementary Therapies in Women), Jean Wyman (principal author for Scheduled Voiding Regimes), Bary Berghmans (principal author for Electrical Stimulation), Tom Yamanishi (principal author for Magnetic Stimulation and Complementary Therapies in Men), and Suzanne Hagan and Lesley Sinclair (principal authors for Conservative Treatment of Pelvic Organ Prolapse). We would also like to acknowledge the secretarial assistance of Debbie Moore in the coordination and preparation of this chapter.
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Services. Public Health Service. Agency for Health Care Policy and Research, 1996. 109. Roe B, Williams K, Palmer M. Bladder training for urinary incontinence in adults. Cochrane Database Syst Rev 2001;4:1–22. 110. Wallace SA, Roe B, Williams K, Palmer M. Bladder training for urinary incontinence in adults [update of Cochrane Database Syst Rev 2000;(2):CD001308; PMID: 10796768]. Cochrane Database Syst Rev 2004;1. 111. Fantl JA, Wyman JF, McClish DK et al. Efficacy of bladder training in older women with urinary incontinence. JAMA 1991;265(5):609–13. 112. Dougherty MC, Dwyer JW, Pendergast JF et al. A randomized trial of behavioral management for continence with older rural women. Res Nurs Health 2002;25(1):3–13. 113. Jarvis GJ, Millar DR. Controlled trial of bladder drill for detrusor instability. BMJ 1980;281(6251):1322–3. 114. McClish DK, Fantl JA, Wyman JF, Pisani G, Bump RC. Bladder training in older women with urinary incontinence: relationship between outcome and changes in urodynamic observations. Obstet Gynecol 1991;77(2):281–6. 115. Jarvis GJ. A controlled trial of bladder drill and drug therapy in the management of detrusor instability. Br J Urol 1981;53(6):565–6. 116. Columbo M, Zanetta B, Scalambrino SEA. Oxybutynin and bladder training in the management of female urinary urge incontinence: a randomized study. Int Urogynecol J 1995;6:63–7. 117. Park JT, Song C, Choo M. The effects of bladder training, tolterodine, and bladder training with tolterodine in female patients with overactive bladder: a prospective randomized study. Neurourol Urodyn 2002;21(4):434–5. 118. Szonyi G, Collas DM, Ding YY, Malone-Lee JG. Oxybutynin with bladder retraining for detrusor instability in elderly people: a randomized controlled trial. Age Ageing 1995;24(4):287–91. 119. Wiseman PA, Malone-Lee J, Rai GS. Terodiline with bladder retraining for treating detrusor instability in elderly people. BMJ 1991;302(6783):994–6. 120. Castleden CM, Duffin HM, Gulati RS. Double-blind study of imipramine and placebo for incontinence due to bladder instability. Age Ageing 1986;15(5):299–303. 121. Mattiasson A, Blaakaer J, Hoye K, Wein AJ. Simplified bladder training augments the effectiveness of tolterodine in patients with an overactive bladder. BJU Int 2003;91(1):54–60. 122. Philp T, Shah PJ, Worth PH. Acupuncture in the treatment of bladder instability. Br J Urol 1988;61(6):490–3.
123. Bergstrom K, Carlsson CP, Lindholm C, Widengren R. Improvement of urge- and mixed-type incontinence after acupuncture treatment among elderly women – a pilot study. J Auton Nerv Syst 2000;79(2–3):173–80. 124. Honjo H, Naya Y, Ukimura O, Kojima M, Miki T. Acupuncture on clinical symptoms and urodynamic measurements in spinal-cord-injured patients with detrusor hyperreflexia. Urol Int 2000;65(4):190–5. 125. Freeman RM, Baxby K. Hypnotherapy for incontinence caused by the unstable detrusor. BMJ (Clin Res Ed) 1982;284(6332):1831–4. 126. Beck RP, McCormick S, Nordstrom L. A 25-year experience with 519 anterior colporrhaphy procedures. Obstet Gynecol 1991;78(6):1011–8. 127. Hagen S, Stark D, Maher C, Adams E. Conservative management of pelvic organ prolapse in women. Cochrane Database Syst Rev 2004(2):CD003882. 128. Adams E, Thomson A, Maher C, Hagen S. Mechanical devices for pelvic organ prolapse in women. Cochrane Database Syst Rev 2004(2):CD004010. 129. Bump RC, Norton PA. Epidemiology and natural history of pelvic floor dysfunction. Obstet Gynecol Clin North Am 1998;25(4):723–46. 130. Poma PA. Nonsurgical management of genital prolapse. A review and recommendations for clinical practice. J Reprod Med 2000;45(10):789–97. 131. Piya-Anant M, Therasakvichya S, Leelaphatanadit C, Techatrisak K. Integrated health research program for the Thai elderly: prevalence of genital prolapse and effectiveness of pelvic floor exercise to prevent worsening of genital prolapse in elderly women. J Med Assoc Thai 2003;86(6):509–15. 132. Jarvis SK, Hallam TK, Dietz HP, Abbott JA, Vancaillie TG. Pre- and post-operative physiotherapy intervention for gynaecological surgery: a single blind randomised controlled trial. In: XIVth Annual Scientific meeting of the Australian Gynaecological Endoscopy Society, May 26–29, 2004. Brisbane, Australia, 2004. 133. Mimura T, Roy AJ, Storrie JB, Kamm MA. Treatment of impaired defecation associated with rectocele by behavioral retraining (biofeedback). Dis Colon Rectum 2000;43(9):1267–72. 134. Hagen S. A feasibility study for an RCT of a pelvic floor muscle training intervention for pelvic organ prolapse. The National Research Register, Publication ID: N0470119684, 2003. 135. Frawley H. The effect of a physiotherapy treatment program on pelvic function following gynaecological surgery [PhD study]. Registered at www.PhdData.org [PhD]. Melbourne: University of Melbourne, 2002.
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30a Outcome measures in women with lower urinary tract symptoms: overactive bladder Catherine E DuBeau, Eboo Versi
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Introduction The definition and standardization of outcome measures is critical to the understanding of the natural history of overactive bladder (OAB) as well as the effects of – and comparisons between – OAB treatments, both in clinical care and evidence-based research. The International Continence Society (ICS) has placed increasing emphasis on the codification and standardization of outcomes in general1 and for particular groups of patients such as the elderly.2 Physiologic measures, such as urodynamic parameters and bladder diary data, have long been used as outcomes. However, due to the increased recognition that OAB is a quality of life (QoL) condition,3,4 the importance and need for patient-centered measures such as QoL scales have markedly increased. While some have classified these different types of measures as ‘objective’ and ‘subjective’, we feel that such terminology is imprecise and implies unsubstantiated value judgments; consequently these terms should be avoided. One of the challenges in discussing OAB outcomes is the fact that OAB is a symptom syndrome and not a specific physiologic entity. Moreover, OAB can coexist with other, more specific symptoms and urodynamically defined conditions such as stress urinary incontinence (SUI). Particularly in the elderly, OAB can be due to factors such as pedal edema and impaired mobility that have nothing to do with an ‘overactive bladder’ per se. Participants in treatment trials often have mixed conditions (e.g. ‘urge-predominant mixed’), rendering condition-specific measures (particularly urodynamics) irrelevant for such subjects. In this chapter, we will review outcome measures of efficacy, tolerability and safety for OAB treatment. We will cover both physiologic and patient-centered outcomes, issues regarding assessment of the placebo response that occurs during treatment for OAB, and factors in the statistical analysis of treatment trials. The primary emphasis will be on outcome measures for use in clinical trials and clinical work, yet these measures could also be used in the evaluation of the natural history of (untreated) OAB.
PRINCIPLES FOR THE EVALUATION OF SYMPTOMS AND TREATMENT OUTCOMES IN OAB Underlying all biomedical research is the need for valid and reliable research tools. Validity refers to the ability of a research tool to accurately measure the specific concept or parameter it is attempting to measure; this is referred to as internal validity. A tool must also have external validity such that the results are generalizable beyond the initial study population. The reliability of a
research tool refers to the reproducibility of the results obtained at each use. A tool that is not reliable will yield different results when administered by different individuals or research groups. When considering appropriate outcome measures for use in OAB research, the type of data collected should also be considered. Data that can be counted, such as number of voids or number of incontinence episodes, can be collected as quantitative or continuous data. Qualitative analysis categorizes data into discrete groupings such as mild, moderate or severe and can be useful in describing patients’ perception of their symptoms. Both types of data can be subjected to statistical analysis and comparison. Finally, the measurement period or treatment interval and sensitivity of the instrument to change should be considered such that the effects of therapeutic interventions can be monitored over relevant time periods of weeks or months.
STATISTICAL EVALUATION Cure versus improvement The natural history of OAB has not been well studied but symptoms tend to wax and wane. Thus improvement may be seen to occur spontaneously but this may only be transient. What degree of improvement should be regarded as clinically significant is also not defined. While many clinicians believe 50% improvement is acceptable, patient acceptance is variable. This should be viewed in the context of a placebo improvement of 25–30%. Cure is probably not an appropriate term in patients with OAB, rather the term remission might be preferable. In this context the duration of diary use is critical: a 3-day diary yields a higher ‘cure’ rate than a 7-day diary.5 Lack of documentation of a symptom on a urinary diary may be regarded as remission for measures of incontinence and urgency; however, urinary frequency and volume voided per micturition cannot be treated in the same way. For these variables, percentage normalized can be used (e.g. percentage of patients who, after treatment, had urinary frequency of 8 or less per day). Again, little is known about patients’ acceptance of such statistical ‘norms’.
Means versus medians If data are normally distributed, parametric statistics can be used to describe the information (means and standard
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deviations); however, if the data are not normally distributed (skewed) then non-parametric statistics should be used (medians and interquartile range or deciles). Most data collected on urinary diaries are not normally distributed and yet most regulatory bodies have accepted data reported as means. This probably stems from the erroneous assumption that normality is approximated when there are a large number of patients in a study. Given the nature of the distribution of response to treatment with incontinence therapy, the median improvement value is invariably numerically higher than the mean value.
Responder analyses Efficacy data are usually presented as an average which hides the heterogeneity of the response. OAB has multiple etiologies and, consequently, any given treatment modality may not equally treat all patients in a given cohort. A lack of understanding of these concepts has led to the erroneous idea that treatments are marginally effective because the average response is not large. However, as every clinician knows, individual responses can be quite impressive so responder analyses should be encouraged when evaluating response to therapy. The search for prognostic indicators would be beneficial in this field.
Baseline severity of disease Treatment effect will depend on severity of the disease prior to treatment in that absolute reductions of incontinence and urgency episodes will be greater for the more severe patients, but the percentage change from baseline when computed for each individual patient may be similar for severe and mild disease.6 For example, a patient with four episodes of incontinence per day will reduce to two, whereas someone with two episodes per day will reduce to one, the reduction still being 50%.
Intention to treat versus per protocol analysis The standard required by regulatory bodies for the treatment of trial dropouts is to use the intention to treat method (ITT), in which all patients randomized to a treatment arm will be included in the analysis for that arm despite later dropout. The last observation is carried forward (LOCF) to represent the end of treatment data point. ITT analysis is necessary to maintain the integrity of the randomization process. This conservative approach is also often used to analyze secondary variables.
By definition, secondary variables are exploratory in that the study would not have been designed and powered to detect differences in the secondary variables and, as such, a per protocol analysis (PPA) would be appropriate for these secondary variables. However, a more conservative statistical approach (ITT) would be warranted if secondary analyses are to be presented as definitive (meaningful).
Non-inferiority Occasionally the goal of a study is to show no difference between two treatments. Unfortunately, one often sees in the literature a claim that two treatments are equal because the ‘p’ value is greater than 0.05. This may simply be the result of underpowering the study or, worse still, not powering it at all! The correct design for such comparisons is a non-inferiority design. This pre-specifies an effect size interval within which both treatments have to fall to be considered the same or the investigational treatment to be non-inferior to the control treatment.
Meta-analyses and systematic review Because OAB treatment results are so variable and because many studies are underpowered because large study populations can be prohibitively expensive, systematic review followed by meta-analysis of the available data is often attempted to increase the power of detection of differences between treatment arms. These methods are not foolproof as they cannot correct for heterogeneity of the study designs that comprise the datasets employed in such analyses. Further, these techniques merely document statistical differences which, given the larger numbers involved, may be significant but clinically irrelevant due to overpowering. A lack of understanding of such limitations can lead to seriously flawed conclusions as was recently demonstrated by Herbison et al.7 These authors set out to perform a meta-analysis of drug effect compared to placebo in the treatment of overactive bladder and found a statistically significant superiority of the antimuscarinic drugs on diary variables. They then went on to conclude that these differences are clinically insignificant even though they did not address any measure of clinical relevance or quality of life.
EFFICACY As noted above, there are multiple domains that should be included in the evaluation of OAB treatment strategies and natural history. These domains include physi431
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ologic, patient-centered, clinician-based and health systems (utilization, compliance, persistence, cost-effectiveness and cost–benefit). While physiologic measures are important for ‘proof of concept’ investigations and studies done for regulatory and registration purposes, and facilitate comparison with the historical literature, they may not be as applicable when the purpose is to define clinical effectiveness. Therefore, patient-centered outcomes are increasingly considered crucial in treatment trials intended to influence clinical practice. Physiologic and patient-centered measures are complementary, and should not be substituted for one another, even when there is established correlation between specific measures. Clinician-based measures should never be used as a substitute for patient-centered outcomes because of the different biases, motivation, frames of reference, and possibly gender, age, cultural and socioeconomic differences between clinicians and patients.
Physiologic measures Urodynamics The main urodynamic test used to evaluate OAB is cystometry. It must be remembered that the assumption in using urodynamic studies to evaluate OAB is that the symptoms are related to detrusor overactivity (Table 30a.1).8 In patients with OAB, efficacy of antimuscarinic therapy has been shown, irrespective of the demonstration of detrusor overactivity.9 This may reflect the inaccuracy of cystometry or that detrusor overactivity is not the only cause of OAB. It has been previously shown that cystometry has a false-negative rate of 45%.10 It is possible that the urodynamic correlate of OAB is sensory urgency but this is not defined by the ICS and it is generally agreed that urodynamic measures should conform to the ICS definitions. While urodynamic studies are important for understanding the effects of treatment on detrusor function, use of urodynamic studies in treatment trials is generally employed
Table 30a.1. International Continence Society definitions of urodynamic bladder sensation and detrusor function Sensation
Definition
First sensation of bladder filling
During filling cystometry, a feeling that the individual has when first becoming aware of the bladder filling
First desire to void
During filling cystometry, a feeling that would lead the individual to pass urine at the next convenient moment, but voiding can be delayed if necessary
Strong desire to void
During filling cystometry, a persistent desire to void without the fear of leakage
Absent bladder sensation
During filling cystometry, the individual has no bladder sensation
Non-specific bladder sensations
During filling cystometry, may make the individual aware of bladder filling, e.g. abdominal fullness or vegetative symptoms
Bladder pain
During filling cystometry, is a self-explanatory term and is an abnormal finding
Urgency
During filling cystometry, is a sudden compelling desire to void
Increased bladder sensation
During filling cystometry, as an early first sensation of bladder filling (or an early desire to void) and/or an early strong desire to void, which occurs at low bladder volume and which persists
Detrusor function Normal detrusor function
Allows bladder filling with little or no change in pressure. No involuntary phasic contractions occur despite provocation
Detrusor overactivity
Urodynamic observation characterized by involuntary detrusor contractions during the filling phase which may be spontaneous or provoked. In everyday life the individual attempts to inhibit detrusor activity until in a position to void. Therefore, when the aims of the filling study have been achieved, and when the individual has a desire to void, normally the ‘permission to void’ is given. That moment is indicated on the urodynamic trace and all detrusor activity before this ‘permission’ is defined as ‘involuntary detrusor activity’
Provocative maneuvers
Techniques used during urodynamics in an effort to provoke detrusor overactivity, e.g. rapid filling, use of cooled or acid medium, postural changes and hand washing
Data from ref. 8.
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Table 30a.2. Components of a typical 1-hour pad test for urinary incontinence Time (min)
Element
Pretest
Determine pretest bladder volume*
0
Apply pre-weighed pad Patient drinks 500 ml sodium-free liquid and rests for 15 minutes
15
Patient walks for 30 minutes, including stair climbing (equivalent of one flight of stairs)
45
Patient performs the following activities during the remaining 15 minutes: • Sit–stand 10 times • Cough vigorously 10 times • Run on the spot for 10 minutes • Pick up a small object from the floor five times • Wash hands under running water for 1 minute
60
Test complete, pad removed and weighed Patient voids and the void volume is recorded
Data from ref. 13. * This element has not been standardized although it appears to improve the reproducibility of the test.104,105
in proof of concept studies rather than those of clinical effectiveness. However, it could be argued that the use of cystometry even in proof of concept studies is inappropriate.
Pad tests As patient perception of incontinence does not correlate well with urodynamic measurements,11,12 alternative methods are required to evaluate urinary incontinence (UI). Pad tests enable the quantification of urine loss as well as an evaluation of the severity of incontinence, and they provide a non-invasive method for evaluating the effect of treatment (Table 30a.2).13 Perineal pads with pad weight testing in the ambulatory patient are the most widely used pad test for the clinical evaluation of UI. Short-duration pad tests of 1 or 2 hours have proved useful in stress incontinence
research.14 However, short-duration pad tests are associated with a high false-negative rate, making them a poor screening tool for incontinence,15 especially urge UI. Protocols for longer duration pad tests (24 and 48 hours) have also been developed for use in the home rather than in the hospital setting. Home pad tests are more relevant than short-duration tests for the evaluation of urge or mixed incontinence associated with OAB where the incontinence episodes are less predictable. However, they are only of value in a third of the OAB population – those with incontinence.16 A normal threshold value for urine loss has been established as 8 g/24 hours and 15 g/48 hours.17,18 Values for incontinence severity have been proposed for the 24-hour pad test as: mild 1.3–20 g/24 hours, moderate 21–74 g/24 hours, and severe >75 g/24 hours (Table 30a.3).19 The reproducibility of both the 24- and 48hour home pad tests have proven to be very good, with correlation coefficients >0.80 for the 24-hour test17,18,20,21 and >0.90 for the 48-hour test.17,22 The 24- and 48-hour tests appear comparable in terms of reproducibility.17,20 Several studies have shown that the home pad test offers greater sensitivity, with a lower false-positive and falsenegative rate.
Bladder diaries Bladder diaries – also referred to as voiding diaries/ records, frequency/volume charts and urinary or incontinence diaries – allow a semi-objective evaluation of the severity of UI (frequency and volume), identification of any associated sensations/events which might help in the diagnosis of the type of incontinence, and association of provocative events (such as coughing, running, etc.). They also allow an estimation of total fluid intake (fluid and food) based on output volume and can be used as part of a bladder retraining program for patients with OAB. These diaries can also be used to monitor ‘warning time’ which measures the interval between first sensation and the void (voluntary or involuntary).23 Unfortunately, this measurement is rather variable given the observed
Table 30a.3. ‘Normal’ urine loss and severity grading of incontinence as assessed by pad weight gain during 1-hour and 24-hour pad tests Test duration
Normal/Dry
Slight to moderate incontinence
Severe incontinence
Very severe incontinence
1 hour
<2 g
2–10 g
10–50 g
>50 g
Mild
Moderate
Severe
1.3–20 g
21–74 g
>75 g
24 hours
8g
Data from refs 13 and 19.
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Date
Time
Measured amount of urine
Are you wet or dry?
Approximate amount of leakage
Comments
a
Your Daily Bladder Diary This diary will help you and your health care scan. Bladder diaries help show the causes of bladder control trouble. The “sample” line (below) will show you how to use the diary.
Your name: Date: A C C I D E N T S
Time
Drinks What kind?
b
Urine How much?
How many times?
Accidental leaks How much? (circle one)
How much? (circle one)
Did you feel a strong urge to go?
What were you doing at the time?
Circle one
Smoking, exercising, having sex, bathing, etc.
Sample
Yes
No
6–7 a.m.
Yes
No
7–8 a.m.
Yes
No
8–9 a.m.
Yes
No
9–10 a.m.
Yes
No
10–11 a.m.
Yes
No
11–12 noon
Yes
No
12–1 p.m.
Yes
No
1–2 p.m.
Yes
No
2–3 p.m.
Yes
No
3–4 p.m.
Yes
No
Figure 30a.1. Bladder diaries. (a) Data from ref. 24. (b) Reproduced from the National Kidney and Urologic Disease Information Clearinghouse. variations in first sensation. Bladder diaries are widely used in both clinical and research settings to assess change during and after therapeutic intervention. They also offer a prospective method for validating patientreported symptoms which, if used correctly, is unbiased by patient recall. A wide variety of diaries are available (Fig. 30a.1) from the most simple, requiring the patient to record only the number and time of UI episodes,24 to the complex, requiring patients to record voided volume, fluid intake and all associated activities (Table 30a.4). The reliability and validity of diary data – and the methods by which to establish reliability and validity – have been questioned. There is an inevitable trade-off between the quantity and quality of the data that can be collected by this method, as ‘diary fatigue’ may distort the results of more complex diaries or those of longer duration.25 Most research bladder diaries are of 7-day duration but patients often have difficulty in maintaining records for this long, raising the possibility that some diaries are filled out in the car park prior to the clinic
visit. Measuring urine volume is particularly onerous and consequently many investigators accept just 2 days’ data for this parameter.26 As independent verification of diary data is not feasible, diary data can only be validated against reported (historical) or cystometrically defined symptomatology. Several studies have found reasonably good agreement between diary data and reported symptom history and, in table 30a.4.
Possible elements of a bladder diary
1. Number and time of urinary incontinence episodes • Associated sensations (e.g. urgency) • Provocative activity (e.g. sneezing, coughing, laughing, running) • Volume of loss (e.g. small, medium, large) 2. Voided volume 3. Number of incontinence pads used 4. Fluid and/or food intake • Type of fluid (e.g. coffee) 5. Time of event (e.g. waking from sleep)
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one study, cystosmetric evaluation.27–29 However, attempts to validate diary-recorded volumes against cystometric or cystoscopic capacity have proved more difficult, with a variety of confounding factors associated with invasive measurement leading to significant discrepancies between the data collected, such as functional bladder capacity (maximum voided volume).10,29 Despite the difficulties in validating diary data against measurable laboratory variables, bladder diaries can be regarded as a valid tool for the assessment of diurnal and nocturnal frequencies as well as functional bladder capacity. Bladder diaries also appear to be reliable measurement tools in patients with urge or mixed UI.30 In a study of men and women with urge and mixed UI, patients were asked to complete 7-day bladder diaries on two occasions separated by at least 1 week. The reliability in terms of measuring micturitions, strong urge sensations and urge incontinence episodes was good to excellent, with reported correlation coefficients ranging from 0.81 to 0.86.30 The same study showed that a 3-day diary is as valid as a 7-day diary30 but when dry rates are determined (no incontinence episodes during diary collection), as would be expected, a 3-day diary yields a higher dry rate.5,31
Electronic diaries Electronic bladder diary devices present both advantages and disadvantages compared with paper diaries. Although it was assumed that entry errors with electronic diaries would be ‘impossible’, this has not been borne out. In a cross-over study in 35 OAB patients (90% women) using 7-day electronic and paper diaries, data entered into the electronic diary could be verified in only 73% of cases, and two patients tried to input electronic data retrospectively.32 In addition, while only 6% of patients found the electronic diary ‘not at all easy to use’, 30% reported feeling ‘initially wary’ because the device was not intuitive. Drug trials using electronic diaries have had large placebo responses:
64% better by patient impression of improvement with placebo versus 74% with duloxetine,33 and 56% reduction in median number of weekly UI episodes with placebo versus 68% with darifenacin.34 These rates may be due to enhanced training effects with a device that is carried constantly.
Patient-centered measures Symptoms OAB encompasses a number of bladder storage symptoms – urgency, frequency, urge incontinence and nocturia. In 2002, the ICS published a standardized definition of OAB that emphasized the need to focus on patient-reported symptoms, symptom-bother and QoL.8 This latest definition of OAB places urgency as the core symptom which patients must experience in order to apply a diagnosis of OAB. The emphasis now placed on urgency as the central characteristic of the OAB symptom complex continues to drive the need for reliable, patient-centered, validated tools for its identification and quantification. Two scales which go some way to meeting this need are the Indevus Urgency Severity Scale (IUSS)35 and the Urgency Perception Scale (UPS).36 The IUSS uses a 4-point qualitative scale and asks patients to rate the severity of the ‘urgency’ they experience prior to voiding (Table 30a.5) while the UPS asks patients to describe their typical response when they feel the need to urinate (Table 30a.6). However, neither scale appears to provide an accurate measure of pathologic urgency as defined by the ICS. Categories 0, 1 and 2 of the IUSS appear to measure normal urge sensations rather than urgency (Table 30a.5). Similarly, one of the three possible responses on the UPS appears to describe normal urge sensations rather than urgency as defined by the ICS (Table 30a.6). The challenge of differentiating and describing urge and urgency sufficiently for them to be recorded accurately,
Table 30a.5. The Indevus Urgency Severity Scale Category
Severity of urgency
0
None: no urgency Mild: awareness of urgency but easily tolerated
2
Moderate: enough urgency/discomfort that it interferes with usual activities/tasks
3
Severe: extreme urgency discomfort that abruptly stops all activities/tasks
Consistency with ICS-defined urgency sensation Normal urge sensations experienced even in the absence of OAB Pathological urgency
Data from ref. 35. ICS, International Continence Society; OAB, overactive bladder.
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Table 30a.6. The Urgency Perception Scale Response code
Patient response when asked to describe their typical response when they felt the desire to urinate
Consistency with ICS-defined urgency sensation
1
I am usually not able to hold urine
Pathological urgency with urge incontinence
2
I am usually able to hold urine until I reach the toilet if I go immediately
Pathological urgency
3
I am usually able to finish what I am doing before going to the toilet
Normal urge sensations
Data from ref. 36. ICS, International Continence Society.
Presumed normal void volume
Void (voluntary and/or involuntary) Normal desire to void Urgency
frequency over a given time period. This latter technique is subject to recall error and may not accurately reflect actual voiding frequency. Similarly, urge UI episode frequency is most often collected using bladder diaries which provide a more accurate picture than patient selfreporting based on recall. Patients with OAB who have an incontinence component (OAB-wet) may experience both an urge UI (urine loss associated with urgency) component and a stress UI component (urine loss associated with defined physical activities such as sneezing, coughing, running, etc.) (Fig. 30a.3). Therefore, assessment of UI in OAB must also identify any associated urgency sensations and provocative activities. The use of antimuscarinics in patients with urge-predominant OAB is effective, but not, apparently, for the stress component.39 Nocturia – waking during the night to urinate – is associated with a number of medical conditions including cardiovascular disease, diabetes mellitus or insipidus, and sleep apnea, and is most common among the elderly. Nocturia should be viewed as a distinct pathologic entity from nocturnal enuresis (urine loss without wakening), which occurs most often in children and is thought to be due to factors unrelated to bladder function such as an immature nervous system leading to impaired arousal during sleep. Nocturia may be the
Reduction of intervoid interval
Intensity
Reduction in volume voided due to urgency
Bladder volume (
)
either in diaries or using quantitative scales, remains. In particular, the fact that antimuscarinics can alter the urge as well as the urgency component of the IUSS35,37 would suggest that this division between urge and urgency is arbitrary. The current definition of urgency may need to be redefined beyond ‘presence’ or ‘absence’ of urgency. One way of overcoming this problem may be to examine the intervoid interval (the time between each void). This interval would be expected to become significantly shorter in patients who experience pathologic urgency and cannot defer voiding for any relevant period of time (Fig. 30a.2). Conceptualizing urgency in this way may allow the development of testable hypotheses about the distinction between normal urge sensation and pathologic urgency, the relationship between urgency and the other symptoms of OAB, and appropriate targets and potential effects of therapeutic intervention.38 Other symptoms of OAB are inherently more categorical in nature, which might be expected to make data collection more straightforward. Frequency is the primary efficacy endpoint preferred by regulators for drug approval when collected in diary form. Bladder diaries allow patients to make a record of each time they visit the bathroom to void. Frequency data can also be collected using a visual analog scale (VAS), with patients being asked to provide an historical estimate of voiding
Figure 30a.2. Relationship between the normal micturition cycle and pathological urgency. (Reproduced from ref. 38 with permission).
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OAB
Stress UI
Mixed UI
Urge UI
Urgency Frequency
Figure 30a.3. Conceptual relationships between the symptoms of overactive bladder (OAB). (UI, urinary incontinence.) result of either overproduction of urine during the night (nocturnal polyuria) or diminished nocturnal bladder capacity, or a combination of the two,40 only the latter two are associated with OAB. Nocturnal polyuria can be diagnosed by straightforward analysis of 24-hour voiding data collected using a bladder diary. Any assessment of nocturia should take into consideration time spent in bed and asleep as this may be subject to considerable individual variation.
Bothersomeness Bothersomeness (or bother) is one type of patientcentered measure of OAB symptom impact. The common definition of bother41 includes to annoy, intrude upon, or cause to be anxious or concerned. Although bother may affect QoL, it should not be confused with – or considered a specific measure of – QoL (see below). The ICS8 and the International Consultation on Incontinence (ICI)42 standardized terminology also separate bother from QoL. Bother also should not be confused with – or considered equivalent to – symptom severity, especially as patient adaptation to even severe symptoms may result in lack of perceived bother. While the concept and measurement of bother has attracted increased attention with regard to OAB symptoms and other lower urinary tract symptoms (LUTS), it remains insufficiently standardized across measures and even as a concept. Questions regarding bother are embedded in gender-specific LUTS measures, such as the American Urological Association (AUA) symptom score,43 the Danish Prostate Symptom Score Schedule (DAN-PSS-1),44 the International Continence Society questionnaire for males (ICSmale),45 and the Bristol Female Lower Urinary Tract Symptoms (BFLUTS) scale,46 generally using Likert-like categorical scaling. Likert scales offer patients the choice of discrete categories (e.g. ‘My symptoms cause me no problems/very minor problems/minor problems/moderate problems/severe problems’). However, Likert measures assume an ordi-
nal scaling that may not correspond to an individual’s internal scaling (which may relate more to ‘thresholds’ or be exponential). The widely used Urogenital Distress Inventory (UDI and UDI-6)47,48 was designed to quantify both specific LUTS and their associated bother, ranked along 4 points from ‘none at all’ to ‘greatly’. While the UDI has good levels of reliability, validity and responsiveness,47 and correlates well with the severity of urodynamically-defined types of UI,49 others have found poor correspondence with severity (pad tests) in communitybased women without urodynamic diagnosis.50 Other OAB outcome studies51,52 include VAS measures. The VAS offers an unconstrained choice and is usually presented as a straight line with opposing choices at either end (e.g. ‘My symptoms cause me no problems’ to ‘My symptoms cause me intolerable problems’). Both methods have been widely used in urogynecologic research. When compared to Likert measures, VAS offers simple, reliable and sensitive measures of patient perception of symptom impact and improvement.53–55 Specific bother ‘subscales’ or questions have been included in OAB- and/or UI-specific QoL questionnaires. One such example is the OABq,56 designed to capture the impact of OAB with and without associated UI (so-called OAB-dry and OAB-wet). Its symptom bother subscale, while internally consistent (Cronbach’s alpha = 0.86), correlated moderately with the other subscales (r = –0.47 to 0.71) and modestly with SF-36 domains (r = –0.18 to –0.34), and showed construct validity regarding urgency, nocturia and patient-rated ‘bladder severity’, but not frequency. Concerns about respondent burden with long questionnaires have led not only to ‘short forms’57 but also to single-state scales of overall symptom ‘severity’. Examples include the Patient Global Impression of Severity (PGIS)58 and a patient perception of bladder condition scale (e.g. ‘My bladder condition: does not cause me problems, causes me some very minor problems, causes me some minor problems, etc.’).59 The PGI-S showed statistically significant construct validity with UI frequency, pad tests and a QoL measure (the I-QoL),60 yet the relationships were not linear and suggested some threshold effects. The ICI Questionnaire-Short Form (ICIQ-SF) includes a question regarding how much urine leakage interferes with everyday life (11 point scale, 0 = none to 10 = great deal).61 There is concern, however, that such measures may sacrifice interpretability for simplicity. Patients may vary widely in what they believe they are answering when asked about their urinary tract or bladder ‘condition’. Indeed, focus on ‘leakage’, as with the ICIQ, may miss other troubling OAB symptoms. Habituation to LUTS, 437
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self-management strategies and assumptions that OAB symptoms are ‘normal’ may lead to reports of minimal interference or bother, and therefore miss important treatment effects. Thus, these measures may be more applicable to the care of individual patients, who serve as their own scaling anchors, rather than to groups of trial subjects.
Improvement Improvement over time is the goal of any therapeutic intervention for OAB. Measuring a patient’s perception of improvement over time requires tools with both temporal validity (reproducibility) and sensitivity to change. Responses on the Patient Global Impression of Improvement (PGI-I) questionnaire have been shown to correlate significantly with measures of symptom severity, including UI episode frequency and a stress pad test as well as a QoL measure, the Incontinence Quality of Life Questionnaire.58 Improvement in patient perception of symptom severity can also be measured using visual analog and Likert scales.
Quality of life The World Health Organization defines QoL as ‘an individual’s perception of his or her position in life in the context of the culture and value system where they live, and in relation to their goals, expectations, standards and concerns … incorporating in a complex way a person’s physical health, psychological state, level of independence, social relationship, personal benefits and relationship to salient features in the environment’. 62 Implicit in this concept is the WHO definition of health
as ‘a state of complete physical, mental, and social wellbeing, and not merely the absence of disease or infirmity’. General health-related QoL (HRQoL) measures capture a number of domains in this ranging concept. However, this breadth often renders HRQoL measures such as the SF-36 or the Sickness Impact Profile insensitive to states related to specific conditions, or changes in those states related to treatment. This has been demonstrated with UI and OAB symptoms, and has led to the development of LUT condition-specific QoL measures. The ICS has codified the importance of QoL as an outcome measure1 that should be reported in all treatment trials. A plethora of LUTS-specific measures now exists; a thorough review of each is beyond the scope of this chapter, and the reader is referred to the 3rd ICI publication and Table 30a.7. The most commonly used instruments differ in terms of how they were derived, domains and derivation and validation populations. Qualitative differences across the measures have not been widely explored, but may be especially important for specific populations, such as the elderly. For example, the 7item Incontinence Impact Questionnaire (IIQ-7) asks about leakage affecting household chores, recreation, entertainment and participation in social activities outside the home. Some older persons, however, may not be involved in household chores, regular exercising or going to movies; they would report therefore that UI does not affect these activities, yet they may experience a significant QoL impact in other domains, such as self-concept,63 that would not be captured by the IIQ. Understanding the nuances of measures and their appli-
Table 30a.7. Commonly used lower urinary tract-specific quality of life measures Scale
Acronym
Gender specificity
Diagnostic specificity
Reference
Incontinence Impact Questionnaire
IIQ-7
Women
Urinary incontinence and related conditions
48
Urge Incontinence Impact Questionnaire
Urge-IIQ
Women
Urge incontinence
106
King’s Health Questionnaire
KHQ
Both
Non-disease specific. Validated in various forms of incontinence and OAB
108
Bristol Female Lower Urinary Tract Symptoms Questionnaire
B-FLUTS
Women
Urinary incontinence
46
Urinary Incontinence Quality of Life Instrument
I-QoL
Both
Urinary incontinence
60
Overactive Bladder Questionnaire
OABq
Both
OAB patients (wet and dry)
56
Urge Impact Scale
URIS
Both
Older persons with urge urinary incontinence
107
OAB, overactive bladder.
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cability to the target population has important implications for their use in treatment trials, as negative results (no response to treatment) may reflect more on the measure than on the efficacy of the treatment.
Function One particular way in which OAB may affect QoL is its impact on activities, including work. While this domain may be included in some QoL measures, it is rarely examined on its own. Target population and precise definitions of activity are important when assessing the functional impact of OAB. For example, Scandinavian women aged 28–80 with existing moderate to high levels of exercise and activity reported no change in activity after UI treatment64 and it may be that hours of participation in an activity may be less sensitive to continence status than whether a woman participates in the activity or not.65 On the other hand, OAB impact on working women may be best assessed by the burden of coping, compensatory strategies and productivity, but not by absences or hours lost. In the US, workplaces must offer bathroom facilities and must also provide workers with an opportunity to use them. Functional impact of OAB in older women likely differs by their overall health. Community-dwelling older women with urge UI report little impact of UI on their activity.63 At the same time, incident UI in older people is associated with a two-fold increased risk of impairment in activities of daily living, instrumental activities of daily living and poor physical performance,66 along with an increased risk of nursing home admission.67 Thus, for frail older women, measures of functional status may be important outcome measures to consider when treating OAB.
Health systems Although there have been rigorous studies of the complex economic cost of illness of OAB,68,69 empiric data regarding the use of economic measures as outcomes of OAB treatment are still sparse. Cost-effectiveness analyses, measuring the marginal cost necessary to achieve a specific amount of treatment effect, may be particularly difficult in OAB, especially because of a lack of standardization in reporting outcomes – including pad use, symptom report, and bladder diary-based symptom frequency – and the relatively short duration of treatment trials.70 One suggestion is to use composite measures such as ‘normal days’ (no leakage or urgency and ‘normal’ frequency rates).70 There are few head-to-head analyses comparing treatment costs with different medications, in part reflecting
their complexity, especially when considered across different health systems and assumptions. Whereas a decision analytic cost-effectiveness model using dryness as an outcome found that expected costs of extended-release oxybutynin were lower than extended-release tolterodine,71 hypothetical per-patient-per-month savings were low (US$0.007–0.026). Similar models using Canadian72 and British73 perspectives found extended-release tolterodine suitably or comparatively effective. Health systembased comparisons will also differ regarding potential cost shifting (e.g. depending on whether patients or the system pays for protective pads and/or drugs). Comparisons across providers of similar treatment should also be considered. For example, an Australian study demonstrated per capita labor costs for treatment by continence advisors were less than those for urogynecologists, with similar dry rate and QoL outcomes.74 Knowledge of the QoL impact of a condition permits QoL-based cost–benefit analyses of different treatments for the same condition. However, if one wants to make comparisons of quality-based costs across conditions (e.g. OAB versus arthritis), the common analytic approach is quality-adjusted life-years (QALYs). QALYs are based on the QoL ratings patients assign to living with a condition, usually measured on a scale from 0 (prefer death) to 1 (prefer living with full health). Such ratings are empirically determined by measures such as time-tradeoffs (time living with the condition), willingness to pay (resources one would spend for a reduction in symptoms) or are inferred from population-based utility scores (e.g. the EuroQol-5D). In one of the few available studies, willingness to pay in Swedish patients with UI was related to the anticipated reduction in urinary frequency and leakage, baseline rates of frequency and UI, and income level.75 A Canadian study found that the cost per QALY with tolterodine was Can$9982, but this was calculated using the Scandinavian utilities75 which may not be an accurate reflection of Canadian patient preferences. More is known about the economic impact of UI costs in long-term care. Although UI in these settings includes symptoms other than OAB, OAB symptoms such as urge UI76 and nocturia77 predominate. Costs of UI in longterm care are driven by nursing labor costs, which result in treatment being more expensive than the status quo (i.e. UI care with protective pads).78 Although some models suggest a cost saving with UI treatment related to decreased incidence of pressure ulcers and urinary tract infections,79 others have not.80 The lack of effective means of targeting treatment and information about patient preferences make such added costs difficult to justify.81 439
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PLACEBO RESPONSE Assessment of the efficacy of any OAB treatment must be placed in the context of the robust placebo response rates consistently demonstrated in randomized, placebocontrolled, double-blind trials (RCTs) of all OAB therapy. Such placebo responses are not limited to bladder diary results, but are also found with urodynamic, patient perception and QoL outcome measures. Potential reasons for high placebo responses are regression to the mean (especially when highly symptomatic patients are enrolled), unintended parallel interventions (e.g. training effects from completing repeated bladder diaries), and time and other effects related to being enrolled in a trial (e.g. patients experiencing early improvement – as is common – may be more likely to perform/continue other behavioral modifications such as modifying fluid intake). One feature of OAB drug therapy that may make it particularly prone to high placebo responses is its adverse effect profile. Symptoms such as dry mouth may alert patients in RCTs as to whether or not they are taking an active drug, especially when possible adverse effects are mentioned in the informed consent process or known from previous experience with OAB drug treatment. Such ‘unblinding’ in OAB RCTs has been empirically demonstrated in two studies, one with immediate-release oxybutynin82 and the other with extended release-tolterodine.83 In both studies, the majority of patients randomized to active drug (96% and 58%) correctly identified their randomization at the end of the trial. Significantly, patients’ perception of their randomization was significantly associated with outcome: patients assuming they took an active drug – regardless of their actual randomization – had significantly better outcomes, whether measured by bladder diary, patient perception of improvement or QoL, and they reported significantly higher rates of dry mouth.
TOLERABILITY Definition In assessing outcomes from treatment, tolerability must be considered as well as efficacy. This has special importance in OAB, as previous studies have indicated that patient compliance with drug therapy falls off markedly by 6 months.84 Tolerability includes not only adverse effects and events, but also other complications such as drug interactions and ease of use (from the perspective of both the clinician and the patient). The latter often are not reported in drug trials, especially open-label
extensions in which they would be most likely to arise. Tolerability of behavioral interventions relate primarily to the burden and time involved in adhering to the specific regimen (see further discussion in Chapter 31). Adverse drug reactions (ADRs) are common with the antimuscarinic agents used to treat OAB, especially among older people.85 For such an important outcome, there is little or no standardization in definitions or ascertainment. Whereas antimuscarinic ADRs are considered primarily bothersome for younger and middleaged women, for older patients they may contribute to serious morbidity, ranging from dental caries and dysphagia to confusion and falls.86 ADRs resulting in cognitive dysfunction may go underdetected in people with dementia (and possibly mild cognitive impairment) who are already at greater risk for cognitive impairment because of decreased central cholinergic transmission. Another important cause of ADRs is drug–drug interaction, often as a consequence of interaction with the cytochrome P450 deactivating system in the liver. Another important but often forgotten consideration is the concomitant use of naturopathic/herbal preparations, which are also potential candidates for drug interactions, especially in countries where these agents are used frequently. Determination of ADRs should not rest with shortterm trials, but should be specifically examined by post-marketing surveillance and medical record databases. Otherwise, important drug–disease interactions (e.g. hepatic or renal disease affecting drug clearance) may be overlooked. In addition, such post-marketing surveillance programs will result in early detection of unexpected serious ADRs – the adverse cardiac effect of terodiline is a prominent example. This was a drug developed for urge UI that was efficacious and tolerable and had gained widespread popularity before being withdrawn from the market because of an association with torsade de pointes (cardiac arrhythmia). The US Food and Drug Administration (FDA) now mandates QTc (a surrogate measure for predicting torsade de pointes) prolongation studies prior to granting approval. In addition, there is a greater move towards instituting risk management plans prior to approval of new drugs in an attempt to prevent such post-launch drug withdrawals.
Measures Spontaneous versus elicited reports Spontaneous self-report is most commonly used in RCTs, yet in clinical practice physicians usually specifically ask patients about possible ADRs. This could lead to underestimation of clinical ADR rates in published data as the
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rate for elicited adverse events is invariable higher. For example, the incidence of dry mouth for the extendedrelease formulation of oxybutynin chloride is given as 61% in the US prescribing information based on the results of dose-escalation studies in which patients were effectively asked about the occurrence of this event.87,88 In subsequent RCTs of this agent the incidence of dry mouth was markedly lower (around half that cited in the prescribing information) when a spontaneous reporting method was employed (Fig. 30a.4).89,90 ADRs may be especially under-reported in older patients in published trials because of selection of healthier subjects, or because an ADR is mistaken as the effects of age-related diseases and aging. Performance measures or specific measurement are infrequently used in ADR ascertainment, which also may lead to underestimation. For example, important but subtle cognitive impairment that could affect tasks such as driving may be not subjectively reported. Furthermore, few studies consider age-related differences in the target measure (e.g. visual accommodation), which would require examination of absolute and not just relative percentage changes in outcome.91 For example, a 25% change in accommodation may significantly impair an older person whose baseline accommodation is poor, yet have little functional effect on a younger person whose baseline accommodation is normal.
Objective tests Table 30a.8 provides an overview of the specific areas suggested as suitable for objective testing when assessing the tolerability of drugs for the treatment of OAB. Cognitive dysfunction While cognitive impairment during antimuscarinic therapy for OAB is of concern, particularly in older patients, there exist few reports in the literature of specific studies
Table 30a.8. Overview of the specific areas suggested as suitable for objective testing when assessing the tolerability of drugs for the treatment of overactive bladder Tolerability outcome Examples of suitable measures Cognitive dysfunction
Test batteries to assess: • consciousness • memory (free, cued, delayed and recall) • attention span • executive function (planning and problem solving) • semantic category fluency • praxis and spatial ability
Reduced visual accommodation
Near point of vision
QTc prolongation
Surface ECG
Dry mouth
Patient reporting (elicited and spontaneous) Unstimulated saliva flow (Stimulated saliva production)
Dry eyes
Schirmer’s test Fluorescein or rose Bengal staining
Altered perspiration
Humidity sensors (whole body or defined areas)
examining this issue. There is a need to more fully define the particular cognitive domains (attention, memory, executive function, reaction time and functional measures such as driving) which may be affected both by any underlying disorder and by therapeutic intervention. Quantitative electroencephalography (qEEG) allows mapping of the electrophysiologic activity of the brain and has been used in the study of a variety of psychiatric conditions including attention deficit disorder, schizophrenia and major depression. However, while
Incidence of dry mouth (%)
70 60 50 40 30 20 10 0
Elicited rate
Spontaneously reported rate
Figure 30a.4. Incidence rates of dry mouth with oxybutynin extended release formulation when elicited by direct questioning87,88 and when spontaneously reported.89 441
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such studies have revealed distinctive patterns of brain activity associated with various pathologic states, the diagnostic value and clinical relevance of this technique remains unclear. One study has been reported of the effect of antimuscarinic therapy on qEEG in healthy volunteers.92 While oxybutynin administration resulted in significant changes in brain activity, no significant changes were detected following oral or intravenous administration of trospium chloride.92 Subsequent studies in adult patients with OAB have extended these results, confirming the apparent lack of effect with trospium chloride, limited effects during tolterodine treatment and significant effects of oxybutynin therapy.93–95 No studies have so far included both qEEG and cognitive function testing. Cognitive function test batteries provide a means of assessing a range of cognitive skills and have been used in a variety of clinical settings to monitor change over time due to disease progression as well as therapeutic intervention. Katz and co-workers reported on cognitive impairment associated with oxybutynin therapy in healthy older people using a battery of cognitive performance tests. The test battery was comprised of 15 cognitive tests including the Buschke Selective Reminding Task, digit span, verbal fluency, reaction time and continuous performance. Significant cognitive decrements were reported on 7 of the 15 tests with oxybutynin compared with placebo, with the Buschke Selective Reminding Task and reaction time being most significantly affected. Most recently, Lipton and co-workers96 reported on the use of a cognitive test battery to assess the impact of darifenacin therapy for OAB in an elderly population. In this study the effect of darifenacin treatment on cognitive function in elderly patients with OAB was compared with that of placebo. A variety of endpoints were assessed, including memory scanning sensitivity, speed of choice reaction time and word recognition sensitivity. The authors reported that there was no difference in performance between patients treated with darifenacin and those who received placebo.96 However, although the authors reported ‘no difference’ from placebo for the active drug, this study was not designed to prove a claim of non-inferiority but rather to detect any benefit with active treatment. Moreover, the authors report the results only from the per-protocol population, thus negating the integrity of the randomization process, and it is unclear whether any differential effect was detected in the ITT population. The results of this study should, therefore, be viewed with caution until additional data from appropriately designed studies in an ITT population are available.
Visual accommodation Only one study has been reported on the effects of antimuscarinic therapy on visual accommodation.97 The study was conducted in 16 healthy adult volunteers and, using a four-way cross-over design, compared the effects of increasing doses of tolterodine and oxybutynin on maximum bladder capacity and visual accommodation (near point of vision). Both agents increased near point vision. A dose-dependent effect was observed with oxybutynin; only a single dose of tolterodine was assessed. The effect of antimuscarinic therapy in older patients who may have underlying age-related impairments in visual accommodation has not yet been reported. QTc measurement Measurement of the QT interval via a surface electrocardiogram (ECG) is required by the FDA in the assessment of all new drugs.98 QTc prolongation can indicate the potential for non-antiarrhythmic drugs to delay cardiac repolarization. Such a delay can lead to the development of cardiac arrhythmias such as torsade de pointes that can degenerate into ventricular fibrillation leading to sudden death. Salivary production The most common ADR with antimuscarinic agents is dry mouth. This was so commonly seen with immediate release oxybutynin that clinicians often considered its presence a marker of therapeutic activity. However, dry mouth can cause difficulty in swallowing, chewing and talking. Saliva is important in the prevention of dental caries and, untreated chronic dry mouth can put individuals at risk of serious tooth decay. Salivary glands are serous, mucous or mixed, and although it is thought that subjective dry mouth is due to a deficiency in production of mucus, this is more difficult to measure. Most often, the incidence of dry mouth is determined only by patients reporting it as an adverse event, although a VAS has been used in the assessment of the extended-release formulation of tolterodine and oxybutynin and revealed a dose-dependent increase in severity for both agents (see Fig. 30a.5).99 In this case, the test may in fact have measured ‘bothersomeness’ of the dry mouth rather than severity, given the wording of the question. Standardized tests are available, although in the clinic dry mouth is most often assessed by simply inspecting the mouth for saliva. The rate of unstimulated saliva production can be determined by asking patients to tilt their head forward and allow saliva to drain into a graduated container for 10 minutes. While flow rates can vary considerably, collection of less than 1 ml in a 10-minute period is considered indicative of
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a
p=0.3 p=0.05 Mean increase in severity of dry mouth
12 10 8 6 4 2 0 b
2 mg 4 mg Tolterodine
5 mg 10 mg Oxybutynin ER
dry mouth.100 More complex tests are available, for example a dye can be injected directly into the salivary glands and the rate of clearance measured. Inhibition of unstimulated saliva production is the most likely cause of dry mouth at rest. Inhibition of the production of the serous type of saliva (produced during eating and in response to stimulation) may also be affected by antimuscarinic therapy. Chewing pre-weighed paraffin tablets for a defined period can be used to assess stimulated salivary production; however, the clinical relevance of inhibition of serous saliva is less clear. Newer antimuscarinics and alternative formulations of oxybutynin (extended-release and transdermal patches) appear to be associated with less resting dry mouth than the immediate-release formulation of oxybutynin88 although this ADR remains a concern with antimuscarinic therapy. Tear production Antimuscarinic therapy may also interfere with tear production and can cause dry eyes. There are several techniques available to assess ocular wetness, the most commonly used of which is Schirmer’s test. This involves placing a small piece of filter paper inside the eyelid and measuring the amount of moisture present after 5 min-
Figure 30a.5. (a) Visual analog scale (10 cm) used to assess the severity of dry mouth associated with treatment for overactive bladder with extended-release formulations of tolterodine and oxybutynin, and (b) the mean increase in severity after 8 weeks of treatment. (Reproduced from ref. 99 with permission.)
utes. Fluorescein and rose Bengal staining can also be used to reveal small scratches and ulcers indicative of chronic dry eye syndromes. Perspiration The relationship between antimuscarinic therapy and perspiration rates is unclear, though there are case reports of heat prostration which may be secondary to reduction in perspiration. Perspiration (whole body or defined areas) can be measured using humidity sensors.101 However, this has not been reported as an objective test of antimuscarinic activity.
EFFICACY–TOLERABILITY RATIOS When prescribing any medication a physician has to weigh the benefits against the risks or efficacy against tolerability and safety (Fig. 30a.6). As OAB is rarely life threatening, when concerns with safety exist, they are likely to trump any other considerations. Thus, for OAB drugs which are safe in the populations studied, in the main, the calculus is an efficacy–tolerability consideration. This ratio is addressed in pharmacology texts as the therapeutic index and more recently has been conceptualized as clinical effectiveness.99 Some assessment 443
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Figure 30a.6. Conceptualization of the therapeutic index.
of clinical effectiveness is increasingly given in reports of controlled clinical trials as well as in efficacy and tolerability reviews.26,102,103 It is generally believed that efficacy is more important and yet tolterodine became more popular than oxybutynin even though the latter had a perception of having greater efficacy. Safety and tolerability considerations become particularly important when drug therapy is being considered for a chronic condition such as OAB which is likely to require longterm, if not continuous, drug therapy.
SAFETY Safety outcomes should not be considered the same as tolerability. In safety assessments, outliers are more important than average measures (as are typically used when evaluating tolerability), in particular because OAB symptoms usually represent benign conditions. For example, while dry mouth rates may be mild to moderate when considered as tolerability outcomes, even a very small number of patients who develop severe caries and tooth loss as a result of dry mouth present a significant safety concern. Similarly, while subtle drug-induced cognitive impairment may not be noticed by a patient and therefore would be ‘tolerable’, it could lead to a major safety issue around driving. RCTs, unless extremely large and of long duration, often will not have adequate power to detect uncommon yet dangerous safety events. Therefore, post-marketing surveillance remains the primary method to assess safety adequately.
SUMMARY Identifying outcome measures for studying the natural history of and effects of therapeutic intervention on OAB is an evolving and, at present, often ad hoc area of research. Standardization of diagnostic terminology by the ICS has permitted the development and incorporation of both physiologic and patientcentered measures into RCTs. Physiologic measures to assess the symptoms of OAB include urodynamics, pad tests and bladder diaries. Increased emphasis has appropriately been placed on patient-centered measures to assess symptoms, bothersomeness, improvement, QoL and function; these measures include questionnaires, often using visual analog and Likert scales. Tolerability assessments should extend beyond reporting in RCTs to include post-marketing surveillance. Objective testing for specified ADRs in drug trials for OAB is also to be encouraged and may include assessment of impact on cognitive functioning, visual accommodation, and saliva, tear and perspiration production. Safety should not be confused with tolerability and, where present, safety concerns should trump any other consideration.
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Committee of the International Continence Society. Neurourol Urodyn 1998;17:249–53. 2. Fonda D, Resnick NM, Colling J et al. Outcome measures for research of lower urinary tract dysfunction in frail older people. Neurourol Urodyn 1998;17:273–81. 3. Coyne KS, Payne C, Bhattacharyya SK et al. The impact of urinary urgency and frequency on health-related quality of life in overactive bladder: results from a national community survey. Value Health 2004;7:455–63. 4. Palmtag H. The patient’s perspective: redefining end points. Urology 2004;64(Suppl 1):17–20. 5. Staskin D, Wein A. Is it possible to make cross-study comparisons of urinary continence rates in patients with overactive bladder? Curr Med Res Opin 2005;21(6):835–7. 6. Landis JR, Kaplan S, Swift S, Versi E. Efficacy of antimuscarinic therapy for overactive bladder with varying degrees of incontinence severity. J Urol 2004;171:752–6. 7. Herbison P, Hay-Smith J, Ellis G, Moore K. Effectiveness of anticholinergic drugs compared with placebo in the treatment of overactive bladder: systematic review. BMJ 2003;326:841–4.
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9. Malone-Lee J, Henshaw DJ, Cummings K. Urodynamic verification of an overactive bladder is not a prerequisite for antimuscarinic treatment response. BJU Int 2003;92:415–7.
25. Tincello D, Williams K, Assassa P, McGrother C. A prospective comparison of data quality from a 3-day urinary diary compared to a 7-day diary [abstract 735]. International Continence Society Annual Meeting, August 25–27, 2004, Paris, France.
10. Diokno AC, Wells TJ, Brink CA. Comparison of selfreported voided volume with cystometric bladder capacity. J Urol 1987;137:698–700. 11. Stanton SL, Ritchie D. Urilos: the practical detection of urine loss. Am J Obstet Gynecol 1977;128:461–3. 12. Frazer MI, Haylen BT, Sutherst JR. The severity of urinary incontinence in women: comparison of subjective and objective data. Br J Urol 1989;63:14–5. 13. Abrams P, Blaivas JG, Stanton SL, Andersen JT. The standardization of terminology of lower urinary tract function. Scand J Urol Nephrol Suppl 1988;114:5–19.
26. Cardozo L, Lisec M, Millard R et al. Randomized, double-blind placebo controlled trial of the once daily antimuscarinic agent solifenacin succinate in patients with overactive bladder. J Urol 2004;172:1919–24. 27. Wyman JF, Choi SC, Harkins SW, Wilson MS, Fantl JA. The urinary diary in evaluation of incontinent women: a test–retest analysis. Obstet Gynecol 1988;71:812–7. 28. Elser DM, Fantl JA, McClish DK. Comparison of ‘subjective’ and ‘objective’ measures of severity of urinary incontinence in women. Neurourol Urodyn 1995;14:311–6.
14. Harvey MA, Versi E. Pad tests. In: Cardozo L, Staskin D (eds) Textbook of Female Urology and Urogynaecology. London: Isis Medical Media, 2001; 175–82.
29. McCormack M, Infant-Rivard C, Schick E. Agreement between clinical methods of measurement of urinary frequency and functional bladder capacity. Br J Urol 1992;69:17–21.
15. Versi E, Cardozo L, Anand D. The use of pad tests in the investigation of female urinary incontinence. J Obstet Gynecol 1988;8:270–3.
30. Brown JS, McNaughton KS, Wyman JF et al. Measurement characteristics of a voiding diary for use by men and women with overactive bladder. Urology 2003;61:802–9.
16. Stewart WF, Van Rooyen JB, Cundiff GW et al. Prevalence and burden of overactive bladder in the United States. World J Urol 2003;20:327–36.
31. Abrams P, Foote J, Lheritier K. Urinary continence during darifenacin therapy for overactive bladder (OAB): pooled data from phase III trials [abstract 229]. Euro Urol 2005;Suppl 4:60.
17. Versi E, Orrego G, Hardy E, Seddon G, Smith P, Anand D. Evaluation of the home pad test in the investigation of female urinary incontinence. Br J Obstet Gynaecol 1996;103:162–7.
32. Quinn P, Goka J, Richardson H. Assessment of an electronic daily diary in patients with overactive bladder. BJU Int 2003;91:647–52.
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33. Millard RJ, Moore K, Rencken R, Yalcin I, Bump RC. Duloxetine vs placebo in the treatment of stress urinary incontinence: a four-continent randomized clinical trial. BJU Int 2004;93:311–8. 34. Haab F, Stewart L, Dwyer P. Darifenacin, an M3 selective receptor antagonist, is an effective and well-tolerated once-daily treatment for overactive bladder. Eur Urol 2004;45:420–9. 35. Dmochowski R, Heit M, Sand P. The effect of anticholinergic therapy on urgency severity in patients with overactive bladder: clinical assessment of a newly validated tool [abstract]. Neurourol Urodyn 2003;22:411–2. 36. Cardozo L, Coyne K, Versi E. Validation of the Urgency Perception Scale (UPS). BJU Int 2005;95:591–6. 37. Zinner N, Harnett M, Sabounjian L, Sandage B Jr, Dmochowski R, Staskin D. The overactive bladdersymptom composite score: a composite symptom score of toilet voids, urgency severity and urge urinary incontinence in patients with overactive bladder. J Urol 2005;173:1639–43. 38. Chapple CR, Artibani W, Cardozo LD et al. The role of urgency and its measurement in the overactive bladder symptom syndrome – current concepts and future prospects. BJU Int 2005;95:335–40. 39. Khullar V, Hill S, Laval KU, Schiotz HA, Jonas U, Versi E. Treatment of urge-predominant mixed urinary incontinence with tolterodine extended release: a randomized, placebo-controlled trial. Urology 2004;64:269–74. 40. Weiss JP, Blaivas JG. Nocturnal polyuria versus overactive bladder in nocturia. Urology 2002;60(Suppl 5A):28–32. 41. Merriam-Webster’s Collegiate® Dictionary, 11th ed. Springfield, MA: Merriam-Webster, 2003. 42. Abrams P, Andersson KE, Artibani W et al. 2nd International Consultation on Incontinence. Recommendations of the International Scientific Committee: Evaluation and treatment of urinary incontinence, pelvic organ prolapse and faecal incontinence. 2002. Online. Available: www.continet.org/documents/ici_pdfs/MENUS/ recomm.pdf. 43. Barry MJ, Fowler FJ Jr, O’Leary MP et al. The American Urological Association symptom index for benign prostatic hyperplasia. The Measurement Committee of the American Urological Association. J Urol 1992;148:1549–57. 44. Meyhoff HH, Hald T, Nordling J, Andersen JT, Bilde T, Walter S. A new patient weighted symptoms score system (DAN-PSS-1). Clinical assessment of indications and outcomes of transurethral prostatectomy for uncomplicated benign prostatic hyperplasia. Scand J Urol Nephrol 1993;27:493–9. 45. Donovan JL, Abrams P, Peters TJ et al. The ICS-‘BPH’ Study: the psychometric validity and reliability of the ICSmale questionnaire. Br J Urol 1996;77:554–62.
46. Brookes ST, Donovan JL, Wright M et al. A scored form of the Bristol Female Lower Urinary Tract Symptoms questionnaire: data from a randomized controlled trial of surgery for women with stress incontinence. Am J Obstet Gynecol 2004;191:73–82. 47. Shumaker SA, Wyman JF, Uebersax JS, McClish D, Fantl JA. Health-related quality of life measures for women with urinary incontinence: the Incontinence Impact Questionnaire and the Urogenital Distress Inventory. Qual Life Res 1994;3:291–306. 48. Uebersax JS, Wyman JF, Shumaker SA, McClish DK, Fantl JA. Short forms to assess life quality and symptom distress for urinary incontinence in women: the Incontinence Impact Questionnaire and the Urogenital Distress Inventory. Neurourol Urodyn 1995;14:131–9. 49. Lemack GE, Zimmern PE. Predictability of urodynamic findings based on the Urogenital Distress Inventory-6 questionnaire. Urology 1999;54:461–6. 50. Harvey MA, Kristjansson B, Griffith D, Versi E. The Incontinence Impact Questionnaire and the Urological Distress Inventory: a revisit of their validity in women without a urodynamic diagnosis. Am J Obstet Gynecol 2001;185:25–31. 51. Davila GW, Daugherty CA, Sanders SW. A short-term multicenter, randomized, double-blind, dose-titration study of the efficacy and anticholinergic side effects of transdermal compared to immediate release oral oxybutynin treatment of patients with urge urinary incontinence. J Urol 2001;166:140–5. 52. Leung HY, Yip SK, Cheon C et al. A randomized controlled trial of tolterodine and oxybutynin on tolerability and clinical efficacy for treating Chinese women with an overactive bladder. BJU Int 2002;90:375–80. 53. Lukacz ES, Lawrence JM, Burchette RJ, Luber KM, Nager CW, Buckwalter JG. The use of a Visual Analog Scale in urogynecologic research: a psychometric evaluation. Am J Obstet Gynecol 2004;191:165–70. 54. Stach-Lempinen B, Kujansuu E, Laippala P, Metsanoja R. Visual analogue scale, urinary incontinence severity score and 15D-psychometric testing of three different healthrelated quality of life instruments for urinary incontinent women. Scand J Urol Nephrol 2001;35:476–83. 55. Melville JL, Miller EA, Fialkow MF, Lentz GM, Miller JL, Fenner DE. Relationship between patient report and physician assessment of urinary incontinence severity. Am J Obstet Gynecol 2003;189:76–80. 56. Coyne K, Revicki D, Hunt T et al. Psychometric validation of overactive bladder symptoms and health-related quality of life questionnaire: the OAB-q. Qual Life Res 2002;11:563–74. 57. Homma Y, Uemura S. Use of the short form of King’s Health Questionnaire to measure quality of life in patients with an overactive bladder. BJU Int 2004;93:1009–13.
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58. Yalcin I, Bump RC. Validation of two global impression questionnaires for incontinence. Am J Obstet Gynecol 2003;189:98–101. 59. Coyne KS, Matza LS. Validation of the perception of bladder condition measure in overactive bladder [abstract]. Value Health 2002;5:464. 60. Wagner TH, Patrick DL, Bavendam TG, Martin ML, Buesching DP. Quality of life of persons with urinary incontinence: development of a new measure. Urology 1996;47:67–71. 61. Karantanis E, Fynes M, Moore KH, Stanton SL. Comparison of the ICIQ-SF and 24-hour pad test with other measures for evaluating the severity of urodynamic stress incontinence. Int Urogynecol J Pelvic Floor Dysfunct 2004;15:111–6. 62. World Health Organization. Statement developed by WHO Quality of Life Working Group, published in the WHO Health Promotion Glossary 1998. WHO/HPR/ HEP/ 98.1, Geneva: WHO, 1994. 63. DuBeau CE, Levy B, Mangione CM, Resnick NM. The impact of urge urinary incontinence on quality of life: importance of patients’ perspective and explanatory style. J Am Geriatr Soc 1998;46:683–92. 64. Stach-Lempinen B, Nygard CH, Laippala P, Metsanoja R, Kujansuu E. Is physical activity influenced by urinary incontinence? BJOG 2004;111:475–80. 65. Fultz NH, Fisher GG, Jenkins KR. Does urinary incontinence affect middle-aged and older women’s time use and activity patterns? Obstet Gynecol 2004;104:1327–34. 66. Thom DH, Haan MN, Van Den Eeden SK. Medically recognized urinary incontinence and risks of hospitalization, nursing home admission and mortality. Age Ageing 1997;26:367–74.
with oxybutynin: a Canadian perspective. Clin Ther 2001;23:2038–49. 73. Hughes DA, Dubois D. Cost-effectiveness analysis of extended-release formulations of oxybutynin and tolterodine for the management of urge incontinence. Pharmacoeconomics 2004;22:1047–59. 74. Moore KH, O’Sullivan RJ, Simons A et al. Randomised controlled trial of nurse continence advisor therapy compared with standard urogynaecology regimen for conservative incontinence treatment: efficacy, costs and two year follow up. BJOG 2003;110:649–57. 75. Johannesson M, O’Conor RM, Kobelt-Nguyen G, Mattiasson A. Willingness to pay for reduced incontinence symptoms. Br J Urol 1997;80:557–62. 76. Resnick NM, Yalla SV, Laurino E. The pathophysiology of urinary incontinence among institutionalized elderly persons. N Engl J Med 1989;320:1–7. 77. Ouslander J, Schnelle J, Simmons S, Bates-Jensen B, Zeitlin M. The dark side of incontinence: nighttime incontinence in nursing home residents. J Am Geriatr Soc 1993;41:371–6. 78. Schnelle JF, Sowell VA, Hu TW, Traighber B. Reduction of urinary incontinence in nursing homes: does it reduce or increase costs? J Am Geriatr Soc 1988;36:34–9. 79. McCormick KA, Cella M, Scheve A, Engel BT. Cost-effectiveness of treating incontinence in severely mobilityimpaired long term care residents. QRB Qual Rev Bull 1990;16:439–43. 80. Schnelle JF, Kapur K, Alessi C et al. Does an exercise and incontinence intervention save healthcare costs in a nursing home population? J Am Geriatr Soc 2003;51:161–8. 81. DuBeau CE. Incontinence in the nursing home: are we FIT to be tied? J Am Geriatr Soc 2005;53:1254–6.
67. Coward RT, Horne C, Peek CW. Predicting nursing home admissions among incontinent older adults: a comparison of residential differences across six years. Gerontologist 1995;35:732–43.
82. DuBeau CE, Miller KM, Bergmann M, Resnick NM. Urge incontinence outcomes in RCTs depend on assumed and not actual drug assignment. Neurourol Urodyn 2000;19:492.
68. Azam U, Castleden M, Turner D. Economics of lower urinary tract symptoms (LUTS) in older people. Drugs Aging 2001;18:213–23.
83. DuBeau CE, Khullar V, Versi E. ‘Unblinding’ in randomized controlled drug trials for urinary incontinence: implications for assessing outcomes when adverse effects are evident. Neurourol Urodyn 2005;24:13–20.
69. Wagner TH, Hu TW. Economic costs of urinary incontinence in 1995. Urology 1998;51:355–61. 70. Kobelt G. Economic considerations and outcome measurement in urge incontinence. Urology 1997;50(Suppl 6A):100–7. 71. Arikian SR, Casciano J, Doyle JJ, Tarride JE, Casiano RN. A pharmacoeconomic evaluation of two new products for the treatment of overactive bladder. Manag Care Interface 2000;13:88–94. 72. O’Brien BJ, Goeree R, Bernard L, Rosner A, Williamson T. Cost-effectiveness of tolterodine for patients with urge incontinence who discontinued initial therapy
84. Kelleher CJ, Cardozo LD, Khullar V, Salvatore S. A medium-term analysis of the subjective efficacy of treatment for women with detrusor instability and low bladder compliance. Br J Obstet Gynaecol 1997;104:988–93. 85. Hanlon JT, Schmader KE, Koronkowski MJ et al. Adverse drug events in high risk older outpatients. J Am Geriatr Soc 1997;45:945. 86. Feinberg M. The problems of anticholinergic adverse effects in older patients. Drugs Aging 1993;3:335–48. 87. Anderson R, Mobley D, Blank B, Saltzstein D, Susset J, Brown JS. Once a day controlled release versus immedi-
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ate release oxybutynin chloride in the treatment of urinary urge incontinence. J Urol 1999;161:1809–12.
accommodation) in healthy volunteers. Drugs in R&D 2002;3:75–81.
88. Versi E, Appell RA, Mobley D, Patton W, Saltzstein D. Dry mouth with conventional and controlled-release oxybutynin in urinary incontinence. Obstet Gynecol 2000;95:718–21.
98. Food and Drug Administration. The clinical evaluation of QT/QTc interval prolongation and proarrhythmic potential for non-antiarrhythmic drugs. Draft 4, June 2004. Online. Available: www.fda.gov/cder/guidance/ 6378dft.htm.
89. Appell RA, Sand P, Dmochowski R et al. Prospective randomized controlled trial of extended-release oxybutynin chloride and tolterodine tartrate in the treatment of overactive bladder: results of the OBJECT study. Mayo Clin Proc 2001;76:358–63.
99. Sussman D, Garely A. Treatment of overactive bladder with once-daily extended-release tolterodine or oxybutynin: the antimuscarinic clinical effectiveness trial (ACET). Curr Med Res Opin 2002;18:177–84.
90. Diokno AC, Appell RA, Sand PK et al. Prospective, randomized, double-blind study of the efficacy and tolerability of the extended-release formulations of oxybutynin and tolterodine for overactive bladder: results of the OPERA trial. Mayo Clin Proc 2003;78:687–95.
100. Screenby L. Saliva-salivary gland hypofunction (SGH). FDI Working Group 10. J Dent Assoc S Afr 1992;47:498– 501.
91. Avorn J, Rochon PA. Principles of pharmacology. In: Cassel C, Leipzig RM, Cohen HJ et al (eds) Geriatric Medicine: An Evidenced Based Approach. New York: Springer, 2003; 65.
102. Dmochowski R, Kell S, Staskin D. Oxybutynin chloride: alternatives in drug delivery and improved therapeutic index. Expert Opin Pharmacother 2002;3:443–54.
92. Pietzko A, Dimpfel W, Schwantes U, Topfmeier P. Influences of trospium chloride and oxybutynin on quantitative EEG in healthy volunteers. Eur J Clin Pharmacol 1994;47:337–43. 93. Katz IR, Sands LP, Bilker W, DiFilippo S, Boyce A, D’Angelo K. Identification of medications that cause cognitive impairment in older people: the case of oxybutynin chloride. J Am Geriatr Soc 1998;46:8–13. 94. Todorova A, Vonderheid-Guth B, Dimpfel W. Effects of tolterodine, trospium chloride, and oxybutynin on the central nervous system. J Clin Pharmacol 2001;41:636–44. 95. Womack KB, Heilman MK. Tolterodine and memory: dry but forgetful. Arch Neurol 2003;60:771–3. 96. Lipton RB, Kolodner K, Wesnes K. Assessment of cognitive function of the elderly population: effect of darifenacin. J Urol 2005;173:493–8. 97. Chapple CR, Nilvebrant L. Tolterodine: selectivity for the urinary bladder over the eye (as measured by visual
101. Ohhashi T, Sakaguchi M, Tsuda T. Human perspiration measurement. Physio Meas 1998;19:449–61.
103. Rovner ES, Wein AJ. Once-daily, extended-release formulations of antimuscarinic agents in the treatment of overactive bladder: a review. Eur Urol 2002;41:6–14. 104. Hahn I, Fall M. Objective quantification of stress urinary incontinence: a short, reproducible, provocative pad test. Neurourol Urodyn 1991;10:475–81. 105. Fantl JA, Harkins SW, Wyman JF, Choi SC, Taylor JR. Fluid loss quantitation test in women with urinary incontinence: a test–retest analysis. Obstet Gynecol 1987;70:739–43. 106. Brown JS, Posner SF, Stewart AL. Urge incontinence: new health-related quality of life measure. J Am Geriatr Soc 1999;46:980–8. 107. DuBeau CE, Kiely DK, Resnick NM. Quality of life impact of urge incontinence in older persons: a new measure and conceptual structure. J Am Geriatr Soc 1999;47:989–94. 108. Reese PR, Pleil AM, Okano GJ, Kelleher CJ. Multinational study of reliability and validity of the King’s Health Questionnaire in patients with overactive bladder. Qual Life Res 2003;12:427–42.
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30b Outcome measures in women with lower urinary tract symptoms: stress incontinence Richard C Bump, Ilker Yalcin
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Background, controversies and standards The majority of outcomes research for female stress urinary incontinence (SUI) has examined the efficacy of various continence surgical procedures. The 1996 US Agency for Health Care Policy and Research Urinary Incontinence Clinical Practice Guidelines Panel concluded that the surgical outcomes literature was deficient in standards ‘for describing…the outcome in different domains’.1 This conclusion was substantiated in a comprehensive systematic review of the surgical literature by Black and Downs that same year.2 In this review, outcome assessment was especially criticized for the use of nonvalidated and non-standardized outcome measures and for failure to obtain patient opinions through the use of valid and reliable clinimetric (e.g. quality of life (QoL) or patient impressions of improvement) methods and questionnaires. Since these unfavorable reviews, a number of professional, governmental, and regulatory groups have developed and published standards for outcomes research in female SUI.3–7 All of these have recognized the complexity of SUI and have emphasized that there is no single measure that adequately captures either the consequences of the condition or the effects of its various treatments. Rather, these guidelines all stress the importable 30b.1.
tance of assessing treatment effects in multiple outcome domains. Table 30b.1 lists the outcome domains proposed by five widely quoted standards. It demonstrates that, while some domains such as quantitation of symptoms with a prospective diary or assessment of QoL are universally recommended, there is no consensus on most domains or measures. There is also no consensus as to the definition of cure of SUI. Some accept only a ‘subjective’ patient-reported definition,7 others accept only an ‘objective’ testing definition,8 while still others require both ‘subjective’ and ‘objective’ proof of cure.5 Hilton has nicely demonstrated the elusive nature of ‘cure’ by reporting outcomes from the UK Tension-Free Vaginal Tape–Burch Colposuspension randomized comparative trial using multiple definitions of cure. Depending on the definition (Fig. 30b.1), he reported cure rates between 6 and 81% from this single study.8 Even more contentious is the definition of clinically important levels of improvement in SUI. This is particularly important for interventions, such as pelvic floor muscle training (PFMT), other behavioral interventions, or pharmacological treatments, which usually decrease rather than completely eliminate SUI. It is also crucial for outcome measures that do not have intuitive clinical interpretability, such as a score on a QoL scale.
Summary of various published outcomes standards for the evaluation of treatments for women with stress urinary incontinence
Outcome domain or measure
ICI3
ICS4
NICHD5
AUA/UDS6
Patient-reported symptom assessment scales
P
P
P
P
Urinary diaries
P
P
P
P
P
Pad test
P
P
±
P
P
P
P
P
±
±
P
Emptying phase testing or post-void residual
P
P
P
Electromyography/electrophysiological testing
P
Stress test Filling phase urodynamic testing
±
Anatomic assessment
P
Pelvic floor muscle assessment
P
Quality of life
P
P
P
Patient-reported global outcome assessment
P
P
P
P
±
P P
Safety and complications Socioeconomic
CHMP7
P
P
P
P
P
P
AUA, American Urologic Association; CHMP, European Agency for the Evaluation of Medicinal Products Committee for Human Medicinal Products; ICI, Second International Consultation on Incontinence; ICS, International Continence Society; NICHD, National Institute of Child Health and Human Development; UDS, Urodynamic Society (now the Society for Urodynamics and Female Urology). P, recommended; ±, equivocal recommendation or noted to be of limited value; blank cells indicate that the domain or variable is not mentioned.
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Patient oBservations symptom scales and symptom assessment As measures of efficacy
Figure 30b.1. Cure rates of tension-free vaginal tape (TVT) and Burch colposuspension procedures from the UK TVT RCT8 using various definitions for cure in the intentto-treat analysis. Cure definitions: A, no urodynamic stress incontinence or negative 1-hour pad test; B, no urodynamic stress incontinence and negative 1-hour pad test; C, no stress incontinence on Bristol Female Lower Urinary Tract (BFLUTS) questionnaire; D, no incontinence under any circumstances on BFLUTS questionnaire; E, combines B and D criteria; F, criteria of the National Institute of Child Health and Human Development (no symptoms of incontinence, negative full bladder cough stress test, and no new symptoms or adverse events). At the center of this question is the relationship between statistical significance and clinical relevance, both when assessing the value of a treatment and when comparing the values of two or more treatments. We have used two terms that, in our opinion, are often misused to imply a hierarchy in the quality or validity of outcome measures: ‘objective’ and ‘subjective’. The term ‘objective’ is often used to imply data that are factual; in contrast, the use of the term ‘subjective’ is often seen as more pejorative, implying data that are more illusory. In the end, ‘objective’ measures (e.g. pad tests or urodynamic measures) are viewed as more valid and reliable than ‘subjective’ measures (e.g. QoL scores or a patient’s impression of improvement). In fact, in terms of reliability, reproducibility, and validity, many subjective measures used in incontinence research are more scientifically robust than objective measures. If used at all, we believe these terms should convey only their traditional medical definitions: ‘subjective’ designating a symptom or condition as perceived by the patient, not by the examiner; ‘objective’ indicating a symptom or condition perceived as a sign of disease by someone other than the patient. We shall now consider various outcome domains and measures in more detail, from both patients’ and examiners’ perspectives.
Self-completed responses to standardized and validated questions that are obviously and understandably descriptive of the symptoms of SUI are the most appropriate way to determine if an individual patient has – or does not have – SUI. There are a number of symptom assessment questionnaires that have been endorsed by the Symptom and Quality of Life Assessment Committee of the 2002 International Consultation on Incontinence (ICI).9 Most of these include standard questions for determining the symptom of SUI. In addition, the ICI has developed the ICIQ-SF (Incontinence Quality of Life Questionnaire – Short Form) that includes two questions in its final item that describe symptoms of SUI.10 Finally, a number of investigators have used single question SUI-focused questions for both clinical and epidemiological research.11 Given the International Continence Society (ICS) definition of the symptom of SUI (‘the complaint of involuntary leakage on effort or exertion, or on sneezing or coughing’),12 there are only a limited number of ways of inquiring about the symptom. A question such as ‘Do you have accidental leakage of urine onto your clothing, underwear, or pad during an activity such as coughing, sneezing, laughing, running, exercising, or lifting?’ has inherent face validity. Any such question that has been shown to be understandable to the tested population, reproducibly answered, correlated with other clinical assessments of the symptom, and, if applicable, meaningfully translated is acceptable for ascertaining the symptom of SUI. Once adequately validated, such a question should be the basis for establishing the existence of the symptom both before as well as during or after treatment. While the question stem options for SUI are limited, there are a number of potential response options. One is a simple yes or no response: ‘Do you have this symptom now?’ or ‘Have you had this symptom during the past month?’ for example. These types of response are applicable only in situations where elimination of the symptom is a reasonable expectation. When improvement in the symptom is more likely than cure, graded responses that assess the level of bother or severity associated with the symptom, or open-ended requests for the number of times per day or week the symptom is experienced, may be more useful. Some instruments, such as the ICIQ-SF combine the frequency, amount, and impact of incontinence into a single composite scale. However, in most 451
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instances, a prospective diary is preferable to retrospective recall when assessing the frequency of incontinent episodes.
As measures of complications Symptom ascertainment may also be used as a measure of safety of an intervention for SUI. In some instances, the same instrument used for efficacy may be applicable. For example, if the instrument asks about symptoms of urge incontinence or emptying phase dysfunction and the intervention is likely to precipitate these new symptoms, the same instrument may be used as a measure of both efficacy and safety. In other instances, where specific other complications are anticipated, the history of their emergence may be prompted by using a list of specific symptoms or adverse events. Finally, in many instances it is most appropriate to ask the study participant to share any new symptoms (positive or negative) using non-probing questions and recording all such events regardless of their perceived causality.
symptom diaries Urinary diaries are self-reported, real-time records of specified lower urinary tract symptoms, kept for a specified period of time, usually from 3 to 7 days. In some instances, for example when attempting to define the onset of action of an intervention, diaries may be kept for longer periods of time. Most commonly the variables recorded include micturition and incontinence episodes, pads used, hours of sleep, and the volumes of fluid intake and urine output. Diaries that include the requirement to measure volumes are generally recorded for shorter periods of time and are more likely to have compliance limitations compared with simpler eventcapture diaries. Paper diaries that record micturition and incontinence episodes (Fig. 30b.2) have proved to be highly reproducible on test–retest analysis in incontinent women, independent of the physiologic subtype of their incontinence (r = 0.86–0.91).13 However, because SUI is inherently variable from day to day due to variations in daily activities or stressful events, a greater num-
SAMPLE DIARY Date: a day you Toilet TIME 12–12:59am 1–1:59am 2–2:59am 3–3:59am 4–4:59am 5–5:59am 6–6:59am 7–7:59am 8–8:59am 9–9:59am 10–10:59am 11–11:59am 12–12:59am 1–1:59pm 2–2:59pm 3–3:59pm 4–4:59pm 5–5:59pm 6–6:59pm 7–7:59pm 8–8:59pm 9–9:59pm 10–10:59pm 11–11:59pm Arise time Bed time # of pads used
Leak
Date: a day you measure Toilet Leak
4
10 4, 9
10
7
11
3, 4 6 8:30am 11:00pm 2
7:00am 10:30pm 3
BLADDER DIARY INSTRUCTIONS TIME 12–12:59am 1–1:59am 2–2:59am 3–3:59am 4–4:59am 5–5:59am 6–6:59am 7–7:59am 8–8:59am 9–9:59am 10–10:59am 11–11:59am 12–12:59am 1–1:59pm 2–2:59pm 3–3:59pm 4–4:59pm 5–5:59pm 6–6:59pm 7–7:59pm 8–8:59pm 9–9:59pm 10–10:59pm 11–11:59pm Arise time Bed time # of pads used
1. Please record each time you empty into the toilet by placing a check mark ( ) under the Toilet column for each day (see ‘a day you ’ sample on back). Measure your urine (using a toilet insert that you will be given) for 2 days during the week. Measure (in fluid ounces) the amount that you urinate every time you go during the entire 24-hour period. In the Toilet column record the number of fluid ounces you void, instead of putting a (see ‘a day you measure’ sample on back). If you void in the toilet, but forget to measure, put a checkmark ( ) for that void only. 2. In the Leak column, record each time you accidentally lose urine (see sample on back). Even a small amount of accidental leakage should be marked each time it occurs. 3. Every time you void or leak, record it next to the time the event occurred. You may put multiple numbers in the same box if needed (see sample on back). 4. At the bottom of the column for each day, indicate the time you get up, the time you go to bed, and the number of pads you used (see sample on back). 5. You may start the diary any day, but try to use it for 7 days in a row.
Figure 30b.2. Sample of a paper diary that can record micturition and incontinence episodes and that can also be used as a frequency–volume chart. 452
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ber of diary days has been shown to reduce variability in the number of incontinence episodes in clinical trials.14 For the study of interventions in women with SUI, volume measurements are generally less critical than for interventions in women with symptoms of bladder overactivity. On the other hand, for interventions that improve but are unlikely to cure SUI, such as PFMT or medications, monitoring micturition frequency is important because improvement in incontinence during a clinical trial could result from more frequent bladder emptying, a behavior learned and reinforced as a consequence of the completion of multiple diaries. There is no single standard for reporting improvements in stress incontinence episode frequency.5 The options include reporting the change in incontinence episodes from baseline with treatment, either as an absolute number or as percent change, or reporting the number of episodes still occurring during treatment. The advantage of reporting the percent reduction is that it normalizes the level of improvement across various levels of baseline severity. However, a patient who experiences a 50% reduction may have only one fewer incontinent episode per week (if the baseline was two per week) or 20 fewer (if the baseline was 40 per week). On the other hand, in this example is it better to end up with one episode or 20 episodes per week? Regardless of how changes in incontinence are reported, they only quantify the treatment response; they do not define the importance of that response. Defining the level of improvement that is clinically important is a critical, though often overlooked, part of SUI outcomes research.
Quality of life instruments Like other forms of urinary incontinence, SUI is not a threat to the life of the sufferer, but can have a significant impact on her quality of life. For this reason, the measurement of incontinence-specific, health-related QoL has been considered an important outcome domain in the assessment of treatments. As noted in Table 30b.1, the quantification of symptoms and their impact on patients, using urinary diaries and QoL instruments, are the two outcome domains recommended in all standards for incontinence research. Health-related QoL instruments translate a patient’s evaluation of the impact of a disease on daily life (e.g. on physical and social functioning) into a score that represents a continuous variable. Instruments should be assessed for face, content, and construct validity, for reliability and reproducibility, and for responsivity to treatment-induced change before they are
accepted as outcome measures in research. The Second International Consultation on Incontinence has rated and recommended several highly validated instruments for use in outcomes research in women with incontinence.9 As is true for changes in incontinence episode frequency, while changes in a QoL score help quantify a response to treatment, they do not define the clinical relevance of that response. Even more than for a reduction in the number of incontinence episodes, it is difficult for a practicing clinician to put these changes in QoL scores into clinical perspective. This is because scores calculated from these instruments are not instinctively interpretable or intuitively meaningful. One concept that allows clinicians to interpret changes in QoL scores is the minimal clinically important difference (MCID). The with in-treatment MCID is defined as the improvement in a score with a treatment at which a patient first recognizes she is improved. For a statistically significant treatment effect to be considered relevant, it should exceed the within-treatment MCID. The between-treatment MCID is the difference between a score change at which a patient first perceives she is improved and the score change at which she perceives no change in her condition. For one treatment’s statistically significant effect to be considered relevantly different from another treatment’s effect, the difference in effects between the two treatments should exceed this between-treatment MCID threshold. Researchers should attempt to define MCIDs for QoL instruments. To date, the within-treatment MCID has been defined for the King’s Health Questionnaire in women with overactive bladder symptoms15 and the within- and between-treatment MCIDs have been defined for the Incontinence Quality of Life (I-QOL) questionnaire in women with SUI symptoms.16
global assessment scales ‘Global scale’ is a term applied to a health-related index that provides a broad overview of a complex phenomenon, using ratings that are not demarcated by stipulated criteria. As a consequence, the selection of a rating is made by the patient based on her feelings, perceptions, opinions or beliefs, using whatever personal standards she deems appropriate. There are two basic categories of global scales based on their stem question: one that measures a general health status at a given point in time (single-state ratings) and a second that measures improvement over a period of time (transition ratings), usually in response to treatment. An example of a stem statement used to assess single-state status at a point in time would be: ‘Check the one response that best describes 453
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how your urinary tract condition is now’; an example of a stem statement used to assess improvement over a period of time would be: ‘Check the one response that best describes how your urinary incontinence is now, compared with how it was before you began treatment in this study.’ Response scales can be binomial categories (e.g. ‘improved’ or ‘not improved’), ordinal categories (e.g. ‘not at all’, ‘somewhat’, ‘moderately’, ‘quite a bit’ or ‘extremely’ bothered) or visual analog (e.g. a 10 cm line with ‘very much worse’ and ‘very much better’ at each extreme). There is no clear superiority demonstrated for either categorical scales or visual analog rating scales; however, the former may be more useful when a clinically interpretable anchor (see later discussion) is required to define a clinically meaningful treatment response threshold. Global indexes that ask an individual patient to rate the severity of a condition or a response to therapy are generally simple, direct, easy to use, and intuitively understandable to the clinician.17 The scientific and clinical goals of the global scale are to get an overall appraisal of a complex phenomenon, not to evaluate every component part of the phenomenon. Multiple-question QoL instruments evaluate many components of a phenomenon and can be used to generate a total score that purports to be an overall appraisal of the condition, but this appraisal is limited by the fact that it is ultimately derived from questions developed by experts rather than from the unique personal perception of the individual patient.18 Global indexes avoid this limitation, but at the cost of uncertainty regarding the precise aspects of the manifestations of the disease severity or improvement that resulted in an individual patient selecting a specific rating.16 Thus, there is an imprecision in a global scale because it has no intrinsic operational criteria for demarcating the ratings; this results in a degree of imprecision across the spectrum of different people who might use it. Nonetheless, global ratings can be quite precise when applied by the same person over time.17 The European Agency for the Evaluation of Medicinal Products has stipulated global assessment scales as their required primary endpoint for studies evaluating medications for the treatment of urinary incontinence.7 While they state that a quantification of symptom changes (such as a change in incontinence episode frequency or in a QoL score) can serve as secondary endpoints, they ‘cannot serve as surrogate end-points for subject perception of effect’. The agency provides three examples of acceptable simple scales:
• an ordinal categorical single-state rating instrument (‘my urinary incontinence causes me no problems,
•
•
very minor problems, minor problems, moderate problems, severe problems, very severe problems’); an ordinal categorical improvement transitional rating instrument (‘my urinary problem has been cured, improved, not changed, or worsened during treatment’); a visual analog single-state rating instrument (a line scale with the two extremes labeled ‘my urinary incontinence causes me no problems’ and ‘my urinary incontinence causes me intolerable problems’).
Two condition-specific global scales have been validated for use in outcomes research for female SUI:19 one (the Patient Global Impression of Severity or PGIS Scale) is a single-state severity rating scale; the other (the Patient Global Impression of Improvement or PGI-I Scale) is a transitional improvement rating scale. The MCID values for QoL scales, considered earlier in this chapter, are generally established by using an ‘anchor-based’ analysis, in which the ‘anchor’ is an understandable measure of minimal improvement. Global scales are ideally suited to this purpose because of their inherent understandability. Both the King’s Health Questionnaire and the I-QOL questionnaire had their MCIDs established using global scales in an anchor-based analysis.15,16
investigator oBservations urodynamic Observations The resolution of the observation of urodynamic stress incontinence is considered one objective definition of cure of SUI.8 However, this criterion is of no use when trying to assess improvement in SUI. Moreover, while urodynamic studies are the only way to observe urodynamic SUI, there is reason to question whether this is the gold standard for establishing the underlying cause of urinary incontinence in an individual woman. The visualization of urine leakage from the uninstrumented urethra at the instant of a cough (the sign of SUI) in a woman who complains of the symptom of SUI may be better evidence of the condition of SUI than a lack of leakage from the catheterized urethra of the same woman is evidence for the absence of the condition of SUI. Thus, urodynamic-based determinations of cure must consider the inherent inaccuracy of urodynamic testing. It is for this reason that most standards do not require a urodynamic study either to
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enroll women into SUI clinical trials or to assess the effect of treatment.3,5,7
Quantitative measures of urethral function Several studies have examined changes in urethral biomechanical parameters with treatments for SUI. Two US National Institute of Health sponsored projects failed to show any significant improvements in various urodynamic parameters despite successful treatment of SUI with bladder training20 and with PFMT.21 Despite a 50% or greater reduction in incontinence episodes by 56% of subjects in the intense 12-week, biofeedback-based PFMT program, no significant or clinically important changes were demonstrated in functional urethral length, maximum or mean urethral closure pressures (MUCPs) at rest, MUCPs during a pelvic floor muscle contraction, or pressure transmission ratios with coughing.21 These results are similar to those of two other randomized controlled trials of PFMT.22,23 In contrast, one randomized trial comparing standard with intensive PFMT did show a statistically significant, though clinically unimportant, 4.6 cm water increase in MUCP with the intensive treatment.24 In summary, even though PFMT is an accepted, widely recommended, and effective treatment for SUI with an acknowledged mode of action that links strengthening the pelvic floor and urethral muscles to improved urethral sphincteric closure, urodynamic tests that are supposed to measure this improvement are largely unchanged despite clinical improvement in SUI. Continence surgery is generally accepted as the SUI treatment that most dramatically changes the urethral continence mechanism by instantly correcting the anatomic defect associated with the condition. Conventional measures of resting urethral resistance (resting functional urethral length and MUCP) have not been shown to change significantly after continence surgery in many surgical series25–27 or have been shown to decrease significantly even when the procedure was successful.28 The one urodynamic measurement that has proved to be most consistently associated with continence surgery outcomes (including success, failure, and complications) is the pressure transmission ratio.25,27–30 Abdominal leak point pressures can be measured in a variety of different ways, under a variety of different circumstances, and with different stressors. Valsalva straining is the most common maneuver used to prompt leakage, although it is also possible to determine a cough leak pressure threshold.31,32 Both methods have shown inconsistent reproducibility with changes in methodology (e.g. they are influenced by different bladder volumes, catheter sizes, sites of pressure measurements, and cough frequencies). Thus, for reproducibility to be good,
the Valsalva leak point pressure needs to be strictly standardized and meticulously performed.31–33 Cough leak point pressures are significantly higher than Valsalva leak point pressures when measured in the same patient.31 Nonetheless, when properly performed, leak point pressures have been shown to be responsive and reflective of clinical improvement as a result of treatment with a vaginal continence device32 and with urethral implants.34 In summary, measures of resting urethral pressure are generally unresponsive to treatments of SUI that have demonstrated clinical efficacy. Dynamic assessments of urethral closure have been more highly related to clinical outcome for procedures or devices that physically result in stress-activated obstruction of the urethra but are prone to significant technique-dependent variability. They are not generally advocated as outcome measures, although they may be informative when examining mechanisms of action of some interventions.7
signs Cough stress test A positive cough stress test represents the sign of SUI and conversion of the full-bladder cough stress test from positive to negative is one of the three National Institute of Child Health and Human Development (NICHD) criteria for the definition of the cure of SUI.5 When performed as an outcome measure, it is important that the test be standardized so that it is performed in the same manner before and after treatment. Variables to be standardized include the bladder volume, subject position, method of ascertainment of leakage, and, as much as possible, the magnitude and number of coughs. The cough stress test (CST) has been shown to be the physical examination or clinical history parameter most highly correlated with a urodynamic observation of SUI, although the CST’s negative predictive value is greater than its positive predictive value.35 However, it may be that the lower positive predictive value is more reflective of the inherent inaccuracy of urodynamic testing to demonstrate SUI than of the inaccuracy of the CST.36 Nonetheless, a negative CST should be considered accurate when it is used to exclude SUI in a treated patient who previously had a positive CST, as long as the second CST is performed under exactly the same conditions as the first. As is true for urodynamic observations, the CST has no value as a criterion to evaluate improvement in SUI.
Stress pad test The conversion of the stress pad test from positive to negative has also been used as a criterion for the cure 455
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of SUI.8 In addition, because the test is quantitative, it has the potential to be used as a measure of improvement in SUI when cure has either not been achieved or has not been the goal of treatment. However, there are many variations of the pad test and it is critical that the test be performed by exactly the same method both before and during or after treatment if it is to be used to measure treatment effects. Even when strictly standardized, it appears that the inherent test–retest variability of ultra-short14 and of the 1-hour37 pad tests is considerable, rendering them unreliable as measures of treatment effect. There is some evidence that the 24-hour pad test may be more reliable than the 1-hour pad test,38 but patient compliance is a greater challenge with the longer test, especially if performed repeatedly. The uncertain role of pad tests as outcome measures in incontinence research is reflected in the conclusions of the NICHD working group:5 ‘Further research is needed to clarify the role of pad tests in quantifying symptom severity and response to treatment; if pad tests are used, the methodology should be described in detail.’
safety surveillance The issue of assessing for symptomatic adverse events related to treatments for SUI has already been addressed. In some instances, investigator observations related to safety may extend to laboratory testing. Examples might include testing for anemia or infection after continence surgery or testing for hepatic or cardiovascular function during pharmacological treatment. Attention might also be directed towards routine testing for evidence of treatment-induced adverse effects on bladder emptying function by performing pre- and post-treatment emptying phase urodynamic studies or by measuring post-void residual urine volumes.
treatment-specific surrogate measures With some interventions, there may be measures that are important surrogate markers of treatment effect that could be included as indirect measures of outcome. Examples of such measures could include anatomic assessments using physical examination or imaging techniques following continence surgery, pelvic floor muscle assessments using grading scales or pressure measurements after a course of PFMT, or urethral sphincter electrophysiological techniques after pharmacological treatments.
economic measures Socioeconomic measures have become increasingly important in the evaluation of all treatments, as relative economic impacts of interventions are emphasized within healthcare systems worldwide. These assessments are not specific or unique for studies of women with SUI and, therefore, the details of such cost-effectiveness, cost-utility, and cost–benefit analyses are not considered further.
summary Female SUI is a complex condition and the effects of its treatment can and should be evaluated in several domains. In most instances, the same outcome measures should be used both before treatment, to characterize the severity and impact of the disease, and during treatment, to quantify the effect of the intervention. The one exception to this rule is the use of global transitional (improvement) scales, which are used only after treatment is started. Primary and secondary outcome variables should be clearly defined a priori before randomized clinical trials are initiated. Definitions of cure and of important clinical responses short of cure should also be pre-specified. Finally, these clinically relevant changes in outcome variables should be used to determine sample sizes to allow for adequately powered studies.
reFerences 1. Department of Health and Human Services (US). Urinary incontinence in adults: acute and chronic management. Report of the Urinary Incontinence Clinical Practice Guideline Panel, HHS, Public Health Service, AHCPR Publication No. 96-0682. Rockville, MD: Agency for Health Care Policy and Research, 1996; 51–2. 2. Black NA, Downs SH. The effectiveness of surgery for stress incontinence in women: a systematic review. Br J Urol 1996;78:497–510. 3. Payne C, Van Kerrebroeck P, Blaivas J et al. Research methodology in urinary incontinence. In: Abrams P, Cardozo L, Khoury S, Wein A (eds) Incontinence. Plymouth: Health Publication, 2002; 1047–77. 4. Lose G, Fantl JA, Victor A, Walter S, Wells TL, Wyman J, Mattiasson A. Outcome measures for research in adult women with symptoms of lower urinary tract dysfunction. Neurourol Urodyn 1998;17:255–62. 5. Weber AM, Abrams P, Brubaker L et al. The standardization of terminology for researchers in female pelvic floor disorders. Int Urogynecol J 2001;12:178–86. 6. Blaivas JG, Appell RA, Fantl JA et al. Standards of efficacy
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for evaluation of treatment outcomes in urinary incontinence: recommendations of the Urodynamic Society. Neurourol Urodyn 1997;16:145–7. 7. Committee for Human Medicinal Products. Note for guidance on the clinical investigation of medicinal products for the treatment of urinary incontinence. London: European Agency for the Evaluation of Medicinal Products, 2002; 1–7. 8. Hilton P. Trials of surgery for stress incontinence – thoughts on the ‘Humpty Dumpty principle’. Br J Obstet Gynaecol 2002;109:1081–8. 9. Donnovan JL, Badia X, Corcos J et al. Symptom and quality of life assessment. In: Abrams P, Cardozo L, Khoury S, Wein A (eds) Incontinence. Plymouth: Health Publication, 2002; 267–316. 10. Avery K, Donovan J, Peters TJ, Shaw C, Gotoh M, Abrams P. ICIQ: a brief and robust measure for evaluating the symptoms and impact of urinary incontinence. Neurourol Urodyn 2004;23:322–30. 11. Sandvik H, Hunskaar S, Vanvik A, Bratt H, Seim A, Hermstad R. Diagnostic classification of female urinary incontinence: an epidemiological survey corrected for validity. J Clin Epidemiol 1995;48:339–43. 12. Abrams P, Cardozo L, Fall M et al. The standardisation of terminology of lower urinary tract function: report from the standardisation sub-committee of the International Continence Society. Neurourol Urodyn 2002;21:167–78. 13. Wyman JF, Choi SC, Harkins SW, Wilson MS, Fantl JA. The urinary diary in evaluation of incontinence in women: a test–retest analysis. Obstet Gynecol 1988;71:812–7. 14. Norton PA, Zinner NR, Yalcin I, Bump RC. Duloxetine versus placebo in the treatment of stress urinary incontinence. Am J Obstet Gynecol 2002;187:40–8.
21. Elser DM, Wyman JF, McClish DK, Robinson D, Fantl JA, Bump RC, and the Continence Program for Women Research Group. The effect of bladder training, pelvic floor muscle training, or combination training on urodynamic parameters in women with urinary incontinence. Neurourol Urodyn 1999;18:427–36. 22. Burns PA, Pranikoff K, Nochajski TH, Hadley EC, Levy KJ, Ory MG. A comparison of effectiveness of biofeedback and pelvic muscle exercise treatment of stress incontinence in older community-dwelling women. J Gerontol 1993;48:M167–M174. 23. Ferguson KL, McKey PL, Bishop KR, Kloen P, Verheul JB, Dougherty MC. Stress urinary incontinence: effect of pelvic muscle exercise. Obstet Gynecol 1990;75:671–5. 24. Bo K, Hagen RH, Kvarstein B, Jorgensen J, Larsen S. Pelvic floor muscle exercise for the treatment of female stress urinary incontinence: III. Effects of two different degrees of pelvic floor muscle exercises. Neurourol Urodyn 1990;9:489–502. 25. Kujansuu E. Urodynamic analysis of successful and failed incontinence surgery. Int J Gynaecol Obstet 1983;21:353– 60. 26. Lalos O, Berglund AL, Bjerle P. Urodynamics in women with stress incontinence before and after surgery. Eur J Obstet Gynecol Reprod Biol 1993;48:197–205. 27. Chen H-Y, Lin W-C, Tsai H-D. Mechanism of continence after endoscopic bladder neck suspension. J Gynecol Surg 1999;15:87–91. 28. Weil A, Reyes H, Bischoff P, Rottenberg RD, Krauer F. Modifications of the urethral rest and stress profiles after different types of surgery for urinary stress incontinence. Br J Obstet Gynaecol 1984;91:46–55.
15. Kelleher CJ, Pleil AM, Reese PR, Burgess SM, Brodish PH. How much is enough and who says so? The case of the King’s Health Questionnaire and overactive bladder. Br J Obstet Gynaecol 2004;111:605–12.
29. Bump RC, Fantl JA, Hurt WG. Dynamic urethral pressure profilometry pressure transmission ratio determinations after continence surgery: understanding the mechanism of success, failure, and complications. Obstet Gynecol 1988;72:870–4.
16. Yalcin I, Patrick D, Summers K, Kinchen K, Bump RC. The minimum clinically important difference in Incontinence Quality of Life Questionnaire (I-QOL) total and subscale scores in women with stress urinary incontinence. Neurourol Urodyn 2004;23:568–70.
30. Bump RC, Hurt WG, Elser DM, Theofrastous JP, Addison WA, Fantl JA, McClish DK, and the Continence Program for Women Research Group. Understanding lower urinary tract function in women soon after bladder neck surgery. Neurourol Urodyn 1999;18:629–37.
17. Feinstein AR. Global indexes and scales. In: Clinimetrics. New Haven, CT: Yale University Press, 1987; 91–103.
31. Bump RC, Elser DM, Theofrastous JP, McClish DK, and the Continence Program for Women Research Group. Valsalva leak point pressures in women with genuine stress incontinence: reproducibility, effect of catheter caliber, and correlations with other measures of urethral resistance. Am J Obstet Gynecol 1995;173:551–7.
18. Gill TM, Feinstein AR. A critical appraisal of the quality of quality-of-life measurements. JAMA 1994;272:619–26. 19. Yalcin I, Bump RC. Validation of two global impression questionnaires for incontinence. Am J Obstet Gynecol 2003;189:98–101. 20. McClish DK, Fantl JA, Wyman JF, Pisani G, Bump RC. Bladder training in older women with urinary incontinence: relationship between outcome and changes in urodynamic observations. Obstet Gynecol 1991;77:281–6.
32. Siltberg H, Larsson G, Victor A. Cough-induced leakpoint pressure – a valid measure for assessing treatment in women with stress incontinence. Acta Obstet Gynecol Scand 1998;77:1000–7. 33. Theofrastous JP, Cundiff GW, Harris RL, Bump RC. The
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effect of vesical volume on Valsalva leak-point pressures in women with genuine stress urinary incontinence. Obstet Gynecol 1996;87:711–4.
tion of a clinical algorithm indicative of urodynamic stress incontinence for use in large-scale clinical trials. J Urol 2004; 171:2321–5.
34. Bent AE, Foote J, Siegel S, Faerber G, Chao R, Gormley EA. Collagen implant for treating stress urinary incontinence in women with urethral hypermobility. J Urol 2001;166:1354–7.
37. Simons AM, Yoong W, Buckland S, Moore KH. Inadequate repeatability of the one-hour pad test: the need for a new incontinence outcome measure. Br J Obstet Gynaecol 2001:108:315–9.
35. Weidner AC, Myers ER, Visco AG, Cundiff GW, Bump RC. Which women with stress incontinence require urodynamics? Am J Obstet Gynecol 2001;184:20–7.
38. Matharu GS, Assassa RP, Williams KS et al. Objective assessment of urinary incontinence in women: comparison of the one-hour and 24-hour pad tests. Eur Urol 2004;45:208–12.
36. Yalcin I, Bump RC, Versi E, Schaefer W, Benson JT. Valida-
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30c Outcome measures in women with lower urinary tract symptoms: pelvic organ prolapse Peggy A Norton
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IntroductIon It is estimated that one in three women have symptoms of pelvic floor disorders, and one in nine undergo surgery for these conditions during their lifetime. While some types of pelvic organ prolapse may be treated conservatively with watchful waiting or pessaries, many cases are treated surgically, and procedures performed in the United States for pelvic organ prolapse outnumber those for stress urinary incontinence 3:1. These procedures are described throughout this textbook, but in this chapter we consider measures for evaluating the outcome of treatments for pelvic organ prolapse, including a brief overview of some of the early nonvalidated outcome measures that are still in use, and then describe more recent tests that have been fully validated. The Standardization Committee of the International Continence Society (ICS)1 recommends that there should be five domains of outcome measures:
Are there normal ranges for these subjective and objective outcomes measures? These are necessary if we are to characterize patients into degrees of mild, moderate, or severe.
SubjectIve outcomeS
Because pelvic organ prolapse shares similar measures for items 4 and 5 discussed in this section, we will consider the first three as they relate to prolapse.
Pelvic organ prolapse (POP) is different from urinary incontinence in that we lack multiple validated subjective and objective outcome measures. Even the definition of normal anatomy is unclear. While questionnaires are useful in assessing urinary incontinence (‘do you leak urine’), their use in POP has been limited. There are multiple symptoms such as ‘bulge’, ‘lump’, ‘pressure’, and ‘dragging’ to describe the sensation of prolapse at or beyond the introitus, and multiple symptoms such as back pain that may or may not be associated with prolapse. Assessment of sexual, urinary, and bowel function is important, because POP can impact each of these, and the surgical treatment for POP may improve these functions if it improves the prolapse. However, the procedure itself can compromise sexual function by making the vagina too short or narrow for coitus, urinary function by unmasking stress incontinence or causing voiding problems, and bowel function by narrowing outlet or damaging autonomic innervation of the lower bowel. The assessment tools available for POP are best used in pre- and postoperative schemes to look for changes in symptoms associated with surgery, but not as symptom screeners in the general population.
How are outcome measures validated?
Generalized questions
1. Patient’s observations (symptoms); 2. Quantification of symptoms; 3. Physician’s observations (anatomical and functional); 4. Quality of life measures; 5. Socioeconomic evaluations.
For both symptom assessment and anatomic/functional outcomes, there is considerable work involved in demonstrating validity, reliability and responsiveness to change after treatment:
• Validity of a test assesses whether the test measures
•
•
what it is supposed to measure, including content/ face validity (does it make sense to patients and clinicians?), construct validity (does it perform in a range of settings and patients groups?) and criterion validity (does it correlate with a ‘gold standard’ that already exists?). Reliability of a test means that it is able to measure quantities with internal consistency (similar items within a questionnaire are answered similarly) and with reproducibility (responses are stable over a short period of time). Responsiveness of a test describes its response to change after treatment.
Weber and colleagues2 used generalized questions to evaluate sexual function in women undergoing surgery for pelvic floor disorders. Sexual function and satisfaction improved or did not change in most women after surgery for either prolapse or urinary incontinence, or both. However, the combination of Burch colposuspension and posterior colporrhaphy was especially likely to result in dyspareunia.
Quality of life The Pelvic Floor Distress Inventory (PFDI) and the Pelvic Floor Impact Questionnaire (PFIQ) were developed from two previously validated questionnaires – the Urinary Distress Inventory (UDI) and the Incontinence Impact Questionnaire (IIQ) – with additional questions regarding pelvic organ prolapse and colorectal dysfunction.3 The PFDI assesses symptom distress in women
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with pelvic floor disorders and has three scales: UDI (28 items), Colorectal–Anal Distress Inventory (17 items), and Pelvic Organ Prolapse Distress Inventory (16 items). The PFIQ assesses life impact and also has three scales: IIQ, Colorectal–Anal Impact Questionnaire, and the Pelvic Organ Prolapse Impact Questionnaire (31 items each). The instrument has been validated with good internal consistency and reproducibility. For POP, the Pelvic Organ Prolapse Distress Inventory and the Pelvic Organ Prolapse Impact Questionnaire significantly correlated with the stage of prolapse (rho = 0.32 and 0.33, respectively, p<0.01 each.) Anatomic changes in POP may not be reflected in symptoms. In a study of 330 women presenting for evaluation of pelvic floor disorders in a university clinic, women with more advanced prolapse were less likely to have stress incontinence and more likely to manually reduce prolapse to void; however, prolapse severity was not associated with sexual or bowel symptoms.4 In several instruments, the number of POP symptoms seems to increase when the leading edge of the prolapse is beyond the hymeneal ring, i.e. (some Stage II and all Stage III–IV).5 This definition of prolapse was recommended by an international National Institutes of Health (NIH) consensus panel on terminology for pelvic floor disorders.6 However, while one would expect posterior compartment defects to cause defecatory dysfunction and anterior defects to cause lower urinary tract dysfunction, symptoms do not always correlate with the anatomic compartment defect.7
Sexual function In creating the Pelvic Organ Prolapse/Urinary Incontinence Sexual Questionnaire (PISQ), Rogers and colleagues8 developed a condition-specific, validated and reliable instrument, containing 31 items divided into three domains, to evaluate sexual functioning in women with urinary incontinence or POP. The PISQ has been validated in a Spanish language format,9 and a short form with 12 questions has been developed that predicts PISQ-31 scores and correlates well with generalized instruments.10 Used in patient populations with pelvic floor distress, the PISQ has demonstrated that prolapse is more likely than urinary incontinence to result in sexual inactivity and to be perceived as affecting sexual relations.3
Symptom screening Developed with NIH funding, the Epidemiology of Prolapse and Incontinence Questionnaire (EPIQ)11 is
condition-specific to POP and urinary incontinence (UI) validated in a large patient population of Caucasians and Hispanics in Southern California, with high reliability and reproducibility. Positive and negative predictive values to detect POP were 76% and 97%, respectively, with similar but slightly lower predictive values for stress urinary incontinence (SUI), overactive bladder (OAB), and fecal incontinence. This instrument is the first psychometrically validated questionnaire that has been shown to identify women at risk of having POP in large undiagnosed populations (i.e. population screening tool).
objectIve outcomeS Objective measures such as pad testing, diaries, and urodynamic testing are available in UI; in POP, however, objective outcomes are defined by the anatomy of the various defects in the anterior, apical, and posterior segments of vaginal support. Although a standardized staging system for prolapse has been accepted by the ICS (POP-Q), there is no consensus as to what level of physical findings defines clinically significant prolapse. Objective measures of anatomic support might seem easier, but in fact we lack definitions of what ‘normal’ anatomy is in patient populations. Consider a woman with an anterior wall defect to 1 cm above the hymeneal ring: some surgeons might recommend surgery for a Stage II anterior wall defect, whereas others consider this to be normal in the absence of other symptoms and defects. In multiple studies, the prevalence of mild-to-moderate anterior wall defects in women who were not seeking treatment for POP has been reported to be as high as 50%. In a study of women enrolled in the Women’s Health Initiative, Handa et al.12 looked at anterior, apical, and posterior wall defects and reported varying degrees of incidence (1.5–9.3 cases per 100 women annually), progression, and even regression of POP in as many as a quarter of subjects. Thus, POP is a dynamic condition with progression and remission, and must be taken into consideration when evaluating short- and long-term outcomes of treatments for POP. This serves to emphasize that prolapse is a dynamic condition, and factors related to progression and remission need further study. What if this same woman is being assessed after surgery for POP? If she had a Stage IV defect and has improved anatomically by two stages, she has a favorable outcome for prolapse surgery; if the procedure was performed for a Stage II defect, the surgery has done little. Anatomic measurements of POP were historically descriptive,13 with terms such as ‘ballooning’ and ‘mas461
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sive’ as initial observations, and ‘nicely reduced’ as outcome descriptors. Important functional outcomes such as sexual function and bowel function were not described.
C
D
3 cm
Ba
vaginal profile (baden–Walker) 14
In 1968, Baden and colleagues described their ‘halfway’ anatomic grading for each element of POP (urethra, bladder, cervix or cuff, cul-de-sac, and rectum; Fig. 30c.1) as Grade 0 (no descent), Grade 1 (half-way to the hymen), Grade 2 (descent to the hymen), Grade 3 (halfway past the hymen) and Grade 4 (maximum descent.) It has also been termed the vaginal profile. The strength of the system is in readily understandable grades from the introitus to complete prolapse; the weakness of the system is that actual measurements of descent are not recorded and thereby subtle differences or improvements cannot be assessed, and that degrees of POP above the introitus are less descriptive. The test has not been validated for reliability or responsiveness. Because Baden–Walker has been in wide use for many years, it is often reported in patient populations whose measurements pre-date the adoption of POP-Q in 1996.
Cervix (cuff) Ischial Halfway to hymen
To the hymen
0
Spines
1 2
Halfway past hymen
3
Maximum descent
4
Figure 30c.1. Badan-Walker vaginal profile. Each element is measured relative to the hymeneal ring in ‘halfway’ terms.
PoP-Q In 1996 the ICS standardization committee published their efforts to standardize reporting of POP, termed the POP-Q15 (Fig. 30c.2). This is a physical recording of defects relative to the hymeneal ring in centimeter gra-
Bp
Aa Ap gh
tvI
pb
Figure 30c.2. Diagram for POP-Q quantification of pelvic organ prolapse. Anterior wall measures (Aa and Ba), posterior wall measures (Ap and Bp), apical measures (C and D) are recorded relative to the hymneal ring in actual centimeters (either above the hymen, designated as minus, or below/beyond the hymen, designated as plus). Additional measures include genital hiatus (gh), perineal body (pb), and total vaginal length (tvl). Stage II exists when the most advanced measure is within 1 cm of the hymeneal ring (minus 1 to plus 1); Stage III exists when the most advanced measure is greater that Stage II; Stage IV is complete eversion of the vagina (or progression to within 2 cm of the entire vaginal length). Any prolapse above Stage II is designated Stage I. dients. These measures are further staged according to the most distal defect as Stage 0 (no descent). The strength of the system is that anatomic measures are precisely recorded in the anterior segments (bladder neck and anterior wall), apex (cervix and cul-de-sac or cuff), posterior segments (distal and proximal), as well as genital hiatus, perineal body, and total vaginal length; the weakness of the system is that clinicians other than researchers may find the multiple measures to be cumbersome and difficult to learn. Nevertheless the system has been validated for reproducibility and reliability. Some of the validation studies performed on POP-Q were carried out by a research team led by Rick Bump, the primary author for the POP-Q source paper.15 In a study by Hall and colleagues,16 the assessment took 2 minutes to accomplish with experienced users and 3 minutes with new users. They found that for each of nine measurements, interobserver reliability was quite good (correlation coefficients [rs] ranging from 0.5 to 0.9) as was intraobserver reliability (0.43–0.93). In the upright position, prolapse was likely to be recorded at a higher stage. The method was highly reproducible for overall staging (tau 0.7) and substaging (0.6): in twothirds of subjects, the staging was identical, and in no
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subject did the stage vary by more than one stage from one evaluation to the next. In a related study, Barber et al.17 compared the stage in supine lithotomy with assessment performed upright, and although the two correlated well, examination in the upright position led to a higher stage in 26% (and a lower stage in 4%). Half of the patients had an increase in one measurement by 2 cm when examined upright. POP-Q was validated in several institutions in Europe and America,18–20 but is available only in abstract form. Koback and colleagues21 studied the interobserver reliability of both the POP-Q and Baden–Walker vaginal profile using both physician and nurse examiners, and found good interobserver reliability using either method.
Is the POP-Q being used by clinicians, or is it only a research tool? Auwad and colleagues22 surveyed members of the societies which have endorsed its use: of the 380 (57%) gynecologist members of the American Urogynecologic Society and International Continence Society who responded, 40.2% routinely use the POP-Q system in their clinical practice. While its use is likely to be much higher in research studies reporting clinical outcomes, Muir et al.23 reviewed the use of grading systems in the peer review literature for two 12-month periods of 1999, and 2001–2002. The POP-Q was used most frequently (22%) followed by the Baden–Walker (19%), but the staging system was not cited or a non-standardized staging system was used in more than half of studies. However, use of POP-Q in reporting did double from the 1999 period to the 2001–2002 period.
Normal ranges Swift et al.24 used POP-Q to evaluate over 1000 women presenting to a university clinic for annual examination. The prevalence of POP quantification stages was 24% (Stage 0), 38% (Stage I), 35% (Stage II), and 2% (Stage III). In contrast, of 330 women presenting for management of pelvic floor, 2.4% had Stage I, 46.1% had Stage II, 48.2% had Stage III, and 3.3% had Stage IV prolapse. Bland and co-workers25 studied perimenopausal women at baseline and again at 1 year, and found apparent increases in prolapse at points C and D (apical measures; see Fig. 30c.2) and total vaginal length, and suggested that this may be due to changes in vaginal size rather than an increase in uterine or vaginal vault prolapse. They concluded that variability may confound the use of the POP-Q staging system in longitudinal studies involving perimenopausal women.
Specific site defects The POP-Q does not distinguish between types of anterior and posterior wall defects, but two studies have demonstrated the difficulty of subtyping defects without the POP-Q. Barber and colleagues26 were unable to accurately predict the presence of lateral wall defects preoperatively in a group of women with anterior wall defects to the hymeneal ring or greater. The sensitivity and negative predictive value for the clinical assessment for paravaginal defects were good on both the right and left sides, whereas the specificity and positive predictive values were poor. Stage of prolapse, previous hysterectomy, or previous anterior colporrhaphy did not significantly affect the accuracy of the clinical examination in predicting fascial defects. Whitesides and co-workers27 examined women with anterior wall POP Stage II or greater to determine whether individual defects (central, right lateral, left lateral, and superior) in the anterior wall could be distinguished. They found poor inter- and intraobserver reliability and reproducibility.
Imaging Radiologic assessment has been recommended for POP, but mainly by non-gynecologic groups who may be less comfortable with the pelvic examination for POP. While they have been proposed, these studies incur significant cost, both in research and clinical use. The expense may be one reason for the lack of validation and reliability studies performed in radiologic assessment of POP compared to clinical examination. In one Swedish study, Altman and his colorectal colleagues28 used cystodefecoperitoneography (CDP) to evaluate the relationship between posterior POP and defecatory symptoms. Although there was a strong association between large rectoceles (>3 cm) at CDP and symptoms of rectal emptying difficulties (p<0.001), severity and prevalence of bowel dysfunction showed poor coherence with clinical prolapse staging and findings at radiologic imaging. Vaginal topography and POP-Q staging predict neither radiologic size nor visceral involvement in posterior vaginal wall prolapse. Their conclusion was that adding radiologic assessment was more likely to assess visceral involvement.
Magnetic resonant imaging Comiter and his urologic co-investigators29 have reported on magnetic resonance imaging (MRI) for POP, using a 2.5 minute acquisition costing US$540 (1998 dollars). They defined an ‘HMO’ classification in 164 consecutive women imaged for pelvic pain (n=39) or POP (n=125). The ‘H-line’ (levator hiatus) measured the distance 463
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from the pubis to the posterior anal canal, the ‘M-line’ (muscular pelvic floor relaxation) measured the descent of the levator plate from the pubococcygeal line, and the ‘O’ classification (organ prolapse) characterized the degree of visceral prolapse beyond the H-line. As would be expected, they found statistically significant differences in the HMO values for POP subjects compared to pain subjects, but there was no validation, reliability, or responsiveness demonstrated. In a British radiologic study using MRI, Singh et al.30 described the ‘midpubic line’ corresponding to the hymeneal ring as their radiologic definition of POP and found moderate correlation (kappa 0.61) with clinical staging by POP-Q. In their hands, MRI was able to measure dynamic descent and prolapse of the pouch of Douglas, and suggested that this method of grading allowed an objective assessment of the results of surgical correction of POP, although no validation, reliability, or responsiveness demonstrated. A small Italian study found good correlation between Baden–Walker and MRI.31
3. Barber MD, Visco AG, Wyman JF, Fantl JA, Bump RC. Continence Program for Women Research Group. Sexual function in women with urinary incontinence and pelvic organ prolapse. Obstet Gynecol 2002;99(2):281–9.
Summary
9. Romero AA, Hardart A, Kobak W, Qualls C, Rogers R. Validation of a Spanish version of the Pelvic Organ Prolapse Incontinence Sexual Questionnaire. Obstet Gynecol 2003;102(5 Pt 1):1000–5.
Reporting outcomes in the treatment of pelvic organ prolapse is complicated by the presence of subjective and objective measures which do not always correlate well. Questionnaires specific to pelvic organ prolapse have recently been developed and validated, and may improve reporting in clinical trials being reported in the future. While objective outcomes may be measured anatomically or radiologically, no perfect system exists that can meet the needs of researchers and clinicians alike. As in all outcomes reporting, it is critical to use the same instrument prior to and following the intervention. Because the surgical treatment of pelvic organ prolapse is functional rather than extirpative, emphasis on long-term evaluation of efficacy (i.e. 5- and 10-year outcomes) must be balanced with the known progression and remission of pelvic floor disorders.
reFerenceS
4. Burrows LJ, Meyn LA, Walters MD, Weber AM. Pelvic symptoms in women with pelvic organ prolapse. Obstet Gynecol 2004;104(5 Pt 1):982–8. 5. Swift SE, Tate SB, Nicholas J. Correlation of symptoms with degree of pelvic organ support in a general population of women: what is pelvic organ prolapse? Am J Obstet Gynecol 2003;189(2):372–7; discussion 377–9. 6. Weber AM, Abrams P, Brubaker L et al. The standardization of terminology for researchers in female pelvic floor disorders. Int Urogynecol J Pelvic Floor Dysfunct 2001;12(3):178–86. 7. Ellerkmann RM, Cundiff GW, Melick CF, Nihira MA, Leffler K, Bent AE. Correlation of symptoms with location and severity of pelvic organ prolapse. Am J Obstet Gynecol 2001;185(6):1332–7. 8. Rogers RG, Kammerer-Doak D, Villarreal A, Coates K, Qualls C. A new instrument to measure sexual function in women with urinary incontinence or pelvic organ prolapse. Am J Obstet Gynecol 2001;184(4):552–8.
10. Rogers RG, Coates KW, Kammerer-Doak D, Khalsa S, Qualls C. A short form of the Pelvic Organ Prolapse/Urinary Incontinence Sexual Questionnaire (PISQ-12). Int Urogynecol J Pelvic Floor Dysfunct 2003;14(3):164–8. 11. Lukacz ES, Lawrence JM, Buckwalter JG, Burchette RJ, Nager CW, Luber KM. Epidemiology of prolapse and incontinence questionnaire: validation of a new epidemiologic survey. Int Urogynecol J Pelvic Floor Dysfunct 2005;16(4):272–84. 12. Handa VL, Garrett E, Hendrix S et al. Progression and remission of pelvic organ prolapse: a longitudinal study of menopausal women. Am J Obstet Gynecol 2004;190:27–32. 13. Brubaker L, Norton P. Current clinical nomenclature for description of pelvic organ prolapse. J Pelvic Surg 1996;7:256–9. 14. Baden WF, Walker TA, Lindsay HJ (1968) The vaginal profile. Tex Med J 64:56–8.
1. Lose G, Fantl JA, Victor A, Walter S, Wells TL, Wyman J, Mattiasson A. Outcome measures for research in adult women with symptoms of lower urinary tract dysfunction. Neurourol Urodyn 1998;17(3):255–62.
15. Bump RC, Mattiasson A, Bo K et al. The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 1996;175(1):10–7.
2. Weber AM, Walters MD, Piedmonte MR. Sexual function and vaginal anatomy in women before and after surgery for pelvic organ prolapse and urinary incontinence. Am J Obstet Gynecol 2000;182(6):1610–5.
16. Hall AF, Theofrastous JP, Cundiff GW, Harris RL, Hamilton LF, Swift SE, Bump RC. Interobserver and intraobserver reliability of the proposed International Continence Society, Society of Gynecologic Surgeons, and American
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Urogynecologic Society pelvic organ prolapse classification system. Am J Obstet Gynecol 1996;175(6):1467–70. 17. Barber MD, Lambers A, Visco AG, Bump RC. Effect of patient position on clinical evaluation of pelvic organ prolapse. Obstet Gynecol 2000;96(1):18–22. 18. Athanasiou S, Hill S, Gleeson C, Anders K, Cardozo L. Validation of the ICS proposed pelvic organ prolapse descriptive system. Neurourol Urodyn 1995;14:414–5. 19. Schussler B, Peschers U. Standardization of terminology of female genital prolapse according to the new ICS criteria: inter-examiner reproducibility. Neurourol Urodyn 1995;14:437–8. 20. Montella J, Cater J. Comparison of measurements obtained in supine and sitting position in the evaluation of pelvic organ prolapse. Int Urogyn J 1995;6:304. 21. Kobak WH, Rosenberger K, Walters MD. Interobserver variation in the assessment of pelvic organ prolapse. Int Urogynecol J Pelvic Floor Dysfunct 1996;7(3):121–4. 22. Auwad W, Freeman RM, Swift S. Is the pelvic organ prolapse quantification system (POPQ) being used? A survey of members of the International Continence Society (ICS) and the American Urogynecologic Society (AUGS). Int Urogynecol J Pelvic Floor Dysfunct 2004;15(5):324–7. 23. Muir TW, Stepp KJ, Barber MD. Adoption of the pelvic organ prolapse quantification system in peer-reviewed literature. Am J Obstet Gynecol 2003;189(6):1632–5; discussion 1635–6. 24. Swift S, Woodman P, O’Boyle A, et al. Pelvic Organ Support Study (POSST): the distribution, clinical definition, and epidemiologic condition of pelvic organ support defects. Am J Obstet Gynecol 2005;192(3):795–806. 25. Bland DR, Earle BB, Vitolins MZ, Burke G. Use of the Pelvic Organ Prolapse staging system of the International Continence Society, American Urogynecologic Society, and Society of Gynecologic Surgeons in perimenopausal women. Am J Obstet Gynecol 1999;181(6):1324–7.
26. Barber MD, Cundiff GW, Weidner AC, Coates KW, Bump RC, Addison WA. Accuracy of clinical assessment of paravaginal defects in women with anterior vaginal wall prolapse. Am J Obstet Gynecol 1999;181(1):87–90. 27. Whiteside JL, Barber MD, Paraiso MF, Hugney CM, Walters MD. Clinical evaluation of anterior vaginal wall support defects: interexaminer and intraexaminer reliability. Am J Obstet Gynecol 2004;191(1):100–4. 28. Altman D, Lopez A, Kierkegaard J, Zetterstrom J, Falconer C, Pollack J, Mellgren A. Assessment of posterior vaginal wall prolapse: comparison of physical findings to cystodefecoperitoneography. Int Urogynecol J Pelvic Floor Dysfunct 2005;16(2):96–103. 29. Comiter CV, Vasavada SP, Barbaric ZL, Gousse AE, Raz S. Grading pelvic prolapse and pelvic floor relaxation using dynamic magnetic resonance imaging. Urology 1999;54(3):454–7. 30. Singh K, Reid WM, Berger LA. Assessment and grading of pelvic organ prolapse by use of dynamic magnetic resonance imaging. Am J Obstet Gynecol 2001;185(1):71–7. 31. Torricelli P, Pecchi A, Caruso Lombardi A, Vetruccio E, Vetruccio S, Romagnoli R. Magnetic resonance imaging in evaluating functional disorders of female pelvic floor. Radiol Med (Torino) 2002;103(5–6):488–500. 32. Barber MD, Kuchibhatla MN, Pieper CF, Bump RC. Psychometric evaluation of 2 comprehensive condition-specific quality of life instruments for women with pelvic floor disorders. Am J Obstet Gynecol 2001;185(6):1388–95. 33. Rogers RG, Kammerer-Doak D, Darrow A, Murray K, Olsen A, Barber M, Qualls C. Sexual function after surgery for stress urinary incontinence and/or pelvic organ prolapse: a multicenter prospective study. Am J Obstet Gynecol 2004;191(1):206–10. 34. Wall LL, Versi E, Norton P, Bump R. Evaluating the outcome of surgery for pelvic organ prolapse. Am J Obstet Gynecol 1998;178(5):877–9.
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31 Behavioral therapies and management of urinary incontinence in women Kathryn L Burgio
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INTRODUCTION Behavioral therapies are a varied group of interventions that improve incontinence by teaching patients skills for preventing urine loss or facilitating changes in their daily habits. In practice, behavioral interventions are generally comprised of multiple components, tailored to the type of incontinence and the individual needs of the patient. Behavioral programs are generally built around one of two approaches: one approach focuses on modifying bladder function through voiding schedules, such as with bladder training; the other approach targets the bladder outlet, such as with pelvic floor muscle training and exercise. Among the techniques included in behavioral treatment programs are: self-monitoring with a bladder diary, pelvic floor muscle training techniques (including biofeedback), pelvic floor muscle exercise regimes, use of pelvic floor muscles for urethral occlusion, urge inhibition training, urge suppression strategies, urge avoidance strategies, scheduled voiding, delayed voiding, fluid management, dietary changes, weight loss, and other lifestyle changes. Behavioral interventions are widely used because their efficacy is well established, although they are not curative in most patients. They are safe and without the risks and side effects common with some other therapies. However, they do require the active participation of a motivated patient and usually require some time and persistence to reach optimum benefit. Behavioral treatments have been recognized as effective by the 1988 Consensus Conference on Urinary Incontinence in Adults1 and the Guideline for Urinary Incontinence in Adults developed by the Agency for Health Care Policy and Research.2
VOIDINg HabITs aND blaDDeR TRaININg Decreasing voiding frequency: bladder training It has long been thought that habitual frequent urination can contribute to reduced bladder capacity and lead to detrusor overactivity, which in turn causes urgency and urge incontinence. Bladder training is a behavioral intervention developed with the goal of breaking the cycle of urgency and frequency, using consistent, incremental voiding schedules. First known as bladder drill, it was an intensive intervention that was often conducted in an inpatient setting. Patients, mostly women, were placed on a strict expanded voiding schedule for 7–10 days to establish a normal voiding interval.3,4 Bladder training is a sequel to this procedure that increases the voiding interval more gradually, over
a longer period of time, and is conducted in the outpatient setting.5–13 Patients are given instructions to void at predetermined intervals and, over time, the voiding interval is gradually increased. To do this, patients must resist the sensation of urgency and postpone urination. This is believed to increase capacity and decrease instability, resulting in improved bladder control. Guidelines for conducting bladder training are outlined in Table 31.1. Several clinical series studies have demonstrated efficacy of outpatient bladder training or a mixture of inpatient and outpatient intervention.5–11,13 The most definitive study is a randomized clinical trial that demonstrated a mean 57% reduction in frequency of incontinence in older women.12 In this trial, bladder training not only reduced incontinence associated with detrusor overactivity, but also incontinence associated with sphincter insufficiency, possibly because patients acquired a greater awareness of bladder function or that the exercise of postponing urination increased the use of pelvic floor muscles.
Increasing voiding frequency It is very common for healthcare providers to advise patients simply to increase their frequency of urination as a way to avoid a full bladder and its increased risk of incontinence. While increased frequency of urination can have an immediate benefit in terms of avoiding incontinent episodes, the long-term result is most likely counterproductive, because the patient can lose the ability to accommodate larger volumes and tolerate bladder fullness. In addition, it feeds the cycle of urgency and Table 31.1
Guidelines for bladder training
1. Review voiding diary with the patient, noting the various voiding intervals 2. Identify with the patient the longest voiding interval that is comfortable for her 3. Patient instructions: Empty your bladder… • first thing in morning • every time your voiding interval passes during the day • just before bed 4. Teach coping strategies to manage urge • Self-statements (affirmations) • Distraction to another task • Relaxation • Urge suppression strategy (using pelvic floor muscle contraction) 5. Gradually increase interval • when patient is comfortable for at least 3 days • by 30-minute intervals or clinical judgment based on patient confidence
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frequency thought to perpetuate overactive bladder and exacerbate urge incontinence in the long run. Increasing the frequency of voiding is generally reserved for patients who clearly void less than normal or in patients with cognitive impairment who are incapable of learning new skills for bladder control. Although we often think of voiding in terms of schedules, most patients have irregular daily voiding patterns. For many patients it is possible to identify times in their day when they are at increased risk of incontinence – for example, 2 hours after morning coffee or during exercise – and they can plan strategic voids before those times.
beHaVIORal TRaININg aND PelVIC FlOOR MUsCle exeRCIse Pelvic floor muscle training was first popularized by Arnold Kegel, a gynecologist who proposed that women with stress incontinence lacked awareness and coordination of their muscles.14 He also demonstrated that women could improve their stress incontinence through pelvic floor muscle training and exercise to improve strength.14,15 Over several decades, this intervention has evolved both as a behavior therapy and a physical therapy, combining principles from both fields into a widely accepted conservative treatment for stress and urge incontinence. The literature on pelvic floor muscle training and exercise has demonstrated that it is effective for reducing stress, urge and mixed incontinence in most outpatients who cooperate with training.16–28 Pelvic floor muscle training and exercise is now a cornerstone of behavioral treatment for both stress and urge urinary incontinence.
Teaching pelvic floor muscle control The goal of behavioral treatment for stress incontinence is to teach patients how to improve urethral closure by voluntarily contracting pelvic floor muscles during whatever physical activities precipitate urine leakage. The first step in training is to identify the pelvic floor muscles properly and to contract and relax them selectively (without increasing intra-abdominal pressure on the bladder or pelvic floor). It is an essential and often overlooked step to confirm that patients have identified the correct muscles. Failure to find the pelvic floor muscles or to exercise them correctly is an important source of failure with this treatment modality. While it is easy to give patients a pamphlet or brief verbal instructions to ‘lift the pelvic floor’ or to interrupt the urinary stream during voiding, this approach does not ensure that the patient understands which muscles to use before she is sent home to exercise
them. This can be accomplished by palpating the vagina during pelvic examination and giving her verbal feedback. Pelvic floor muscle control can also be taught using biofeedback or electrical stimulation. Biofeedback is a teaching technique that helps patients learn by giving them instantaneous accurate feedback of their pelvic floor muscle activity. In his original work, Kegel used a biofeedback device he designed and named the perineometer.14 It consisted of a pneumatic chamber (which was placed in the vagina) and a hand-held pressure gauge, which displayed the pressure generated by circumvaginal muscle contraction. This device provided immediate visual feedback of pelvic floor muscle contraction to the woman learning to identify her muscles and monitor her practice. Most biofeedback instruments in current use are computerized and display feedback visually on a computer monitor. Pelvic floor muscle activity can be measured by manometry or electromyography, using vaginal or anal probes or surface electrodes. Signals are augmented through the computer, and immediate feedback is provided on a monitor for visual feedback or via speakers for auditory feedback. When patients observe the results of their attempts to control bladder pressure and pelvic floor muscle activity, learning occurs by means of operant conditioning (trial and error learning). Biofeedbackassisted behavioral training has been tested in several studies, producing mean reductions of incontinence ranging from 60 to 85%.16,17,20,27–32 A common problem encountered in learning to control the pelvic floor muscles is that patients tend to recruit other muscles, such as the rectus abdominis muscles or gluteal muscles, when they contract the pelvic floor muscles. Contracting certain abdominal muscles can be counterproductive, when it increases pressure on the bladder or pelvic floor, and therefore tends to push urine out rather than holding it in. Thus, it is important to observe for this bearing down Valsalva response and to help patients exercise pelvic floor muscles selectively while relaxing these abdominal muscles.
Daily pelvic floor muscle exercise Once patients learn to contract and relax the pelvic floor muscles both properly and selectively, a regime of daily practice and exercise is recommended. The purpose of this regime is not only to increase muscle strength, but also to enhance motor skills through practice. Exercise regimes vary considerably in frequency and intensity, and the optimal exercise regime has yet to be determined. However, good results are generally achieved using 45–50 exercises per day.16,27 It 469
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is usually recommended that patients space the exercises across the day, typically in two to three sessions per day, in order to avoid muscle fatigue. Practicing the exercises while in the lying position is often recommended at first, but it is important to progress patients to sitting or standing positions as well, so that they become comfortable and skilled using their muscles to avoid accidents in any position. To improve muscle strength, contractions should be sustained for 2–10 seconds,33,34 depending on the patient’s initial ability. Exercise regimes can be individualized so that patients begin with a comfortable duration and gradually progress to 10 seconds.34 Each exercise consists of muscle contraction followed by a period of relaxation using a 1:1 or 1:2 ratio.34 This allows the muscles to recover between contractions (see Chapter 32 for more information on pelvic floor muscle training.)
Using muscles to prevent accidents: stress strategies Although exercise alone has been known to improve urethral pressure and structural support and to reduce incontinence,35 the best results seem to be achieved when patients consciously use their muscles to prevent urine loss before and during coughing, sneezing or any other activities that have caused urine loss.27,36 Initially, this new skill requires a conscious effort but, with consistent practice, patients can develop the habit of automatically contracting their muscles to occlude the urethra in situations of physical exertion. This skill has been referred to varyingly as the ‘stress strategy’,27 ‘counterbracing’, ‘the Knack’,36 and ‘the perineal blockage before stress technique’.37 Even when their muscles are weak, some women will benefit from simply learning how to control their pelvic floor muscles and use them to prevent accidents. Others will need a more comprehensive program of pelvic floor muscle rehabilitation to increase strength in addition to skill.
beHaVIORal TRaININg FOR URge INCONTINeNCe
bition can be taught and documented in the clinic (Fig. 31.1). Patients are then encouraged to practice this urge suppression technique to manage urge and prevent incontinent episodes in their daily lives. This technique is now used in many centers as a component in the treatment of urge incontinence. Further, patients can be taught a new way to respond to the sensation of urgency. Most patients with urge incontinence feel compelled to rush to the toilet to void. This behavior can make matters worse because it increases intra-abdominal pressure on the bladder and when the patient reaches the vicinity of the toilet, she is exposed to visual cues that can trigger incontinence. The urge suppression strategy encourages patients to pause, sit down if possible, relax the entire body, and contract pelvic floor muscles repeatedly to diminish urgency, inhibit detrusor contraction and prevent urine loss. After the urge sensation subsides, they are to proceed to the toilet at a normal pace.39 Behavioral training for urge incontinence has been tested in several clinical series utilizing pre-post designs. Mean reductions of incontinence range from 76 to 86%.16,28–30,32,38 In randomized controlled trials using intention-to-treat models, mean reduction of incontinence ranges from 60 to 80%.28,29,38 This urge suppression strategy can be combined with bladder training as one of several coping techniques that can help patients make it to their next scheduled void. It can also be combined with a delayed voiding approach, in which patients are encouraged to wait a specified period of time after they have suppressed the urge. Beginning with short delays (5 minutes) and increasing them incrementally, it is possible to expand the voiding interval and bladder capacity.
Anal sphincter
Using muscles to prevent urge accidents: urge suppression strategies Historically, pelvic floor muscle training and exercise has been used almost exclusively for the treatment of stress incontinence. In the 1980s, however, it became evident that voluntary pelvic floor muscle contraction can also be used not only to occlude the urethra, but also to inhibit detrusor contraction.16,28,38 Detrusor inhi-
Bladder
Figure 31.1. Voluntary contraction of pelvic floor muscles (anal sphincter) accompanied by detrusor inhibition.
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THe blaDDeR DIaRy The bladder or voiding diary is used widely as a tool in the evaluation of incontinence in women. It provides information that helps the clinician to understand the type and severity of urine loss, and to plan appropriate components of behavioral intervention. It is less often recognized for its value in the treatment phase when it can be monitored to determine the efficacy of various treatment components and guide the intervention. In addition to its value for the clinician, completing a daily diary can have direct benefit to the patient. Its self-monitoring effect enhances the patient’s awareness of voiding habits and patterns of incontinence, and facilitates the patient’s recognition of how their incontinence is related to their activities. In particular, understanding clearly the precipitants of urine leakage optimizes the patient’s readiness to implement the continence skills learned through behavioral treatment. At a minimum, the patient should record the time of each incontinent episode and the circumstances or reasons for the accident.39 In behavioral treatment, the circumstances of each incontinent episode noted in the dairy can be reviewed with the patient and used to develop instructions that are specific to the patient’s situation. Through the process of reviewing the bladder diary, patients can identify certain times when they are more likely to have incontinence and activities that seem to trigger incontinence. For example, patients can be made more aware of the antecedents of stress incontinence (e.g. coughing, sneezing) and develop the habit of contracting their pelvic floor muscles in preparation for these situations. In addition to documenting incontinence, it is also very useful to have the patient record the times she urinates, both during the day and at night. These recordings can be used to identify patients who urinate too frequently and to establish appropriate voiding intervals for interventions like bladder training and delayed voiding.
lIFesTyle CHaNges Lifestyle changes are generally used as adjuncts to a primary behavioral intervention in selected cases. Lifestyle changes include fluid management, caffeine reduction, weight loss, and bowel management.
Fluid management Fluid management is a common practice used to make it easier for patients to control their bladder.
Recommendations include alterations in the volume or type of fluids that patients consume. Many patients with incontinence restrict fluid intake as a self-management technique to help avoid incontinence. In some cases, particularly among older women, this results in an inadequate intake of fluid and places them at risk of dehydration. It is important to recognize these cases and to encourage patients, for their overall health and wellbeing, to consume an adequate amount of fluid each day, such as the often recommended 6–8 glasses of fluid per day. In patients who consume an abnormally high volume of liquids, fluid restriction is often appropriate. Some patients maximize their fluid intake deliberately in the belief that they need to ‘flush’ their kidneys, or in an effort to lose weight, or out of concern that they will become dehydrated. In these cases, reducing excess fluids can relieve problems with sudden bladder fullness and urgency. Avoiding fluids in the evening hours is also helpful for reducing nocturia. Caffeinated beverages in particular can exacerbate incontinence because, in addition to being a diuretic, caffeine seems to be a bladder irritant for many people. Although it is very difficult for most coffee drinkers to completely eliminate it from their diet, provided with the knowledge that caffeine may be aggravating their incontinence, many will be willing to reduce caffeine intake. This can be done gradually by mixing decaffeinated beverages with caffeinated beverages in increasing increments. For example, coffees can be mixed to consist of a quarter decaffeinated coffee in week 1, half in week 2, three-quarters in week 3, and full decaffeinated coffee in week 4. Although data are lacking on the role of sugar substitutes, there are clinical cases in which these substances appear to be aggravating incontinence, and reduction of diet drinks has provided clinical improvement.
Weight loss Obesity is an established risk factor for urinary incontinence. Women with a higher body mass index (BMI) are not only more likely to develop incontinence, but they also tend to have more severe incontinence than women with a lower BMI. Research on the relationship between BMI and incontinence reports that each fiveunit increase in BMI increases the risk of daily incontinence by approximately 60%.40,41 Intervention studies of morbidly obese women report significant improvement in symptoms of incontinence with weight loss of 45–50 kg following bariatric surgery.42,43 Similarly, significant improvements in continence status have been demon471
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strated with as little as 5% weight reduction in more traditional weight loss programs.44 Because this is an achievable goal for many women, it is rational to recommend weight loss as part of a comprehensive program to treat incontinence in overweight women.
bowel management Fecal impaction and constipation have been cited as factors contributing to urinary incontinence in women, particularly in nursing home populations.45 In severe cases, fecal impaction can be an irritating factor in overactive bladder or obstruct normal voiding, causing incomplete bladder emptying and overflow incontinence. Disimpaction relieves symptoms for some patients, but it can recur in the absence of a bowel management program. Bowel management may consist of recommendations for a normal fluid intake and dietary fiber (or supplements) to maintain normal stool consistency and regular bowel movements. When hydration and fiber are not enough, enemas may be used to stimulate a regular daily bowel movement, preferably after a regular meal such as breakfast to take advantage of postprandial motility.
eNCOURagINg PaTIeNT PaRTICIPaTION The success of behavioral treatment depends on the active participation of a motivated patient, and this reliance on patient behavior change represents the major limitation of this treatment approach. Like any new habit or skill, changing daily bladder habits and learning new skills requires some effort and persistence over time. It can be challenging to remember to use muscles strategically in daily life, as well as to maintain a regular exercise regime for strength and skill. Unlike with some therapies, progress with behavioral treatment is often gradual, presenting the primary challenge for behavioral treatment – how to sustain the patient’s motivation for a long enough time that she will experience noticeable change in her bladder control. A key ingredient in addressing this problem is to maintain contact with the patient during the period when her benefit is not yet appreciable. Rather than leaving the patient on her own, it is essential that clinicians support her efforts to persist by scheduling follow-up appointments to review and reinforce her progress, and to make any needed adjustments to her daily regime. In addition, when initiating behavioral treatment, it is important to make it clear to the patient that her improvement, as with any new skill, will likely be gradual, and that it will depend on her consistent practice.
The patient who expects this course of treatment will be better prepared to persist over time until results can be achieved.
ReFeReNCes 1. NIH Consensus Conference. Urinary incontinence in adults. JAMA 1989;261:2685–96. 2. Fantl JA, Newman DK, Colling J et al. Urinary incontinence in adults: acute and chronic management. Clinical Practice Guideline, No. 2 1996 Update; Rockville, MD: U.S. Department of Health and Human Services. Public Health Service, Agency for Health Care Policy and Research. AHCPR Publication No. 96-0682. 3. Frewen WK. Role of bladder training in the treatment of the unstable bladder in the female. Urol Clin North Am 1979;6:273–7. 4. Frewen WK. A reassessment of bladder training in detrusor dysfunction in the female. Br J Urol 1982;54:372–3; Gynaecology 1979;96:607–12. 5. Elder DD, Stephenson TP. An assessment of the Frewen regime in the treatment of detrusor dysfunction in females. Br J Urol 1980;52:467–71. 6. Jarvis GJ, Millar DR. Controlled trial of bladder drill for detrusor instability. Br Med J 1980;281:1322–3. 7. Jarvis GJ. A controlled trial of bladder drill and drug therapy in the management of detrusor instability. J Urol 1981;53:565–6. 8. Jarvis GJ. The management of urinary incontinence due to primary vesical sensory urgency by bladder drill. Br J Urol 1982;54:374–6. 9. Pengelly AW, Booth CM. A prospective trial of bladder training as treatment for detrusor instability. Br J Urol 1980;52:463–6. 10. Svigos JM, Matthews CD. Assessment and treatment of female urinary incontinence by cystometrogram and bladder retraining programs. Obstet Gynecol 1977;50:9–12. 11. Jeffcoate TNA, Francis WJ. Urgency incontinence in the female. Am J Obstet Gynecol 1966;94:604–18. 12. Fantl JA, Wyman JF, McClish DK et al. Efficacy of bladder training in older women with urinary incontinence. JAMA 1991;265:609–13. 13. Colombo M, Zanetta G, Scalambrino S, Milani R. Oxybutynin and bladder training in the management of female urinary urge incontinence: a randomized study. Int Urogynecol J 1995;6:63–7. 14. Kegel AH. Progressive resistance exercise in the functional restoration of the perineal muscles. Am J Obstet Gynecol 1948;56:238–48. 15. Kegel AH. Stress incontinence of urine in women: physiologic treatment. J Int Coll Surg 1956;25:487–99. 16. Burgio KL, Whitehead WE, Engel BT. Urinary incon-
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tinence in the elderly: bladder-sphincter biofeedback and toileting skills training. Ann Intern Med 1985;104:507–15. 17. Burns PA, Pranikoff K, Nochajski TH, Hadley EC, Levy KJ, Ory MG. A comparison of effectiveness of biofeedback and pelvic muscle exercise treatment of stress incontinence in older community-dwelling women. J Gerontol 1993;48:167–74. 18. Wells TJ, Brink CA, Diokno AD, Wolfe R, Gillis GL. Pelvic muscle exercise for stress urinary incontinence in elderly women. J Am Geriatr Soc 1991;39:785–91. 19. Dougherty M, Bishop K, Mooney R, Gimotty P, Williams B. Graded pelvic muscle exercise. Effect on stress urinary incontinence. J Reprod Med 1993;39:684–91. 20. Berghmans LCM, Frederiks CMA, de Bie RA. Efficacy of biofeedback when included with pelvic floor muscle exercise treatment for genuine stress incontinence. Neurourol Urodyn 1996;15:37–52. 21. Nygaard IE, Kreder KJ, Lepic MM, Fountain KA, Rhomberg AT. Efficacy of pelvic floor muscle exercises in women with stress, urge, and mixed urinary incontinence. Am J Obstet Gynecol 1996;174:120–5. 22. Bo K, Talseth T. Single blind randomized controlled trial of pelvic floor exercises, electrical stimulation, vaginal cones, and no treatment in management of genuine stress incontinence in women. BMJ 1999;318:487–93. 23. Wilson PD, Herbison GP. A randomized controlled trial of pelvic floor muscle exercises to treat postnatal urinary incontinence. Int Urogynecol J 1998;9:257–64. 24. Wilson PD, Herbison GP, Glazener CMA, Lang G, Gee H, MacArthur C. Postnatal incontinence: a multicenter, randomized controlled trial of conservative treatment. Neurourol Urodyn 1997;16:349–50. 25. Glazener CM, Herbison GP, Wilson PD, MacArthey C, Lang GD, Gee H, Grant A. Conservative management of persistent postnatal urinary and faecal incontinence: a randomized controlled trial. BMJ 2001;323:1–5. 26. Morkved S, Bo K. Effect of postpartum pelvic floor muscle training in prevention and treatment of urinary incontinence: a one-year follow-up. Br J Obstet Gynaecol 2000;107:1022–8. 27. Goode PS, Burgio KL, Locher JL et al. Effect of behavioral training with or without pelvic floor electrical stimulation on stress incontinence in women: a randomized controlled trial. JAMA 2003;290:345–52.
ing urinary incontinence in community-residing elderly persons. Gerontologist 1989;29(2):229–33. 31. Burgio KL, Robinson JC, Engel BT. The role of biofeedback in Kegel exercise training for stress urinary incontinence. Am J Obstet Gynecol 1986;157:58–64. 32. McDowell BJ, Burgio KL, Dombrowski M, Locher JL, Rodriguez E. Interdisciplinary approach to the assessment and behavioral treatment of urinary incontinence in geriatric outpatients. J Am Geriatr Soc 1992;40:370–4. 33. American College of Sports Medicine. ACSM’s Guidelines for Exercise Testing and Prescription, 2nd ed. Philadelphia: Lea & Febiger, 1993. 34. Kisner C, Colby LA. Therapeutic Exercise. Foundations and Techniques, 4th ed. Philadelphia: FA Davis, 2003. 35. Bo K. Pelvic floor muscle exercise for the treatment of stress urinary incontinence: an exercise physiology perspective. Int Urogynecol J 1995;6:282–91. 36. Miller JM, Ashton-Miller JA, DeLancey J. A pelvic muscle pre-contraction can reduce cough-related urine loss in selected women with mild SUI. J Am Geriatr Soc 1998;46:870–4. 37. Bourcier AP, Juras JC, Jacquetin B. Urinary incontinence in physically active and sportswomen. In: Appell RA, Bourcier AP, La Torre F (eds) Pelvic Floor Dysfunction: Investigations and Conservative Treatment. Rome: C.E.S.I., 1999; 9–17. 38. Burton JR, Pearce KL, Burgio KL, Engel BT, Whitehead WE. Behavioral training for urinary incontinence in elderly ambulatory patients. J Am Geriatr Soc 1988;36:693–8. 39. Burgio KL, Pearce KL, Lucco AJ. Staying Dry: A Practical Guide to Bladder Control. Baltimore: Johns Hopkins University Press, 1989. 40. Brown J, Seeley D, Feng J et al. Urinary incontinence in older women: who is at risk? Study of Osteoporotic Fractures Research Group. Obstet Gynecol 1996;87:715–721. 41. Brown J, Grady D, Ouslander J, Herzog A, Varner RE, Posner S. Prevalence of urinary incontinence and associated risk factors in postmenopausal women. Heart & Estrogen/ Progestin Replacement Study (HERS) Research Group. Obstet Gynecol 1999;94:66–70. 42. Bump R, Sugerman H, Fantl J et al. Obesity and lower urinary tract function in women: effect of surgically induced weight loss. Am J Obstet Gynecol 1992;166:392–9.
28. Burgio KL, Locher JL, Goode PS et al. Behavioral versus drug treatment for urge incontinence in older women: a randomized clinical trial. JAMA 1998;23:1995–2000.
43. Deitel M, Stone E, Kassam HA et al. Gynecologic–obstetric changes after loss of massive excess weight following bariatric surgery. J Am Coll Nutr 1988;7:147–53.
29. Burgio KL, Goode PS, Locher JL et al. Behavioral training with and without biofeedback in the treatment of urge incontinence in older women: a randomized controlled trial. JAMA 2002;288:2293–9.
44. Subak LL, Johnson CEW, Boban D et al. Does weight loss improve incontinence in moderately obese women? Int Urogynecol J Pelvic Floor Dysfunct 2002;13:40–3.
30. Baigis-Smith J, Smith DAJ, Rose M, Newman DK. Manag-
45. Ouslander JG, Schnelle JF. Incontinence in the nursing home. Ann Intern Med 1995;122:438–49.
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32 Physiotherapy for urinary incontinence Jeanette Haslam
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IntroductIon Physiotherapists in the UK have been involved in the treatment of pelvic floor conditions for many years.1 Over time, ‘Women’s Health Physiotherapy’ has developed into a postgraduate specialty with specific continence training encompassing muscular rehabilitation and other behavioral therapies to ensure optimum holistic care. Physiotherapists are trained to have good communication skills and are part of the multiprofessional team that provides continence advice. There are many modalities available to physiotherapists to rehabilitate the pelvic floor musculature and to affect the continence mechanism. Outcomes depend on the integrity of the neurologic system and urethral sphincter mechanism, collagen type, and any damage to the pelvic floor muscles (PFM). Other relevant factors are patient mobility, manual dexterity, environment, likely adherence to therapy, and the therapist’s availability, knowledge, expertise, and ability to motivate the woman. Conservative therapies are recommended as first line treatment by many authorities.2,3
PhysIotheraPeutIc InterventIons Although physiotherapy skills can be employed to some extent in all forms of incontinence, the principal types treated are stress urinary incontinence (SUI), urge urinary incontinence (UUI), and mixed urinary incontinence. The main modalities of treatment employed are pelvic floor muscle exercise (PFME), a variety of forms of biofeedback, and neuromuscular stimulation. There are also other treatment modalities that are increasingly being used, but as yet do not have good research-based evidence to underpin their use in the female incontinent population. A systematic review of randomized clinical trials on the conservative treatment of SUI found strong evidence to suggest that PFME is an effective therapy in the treatment of SUI.4 Biofeedback in combination with PFME was not found to be a more effective adjunct to PFME alone in the treatment of SUI. However, a later meta-analysis concluded that biofeedback might be an important adjunct to PFME.5 Evidence of the effectiveness of electrical stimulation is clouded by the different parameters chosen for studies. The Cochrane review group concluded that PFM training was better than no treatment or placebo treatment, that intensive exercise was better than standard PFM training, and that the effect of adding PFM training to other therapies to the pelvic floor is not clear.6
assessment verbal assessment All women, whatever their type of urinary incontinence, need to have an appropriate examination and assessment prior to the commencement of therapy. There is an increasing interest in the use of assessment proforma that can move with the patient rather than them being asked the same questions by different health professionals when visiting different departments. However, the time taken to ascertain a full patient history can assist in establishing a good therapeutic relationship with the woman, as well as to eventually assist with motivation and compliance with the recommended therapy. The history taking should be able to elicit relevant factors from the patient’s obstetric, gynecologic, medical, surgical, and family history. It is also necessary to determine the way that their urinary problem has affected their quality of life and also their expectations of therapy. Full details of history taking can be found in Laycock.7 Urinalysis should be considered mandatory if there are any symptoms of urgency or frequency. A bladder diary (frequency/volume chart) noting types, volumes, and times of fluid taken, and times and amounts of urine voided should also be completed by the woman, with episodes of leakage and possible cause noted (for further details, see Chapter 13). After valid consent8 has been obtained, a physical examination is essential. It has been shown9,10 that verbal and written instructions are insufficient for some women to be able to perform adequate PFM contractions; some women bear down, believing that they are contracting their PFM. Therefore, only providing a leaflet or describing PFME may be useless or even harmful. Prior to any examination it should be ensured that there are private facilities for the patient to undress and for the examination to take place.11 The Royal College of Obstetricians and Gynaecologists (RCOG) further recommend that ideally a professional chaperone should be available, not a relative or friend.12 However, the General Medical Council13 have advised that whenever possible a patient should be offered a chaperone, but alternatively they may be invited to bring a friend or relative to the consultation. Most physiotherapy practices would be unable to provide a ‘professional chaperone’, but all patients should be advised that they are welcome to bring someone with them if they so wish. Professional interpreters should be used if there is a need; family members should not be used. In order to gain valid consent, the relevant anatomy should be explained prior to examination; it should also be made clear that consent can be withdrawn at any time
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without need for explanation. It is also sensible to give verbal instructions regarding PFM contractions prior to the examination. A thorough PFM assessment is necessary to ensure that any prescribed exercise regime is possible and appropriate to the individual, and also to determine if the woman is suitable for devices such as vaginal cones or electrodes. Examination of the abdomen and vagina is required to determine if there are any other possible contributory factors such as an abdominal mass (constipation, pregnancy or tumor) or prolapse. If there is cause for concern after testing the relevant dermatomes and myotomes (S2–4),7 the woman should be referred for a further neurologic assessment. The assessment leads to appropriate therapy for SUI with the aim of teaching ‘the knack’14 and improving muscle volume and structural support.15 For UUI the aim is to determine appropriate therapy to improve reflex activity,16 and to provide other behavioral therapy (see Chapter 31).
digital assessment Any known latex allergy should be ascertained prior to digital assessment and appropriate gloves used. The woman should be made comfortable in crook supine lying, suitably covered. Assessment should take place in good light so that skin condition can be observed and any lesions, excoriation, soreness or signs of irritation seen. The labia need to be separated so that a full examination can take place, with any odors, discharge, introital gaping, prolapse or atrophic vaginitis being noted. A cough can reveal any effect on perineal descent, urine loss, and prolapse status. The woman should then be asked to contract her PFM; a perineal lift denotes at least a grade 3 contraction on the Oxford scale;17 any breath holding or co-contraction of other muscle groups should be noted. The lubricated index finger is then introduced 3–5 cm into the vagina to palpate the full 360° of the vagina. Any areas of tenderness, soreness, scarring, reduced or lack of sensation, spasm, laxity, narrowing or other irregutable 32.1.
larities are ascertained, with differences between the left and right noted. During a cough, the examining finger can be hooked over the PFM to palpate any reflex contraction, or palpate the anterior vaginal wall to detect any bladder neck descent. Specific PFM examination then determines the grade, contractility, and endurance, and the appropriate starting point for an exercise regime. The PFM are composed of striated fibers – both slow-twitch (tonic) fibers and fast-twitch (phasic) fibers – under voluntary control. Some women have little sensory awareness or motor ability to contract the PFM, and some carry out other accompanying accessory movements. Palpation during the examination can increase cerebral awareness; therefore the assessment is not only the time of determining muscle grade and exercise regime but also the time for correcting technique with application to teaching the ‘knack’. Further assessment techniques can be found in Laycock.7 The modified Oxford scale17 is found useful in clinical practice when examining a woman despite the viewpoint that it is not well enough validated. The modified Oxford scale (Table 32.1) has been shown to correlate well with surface electromyography and manometry of the PFM.18 Contrary to previous beliefs that the pudendal nerve supplies all of the PFM, it has been found that the pudendal nerve (S2–4 nerve root) supplies the urethral sphincter and superficial PFM, whilst the levator ani (S3–5) is said to have a separate nerve supply.19 Although this should make no difference to the way that the pelvic floor is assessed, additional note should perhaps be made of superficial pelvic floor muscle activity.
theraPeutIc InterventIons Pelvic floor muscle exercise Training of the PFM should be initially considered as it is an effective, low risk intervention that will significantly
The modified Oxford scale for the pelvic floor muscles (PFM)
Muscle grade
External observation
Internal examination explanation
0
No indrawing movement of the perineal body
No activity detected
An indrawing movement of the perineal body
A moderate PFM lift but without resistance
1 2 3 4 5
A mere flicker of activity A weak contraction without PFM lift A good capability to lift PFM against some resistance An ability to lift PFM against more resistance with a strong grip of the examining digit
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contribute towards reducing incontinence.2 However, there is little point in embarking on an exercise regime without having ascertained the likely adherence and motivation of the woman.20 Realism is essential, and the woman must realize that there is no ‘quick fix’. There is no randomized controlled trial that has determined the most efficacious PFM exercise regime. The exercise science literature of DiNubile21 – which recommends three sets of 8–12 slow velocity maximum PFM contractions sustained for 6–8 seconds each, performed three to four times a week for at least 15–20 weeks – is often cited. It should not, however, be assumed that this is an appropriate regime for all women, as DiNubile21 viewed muscle training from an orthopedic view regarding athletic performance, not specifically for the needs of individual women with PFM dysfunction. He did, however, discuss the need to consider overload and specificity in order to strengthen muscle; that is, muscles need to be made to work harder than usual and exercised in a way that is specific and similar to normal usage, i.e. functionally. Therefore, a starting point needs to be decided, depending on the fatigability of the PFM. There is a need to determine the number of sustained contractions that can be held for up to 10 seconds, with at least a 4-second rest between each contraction; in some women this may be as little as 2-second contractions repeated twice. After a short rest of approximately 1 minute the woman is then asked to attempt 1-second maximum holds as quickly and strongly as she can (up to ten contractions). These tonic and phasic contractions form the basis for a personalized exercise plan. Progression over the following weeks is made by increasing the length of PFM hold, shortening the rest phase between the contractions and increasing the number of contractions at each exercise session. Women are best advised to exercise in functional positions – such as sitting or standing – with concentrated effort three times a day. If requested to exercise too frequently women often forget and then have a resulting sense of failure. Goal setting and discussing the appropriate times to exercise will increase patient motivation;20 this may be significantly affected by the physiotherapist’s enthusiasm, realism, and knowledge. The purpose of PFM strength training is to form a better structural support by hypertrophying the PFM, and increasing PFM and the connective tissue stiffness, hence facilitating more effective motor unit firing.15 It has been shown that women who are taught to use a pretimed PFM contraction prior to occasions of increased intra-abdominal pressure (known as ‘the knack’) have decreased vesical neck mobility.22 Therefore a PFM contraction timed prior to the stress activity can aug-
ment proximal urethral support during that activity. It may be by practicing ‘the knack’ that reflex activity is encouraged.23 All referred women need to be seen on an individual basis for both initial assessment and progress update. However, PFM exercise groups have become popular as an initial meeting point to impart information, to give peer group support, and to use as group activity sessions to improve motivation and adherence. It has also been shown that 6 months of PFM classes can also successfully contribute to an improvement in quality of life and sex life.24 Pragmatically, the physiotherapist has to work within given resources; this may include an exercise group. Women should be encouraged to exercise three times a day regardless of whether they attend a group or not. There may be some early improvement in the first 6 weeks due to improved cortical awareness of the PFM and the use of ‘the knack’, although it is generally recognized that to gain maximal effect, muscle training requires 20 weeks. However, it has been shown by Balmforth et al.25 that an intensive training period of 14 weeks, consisting of individualized PFM program and behavioral modification resulted in a statistically significant elevation of the bladder neck at rest, maximum PFM contraction, and on Valsalva. This suggests improvement of the PFM and in the overall ‘stiffness’ of the connective tissue sheaths as discussed by Bø.15 If little or no PFM contraction can be elicited by instruction, verbal feedback, and proprioception, neuromuscular electrical stimulation (NMES) is likely to be considered appropriate.
neuromuscular electrical stimulation Neuromuscular electrical stimulation (NMES) can be used to achieve awareness of appropriate activity. This ‘awareness’ can be utilized by the woman to make a conscious attempt to join in with the stimulated contraction. The aim is one of being able to eventually initiate a PFM contraction herself and be able to participate in a PFM exercise program. It has been found that voluntary contraction of the PFM is twice as effective as an electrically stimulated contraction at increasing urethral pressure.26 It has also been shown that a structured program of PFME is more effective than a course of NMES.27 This may be because there is a fundamental difference between exercise and NMES. A vaginal electrode ensures that there is close proximity to the PFM to be stimulated. However, the effectiveness of the stimulation is limited by the intensity of current tolerated by the patient. Current will always take the easiest pathway which is via the largest nerve fibers close to the electrode causing a
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synchronous contraction of the muscle fibers supplied (Table 32.2). The research-based evidence for NMES is inconclusive, with many different parameters being used but with authors claiming success. Wilson et al.28 conclude that there is insufficient evidence to judge if NMES is better than no treatment for women with SUI; further research is necessary to provide proof of worth for a specific regime. A review of the various types of stimulation concluded that there is a 30–50% clinical success on intent to treat basis.29 Any clinician deciding to use NMES for incontinence must fully understand the rationale behind the different parameters used. Despite the lack of definitive research evidence for a specific regime, clinicians still need to use NMES for those women in whom other methods of eliciting a PFM contraction have failed. Care must be taken regarding contraindications and precautions (Table 32.3). The recommendation in the UK for comfort and effectiveness is for CE marked equipment to be used (to ensure that the product meets the essential requirements of all relevant European Directives), providing a biphasic rectangular pulse with constant current. Parameters advocated for SUI are a frequency of 35– 40 Hz, 250 microseconds pulse duration, to produce a forceful contraction while minimizing any possible adverse affects due to fatigue.30 The duty cycle should be such that the off time is double the on time. The treatment duration is determined on an individual basis, but the clinician is well advised to start with 5 minutes NMES and monitor any adverse effects, then gradually build up the treatment time to 25–30 minutes. The parameters recommended for treating UUI, however, are 5–10 Hz, 500 microseconds pulse duration, with a continuous duty cycle or one with short rest periods.30 The woman should be encouraged to have maximum stimulation of up to 80 mA rms. The aim is one of reflex activation of sympathetic hypogastric inhibitory neurons and reflex central inhibition of pelvic parasympathetic excitatory neurons.31 Home treatment units make daily therapy table 32.2.
Differences between exercise and neuromuscular electrical stimulation (NMES)
Recruitment depends on
Exercise
NMES
Size of motor nerves
Small to large
Large to small
Depth of muscle
Deep to superficial
Superficial to deep
Firing of motor units
Asynchronous
Synchronous
table 32.3.
Contraindications and precautions to neuromuscular electrical stimulation (NMES)
1. Contraindications • Lack of valid consent: this includes any inability to understand the treatment • Implanted pacemaker • Known pregnancy • Recent hemorrhage, hematoma, vaginal or perineal tissue damage • Infection or inflammation of the vagina or vulva • Lack of sensation • Malignancy in the area undergoing active treatment • Allergic reaction to electrode or gel 2. Treat prior to any NMES • Atrophic vaginitis • Urinary tract infection 3. Precautions • History of sexual abuse: unlikely that NMES is appropriate – but external electrodes may be considered appropriate • Diabetes: do not use if poor tissue quality or nerve damage • Epilepsy: ensure that the woman is not alone during treatment • Hypotension or hypertension – ensure that the blood pressure is controlled
possible with NMES, whereas the need to attend a clinic will probably limit treatment to two to three times per week. The vaginal electrodes that are used must be CE marked, be able to have good contact with the tissues, and be used with a water-based gel. If electrodes are for single patient multiple use, they must be cleansed and stored appropriately.32 Magnetic stimulation has also been used in some research studies33,34 but at present it is not in common use and there is insufficient robust evidence to prove its value.
Biofeedback Urinary incontinence normally occurs in an upright position; it is therefore necessary to ensure that the woman is able to exercise her PFM in sitting, standing, and during activities. It is for this reason that a variety of methods of biofeedback have been found useful. Biofeedback in essence is the utilization of any of the senses to gain further knowledge of bodily processes. This can be by the initial feedback given during vaginal assessment to the use of more complicated computerized equipment as shown in Figure 32.1. 479
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Figure 32.1. Myomed biofeedback equipment (Enraf Nonius, Netherlands).
In the UK, biofeedback is used extensively by clinicians to give women a greater insight into their PFM activity and is always associated with an appropriate PFME regime.
Vaginal palpation Vaginal palpation can be used to give increased proprioception to ensure that a woman is able to understand which muscles to contract. Putting the PFM on the stretch in a posterolateral direction during the vaginal assessment can enhance the proprioception. Self-examination may also be taught, but it should not be assumed that all women would be happy to do this.35
of the cone is increased and the procedure starts again. Cones can also be used as resistance exercise tools. However, it has been shown radiographically that vaginal cones can be retained by assuming a horizontal position in a flaccid vagina rather than by PFM activity.39 There are no studies that show cones to be effective as a preventive therapy for incontinence.
The pelvic floor educator This device (Neen, Mobilis healthcare group) was developed from the Periform (Neen, Mobilis health-
Vaginal cones Vaginal cones were first reported as a successful therapeutic intervention in 1985.36 This was followed by a 1-month study of 39 women, with a 70% subjective improvement being reported by the 30 women completing the study.37 A Cochrane Review of all vaginal cone studies concluded that vaginal cones are similar in effect to PFM training and NMES, but that larger high quality studies are necessary.38 There are a variety of cones on the market of different sizes and weights (Fig. 32.2). The clinician has to ensure by assessment that the appropriate weight and shape of cone is used. In clinical practice, the appropriate weight of cone is determined (the one that a woman can retain in the vagina while walking for 1 minute), then the woman attempts to retain the cone for increasing lengths of time and increasing levels of activity. When she is able to retain the cone for 15 minutes, the weight
Figure 32.2. Aquaflex vaginal cones (Neen, Mobilis healthcare group).
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care group) vaginal electrode in the late 1990s. The body of the educator is retained within the vagina, with an external indicator (Fig. 32.3). A downward deflection of the indicator shows an appropriate PFM contraction, whereas an incorrect Valsalva maneuver results in an upward deflection. This utilizes similar principles to those espoused in the intraurethral ‘Q tip-test’.40 Although there is no research base to the use of the educator, many women find it a useful self-help strategy to ensure that they are performing a correct PFM contraction. Some clinicians have used the same principle when using a vaginal Periform electrode for stimulation; the external indicator can be seen to move downwards when there is sufficient stimulation to the PFM.
Manometry Manometry has been used extensively as a method of biofeedback. Kegel41 was responsible for the earliest vaginal manometers, and these have been further developed over many years into sophisticated computerized devices. There can be many problems with manometry, the greatest being that of ensuring an accurate maintained position. If the probe is badly positioned in the upper vagina it is likely to be recording intra-abdominal
pressure and not that generated by the PFM.42 There may also be problems with the degree of pressure probe inflation. Due to problems with both this and the use of manometry in functional upright positions, it now tends to have been superseded by the use of electromyography (EMG).
Electromyography EMG records muscle bioelectrical activity and is a practical indicator of muscle contractility.43 Surface EMG is a monitor of, and not a measure of, activity; each machine is its own reference and there can be no transferability of outcomes between machines with variable electrode placement giving different readings. EMG can therefore be very usefully employed as an additional visual and auditory method of giving women further insight into PFM activity but cannot be used to provide outcome measures. The main advantages to surface EMG is that it is easy to use, is painless, functional positions can be used, and women can focus on the appropriate PFM activity while performing different functional activities. It can be seen in Figure 32.4a that there is a sluggish, poorly held contraction, whereas in Figure 32.4b there is a good contraction shown on surface EMG using a Periform electrode. Again using a Periform electrode, Figure 32.5a shows poorly controlled fast contractions, with Figure 32.5b showing good fast contractions. These studies illustrate how surface EMG can be utilized to increase a woman’s awareness of her PFM ability.
Real time ultrasound This technique is increasingly being used as a tool for biofeedback. It has the advantage of actually visualizing PFM activity. To date it has been used extensively as a research tool for recording bladder neck movement during a variety of activities. It has also been used as a tool for teaching PFME.44 Currently there is increasing clinical use of ultrasound biofeedback but as yet there is no substantial study that shows its effectiveness as a reliable tool for biofeedback therapy.
other physiotherapy techniques
Figure 32.3. The pelvic floor educator (Neen, Mobilis healthcare group).
Other techniques that are employed have insufficient rigorous research as yet to prove their clinical effectiveness. The main technique espoused by physiotherapists is that of co-contraction of the transversus abdominis muscles to either reinforce or even activate a PFM contraction. However, the studies so far are all small in number in a largely continent population. Bø15 reviewed the literature and concluded that there should be caution 481
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a
a
b
b
Figure 32.4. (a) Surface EMG sluggish, poorly held contraction; (b) surface EMG good contraction.
in transferring the findings of small studies of the continent population to that of incontinent women. It is being increasingly believed that an assessment of the whole pelvic girdle and its joints may also be essential; any misalignments can then be corrected and appropriate exercise advised. Other modalities used include connective tissue mobilization, proprioceptive neuromuscular facilitation, and the use of breathing patterns, reflex therapy and acupuncture as useful adjuncts to treatment. Again there is no substantial research-based evidence as yet to show the value of any of these therapies. The next decade or so will hopefully see further high quality research taking place to determine which techniques are truly effective. The physiotherapist should be encouraged to participate in such relevant research and not merely rely on evidence-based practice.
Figure 32.5. (a) Surface EMG poorly controlled fast contractions; (b) surface EMG good quality fast contractions.
reFerences 1. Haslam J. Margie Polden Memorial lecture. The continuing challenge of childbirth and the pelvic floor. J Assoc Chartered Physiother Women’s Health 2004;94:4–10. 2. Fantl JA, Newman DK, Colling J et al. Urinary Incontinence in Adults: Acute and Chronic Management. Clinical Practice Guideline No. 2, 1996 Update. Rockville, MD: U.S. Department of Health and Human Services. Public Health Service, Agency for Health Care Policy and Research. AHCPR Publication No. 96-0682. 1996; 36–8. 3. Department of Health. Good practice in continence services. London: Department of Health, 2000; 10–6. 4. Berghmans LCM, Hendriks HJM, Bø K et al. Conservative treatment of stress urinary incontinence in women: a
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systematic review of randomized clinical trials. Br J Urol 1998;82:181–91. 5. Weatherall M. Biofeedback or pelvic floor muscle exercises for female genuine stress incontinence: a metaanalysis of trials identified in a systematic review. BJU Int 1999;83:1015–6. 6. Hay-Smith EJC, Bø K, Berghmans LCM et al. Pelvic floor muscle training for urinary incontinence in women (Cochrane Review). In: The Cochrane Library, Issue 4, 2002. Oxford: Update Software. 7. Laycock J. Patient assessment. In: Laycock J, Haslam J (eds) Therapeutic Management of Incontinence and Pelvic Pain. London: Springer, 2002; 45–54. 8. Department of Health. Reference guide to consent for examination or treatment. London: Department of Health, 2001; 4–11. 9. Bø K, Larsen S, Oseid S et al. Knowledge about and ability to correct pelvic floor muscle exercises in women with stress urinary incontinence. Neurourol Urodyn 1988;69:261–2. 10. Bump RC, Hurt WG, Fantl JA, Wyman JA. Assessment of Kegel pelvic muscle exercise performance after brief verbal instruction. Am J Obstet Gynecol 1991;165:322–9. 11. Royal College of Obstetricians and Gynaecologists. Intimate examinations: report of a working party. London: RCOG Press, 1997; 3–5. 12. Royal College of Obstetricians and Gynaecologists. Gynaecological examinations: guidelines for specialist practice. London: RCOG Press, 2002; 2–4, 25.
22. Miller JM, Perucchini D, Carchidi LT, DeLancey JO, Ashton-Miller J. Pelvic floor muscle contraction during a cough and decreased vesical neck mobility. Obstet Gynecol 2001;97:255–60. 23. Constantinou CE, Govan DE. Spatial distribution and timing of transmitted and reflexly generated urethral pressures in healthy women. J Urol 1982;127:964–9. 24. Bø K, Talseth T, Vinsnes A. Randomized controlled trial on the effect of pelvic floor muscle training on quality of life and sexual problems in genuine stress incontinent women. Acta Obstet Gynecol Scand 2000;79:598–603. 25. Balmforth J, Bidmead J, Cardozo L et al. Raising the tone: a prospective observational study evaluating the effect of pelvic floor muscle training on bladder neck mobility and associated improvement in stress urinary incontinence. Neurourol Urodyn 2004;23:553–4. 26. Bø K, Talseth T. Change in urethral pressure during voluntary pelvic floor muscle contraction and vaginal electrical stimulation. Int Urogynaecol J 1997;8:3–7. 27. Bø K, Talseth T, Holme I. Single blind, randomised controlled trial of pelvic floor exercises, electrical stimulation, vaginal cones, and no treatment in management of genuine stress incontinence in women. BMJ 1999;318:487–93. 28. Wilson PD, Bø K, Hay-Smith J et al. Conservative treatment in women. In: Abrams P, Cardozo L, Khoury S, Wein A (eds) Incontinence, 2nd ed. London: Health Publication, 2002; 573–624.
13. General Medical Council. Online. Available: www.gmcuk.org.
29. Van Balken MR, Vergunst H, Bemelmans BLH. The use of electrical devices for the treatment of bladder dysfunction: a review of methods. J Urol 2004;172:846–51.
14. Miller JM, Ashton-Miller JA, DeLancey JOL. A pelvic muscle pre-contraction can reduce cough related urine loss in selected women with mild SUI. JAGS 1998;46:870–4.
30. Laycock J, Vodusek DB. Electrical stimulation. In: Laycock J, Haslam J (eds) Therapeutic Management of Incontinence and Pelvic Pain. London: Springer, 2002; 85–9.
15. Bø K. Pelvic floor muscle training is effective in treatment of female stress urinary incontinence, but how does it work? Int Urogynaecol J 2004;15:76–84.
31. Lindstrom S, Fall M, Carlsson CA et al. The neurophysiological basis of bladder inhibition in response to intravaginal electrical stimulation. J Urol 1983;129;405–10.
16. Mahoney DT, Laferte OR, Blais DJ. Integral storage and voiding reflexes. Urology 1980;IX:95–106. 17. Laycock J, Jerwood D. Pelvic floor assessment: the PERFECT scheme. Physiotherapy 2001;87:631–42.
32. Barkess-Jones L, Haslam J. Infection control issues. In: Laycock J, Haslam J (eds) Therapeutic Management of Incontinence and Pelvic Pain. London: Springer, 2002; 243–8.
18. Haslam J. Evaluation of pelvic floor muscle assessment, digital, manometric and surface electromyography in females. MPhil Thesis. University of Manchester, 1999.
33. Galloway NT, El-Galley RE, Sand PK et al. Extracorporeal magnetic innervation therapy for stress urinary incontinence. Urology 1999;53:1108–11.
19. Barber MD, Bremer RE, Thor KB et al. Innervation of the female levator ani muscles. Am J Obstet Gynecol 2002;187:64–71.
34. Unsal A, Saglam R, Cimentepe E. Extracorporeal magnetic stimulation for the treatment of stress and urge incontinence in women – results of 1-year follow-up. Scand J Urol Nephrol 2003;37:424–8.
20. Chiarelli P. Improving patients’ adherence. In: Laycock J, Haslam J (eds) Therapeutic Management of Incontinence and Pelvic Pain. London: Springer, 2002; 73–4. 21. DiNubile NA. Strength training. Clin Sports Med 1991;10:33–62.
35. Prashar S, Simons A, Bryant C et al. Attitudes to vaginal/ urethral touching and device placement in women with urinary incontinence. Int Urogynecol J Pelvic Floor Dysfunct 2000;11:4–8.
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36. Plevnik S. New method for testing and strengthening of pelvic floor muscles. In: Proceedings of the 15th Annual Meeting, International Continence Society, 1985; 267–8. 37. Peattie AB, Plevnik S. Vaginal cones: a conservative method of treating genuine stress incontinence. BJOG 1988;95:1049–53. 38. Herbison P, Plevnik S, Mantle J. Weighted vaginal cones for urinary incontinence (Cochrane Review). In: The Cochrane Library, Issue 4, 2001. Oxford: Update Software. 39. Hahn I, Milson I, Ohlsson B et al. Comparative assessment of pelvic floor function using vaginal cones, vaginal digital palpation and vaginal pressure measurements. Gynecol Obstet Invest 1996;41:269–74.
40. Crystal D, Charme L, Copeland W. Q-tip test in stress urinary incontinence. Obstet Gynecol 1971;38:313–5. 41. Kegel AH. Progressive resistance exercises in the functional restoration of the perineal muscles. Am J Obstet Gynecol 1948;36:238–48. 42. Whyte TD, McNally DS, James ED. Six-element sensor for measuring vaginal pressure profiles. Med Biol Eng Comput 1993;31:184–6. 43. Vodusek D. Electrophysiology. In: Schussler B, Laycock J, Norton P, Stanton J (eds) Pelvic Floor Re-education. London: Springer, 1994; 83–97. 44. Dietz HP, Wilson PD, Clarke B. The use of perineal ultrasound to quantify levator activity and teach pelvic floor muscle exercises. Int Urogynecol J Pelvic Floor Dysfunct 2001;12:166–8.
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33 Drug treatment of voiding dysfunction in women Alan J Wein, M Louis Moy
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IntroductIon The lower urinary tract has two basic functions: the storage and the emptying of urine. The physiology and pharmacology of micturition have been described by many qualified authors, each of whom has reported his or her own particular concept of the neuroanatomy, neurophysiology, and neuropharmacology of the smooth and striated muscle structures involved; of the peripheral, autonomic and somatic neural factors; and of the spinal and supraspinal influences that are necessary for normal function.1–5 Although there are significant disagreements about the finer details, it is important to realize that exact agreement about neuromorphology, neurophysiology, and neuropharmacology is not necessary for an understanding of the pharmacologic principles and applications involved in drug-induced alterations of voiding function and dysfunction. Despite such disagreements, all ‘experts’ would agree that, for the purposes of description and teaching, one can succinctly summarize the two phases of micturition from a conceptual point of view. Bladder filling and urine storage require:
• accommodation of increasing volumes of urine at • •
a low intravesical pressure and with appropriate sensation; a bladder outlet that is closed at rest and remains so during increases in intra-abdominal pressure; absence of involuntary bladder contractions (IVCs) – non-neurogenic or neurogenic detrusor overactivity (DO).
Bladder emptying requires:
• a coordinated contraction by the bladder smooth •
•
musculature of adequate magnitude and duration; concomitant lowering of resistance at the level of the smooth sphincter (the smooth muscle of the bladder neck and proximal urethra) and of the striated sphincter (the periurethral and intramural urethral striated musculature); absence of anatomic obstruction.
This simple overview implies that any type of voiding dysfunction (i.e. of storage, emptying, or a combination of these) must result from an abnormality of one or more of the factors listed. This description provides a logical framework for the discussion and classification of all types of voiding dysfunction. In addition, all aspects of urodynamic, radiologic, and videourodynamic evaluation can be conceptualized within this scheme in regard to exactly what they evaluate in terms of either bladder or outlet activity during filling, storage or emptying.
Likewise, one can easily classify all known treatments for voiding dysfunction under the broad categories of facilitating either filling, storage or emptying, and achieving this by acting primarily on the bladder or one or more of the components of the bladder outlet (Table 33.1). As a result of advances in the knowledge of the neuropharmacology and neurophysiology of the lower urinary tract, effective pharmacologic therapy now exists for the management of many types of voiding dysfunction. Because of the number of drug therapies available, along with the varying quality and quantity of studies performed using them, the International Consultation on Incontinence has assessed many of the different available agents for voiding dysfunction and made their recommendations regarding their use (Table 33.2). This chapter summarizes the treatments available for female voiding dysfunction within this functional classification. As an apology to others in the field whose works have not been specifically cited in this chapter, it should be noted that citations have generally been chosen primarily because of their review or informational content or sometimes their controversial nature, and not because of their originality or initial publication on a particular subject.
clInIcal uropharmacology of the lower urInary tract: some useful concepts Clinical uropharmacology of the lower urinary tract is based primarily on an appreciation of the innervation and receptor content of the bladder and its related anatomic structures. The targets of pharmacologic intervention in the bladder body, base or outlet include nerve terminals that alter the release of specific neurotransmitters, receptor subtypes, cellular second-messenger systems, and ion channels identified in the bladder and urethra. Peripheral nerves and ganglia, spinal cord and supraspinal areas are also sites of action of some agents discussed. Because autonomic innervation and receptor content are ubiquitous throughout the human body’s organ systems, there are no agents in clinical use that are purely selective for action on the lower urinary tract. The majority of side-effects attributed to drugs facilitating bladder storage or emptying are collateral effects on organ systems that share some of the same neurophysiologic or neuropharmacologic characteristics as the bladder. Generally speaking, the simplest and least hazardous form of treatment should be tried first. A combination of therapeutic maneuvers or pharmacologic agents can sometimes be used to achieve a particular effect, especially if their mechanisms of actions are different and
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table 33.1. Treatment options depending on cause of lower urinary tract voiding dysfunction
table 33.1. Treatment options depending on cause of lower urinary tract voiding dysfunction (cont.)
Increasing intravesical pressure or bladder contractility 1. External compression, Valsalva maneuver 2. Promotion or initiation of reflex contractions • Trigger zones or maneuvers • Bladder training, tidal drainage 3. Pharmacologic therapy • Parasympathomimetic agents • Prostaglandins • Blockers of inhibition a. α-Adrenergic antagonists b. Opioid antagonist 4. Electrical stimulation • Directly to the bladder or spinal cord • To the nerve roots • Transurethral intravesical electrotherapy 5. Reduction cystoplasty
Inhibiting bladder contractility, decreasing sensory input, or increasing bladder capacity 1. Habit training (timed voiding); prompted voiding 2. Bladder training (± biofeedback) 3. Pharmacologic therapy • Anticholinergic agents • Musculotropic relaxants • Calcium antagonists • Potassium-channel openers • Prostaglandin inhibitors β-Adrenergic agonists • Tricyclic antidepressants • Dimethyl sulfoxide (DMSO) 4. Bladder overdistension 5. Electrical stimulation (reflex inhibition) 6. Acupuncture 7. Interruption of innervation • Central (subarachnoid block) • Peripheral (sacral rhizotomy, selective sacral rhizotomy) • Dorsal • Perivesical (peripheral bladder denervation) 8. Augmentation cystoplasty
Decreasing outlet resistance 1. At a site of anatomic obstruction • Prostatectomy, (diathermy, laser, heat) • Balloon dilation • Intraurethral stent • Pharmacologic decrease in prostate size or tone a. Luteinizing hormone-releasing hormone agonists b. Antiandrogens c. 5α-Reductase inhibitors d. α-Adrenergic antagonists • Urethral stricture repair or dilation 2. At the level of the smooth sphincter • Pharmacologic therapy a. α-Adrenergic antagonists b. β-Adrenergic agonists • Transurethral resection or incision of the bladder neck • Y-V plasty of the bladder neck 3. At the level of the striated sphincter • Pharmacologic therapy a. Skeletal muscle relaxants 1. Benzodiazepines 2. Baclofen 3. Dantrolene • α-Adrenergic antagonists • Urethral overdilation • Surgical sphincterotomy, botulinum toxin • Urethral stent • Pudendal nerve interruption • Psychotherapy, biofeedback Circumventing the problem 1. Intermittent catheterization 2. Continuous catheterization 3. Urinary diversion
Increasing outlet resistance 1. Physiotherapy (± biofeedback) 2. Electrical stimulation of the pelvic floor 3. Pharmacologic therapy • α-Adrenergic agonists • Tricyclic antidepressants • β-Adrenergic antagonists • Estrogens • β-Adrenergic agonists 4. Vesicourethral suspension (SUI) • Transvaginal • Transabdominal 5. Bladder outlet reconstruction 6. Surgical mechanical compression • Sling procedures • Artificial urinary sphincter • Periurethral collagen, Polytef, fat injection 7. Non-surgical mechanical compression • Occlusive devices (hydrophilic urethral patch/suction cup/urethral insert) • Compressive devices (pessaries) Circumventing the problem 1. Antidiuretic-hormone-like agents 2. Intermittent catheterization 3. Continuous catheterization 4. Urinary diversion 5. External collecting devices 6. Absorbent product SUI, stress urinary incontinence.
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table 33.2.
International Consultation on Incontinence assessments of pharmacotherapy for voiding dysfunction 2004 Level
Grade
Tolterodine
1
A
Trospium
1
A
Darifenacin
1
A
Solifenacin
1
A
Propantheline
2
B
Atropine, hyoscyamine
3
C
Oxybutynin
1
A
Propiverine
1
A
Dicyclomine
3
C
Flavoxate
2
D
3
C
1
A
3
C
Antimuscarinics
Drugs with mixed actions
Antidepressants Imipramine Vasopressin analogs Desmopressin α-AR antagonists (alfuzosin, doxazosin, terazosin, tamsulosin)
facIlItatIon of bladder emptyIng Absolute or relative failure to empty results from decreased bladder contractility, increased outlet resistance, or both.6 Failure of adequate bladder contractility may result from temporary or permanent alteration in any one of the neuromuscular mechanisms necessary for initiating and maintaining a normal detrusor contraction. In a neurologically normal individual, inhibition of the micturition reflex may be secondary to painful stimuli, especially stimuli from the pelvic and perineal areas, or it may be psychogenic. Some drug therapies may inhibit bladder contractility through neurologic or myogenic mechanisms. Bladder smooth muscle function may be impaired from overdistension, severe infection or fibrosis. Increased outlet resistance is generally secondary to anatomic obstruction but may be secondary to a failure of coordination of the smooth or striated sphincter during bladder contraction. Treatment of failure to empty consists of attempts to increase intravesical pressure, to facilitate the micturition reflex or to decrease outlet resistance – or some combination of the above.
Increasing intravesical pressure or facilitating bladder contraction Parasympathomimetic agents
β-AR agonists (terbutaline, salbutamol, clenbuterol)
3
C
Baclofen
3
C
Capsaicin
2
C
Resiniferatoxin
2
C
Botulinum toxin
2
B
Level: 1, systematic reviews, meta-analyses, good quality randomized controlled clinical trials 2, randomized controlled trials, good quality prospective cohort studies 3, case-controlled studies, case series 4, expert opinion. Grade: A, based on level 1 evidence (highly recommended) B, consistent level 2 or 3 evidence (recommended) C, level 4 studies or ‘majority evidence’ (optional) D, evidence inconsistent/inconclusive (no recommendation possible).
their side-effects are not synergistic. At the outset it should be noted that, in our experience, although great improvement often occurs with rational pharmacologic therapy, a perfect result (restoration to ‘normal’ status) is seldom, if ever, achieved.
Because a major portion of the final common pathway in physiologic bladder contraction is the stimulation of parasympathetic postganglionic muscarinic cholinergic receptor sites, agents that imitate the actions of acetylcholine (ACh) might be expected to be effective in treating patients who cannot empty because of inadequate bladder contractility. ACh itself cannot be used for therapeutic purposes because of its actions at central and ganglionic levels and because of its rapid hydrolysis by acetylcholinesterase and butyrylcholinesterase.7 Many ACh-like drugs exist, but only bethanechol chloride (BC) has a relatively selective action in vitro on the urinary bladder and gut, with little or no nicotinic action.7 BC in vitro causes a contraction of smooth muscle from all areas of the bladder.8,9 For more than 50 years BC has been recommended for the treatment of the atonic or hypotonic bladder,10 and it has been reported to be effective in achieving ‘rehabilitation’ of the chronically atonic or hypotonic detrusor.11 When so used, it is recommended that the drug be initially administered subcutaneously in a dose of 5–10 mg (usually 7.5 mg) every 4–6 hours, along with an intermittent bladder-decompression regimen. The patient is asked to try to void 20–30 minutes after each dose. When the residual urine volume has decreased to
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an acceptable level, the dose is gradually decreased and ultimately changed to an oral dose of 50 mg four times daily. In cases of partial bladder emptying, a therapeutic trial with an oral dose of 25–100 mg four times daily may be utilized in conjunction with attempted voiding every 4 hours. BC has also been used to stimulate or facilitate the development of reflex bladder contractions in patients with spinal shock secondary to suprasacral spinal cord injury.12 Although anecdotal success in using BC in patients with voiding dysfunction is reported, there is little or no evidence to support its success in facilitating bladder emptying in series of patients in which the drug (BC) was the only variable.13 Short-term studies in which the drug was the only variable have generally failed to demonstrate significant efficacy in terms of flow and residual urine volume data.14 Farrell and colleagues conducted a randomized, double-blind trial that looked at the effects of two catheter-management protocols and the effect of BC on postoperative urinary retention following gynecologic incontinence surgery,15 and concluded that BC was not at all helpful in this setting. Although BC is capable of eliciting an increase in bladder smooth muscle tension, as would be expected from studies in vitro, its ability to stimulate or facilitate a coordinated and sustained physiologic bladder contraction in patients with voiding dysfunction has been unimpressive.13 Similar sentiments have been expressed by others.9 However, due to the paucity of pharmacotherapy to improve bladder emptying, many clinicians continue to use BC in the hope of improving emptying as long as the medication is tolerated without adverse effect by the patient or is contraindicated. The potential side-effects of cholinomimetic drugs include flushing, nausea, vomiting, diarrhea, gastrointestinal cramps, bronchospasm, headache, salivation, sweating and difficulty with visual accommodation.7 Intramuscular and intravenous use can precipitate acute and severe side-effects, resulting in acute circulatory failure and cardiac arrest, and is therefore prohibited. Contraindications to the use of this general category of drug include bronchial asthma, peptic ulcer, bowel obstruction, enteritis, recent gastrointestinal surgery, cardiac arrhythmia, hyperthyroidism and any type of bladder outlet obstruction. One potential avenue of increasing bladder contractility is cholinergic enhancement or augmentation. Such an action might be useful as above or in combination with a parasympathomimetic agent. Metoclopramide is a dopamine antagonist with cholinergic properties. Its effects seem to be related to its ability to antagonize the inhibitory action of dopamine, to augment ACh release,
and to sensitize the muscarinic receptors of gastrointestinal smooth muscle.16 Experiments on dogs suggest that this agent can increase detrusor contractility,17 and there is one anecdotal case report of improved bladder function in a diabetic patient treated originally with this agent for gastroparesis.18 Cisapride is a substituted synthetic benzamide that enhances the release of ACh in Auerbach’s plexus (in the gastrointestinal tract). In 15 patients with complete spinal cord injury treated with 10 mg cisapride three times a day for 3 days, Carone and associates noted earlier and higher amplitude reflex contractions in those with hyperactive bladders; in those with hypoactive bladders there was a significant decrease in compliance.19 There was also increased activity and decreased compliance of the anorectal ampulla, with no alteration in striated sphincter activity. In another study in paraplegic patients, cisapride was found to decrease colonic transit time and maximal rectal capacity; an incidental decrease in residual urine was also noted (although only from 51.5 to 27.7 ml).20 Conversely, in a double-blind placebocontrolled study, Wyndaele and Van Kerrebroeck looked at the effects of 40 mg cisapride daily in 21 patients with clinically complete spinal cord injuries. After 4 weeks of therapy, the authors noted a trend towards a ‘stimulating effect’ of cisapride on the bladder; however, no statistically significant differences were noted between the treated and placebo groups in any urodynamic parameter measured.21 Cisapride has now been withdrawn from general use because of its cardiotoxic side effects (QT interval prolongation, ventricular arrhythmias and death).
Prostaglandins The reported use of prostaglandins (PGs) to facilitate emptying is based on the hypothesis that these substances contribute to the maintenance of bladder tone and bladder contractile activity.1,5 PGE2 and PGF2α cause bladder contractile responses in vitro and in vivo. PGE2 seems to cause a net decrease in urethral smooth muscle tone; PGF2α causes an increase. Bultitude and colleagues reported that instillation of 0.5 mg PGE2 into the bladders of women with varying degrees of urinary retention resulted in acute emptying and in improvement of longer-term emptying (several months) in two-thirds of the patients studied (n=22).22 In general, they reported a decrease in the volume at which voiding was initiated, an increase in bladder pressure and a decrease in residual urine. Desmond and coworkers reported the results of intravesical use of 1.5 mg of PGE2 (diluted with 20 ml 0.2% neomycin solution) in patients whose bladders exhibited no 489
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contractile activity or in whom bladder contractility was relatively impaired.23 Of 36 patients, 20 showed a strongly positive response, and six showed a weakly positive immediate response; 14 patients were reported to show prolonged beneficial effects, all but one of whom had shown a strongly positive immediate response. The authors noted additionally that the effects of PGE2 appeared to be additive or synergistic with cholinergic stimulation in some patients. Vaidyanathan and colleagues reported that intravesical instillation of 7.5 mg PGF2α produced reflex voiding in some patients with incomplete suprasacral spinal cord lesions.24 The favorable response to a single dose of drug, when present, lasted from 1.0 to 2.5 months. Tammela and associates reported that one intravesical administration of 10 mg PGF2α facilitated voiding in women who were in retention 3 days after surgery for stress urinary incontinence (SUI).25 The drug was administered in 50 ml saline as a single dose and retained for 2 hours. It should be noted, however, that in these ‘successfully’ treated patients, the average maximum flow rate was 10.6 ml/s with a mean residual urine volume of 107 ml; furthermore, the authors state that ‘bladder emptying deteriorated in most patients on the day after treatment’. Jaschevatzky and colleagues reported that 16 mg PGF2α in 40 ml saline given intravesically reduced the frequency of urinary retention in a group of women undergoing gynecologic surgery but, inexplicably, only in women undergoing vaginal hysterectomy with vaginal repair – not in those undergoing vaginal repair with urethral plication or vaginal repair alone.26 Koonings and colleagues reported that daily intravesical doses of PGF2α and intravaginal PGE2 reduced the number of days required for catheterization after stress incontinence surgery compared with a control group receiving intravesical saline.27 Other investigators, however, have reported conflicting (negative) results. Stanton and associates28 and Delaere and co-workers29 reported no success using intravesical PGE2 at doses similar to those reported earlier; Delaere and co-workers29 similarly reported no success using PGF2α in a group of women with emptying difficulties of various causes, although it should be noted that they used lower doses than those reported earlier. Wagner and colleagues30 used PGE2 at doses of 0.75–2.25 mg and reported no effect on urinary retention in a group of patients who had undergone anterior colporrhaphy. Schussler31 reported that both intravesical PGE2 and sulprostone (a derivative) caused a strong sensation of urgency in normal female volunteers, resulting in reduced bladder capacity and instability. Both agents also decreased resting urethral
closure pressure. PGE2 increased detrusor pressure at opening and during maximum flow; sulprostone slightly decreased these two parameters. All effects had disappeared 24 hours after administration. Prostaglandins have a relatively short half-life, and it is difficult to understand how any effects after a single application can last as long as several months. If such an effect does occur, it must be the result of a ‘triggering effect’ on some as yet unknown physiologic or metabolic mechanism. Because of the number of conflicting positive and negative reports with various intravesical preparations, double-blind placebo-controlled studies would obviously be helpful to determine whether there are circumstances in which prostaglandin usage can reproducibly facilitate emptying or treat postoperative retention. Potential side-effects of prostaglandin usage include vomiting, diarrhea, pyrexia, and hyper- and hypotension.32
Blockers of inhibition De Groat and co-workers1,4,33 have demonstrated a sympathetic reflex during bladder filling that, at least in the cat, promotes urine storage partly by exerting an α-adrenergic inhibitory effect on pelvic parasympathetic ganglionic transmission. Some investigators have suggested that α-adrenergic blockage, in addition to decreasing outlet resistance, may in fact facilitate transmission through these ganglia and thereby enhance bladder contractility. Although such an effect may be due solely to an α-adrenergic effect on the outlet, it may be that α-adrenergic blockade can, under certain circumstances, facilitate the detrusor reflex, through either a direct effect on parasympathetic ganglia or an indirect one (a mechanism associated with a decrease in urethral resistance).
Opioid antagonists Recent advances in neuropeptide physiology and pharmacology have provided new insights into lower urinary tract function and its potential pharmacologic alteration. It has been hypothesized that endogenous opioids may exert a tonic inhibitory effect on the micturition reflex at various levels,1,3 and agents such as narcotic antagonists may, therefore, offer possibilities for stimulating reflex bladder activity. However, Wheeler and colleagues34 noted no significant cystometric changes in a group of 15 patients with spinal cord injury following intravenous naloxone, and 11 of these patients showed decreased perineal electromyographic (EMG) activity. Although this issue is intriguing, it is of little practical use at present.
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decreasing outlet resistance at the level of the smooth sphincter α-Adrenergic antagonists Whether or not one believes that there is significant innervation of the bladder and proximal urethral smooth musculature by postganglionic fibers of the sympathetic nervous system, one must acknowledge the existence of α- and β-adrenergic receptor sites in these areas.1,5 The smooth muscle of the bladder base and proximal urethra contains predominantly α-adrenoceptors. The bladder body contains both types of adrenoceptor, the β type being more common. The implication that α-adrenergic blockade could be useful in certain patients who cannot empty the bladder was first made by Kleeman in 1970.35 Krane and Olsson36,37 were among the first to endorse the concept of a physiologic internal sphincter that is partially controlled by tonic sympathetic stimulation of contractile α-adrenoceptors in the smooth musculature of the bladder neck and proximal urethra. Furthermore, they hypothesized that some obstructions that occur at this level during detrusor contraction result from an inadequate opening of the bladder neck or an inadequate decrease in resistance in the area of the proximal urethra. They also theorized and presented evidence that α-adrenergic blockade could be useful in promoting bladder emptying in such a patient – one with an adequate detrusor contraction but without anatomic obstruction or detrusor striated sphincter dyssynergia. Abel and colleagues38 called attention to the fact that such a functional obstruction (which they, too, assumed to be mediated by the sympathetic nervous system) could be maximal at a urethral rather than bladder neck level, and coined the term ‘neuropathic urethra’. Many others have subsequently confirmed the utility of α-blockade in the treatment of what is now usually referred to as smooth sphincter or bladder neck dyssynergia or dysfunction. Successful results – usually defined as an increase in flow rate, a decrease in residual urine, and an improvement in upper tract appearance (when that is pathologic) can often be correlated with an objective decrease in urethral profile closure pressures. One would expect such success with α-adrenergic blockade in treating emptying failure to be least evident in patients with detrusor striated sphincter dyssynergia, as reported by Hachen.39 Although most would agree that α-blockers exert their favorable effects on voiding dysfunction primarily by affecting the smooth muscle of the bladder neck and proximal urethra, some information suggests that they may affect (decrease) striated sphincter tone as well. Other data suggest that they may
exert some effects on the symptoms of voiding dysfunction in certain circumstances by decreasing bladder contractility. Much of the confusion about whether α-blockers have a direct (as opposed to an indirect) inhibitory effect on the striated sphincter relates to the interpretation of observations of their effect on urethral pressure and periurethral striated muscle EMG activity in the region of the urogenital diaphragm. It is impossible to tell from pressure tracings alone whether a decrease in resistance in one area of the urethra is secondary to a decrease in smooth or striated muscle activity. Nanninga and colleagues40 found that EMG activity of the external sphincter decreased after administration of phentolamine in three paraplegic patients; they attributed this to direct inhibition of a sympathetic action on the striated sphincter. Nordling and colleagues41 demonstrated that clonidine and phenoxybenzamine (POB), both of which pass the blood–brain barrier, also decreased urethral pressure in this area but had no effect on EMG activity. They concluded:
• that the effect of phentolamine was due to smooth • •
muscle relaxation alone; that the effect of clonidine and possibly of POB was elicited mostly through centrally induced changes in striated urethral sphincter tonus; that these agents also had an effect on the smooth muscle component of urethral pressure.
None of the three drugs, however, affected the reflex rise in either urethral pressure or EMG activity that was seen during bladder filling, and none decreased the urethral pressure or EMG activity response to voluntary contraction of the pelvic floor striated musculature. Pedersen and associates42 showed that thymoxamine (an α-adrenergic antagonist that crosses the blood–brain barrier) decreased peak urethral pressure and striated sphincter EMG activity in patients with spastic paraplegia; they speculated that the drug acted on the striated sphincter via a central mechanism. Gajewski and colleagues43 concluded that α-blockers do not influence the pudendal nerve-dependent urethral response in the cat through a peripheral action, but that prazosin, at least, can significantly inhibit this response at a central level. Thind and co-workers44 reported on the effects of prazosin on static urethral sphincter function in 10 healthy women: they found that function was diminished, predominantly in the midurethral area, and hypothesized that this response was due to a decrease in both smooth and striated sphincter muscle tone, the latter as a result of a reduced somatomotor output from the central nervous system (CNS). 491
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α-Adrenergic blocking agents have also been used to treat both bladder and outlet abnormalities in patients with so-called autonomous bladders.45 These include those with myelodysplasia, sacral or infrasacral spinal cord neural injury, and voiding dysfunction following radical pelvic surgery. Parasympathetic decentralization has been reported to lead to a marked increase in adrenergic innervation of the bladder, resulting in conversion of the usual β (relaxant) bladder response to sympathetic stimulation to an α (contractile) response.46 Although the alterations in innervation have been disputed, the alterations in receptor function have not. Koyanagi47 demonstrated urethral supersensitivity to α-adrenergic stimulation in a group of patients with autonomous neurogenic bladders, implying that a change had occurred in adrenergic receptor function in the urethra following parasympathetic decentralization. Parsons and Turton48 observed the same phenomenon but ascribed the cause to adrenergic supersensitivity of the urethral smooth muscle caused by sympathetic decentralization. Nordling and colleagues49 described a similar phenomenon in women who had undergone radical hysterectomy and ascribed this change to damage to the sympathetic innervation. Decreased bladder compliance is often a clinical problem in such patients, and this, together with a fixed urethral sphincter tone, results in the paradoxical occurrence of both storage and emptying failure. Norlen45 has summarized the supporting evidence for the success of α-adrenolytic treatment in these patients. POB is capable of increasing bladder compliance (increasing storage) and decreasing urethral resistance (facilitating emptying). Andersson and co-workers50 used prazosin in such patients and found that maximum urethral pressure (MUP) during filling was decreased, whereas ‘autonomous waves’ were reduced. McGuire and Savastano51 reported that POB decreased filling cystometric pressure in the decentralized primate bladder. α-Adrenergic blockade can also decrease bladder contractility in patients with voiding dysfunction by another mechanism. Jensen52–54 reported an increase in the ‘α-adrenergic effect’ in bladders characterized as ‘uninhibited’. Short- and long-term prazosin administration increased bladder capacity and decreased the amplitude of contractions. Thomas and colleagues55 found that intravenous phentolamine produced a significant reduction in maximum voiding detrusor pressure, voiding volumes and peak flow rates in patients with suprasacral spinal cord injury with no reduction of outflow obstruction. Rohner and associates56 found that the normal β response of canine bladder-body smooth
musculature was changed to an α response after bladder outlet obstruction. Swierzewski and colleagues57 prospectively studied the effects of terazosin on 12 patients with spinal cord injuries and decreased compliance. All patients were refractory to medical therapy and intermittent catheterization. Urodynamic studies were conducted before, during and at the conclusion of 4 weeks of therapy with 5 mg terazosin daily. The authors found statistically significant improvements in bladder compliance, ‘safe bladder volume’ and bladder pressure in all patients, with the additional benefits of decreased episodes of both urinary incontinence and autonomic dysreflexia. They speculated that the improvement was due either to a direct effect on the α-receptors of the detrusor or to a central effect, but not to any effects on outlet resistance. POB was the α-adrenolytic agent originally used for the treatment of voiding dysfunction; like phentolamine, it has blocking properties at both α1- and α2-receptor sites. The initial adult dosage of this agent is 10 mg/day, and the usual daily dose for voiding dysfunction is 10–20 mg. Daily doses larger than 10 mg are generally divided and given every 8–12 hours. After the drug has been discontinued, the effects of administration may persist for days because the drug irreversibly inactivates α-receptors, and the duration of effect depends on the rate of receptor resynthesis.58 Potential side-effects include orthostatic hypotension, reflex tachycardia, nasal congestion, diarrhea, miosis, sedation, nausea and vomiting (secondary to local irritation). Those who still use POB for long-term therapy should be aware that it has mutagenic activity in the Ames test and that repeated administration to animals can cause peritoneal sarcomas and lung tumors.58 Furthermore, the manufacturer has reported a doserelated incidence in rats of gastrointestinal tumors,59 the majority of which were in the non-glandular portion of the stomach. Although this agent has been in clinical use for some 35 years without clinically apparent oncologic associations, one must now consider the potential medicolegal ramifications of long-term therapy, especially in younger persons. Prazosin hydrochloride is a potent selective α1-antagonist,58 and its clinical use to lower outlet resistance has already been mentioned. The duration of action is 4–6 hours; therapy is generally begun in daily divided doses of 2–3 mg. The dose may be gradually increased to a maximum of 20 mg daily, although seldom is more than 9–10 mg daily used for voiding dysfunction. The potential side-effects of prazosin are a consequence of its α1-blockade. Occasionally, a ‘first-dose’ phenomenon occurs, a symptom complex of faintness, dizziness, pal-
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pitations and (infrequently) syncope, thought to be due to acute postural hypotension. The incidence of this phenomenon can be minimized by restricting the initial dose of the drug to 1 mg and administering this at bedtime. Other side-effects associated with chronic prazosin therapy are generally mild and rarely necessitate withdrawal of the drug. Terazosin and doxazosin are two selective postsynaptic α1-blocking drugs. They are readily absorbed and have a high bioavailability and a long plasma half-life, enabling their activity to be maintained over 24 hours following a single dose.60,61 They are most often used for the treatment of voiding dysfunction secondary to benign prostatic hyperplasia (BPH) consequent on the α1-receptor content of the prostatic stroma and capsule. Their side-effects are similar to those of prazosin.62 Daily doses range from 1 to 10 mg, generally given at bedtime, a convenient advantage over the three-times-daily dosage schedule necessary for prazosin. Terazosin is said to have the same affinity for α1-receptors in genitourinary as in vascular tissue and a four-fold greater selectivity for α1-receptors than doxazosin. Alfuzosin is a new agent that is reported to be a selective and competitive antagonist of α1-mediated contraction of the prostate capsule, bladder base and proximal urethral smooth muscle, with efficacy similar to that of prazosin.63 It is said to be more specific for receptors in the genitourinary tract than in the vasculature, raising the possibility that voiding may be facilitated by doses that have minimal vasodilatory effects, thus minimizing postural hypotension.64 The drug requires three-times-daily dosing (7.5–10 mg total). A sustained-release form of the drug, which allows convenient once-daily dosing, is also now available. In a placebo-controlled study,65 sustained-release alfuzosin was shown to have no significant incidence of adverse effects above that due to placebo. In addition, effects on blood pressure (orthostatic hypotension) were minimal, supporting its selectivity of the lower urinary tract over the vasculature. Finally, recent molecular characterization of the α1-receptor has led to the recognition, classification and cloning of a number of α1-receptor subtypes. In the human prostate, there appears to be some tissue specificity in that the majority of the stromal α1-receptors are of the α1a subtype.66 A drug that is selective for the α1a-receptor subtype would be expected to cause fewer undesired (and dose-limiting) effects than the less selective drugs while maintaining clinical efficacy. Tamsulosin is an α1-blocking agent that is selective for the α1a- and α1d-receptor subtypes over the α1b subtype.67 It appears to have no statistically significant drug-related adverse effects over placebo68 and has less
effect on blood-pressure parameters than alfuzosin.69 It is unclear whether highly selective α1a-antagonists will have similar effects in women, as virtually all of the studies reported in the peer-reviewed literature have studied the effects of these agents on benign prostatic obstruction in men. Agents with α-adrenergic blocking properties at various levels of the neural organization have been used in patients with very varied types of voiding dysfunction – functional outlet obstruction, urinary retention, decreased compliance, and neurogenic and idiopathic DO. Although there remains a paucity of data regarding the use of α-adrenergic agonists in women, our experience suggests that a trial of such an agent is certainly worthwhile, because its effect or non-effect will become obvious in a matter of days and the pharmacologic sideeffects are, of course, reversible. However, our results with such therapy for non-BPH-related voiding dysfunction have been somewhat less spectacular than those of (at least some) other investigators.
Other potential non-specific therapy
β-Adrenergic stimulation has been shown experimentally to decrease the urethral pressure profile and, by inference, urethral resistance.70 Vaidyanathan et al.71 reported a decrease in urethral closure pressure after the administration of terbutaline, a relatively specific β2-agonist. Other investigators have reported that β2-agonists potentiate periurethral striated muscle contraction in vitro. It seems doubtful that a β-agonist will prove clinically useful in facilitating bladder emptying by decreasing outlet resistance. Progesterone has been suggested as a possible treatment for emptying abnormalities in women. In a study of normal women looking at the effects of estrogen alone versus estrogen plus progesterone, maximum flow in the estrogen-only group increased from 26 to 38 ml/s. A sphincteric effect was hypothesized.72 Finally, nitric oxide (NO) has been suggested to be a mediator of non-adrenergic, non-cholinergic (NANC) relaxation of the smooth muscle of the bladder outlet that occurs with bladder contraction.5 Whether this means that analogs or substances that release NO in vivo will prove useful in decreasing smooth-muscle-related outlet resistance in humans remains to be seen. If so, one could envisage a role for NO synthetase inhibitors to stabilize urethral pressure or increase outlet resistance as well. NO is a ubiquitous molecule, however, and also exerts inhibitor effects on the detrusor body in vitro. Opposite functional effects on the bladder and outlet (on contractility and resistance) could well frustrate any clinical application. 493
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decreasing outlet resistance at the level of the striated sphincter No class of pharmacologic agents selectively relaxes the striated musculature of the pelvic floor. Three different types of drug have been used to treat voiding dysfunction secondary to outlet obstruction at the level of the striated sphincter: the benzodiazepines (diazepam), dantrolene, and baclofen. All are characterized generally as antispasticity drugs.73 Baclofen and diazepam act predominantly within the CNS, whereas dantrolene acts directly on skeletal muscle. Although these drugs are capable of providing variable relief in specific circumstances, their efficacy is far from complete, and troublesome muscle weakness, adverse effects on gait and other side-effects limit their overall usefulness. Benzodiazepines and baclofen are thought to exert their effects on the lower urinary tract through interactions with inhibitory neurotransmitters. γ-Aminobutyric acid (GABA) and glycine have been identified as major inhibitory neurotransmitters in the CNS.74 Evidence favors glycine as the mediator of intraspinal postsynaptic inhibition and the most likely inhibitory transmitter in the reticular formation. GABA appears to mediate presynaptic inhibition in the spinal cord and the inhibitory action of local interneurons in the brain. The specific substrate for spinal cord inhibition consists of the synapses located on the terminals of the primary afferent fibers. GABA is the transmitter secreted by these synapses and activates specific receptors, resulting in a decrease in the amount of excitatory transmitter released by impulses from primary afferent fibers, consequently reducing the amplitude of the excitatory postsynaptic potentials.
Benzodiazepines The benzodiazepines potentiate the action of GABA at pre- and postsynaptic sites in the brain and spinal cord.75,76 When GABA recognition sites are activated, increased chloride conductance across the neuronal membrane produces inhibitory effects. The benzodiazepines increase the affinity of the GABA receptor sites on CNS membranes, and the increased binding increases the frequency with which the chloride channels open in response to a given amount of GABA. Presynaptic inhibition is augmented, and it is thought that this reduces the release of excitatory transmitters from afferent fibers, thereby reducing the gain of the stretch and flexor reflexes in patients with bladder spasticity. This is a postulated mechanism of action of the muscle relaxant properties of diazepam at least.75 Side-effects of benzodiazepines include nonspecific CNS depression, manifested as sedation, leth-
argy, drowsiness, slowing of thought processes, ataxia, and decreased ability to acquire or store information.77 Some authors believe that any muscle relaxant effect in clinically used doses is due to the CNS depressant effects and cite a lack of clinical studies showing any advantages of these agents over placebo or aspirin in this regard.78 Effective total daily doses of diazepam, the most widely used agent of this group, range from 4 to 40 mg. Other benzodiazepine anxiolytic agents include chlordiazepoxide, clorazepate, prazepam, halazepam, clonazepam, lorazepam, oxazepam, and alprazolam. There are few available published papers that provide valuable data on the use of any of the benzodiazepines for treatment of functional obstruction at the level of the striated sphincter. In view of the information previously cited on the use of α-adrenergic blocking agents for treating or preventing postoperative urinary retention, it is interesting to note that one of the few articles that specifically mentions diazepam reports that it is more effective than oral POB, intravesical PGE or oral BC in promoting spontaneous voiding after colposuspension surgery.79 We have not found the recommended oral doses of diazepam effective in controlling the classic type of detrusor striated sphincter dyssynergia secondary to neurologic disease. If the cause of incomplete emptying in a neurologically normal patient is obscure, and the patient has what appears urodynamically to be inadequate relaxation of the pelvic floor striated musculature (e.g. occult neuropathic bladder, the Hinman syndrome), a trial of such an agent may be worthwhile. The rationale for its use is either relaxation of the pelvic floor striated musculature during bladder contraction, or that such relaxation removes an inhibitory stimulus to reflex bladder activity. However, improvement under such circumstances may simply be due to the antianxiety effect of the drug or to the intensive explanation, encouragement, and modified biofeedback therapy that usually accompanies such treatment in these patients. Finally, diazepam may also have effects on the smooth muscle of the detrusor. Peripheral benzodiazepine receptors have been demonstrated in the rabbit detrusor,80 although the clinical significance is, at present, unknown. In addition, administration of diazepam resulted in smooth muscle relaxation in the rat detrusor in a GABA-independent fashion through interference with calcium transport.81 It is unclear whether this effect occurs at physiologic doses of diazepam or whether this action has any clinical relevance in humans.
Baclofen Baclofen depresses mono- and polysynaptic excitation of motor neurons and interneurons in the spinal cord and
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was originally thought to function as a GABA agonist.73,75 However, its electrophysiologic and pharmacologic profiles differ radically from those of GABA. Although its effects superficially resemble those of GABA, some specific GABA inhibitors (e.g. bicuculline) do not antagonize the actions of baclofen. Baclofen does not cause depolarization of primary afferent nerve terminals, and there is no evidence that baclofen increases chloride conduction, the most prominent action of GABA. Because both GABA and baclofen can produce some effects that are insensitive to blockade by classic GABA antagonists, two classes of GABA receptors have been proposed: the GABAA receptor (the classic receptor) and the GABAB receptor. Baclofen does not bind strongly or specifically to classic GABAA receptors but does to GABAB receptors in brain and spinal membranes. Currently, it is thought that activation of the GABA receptors by baclofen causes a decrease in the release of excitatory transmitters onto motor neurons by increasing potassium conductance or by inhibiting calcium influx. The primary site of action of baclofen is in the spinal cord, but it is also reported to be active at more rostral sites in the CNS. Milanov82 states that, like a GABAB agonist, baclofen suppresses excitatory neurotransmitter release but also has direct GABA-ergic activity. Its effect in reducing spasticity is caused primarily by normalizing interneuron activity and decreasing motor neuron activity (perhaps secondary to normalizing interneuron activity).82 Baclofen has been found useful for the treatment of skeletal spasticity due to a variety of causes (especially multiple sclerosis and traumatic spinal cord lesions).73 In regard to its use in treating voiding dysfunction, Hachen and Krucker83 found that a daily oral dose of 75 mg was ineffective in patients with striated sphincter dyssynergia and traumatic paraplegia, whereas a daily intravenous dose of 20 mg was highly effective. Leyson and associates84 reported that 73% of their patients with voiding dysfunction secondary to acute and chronic spinal cord injury had lower striated sphincter responses and decreased residual urine volume following baclofen treatment, but only with an average daily oral dose of 120 mg. Potential side-effects of baclofen include drowsiness, insomnia, rash, pruritus, dizziness, and weakness. It may impair the ability to walk or stand, and is not recommended for the management of spasticity due to cerebral lesions or disease. Sudden withdrawal has been shown to provoke hallucinations, anxiety, and tachycardia; hallucinations due to reductions in dosage during treatment have also been reported.85 Drug delivery often frustrates adequate pharmacologic treatment, and baclofen is a good example of this.
GABA’s hydrophilic properties prevent its crossing the blood–brain barrier in sufficient amounts to make it therapeutically useful. For oral use, a more lipophilic analog, baclofen, was developed. However, its passage through the barrier is likewise limited, and it has proved to be a generally insufficient drug when given orally to treat severe somatic spasticity and micturition disorders secondary to neurogenic dysfunction.86 Intrathecal infusion bypasses the blood–brain barrier: cerebrospinal fluid levels 10 times higher than those reached with oral administration are achieved with infusion amounts 100 times less than those taken orally.87 Direct administration into the subarachnoid space by an implanted infusion pump has shown promising results, not only for skeletal spasticity but also for striated sphincter dyssynergia and DO. Nanninga and colleagues88 reported on such administration to seven patients with intractable bladder spasticity: all patients experienced a general decrease in spasticity and the amount of striated sphincter activity during bladder contraction decreased; six showed an increase in bladder capacity. Four previously incontinent patients were able to stay dry with clean intermittent catheterization (CIC). The action of baclofen on bladder overactivity is not unexpected, given its spinal cord mechanism of action, and this inhibition of bladder contractility when the drug is administered intrathecally may, in fact, prove to be its most important benefit. Loubser and colleagues89 studied nine patients with spinal cord injury and refractory spasticity, using an external pump to test the initial response: eight showed objective improvement in functional ability; three of seven studied urodynamically showed an increase in bladder capacity. Development of tolerance to intrathecal baclofen with a consequent requirement for increasing doses may prove to be a problem with long-term chronic usage. Mertens and colleagues90 reported on the longterm use of intrathecal baclofen in a series of 17 patients with mixed spinal cord lesions and severe refractory limb spasticity. Average follow-up was 37.5 months (range 5–69 months). Intrathecal dose was adjusted every 3 months as needed to maintain ‘good clinical and functional condition’ with regard to limb spasticity, hypertonia, pain, and functional disability, and not necessarily for its effects on the lower urinary tract. The authors noted that the dosage necessary to gain an initial ‘satisfactory effect’ varied considerably between patients, with dosage titration increasing over the first few months in the majority of patients but ‘usually’ stabilizing after the first year. Unfortunately, quantitative data (actual dosage adjustment, number of patients requiring adjustment, etc.) were not provided. Only 12 495
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of the 17 patients had an associated neurogenic bladder and underwent urodynamic study. Long-term effects on the lower urinary tract were inconsistent: five of nine patients with decreased functional bladder capacity had significant improvement, and uninhibited contractions were reduced or suppressed in 50% of those with neurogenic DO at presentation. The authors attribute these inconsistent results as potentially due to inadequate dose titration for effects on the lower urinary tract. They speculated that the ‘effective dose’ to improve lowerextremity hypertonia (the endpoint in this study) was perhaps not sufficient to improve the lower urinary tract parameters in the majority of patients. Further studies on the long-term efficacy of intrathecal baclofen specifically on the lower urinary tract in patients with neurogenic bladder are anticipated.
Dantrolene Dantrolene exerts its effects by direct peripheral action on skeletal muscle.73,75 It is thought to inhibit the excitation-induced release of calcium ions from the sarcoplasmic reticulum of striated muscle fibers, thereby inhibiting excitation–contraction coupling and diminishing the mechanical force of contraction. The blockade of calcium release is not complete, however, and contraction is not completely abolished. It reduces reflex more than voluntary contractions, probably because of a preferential action on fast-twitch rather than slow-twitch skeletal muscle fibers. The drug improves voiding function in some patients with classic detrusor striated sphincter dyssynergia and was initially reported to be very successful in doing so.91 In adults, the recommended starting dose is 25 mg daily, gradually increasing by increments of 25 mg every 4–7 days to a maximum oral dose of 400 mg given in four divided doses. Hackler and colleagues92 reported improvement in voiding function in approximately half of their patients treated with dantrolene but found that such improvement required oral doses of 600 mg daily. Although no inhibitory effect on bladder smooth muscle seems to occur,93 the generalized weakness that dantrolene can induce is often sufficiently significant to compromise its therapeutic effects. Potential side-effects other than severe muscle weakness include euphoria, dizziness, diarrhea, and hepatotoxicity. Fatal hepatitis has been reported in 0.1–0.2% of patients treated with the drug for 60 days or longer, and symptomatic hepatitis may occur in 0.5% of patients treated for more than 60 days; chemical abnormalities of liver function are noted in up to 1%. The risk of hepatic injury is two-fold greater in women.94 One use of dantrolene for which agreement exists is the acute management of malignant hyperthermia.
Other agents
β-Adrenergic agonists, especially those with prominent β2 characteristics, are able to produce relaxation of some skeletal muscles of the slow-twitch type.95,96 This action could be significant in view of the fact that the portion of the external urethral sphincter comprising the outermost urethral wall is said to consist exclusively of slow-twitch fibers,97 whereas the striated muscle fibers of the levator ani contain both fast- and slow-twitch fibers, although the majority are of the slow-twitch type. This type of action may account at least in part for the decrease in urethral profile parameters seen with terbutaline. This area of pharmacology and its clinical relevance is somewhat confusing at the moment because β2-adrenergic drugs have been reported to potentiate periurethral striated muscle contraction, albeit in a different in vitro system. Botulinum toxin (BTX) (a potent inhibitor of ACh release at the neuromuscular junction of striated muscle) has been injected directly into the striated sphincter to treat dyssynergia to cause relaxation of the muscle.98 This application has led to the use of BTX in treating neurogenic and non-neurogenic causes of urethral sphincter hypertonicity which may lead to retention. Although there are number of subtypes, botulinum A toxin (BTX-A) is the one which has been most studied and is most commonly used and available. Injections of 100 units carried out weekly for 3 weeks can achieve a duration of effect averaging 6–9 months. The number of patients tested thus far is small, and more information is needed about criteria for success and side-effects. Fowler and colleagues99 used BTX injections in six women with difficult voiding or urinary retention secondary to abnormal myotonus-like EMG activity in the striated urethral sphincter. Although voiding did not improve in any patient (attributed to the type of repetitive discharge activity present), three patients developed transient stress incontinence, indicating that the sphincter muscle had, indeed, been weakened. Phelan and colleagues100 performed a prospective study to assess the efficacy of injecting 80–100 units of BTX into the external sphincter of 13 women and 8 men with voiding dysfunction due to various causes, including detrusor sphincter dyssynergia, pelvic floor spasticity, and bladder hypocontractility. All the patients except one were able to void spontaneously, and all but two were able to discontinue catheterizations. Similarly, Kuo injected 50 or 100 units BTX into the urethra of 103 patients (55 women) with chronic urinary retention or severe difficulty in urinating.101 The reasons for the lower urinary tract voiding dysfunction were quite heterogeneous: detrusor sphincter dyssynergia, dysfunc-
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tional voiding, non-relaxing urethral sphincter, cauda equina lesion, peripheral neuropathy, and idiopathic detrusor underactivity. Subjectively, 39% had ‘excellent’ results and 46% had ‘significant’ improvement. There was a statistically significant decrease in maximum voiding pressure, maximal urethral closure pressure, and post void residual. In a small double-blind controlled study, the efficacy of BTX-A was compared with lidocaine. This study by de Seze and colleagues102 was performed in 13 patients with detrusor sphincter dyssynergia secondary to spinal cord injury. The injections were performed transperineally. BTX-A was superior to lidocaine, resulting in decreased post void residual and maximal urethral pressure. Those treated with BTX-A also had an increase in patient satisfaction. Clonidine is the prototypical α2-adrenergic receptor agonist. It is considered to be a centrally acting agent with a variety of associated systemic effects including antihypertensive, antinociceptive, and antispasmodic effects. Potential effects on relaxation of the external urethral sphincter have been reported previously.103,104 Herman and Wainberg105 administered oral clonidine (400 mcg) in three divided doses over a 16-hour period under monitored inpatient conditions to five spinal cord injury patients with neurogenic DO and quantified the effects on the external urethral sphincter (EUS) via needle electrodes. They found that clonidine had a profound suppressive effect on volume-induced EMG activity in the EUS in four of five patients. The one patient in whom there were only minimal effects on the EUS had received an intrathecal dose of morphine 2 days before, which the authors feel may have confounded the effects of clonidine in this patient. The authors speculate that the somewhat selective effect of clonidine on the EUS is attributable to postsynaptic suppression of excitatory spinal interneurons (unmasked by the spinal lesion) via the α2-agonist activity of clonidine. Adverse effects included significant reductions in systolic and diastolic blood pressure as well as sedative effects. Further clinical studies on the effects of clonidine on the lower urinary tract and striated sphincter (as well as its clinical utility) may be limited owing to its significant effects on blood pressure.
facIlItatIon of urIne storage The pathophysiology of failure of the lower urinary tract to fill with or to store urine adequately may be secondary to problems related to the bladder, the outlet or both.6 DO can be expressed as discrete involuntary contractions or as reduced compliance with or without phasic
contractions. It may manifest itself symptomatically as overactive bladder (OAB), a syndrome of urgency which may be associated with frequency and nocturia. IVCs are most commonly associated with inflammatory or irritating processes in the bladder wall or with bladder outlet obstruction, or they may be idiopathic. Decreased compliance during filling may be secondary to the sequelae of neurologic injury or disease but may also result from any process that destroys the elastic or viscoelastic properties of the bladder wall. Purely sensory urgency may result from inflammatory, infectious, neurologic or psychological factors, or it may be idiopathic. A fixed decrease in outlet resistance may result from degeneration of or damage to innervation of the structural elements of the smooth or striated sphincter or from neurologic disease or injury, surgical or other mechanical trauma, or aging. Classic SUI or genuine SUI in women implies a failure of the normal transmission of increases in intraabdominal pressure to the area of the bladder neck and proximal urethra due to changes in the anatomic position of the vesicourethral junction and proximal urethra during increases in intra-abdominal pressure (hypermobility). The pathophysiology of SUI may also involve a decrease in the reflex striated sphincter contraction, which occurs with a number of maneuvers that increase intra-abdominal pressure. Treatment of abnormalities related to the filling or storage phase of micturition are directed towards inhibiting bladder contractility, increasing bladder capacity, decreasing sensory input during filling or increasing outlet resistance, either continuously or only during abdominal straining.
decreasing bladder contractility Anticholinergic agents Physiologic bladder contractions are thought to be primarily triggered by ACh-induced stimulation of postganglionic parasympathetic muscarinic cholinergic receptor sites on bladder smooth muscle.1,5 Atropine and atropine-like agents should depress normal bladder contractions and IVC of any cause.52,106,107 In such patients, the volume to the first IVC is generally increased, the amplitude of the IVC decreased, and maximum bladder capacity increased. However, although the volume and pressure thresholds at which an IVC is elicited may increase, the ‘warning time’ (the time between the perception of an IVC about to occur and its occurrence) and the ability to suppress an IVC are not increased. Thus, urgency and incontinence still occur unless such therapy is combined with a regime of timed voiding or toi497
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leting. McGuire and Savastano51 reported that atropine increased both the compliance and the capacity of the neurologically decentralized primate bladder, and that both of these effects were additive to those produced by POB.50 However, the effect of pure antimuscarinics in those who exhibit only decreased compliance has not been well studied. Outlet resistance, at least as reflected by urethral pressure measurements, does not seem to be clinically affected by anticholinergic therapy. Although antimuscarinic agents can produce significant clinical improvement in patients with IVCs and associated symptoms, only partial inhibition results. In many animal models, atropine only partially antagonizes the response of the whole bladder to pelvic nerve stimulation and of bladder strips to field stimulation, although it does completely inhibit the response of bladder smooth muscle to exogenous cholinergic stimulation. Of the theories proposed to explain this phenomenon, termed ‘atropine resistance’, the most attractive and most commonly cited is the idea that a portion of the neurotransmission involved in the final common pathway of bladder contraction is non-adrenergic, non-cholinergic (NANC), i.e. secondary to a release of a transmitter other than ACh or noradrenaline.1,2,5 Although the existence of atropine resistance in human bladder muscle is by no means agreed on, this concept is the most common hypothesis invoked to explain clinical difficulty in abolishing IVCs with anticholinergic agents alone, and it is also used to support the rationale of treatment of such types of bladder activity with agents that have different mechanisms of action. Brading108,109 and Andersson5 both discuss the difficulty of evaluating apparently conflicting data in the literature with respect to atropine resistance. Brading109 states that the size of the atropine-resistant component varies markedly among different species and, in a given preparation, also depends on the frequency of nerve stimulation. Andersson5 states that ‘most probably normal human detrusor muscle exhibits little atropine resistance’, but does not exclude its existence in morphologically or functionally abnormal bladders. At least five different genetically established (by cloning) muscarinic subtypes exist (muscarinic receptor genes designated M1–M5).110 The nomenclature M1–M4 describes the protein products of the M1–M5 coding regions (the actual muscarinic receptor subtypes) which are each defined pharmacologically using receptor subtype agonists and antagonists.5,111,112 A physiologic role for the product of the M5 coding region remains undefined.112 Pirenzepine (a selective muscarinic blocker) was originally used to subdivide muscarinic receptors
into M1 and M2 categories; using this subclassification, detrusor muscarinic receptors were classified as the M2 type.5,113,114 On further analysis of the M2 receptor population, a small proportion of glandular M2 receptors were found which could represent the pharmacologic type responsible for muscarinic agonist-induced contractions. This subtype is now called the M3 receptor.5,111 Although it appears that the majority of the muscarinic receptors in human smooth muscle (including bladder) are of the M2 subtype,115 in vitro data indicate that most smooth muscle contraction, including that of the urinary bladder, is mediated by the M3 receptor subtype.115,116 Muscarinic receptor subtyping becomes important when considering the possibility of pharmacologically selecting (and blocking) those receptors responsible for urinary bladder smooth muscle contraction while minimally affecting other muscarinic receptor sites throughout the body. Ideally, this approach would effectively treat the underlying problem (detrusor overactivity) while eliminating the unpleasant systemic side-effects of most non-specific antimuscarinic agents (dry mouth, constipation, blurred vision, etc.) which, in many cases, are worse than the problem they are treating and result in patient non-compliance.
Specific drugs Propantheline bromide Propantheline bromide is the classically described oral agent for producing an antimuscarinic effect in the lower urinary tract. The usual adult oral dose is 15–30 mg every 4–6 hours, although higher doses are often necessary. Propantheline is a quaternary ammonium compound that is poorly absorbed after oral administration. No available oral drug has a direct in vitro antimuscarinic binding potential that is closer to that of atropine than propantheline bromide.117,118 There is a surprising lack of valuable data on the effectiveness of propantheline for the treatment of bladder overactivity. As Andersson107 points out, anticholinergic drugs in general have been reported to have both great and poor efficacy for this indication. To show the range of variation, Zorzitto and colleagues119 concluded that propantheline bromide administered orally in doses of 30 mg four times a day to a group of institutionalized incontinent geriatric patients had marginal benefits that were outweighed by the sideeffects. Blaivas and colleagues,106 on the other hand, by increasing the dose of propantheline (up to 60 mg four times a day) until incontinence was eliminated or side-effects precluded further use, obtained a complete response in 25 of 26 patients with IVCs. Differences in bioavailability, selective drug delivery, receptor selectivity, receptor density, atropine resistance, pathophysiology,
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susceptibility to dose-limiting side-effects, and mental status are all potential factors that could explain such disparate results. The Agency for Health Care Policy and Research (AHCPR) Clinical Practice Guidelines120 list five randomized controlled trials for propantheline, in which 82% of the patients were women. Percentage cures (all figures refer to percentage minus percentage on placebo) are listed as 0–5, percentage reduction in urge incontinence as 0–53, percentage side-effects 0–50, and percentage dropouts 0–9. Atropine Atropine is reported to be available in a 0.5 mg tablet, although we have yet to find it. Atropine and all related belladonna alkaloids are well absorbed from the gastrointestinal tract. Atropine is said to have almost no detectable CNS effects at clinically used doses.121 It has a half-life of about 4 hours. Scopolamine Scopolamine is another belladonna alkaloid marketed as a soluble salt. It has prominent central depressive effects at low doses, probably because of its greater penetration (compared with atropine) through the blood–brain barrier. Transdermal scopolamine has been used for treating IVCs.122 The ‘patch’ provides continuous delivery of 0.5 mg daily to the circulation for 3 days. Cornella and associates,123 however, reported poor results with using this in treating 10 patients with DO: only two patients showed a positive response; one showed a slight improvement, and the drug was discontinued in eight patients because of side-effects. Side-effects were related to the CNS (ataxia, dizziness) and included blurred vision and dry mouth. A doubleblind placebo-controlled study using transdermal scopolamine was performed on 20 patients with DO: after a 14-day treatment period, the 10 patients randomized to transdermal scopolamine treatment showed statistically significant improvements in frequency, nocturia, urgency, and urge incontinence over the placebo group; no adverse effects of the therapy were reported.124 A double-blind placebo study on the effects of transdermal scopolamine in patients who had undergone suprapubic prostatectomy was performed to investigate its use in the treatment or prevention of pain, IVCs, urgency, and bladder pressure rises of 15 cmH2O. No statistical differences were found.125 In our experience of treating patients with IVCs with this method, results were very erratic and skin irritation with the patch was a problem for some patients. Caution should be exercised in the use of the patch in the elderly and young, because of the fixed dose.
Hyoscyamine Hyoscyamine and hyoscyamine sulfate are reported to have similar anticholinergic actions and side-effects as other belladonna alkaloids. Hyoscyamine sulfate is available as a sublingual formulation, a theoretical advantage, but controlled studies of its effects on bladder overactivity are lacking. Glycopyrrolate Glycopyrrolate is a synthetic quaternary ammonium compound that is a potent inhibitor of both M1 and M2 receptors but has a preference for the M2 subtype.126 It is available in both oral and parenteral preparations, the latter being commonly used as an antisialogogue during anesthesia. An anticholinergic agent with a significant ganglionic-blocking action as well as such action at the peripheral receptor level might be more effective in suppressing bladder contractility. Methantheline Although methantheline has a higher ratio of ganglionic-blocking to antimuscarinic activity than propantheline, the latter drug seems to be at least as potent in each respect, clinical dose for dose. Methantheline does have similar effects on the lower urinary tract, and some clinicians still prefer it over other anticholinergic agents. Few real data are available regarding its efficacy. The potential side-effects of all antimuscarinic agents include inhibition of salivary secretion (dry mouth), blockade of the ciliary muscle of the lens to cholinergic stimulation (blurred vision for near objects), tachycardia, drowsiness, and inhibition of gut motility. Those agents that possess some ganglionic-blocking activity may also cause orthostatic hypotension and erectile dysfunction at high doses (at which nicotinic activity becomes manifest). Antimuscarinic agents are contraindicated in patients with narrow-angle glaucoma and should be used with caution in patients with significant bladder outlet obstruction because complete urinary retention may be precipitated. A lack of selectivity is a major problem with all antimuscarinic compounds as they tend to affect parasympathetically innervated organs in the same order; generally, larger doses are required to inhibit bladder activity than to affect salivary, bronchial, nasopharyngeal, and sweat secretions. Several new receptor antagonists with varying degrees of specificity for the lower urinary tract show some promise in decreasing the side-effect profiles of this class of medications without compromising efficacy. 499
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Tolterodine Tolterodine and its primary metabolite PNU-200577127 show some selectivity for bladder tissue over salivary tissue in vitro and in vivo in the anesthetized cat.128,129 These tissue-selective effects do not appear to be due to muscarinic receptor subtype selectivity127,128 but may be related to differential affinities of the receptors in the salivary gland and detrusor muscle for tolterodine compared with oxybutynin. Although it appears that the binding affinity of tolterodine and oxybutynin to muscarinic receptors in the urinary bladder (in the guinea pig) are very similar, the affinity of tolterodine for muscarinic receptors in the parotid gland is eight times lower than that of oxybutynin.130 Tolterodine is available in two formulations: an immediate-release (IR) form (2 mg twice daily) and an extended-release (ER) form (2 or 4 mg once daily). In a pilot study in 12 healthy males, tolterodine was shown to have a greater objective and subjective effect 131 on bladder function than on salivation. Jonas and colleagues132 looked at the urodynamic effects of tolterodine in a multicenter, randomized, double-blind, placebo-controlled study: 242 patients were enrolled and treated over a 4-week period with 1 or 2 mg tolterodine or placebo twice daily. Compared with placebo, 2 mg tolterodine (but not 1 mg) showed statistically significant improvements in:
• mean volume to first IVC: 141 to 230 ml, 142 to 210 ml, and 140 to 181 ml;
• mean maximal strength of IVC: 52 to 37 cmH2O, 41 to 35 cmH2O, and 47 to 40 cmH2O;
• maximal cystometric capacity: 272 to 316 ml, 276 to 294 ml, and 264 to 268 ml; in the 2 mg, 1 mg, and placebo groups, respectively. The proportion of adverse effects between the treated groups and placebo was not statistically significant; however, dry mouth was the most commonly reported event (9% of treated patients) – significantly less than the 50% incidence reported in the literature for other commonly used anticholinergic preparations.133 Furthermore, the dry mouth was classified as ‘severe’ by only 1% of patients. At higher doses, the incidence of side-effects of tolterodine may be more significant and approach that of other commonly used anticholinergic drugs. Rentzhog and colleagues134 noted that, at a dose of 2 mg or less, the incidence of adverse effects (including dry mouth) due to tolterodine was comparable to that of placebo (2/13 patients in the placebo group versus 9/51 patients in the tolterodine group reported dry mouth); however, when the dose of tolterodine was increased
to 4 mg, a substantial increase in the incidence of dry mouth occurred (9/16 patients). Overall, it appears that tolterodine is safe and efficacious for the treatment of DO. A favorable side-effect profile exists at lower doses (less effect on salivary glands), which may diminish in a dose-dependent fashion. There have been several randomized controlled studies documenting the effectiveness of tolterodine in reducing micturition frequency and incontinence episodes.135,136 There have also been trials comparing it to other agents. The OBJECT (Overactive Bladder: Judging Effective Control and Treatment) trial performed by Appell and colleagues137 compared tolterodine IR 2 mg twice daily to oxybutynin ER 10 mg daily. This was a randomized, double-blind, parallel-group study which included 378 patients with OAB. Patients were treated for 12 weeks. The outcome measures included the number of episodes of urge incontinence, total incontinence, and micturition frequency. The study showed oxybutynin ER to be significantly more effective than tolterodine in each of the outcome measures when adjusted for baseline. The most common adverse event was dry mouth which was reported by 28% and 33% of those taking oxybutynin ER and tolterodine IR, respectively. Rates of other adverse events including CNS side-effects were generally low and comparable between the two groups. In the OPERA (Overactive Bladder: Performance of Extended Release Agents) study, Diokno and colleagues138 compared tolterodine ER 4 mg daily to oxybutynin ER 10 mg daily in 790 women with OAB symptoms. This too was a randomized, double-blind study with a duration of 12 weeks. 24-hour voiding diaries were kept to document the number of incontinence episodes (primary outcome), total incontinence, and micturition frequency at weeks 2, 4, 8, and 12. Improvements in weekly urge incontinence episodes were similar between the two treatment groups. Oxybutynin ER was more effective in reducing micturition frequency, and 23.0% of women taking it reported no episodes of urinary incontinence compared to 16.8% of women taking tolterodine ER. Dry mouth was more common in the oxybutynin ER group, with both groups having similar discontinuation rates. The conclusions were that both drugs had similar reductions in weekly urge incontinence and total incontinence episodes. Those taking oxybutynin ER had more dry mouth, but the tolerability between the two drugs was comparable. In the ACET (Antimuscarinic Clinical Effectiveness Trial), Sussman and Garely139 performed an open label study in 1289 patients with OAB, comparing tolterodine ER 2 or 4 mg to oxybutynin ER 5 or 10 mg. After 8 weeks,
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70% of patients taking tolterodine ER 4 mg perceived an improved bladder condition compared to approximately 60% perceived improvement in the other groups. There were fewer withdrawals from the study in the tolterodine ER 4 mg group (12%) than in either oxybutynin ER 5 or 10 mg (19% and 21%, respectively). Patients taking tolterodine ER 4 mg reported significantly less dry mouth than those on oxybutynin ER 10 mg. Although the findings suggest that tolterodine ER 4 mg may have improved clinical efficacy and tolerability to oxybutynin ER 10 mg, the open label design of this study makes for a less convincing conclusion. Zinner and colleagues140 performed a 12-week randomized, double-blind, placebo-controlled study to evaluate the efficacy, safety, and tolerability of tolterodine ER in treating OAB symptoms in older (≥65 years) and younger (<65 years) patients. Objective measures by micturition diaries as well as subjective measures were evaluated. There were significant improvements in patients on tolterodine ER in their micturition chart variables compared to placebo. There were no agerelated differences. Dry mouth was the most common adverse event in both arms. No CNS or cardiac events were seen. Tolterodine ER appeared to be well tolerated by both age groups. Freeman et al.141 presented a secondary analysis of a double-blind, placebo-controlled study looking at the effects of tolterodine ER 4 mg on the symptoms of urinary urgency in patients with OAB: 772 patients with ≥8 micturitions/24 hours and urge incontinence (≥5/week) were randomized to drug or placebo and treated for 12 weeks. Efficacy was assessed by using patient perception evaluations. Patients on tolterodine ER 4 mg had a greater improvement in urgency (44% versus 32%) and bladder symptoms (62% versus 48%) than placebo. Patients taking tolterodine ER 4 mg were also significantly more likely to hold their urine after experiencing urgency than those on placebo. Darifenacin and solifenacin Recently, several pharmacologic agents have been approved for use by the FDA in the United States, including darifenacin and solifenacin. Darifenacin, a tertiary amine, is a selective muscarinic M3 receptor antagonist. Its theoretical advantage is its ability to selectively block the M3 receptor, which is the most important in bladder contraction, thereby decreasing the adverse events related to the blockade of other muscarinic subtypes. Darifenacin has been studied in several randomized controlled studies. Haab and colleagues performed a multicenter, randomized, double-blind, placebo-con-
trolled study comparing darifenacin 3.75 mg, 7.5 mg, 142 15 mg, and placebo once daily. The treatment period was 12 weeks. Using an electronic voiding diary, patients recorded daily incontinence episodes, micturition frequency, volume voided, frequency and severity of urgency, incontinence episodes necessitating a change of clothing or pads, and nocturnal awakenings due to bladder symptoms. The 7.5 and 15 mg doses of darifenacin had a quick onset of action with significant improvements over placebo being seen at week 2. The clinical parameters in which the treatment arm were significantly better than placebo included improvements in micturition frequency, bladder capacity, frequency of urgency, severity of urgency, and number of incontinence episodes. No significant change occurred in nocturnal awakening due to bladder symptoms. The most common side-effects seen were mild-to-moderate dry mouth and constipation. No patients withdrew from the study due to dry mouth, and the discontinuation rate due to constipation was low (0.9% for darifenacin versus 0.6% for placebo). The CNS and safety profiles were similar to placebo. An analysis of the pooled data from phase III trials was performed by Chapple,143 with 1059 patients (85% female) with symptoms of urgency, urge incontinence, and frequency being randomized into three arms: darifenacin 7.5 mg, 15 mg, or placebo daily for 12 weeks. Once again, patient voiding diaries were maintained electronically. The parameters monitored included incontinence episodes, frequency and severity of urgency, micturition frequency, and volume voided. Compared to baseline, there was a significant dose-related decrease in the number of incontinence episodes per week, with darifenacin 7.5 mg reducing episodes by 8.8, and darifenacin 15 mg reducing episodes by 10.6. Significant decreases in the frequency and severity of urgency, micturition frequency, and number of incontinence episodes requiring a change of clothing or pads were seen, as well as an increase in bladder capacity. Although the most common side-effect was dry mouth, this led to few discontinuations (darifenacin 7.5 mg 0.5%, 15 mg 2.1%, and placebo 0.3%). The incidence of CNS and cardiovascular adverse events was similar to placebo. Cardozo et al.144 performed a study to determine the effects of darifenacin on ‘warning time’, or the ability of the medication to allow patients to postpone micturition once urge was sensed. This was a multicenter, randomized, double-blind, placebo-controlled study with a 2-week treatment phase of darifenacin 30 mg daily or placebo. Darifenacin treatment resulted in a significant increase in the mean warning time, with a median increase of 4.3 minutes compared to placebo. 501
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Overall, 47% of darifenacin-treated subjects compared with 20% of those receiving placebo achieved a >30% increase in mean warning time. Although this study utilized a higher than usual dose of therapeutic agent and the treatment period was short, it is the first to evaluate changes in warning time. This may be particularly germane to patients with severe symptoms of urgency and urge incontinence. Solifenacin (YM-905) is a tertiary amine, once-a-day antimuscarinic. It is well absorbed from the gastrointestinal tract and undergoes significant hepatic metabolism by the cytochrome P450 enzyme system. There have been several large trials examining the effects of solifenacin. Chapple and colleagues145 performed a multinational study comparing various doses of solifenacin (2.5, 5, 10, and 20 mg) to tolterodine IR 2 mg twice daily and placebo in patients with OAB. A total of 225 patients were treated for 4 weeks and followed for an additional 2 weeks. To be included in the study all patients had to have ≥8 micturitions/24 hours and one episode of incontinence or one episode of urgency daily as recorded by a 3-day voiding diary. Micturition frequency was the primary outcome. In patients treated with solifenacin, there was a statistically significant reduction in micturition frequency for those taking 5, 10, and 20 mg. This was not seen in the other two arms of the study. Additionally, these doses of solifenacin, when compared to placebo, resulted in a significant increase in volume voided, and a reduction in episodes of frequency and incontinence. The onset of action was rapid, occurring at 2 weeks, the earliest follow-up in the study. Discontinuation rates were similar among the different treatments except for solifenacin 20 mg which was higher. The 5 and 10 mg doses of solifenacin had a lower rate of dry mouth than tolterodine. Another dose-ranging, placebo-controlled study of solifenacin 2.5–20 mg was performed by Smith and colleagues in the United States.146 The treatment duration was 4 weeks with 2 weeks of follow-up. There was a significant reduction in micturition frequency in the solifenacin 10 and 20 mg groups over placebo. The onset of efficacy was seen at 7 days, with continued improvement at 28 days. Significant increases in the volume voided were seen in those taking 5, 10, and 20 mg of solifenacin. Those taking the 10 mg solifenacin dose also had a significant decrease in incontinent episodes. There were four phase III trials to evaluate efficacy, safety, and tolerability of solifenacin in adult patients with OAB. The primary outcome in all the studies was 24-hour micturition frequency. Secondary outcomes included change in number of urgency and incontinence episodes and mean volume voided.
Chapple and colleagues147 performed a multicenter, randomized, placebo-controlled and tolterodine-controlled study. Subjects were treated for 12 weeks with either solifenacin 5 or 10 mg daily, tolterodine IR 2 mg twice a day, or placebo. Those taking both doses of solifenacin had a significant decrease in urgency episodes in 24 hours compared to placebo, whereas tolterodine did not. In the solifenacin group, there was a significant decrease in incontinence episodes, and the mean number of voids in 24 hours was significantly lower in all three active treatment arms. As with most antimuscarinics, the most common side-effect was dry mouth in 14% in the solifenacin 5 mg group and 21.3% in the 10 mg group. Cardozo and colleagues148 performed a multicenter, randomized, placebo-controlled study comparing solifenacin 5 and 10 mg once daily to placebo. They found that both the 5 and 10 mg doses significantly improved frequency over placebo. Solifenacin was also better than placebo in improving urgency, volume voided, and decreasing incontinence episodes over 24 hours. The reduction in urgency was slightly greater than 50% for both doses of solifenacin, whereas placebo had a reduction of 33%. The percent increase in voided volume per micturition was 25.4, 29.7, and 11% for solifenacin 5 mg, 10 mg, and placebo, respectively. The percent decrease in overall incontinence episodes was 60.7, 51.9, and 27.9% in solifenacin 5 mg, 10 mg, and placebo, respectively. The majority of patients completed the study with only a small percentage (2–4%) not completing due to adverse events which was comparable in all groups. The incidence of dry mouth was 2.3, 7.7, and 23.1% in placebo, solifenacin 10 mg and 20 mg, respectively. There were no changes in ECG parameters. There were two randomized, placebo controlled, double-blind studies performed in the United States in which a total of 1208 patients participated.149 Findings included a reduction in the number of micturitions/24 hours, decrease in the number of incontinence and urgency episodes/24 hours, and an increase in the volume voided per micturition. Among the patients who were incontinent at baseline, a significant number on solifenacin became continent when compared to placebo (53% versus 31%, respectively).
Musculotropic relaxants Musculotropic relaxants affect smooth muscle directly at a site that is metabolically distal to the cholinergic or other contractile receptor mechanism. Although the agents discussed in this section do relax smooth muscle in vitro by papaverine-like (direct) action, all have also been found to possess variable anticholinergic and local
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anesthetic properties. There is still some uncertainty about how much of their clinical efficacy is due only to their atropine-like effect. If, in fact, any of these agents do exert a clinically significant inhibitory effect that is independent of antimuscarinic action, a therapeutic rationale exists for combining them with a relatively pure anticholinergic agent. Oxybutynin Oxybutynin chloride is a moderately potent anticholinergic agent that has strong independent musculotropic relaxant activity as well as local anesthetic activity. The recommended oral adult dose is 5 mg three or four times a day; side-effects are antimuscarinic and dose related. Initial reports documented success in depressing neurogenic DO,150 and subsequent reports documented success in inhibiting other types of bladder overactivity as well.107 A randomized, double-blind, placebo-controlled study comparing 5 mg oxybutynin three times a day with placebo in 30 patients with DO was carried out by Moisey and colleagues:151 17 of 23 patients who completed the study with oxybutynin had symptomatic improvement and nine showed evidence of urodynamic improvement, mainly an increase in maximum bladder capacity. Hehir and Fitzpatrick152 reported that 16 of 24 patients with neuropathic voiding dysfunction secondary to myelomeningocele were cured or improved (17% dry, 50% improved) with oxybutynin treatment: average bladder capacity increased from 197 to 299 ml (with drug) versus 218 ml (with placebo); maximum bladder filling pressure decreased from 47 to 37 cmH2O (with drug) versus 45 cmH2O (with placebo). In a prospective randomized study of 34 patients with voiding dysfunction secondary to multiple sclerosis, Gajewski and Awad153 found that 5 mg oral oxybutynin three times a day produced a good response more frequently than 15 mg propantheline three times a day; they concluded that oxybutynin was more effective in the treatment of neurogenic DO secondary to multiple sclerosis. Holmes and associates154 compared the results of oxybutynin and propantheline in a small group of women with DO. The experimental design was a randomized crossover trial with a patient-regulated variable dose regimen. This kind of dose-titration study allows the patient to increase the drug dose to whatever is perceived to be the optimum ratio between clinical improvement and side-effects – an interesting way of comparing two drugs while minimizing differences in oral absorption. Of the 23 women in the trial, 14 reported subjective improvement with oxybutynin as opposed to 11 with propantheline. Both drugs significantly increased the maximum cystometric capacity and reduced the maximum detrusor pressure
on filling. The only significant objective difference was a greater increase in the maximum cystometric capacity with oxybutynin. The mean total daily dose of oxybutynin tolerated was 15 mg (range 7.5–30) and that of propantheline was 90 mg (range 45–145). Thuroff and colleagues155 compared oxybutynin with propantheline and placebo in a group of patients with symptoms of instability and either neurogenic or nonneurogenic DO. Oxybutynin (5 mg three times a day) performed best, but propantheline was used at a relatively low dose – 15 mg three times a day. The incidence of side-effects was higher for oxybutynin at just about the level of clinical and urodynamic improvement. The mean grade of improvement on a visual analog scale was higher for oxybutynin (58.2%) than for propantheline (44.7%) or placebo (43.4%). Urodynamic volume at the first IVC increased more with oxybutynin (51 versus 11.2 versus 9.7 ml), as did the change in maximum cystometric capacity (80.1 versus 48.9 versus 22.5 ml). Residual urine volume also increased more (27.0 versus 2.2 versus 1.9 ml). The authors further subdivided their overall results into excellent (>75% improvement), good (50– 74%), fair (25–49%) and poor (<25%). Percentages for treatment with oxybutynin were, respectively, 42, 25, 15, and 18%. The authors compared their 67% rate of good or excellent results with those reported in seven other oxybutynin series in the literature (some admittedly poorer studies included) and concluded that their results compared favorably with the range of results calculated from these studies (61–86%). The results of propantheline treatment generally ranked between those of oxybutynin and placebo but did not reach significant levels over placebo in any variable. Subdivision of propantheline results into excellent, good, fair, and poor categories yielded percentages of 20, 30, 14, and 36%, respectively. The authors compared their 50% ratio of good or excellent results with those achieved in six other propantheline studies reported in the literature (30– 57%) and concluded that their results were consistent with these. Although this study is better than most in the literature, it does have drawbacks, and anyone using it in a meta-analysis would be well advised to read it and the other cited studies very carefully. Zeegers and colleagues156 reported on a double-blind, prospective, crossover study comparing oxybutynin, flavoxate, emepronium, and placebo. Although there was a high dropout rate (19 of 60 patients) and the entry criteria were vague (frequency, urgency, urge incontinence), the results were scored as 5 (excellent overall effect) to 1 (no improvement) by both patient and physician, and the results were combined into a single number. The percentages of results in categories 3–5 for the agents 503
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used were oxybutynin 61%, placebo 41%, emepronium 34%, and flavoxate 31%. The results of the first treatment gave corresponding percentages of only 63, 29, 18 (probably reflecting eight dropouts due to side-effects), and 44%, respectively. Ambulatory urodynamic monitoring and pad weighing were used by van Waalwijk van Doorn and Zwiers157 to assess the effects of oxybutynin on DO. The 24-hour average frequency of IVCs decreased from 8.7 to 3.4, the maximum contraction amplitude decreased from 32 to 22 cmH2O, and the duration of the average IVC decreased from 90 to 60 seconds. However, the daily micturition frequency did not change (11–10), nor did the amount of urine lost – findings the authors try to minimize by pointing out that some patients also had sphincteric incontinence and that, during treatment, there may have been a higher fluid intake. The AHCPR guidelines120 list six randomized controlled trials for oxybutynin; 90% of patients were women. The percentage of cures (all figures refer to percentage minus percentage on placebo) is listed as 28–44%, percentage of reduction in urge incontinence is 9–56%, and the percentages of side-effects and dropouts are 2–66% and 3–45%, respectively. There are some negative reports on the efficacy of oxybutynin. Zorzitto and colleagues158 came to conclusions similar to those resulting from their study of propantheline in a double-blind, placebo-controlled trial conducted in 24 incontinent geriatric institutionalized patients: oxybutynin 5 mg twice a day was no more effective than placebo with scheduled toileting in treating incontinence in this type of population with DO. An incontinence profile was used to assess results: the only significant difference noted was an increase in residual urine volume (159 versus 92 ml). Ouslander and colleagues159 reported similar conclusions in a smaller study of geriatric patients and, in an accompanying article, they concluded simply that the drug is safe for use in the elderly at doses of 2.5–5 mg three times a day.159,160 An ER form of oxybutynin is available which releases the active compound over a period of 24 hours. Aside from the ease of once-daily administration, the potential benefit of the ER formulation is that stabilization of serum levels throughout the day should lower the incidence of side-effects.161 Another theoretical advantage may be that less absorption occurs in the proximal portion of the gastrointestinal tract draining into the portal system so that there is less first-pass metabolism. IR and ER oxybutynin have been compared in a multicenter, randomized, double-blind trial of 106 patients, all of whom had previously responded to IR oxybutynin.162 For patients currently on anticholinergic
therapy, after a 1-week washout period, a dose-titration schedule was used to reach the maximum allowable dose (20 mg IR or 30 mg ER daily), or to the dose at which no urge urinary incontinence (UUI) episodes occurred over the course of 2 days (as measured from a diary) or until a dose was reached with intolerable sideeffects (at which point the final dose was decreased by 5 mg). Thirteen patients discontinued therapy during the trial, four because of anticholinergic events. Overall, similar efficacy was noted for both formulations of oxybutynin in the overall number of episodes (27.4 to 4.8 for ER and 23.4 to 3.1 for IR), the percentage decrease in weekly UUI episodes (84% ER and 88% IR), and overall incontinence episodes (urge, stress and mixed). The number and proportion of patients achieving continence was also similar between the groups (41% ER and 40% IR). Curiously, voiding frequency increased in both groups, with a statistically significant percentage increase of voiding frequency in patients receiving the ER compared with those receiving the IR formulation (54% versus 17%; p<0.001). Anticholinergic sideeffects were noted in both groups. Dry mouth was the most frequent, occurring in the majority of patients. Dry mouth was reported as moderate or severe by 25% and 46% of patients receiving the ER and IR formulations, respectively (p=0.03). Other anticholinergic side-effects were reported with similar frequency in the ER and IR groups: somnolence (38% versus 40%), blurred vision (28% versus 17%), constipation (30% versus 31%), dizziness (28% versus 38%), impaired urination (25% versus 29%), nervousness (25% versus 23%), and nausea (19% versus 17%). In an open-label trial163 with 256 patients (23.4% of whom were on anti-incontinence medication at baseline and switched over to oxybutynin ER for the study), oxybutynin ER reduced the number of incontinence episodes per week from 18.8 at baseline to 2.8 at the end of the study (83.1% reduction); 31% of patients remained free of UUI throughout the study. A 14.7% reduction in voiding frequency was noted on therapy compared with baseline, as measured from the voiding diary. Dry mouth was reported by 58.6% of patients, 23.0% reporting moderate or severe dry mouth. Only 1.6% of patients discontinued therapy because of dry mouth. Overall, 7.8% of patients discontinued therapy because of adverse events, of which nausea, dry mouth, and somnolence were the most frequent. Topical application of oxybutynin and other agents to normal or intestinal bladders has been suggested and implemented.164 This conceptually attractive form of alternative drug administration, delivered by periodic intravesical instillation of either liquid or timed-released
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pellets, awaits further clinical trials and the development of preparations specifically formulated for this purpose. Several non-randomized, unblinded, and non-placebocontrolled studies have demonstrated the efficacy of this therapy in a variety of patients with neurogenic bladders, showing statistically significant improvements in cystometric capacity, volume at first IVC, bladder compliance, and overall continence.165–167 Madersbacher and Jilg reviewed the intravesical usage of 5 mg of oxybutynin dissolved in 30 ml distilled water in 13 patients with complete suprasacral cord lesions who were on CIC.168 Of the 10 patients who were incontinent, nine remained dry for 6 hours. For the group, the changes in bladder capacity and maximum detrusor pressure were statistically significant. Some of the more interesting data were given in a figure showing plasma oxybutynin levels in a group of patients in whom administration was intravesical or oral. The level following an oral dose rose to 7.3 mg/ ml within 2 hours and then precipitously dropped to slightly less than 2 mg/ml at 4 hours. Following intravesical administration, the level rose gradually to a peak of approximately 6.2 mg/ml at 3.5 hours, but at 6 hours it was still greater than 4 mg/ml, and at 9 hours it was still between 3 and 4 mg/ml. From these data it is unclear whether the intravesically applied drug acted locally or systemically. In a later study, Madersbacher and Knoll169 administered oxybutynin intravesically and then, 1 week later, orally in six patients with neurogenic bladders in order to study the pharmacokinetics of the drug and investigate the pharmacologic properties responsible for its clinical effects; serum drug levels were correlated with urodynamic effects 20 minutes and 2 hours after administration of the drug. The authors concluded that the main effect of intravesical oxybutynin is due to systemic absorption; however, a secondary direct local effect (smooth muscle relaxation or topical anesthetic effect) could not be excluded. Weese and colleagues170 reported on a similar dose of oxybutynin (5 mg in 30 ml sterile water) to treat 42 patients with IVCs in whom oral anticholinergic therapy had failed (11 patients) or who had intolerable sideeffects (31 patients): 20 had neurogenic DO, 19 had non-neurogenic DO, and three had bowel or DO after augmentation. The drug was instilled two or three times each day for 10 minutes by catheter. Nine patients (21%) withdrew from the study because they were unable to tolerate CIC or retain the solution properly, but there were no reported side-effects. Of the 33 patients able to follow the protocol, 18 (55%) reported at least a moderate subjective improvement in incontinence and urgency.
Nine patients became totally continent and experienced complete resolution of their symptoms; 18 patients improved and experienced a decrease of 2.5 pads per day. There were no urodynamic data. Follow-up ranged from 5 to 35 months (mean 18.4 months). The lack of side-effects prompted some speculation about the mechanism of drug action: one possibility suggested was simply a more prolonged rate of absorption; another was a decreased pass through the liver and therefore a decrease in metabolites, the hypothesis being that perhaps the metabolites and not the primary compound are responsible for the side-effects. Enzelsberger et al.171 reported on the use of intravesical oxybutynin in the treatment of DO in 52 women. In the only randomized, double-blind, placebo-controlled study published on the use of intravesical oxybutynin, patients received once-daily intravesical oxybutynin (20 mg in 40 ml sterile water) or placebo for 12 days. The results revealed statistically significant differences in first desire to void (from 95 ml [pretreatment] to 150 ml [post-treatment]), cystometric capacity (205 to 310 ml), maximal pressure during filling (16 to 9 cmH2O), daytime frequency (7.5 to 4), and nocturia (5.1 to 1.8). Sideeffects were similar in the treated and placebo groups (17% versus 10%, respectively). For unexplained reasons, 19/23 patients in the treated group continued to have symptomatic relief after termination of the study. In an increasing effort to maintain or improve the efficacy of oxybutynin while minimizing its sideeffects, the use of transdermal oxybutynin (OXY-TDS) has been studied. In one study,172 the daily dose patch significantly reduced the number of weekly incontinence episodes while reducing average daily urinary frequency by an increased average voided volume. Dry mouth rates were similar to placebo (7% versus 8.3%). A recent study173 comparing OXY-TDS and oxybutynin IR demonstrated equivalent reduction in incontinent episodes, but significantly less dry mouth with OXY-TDS (38%) versus oxybutynin IR (94%). In a third study,174 OXY-TDS was compared to placebo and tolterodine ER. Both drugs had similarly significant reduced daily incontinence episodes and increased voided volume, but tolterodine ER was associated with a higher rate of antimuscarinic adverse events. The major side-effect for OXY-TDS was pruritus at the application site in 14% and erythema in 8.3%. Dicyclomine Dicyclomine hydrochloride is also reported to exert a direct relaxant effect on smooth muscle in addition to an antimuscarinic action.175 An oral dose of 20 mg three times a day in adults has been reported to increase blad505
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der capacity in patients with neurogenic DO.176 Beck and co-workers177 compared the use of 10 mg dicyclomine, 15 mg propantheline, and placebo three times a day in patients with DO:178 the cure or improved rates, respectively, were 62, 73, and 20%. Awad and associates179 reported that 20 mg dicyclomine three times a day caused resolution or significant improvement in 24 of 27 patients with IVCs. Flavoxate Flavoxate hydrochloride has a direct inhibitory action on smooth muscle but very weak anticholinergic properties.107,180 In cats, at least, there is some evidence that flavoxate may have central effects on the inhibition of the micturition reflex in addition to its effects on the relaxation of smooth muscle.181 Clinical studies addressing the efficacy of flavoxate in the treatment of DO have been mixed. Milani and colleagues182 performed a double-blind, crossover study comparing flavoxate 1200 mg daily with oxybutynin 15 mg daily in 41 women with idiopathic motor or sensory urgency, utilizing clinical and urodynamic criteria. Both drugs had similar efficacy, with flavoxate having fewer side-effects. However, Briggs and colleagues183 reported that this drug had essentially no effect on non-neurogenic DO in an elderly population, an experience that coincides with the laboratory effects obtained by Benson and associates.184 There were few reported side-effects. Although the efficacy compared to other agents in this group has not been proven, a short clinical trial may be worthwhile. Trospium and propiverine Trospium and propiverine are classified as predominantly antispasmodic agents (smooth muscle relaxants) with some anticholinergic effects as well. Although both drugs have been used in Europe for years, trospium chloride has now been approved by the FDA and is available for use in the United States. It is a quaternary amine and has limited ability to cross the blood–brain barrier, therefore in theory leading to minimal cognitive dysfunction.185–187 Trospium has no selectivity for a muscarinic subtype. There have been several randomized controlled trials which have shown the beneficial effects of trospium188,189 in both neurogenic and non-neurogenic DO.190–194 Stohrer and colleagues performed a multicenter, double-blind, placebo-controlled study to determine the effects of trospium on urodynamic parameters in patients with neurogenic DO secondary to spinal cord injury.188 Patients were randomized to either trospium 20 mg twice daily or
placebo for 3 weeks. In the treatment group, there was an increase in maximum cystometric capacity, decreased maximal detrusor pressure, and increased compliance. No such effects were seen in the placebo group. In a similar study, Madersbacher et al.189 compared the use of trospium and oxybutynin in the treatment of neurogenic detrusor overactivity. Both medications appeared to have equal effects, but the patients on trospium had fewer side-effects. The effectiveness of trospium in the treatment of non-neurogenic detrusor overactivity has also been well documented. Alloussi and colleagues190 performed a randomized, double-blind, placebo-controlled study in 309 patients with non-neurogenic DO. The treatment group received trospium 20 mg twice daily, and the study length was 3 weeks. They found a significant increase over placebo in volume at first involuntary detrusor contraction and in maximum bladder capacity. Cardoza et al.191 also performed a randomized, double-blind, placebo-controlled study in patients with non-neurogenic DO. The 208 patients participating in the study were given placebo or trospium 20 mg twice daily for 2 weeks. This study similarly found an increase in volume at which the first involuntary detrusor contraction took place as well as an increase in maximum cystometric capacity. In a study comparing the efficacy of trospium 20 mg twice daily with tolterodine 2 mg twice daily and placebo in patients with urodynamically proven DO, Junemann and colleagues found trospium to be significantly more effective in decreasing the frequency of micturition than either tolterodine or placebo.192 The use of trospium was also found to cause a greater reduction in the number of incontinence episodes and had similar rates of dry mouth as tolterodine. Halasaka et al.193 performed a long-term tolerability and efficacy study comparing trospium 20 mg twice daily and oxybutynin 5 mg twice daily in patients with DO. Patients were treated for 52 weeks. Urodynamics were performed at baseline, 26 weeks, and 52 weeks, and patient voiding diaries were also kept at baseline, 2, 26, and 52 weeks. There was found to be a significant increase in mean maximum cystometric capacity of 92 ml at 26 weeks and 115 ml at 52 weeks in the trospium group. No other significant difference in urodynamic parameters was noted between the two treatment groups. Voiding diaries revealed a decrease in frequency, frequency of incontinence, and urgency episodes in both groups. At least one adverse event occurred in the majority of patients: 64.8% and 76.6% in the trospium and oxybutynin groups, respectively. The most common side-effect in both groups was dry mouth. Overall, both drugs were comparable in the efficacy in improving urinary symp-
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toms, but trospium had a better benefit–risk ratio than oxybutynin due to better tolerability. In a large multicenter, randomized, placebo-controlled, parallel study, Zinner and colleagues from the Trospium Study Group194 compared the effects of trospium 20 mg twice daily and placebo in patients with OAB and urge incontinence. The study length was 12 weeks, with the primary endpoints being a change in the mean number of voids and change in urge incontinence episodes in a 24-hour period. Other variables such as mean volume per void, urge severity, diurnal and nocturnal micturition episodes, and onset of action were also examined. Compared to placebo, trospium had a significant reduction in the mean frequency of toilet voids and urge incontinence episodes. A significant increase in volume voided and decrease in urge severity and diurnal frequency were also seen. The effects were seen after 1 week of treatment and were maintained throughout the remainder of the study. Once again, the most common side-effect was dry mouth, occurring in 21.8%, followed by constipation in 9.5%, and headache in 6.5%. Similar results were confirmed by Rudy and colleagues195 in a large multicenter study in the United States which included 658 patients. Propiverine Propiverine is a musculotropic smooth muscle relaxant with anticholinergic activity. It is rapidly absorbed and has a high first pass metabolism.196 Thuroff et al.197 reviewed nine randomized studies on a total of 230 patients, and found reductions in frequency and micturitions per 24 hours of 30% and 17%, respectively. There was a 77% subjective improvement, and side-effects were found in 14%. In a study by Stohrer and colleagues,198 the superiority of propiverine over placebo was found in patients with neurogenic DO. In controlled trials comparing propiverine, flavoxate, and placebo, and propiverine, oxybutynin, and placebo,199 they have confirmed the efficacy of propiverine and suggested that the drug may have equal efficacy and fewer side-effects than oxybutynin. Madersbacher et al.200 compared the tolerability and efficacy of propiverine (15 mg three times a day), oxybutynin (5 mg twice daily) and placebo in 366 patients with urgency and urge incontinence in a randomized, double-blind, placebo-controlled clinical trial. The urodynamic efficacy of propiverine was similar to that of oxybutynin, but the incidence and severity of dry mouth was less with propiverine than oxybutynin. Dorschner and colleagues201 performed a multicenter, randomized, double-blind, placebo-controlled study to test the efficacy and cardiac safety of propiverine in elderly patients with urgency, urge, or mixed incontinence: 98 patients with a
mean age of 68 years received propiverine 15 mg or placebo three times daily for 4 weeks. Propiverine resulted in a significant reduction in micturition frequency and a decrease in incontinence episodes. Adverse events were very low. Therefore, propiverine appears to have an acceptable side-effect profile and reasonable efficacy.
Calcium antagonists The role of calcium as a messenger in linking extracellular stimuli to the intracellular environment is well established, including its involvement in excitation–contraction coupling in striated, cardiac, and smooth muscle.1,5 Interference with calcium inflow or intracellular release is a very potent potential mechanism for bladder smooth muscle relaxation. Nifedipine Nifedipine has been shown to be an effective inhibitor of contraction induced by several mechanisms in 107,202 human and guinea pig bladder muscle. It has also been shown to block completely the non-cholinergic portion of the contraction produced by electrical field stimulation in rabbit bladder.203 Nifedipine more effectively inhibited those contractions induced by potassium than those by carbachol in rabbit bladder strips, whereas terodiline, an agent with both calcium-antagonistic and anticholinergic properties, had the opposite effect. However, terodiline did cause complete inhibition of the response of rabbit bladder to electrical field stimulation. At low concentrations, terodiline has mainly an antimuscarinic action, whereas at higher concentration a calcium-antagonistic effect becomes evident. Experiments in vitro appeared to show that these two effects were at least additive with regard to bladder contractility. Other experimental studies have confirmed the inhibitory effect of the calcium antagonists nifedipine, verapamil and diltiazem on a variety of experimental models of the activity of spontaneous and induced bladder muscle strips and whole bladder preparations.204,205 Andersson and colleagues206 showed that nifedipine effectively (and with some selectivity) inhibited the nonmuscarinic portion of the contraction of rabbit detrusor strips, whereas verapamil, diltiazem, flunarizine, and lidoflazine caused a marked depression of both the total and the non-muscarinic parts of contraction, suggesting that differences exist between various calcium-channel blockers with respect to their effects on at least electrically induced bladder muscle contraction. These results were used as support for the view that, even if ‘atropineresistant’ contractions in rabbit and human bladder had different causes, combined muscarinic-receptor and calcium-channel blockade might offer a more effective way 507
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of treating bladder overactivity than the single-mechanism therapies currently available. Terodiline A number of clinical studies on the inhibitory action of terodiline on bladder overactivity have shown clinical effectiveness.207 In a double-blind crossover study of 12 women with motor urge incontinence, Ekman and colleagues208 reported increases in bladder capacity and the volume at which sensation of urgency was experienced in all but one of the patients treated with terodiline, whereas placebo treatment had no objective or subjective effect. Peters and associates209 reported the results of a multicenter study that ultimately included data from 89 patients (from an original 128) and compared terodiline and placebo in women with motor urge incontinence. The daily dose in this study was 12.5 mg in the morning and 25 mg at night. The authors concluded that terodiline was more effective than placebo, but noted that this improvement was much more apparent on subjective than on objective assessment of cystometric and micturition data: 63% of patients preferred terodiline, regardless of treatment sequence; although statistically significant objective differences between terodiline and placebo were recorded, they were not very impressive. Tapp and colleagues210 reported on a double-blind, placebo-controlled study, using a dose-titration technique, that included 70 women with urodynamically proven DO and bladder capacities of less than 400 ml. Of the 34 women in the terodiline group, 62% considered themselves improved, and 38% were unchanged; of the 36 women in the placebo group, 42% considered themselves improved, 47% unchanged and 11% worse – a statistically significant response in favor of terodiline with regard to the improvement percentage. Micturition variables of daytime frequency, daytime incontinence episodes, number of pads used, and average voided volumes were statistically changed in favor of terodiline, but the absolute changes were relatively small (e.g. a change in daytime incontinence episodes in patients on placebo from 2.5 to 1.9 per day as opposed to 3.7 to 1.6 for those taking terodiline). Urodynamic data, although showing a trend in favor of terodiline in each parameter, showed no statistically significant differences in any category. Side-effects were noted in a large number and with equal frequency in both groups after the dose-titration phase. However, the incidence of anticholinergic side-effects was higher in the drug group: 29% of the terodiline patients versus 11% of the placebo patients spontaneously complained of a dry mouth, and 20% of the terodiline patients but none of the placebo patients complained of blurred vision.
The AHCPR guidelines120 list seven randomized controlled trials for terodiline; 94% of patients were women. The percentage of cures (all figures refer to percentage minus percentage on placebo) is listed as 18–33%, percentage of reduction in urge incontinence as 14–83%, and the percentages of side-effects and dropouts are 14–40% and 2–8%, respectively. Terodiline also exhibits an inhibitory effect on experimental neurogenic DO in the rabbit whole-bladder model, suggesting a possible role for local administration as well.211 Terodiline is almost completely absorbed from the gastrointestinal tract and has a low serum clearance. The recommended dosage in adults is 25 mg twice a day, reduced to an initial dose of 12 mg twice a day in geriatric patients. The half-life is around 60 hours. On this basis, Abrams207 logically proposes a once-daily dose but emphasizes the necessity of dose titration for each patient. The common side-effects seen with calcium antagonists (hypotension, facial flushing, headache, dizziness, abdominal discomfort, constipation, nausea, rash, weakness, and palpitations) have not been reported in larger initial clinical studies with terodiline, side-effects consisting primarily of those consequent on its anticholinergic action. However, questions have been raised about the occurrence of a rare arrhythmia (torsade de pointes) in patients taking terodiline simultaneously with antidepressants or antiarrhythmic drugs.213,214 Stewart and colleagues215 reported a prolongation of QT and QTc intervals and a reduction in heart rate in elderly patients taking 12.5 mg terodiline twice a day; these effects were apparent after 1 week but not after 1 day of therapy. These investigators also reported polymorphic ventricular tachycardia in four patients (three over age 80) receiving the drug. They advised avoidance of the drug in patients with cardiac disease requiring cardioactive drugs or those with hypokalemia, or in combination with other drugs that can prolong the QT interval, such as tricyclic antidepressants or antipsychotics. After other reports of apparent cardiac toxicity, the drug was voluntarily withdrawn by the manufacturer pending the results of further safety studies. The studies conducted for approval by the FDA were likewise voluntarily halted by the manufacturer pending the results of further safety studies. Other calcium-antagonist drugs have not been widely used to treat voiding dysfunction. A bladder-specific membrane calcium channel is not known to exist, and there is no agent that will specifically block intracellular calcium release only in bladder smooth muscle cells. Available information does not suggest that systemic therapy with calcium antagonists is an effective way to treat DO.
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Potassium-channel openers Potassium-channel openers relax various types of smooth muscle, including the detrusor, by increasing potassium efflux, resulting in membrane hyperpolarization.107 Hyperpolarization reduces the opening probability of ion channels involved in membrane depolarization, and excitation is reduced. Andersson216 summarized studies showing that, in isolated human and animal detrusor muscle, potassium-channel openers reduce spontaneous contractions and contractions occurring in response to electrical stimulation, carbachol and low (but not high) external potassium concentrations. There are some suggestions that bladder instability – at least that associated with intravesical obstruction and detrusor hypertrophy – may be secondary to supersensitivity to depolarizing stimuli. Theoretically, then, potassium-channel openers might be an attractive alternative for the treatment of DO in such circumstances without inhibiting the normal voluntary contractions necessary for bladder 217 emptying. Pinacidil is a compound that, in a concentrationdependent fashion, inhibits not only spontaneous myogenic contractions but also contractile responses induced by electrical field stimulation and carbachol in isolated human detrusor218 and in normal and hypertrophied rat detrusor muscle. Unfortunately, a preliminary study of this agent in a double-blind crossover format produced no effects on symptoms in nine patients with DO and bladder outlet obstruction.219 Nurse and associates220 reported on the use of cromakalim, another potassium-channel opener, in 17 patients who had refractory DO or neurogenic DO or had stopped other drug therapy because of intolerable side-effects. Of the 16 patients who completed the study, six (37.5%) showed a decrease in frequency and an increase in voided volume. Long-term observation was not possible because the drug was withdrawn owing to reported adverse effects of high doses in animal toxicology studies. Levcromakalim (the pharmacologically active enantiomer of cromakalim) was administered intravenously to six patients with high spinal cord lesions and reflex micturition:221 other than an increase in the duration of the detrusor contraction, no other urodynamic parameters associated with the neurogenic DO were significantly affected. Levcromakalim resulted in a rapid and significant drop in blood pressure which precluded studies at a higher dose. Overall, potassium-channel openers are not at present very specific for the bladder and are more potent in relaxing other tissues – hence their potential utility in the treatment of hypertension, asthma, and angina.
If tissue-selective potassium-activator drugs can be developed, they may prove very useful for the treatment of DO, irritable bowel syndrome, and epilepsy.222 Intravesical use has also been suggested221,222 as a method of potentially eliminating some of the intolerable systemic side-effects that limit the clinical utility of these agents. Side-effects of pinacidil have been studied best: they include headache, peripheral edema (in 25–50% of patients and dose related), weight gain, palpitations, dizziness, and rhinitis. Hypertrichosis and symptomatic T-wave changes have also been reported (30%). Fewer data are available on cromakalim, which can produce dose-related headache but rarely edema.216
Prostaglandin inhibitors PGs are ubiquitous compounds that have a potential role in the excitatory neurotransmission to the bladder, the development of bladder contractility or tension occurring during filling, the emptying contractile response of bladder smooth muscle to neural stimulation, and even the maintenance of urethral tone during the storage phase of micturition, as well as the release of this tone during the emptying phase. Downie and Karmazyn223 suggest a different type of contractile influence of PGs on detrusor muscle. They found that mechanical irritation of the epithelium of rabbit bladder increased basal tension and spontaneous activity in response to electrical stimulation and that these responses, related to the intensity of the irritative trauma, were mimicked by PGs. The effect was significantly reduced by pretreatment of the epithelium, but not the muscle, with PG synthetase inhibitors. Andersson107 suggests a possible sensitization of sensory afferent nerves by PGs, increasing afferent input at a given degree of bladder filling and contributing to the triggering of IVCs at a small bladder volume. Thus, there are many mechanisms whereby PG synthesis inhibitors might decrease bladder contractility in response to various stimuli; however, objective evidence that such can occur is scant. Cardozo and colleagues224 reported a double-blind, placebo-controlled study on the effects of 50 mg flurbiprofen (a PG synthetase inhibitor) three times a day on 30 women with DO. They concluded that the drug did not abolish IVCs or abnormal bladder activity but did delay the intravesical pressure rise to a greater degree of distension. Of these patients, 43% experienced sideeffects – primarily nausea, vomiting, headache, indigestion, gastric distress, constipation, and rash. Cardozo and Stanton225 reported symptomatic improvement in patients with detrusor instability who were given indo509
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metacin in doses of 50–200 mg daily, but this was a shortterm study with no cystometric data, and the drug was compared only with bromocriptine. The incidence of side-effects was high (19 of 32 patients), although no patient had to stop treatment because of them. Numerous PG synthetase inhibitors exist, most of which belong in the category of non-steroidal antiinflammatory drugs, and every clinician has a favorite. It should be remembered that these drugs can interfere with platelet function and contribute to excess bleeding in surgical patients; some may also have adverse renal effects.226
β-Adrenergic agonists
The presence of β-adrenoceptors in human bladder muscle has prompted attempts to increase bladder capacity with β-adrenergic stimulation. Such stimulation can cause significant increases in the capacity of animal bladders, which contain a moderate density of β-adrenoceptors.1 Studies in vitro show a strong dose-related relaxant effect of β2-agonists on the bladder body of rabbits but little effect on the bladder base or proximal urethra. Terbutaline, in oral doses of 5 mg three times a day, has been reported to have a ‘good clinical effect’ in some patients with urgency and urgency incontinence, but no significant effect on the bladders of neurologically normal humans without voiding difficulty.227 Although these results are compatible with those seen in other organ systems (β-adrenergic stimulation causes no acute change in total lung capacity in normal humans but does favorably affect patients with bronchial asthma), there are few adequate studies of the effects of β-adrenergic stimulation in patients with DO. Lindholm and Lose228 used 5 mg terbutaline three times a day in eight women with motor and seven with sensory urge incontinence; after 3 months of treatment, 14 patients claimed to have experienced beneficial effects, and 12 became subjectively continent. In six of eight cases, the detrusor became stable on cystometric examination. The volume at first desire to void increased in the patients with originally unstable bladders from a mean of 200 to 302 ml, but the maximum cystometric capacity did not change. Nine patients had transient side-effects – including palpitations, tachycardia, or hand tremor – and in three of these the sideeffects continued but were acceptable to the patient. The drug was discontinued in one patient because of severe adverse symptoms. Gruneberger,229 in a doubleblind study, reported that clenbuterol had produced a good therapeutic effect in 15 of 20 patients with motor urge incontinence.
Unfavorable results of β-agonist usage for bladder overactivity were published by Castleden and Morgan230 and Naglo and associates.231 As yet there have been no controlled clinical trials on the treatment of overactive bladder with b agonists.
Tricyclic antidepressants Many clinicians have found that tricyclic antidepressants, particularly imipramine hydrochloride, are useful for facilitating urine storage, both by decreasing bladder contractility and by increasing outlet resistance.9 These agents have been the subject of extensive and highly sophisticated pharmacologic investigation to determine the mechanisms of action responsible for their varied effects.78,232,233 Most data have been accumulated as a result of trying to explain the antidepressant properties of these agents and consequently involve primarily CNS tissue. Although the results, conclusions and speculations based on the data are extremely interesting, it should be emphasized that it is essentially unknown whether they apply to, or have relevance for, the lower urinary tract. In varying degrees, all of these agents have at least three major pharmacologic actions:
• they have central and peripheral anticholinergic effects at some (but not all) sites;
• they block the active transport system in the
•
presynaptic nerve ending that is responsible for the reuptake of the released amine neurotransmitters noradrenaline and serotonin; they are sedatives, an action that occurs presumably on a central basis but is perhaps related to antihistaminic properties (at H1 receptors, although they also antagonize H2 receptors to some extent).
There is also evidence that these agents desensitize at least some α2- and some β2-adrenoceptors. Paradoxically, they also have been shown to block some α- and serotonin-1 receptors. Imipramine Imipramine has prominent systemic anticholinergic effects but only a weak antimuscarinic effect on bladder smooth muscle.234,235 It does have a strong direct inhibitory effect on bladder smooth muscle, however, that is neither anticholinergic nor adrenergic.232,236,237 This may be due to a local anesthetic-like action at the nerve terminals in the adjacent effector membrane – an effect that seems to occur also in cardiac muscle238 – or it may be due to an inhibition of the participation of calcium in the excitation–contraction coupling process.234,236
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Akah239 has provided supportive evidence in the rat bladder that desipramine, the active metabolite of imipramine, depresses the response to electrical field stimulation by interfering with calcium movement (perhaps not only extracellular calcium movement but also internal translocation and binding). Direct evidence suggesting that the effect of imipramine on noradrenaline reuptake occurs in lower urinary tract tissue as well as brain tissue in the rabbit has been provided by Foreman and McNulty.240 In addition, they describe a significantly greater but similar effect of tomoxetine in the bladder and urethra in this model. Tomoxetine inhibits noradrenaline reuptake selectively, whereas imipramine has a non-selective effect. This fact suggests a potential new clinical approach to the use of more selective and potent reuptake inhibitors for the treatment of incontinence. In attempting to correlate clinical effects with mechanisms of action, one might also postulate a β-receptor-induced decrease in bladder body contractility if peripheral blockade of noradrenaline reuptake does occur there owing to the increased concentration of β-receptors compared with α-adrenoceptors in that area. An enhanced α-adrenergic effect in the smooth muscle of the bladder base and proximal urethra, where α-receptors outnumber β-receptors, is generally considered the mechanism whereby imipramine increases outlet resistance. Clinically, imipramine seems to be effective in decreasing bladder contractility and increasing outlet resistance.241–244 Castleden and colleagues244 began therapy in elderly patients with DO with a single 25 mg nighttime dose of imipramine, which was increased every third day by 25 mg until the patient was continent or had side-effects, or a dose of 150 mg was reached. Six of 10 patients became continent and, in those who underwent repeated cystometry, bladder capacity increased by a mean of 105 ml and bladder pressure at capacity decreased by a mean of 18 cmH2O. MUP increased by a mean of 30 cmH2O. Although our subjective impression242 was that the bladder effects became evident only after days of treatment, some patients in the Castleden series became continent after only 3–5 days of therapy. Our usual adult dose for treatment of voiding dysfunction is 25 mg four times a day; less frequent administration is possible because of the drug’s long half-life. Half that dose is given in elderly patients, in whom the drug half-life may be prolonged. In our experience, the effects of imipramine on the lower urinary tract are often additive to those of atropine-like agents; consequently, a combination of imipramine and an antimuscarinic or an antispasmodic is sometimes especially useful for decreasing bladder contractility.242 If imipramine is used
in conjunction with an atropine-like agent, it should be noted that the anticholinergic side-effects of the drugs may be additive. It has been known for many years that impramine is relatively effective for the treatment of nocturnal enuresis in children. Doses for this condition range from 10 to 50 mg daily. It is not known whether the mechanisms of drug action in this situation are the same as those for decreasing bladder contractility. Korczyn and Kish245 have presented evidence that the mechanism of the antienuretic effect differs from that of the peripheral anticholinergic effect and the drug’s antidepressant effect. The antienuretic effect occurs soon after initial administration, whereas the antidepressant effects generally take 2–4 weeks to develop. Doxepin Doxepin is another tricyclic antidepressant that has been found (using rabbit bladder strips in vitro) to be more potent than other tricyclic compounds with respect to antimuscarinic and musculotropic relaxant activity.238 Lose and colleagues,246 in a randomized double-blind crossover study of women with IVCs and frequency, urgency or urge incontinence, found that this agent caused a significant decrease in control over night-time frequency and incontinence episodes, and a near-significant decrease in urine loss (by the pad-weighing test) and in the cystometric parameters of first sensation and maximum bladder capacity. The dose of doxepin used was either a single 50 mg bedtime dose or this dose plus an additional 25 mg in the morning. The number of daytime incontinence episodes decreased in both doxepin and placebo groups, but the difference was not statistically significant. Doxepin treatment was preferred by 14 patients, whereas two preferred placebo; three patients had no preference. Of the 14 patients who stated a preference for doxepin, 12 claimed that they became continent during treatment and two claimed improvement; the two patients who preferred placebo also claimed improvement. The AHCPR guidelines120 combine results for imipramine and doxepin, citing only three randomized controlled trials, with an unknown percentage of women patients. The percentage of cures (all figures refer to percentage minus the percentage on placebo) are listed as 31%, percentage of reduction in urge incontinence as 20–88%, and percentage of side-effects as 0–70%. Side-effects of tricyclic antidepressants When the tricyclic antidepressants are used in the generally larger doses employed for antidepressant effects, their most frequent side-effects are those attributable to 511
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their systemic anticholinergic activity.78,232 Allergic phenomena – including rash, hepatic dysfunction, obstructive jaundice, and agranulocytosis – may also occur but are rare. CNS side-effects may include weakness, fatigue, parkinsonian effects, fine tremors (noted mostly in the upper extremities), a manic or schizophrenic picture, and sedation, probably from an antihistaminic effect. Postural hypotension may also be seen, presumably due to selective blockade (a paradoxical effect) of α1-adrenoceptors in some vascular smooth muscle. Tricyclic antidepressants may also cause excess sweating of obscure origin and a delay in orgasm or orgasmic impotence, the cause of which is likewise unclear. They may also produce arrhythmias and can interact in deleterious ways with other drugs; thus, caution must be observed in using these drugs in patients with cardiac disease.78 Whether cardiotoxicity will prove to be a legitimate concern in patients receiving smaller doses (smaller than those used for treatment of depression) for lower urinary tract dysfunction remains to be seen, but is a matter of potential concern. Consultation with a patient’s physician or cardiologist is always helpful before such therapy is instituted in questionable situations. The use of imipramine is contraindicated in patients receiving monoamine oxidase inhibitors because severe CNS toxicity can be precipitated, including hyperpyrexia, seizures, and coma. Some potential side-effects of antidepressants may be especially significant in the elderly – specifically weakness, fatigue and postural hypotension. If imipramine or any of the tricyclic antidepressants is to be prescribed for the treatment of voiding dysfunction, the patient should be thoroughly informed about the fact that this is not the usual indication for this drug and that potential side-effects exist. Reports of significant side-effects (severe abdominal distress, nausea, vomiting, headache, lethargy and irritability) following abrupt cessation of high doses of imipramine in children suggest that the drug should be discontinued gradually, especially in patients receiving high doses. Botulinum toxin Botulinum toxin (BTX) is a presynaptic inhibitor of ACh release and the release of other neurotransmitters. It was previously discussed in its use to facilitate emptying by relaxing the striated sphincter. Similarly, the same effects of decreasing muscle contractility can be applied to the bladder by cystoscopic injection of BTX directly into the detrusor muscle. This produces a chemical denervation which is reversible after about 6 months. Of the seven subtypes of botulinum toxin which have been identified, botulinum A toxin (BTX-A) is the most com-
monly used, with botulinum B toxin (BTX-B) being the next most commonly used. There have been some open label and few doubleblind studies reporting its use in the treatment of neurogenic and idiopathic DO. Although preliminary studies using BTX-A look promising, the use of BTX-B is too early to tell. Schurch247 evaluated the use of BTX-A in patients with neurogenic DO secondary to spinal cord injury who were on intermittent catheterization. The study was prospective but non-randomized. A total of 21 patients received 200–300 units of BTX-A. At 6 weeks, 17 of 19 patients were completely continent and could decrease or stop oral agents for their DO. The two who did not improve were given the lower dose of BTX-A (200 units). Urodynamics also demonstrated an increase in mean bladder capacity, post void residual, and a decrease in maximum voiding pressure. In some of the patients, the improvements were still durable out to 36 weeks. Reitz and colleagues from Europe describe the European experience with BTX-A.248 This retrospective study examined the data on 200 patients with neurogenic DO. At 12 weeks, there was a significant increase in the mean maximum cystometric bladder capacity, post void residual, and compliance. A majority of the patients could reduce or discontinue their anticholinergic medications. Data at 36 weeks revealed continued improvement. Two studies investigated the use of BTX for the treatment of non-neurogenic DO. Rapp and colleagues249 performed BTX-A intradetrusor injections in 35 patients (29 women and 6 men) with frequency, urgency, and/ or urge incontinence. They used 300 units of BTX-A injected transurethrally into 30 different sites within the bladder. There was a significant decrease in the scores recorded by the Incontinence Impact Questionnaire and Urinary Distress Inventory short forms. Overall, 60% of patients reported a slight to complete improvement in symptoms. Improvement was seen for at least 6 months. Dykstra et al.250 used escalating doses of BTX-B in a similar cohort of patients; 14 of 15 patients reported decreased frequency of urination and subjective improvement. BTX does appear to be a promising new therapy for facilitating bladder storage. Further placebo-controlled studies need to be carried out to appreciate its true efficacy, as well as determine the optimum dosages and locations of injections.
Dimethyl sulfoxide Dimethyl sulfoxide (DMSO), a naturally occurring organic compound used as an industrial solvent for
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many years, has multiple pharmacologic actions (membrane penetration, anti-inflammatory, local analgesic, bacteriostatic, diuretic, cholinesterase inhibitor, collagen solvent, vasodilator) and has been used for the treatment of arthritis and other musculoskeletal disorders. The formulation for human intravesical use is a 50% solution. Sant251 has summarized the pharmacology and clinical usage of DMSO and has tabulated good-to-excellent results in 50–90% of collected series of patients treated with intravesical instillations for interstitial cystitis. However, DMSO has not been shown to be useful in the treatment of neurogenic and non-neurogenic DO, or in any patient with urgency or frequency without interstitial cystitis.
Polysynaptic inhibitors Baclofen has been discussed previously with agents that decrease outlet resistance secondary to striated sphincter dyssynergia. It is also capable of depressing neurogenic detrusor overactivity due to spinal cord injury.252 Taylor and Bates,253 in a double-blind crossover study, reported that it was very effective in decreasing both day and night urinary frequency and incontinence in patients with idiopathic DO. Cystometric changes were not recorded, however, and considerable improvement was also obtained in the placebo group. The intrathecal use of baclofen for treatment of DO is a potentially exciting area, and further reports are awaited.
Other potential agents NO is hypothesized to be a mediator of the NANC relaxation of the outlet smooth muscle that occurs with bladder contraction.5 Evidence exists that it is also involved in relaxation of bladder body smooth muscle,254 and this provides interesting fodder for speculation – is relaxation impaired in some types of overactivity and can NO analogs or synthetase stimulators be developed as agents to inhibit detrusor contractility? Glyceryl trinitrate releases NO in vivo and achieves its cardiovascular effects by relaxing vascular smooth muscle. A pilot study of 10 patients with DO given transdermal NO showed significant decreases in episodes (per 24 hours) of frequency (from 9.7 to 6.7), nocturia (from 1.84 to 1.09), and incontinence (from 0.6 to 0.36).234 Although the ubiquity of NO might seem to mitigate its potential use in treating bladder overactivity (unless more organspecific substrates or receptors are found), randomized controlled trials should be conducted. Soulard and colleagues255 have described the effects of JO1870 on bladder activity in the rat. This nonanticholinergic probable opioid agonist increased bladder capacity and threshold pressure responsible for
micturition in a dose-dependent fashion, raising the possibility of the use or development of opioid agonists with selectivity for receptors involved in the micturition reflex. Constantinou256,257 described the effects of thiphenamil hydrochloride on the lower urinary tract of healthy female volunteers and those with detrusor incontinence. This drug was said to be a ‘synthetic antispasmodic’. In a randomized controlled trial, based on diary records from 14 patients with DO, it was reported that voiding frequency per day decreased significantly (from 10.3 to 8.0 times), but placebo values were not given. Daily incontinence episodes decreased in nine analyzable patients from 2.3 to 1.6 (not significant, placebo values not given), with pad dryness (rated on a 0–4 scale) improving from 1.6 to 1.2 (significant, but no placebo data given). Objective urodynamic results (in 16 patients) showed no flowmetry changes, no changes in bladder capacity, some increase in first sensation of fullness, and a significant decrease in detrusor voiding pressure (from 46.1 to 31.9 cmH2O) over placebo. The data and interpretation in this article are confusing, especially because the study of healthy volunteers showed no urodynamic differences except an increase in maximum flow rate (from 16.9 to 27.7 ml/s) at a drug dose of 800 mg. The most that can be said about the clinical use of thiphenamil is that, now a question has been raised, it needs to be addressed by further ‘cleaner’ studies with internally consistent results.
Increasing bladder capacity by decreasing sensory (afferent) input Vanilloids: capsaicin and resiniferatoxin Decreasing afferent input peripherally is the ideal treatment for both sensory urgency and DO in a bladder with relatively normal elastic or viscoelastic properties in which the sensory afferents constitute the first limb in the abnormal micturition reflex. Maggi has written extensively about this type of treatment, specifically with reference to the properties of capsaicin (CAP).258–260 CAP is an irritant and algogenic compound obtained from hot red peppers that has highly selective effects on a subset of mammalian sensory neurons, including polymodal receptors and warm thermoreceptors.261 CAP produces pain by selectively activating polymodal nociceptive neurons by membrane depolarization and opening a cation-selective ion channel, which can be blocked by ruthenium red. Repeated administration induces desensitization and inactivation of sensory neurons by several mechanisms. Systemic and topical CAP produce a reversible antinociceptive and anti-inflamma513
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tory action after an initially undesirable algesic effect. Local or topical application blocks C-fiber conduction and inactivates neuropeptide release from peripheral nerve endings, accounting for local antinociception and reduction of neurogenic inflammation. Resiniferatoxin (RTX) is an analog of CAP, and is approximately 1000 times more potent for desensitization than CAP,262 but only a few hundred times more potent for excitation.263 Systemic CAP produces antinociception by activating specific receptors on afferent nerve terminals in the spinal cord; spinal neurotransmission is subsequently blocked by a prolonged inactivation of sensory neurotransmitter release. With local administration (intravesical), the potential advantage of CAP is a lack of systemic side-effects. The actions are highly specific when the drug is applied locally – the compound affects primarily small-diameter nociceptive afferents, leaving the sensations of touch and pressure unchanged, although heat (not cold) perception may be reduced; motor fibers are not affected.264 The effects are reversible, although it is not known whether initial levels of sensitivity are regained. Maggi260 reviewed the therapeutic potential of capsaicin-like molecules. Capsaicin-sensitive primary afferents (CSPAs) innervate the human bladder, and intravesical instillation of capsaicin into human bladder produces a concentration-dependent decrease in first desire to void, decreased bladder capacity, and a warm burning sensation. Maggi and colleagues258 used doses of 0.01, 1.0, and 10 µmol, administered in ascending order at intervals of 10–15 minutes as constant infusions of 20 ml/minute until micturition occurred. Five capsaicin-treated patients with ‘hypersensitive disorder’ reported either a complete disappearance of symptoms (four patients) or marked attenuation of symptoms (one patient), beginning 2–3 days after administration and lasting for 4–16 days; after that time the symptoms gradually reappeared but were no worse. Fowler and colleagues99 found that considerably higher doses (up to 1–2 mm for 30 minutes) were necessary to produce an effect in humans;98 however, these investigators reported that bladder control improved within 2 days, and the improvement lasted for 3–6 months. Lower doses (0.1– 100 µmol) produced ‘no long lasting benefit’. In a later study, Fowler and colleagues265 administered intravesical CAP to 14 patients with DO and intractable urinary incontinence, 12 of whom had known spinal cord disease. A single intravesical instillation of 1 or 2 mmol capsaicin revealed a response in nine patients (all of whom had spinal cord disease), with four of these patients having only a ‘partial’ response and five patients having complete and durable (3 weeks to 6 months)
responses, defined as complete continence on intermittent catheterization. In the nine patients who responded to treatment, mean bladder capacity increased from 106 to 302 ml and maximum detrusor pressure decreased from 54 to 36 cmH2O. There were no long-term adverse effects from the therapy. Similar results were noted by Das and colleagues,266 who treated seven patients with neurogenic bladders with four increasing doses of intravesical capsaicin over a period of several weeks (100 µmol, 500 µmol, 1 mmol and 2 mmol). Only five of seven patients were able to complete the therapy, owing to the discomfort induced by the instillation. Of these five patients, three had symptomatic and urodynamic improvement. Geirsson and associates267 treated 10 patients with traumatic spinal cord injury and neurogenic bladder with 2 mmol intravesical capsaicin; urodynamic improvement (decreased voiding pressure and increased bladder capacity) was noted in 9/10 patients at 6 weeks. Subjective improvement was noted in 4/10 patients at 2–7 months after therapy, two of whom became continent. All 10 patients had no improvement or a worsening of symptoms during the first 1–2 weeks after instillation. Adverse reactions included severe burning on instillation in those patients with partial spinal lesions, precipitation of autonomic dysreflexia in several other patients, and gross hematuria in four patients. Chandiramani and colleagues268 were able to reduce significantly the short-term toxicity (triggering of involuntary detrusor contractions) and discomfort of intravesical capsaicin therapy by pretreatment with an instillation of 2% topical lidocaine. Pretreatment with lidocaine did not alter the therapeutic efficacy of the capsaicin. An efferent function of CSPAs is the release of neurotransmitters from the peripheral endings of these sensory neurons, such as tachykinins and calcitonin gene-related peptide.258 These neurotransmitters can produce events collectively known as neurogenic inflammation, which can include smooth muscle contractions, increased plasma protein extravasation, vasodilation, mast cell degranulation, facilitation of transmitter release from nerve terminals, and recruitment of inflammatory cells. This is another reason why intravesical capsaicin could theoretically be useful in treating the pain and related problems of interstitial cystitis and certain types of bladder overactivity that originate in primary afferents. The peripheral terminals of CSPAs form a dense plexus just below the bladder urothelium, and fibers penetrating the urothelium come into contact with the lumen. This location, combined with their peculiar chemosensitivity, permits CSPAs to detect ‘backflow’ of
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chemicals across the urothelium, which is thought to occur during conditions leading to breakdown of the ‘barrier function’ of the urothelium.260 If the ‘barrier’ theory or the ‘leaky urothelium’ theory of the pathogenesis of the interstitial cystitis is true, for some or many of the patients with this condition, the CSPAs in such patients may be stimulated by urine constituents leaking back across the urothelium, and, under these circumstances, a local release of neuropeptides may well contribute to the production of neurogenic inflammation. If this is so, as Maggi suggests,260 a local treatment leading to desensitization of CSPAs would be doubly advantageous. With capsaicin, however, excitation precedes desensitization, somewhat limiting the potential for therapy in humans. A preferable analog would produce the latter action while reducing or eliminating the former. Last, Maggi260 discusses the possible long-term disadvantages of such therapy as related to the potential physiologic roles – trophic or protective – of CSPAs and their secretions in response to stimulation. RTX has been shown to be beneficial in several studies.269–273 de Seze and colleagues269 compared the efficacy and tolerability of non-alcohol CAP (1 mmol) versus RTX (100 nmol) in 10% alcohol in a randomized, double-blind, parallel group study in 39 spinal cord injured patients with neurogenic DO. Follow-up was 3 months. On day 30, similar clinical and urodynamic improvement was found in 78% and 83% of patients with CAP and 80% and 60% with RTX, respectively. The benefit remained in two-thirds of the two groups after 3 months. There was no difference in side-effects in the two groups. Overall, intravesical capsaicin and RTX treatment may be a promising therapy for DO, and possibly sensory dysfunction of the lower urinary tract; however, many problems exist. Optimal dosage, method and timing of delivery, as well as delivery vehicle (diluent) remain unclear. The patients likely to respond to this therapy are not yet defined, and randomized, placebocontrolled studies to determine overall efficacy have not yet been performed. Finally, discomfort and triggering of involuntary bladder activity with instillation and postinstillation gross hematuria may be problematic.
Increasing outlet resistance α-Adrenergic agonists The bladder neck and proximal urethra contain a preponderance of α-adrenergic receptor sites, which, when stimulated, produce smooth muscle contraction.1,2,5 The static infusion urethral pressure profile is altered by such stimulation, producing an increase in MUP and maxi-
mum urethral closure pressure (MUCP). α-Adrenergic stimulants generally increase outlet resistance to a variable degree but are most often limited by their potential side-effects including blood pressure elevation, anxiety and insomnia due to stimulation of the CNS, headache, tremor, weakness, palpitations, cardiac arrhythmia, and respiratory difficulties. All such agents should be used with caution in patients with hypertension, cardiovascular disease or hyperthyroidism.274 The use of ephedrine to treat SUI was mentioned as early as 1948.272 This is a non-catecholamine sympathomimetic agent that enhances release of noradrenaline from sympathetic neurons and directly stimulates both α- and β-adrenoceptors.250 The oral adult dosage is 25– 50 mg four times a day. Some tachyphylaxis develops in response to its peripheral actions, probably as a result of depletion of noradrenaline stores. Pseudoephedrine, a stereoisomer of ephedrine, is used for similar indications and carries similar precautions. The adult dosage is 30–60 mg four times a day, and the 30 mg dose form is available in the United States without prescription. Diokno and Taub275 reported a ‘good-to-excellent’ result in 27/38 patients with sphincteric incontinence treated with ephedrine sulfate. Beneficial effects were most often achieved in those with minimal-to-moderate wetting; little benefit was achieved in patients with severe stress incontinence. A dose of 75–100 mg of norephedrine chloride has been shown to increase MUP and MUCP in women with SUI.276 At a bladder volume of 300 ml, MUP rose from 82 to 110 cmH2O, and MUCP rose from 63 to 93 cmH2O. The functional profile length did not change significantly. Obrink and Bunne,277 however, noted that 100 mg norephedrine chloride given twice a day did not improve severe stress incontinence sufficiently to offer it as an alternative to surgical treatment. They further noted in their group of 10 such patients that the MUCP was not influenced at rest or with stress at low or moderate bladder volumes. Lose and Lindholm278 treated 20 women with stress incontinence with norfenefrine, an α-agonist, given as a slow-release tablet: 19 patients reported reduced urinary leakage; 10 reported no further stress incontinence. MUCP increased in 16 patients during treatment, the mean rise being 53–64 cmH2O. It is interesting and perplexing that most patients reported an effect only after 4 days of treatment. This delay is difficult to explain on the basis of drug action, unless one postulates a change in the number or sensitivity of α-adrenoceptors. The group at Kolding Hospital in Denmark has published three other articles of note on the use of norfenefrine for sphincteric incontinence, with interesting 515
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results. Forty-four patients with SUI were randomized to treatment with norfenefrine (15–30 mg three times a day) versus placebo for 6 weeks.279 Subjectively, 12/23 (52%) of the norfenefrine group reported improvement as opposed to 7/21 (33%) of the placebo group – a difference that was not significant. Continence was reported by six (26%) norfenefrine patients and three (14%) placebo patients (not significant). Judged by a stress test, seven patients in each group became continent; 11/23 (48%) improved both subjectively and objectively in the norfenefrine group as opposed to 5/21 (24%) in the placebo group (p=0.09). MUCP increased significantly, from 50 to 55 cmH2O in the norfenefrine group, and from 55 to 65 cmH2O in the placebo group! Although the patients were said to have ‘genuine stress incontinence’, 5/12 with ‘urge incontinence’ were reported cured with norfenefrine, and 4/7 with placebo! Diernaes and associates280 reported on the results of a 1-hour pad test in 33 women with either SUI or combined stress incontinence and urgency treated with 30 mg norfenefrine three times a day. Leakage of more than 10 g was required for entry into the study. Subjective improvement was reported by 10 patients (30%). Continence as shown by pad test was found in six patients (18%). Pad tests were graded on a scale of 1–4. At 12 weeks, 20 patients (61%) had improved by at least one grade (p<0.05), but at 3 weeks the number was 13 (39%; not significant). Lose and colleagues281 studied 44 women scheduled for operation for SUI who were treated with 15–30 mg norfenefrine three times a day versus placebo for 3–4.5 months and were then evaluated for outcome after a median observation period of 30 months. The description and categorization of results were somewhat confusing, but the results were interesting. Originally 23 patients were allocated to the norfenefrine group and 21 to placebo. Results were categorized as follows:
• cured or much improved with no further treatment • • • •
wanted; underwent surgery for relief; wanted medical therapy reinstituted; uncertain about what kind of treatment they wanted; used pads or pelvic floor exercises.
At the end of a 6-week initial treatment period and reevaluation, patients whose initial treatment had had no effect at all were crossed over to the other group. It is obvious that a powerful placebo effect occurred, for reasons unknown, and therefore caution must be exercised in the evaluation of all modalities of therapy for sphincteric (and detrusor) incontinence.
Phenylpropanolamine (PPA) hydrochloride shares the pharmacologic properties of ephedrine and is approximately equal in peripheral potency while causing less central stimulation.282 It is available in tablets of 25 or 50 mg, and 75 mg timed-release capsules, and is a component of numerous proprietary mixtures marketed for the treatment of nasal and sinus congestion (usually in combination with an H1 antihistamine) and as appetite suppressants. Using doses of 50 mg three times a day, Awad and associates283 found that 11/13 women and 6/7 men with stress incontinence were significantly improved after 4 weeks of therapy. MUCP increased from a mean of 47 to 72 cmH2O in patients with an empty bladder and from 43 to 58 cmH2O in patients with a full bladder. Using a capsule (Ornade) containing 50 mg PPA, 8 mg chlorpheniramine (an antihistamine) and 2 mg isopropamide (an antimuscarinic), Stewart and colleagues284 found that, of 77 women with SUI, 18 were ‘completely cured’ with one sustained-release capsule, 28 patients were ‘much better’, 6 were ‘slightly better’, and 25 were ‘no better’. In 11 men with stress incontinence after prostatectomy, the numbers in the corresponding categories were one, two, one and seven. The formulation of Ornade has now been changed, and each capsule of drug now contains 75 mg PPA and 12 mg chlorpheniramine. Collste and Lindskog285 reported on a group of 24 women with SUI treated with PPA or placebo with a crossover after 2 weeks. Severity of SUI was graded 1 (slight) or 2 (moderate). Average MUCP overall increased significantly with PPA compared with placebo (48–55 versus 48–49 cmH2O). This was a significant difference in grade 2 but not in grade 1 patients. The average number of leakage episodes per 48 hours was reduced significantly overall for PPA patients but not in placebo patients (five to two versus five to six). This was significant for grade 1 but not for grade 2 patients. Subjectively, six of 24 patients thought that both PPA and placebo were ineffective. Among the 18 patients (of 24) who reported a subjective preference, 14 preferred PPA and four placebo. Improvements were rated subjectively as good, moderately good and slight. Improvements obtained with PPA were significant compared with those for placebo for the entire population and for both groups separately. The AHCPR guidelines120 reported eight randomized controlled trials with PPA 50 mg twice a day for SUI in women. Percentage cures (all figures refer to percentages minus percentages on placebo) are listed as 0–14, percentage reduction in incontinence as 19–60, and percentage side-effects and percentage dropouts as 5–33 and 0–4.3, respectively.
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Some authors have emphasized the potential complications of PPA. Mueller286 reported on a group of 11 patients who had significant neurologic symptoms (acute headache, psychiatric symptoms or seizures) after taking ‘look-alike pills’ thought to contain amfetamines but actually containing PPA. Biaggioni et al.287 emphasized the possibility of blood pressure elevation, especially in patients with autonomic impairment. Lasagna288 pointed out that previously reported blood pressure elevations occurred with a product that differed from American PPA and probably contained a different and much more potent isomer. He noted that although a huge volume of PPA has been consumed in the form of decongestants and anorectic medications, the world literature has reported only a minimum number of possible toxic reactions, most of which involved excessively high doses in combination medications. Liebson and colleagues289 found no cardiovascular or subjective adverse effects with doses of 25 mg three times a day or a 75 mg sustainedrelease preparation in a population of 150 healthy normal volunteers. Blackburn and colleagues,290 in a larger series of healthy subjects using many over-the-counter formulations, concluded that a statistically significant but clinically unimportant pressor effect existed during the first 6 hours after administration of PPA and that this was greater with sustained-release preparations. Caution should still be exercised in individuals known to be significantly hypertensive and in elderly patients, in whom pharmacokinetic function may be altered. Midodrine is a long-acting α-adrenergic agonist reported to be useful in the treatment of seminal emission and ejaculation disorders following retroperitoneal lymphadenectomy. Treatment with 5 mg twice a day for 4 weeks in 20 patients with stress incontinence produced a cure in one and improvement in 14.291 The MUCP rose by 8.3%, and the planometric index of the continence area on profilometry increased by 9%. The actions of imipramine have already been discussed. On a theoretical basis, an increase in urethral resistance might be expected if, indeed, an enhanced α-adrenergic effect at this level resulted from an inhibition of noradrenaline reuptake. However, as mentioned previously, imipramine also causes α-adrenergic blocking effects, at least in vascular smooth muscle. Many clinicians have noted improvement in patients treated with imipramine primarily for bladder overactivity but who had in addition some component of sphincteric incontinence. Gilja and colleagues292 reported a study of 30 women with stress incontinence who were treated with 75 mg imipramine daily for 4 weeks: 21 women subjectively reported continence; the mean MUCP for the group increased from 34.06 to 48.23 mmH2O.
Although some clinicians have reported spectacular cure and improvement rates with α-adrenergic agonists and agents that produce an α-adrenergic effect in the outlet of patients with sphincteric urinary incontinence, our own experience coincides with those who report that such treatment often produces satisfactory or some improvement in mild cases but rarely total dryness in patients with severe or even moderate stress incontinence. Nevertheless, a clinical trial, when possible, is certainly worthwhile, especially in conjunction with pelvic floor physiotherapy or biofeedback.
β-Adrenergic antagonists and agonists
Theoretically, β-adrenergic blocking agents might be expected to ‘unmask’ or potentiate an α-adrenergic effect, thereby increasing urethral resistance. Gleason and colleagues293 reported success in treating certain patients with SUI with propranolol, using oral doses of 10 mg four times a day: the beneficial effect became manifest only after 4–10 weeks of treatment. Cardiac effects occur rather promptly after administration of this drug, but hypotensive effects do not usually appear as rapidly, although it is difficult to explain such a long delay in onset of the therapeutic effect on incontinence on this basis. Kaisary294 also reported success with propranolol in the treatment of stress incontinence. Although such treatment has been suggested as an alternative to α-agonists in patients with sphincteric incontinence and hypertension, few, if any, subsequent reports of such efficacy have appeared. Others have reported no significant changes in urethral profile pressures in normal women after β-adrenergic blockade.295 Although 10 mg four times a day is a relatively small dose of propranolol, it should be recalled that the major potential side-effects of the drug are related to the therapeutic β-blocking effects. Heart failure may develop, as well as an increase in airway resistance, and asthma is a contraindication to its use. Abrupt discontinuation may precipitate an exacerbation of anginal attacks and rebound hypertension.282 β-Adrenergic stimulation is generally conceded to decrease urethral pressure, but β2-agonists have been reported to increase the contractility of fast-contracting striated muscle fibers (extensor digitorum longus) from guinea pigs and suppress that of slow-contracting fibers (soleus).296 Clenbuterol, a selective β2-agonist, has been reported to potentiate, in a dose-dependent fashion, the field stimulation-induced contraction in isolated periurethral muscle preparation in the rabbit. The potentiation is greater that that produced by isoprenaline and is suppressed by propranolol. Kishimoto and colleagues297 reported an increase in urethral pressure with clinical 517
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use of clenbuterol and speculated on its promise in the treatment of sphincteric incontinence. Although the differential effects on the smooth and striated musculature of the outlet and even on different fiber types of the striated sphincter may be functionally antagonistic, one should not ignore the possibility of an augmentative effect on outlet resistance by a drug such as clenbuterol under certain physiologic conditions. Other β2-agonists are salbutamol and terbutaline.
Duloxetine Duloxetine, a combined serotonin- and norepinephrinereuptake inhibitor, increases sphincteric muscle activity during the filling and storage phase of micturition in the model of the irritated bladder in the cat. This relatively new pharmacologic agent has been used clinically as an antidepressant.298 In a study of its effects on the lower urinary tract in the cat, Thor and Katofiasc299 noted that duloxetine significantly increased bladder capacity (probably through a CNS effect), as well as enhanced external urethral sphincter activity with no effect on sphincter activity during voiding. To date, there have been several randomized controlled studies documenting the effects of duloxetine in the treatment of stress incontinence. Dmochowski and colleagues300 enrolled 683 patients in a doubleblind, placebo-controlled study comparing duloxetine 40 mg twice daily to placebo. There was a significantly greater decrease in incontinence episode frequency in the duloxetine group (50%) compared to the placebo group (27%), as well as improvement in quality of life. The improvements with duloxetine were associated with significant increases in the voiding interval (20 minutes versus 2 minutes) compared to placebo. The discontinuation rate was higher in the duloxetine group (24%) than placebo (4%), most frequently due to nausea (6.4%) which was usually transient. Similar results were reported by Millard et al.301 and van Kerrebroeck et al.302 investigating the effects of duloxetine in the treatment of SUI outside the United States. At the present time this medication is not indicated for the use of SUI in the United States.
Estrogens Although estrogens have been recommended for the treatment of female urinary incontinence as early as 1941,295 there is still controversy over their use and benefit–risk ratio for this purpose. Although numerous clinical studies exist, there has been little consistency in methodology, many of the studies have been observational, different formulations of estrogens have been tested, and the data can be conflicting. In some cases,
raw data seem to be ignored in favor of statistics; however, as always, there is no lack of opinions. Significant work has been done on the effects of estrogenic hormones on the lower urinary tract. Hodgson and associates303 reported that the sensitivity of the rabbit urethra to α-adrenergic stimulation was estrogen dependent. Levin and co-workers304,305 showed that parenteral estrogen administration can change the autonomic receptor content and the innervation of the lower urinary tract of immature female rabbits, increasing the response to α-adrenergic, muscarinic and purinergic stimulation in the bladder body but not the base, and significantly increasing the number of α-adrenergic and muscarinic receptors in the bladder body but not the base. Other work5 has shown a decrease in muscarinic receptor density following estradiol treatment of mature female rabbits, and either no change or a decreased detrusor response to cholinergic and electrical stimulation. Levin and co-workers305 concluded that pregnancy induced an increase in the purinergic and a decrease in the cholinergic responses of the rabbit bladder to field stimulation, and Tong and colleagues306 reported a decrease in the α-adrenergic response of the mid-part and base of the bladder of pregnant as opposed to virgin rabbits. Larsson and associates307 reported that estrogen treatment of the isolated female rabbit urethra caused an increased sensitivity to noradrenaline. The mechanism was postulated to be related to a more than two-fold increase in the α-adrenergic receptor number. Callahan and Creed308 reported that pretreatment with estrogen of oophorectomized dogs and wallabies did increase sensitivity of urethral strips to α-adrenergic stimulation, but that this did not occur in the rabbit or guinea pig. Bump and Friedman309 reported that sex hormone replacement with estrogen, but not testosterone, enhanced the urethral sphincter mechanism in the castrated female baboon by effects that were unrelated to skeletal muscle. They added that these effects might be related not just to changes in the urethral smooth musculature but also to changes in the urethral mucosa, submucosal vascular plexus, and connective tissue. Estrogens have been considered in the treatment for SUI as the urethra has four estrogen-sensitive layers which may play a role in maintaining a positive urethral pressure: 1) epithelium; 2) vasculature; 3) connective tissue; 4) musculature. Two meta-analyses have shed some light on the use of estrogen therapy in the treatment of SUI. In the first, a report by the Hormones and Urogenital Therapy Committee, the use of estrogens to treat all causes of incontinence in postmenopausal women was examined.310 Of 166 articles reviewed, there were only 6
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controlled and 17 uncontrolled series. Although they showed that there was a subjective improvement in urinary incontinence, when an objective parameter – the amount of urine loss – was examined, there was no significant change. Maximum urethral closure pressure was also increased in one study. In a second study, Sultana and Walters311 found that estrogens were not efficacious in the treatment of SUI. They did, however, believe that estrogens may be useful in the treatment of urgency and urge incontinence. Estrogen alone may not be effective treatment for urinary incontinence; however, in combination with other therapies, both pharmacologic and pelvic floor exercises, it may be more efficacious and useful. Estrogen therapy certainly seems to be capable of facilitating urinary storage in some postmenopausal women. Whether this effect is related just to changes in the autonomic innervation, receptor content or function of the smooth muscle, or to changes in estrogen-binding 312 sites or in the vascular or connective tissue elements of the urethral wall, has not been defined. After menopause, urethral pressure parameters normally decrease slightly,313 and although this change is generally conceded to be related in some way to decreased estrogen levels, it is still largely a matter of speculation whether the actual changes occur in smooth muscle, blood circulation, supporting tissues or the ‘mucosal seal mechanism’. Versi and associates314 describe a positive correlation between skin collagen content (which does decline with declining estrogen status) and parameters of the urethral pressure profile, suggesting that the estrogen effect on the urethra may be predicted, at least in part, by changes in the collagen component. Beisland and colleagues315 carried out a randomized open comparative crossover trial in 20 postmenopausal women with urethral sphincteric insufficiency: both oral PPA, 50 mg twice a day, and estriol vaginal suppositories, 1 mg daily, significantly increased the MUCP and the continence area on profilometry. PPA was clinically more effective than estriol but not sufficiently so to obtain complete continence. However, with combined treatment, eight patients became completely continent, nine were considerably improved, and only one remained unchanged. Two patients dropped out of the study because of side-effects. Bhatia and colleagues316 used 2 g conjugated-estrogen vaginal cream daily for 6 weeks in 11 postmenopausal women with SUI: six were cured or improved significantly. Favorable response was correlated with increased closure pressure and increased pressure transmission. Negative effects from estrogen alone on stress incontinence were reported by Walter and colleagues,317 Hilton
and Stanton318 and Samsioe and associates;319 however, in each of these studies urge symptomatology was favorably affected. In a review article, Cardozo320 concluded that ‘there is no conclusive evidence that estrogen even improves, let alone cures, stress incontinence’, although it ‘apparently alleviates urgency, urge incontinence, frequency, nocturia and dysuria’. Kinn and Lindskog321 described the results of treatment of 36 postmenopausal women with SUI with oral estriol and PPA, alone and in combination, in a double-blind trial after a 4-week run-in period with PPA. Although some of the data are difficult to interpret, the authors concluded that PPA alone and PPA plus estriol raised the intraurethral pressure and reduced urinary loss by 35% (significant) in a standardized physical strain test. Leakage episodes and amounts were significantly reduced by estriol and PPA given separately (28%) or in combination (40%); the authors found no evidence of a synergistic effect but did indicate that an additive 322 effect was present. Walter and colleagues completed a complicated but logical study of 28 (out of 38 original subjects) postmenopausal women with SUI. After 4 weeks of a placebo run-in, patients were randomized to oral estriol or PPA alone for 4 weeks and then to combined therapy for 4 weeks. In the group that sequentially received placebo, PPA and PPA/estriol, the percentages reporting cure or improvement, respectively, were 0 and 13%, 13 and 20%, and 21 and 14%. In the group receiving placebo, estriol and estriol/PPA, the corresponding percentages were 0 and 0%, 14 and 29%, and 64 and 7%. Objective parameters showed the following: the number of leak episodes per 24 hours in patients treated with PPA first showed a 31% decrease (~3 to 2) compared with placebo (p<0.003). For those treated with estriol first, the change was not significant (~1.5 to 0.8). Combined treatment produced a mean decrease of 48% over placebo. There was a greater effect with estriol/ PPA than with PPA/estriol. Pad weights (in grams in a 1hour test) decreased significantly with PPA alone (~27 to 6 g), but there was no difference between PPA and PPA/ estriol. Estriol alone significantly decreased pad weights (~47 to 15 g). Although estriol/PPA was not significantly different, there was further numerical loss from ~15 to 3 g. The overall conclusions were that estriol and PPA are each effective in treating SUI in postmenopausal women, and, on the basis of the subjective data, combined therapy is better than either drug alone. This conclusion was substantiated by a significant decrease in the number of leak episodes in the patients in whom estriol was given before PPA but was not confirmed statistically by pad-weighing tests. 519
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Confusing the data on the potential benefits of estrogen is a recent study by Hendrix and colleagues.323 They reviewed data from 27,347 postmenopausal women participating in the Women’s Health Initiative which was a randomized, double-blind, placebo-controlled study of menopausal hormone therapy to assess its effects on stress, urge, and mixed incontinence. Depending on the presence or absence of a uterus, patients were treated with placebo, 0.625 mg/d of conjugated equine estrogen (CEE), or a combination of 0.625 mg/d CEE and 2.5 mg/d of medroxyprogesterone acetate (MPA). They evaluated 23,296 women whose urinary incontinence symptoms were known. They found that hormone therapy increased all types of urinary incontinence, with stress urinary incontinence being the most common, in women who were continent at baseline after 1 year of use. For those women with urinary incontinence at baseline, frequency worsened with both CEE alone and the combination of CEE and MPA. 324 Session and associates reviewed the benefits and risks of estrogen-replacement therapy. Improvements in vasomotor symptomatology and osteoporosis prevention are well established. There is also substantial evidence of a decreased risk of cardiovascular disease, perhaps because of an effect on the lipid profile. There is little question, however, that unopposed estrogen use in those with an intact uterus increases the risk of endometrial cancer. Progestogen treatment exerts a protective effect, and daily administration of an estrogen and a progestogen provides an attractive alternative because of a lack of withdrawal bleeding (with sequential therapy) and consequent increased patient compliance. Whether progestogen administration adversely affects the results of estrogen treatment of SUI is unknown but must be considered. Progestogens may also cause mastalgia, edema, and bloating. It is concluded, further, that there is no evidence for an increase in thromboembolism or hypertension with estrogen replacement. Transdermal administration of estrogen avoids any theoretical problems associated with the first-pass effect through the liver with oral administration (alteration in clotting factors and increase in renin substrate). The evidence does suggest an association between breast cancer and estrogen replacement therapy, but only for those who have received such therapy for more than 15 years. A preventive role of progestogens in this regard is controversial, as is the dose of estrogen necessary to produce this effect. Grodstein and colleagues325 looked at the relationship between long-term postmenopausal hormone replacement therapy and overall mortality in a cohort of nurses over an 18-year period. Although they noted an overall lower risk of death (relative risk
0.63) for active estrogen users as compared to subjects who had never taken hormones, the apparent benefit decreased somewhat (relative risk 0.80) after 10 years of therapy owing to an increased mortality from breast cancer in the hormone-treated group. As to the type of estrogen preparation preferred, transdermal seems to be as effective as oral, and subcutaneous implants appear to produce physiologic serum levels. Percutaneous and intramuscular estrogen seem to produce variable serum levels. Vaginal creams are said to produce variable serum levels but physiologic estradiol– estrone ratios.324 We agree that ‘hands on’ application to the ‘affected area’ may have a psychological benefit as well, as suggested by Murray.326 A unique new method for delivering vaginal estrogen involves a silicone ring with an estradiol-loaded core containing 2 mg of 17βestradiol inserted into the vagina, by the patient or the physician. A low, constant dose (5–10 g/24 hours) is delivered over a period of 90 days. This mode of admin327 istration is not only more acceptable to certain women but also offers a more continuous delivery of estrogen to the affected tissues.328
cIrcumVentIng the problem Antidiuretic-hormone-like agents The synthetic antidiuretic hormone (ADH) peptide analog desmopressin acetate (DDAVP; 1-desamino-8d-arginine vasopressin) has been used for the symptomatic relief of refractory nocturnal enuresis in both children and adults.326,329 The drug can be administered conveniently by intranasal spray at bedtime (in a dose of 10–40 mcg) and effectively suppresses urine production for 7–10 hours. Its clinical long-term safety has been established by continued use in patients with diabetes insipidus. Normal water-deprivation tests, as described by Rew and Rundle,330 indicate that long-term use does not cause depression of endogenous ADH secretion, at least in patients with nocturnal enuresis. Changes in diuresis during 2 months of treatment in an elderly group of six men and 12 women with increased nocturia and decreased ADH secretion were reported by Asplund and Aberg:331 nocturia decreased 20% (in milliliters) in men and 34% in women; however, the number of voids from 20:00 to 08:00 hours decreased from 4.5 to 4.3 in men and from 3.5 to 2.8 in women, but the drug was not given until 20:00 hours. At present, this novel circumventive approach to the treatment of urinary frequency and incontinence has been largely restricted to those with nocturnal enuresis and diabetes insipidus. The fact that the drug seems to be much more effective than simple fluid restriction alone
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for the former condition is perhaps explained by relatively recent reports suggesting a decreased nocturnal secretion of ADH by such patients.329 Recently, suggestions have been made that desmopressin might be useful in patients with refractory nocturnal frequency and incontinence who do not belong in the category of primary nocturnal enuresis. Kinn and Larsson332 reported that micturition frequency ‘decreased significantly’ in 13 patients with multiple sclerosis and urge incontinence who were treated with oral tablets of desmopressin and that less leakage occurred. The actual approximate average change in the number of voids during the 6 hours after drug intake was from 3.2 to 2.5. A similar circumventive approach is to give a rapidly acting loop diuretic 4–6 hours before bedtime. This, of course, assumes that the nocturia is not due to obstructive uropathy. A randomized, double-blind, crossover study of this approach using bumetanide in a group of 14 general practice patients was reported by Pedersen and Johansen.333 Control nocturia episodes per week averaged 17.5; with placebo, this decreased to 12(!), and with drug to 8. Bumetanide was preferred to placebo by 11 of 14 patients.
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235. Levin RM, Staskin D, Wein AJ. Analysis of the anticholinergic and musculotropic effects of desmethylimipramine on the rabbit urinary bladder. Urol Res 1983;11:259–62. 236. Levin RM, Wein AJ. Comparative effects of five tricyclic compounds on the rabbit urinary bladder. Neurourol Urodyn 1984;3:127–35. 237. Delaere KJP, Michiels HGE, Debruyne FMJ et al. Flavoxate hydrochloride in the treatment of detrusor instability. Urol Int 1977;32:377–81. 238. Bigger J, Giardino E, Perel JE. Cardiac antiarrhythmic effect of imipramine hydrochloride. N Engl J Med 1977;296:206–8. 239. Akah PA. Tricyclic antidepressant inhibition of the electrical evoked responses of the rat urinary bladder strip – effect of variation in extracellular Ca concentration. Arch Int Pharmacodyn 1986;284:231–8. 240. Foreman MM, McNulty AM. Alterations in K(+)-evoked release of 3H-norepinephrine and contractile responses in urethral and bladder tissues induced by norepinephrine reuptake inhibition. Life Sci 1993;53:193–200. 241. Cole A, Fried F. Favorable experiences with imipramine in the treatment of neurogenic bladder. J Urol 1972;107:44–5. 242. Raezer DM, Benson GS, Wein AJ, Duckett JW Jr. The functional approach to the management of the pediatric neuropathic bladder: a clinical study. J Urol 1977;117:649–54. 243. Tulloch AG, Creed KE. A comparison between propantheline and imipramine on bladder and salivary gland function. Br J Urol 1979;51:359–62. 244. Castleden CM, George CF, Renwick AG, Asher MJ. Imipramine – a possible alternative to current therapy for urinary incontinence in elderly. J Urol 1981;125:318–20. 245. Korczyn AD, Kish I. The mechanism of imipramine in enuresis nocturna. Clin Exp Pharmacol Physiol 1979;6:31–5. 246. Lose G, Jorgensen L, Thunedborg P. Doxepin in the treatment of female detrusor overactivity: a randomized double-blind crossover study. J Urol 1989;142:1024–6. 247. Schurch B. Botulinum-A toxin for treating detrusor hyperreflexia in spinal cord injured patients: a new alternative to anticholinergic drugs? Preliminary results. J Urol 2000;164:692–7. 248. Reitz A, Stohrer M, Kramer G et al. European experi-
250. Dykstra D, Enriquez A, Valley M. Treatment of overactive bladder with botulinum toxin type B: a pilot study. Int Urogynecol J Pelvic Floor Dysfunct 2003;14:424–6. 251. Sant GR. Intravesical 50% dimethyl sulfoxide (Rimso50) in treatment of interstitial cystitis. Urology 1987;4(Suppl):17–21. 252. Kiesswetter H, Schober W. Lioresal in the treatment of neurogenic bladder dysfunction. Urol Int 1975;30:63–71. 253. Taylor MC, Bates CP. A double-blind crossover trial of baclofen: a new treatment for the unstable bladder syndrome. Br J Urol 1979;51:504–5. 254. James MJ, Birmingham AT, Hill SJ. Partial mediation by nitric oxide of the relaxation of human isolated detrusor strips in response to electrical field stimulation. Br J Clin Pharmacol 1993;35:366–72. 255. Soulard C, Pascaud X, Roman FJ et al. Pharmacological evaluation of JO-1870 – relation to the potential treatment of urinary bladder incontinence. J Pharmacol Exp Ther 1992;260:1152–8. 256. Constantinou CE. Pharmacologic treatment of detrusor incontinence with thiphenamil HCl. Urol Int 1992;48:42–7. 257. Constantinou CE. Pharmacologic effect of thiphenamil HCl on lower urinary tract function of healthy asymptomatic volunteers. Urol Int 1992;48:293–8. 258. Maggi CA, Barbanti G, Santicioli P et al. Cystometric evidence that capsaicin-sensitive nerves modulate the afferent branch of micturition reflex in humans. J Urol 1989;142:150–4. 259. Maggi CA. Capsaicin and primary afferent neurons: from basic science to human therapy? J Auton Nerv Syst 1991;33:1–14. 260. Maggi CA. Therapeutic potential of capsaicin-like molecules – studies in animals and humans. Life Sci 1992;51:1777–81. 261. Dray A. Mechanism of action of capsaicin-like molecules on sensory neurons. Life Sci 1993;51:1759–65. 262. Ishizuka O, Mattiasson V, Andersson KE. Urodynamic effects of intravesical resiniferatoxin and capsaicin in conscious rats with and without outflow obstruction. J Urol 1995;154:611–16. 263. Szallasi A, Blumberg PM. Vanilloid receptors: new insights enhance potential as a therapeutic target. Pain 1996;68:195–208.
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264. Craft RM, Porreca F. Treatment parameters of desensitization to capsaicin. Life Sci 1992;51:1767–75. 265. Fowler CJ, Beck RO, Gerrard S et al. Intravesical capsaicin for treatment of detrusor hyperreflexia. J Neurol Neurosurg Psychiatry 1994;57:169–73. 266. Das A, Chancellor M, Watanabe T et al. Intravesical capsaicin in neurologic impaired patients with detrusor hyperreflexia. J Spinal Cord Med 1996;19:190–3. 267. Geirsson G, Fall M, Sullivan L. Clinical and urodynamic effects of intravesical capsaicin treatment in patients with chronic traumatic spinal detrusor hyperreflexia. J Urol 1995;154:1825–9. 268. Chandiramani VA, Peterson T, Duthie GS et al. Urodynamic changes during therapeutic intravesical instillations of capsaicin. Br J Urol 1996;77:792–7. 269. de Seze M, Wiart L, de Seze MP et al. Intravesical capsaicin versus resiniferatoxin for the treatment of detrusor hyperreflexia in spinal cord injured patients: a double-blind, randomized, controlled study. J Urol 2004;171:251–5. 270. Kim JH, Rivas DA, Shenot PJ et al. Intravesical resiniferatoxin for refractory detrusor hyperreflexia: a multicenter, blinded, randomized, placebo-controlled trial. J Spinal Cord Med 2003;26:358–63. 271. Kuo HC. Effectiveness of intravesical resiniferatoxin in treating detrusor hyperreflexia and external sphincter dyssynergia in patients with chronic spinal cord lesions. BJU Int 2003;92:597–601. 272. Watanabe T, Yokoyama T, Sasaki K et al. Intravesical resiniferatoxin for patients with neurogenic detrusor overactivity. Int J Urol 2004;11:200–5. 273. Giannantoni A, Di Stasi SM, Stephen RL et al. Intravesical resiniferatoxin versus botulinum-A-toxin injections for neurogenic detrusor overactivity: a prospective randomized study. J Urol 2004;172:240–3. 274. Rashbaum M, Mandelbaum CC. Non-operative treatment of urinary incontinence in women. Am J Obstet Gynecol 1948;56:777. 275. Diokno A, Taub M. Ephedrine in treatment of urinary incontinence. Urology 1975;5:624–5 276. Ek A, Andersson KE, Gullberg B et al. The effects of long-term treatment with norephedrine on stress incontinence and urethral closure pressure profile. Scand J Urol Nephrol 1978;12:105–10. 277. O’Brink A, Bunne G. The effect of alpha adrenergic stimulation in stress incontinence. Urol Int 1978;12:205–8. 278. Lose G, Lindholm D. Clinical and urodynamic effects of nofenefrine in women with stress incontinence. Urol Int 194;39:298–302. 279. Lose G, Rix P, Diernaes E, Alexander N. Norfenefrine in the treatment of female stress incontinence. A double blind trial. Urol Int 1988;43:11–15.
280. Diernaes E, Rix P, Sorensen T, Alexander N. Norfenefrine in the treatment of female urinary stress incontinence assessed by one hour pad weighing test. Urol Int 1989;44:28–31. 281. Lose G, Diernaes E, Rix P. Does medical therapy cure female stress incontinence? Urol Int 1989;44:25–7. 282. Hoffman BB, Lefkowitz RJ. Catecholamines and sympathomimetic drugs. In: Gilman AG, Rall TW, Nies AS, Taylor P (eds) Goodman and Gilman’s The Pharmacological Basis of Therapeutics, 8th ed. New York: Pergamon Press, 1990; 187–220. 283. Awad SA, Downie J, Kiruluta J. Alpha-adrenergic agents in urinary disorders of the proximal urethra. Part I. Sphincteric incontinence. Br J Urol 1978;50:332–5. 284. Stewart B, Banowsky L, Montague D. Stress incontinence: conservative therapy with sympathomimetic drugs. J Urol 1976;115:558–9. 285. Collste L, Lindskog M. Phenylpropanolamine in treatment of female stress incontinence. Double blind placebo controlled study in 24 patients. Urology 1987;30:398–403. 286. Mueller SM. Neurologic complications of phenylpropanolamine use. Neurology 1983;33:650–2. 287. Biaggioni I, Onrot J, Stewart CK, Robertson D. The potent pressor effect of phenylpropanolamine in patients with autonomic impairment. J Am Med Assoc 1987;258:236–9. 288. Lasagna L. Phenylpropanolamine and blood pressure. J Am Med Assoc 1985;253:2491–3. 289. Liebson I, Bigelow G, Griffiths RR, Funderburk FR. Phenylpropanolamine: effects on subjective and cardiovascular variables at recommended over-the-counter dose levels. J Clin Pharmacol 1987;27:685–93. 290. Blackburn GL, Morgan JP, Lavin PT et al. Determinants of the pressor effect of phenylpropanolamine in healthy subjects. J Am Med Assoc 1989;261:3267–72. 291. Kiesswetter H, Hennrich F, Englisch M. Clinical and pharmacologic therapy of stress incontinence. Urol Int 1983;38:58–63. 292. Gilja I, Radej M, Kovacic M, Parazajder J. Conservative treatment of female stress incontinence with imipramine. J Urol 1984;132:909–11. 293. Gleason D, Reilly R, Bottaccini M, Pierce MJ. The urethral continence zone and its relation to stress incontinence. J Urol 1974;112:81–8. 294. Kaisary AV. Beta adrenoceptor blockade in the treatment of female stress urinary incontinence. J Urol (Paris) 1984;90:351–3. 295. Donker P, Van Der Sluis C. Action of beta adrenergic blocking agents on the urethral pressure profile. Urol Int 1976;31:6–12. 296. Fellenius E, Hedberg R, Holmberg E, Waldbeck B.
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Functional and metabolic effects of terbutaline and propranolol in fast and slow contracting skeletal muscle in vitro. Acta Physiol Scand 1980;109:89–95. 297. Kishimoto T, Morita T, Okamiyo Y. Effect of clenbuterol on contractile response in periurethral striated muscle of rabbits. Tohoku J Exp Med 1991;165:243–5. 298. Berk M, du Plessis AD, Birkett M et al. An open-label study of duloxetine hydrochloride, a mixed serotonin and noradrenaline reuptake inhibitor, in patients with DSM-III-R major depressive disorder. Int Clin Psychopharmacol 1997;12:137–40. 299. Thor KB, Katofiasc MA. Effects of duloxetine, a combined serotonin and norepinephrine reuptake inhibitor, on central neural control of lower urinary tract function in the chloralose-anesthetized female cat. J Pharmacol Exp Ther 1995;274:1014–24. 300. Dmochowski RR, Miklos JR, Norton PA et al. Duloxetine versus placebo for the treatment of North American women with stress urinary incontinence. J Urol 170;170:1259–63. 301. Millard RJ, Moore K, Rencken R et al. Duloxetine versus placebo in the treatment of stress urinary incontinence: a four-continent randomized clinical trial. BJU Int 2004;93:311–18. 302. van Kerrebroeck P, Abrams P, Lange R et al. Duloxetine versus placebo in the treatment of European and Canadian women with stress urinary incontinence. BJOG 2004;111:249–57.
management of urinary incontinence in postmenopausal women: a meta-analysis. First report of the Hormones and Urogenital Therapy Committee. Obstet Gynecol 1994;83:12–8. 311. Sultana CJ, Walters MD. Estrogen and urinary incontinence in women. Maturitas 1994;20:129–38. 312. Batra SC, Iosif CS. Female urethra: a target for oestrogen action. J Urol 1983;129:418–20. 313. Rud T. Urethral pressure profile in continent women from childhood to old age. Acta Obstet Gynecol Scand 1980;59:331–5. 314. Versi E, Cardozo L, Brincat L et al. Correlation of urethral physiology and skin collagen in postmenopausal women. Br J Urol Gynaecol 1988;95:147–52. 315. Beisland HO, Fossberg E, Moer A, Sander S. Urethral sphincteric insufficiency in postmenopausal females: treatment with phenylpropanolamine and estriol separately and in combination. Urol Int 1984;39:211–16. 316. Bhatia NN, Bergman A, Karram MM. Effects of oestrogen on urethral function in women with urinary incontinence. Am J Obstet Gynecol 1989;160:176–81. 317. Walter S, Wolf H, Barleto H, Jensen HK. Urinary incontinence in post menopausal women treated with oestrogens. Urol Int 1978;33:135–43. 318. Hilton P, Stanton SL. The use of intravaginal oestrogen cream in genuine stress incontinence. Br J Obstet Gynaecol 1983;90:940–4.
303. Hodgson BJ, Dumas S, Bolling DR et al. Effect of oestrogen on sensitivity of rabbit bladder and urethra to phenylephrine. Invest Urol 1978;16:67–9.
319. Samsioe G, Jansson I, Mellström D et al. Occurrence, nature and treatment of urinary incontinence in a 70year-old female population. Maturitas 1985;7:335–42.
304. Levin RM, Shofer FS, Wein AJ. Oestrogen-induced alterations in the autonomic responses of the rabbit urinary bladder. J Pharmacol Exp Ther 1980;215:614–18.
320. Cardozo L. Role of oestrogens in the treatment of female urinary incontinence. J Am Geriatr Soc 1990;38:326–8.
305. Levin RM, Zderic SA, Ewalt DH et al. Effects of pregnancy on muscarinic receptor density and function in the rabbit urinary bladder. Pharmacology 1991;43:69–77. 306. Tong Y, Wein AJ, Levin RM. Effects of pregnancy on adrenergic function in the rabbit urinary bladder. Neurourol Urodyn 1992;11:525–8. 307. Larsson B, Andersson K, Batra S et al. Effects of estradiol on norepinephrine-induced contraction, alpha adrenoceptor number and norepinephrine content in the female rabbit urethra. J Pharmacol Exp Ther 1984;229:557–63.
321. Kinn AC, Lindskog M. Oestrogens and phenylpropanolamine in combination for stress urinary incontinence in postmenopausal women. Urology 1988;32:273–80. 322. Walter S, Kjærgaard B, Lose G et al. Stress urinary incontinence in postmenopausal women treated with oral oestrogen (estriol) and an alpha-adrenoceptor-stimulating agent (phenylpropanolamine): a randomized doubleblind placebo-controlled study. Int Urogynecol J 1990;1:74–9. 323. Hendrix SL, Cochrane BB, Nygaard IE et al. Effects of estrogen with and without progestin on urinary incontinence. JAMA 2005;293:935–48.
308. Callahan SM, Creed KE. The effects of oestrogens on spontaneous activity and responses to phenylephrine of the mammalian urethra. J Physiol 1985;358:35–46.
324. Session DR, Kelly AC, Jewelewicz R. Current concepts in oestrogen replacement therapy in the menopause. Fertil Steril 1993;59:277–84.
309. Bump RC, Friedman CI. Intraluminal urethral pressure measurements in the female baboon: effects of hormonal manipulation. J Urol 1986;136:508–11.
325. Grodstein F, Stampfer MJ, Colditz GA et al. Postmenopausal hormone therapy and mortality. N Engl J Med 1997;336:1769–75.
310. Fantl JA, Cardozo L, McClish DK. Estrogen therapy in the
326. Murray K. Medical and surgical management of female
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voiding difficulty. In: Drife JO, Hilton P, Stanton SL (eds) Micturition. London: Springer-Verlag, 1990; 179. 327. Ayton RA, Darling GM, Murkies AI et al. A comparative study of safety and efficacy of continuous low dose estradiol released from a vaginal ring compared with conjugated equine oestrogen vaginal cream in the treatment of postmenopausal urogenital atrophy. Br J Obstet Gynaecol 1996;103:351–8. 328. Johnston A. Estrogens: pharmacokinetics and pharmacodynamics with special reference to vaginal administration and the new estradiol formulation – Estring. Acta Obstet Gynecol Scand 1996;165:16–25. 329. Norgaard JP, Rillig S, Djurhuus JC. Nocturnal enuresis: an approach to treatment based on pathogenesis. J Pediatr 1989;114:705–10.
330. Rew DA, Rundle JSH. Assessment of the safety of regular DDAVP therapy on primary nocturnal enuresis. Br J Urol 1989;63:352–3. 331. Asplund R, Aberg H. Desmopressin in elderly subjects with increased nocturnal diuresis: a 2 month treatment study. Scand J Urol Nephrol 1993;27:77–82. 332. Kinn AC, Larsson PO. Desmopressin: a new principle for symptomatic treatment of urgency and incontinence in patients with multiple sclerosis. Scand J Urol Nephrol 1990;24:109–12. 333. Pedersen PA, Johansen PB. Prophylactic treatment of adult nocturia with bumetanide. Br J Urol 1988;62:145–7.
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34 Pessaries and devices for non-surgical treatment of pelvic organ prolapse and stress incontinence Ingrid E Nygaard
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IntroductIon Various types of pessary have been used to reduce prolapse for centuries. Hippocrates reportedly placed pomegranates to reduce prolapsed uteri and subsequent physicians used wool, sponges, cork, and gold.1 As modern surgical techniques became more available and safer, pessaries fell out of favor for a period of time. However, pessaries do fill an important niche in the treatment armamentarium of pelvic floor disorders. Physicians are becoming more conscious of the long-term risks and failure rate of surgical procedures for pelvic organ prolapse and urinary incontinence, and patients are becoming more interested in considering all options for their problem. In addition, pessaries may be useful when prolapse or uterine malposition complicate a pregnancy; in such cases, a pessary can prevent progression and can be removed in the fourth or fifth month of gestation when there is little chance of prolapse. In a questionnaire study published in 2001 (response rate 47.3%),2 86% of American gynecologists queried prescribed pessaries, though most received minimal training in this area in their residencies. Only 12% believed that pessaries were an effective treatment for stress incontinence. In another study,3 48% of members of the American Urogynecologic Society responded to a questionnaire about pessary use. Seventy-seven percent used pessaries as first-line therapy for prolapse, while 12% used pessaries only when surgery was contraindicated. While an Australian study4 found that only 21% of 104 women who presented to a community continence clinic stated that they felt very comfortable about inserting a device into the vagina (and half felt uncomfortable), we found that two-thirds of 190 women (mean age 57.4 years, range 15–89) offered a trial of pessary to manage stress or mixed incontinence were interested in pursuing this modality.5 Some patients choose to wear a pessary as the primary therapy for their pelvic floor disorder, while others use one temporarily, while awaiting surgery. For some women, the option of a pessary allows flexibility in scheduling surgery; for example, a woman with small children may achieve some comfort for several years and then undertake surgery when practical for her life. Some women may wear a pessary or device for urinary incontinence only when undertaking an activity that causes symptoms, such as exercise. Offering appropriate candidates the choice of expectant management – a pessary or other device, or surgery – constitutes good informed consent. In addition, a pessary can be a useful diagnostic tool for the clinician. By reducing prolapse for several weeks with a pessary, the
patient and clinician can obtain clues about whether similar surgical reduction of prolapse is likely to resolve symptoms the patient may have, such as pelvic and back pain, urinary urgency and frequency, or voiding dysfunction, or whether symptoms of stress incontinence will appear. This in turn will help to ensure that the patient has reasonable expectations of postoperative results. There are limited data that suggest that wearing a pessary may have a therapeutic effect in women with pelvic organ prolapse. In one study,6 19 of 56 women fitted with a pessary continued its use for at least 1 year. Four women had an improvement in stage of prolapse and no women had worsening.
choosIng a pessary Today, many pessaries are available to treat pelvic organ prolapse and stress urinary incontinence. In the 20th century, pessaries were largely made of rubber, nowadays, however, most pessaries are made from medicalgrade silicone, which has various advantages: it is not allergenic or toxic, does not absorb odors, can be sterilized, and lasts for several years. Some pessaries are easier for a woman to manage herself than others. Pessaries can be loosely grouped into supportive pessaries, in which levator muscle tone is needed to keep the pessary in place (Fig. 34.1), or spaceoccupying pessaries (Fig. 34.2) which, as their name implies, keep prolapse reduced by filling the vagina. All of the commonly used pessaries for stress urinary incontinence are supportive pessaries (Fig. 34.3). In the survey
Figure 34.1. Support pessaries used to treat pelvic organ prolapse. Top row: (left) ring with support (Milex Inc., Chicago, IL); (right) Shaatz (Mentor Corp., Santa Barbara, CA). Middle row: oval with support (Mentor). Bottom row: (left) Gehrung (Milex); (right) Hodge (Milex).
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Figure 34.2. Space-occupying pessaries used to treat pelvic organ prolapse. Top row: (left) Gellhorn (Mentor Corp., Santa Barbara, CA); (middle) inflataball (Milex Inc., Chicago, IL); (right) cube with drainage holes (Mentor). Bottom row: (left) Mar-Land; (middle) donut; (right) cube (all three by Milex).
Space-occupying pessaries are particularly useful for women with advanced pelvic organ prolapse who have minimal levator muscle tone and wide genital hiatuses. However, once in a while, we are surprised to see that a woman with no apparent muscle support retains a ring pessary with support. Because these types of pessary are much easier for the patient to manage on her own than the space-occupying ones, we start our fitting session with a supportive pessary (such as a ring with support). If quickly expelled, we move on to space-occupying ones. A similar management strategy was employed by Wu et al.,7 who always used a flexible ring pessary as the first pessary tried. Seventy percent of women were successfully fitted with a size 3, 4, or 5 ring pessary. In the questionnaire survey by Pott-Grinstein and Newcomer,2 physicians reported that ring and donut pessaries were the most common pessaries used. However, others use different strategies. Sulak et al.8 used a Gellhorn pessary in 96 of 107 women with symptomatic pelvic organ prolapse. The authors provide the following opinions on why they chose this pessary:
• the design makes it easy to insert and remove; • the base of the pessary is large enough to support •
Figure 34.3. Incontinence pessaries. Clockwise from top: Suarez ring (Cook Urological, Spencer, IN); PelvX ring (DesChutes Medical Products, Bend, OR); incontinence dish (Milex Inc., Chicago, IL); incontinence dish with support (Milex Inc., IL); Introl prosthesis (was Johnson and Johnson; currently not available); Incontinence ring with support (Milex). Middle: Incontinence dish with support (Mentor, Santa Barbara, IL). of members of the American Urogynecologic Society,3 22% used the same pessary, usually a ring pessary, for all support defects. In the remainder that tailored the pessary to the defect, a ring pessary was more common for anterior and apical defects, a Gellhorn was more common for complete procidentia, and a donut was more common for posterior defects.
the proximal prolapse without exerting excessive pressure on any particular area; the concave base provides suction.
The authors note that this pessary can be removed by the patient ‘with minimal discomfort’. Patients were instructed to remove the pessary once or twice weekly, leave it out overnight, and clean it and lubricate it with estrogen cream before reinsertion. In our clinic, women have been less able to manage this pessary on their own than others, and we use it infrequently. In a prospective cohort study, Clemons et al.9 studied the outcome of pessary fitting in 100 consecutive women with symptomatic pelvic organ prolapse. At the first visit, 94 of the 100 were successfully fitted in the office, while two women had pain, and four expelled all pessaries tried. Clinicians tried a mean of 2.2 pessaries per patient to achieve the best fit. The strategy of the clinic was to try a ring pessary with support first, followed by a Gellhorn if the ring was expelled; 71% were fitted with a ring pessary with support and 28% with a Gellhorn. One week later, 54% of women were satisfied with the pessary, whereas in 29% the pessary was expelled and 17% of the women had pain or discomfort. Of the dissatisfied women, 29 were refit, 76% successfully. Overall, 73% of women had a successful 2-week pessary fitting trial. Women with a vaginal length of 6 cm or less and those with a wide introitus (four fingerbreadths wide 535
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or greater) had a lower chance of being successfully fitted. Ring pessaries with support were used in 100% of women with stage II prolapse and 71% of women with stage III prolapse. Gellhorn pessaries were used in 64% of women with stage IV prolapse.
pessary care Prior to a pessary fitting session, we treat women that demonstrate vaginal atrophy for 6 weeks with estrogen cream. Women are instructed to come to the fitting session with a moderately full bladder. For women with stress incontinence, this allows testing the efficacy of the pessary, and for women with prolapse, determines whether reducing the prolapse is accompanied by incontinence. We instruct women to do vigorous activity in the clinic area (such as brisk walking, jumping jacks, straining) and the patient is then sent home with the best fit. Women attempt to void with the pessary in place before leaving the office. In an informal survey of our practice, we find that once home, the best fit in the office fails for approximately one-quarter of women, who then return for further fitting. We recommend that women remove the pessary at least weekly, leave it out overnight, and then reinsert in the morning. When removed, the pessary is simply washed with warm water. In our experience, women rarely encounter excessive or malodorous vaginal discharge using this approach and thus have little use for creams other than estrogen. If women are unwilling or unable to remove the pessary this frequently, we try to estimate the appropriate interval between pessary removals in the following manner:
• We examine women first at 2 weeks after initial pessary insertion.
• If discharge is minimal and no erosions are present, we examine next at 4 weeks.
• Similarly, if the examination is reassuring, we examine again after 6 weeks, and so on. The appropriate pessary interval is either a maximum of 3 months or the interval at which we see foul-smelling discharge or early erosions. Visiting nurses can be an invaluable resource for women unable to care for the pessary on their own. They are often able to visit the woman at home, remove the pessary in the evening and return in the morning to replace it. Excessive foul-smelling discharge or bleeding signals a need to arrange medical follow-up. After an initial 2-week and 3-month check, we examine women who manage their own pessary without diffi-
culty yearly. In women who retain the pessary for several months at a time, we believe that a visual inspection of the vagina should occur at least twice yearly. It is important to inspect the anterior and posterior vaginal walls during the examination (by turning the speculum 90 degrees), as well as the obvious lateral walls that are visible when the speculum is placed in the usual fashion. We have seen several women with large rectovaginal or vesicovaginal fistulae caused by pessaries; in all cases they were undergoing regular examinations by a physician. It is possible that unseen erosions under the speculum blades may have heralded the beginnings of such pressure ulcers. Wu et al.7 used a different care program in 81 women. After fitting, women were seen again in 2 weeks. While self-care of the pessary was encouraged, most women opted to return for office visits every 3 months. At each visit, the pessary was removed, rinsed with tap water and dried. The vagina was examined, and if satisfactory, the pessary was reinserted. Pessaries were replaced yearly. After 1 year, if women had no problems, the follow-up interval was extended to 6 months. The authors note that women using a cube pessary were managed by a different protocol.
other devIces The information above summarizes the most commonly used devices (pessaries) for pelvic organ prolapse and stress urinary incontinence. A sampling of other devices either currently available or recently marketed in the US that may improve continence are shown in Figure 34.4. The Introl device (not currently available; see Fig. 34.3), marketed as a prosthesis rather than a pessary, attempts anatomically to mimic the results from a retropubic urethropexy. Numerous sizes were available, varying the size of the ring and the size and angle of the periurethral prongs. The FemAssist® (also not currently available) is a hat-shaped silicone device that adheres by applying an adhesive gel to the edge of the device, squeezing the central dome and creating a vacuum. This patch can be reapplied after voids and reused for up to a week. Urethral inserts are sterile inserts placed into the urethra by the patient and removed before a void, after which a new sterile insert is introduced. Such inserts are appropriate for women with relatively pure stress incontinence, no history of recurrent urinary tract infections, and no serious contraindications to bacteriuria (e.g. artificial heart valves). At this time, only the FemSoft® insert (Rochester Medical, Inc., Stewartville, MN, USA)
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Figure 34.4. Examples of devices used to treat stress incontinence that are not pessaries. Top row: (left) urethral suction cap (was marketed by Uromed, currently not available); (right) contraceptive diaphragm. Bottom row: (left) urethral insert (Rochester Medical, Inc., Stewartville, MN); (right) menstrual tampon.
at the time of manuscript preparation, 4% had died, 26% underwent surgery and 21% had discontinued use without surgery. Of those still using the pessary, the average length of use was 16 months. Clemons et al.16 prospectively followed the 73 of 100 women with symptomatic pelvic organ prolapse who were fitted successfully with a pessary. Two months after fitting, only 3% of women described feeling a bulge, compared to 90% at baseline. Other symptoms that improved included pressure, discharge, and splinting. Of the 27% of women with stress incontinence symptoms at baseline, leakage persisted in 55% and improved or resolved in 45%. Of those without stress incontinence symptoms at baseline (73%), 21% developed this symptom after using the pessary. One-third of women had urge incontinence at baseline; this improved in 54%. Twenty-three percent had voiding difficulty at baseline which improved in half. At 2 months, 92% were either very or somewhat satisfied with their pessary.
for stress urinary incontinence Vaginal devices
is being marketed. Standard menstrual tampons are widely available. Other devices (not pictured) available in a limited number of countries include polyurethane foam tampons,10–12 and a non-allergenic thermoplastic rubber hollow tampon,13 each placed in the vagina. In addition, devices that were previously marketed in the US but are not currently available include a single use triangularly shaped foam device with an adhesive hydrogel14 that adheres to the perimeatal area to keep urine from exiting the urethral meatus, and a hat-shaped silicone patch15 that adheres by applying an adhesive gel to the edge of the device, squeezing the central dome and creating a vacuum. This patch can be reapplied after voids and reused for up to a week.
effectIveness of treatment for prolapse In the study by Wu et al.,7 of 110 women (mean age 65 years) who opted for pessary management, 74% were fitted successfully. For the 62 women that used a pessary for more than 1 month, 66% were still using it after 12 months. No clear factors were identified that correlated with unsuccessful pessary use. In the series by Sulak et al.,8 of the 107 women fitted (mean age 69.5 years), 49% continued to use the pessary
Most studies evaluating the effectiveness of devices for stress incontinence are small and short. In a prospective, randomized laboratory-based study,17 18 women did three 40-minute standardized aerobics sessions, wearing either a Hodge pessary, a ‘super’ sized menstrual tampon, or no device; volume of urine loss was measured while wearing a pad. Six of 14 were cured and two of 14 improved while exercising with tampons. Nine of 12 women had resolution of stress incontinence while wearing a contraceptive diaphragm during urodynamic testing.18 Four of 10 women wearing a contraceptive diaphragm for 1 week had improved continence.19 We retrospectively evaluated 190 women presenting to a tertiary care center with symptoms of stress or mixed urinary incontinence who were offered pessary management.5 Of the 63% that chose to undergo fitting, 89% achieved a successful fit in the office. Of the 106 women who took a pessary home, follow-up was available on 100. Fifty-five women used the pessary for at least 6 months as their primary method of managing urinary incontinence (median duration 13 months). Of the remaining 45 women who discontinued use before 6 months, most did so by 1 month. Several investigators studied the Introl device. In 30 women using this device for 1 month, 83% were dry with it in place.20 In a study in which 53 of 70 enrolled women completed 1 month follow-up,21 the number of incontinence episodes per week decreased from 28.6 to 16.6 in 537
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women with stress urinary incontinence and from 30.2 to 15 per week in women with mixed incontinence. Of 21 women with mixed incontinence,22 16 were fitted successfully with the Introl. In the 14 women still using it at 4 weeks, the median number of leaks per week decreased from 4.3 to 1.0. In another study of 65 women with urodynamic stress incontinence fitted with the device, 39 (60%) withdrew from the study.23 In the remaining 26 women, the median pad weight decreased from 19 g at baseline to 2 g, and 62% were continent. Six months later, 18 of these 26 (thus 18/65) still wore the device. At 2 years, 14 women still wore the device. In another longer term study,24 6 months after being fitted with the Introl device, 22 women (29%) reported complete continence, and 39 had at least a 50% decrease in incontinence severity. Other vaginal devices have also been studied, particularly in Europe. Forty-one of 55 women (74.5%) completed a 3-month study25 to evaluate the Continence Guard, a disposable polyurethane device. In an intentto-treat analysis, 20% of women were subjectively cured and 49% improved. In a randomized trial comparing two vaginal tampons,26 one shaped like a clam and one like a traditional tampon, 62 of 94 women completed the study. Both devices decreased urine loss significantly, but 73% preferred the ‘tampon’ type design for its ease of use.
Urethral occlusive devices In several studies with follow-up ranging from 4 weeks to 3 months, external urethral occlusive devices had varying efficacy, with continence rates of approximately 50%.15,27,28 However, in one study of the external meatus suction cap,29 only 5% of women completed the 3-month study, while the remainder dropped out for various reasons generally related to dissatisfaction with the device.
Intraurethral devices Studies of previously available intraurethral inserts showed that most women who use intraurethral devices are dry or improved (66–95%) when the device is in place.30–33 Women reported improved comfort and ease of use over time. In one study, women exercised with and without a urethral insert.34 The volume of urine lost decreased from a median of 20 cc to 2.6 cc when the insert was worn. Of 150 women enrolled in a study assessing the effectiveness of the FemSoft® urethral insert,35 51% withdrew from the trial by the mean follow-up interval (15 months). Of women still in the trial, the median time per day the device was worn was 5.7 hours, and the mean number of devices used per day was 1.22. At 12 months
follow-up (n=91), 93% of women were continent, based on a pad test, with the insert in place, compared to 14% without the insert.
adverse events In Wu et al’s series,7 in which pessaries were generally kept in situ for 3 months at a time, eight women developed vaginal erosions: five were using a cube, and three others a ring pessary. Overall, five of six women using cube pessaries developed vaginal erosions, compared to three of 101 using ring pessaries. Overall 10 women had pelvic pain with the pessary in place; three were using cube pessaries and seven ring pessaries. Only two women discontinued pessary use because of discharge, while one did so because of difficulty evacuating the rectum. Clemons et al.16 reported that six of 73 women (8%) using a pessary for pelvic organ prolapse for 2 months discontinued using the pessary within the 2-month study period because of severe stress incontinence (4), de novo voiding difficulty (1), and de novo defecation difficulty (1). Two women developed vaginal erosions which subsequently resolved with daily vaginal estrogen cream and continued pessary use. Side effects of the Introl device in a study of 53 women21 included five urinary tract infections and 23 cases of vaginal mucosal soreness or mild irritation. The study by Wu et al.7 highlights the need for extra caution when using a cube pessary. The suction cups on each side of the cube allow this pessary to retain its intravaginal position when other pessaries fall out; the same suction cups can cause significant ulceration in the vagina. We have seen several postmenopausal women who developed large, weeping ulcers after wearing the cube pessary for only 2 or 3 days. Anecdotally, some colleagues have not had similar experiences; however, based on ours, we now reserve the use of this type of pessary for women with healthy vaginal tissue who are able to remove it nightly. Patients and clinicians must take care to release the suction by sweeping a finger between the pessary and the upper vaginal wall before attempting removal. Not surprisingly, urinary tract infections are the primary adverse event associated with use of urethral inserts. In women using the Reliance insert,32 treatment for positive urine cultures was undertaken in 20% of symptomatic and 11% of asymptomatic patients; 39% of patients had positive cultures which were not treated and 30% had negative cultures at all monthly intervals for the 4-month study. In another study of this insert, one or more episodes of gross hematuria (24%), cystoscopic findings of mucosal irritation at 4 or 12 months
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(9%), and asymptomatic bacteriuria (30%) on monthly cultures were also documented.36 In a prospective study of the FemSoft® insert,35 31.3% of women had a symptomatic, 24.7% had urinary symptoms, and 3.3% hematuria. There were two cases of device migration (1.3% of subjects, 0.0023% of devices used), one into the urethra, which was spontaneously expelled, and one into the bladder which was removed cystoscopically. Of note, the rate of symptomatic urinary tract infection was highest in the first 30 days of use and decreased markedly thereafter.
conclusIon Pessaries and other devices are an important part of the treatment armamentarium for pelvic organ prolapse and stress urinary incontinence. Further research is needed to delineate women most likely to respond to this form of treatment. Long-term studies of both effectiveness and adverse events associated with various devices are essential to better understand the risk–benefit ratio.
references 1. Deger RB, Menzin AW, Mikuta JJ. The vaginal pessary: past and present. Postgrad Obstet Gynecol 1993;13(18):1–6. 2. Pott-Grinstein E, Newcomer JR. Gynecologists’ patterns of prescribing pessaries. J Reprod Med 2001;46:205–8. 3. Cundiff GW, Weidner AC, Visco AG et al. A survey of pessary use by members of the American Urogynecologic Society. Obstet Gynecol 2000;95:931–5. 4. Prashar S, Simons A, Bryant C, Dowell C, Moore KH. Attitudes to vaginal/urethral touching and device placement in women with urinary incontinence. Int Urogynecol J 2000;11:4–8. 5. Donnelly MJ, Powell-Morgan S, Olsen AL et al. Vaginal pessaries for the management of stress and mixed urinary incontinence. Int Urogynecol J 2004;15:302–7. 6. Handa VL, Jones M. Do pessaries prevent the progression of pelvic organ prolapse? Int Urogynecol J 2002;13:349– 52. 7. Wu V, Farrell SA, Baskett TF, Flowerdew G. A simplified protocol for pessary management. Obstet Gynecol 1997;90:990–4. 8. Sulak PJ, Kuehl TJ, Shull BL. Vaginal pessaries and their use in pelvic relaxation. J Reprod Med 1993;38:919–23. 9. Clemons JL, Aguilar VC, Tillinghast TA, Jackson ND, Myers DL. Risk factors associated with an unsuccessful pessary fitting trial in women with pelvic organ prolapse. Am J Obstet Gynecol 2004;190:345–50. 10. Thyssen H. New disposable vaginal device (continence guard) in the treatment of female stress incontinence:
design, efficacy and short term safety. Acta Obstet Gynecol Scand 1996;75:170–3. 11. Thyssen H, Lose G, Andersen JT. Effect of a vaginal device on quality of life with genuine stress incontinence. Obstet Gynecol 1999;93(3):407–11. 12. Hahn I, Milson I. Treatment of female genuine stress incontinence with a new anatomically shaped vaginal device (Conveen Continence Guard). Br J Urol 1996;77(5):711–5. 13. Morris AR, Moore KH. The Contiform incontinence device – efficacy and patient acceptability. Int Urogynecol J 2003;14:412–7. 14. Brubaker L, Harris T, Gleason D et al. The external urethral barrier for stress incontinence: a multicenter trial of safety and efficacy. Miniguard Investigators Group. Obstet Gynecol 1999;93(6):932–7. 15. Versi E, Griffiths DJ, Harvey MA. A new external urethral occlusive device for female urinary incontinence. Obstet Gynecol 1998;2:286–91. 16. Clemons JL, Aguilar VC, Tillinghast TA, Jackson ND, Myers DL. Patient satisfaction and changes in prolapse and urinary symptoms in women who were fitted successfully with a pessary for pelvic organ prolapse. Am J Obstet Gynecol 2004;190:1025–9. 17. Nygaard I. Prevention of exercise incontinence with mechanical devices. J Reprod Med 1995;40:89–94. 18. Suarez G. Use of a standard contraceptive diaphragm in management of genuine stress incontinence. Urol 1991;37(2):119–22. 19. Realini JP, Walters MD. Vaginal diaphragm rings in the treatment of stress incontinence. J Am Board Fam Pract 1990;3(2):99–103. 20. Davila GW, Osterman KV. The bladder neck support prosthesis: a nonsurgical approach to stress incontinence in adult women. Am J Obstet Gynecol 1994;171:206–11. 21. Davila GW, Neal D, Horbach N et al. A bladder-neck support prosthesis for women with stress and mixed incontinence. Obstet Gynecol 1999;93(6):938–42. 22. Moore KH, Foote A, Siva S et al. The use of the bladder neck support prosthesis in combined genuine stress incontinence and detrusor instability. Aust N Z J Obstet Gynecol 1997;37:440–5. 23. Moore KH, Foote AJ, Burton G et al. An open study of the bladder neck support prosthesis in genuine stress incontinence. Br J Obstet Gynaecol 1999;106:42–9. 24. Kondo A, Yokoyama E, Koshiba K et al. Bladder neck support prosthesis: a non operative treatment for stress or mixed urinary incontinence. J Urol 1997;157:824–7. 25. Sander P, Thyssen H, Lose G, Andersen JT. Effect of a vaginal device on quality of life with urinary stress incontinence. Obstet Gynecol 1999;93(3):407–11.
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26. Thyssen H, Bidmead J, Lose G, Moller Bek K, Dwyer P, Cardozo L. A new intravaginal device for stress incontinence in women. Br J Urol Int 2001;88:889–92. 27. Brubaker L, Harris T, Gleason D et al. The external urethral barrier for stress incontinence: a multicenter trial of safety and efficacy. Miniguard Investigators Group. Obstet Gynecol 1999;93(6):932–7. 28. Bellin P, Smith J, Poll W et al. Results of a multicentre trial of the CapSure Continence shield on women with genuine stress incontinence. Urol 1998;51(5):697– 706. 29. Tincello DG, Adams EJ, Bolderson J et al. A urinary control device for management of female stress incontinence. Obstet Gynecol 2000;95(3):417–20. 30. Neilsen KK, Walter S, Maeffaard E et al. The urethral plug II: an alternative treatment in women with genuine stress incontinence. Br J Urol 1993;72(4):428–32. 31. Peschers U, Zen Ruffinen F, Schaer GN et al. The VIVA urethral plug: a sensible expansion of the spectrum for
conservative therapy of genuine stress incontinence? Geburtshilfe Frauenheilkd 1996;56(3):118–23. 32. Staskin DR, Bavendam T, Miller J et al. Effectiveness of a urinary control insert in the management of genuine stress incontinence: early results of a multicenter study. Urology 1996;47(5):629–36. 33. Sand PK, Staskin D, Miller J et al. Effect of a urinary control insert on quality of life in incontinent women. Int Urogynecol J Pelvic Floor Dysfunc 1999;10(2):100–5. 34. Dunn M, Brandt D, Nygaard I. Treatment of exercise incontinence with a urethral insert: a pilot study. Phys Sportsmed 2002;30:45–8. 35. Sirls LT, Foote JE, Kaufman JM et al. Long-term results of the FemSoft® urethral insert for the management of female stress urinary incontinence. Int Urogynecol J 2002;13:88–95. 36. Miller JL, Bavendam T. Treatment with the Reliance urinary control insert: one-year experience. J Endourol 1996;10(3):287–92.
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35 Catheters; pads and pants; appliances Kate Anders, Su Foxley
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IntroductIon Incontinence is a common and complex condition affecting women of all ages and of all social and cultural backgrounds. Unfortunately, for some, treatment is ineffective, or diagnosis and treatment of the condition can take some time to establish; their incontinence or their inability to micturate normally therefore must be contained or managed. Many products are marketed worldwide for this purpose, but these must be carefully and appropriately selected for each individual, with consideration to their needs, wishes, and social circumstances. Products fall into three main categories: catheters, pads and pants, and aids and appliances. This chapter attempts to provide an overview of what is available and how these can be applied in practice.
cAtHEtErS Catheters are used for effective drainage of the bladder, either temporarily or permanently, in the presence of physiologic and anatomic defects or obstruction of the lower urinary tract. The word catheter derives from the Greek word katheter meaning ‘to set down’ or ‘let down into’ and its usage is said to date back to the Sumerian culture in 3000 BC. It was suggested that gold was used as it was easily molded and was suited to drain urine from the bladder.1 Today, catheters are an integral part of patient care and the prevalence rate for short-term catheterization2 among hospitalized patients in the UK is 12.6% (median 4 days) and around 4% in patients in the community.3 Catheters are used for a variety of reasons, which are summarized below. They are not without associated complications including urinary tract infection, encrustation, trauma, stricture formation, urethral perforation, bladder calculi, and even neoplastic changes.4 Catheterization, therefore, should be undertaken only after full consideration of the implications of the procedure, all other avenues of treatment have table 35.1.
been explored, and with valid consent from the person or their legal guardian to be catheterized.5 Reasons for catheterization are as follows:
• Prophylaxis; to maintain bladder drainage during
•
• •
and following surgery or epidural anesthetic administration, thus minimizing the risk of distension injury to the bladder; Investigations; during urodynamic investigations; for accurate urine output measurement (e.g. in intensive care units); measurement of postmicturition residuals; Treatment; to relieve urinary retention; bladder irrigation; for chemotherapy or other drug instillation; Intractable incontinence; only as a final option for containment.
Catheter insertion falls into two main groups: urethral and suprapubic. Urethral catheterization can be indwelling (or self-retaining) or intermittent/single use (or non-retaining), for example clean intermittent selfcatheterization (CISC).
urethral catheterization A self-retaining catheter was first described by Reybard in 1853,6 but it was not until the 1930s that Frederick Foley7 perfected a method of devising a latex catheter with an integrated balloon that did not disintegrate. With modern techniques and the development of new materials, there is now an extensive range that can be utilized for both short- and long-term use (Table 35.1). The urethral catheter is still the most commonly used catheter for the drainage of urine as it can be quickly and easily inserted. Female urethral catheterization is an accepted aseptic procedure and should be undertaken under the guidance of strict local hospital or community infection-control policies. It is important to take note of guides on good practice.8
Catheter materials
Short-term use (max. 7 days)
Medium use (max. 4 weeks)
Long-term use (max. 12 weeks)
Specialist
• •
•
•
•
•
Latex rubber Siliconized latex (used to facilitate insertion only) Plastic/PVC (used when there is extensive debris in the urine, particularly postoperatively)
•
Latex coated with Teflon/PTFE Silver alloy hydrogel-coated latex
• • •
Silicone elastomerencapsulated (coated) latex Hydrogel-coated latex (hydrogels facilitate insertion and have similar properties to silicone) 100% silicone Hydrogel-coated silicone
• •
Roberts (Teflon-coated with one eye below the balloon for drainage) Three-way irrigation (plastic or latex rubber, usually with reinforcement to prevent collapse with suction) Whistle-tip catheter
PTFE, polytetrafluoroethylene.
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catheter selection With different modes of catheterization and the availability of different materials, it is important to make the right choice for each individual’s needs. Not surprisingly, a review of hospitals (in the UK)9 found that many staff had insufficient knowledge of, and inadequate training in, the selection of catheters.
Designs and materials (Table 35.1) Plastic or PVC and latex rubber should be used for only a very short time and are generally used only in immediate postoperative circumstances. Although cheap, plastic catheters are rigid and uncomfortable, causing bladder spasm and bypassing (urine leaking around the outside of the catheter).10 Both plastic and latex catheters tend to attract surface deposits, causing encrustation and fractures within the catheter. Following reports that some catheters were associated with cytotoxity,11 all catheters in the UK must now conform to British Standards. Attempts to improve on the latex catheter include ‘siliconizing’ the surface of the catheter, producing a lubricant effect to facilitate insertion. Latex has also been coated in Teflon (polytetrafluoroethylene or PTFE) to make it more inert, and giving it a smoother surface in an attempt to reduce urethritis and encrustation. Silver alloy hydrogel-coated latex catheters have been advocated for the inhibition of bacterial growth,12 and are more effective than standard catheters in reducing the incidence of bacteriuria in short-term catheterization (up to 4 weeks).13 The introduction of a silver alloy hydrogel-coated urinary catheter does seem to be associated with a significant decline in nosocomial urinary tract infection and thus ensuing savings in cost of patient treatment and management. Additionally, there does not appear to be any antimicrobial resistance to silver.14 Silicone elastomer-encapsulated (coated) latex catheters differ from the ‘siliconized’ catheters described above and are recommended for use in the long term. Silicone is an inert material, reducing the incidence of trauma, urethritis, and encrustation, and therefore can be used long term (i.e. up to 3 months). Hydrogel catheters are similar to silicone catheters but they become smoother when hydrated. A comparison of urethral reactions to 100% silicone catheters, hydrogel-coated catheters, and siliconized latex catheters demonstrated that 100% silicone catheters had the lowest incidence of urethral inflammation, hydrogel catheters proved to be the most superior in preventing encrustation, and the siliconized latex catheters were the least effective in preventing both urethral inflammation and encrustation.15
Hydrogel-coated latex catheters are not only biocompatible but have low surface friction, resulting in improved comfort and less irritation for the user. Additionally, they have been shown to be resistant to bacterial adherence and encrustation.16 It stands to reason that, for longterm catheterization, the first choice for both urethral and suprapubic catheter use should be hydrogel-coated latex whenever possible.17 The majority of catheters have a semi-rigid rounded tip with two drainage eyes, placed either laterally or opposed. Opposite drainage eyes generally facilitate better drainage with fewer blockages. There are some variations, including the Tiemann catheter, which is curved at the tip, although this is not usually used in women as the curve is designed to facilitate insertion past an enlarged prostate. A whistle-tipped catheter aids drainage of urine containing large amounts of debris because of its open-ended tip (Fig. 35.1). Other specialist catheters include the Roberts catheter, which has two drainage eyes, on either side of the balloon of the catheter. The design allows urine to drain through the distal eye, rather than bypassing the catheter. This is particularly useful in patients with abnormal detrusor activity or when the catheter is susceptible to blockage.
Catheter size and length To develop a standard measurement, a French instrument maker, J.F.B. Charriere, suggested a scale based on the metric system. This measurement is termed as either ‘French gauge’ (Fg; written as ‘F’ or ‘Fr’) or ‘Charriere’ (Ch). It is the measurement of the external circumference in millimeters, which is approximately equal to three times the external diameter. Catheters used in women should range from size 12 to 16 Fr, with
a
b
c
d
Figure. 35.1. Catheter tips: (a) whistle; (b) Tiemann; (c) round; (d) Roberts. 543
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a small balloon that holds 10 ml sterile water or saline.18 All 10 ml must be instilled to ensure correct inflation of the balloon, as underinflation may cause distortion of the balloon and deflection of the catheter tip. Catheters are available with a pre-filled balloon which can be easy to use and eliminate the need for additional fluid and syringes to fill the balloon manually. Many healthcare professionals continue to use larger-diameter catheters even though there is evidence that larger catheters are associated with discomfort and bypassing.19,20 There is also evidence that too large a catheter will block the paraurethral glands, causing a build-up of secretions which in turn become infected and lead to abscess and stricture21 (Fig. 35.2). Larger catheters, however, are useful for draining heavy hematuria. The 30 ml balloon associated with a larger catheter was developed to aid homeostasis and therefore is useful only following prostate surgery in men. Catheters are available in three categories of length: 40–45 cm (male length); 20–26 cm (female length); and a pediatric catheter (30–31 cm). A longer male-length catheter may be more suitable for women who are obese or wheelchair bound.
catheter-associated problems Infection The incidence of urinary tract infection (UTI) is high with long-term urinary catheter use and is the most common complication with indwelling catheters. Most users of a catheter will have bacteria in the urine within 3 days22 and, because of overgrowth of resistant bacteria, prophylactic antibiotics are discouraged23 unless the patient develops systemic symptoms. Similarly, although irrigation of the bladder with antibiotic and antiseptic Urethra Catheter
a
Para urethral glands
Blocked gland
b
Figure. 35.2. (a) Use of too large a catheter, leading to blockage of paraurethral glands; (b) use of appropriate-sized catheter.
agents continues to be used,24,25 such management is generally of limited value.26 In particular, the readily available pre-packed chlorhexidine has not been shown to be effective in long-term usage against a number of frequently occurring pathogens: it has been shown to remove sensitive bacteria in the normal urethral flora and thus to allow subsequent colonization by resistant organisms.27 One of the main reasons why infections are so difficult to eradicate is the growth of bacterial populations as an adherent biofilm on the catheter surface. Common pathogens, such as Escherichia coli, may be eliminated from the urine, but persist in the biofilm and restart the cycle of infection.28 Laboratory tests have been performed on ‘an infection-inhibiting’ urinary catheter material with promising results. A silicone rubber elastomer catheter compounded with chlorhexidine gluconate was found to be effective for 4 weeks against E. coli, Proteus mirabilis, and Staphylococcus epidermidis.29 However, a study comparing 18 types of catheter in current use found that none was capable of resisting encrustation by P. mirabilis biofilms.30
Catheter leakage, bypassing and blockage Too large a catheter, detrusor spasm, blockage, debris or the presence of bladder calculi are all reasons for catheter failure. Blockage is frequently the result of a UTI leading to encrustation. The incidence of catheter blockage and bypassing in long-term catheterization is approximately 48% and 37%, respectively,31 and this may indicate a need for early changing. The use of a large catheter often irritates the bladder, causing it to contract and squeeze urine out past the catheter. The use of an appropriate smaller catheter will reduce the incidence of abnormal bladder contractions, although some may benefit from anticholinergic therapy if there is concomitant detrusor overactivity. In an attempt to avoid any systemic side-effects, such therapy can be instilled intravesically.32 Urinary catheters also tend to become blocked when biofilm from urease-producing organisms builds up on the catheter surface. This will be indicated by an alkaline urine which precipitates crystals, encrusts the catheter and reduces the catheter lumen, eventually resulting in blockage. The obstruction of the flow of urine through a catheter can induce serious complications. Urine either leaks around the outside of the catheter (bypassing) causing women to become incontinent or it is retained in the bladder resulting in distension of the bladder and possibly ureteric reflux. This in turn could cause pyelonephritis, septicemia, and even shock. Approximately 50% of patients suffer from recurrent encrustation of their
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urinary catheters,20,33–35 and regular bladder washouts are advocated in the prevention and treatment of blockage (see Table 35.2 for types of solution used). There is a wide variation of practice in bladder instillations across the UK when managing indwelling catheters.36 The use of solutions has been contentious but there remains evidence that supports the use of maintenance solutions in certain circumstances.37 Nevertheless, if a patient’s catheter repeatedly becomes blocked, excessive bladder washouts are not always the answer and the catheter should, perhaps, be changed more frequently in an effort to pre-empt blockage. One unique way to control for encrustation is to use an antimicrobial solution to fill the retention balloon rather than water. It would appear that certainly in a laboratory model, antibacterial agents (triclosan) can diffuse through the catheter inflation line and balloon into urine.38 To protect against blockage it is vital to increase the fluid intake. A reduction in acidic fluids (e.g. fruit juice), calcium-rich foods and supplements, and a reduction in alcohol (which may lead to dehydration) is recommended.39 Debris in the urine is almost inevitable in any woman who has a long-term catheter. General mobilization can protect against debris accumulating and subsequently blocking the drainage eyes of the catheter. In women who are immobile, assisted regular change of position will reduce the incidence of this accumulation. Constipation should be avoided as this can cause leakage and bypassing. Straining on defecation can also contribute to the expulsion of the catheter.
advantage and can lead to the development of resistant organisms.40 Routine daily bathing or showering is generally all that is needed.41 However, women need to be instructed in correct perineal cleaning after bowel motions (i.e. to wipe toilet paper away from the urethral opening [front to back]). Talcum powder should be avoided as it can become clogged around the catheter. Care and maintenance of the drainage system is discussed in the section on drainage bags and valves (see next page).
Suprapubic catheterization Suprapubic catheterization is the insertion, under a general or local anesthetic, of a catheter into the bladder lumen just above the symphysis pubis (Fig. 35.3), for a variety of reasons (Table 35.3). Suprapubic catheters are particularly useful following urogynecologic or urologic procedures. They allow safe drainage of the bladder during attempts at postoperative voiding, without the trauma of reinsertion of a urethral catheter each time if
Inflated balloon Catheter
Urethral catheter care For both short- and long-term catheterized patients, advice is needed on careful meatal cleansing. A mild unscented soap with water is sufficient, as antiseptic solutions for long-term catheter care have no proven table 35.2.
Commonly used bladder washout solutions
Type
Indications for use
Citric acid (3.23%)
To prevent/dissolve crystals forming in the catheter or bladder
Citric acid (6%)
Dissolves persistent crystals in the catheter or bladder Minimizes trauma on catheter removal Unblocks an encrusted catheter
Chlorhexidine (0.2%) Reduces growth of bacteria especially E. coli and Klebsiella (short-term use only) Saline (0.9%)
Mechanical effect to remove blood clots and debris
Pubic bone
Figure. 35.3. table 35.3.
• • • • • • • • •
Bladder
Position of suprapubic catheter. Indications for suprapubic catheterization
Urogynecologic /gynecologic (e.g. colposuspension, anterior colporrhaphy, pelvic floor repair, vaginal hysterectomy) Urologic (e.g. urethral stricture/trauma, ileal augmentation, cecocystoplasty (open prostatectomy) Anorectal surgery Neurogenic bladder Cardiothoracic surgery Acute retention Inability to self-catheterize Need for long-term catheterization Intractable incontinence
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attempts are unsuccessful, or if there is a large postmicturition residual. The suprapubic catheter can be clamped and unclamped according to the patient’s progress.42 This also applies to women in acute retention, as voiding can be tried without removal of the catheter. Following major abdominal surgery, suprapubic catheters have been found to be the method of choice for urinary drainage, with a lower incidence of bacteriuria and discomfort than with urethral catheterization.43 Suprapubic catheterization can be used in women who have intractable incontinence, but this should be a last resort, when all other treatment and forms of containment have failed. For long-term catheterization it is the preferred route, especially in wheelchair users and for those who are sexually active. A proper explanation of the procedure must be given and valid consent must be obtained. Unexplained hematuria is perhaps the only real contraindication for suprapubic catheterization, because of the risk of placing a catheter through a bladder tumor. In women suffering from voiding difficulties or incomplete bladder emptying, every effort should be made to teach them intermittent self-catheterization (ICS) first. Unfortunately, there are some for whom the procedure may be technically difficult and therefore a permanent catheter may be the only answer to maintain adequate bladder drainage. The choice of suprapubic catheter will depend on whether it is to be used short term (e.g. following surgery) or long term. Suprapubic catheter insertion via an open technique (i.e. cystotomy into the bladder dome under direct vision) can be used following a retropubic procedure. To insert a suprapubic catheter percutaneously or using a ‘closed’ technique safely, and without injury to the bowel (as this could lie between the bladder and the anterior abdominal wall), the bladder should be filled to at least 300 ml (transurethrally) with the patient in the Trendenlenburg position. When a suprapubic catheter is used as a first line of management in the case of acute retention, it is advisable to use ultrasonography to assess the bladder volume before insertion. Catheters for short-term use, such as the Bonnano catheter, should be used for only 2–3 weeks. They are commonly held in place by skin sutures, which can pull on the skin, fall out or cause discomfort; the insertion site is, therefore, susceptible to infection if the catheter is used for too long. Suprapubic catheters used long term should be Foley catheters (i.e. held in place with a fluid-filled balloon), ideally hydrogel coated. Medium-sized catheters (14–16 Fr) can be used. They can be changed every 3 months with little effort once a ‘track’ or ‘fistula’ has
been formed, although some may need more frequent changes owing to encrustation or blockage. It is not uncommon for the first change to be undertaken in the acute-care setting, but subsequent changes can be done routinely within the community. Nevertheless, if there is delay in reinsertion and the catheter fistula is allowed to close, the suprapubic catheter may need to be re-sited. Insertion sites, once healed, should not require a dressing. Other types of self-retaining catheters used in suprapubic catheterization include the Malecot and de Pezzer catheters, which have ‘wings’ to keep them in situ. Suprapubic catheters, as with urethral catheters, drain urine via a ‘closed system’ into a drainage bag, although valves are being used as an alternative for some women.
catheters and sexual health There is little work on the use of catheters, either urethral or suprapubic, and their effect on sexual health. In clinical practice, it is something frequently glossed-over or possibly not even discussed with the patient at all. What does seem to be apparent is that beliefs about the sexual attitudes and behaviors of older people seem to be based on stereotyped views of aging and sexuality.44 As many women who have long-term catheters are older in age, it may be because of this that it is avoided in assessment and subsequent management. Nonetheless, whatever the reason, it remains the healthcare professional’s responsibility to address this sensitive issue and discuss with the patient that having a long-term catheter does not mean that they are unable to have a sexual relationship, although suprapubic catheters are more suitable.
catheter drainage bags Catheter drainage bags connected directly to a catheter should have a non-return valve to prevent any refluxing of urine once it has entered the bag. Prior to the 1960s, catheters had an open drainage system with the end of the catheter draining into an open non-sterile container. This was the main cause of ascending infection, and the introduction of a ‘closed drainage system’, in which urine drains directly into a sealed sterile drainage bag (Fig. 35.4) has reduced the incidence of bacteriuria dramatically from 97% to 8–15%.45,46 This system was further developed by replacing the drainage spigot with a non-return outlet tap. It is still possible for bacteria to migrate upwards from the bag, past a non-return valve system, in the form of biofilms;47 however, if catheter bags are changed once a week, the risk of infection caused by biofilm build-up is minimized.48 Strict care must be taken when chang-
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a
b
c
d
Figure. 35.4. Closed drainage system with a night bag attached to the leg bag; note the short female catheter. ing bags, with scrupulous attention to hand-washing. Breakage of a closed urinary drainage system should be kept to a minimum; therefore, if a sample of urine is needed, the sampling port must be used, in order to avoid breaking the system.49 Women, especially those who are ambulant, should be offered a small body-worn drainage bag (e.g. ‘the leg bag’). They come in different sizes (capacity 350, 500 or 750 ml) with long, medium or short tubing (Fig. 35.5). Manufacturers have developed a wide variety of methods to keep leg drainage bags in place, including fabric ties, G-straps, Velcro straps, ‘sporran’ belts and integrated pockets or sleeves (e.g. the urisleeve which gives even distribution of pressure, keeping it secure on the leg) (Fig. 35.6). Leg bags, however, do not have the capacity for drainage of urine while the user is asleep. So that the closed system is not broken, a ‘night bag’ is fit-
Figure. 35.5. Different lengths of leg bags, ranging from 350 to 750 ml in capacity, and suspensory systems: (a) short-tube bag; (b) medium-tube bag; (c) long-tube bag; (d) alternative method of suspension. ted to the tap of the ‘leg bag’, so that the urine can flow from the smaller leg bag into the larger, 2-liter, night bag (see Fig. 35.4). Newer bags include the ‘belly bag’, which, as its name suggests, is worn on the belly, with a belt around the waist to hold it in place. There is no need for an additional night bag as they have a capacity for 1000 ml. These may be useful in women who are wheelchair bound but care needs to be taken that urine is draining correctly into the bag (Fig. 35.7). 547
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Figure. 35.6.
Urisleeve (Bard Ltd)
a
b
c
Figure. 35.8. Examples of catheter valves: (a) EMS Medical; (b) Bard Flip-Flo; (c) Sims Portex Uro-Flo.
Figure. 35.7.
Bellybag® in situ.
Valves The use of valves (Fig. 35.8) instead of continuous drainage bags is increasing in popularity. Release of the valve is dependent on fluid intake and bladder capacity. Release every 3–4 hours may maintain bladder tone, as the bladder will fill and empty as under normal conditions. This may also protect against the erosion of the bladder wall that is associated with the permanent collapse of the bladder in long-term catheterization, although more research is needed in this area. The benefits of cathetervalve use appear to be well recognized in clinical practice, such as a reduction in UTI due to the ‘flushing’ effect, but there is limited evidence to back this. Current opinion suggests that women with detrusor overactivity,
impaired bladder sensation or confusion may do less well with catheter valves. The use of valves is particularly useful for women with voiding difficulties who are unable to perform CISC and who do not wish to use a drainage bag. It is certainly more discreet for the user, although it is not suitable for everyone (Table 35.4). A multicenter comparative evaluation of catheter valves concluded that prescribers need to be aware of the strengths and limitations of the different types of valve. The ideal valve should be easily manipulated, leak free, comfortable, and inconspicuous.50 Whereas 94% of those using catheter valves preferred this to a standard drainage system, 35% of those who used a bag were happy to continue to do so. In this study, no significant difference was found in the incidence of UTI.51
table 35.4.
• • • • •
Contraindications for the use of catheter valves
Poor manual dexterity Poor mental awareness Uncontrolled detrusor overactivity/hyperreflexia Compromised renal function Low bladder capacity
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clean intermittent self-catheterization (cISc) Intermittent catheterization is a technique mainly taught to patients to facilitate bladder emptying, although it can also be used to enable a patient to instill drugs (e.g. oxybutynin) intravesically, and therefore is appropriate not only for those with voiding difficulties but also for women who have concomitant detrusor overactivity or detrusor overactivity of neurogenic origin.52 CISC (Fig. 35.9) was first introduced by Lapides et al. in 1972.53 It greatly reduces the incidence of UTI by removing any residual urine and the complications associated with it. It allows women to regain control over their bladders, rather than their bladders controlling them.54 CISC should be taught in a relaxed manner by professionals who have an adequate understanding of normal lower urinary tract function and bladder dysfunction. Proper assessment, reassurance, and continuing support are vital if women are to be motivated to perform catheterization themselves. Criteria for women performing CISC are summarized in Table 35.5. CISC can be used in the following voiding disorders and conditions:
• • • •
Neurogenic bladder Hypotonic bladder Obstruction After surgery.
Neurogenic bladder CISC is commonly used by women who have urinary dysfunction due to neurologic damage from either trauma or a disease such as multiple sclerosis. Recurrent UTIs from persistent residual urine, upper tract damage due to ureteric reflux from high intravesical pressures caused by detrusor overactivity of neurogenic origin, and subsequent incontinence are prevalent. By the introduction of CISC and thus removal of any persistent urinary residual, all these problems can become greatly reduced. Anticholinergics in addition to CISC are advantageous in this group of women and can be instilled intravesically via the catheter to reduce systemic side effects.
Hypotonic bladder Women who have little or no sensation of bladder filling or emptying often experience persistent residual urine, giving rise to recurrent UTIs and, in some cases, overflow incontinence. By emptying the bladder at pre-set times (‘by the clock’), rather than by desire, they ensure that the bladder capacity is kept within normal limits.
Obstruction Voiding difficulties caused by urethral stenosis or stricture can be managed temporarily by CISC. Biweekly CISC may help keep the urethra patent and eliminate the need for repeat procedures, such as urethrotomy. It can also be useful for bladder emptying in the presence of an obstructive prolapse or pelvic mass (e.g. large fibroid).
After surgery
Figure. 35.9. table 35.5.
• • • • • •
Self-catheterization by a woman. Criteria for women performing clean intermittent self-catheterization
Motivation Acceptability Adequate manual dexterity Adequate mental awareness Ability to position themselves to gain access to the urethra Sufficient bladder capacity
Many surgical techniques used in an attempt to cure urodynamically proven stress incontinence are obstructive in nature.55 If voiding difficulties do develop, these can easily be managed by CISC. It is important that women are warned of this potential postoperative complication before they consent to such procedures. There is no set rule as to how long a woman will need to perform CISC, but residuals do tend to decrease with time, unless there was preoperative evidence of voiding difficulties. If women are identified preoperatively (i.e. at urodynamic investigation), it is advisable to teach them CISC before they undergo any surgery. This ensures that they are aware of what is involved should the need to self-catheterize arise. CISC is not suggested to replace immediate postsurgical bladder drainage via 549
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a usual indwelling catheter, as continuous bladder drainage may result in quicker or normal voiding.56
catheter types PVC is frequently used for CISC with a lubricant to facilitate insertion. Plastic catheters can be reused, for up to a week, as long as the user is infection free and has a good technique. Other materials used, although less commonly, include stainless steel and silver. Currently there is a highly competitive market in catheter types, making it often difficult for both healthcare professional and user to make a choice in what to use. Ultimately, catheter choice will depend on the individual and what is available. Manufacturers have developed self-lubricating (hydrophilic) catheters, with evidence that the higher the osmolality within the catheter the less friction there is on insertion.57 The disadvantages associated with these catheters are that they are more expensive and can be used only once. However, these catheters have gained popularity over recent years and most of the evidence on advocating their use suggests that, in the long term, there is less trauma to the urethral mucosa. Other advances include silicone-coated catheters that ‘pick-up’ a watersoluble lubricating gel as the catheter passes through the sterile packaging and guide mechanism. Most women will use a size 10–12 Fr. It is quite reasonable for women to use a longer ‘male’ length catheter if they find it easier. Many manufacturers are now designing catheters to fit in with women’s busy lives, advocating discreet, easy and ready-to-use catheters, advertising them as ‘no bigger than a lipstick’. Additionally, it is possible to have catheters with attached bags to drain urine into and some catheters even have an antimicrobial coating to minimize device-associated infections. How effective these are in real terms is debatable. If women have difficulty in directing the catheter into the urethra there are aids to guide them.
Summary Careful consideration is necessary before any type of catheterization is used as a long-term form of management. If catheterization is the only feasible solution after appropriate investigation, the choice of catheter should follow comprehensive assessment of the individual.
PAdS And PAntS Incontinence is frequently accepted as an unavoidable female condition. The use of incontinence pads and pants is, for many women, the first method of control.
Women may be unaware of their local continence services and have enormous trouble finding information to help them make a choice;58 consequently, they buy their own products, frequently sanitary towels, which are often unsuitable. Nonetheless, today there is a wide range of products available from a variety of sources, including the internet, mail order, and even supermarkets. The need for appropriate assessment is vital so that the best available treatment or management can be obtained. In the last 30 years there has been a huge growth in the market of reusable and disposable products. In 1974, Australian Bill Kylie devised an oblong absorbent pad, which became the forerunner of the disposable pad industry. Products are continuously changing and developing, with companies endeavoring to ensure that their products suit the users’ needs. It is difficult even for a specialist continence nurse to keep up with the choice available. Certainly, gaps in knowledge seem to exist about the uses, best practices, quality of life factors, and problems associated with absorbent products, as well as other devices, catheters, and skin care products. It has been suggested that collaboration among public and private sectors would result in a greater likelihood of higher quality research that has sufficient power and integrity, more efficient use of resources special to each setting, and therefore expedite application of technologies for patient use.59 It is certainly not unusual for many products not to be assessed in quality trials and it is equally not uncommon that those that are assessed have been changed before the results are published. Because the task of selecting continence products is so often overwhelming, the Continence Product Evaluation (CPE) network, funded by the Medical Devices Agency, has been set up in the UK to provide an evidence base for product selection, including pads and pants.60
Pads Although incontinence is not a life-threatening condition, the social stigma associated with it can put enormous pressure on the individual. Pads may be required as a temporary measure while investigations are undertaken or treatment is awaited. They should not, however, be used as an alternative to effective continence promotion strategies. Their use should not be considered as the first line of treatment except for the severely incontinent person where containment will be a priority. Accurate assessment of the patient’s needs (Table 35.6) should ensure that the correct product to contain incontinence is supplied. For women, absorbent pads are still the most popular form of management and are manufactured in various shapes and sizes (Fig. 35.10). An absorbent pad
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table 35.6.
Guidelines when assessing product provision Individual assessment considerations
Key feature for the ‘perfect product’
Requirement
Linked to
Options/variables
Absorbent
Able to receive the loss with no or low leakage
Speed of urine entry and spread Type of pulp in core, e.g. pulp with Absorbent capacity super-absorber Core remaining intact Reusable
Safe
Able to receive and contain the loss with no or low leakage for a reasonable period
Absorbent capacity Good fit of pad Pad staying in place Retention of shape Posture of user
Type of pulp in core, e.g. pulp with super-absorber Reusable
Comfort (wet and dry)
Able to be worn dry or wet without being felt unduly and without irritating the skin
Good fit Compliance Retention of shape Low bulk Dry and wet surface texture Core remaining intact
Length, width, thickness Rectangular/shaped Backed/unbacked Method of securing Surface and core materials Disposable/reusable products
Discreet
Won’t show Won’t rustle Won’t smell Won’t look different
Low bulk Discreet outline No rustle noise Normal appearance Discreet packaging and delivery Discreet disposal or laundering
With/without super-absorber Rectangular/shaped Reusable pant with integral pad Disposable/reusable system Delivery/mail order
Easy to change
Ease when putting on Ease when taking off Convenient storage immediately before and after use
User disability: mobility; dexterity Facilities
Disposable/reusable system; disposable/reusable materials; pad rectangular, shaped or pants with integral pad; pad pouched, pocketed or loose; adhesive tabs, press-studs or Velcro closures
Secure in position
Won’t shift when user moves, walks or transfers
User mobility Pad shape Pad design Method of securing pad
Pad rectangular, shaped or pants with integral pad; pad pouched, pocketed or loose; adhesive tabs, press-studs or Velcro closures
Convenient
Easily used without excessive effort, frustration or anxiety
Availability; storage, temporary and immediate; disposal, immediate and temporary; laundering, ability and facilities; environment, domestic/ communal; indoors/out of doors
Disposable/reusable products Disposable/reusable usage cycle
Economical
Able to be used in a costeffective, non-wasteful manner
Disposables: staying intact to permit reuse if dry Reusables: effect of wash and wear on product life Durability: seam strength; edgestitching strength; stability of core; stability of dimensions
Disposables: pulp quality; coverstock strength Reusables: surface, core and backing materials; various qualities of workmanship
Reproduced by kind permission of Nursing Times, where this table first appeared in the Continence Supplement on 21 April 1993.
worn (or incorporated) inside a retaining garment is the most common way of managing incontinence.61 The ideal pad should be ‘simple to use, reliable to wear and pleasing in appearance’,62 although the most
important purpose is that the pad should contain the incontinence. Each type of pad has been developed with a particular need in mind (Table 35.7): small pads are used 551
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Adhesive strips
Elastication Elastication aids fitting to groin
Shaping
Wetness indicator
a
Figure. 35.10. table 35.7.
b
Examples of absorbent pads: (a) insert pads; (b) heavy incontinence pads (used with net pants). Selection of a product
Type of continence
Loss
Recommended product
Urinary
Light (0–50 ml)
Small, slim waterproof-backed disposable/reusable liner Washable pad built into normal pants Male dribble pouch, disposable/reusable
Moderate (200 ml)
Rectangular or shaped Waterproof-backed disposable/reusable liner
Severe (>300 ml)
Shaped waterproof-backed disposable pad Booster pad with above All-in-one disposable/reusable pad Female urinary pouch Male retracted urinary pouch
Fecal
Staining
Panty liner Disposable pants Cotton-top reusable slim pad
Light
Shaped disposable waterproof-backed pad
Severe
Fecal pouch
in cases of light incontinence or when a pad can be changed frequently; large pads are used when there is severe incontinence or where toileting is not an option.63
Disposable pads Disposable products are usually made up of two or three layers. The top layer, which is worn next to the skin, is made of a hydrophobic cover which allows urine to pass through to a second absorbent layer composed of a mixture of chemicals and mechanically made pulps, often with added super-absorbent. The third layer, when used, is a waterproof backing to prevent leakage.
The product can also contain a deodorizer. Some pads have elasticated sides, especially around the gusset or crotch area, thus ensuring a good fit. A peel-off sticky strip is often integrated into the backing of smaller pads, which attaches to the pants and enables use with normal underclothes or with specially designed net underpants. One of the major disadvantages with pads is that they can ‘bulk up’; in addition, the outside covering comes apart if the pads are not changed often enough.64 A multicenter comparative evaluation of disposable pads for women with light incontinence was undertaken by the CPE network. They found statistically significant differ-
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ences in 13 of the 17 performance aspects (e.g. ability to hold urine without leaking and the fit of the pad).65 In practice, this may mean that the suitability of many pads for each individual may end up down to trial and error.
Disposable absorbent roll Like the pouch pad, the absorbent roll has no waterproof backing and therefore needs to be used with pants with a waterproof lining. It has the advantage that it can be cut to suit individual requirements, but it is useful only for light incontinence.
Disposable pad-and-pants system Plastic-backed pads used with net pants come in many sizes and shapes (see Fig. 35.10) and are recommended for patients who are able to undertake toileting.
Disposable all-in-one pads All-in-one pads (Fig. 35.11) are worn without additional pants. Some have side fastenings and the size required is determined by the hip size of the patient. They are not necessarily more absorbent than a pad with separate pants but, if well fitted, can be particularly effective in containing urine and poorly formed feces. They are often used for the severely disabled, bed-fast patient, or when toileting is difficult or not appropriate.
Disposable pouch pads Pouch pads have no waterproof backing; they are designed to be placed in the pouch of a washable pair of pants. The outside of the pouch is lined with a waterproof gusset. The size of the pad required is dependent upon the size of pouch and the degree of absorbency required (Fig. 35.12).
Resealable tapes
Disposable bed pads Disposable bed pads are available in a range of sizes and absorbencies. They have a liquid-permeable top cover, a cellulose wadding or fluffy pulp middle layer, and a waterproof backing. They are designed as bed protection when there is the added risk of soiling or when a body-worn pad is not suitable (Fig. 35.13).
Reusable pads The decision whether to use reusable incontinence products rather than disposables is a complex one that will depend on individual needs and preferences. There is a small pilot study on how washable and disposable products perform and how nurses can enable their patients to use washable products appropriately.66 The availability of suitable laundry facilities will be an important factor.67
Reusable body-worn pads Reusable body-worn pads can be a pad-and-pants system or an all-in-one system. The surface next to the skin can be a smooth or a quilted fabric. Both systems allow urine to pass through to an absorbent layer. Reusable pads are available with or without a waterproof backing. A comparative evaluation of reusable all-in-one pad and pants, for light incontinence, found that although many performed similarly, there were statistical differences in other aspects (e.g. fit and discreetness).68
Reusable bed and chair pads
Tear-away side seam for easy removal
Figure. 35.11.
Most reusable bed and chair pads are available with or without ‘tuck-in’ flaps or waterproof backings; some are non-slip (Fig. 35.14). These pads, like the disposable pads, have a hydrophobic upper layer allowing urine to pass into the absorbent layer below so that the patient’s skin stays dry; her skin can therefore remain in direct contact with the pad. The use of disposable underpads or bed protection (see Fig. 35.13) has diminished over the years with the advent of washable bed protectors and more sophisticated disposable and reusable body-worn pads. The advantages and limitations of reusable and disposable products are outlined in Table 35.8.
All-in-one pads. 553
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Elasticated waist and legs
Absorbent pad
Waterproof gusset
a
Waterproof pouch (alternatively may be inside pants)
b
Waistband keeps pants in place Velcro tabs for fastening Hand-held urinal
Front can be dropped to use urinal c
d
Figure. 35.12. Pouch pads and pants: (a) pouch pants; (b) stretch pants with waterproof gusset; (c) stretch pants for use with plastic-backed pad; (d) drop-front pants.
a b
Waterproof sheet should be placed underneath
a
Figure. 35.14. Reusable bed and chair protection: (a) reusable bed pad; (b) reusable chair pad.
b
Cotton flap each side to tuck in (or fold under one side if using double bed)
Figure. 35.13. Disposable and washable types of bed protection: (a) disposable bed pad; (b) washable bed sheet.
Pants Many designs are available to suit varying degrees of incontinence. Most have an integrated waterproof gusset and can be used with or without a pouch pad (see Fig. 35.12).
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table 35.8.
Advantages and limitations of reusable and disposable products
Type of product
Advantages
Limitations
Reusable
Cannot be torn apart Retain better shape Do not break up Potential for more design options Facilitate independence from supply system Eliminate the need for storage Can be reused if remain dry
Require washing Initial capital outlay ? Unacceptable to users (especially if menstruating or fecally incontinent)
Disposable
Flexibility for experimentation to match user’s requirements No need to launder Materials better suited to fecal incontinence
Tendency for pulp compression Tendency for pulp break-up Can be torn apart
Skin care The prevention and treatment of any skin condition caused by incontinence are very important. If urine is in contact with the skin, the area should be regularly cleaned and dried. The use of talcum powder is not advocated. Thick barrier creams are not recommended for use with pads as this affects absorption.69 Urinary incontinence in people with poor skin condition and pressure sores needs careful management. Collier70 describes how ‘moisture predisposes skin to pressure sores because of the effects of skin maceration, which in turn leads to excoriation, increasing the risk of abrasion by friction’. Skin problems associated with incontinence can vary, and need treatment according to the severity of the condition.71 A recent study examined the effects of two different pad-changing regimes, at night, on skin health. The authors wanted to answer the question of whether a change at 4-houly intervals rather than 8-hourly meant less deterioration in skin health. Although there was no statistical evidence to support that more frequent changing resulted in less erythema/dermatitis, there was evidence that when the skin remained wetter for longer it made it more vulnerable to abrasion damage.72 Lastly, it is worth noting that absorbent pads do seem to have a substantial adverse effect on the pressure redistribution properties of pressure-management mattresses. Folds within the pad appear to contribute to this effect.73 Holistic patient assessment is the key to achieving a containment of incontinence by pads and pants, with regular review to ensure that the patient’s needs are met. No one pad suits everyone; some pads are more susceptible to misuse than others, but all work best if the wearers and carers receive proper instruction and ongoing support.74
AIdS And APPLIAncES The female anatomy does not allow easy application of aids and appliances to maintain dryness. For this reason the number of products available for women is far more limited than it is for men. For many women, incontinence will be an ongoing and sometimes intractable problem. It is, therefore, important that women are provided with full information on the range of products available and how to obtain them. The ‘range of products and their provision is bewildering to professionals and consumers alike’.75 The United Kingdom Continence Foundation Continence Products Directory,76 which can also be found online (www.continence-foundation.org.uk), lists over a thousand items, ranging from special toilet seats to assist toilet training to odor-control products for use by those with fecal incontinence or who are unable to maintain prompt personal hygiene. When advising patients or carers about aspects of care on particular aids and appliances, there are several important factors to consider, as shown in Table 35.9.77 Ideally, the choice of products should be made following full consultation with the user and, where appropriate, with the carers. The opportunity should be given, where possible, for a trial of the aid or appliance prior to purchase. Full explanation of the product’s use with supporting written information is needed, together with ongoing support to ensure that the product is meeting the user’s needs. table 35.9.
• • • • • •
Implications for the selection of aids and appliances
Personal preference Mobility Manual dexterity Local anatomy Eyesight Mental function
• • • • •
Hygiene Environment Financial implications Laundry or disposal facilities Available helpers (relatives, carers, professionals)
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Aids in the toilet
floor. Some are designed to swing out of the way to give adequate access for wheelchair users.
For those with difficulty in bending or managing in the toilet, a raised lavatory seat facilitates sitting down and getting up78 (Fig. 35.15). Support rails, suitably placed, can also assist elderly or disabled patients to position themselves on the toilet and to manage clothing after voiding. Rails can be positioned on walls or fixed to the
Aiding toileting: clothing The Disabled Living Foundation guidelines for management of incontinence79 comment that ‘the selection of appropriate clothing can make continence so much easier to achieve’ (Fig. 35.16). The general recommendations are as follows:
• The fewer the layers of clothing, the easier to manage;
• Loose-fitting clothes are easier to manage than tight • Raised seat
• •
Adjustable surround
• •
Figure. 35.15.
ones; Light, slippery fabrics cling less and are therefore easier to adjust; Short vests, shirts or blouses are less likely to get in the way; Fabrics that are easy to launder and do not retain odor should be chosen; Thumb or hand loops attached to waistbands may help those who cannot remove trousers or skirts easily; Clothes that disguise the chosen method of management (i.e. easy access for toileting or changing pads) are recommended.
Aids in the toilet.
Flaps can be tucked into waistband for toileting
a Wide leg can be pulled to one side for toileting b Ensure generous overlap
c
Figure. 35.16.
Front
d Back
Drop-front gusset secured by Velcro tabs
Selection of clothing: (a) French knickers; (b) wrap-around skirt; (c) open-crotch knickers; (d) camiknickers.
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commodes When the lavatory is not easily accessible, a number of items of equipment can assist in maintaining continence. Commodes and chemical toilets can be used as a substitute to the lavatory (Fig. 35.17). Commodes can be obtained with a variety of properties, including adjustable-height legs and removable arms and backs.80 Many look like well-designed chairs and can be kept in a bedroom or living room as part of the ordinary furniture.81 Chemical toilets have the advantage that they need emptying less often.
Female urinals McIntosh82 described the major problems that women with incontinence have in managing toileting in the community, and felt that female urinals could offer a
solution for toileting problems and may therefore be the management method of choice. As a viable alternative to commodes, they are particularly helpful for those who cannot get to the toilet in time (Fig. 35.18); this would include women with overactive bladder, frailty due to old age, poor mobility, being without assistance (especially at night), having an inaccessible toilet, and being wheelchair dependent. They also benefit women on social outings and during travel. A wide range of urinals is available for use in different positions (standing; lying down in bed; lying prone; lying on the side; sitting in bed leaning back or sitting up; sitting up, forwards or backwards in a chair or wheelchair). In addition, small slipper-pan urinals, jug-type urinals (see Fig. 35.18), and simple home-made collecting devices can be used. Urinals for women are products that are, however, little used, little known, and undervalued.82 In order to meet this problem, the CPE network carried out an evaluation of these products in 1999, and found that although many of the urinals were successful in the standing/crouching and sitting on the edge (of bed/chair) positions, comparatively few were successful in the lying position. They found that women
b
a a c
d
e b
Figure. 35.17. Commode and chemical toilet: (a) typical commode; (b) raised, contoured toilet seat over a chemical commode.
Figure. 35.18. Female urinals: (a) bridge urinal with Ushaped cushion; (b) St Peter’s boat; (c) female urinal connected to drainage bag; (d) swan-neck urinal; (e) pan-type urinal connected to drainage bag. 557
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with higher dependency needs found fewer urinals suitable for their needs without assistance.83 It is really the responsibility of the continence specialist to have access to the different types of urinal and be in a position to offer the most appropriate. Nevertheless, this may well be through trial and error.
Body-worn female devices There are two body-worn female devices: a female urinary pouch with adhesive backing and a device kept in place with straps. These are rarely used and are no longer considered satisfactory appliances for women with urinary incontinence.
Alarms Three types of alarm are used to promote continence (Fig. 35.19), as follows:
• Body-worn alarm with audible, vibrating or flashing alarm signals;
• Bed alarm with audible alarm signals;
• Toilet bowl or potty alarms with musical signals. Body-worn and bed alarms are condition devices used to prompt ‘wake up’ and ‘hold on’ to the sensation of a full bladder from sleep. Body-worn alarms can also be used during the day as an aid to bladder retraining or toileting, alerting the patient or her carers to incontinence. Musical toilet bowls or potty alarms are particularly useful for toilet training for children or for adults with learning difficulties. Every time urine is passed into the toilet or potty, a tune is played; this encourages the recognition of the use of the toilet with the emergence of urine. There is substantial evidence that although alarms have less immediate effect on nocturnal enuresis than drugs, such as desmopressin, they do appear more effective by the end of a course of treatment.84 Additionally, treatment with an alarm system has been associated with a significant increase in bladder storage capacities (maximum nocturnal bladder capacity, maximum functional bladder capacity and mean daytime bladder capacity).85
Furniture protection Women with intractable incontinence who have nocturnal enuresis may require waterproof mattress covers to prevent damage to the mattress (see Figs 33.13, 33.14). Also available are waterproof drawsheets, pillowcases and duvet covers.86
Control box
Sensor pad
odor control
b Control box
Sensor mat
a
c
People who have an incontinence problem often become obsessed by a fear of smelling offensive. This is an unnecessary fear as, with reasonable care, odor need not arise.87 Good personal hygiene, prompt disposal and storage of products, together with good ventilation, should be all that is needed. Aids and appliances must be cleaned frequently to reduce the risk of crystalline deposits building up and causing a smell. Where possible, it would be an advantage to have two appliances so that one can be cleaned and thoroughly dried before use again.79 A neutralizing deodorant will help if added to the water when washing appliances, commodes, urinals, chairs, and carpets. It is also possible to put a drop or two onto protective padding or onto appliances.
d
SuMMArY Figure. 35.19. Alarms: (a) mini-personal alarm; (b) bed alarm; (c) potty alarm; (d) toilet bowl alarm.
There are many products to suit a variety of urinary complaints. However, it is crucial that all women with
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urinary dysfunction are comprehensively assessed and investigated before any form of containment becomes long-term management. For those unfortunate enough to have to rely on catheters, pads and pants, or aids and appliances, the right product or mode of containment must be suitable for the individual. The aim with all these products is primarily to improve the individual’s quality of life.
rEFErEncES 1. Mattelaer JJ, Billet I. Catheters and sounds: the history of bladder catheterization in the early management of traumatic paraplegia and tetraplegia. Paraplegia 1995;33:429–33. 2. Crow RA, Chapman RG, Roe BH, Wilson JH. Study of Patients with an Indwelling Urinary Catheter and Related Nursing Practice. Guildford, UK: Nursing Practice Research Unit, University of Surrey, 1986. 3. Roe BH. Catheters in the community. Nurs Times 1989;85(36):43–4. 4. Lowthian P. The dangers of long-term catheter drainage. Br J Nurs 1998;7(7):366–79. 5. Department of Health. Reference guide to consent for examination or treatment. London: Department of Health, 2001. 6. Reybard JF. Traité Pratique des Rétrécissements du Canal de l’Urètre. Paris: Labe, 1853. 7. Foley FEB. A self-retaining bag catheter for use as indwelling catheter for constant drainage of the bladder. J Urol 1937;38:140–3. 8. Association for Continence Advice (ACA). Notes on good practice. Urethral catheters. Glasgow: ACA, 2004. 9. Henry, M. Catheter confusion. Nurs Times 1992;88(42): 65–72. 10. Blannin J, Hobden J. The catheters of choice. Nurs Times 1980;76(48):2092–3. 11. Ruuta M, Alfhan, O, Anderson LC. Cytotoxicity of latex urinary catheters. Br J Urol 1985;57:82–7. 12. Liedberg H, Lunberg T. Silver alloy catheters reduce catheter-associated bacteriuria. Br J Urol 1990;65:379–81. 13. Rosier PK. Review: silver alloy catheters are more effective than standard catheters for reducing bacteriuria in adults in hospital having short term catheterization. Evid Based Nurs 2004;7(3):85. 14. Rupp ME, Fitzgeral T, Marion N, Helger V, Puumal S, Anderson JR, Fey PD. Effect of silver-coated urinary catheters: efficacy, cost-effectiveness, and antimicrobial resistance. Am J Infect Control 2004;32(8):445–50. 15. Talji M, Korpela A, Jarvi K. Comparison of urethral reactions to full silicone, hydrogel coated and siliconized latex catheters. Br J Urol 1990;66:652–7.
16. Seth C. Catheters ring the changes. Community outlook. May 1998;12–4 [Cox AJ, Huskin DUL, Sutton TM. Comparison of in vitro encrustation on silicone and hydrogel coated latex catheters during eighteen weeks. Br J Urol 1998;61:151–61.] 17. Parkin J, Scanlan J, Woolley M, Grover D, Evans A, Feneley RC. Urinary catheter ‘deflation cuff’ formation: clinical audit and quantative in vitro analysis. BJU Int 2002;90(7):666–71. 18. Hiu J, Ng CF, Chan LW, Chan PS. Can normal saline be used to fill the balloon of a Foley catheter? The experience of a prospective randomized study in China. Int J Urol 2004;11(10):845–7. 19. Kennedy AP, Brocklehurst JC, Lye MDW. Factors related to the problems of long-term catheterization. J Adv Nurs 1983;8:207–12. 20. Roe BH, Brocklehurst JC. Study of patients with indwelling catheters. J Adv Nurs 1987;12:713–8. 21. Blandy JP. How to catheterise the bladder. Br J Hosp Med 1981;26:58–60. 22. Bach D, Hess EA, Prauge CH. Prophylaxis against encrustation and urinary tract infection with indwelling transurethral catheters. Urol Nephrol 1990;2:25–32. 23. Warren JW. Catheter-associated bacteriuria. Clin Geriat Med 1992;8:805–19. 24. Roe BH. Use of bladder washouts: a study of nurse’s recommendations. J Adv Nurs 1989;14:494–500. 25. Getliffe KA. The characteristics and management of patients with recurrent blockage of long-term urinary catheters. J Adv Nurs 1994;20:140–9. 26. Gopal Rao G, Elliot TSJ. Bladder irrigation. Age Ageing 1988;17:373–8. 27. Davies AJ, Desai HN, Turton S, Dyas A. Does instillation of chlorhexidine into the bladder of catheterised geriatric patients help reduce bacteriuria? J Hosp Infect 1987;9: 72–5. 28. Stickler DI, Chawia IC. The role of antiseptics in the management of patients with long term indwelling bladder catheters. J Hosp Infect 1987;10:219–28. 29. Whalen RL, Cai C, Thompson LM et al. An infectioninhibiting urinary catheter material. ASAIO J 1997;43: M842–M847. 30. Morris NS, Stickler DJ, Winters C. Which indwelling urethral catheters resist encrustation by Proteus mirabilis biofilms? Br J Urol 1997;80:58–63. 31. Kohler-Ockmore J, Feneley RC. Long-term catheterization of the bladder: prevalence and morbidity. Br J Urol 1996;77:347–51. 32. O’Flynn KJ, Thomas DG. Intravesical instillation of oxybutynin hydrochloride for detrusor hyperreflexia. Br J Urol 1993;72:566–70.
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33. Brocklehurst J, Brocklehurst S. The management of indwelling catheters. Br J Urol 1978;50:102–5.
domised study comparing a catheter valve with a standard drainage system. Br J Nurs 1997;80:915–7.
34. Kohler-Ockmore J. Urinary catheter complications. J Dist Nurs 1992;10(8):18–20.
52. O’Flynn KJ, Thomas DG. Intravesical instillation of oxybutynin hydrochloride for detrusor hyperreflexia. Br J Urol 1993;72:566–70.
35. Getliffe KA. The characteristics and management of patients with recurrent blockage of long-term urinary catheters. J Adv Nurs 1994:20;140–9. 36. Pomfret I, Bayait F, Mackenzie R, Wells M, Winder A. Using bladder instillations to manage indwelling catheters. Br J Nurs 2004;13(5):261–7.
53. Lapides J, Dionko AC, Silber SJ, Lowe BS. Clean intermittent catheterization in the treatment of urinary tract disease. J Urol 1972;107:458–61. 54. Moore K. Intermittent self catheterization. Researchbased practice. Br J Nurs 1995;4:1057–62.
37. Getliffe KA, Hughes SC, Le Claire M. The dissolution of urinary catheter encrustation. BJU Int 2000;85(1):60–4.
55. Smith R, Cardozo L. Early voiding difficulties after colposuspension. Br J Urol 1997;80:911–4.
38. Stickler DJ, Jones GL, Russell AD. Control of encrustation and blockage of Foley catheters. Lancet 2003;361(9367):1435–7.
56. Gandhi S, Beaumont JL, Goldberg RP, Kwon C, Abramov Y, Sand PK. Foley versus intermittent self-catheterisation after transvaginal sling surgery: which works best? Urology 2004;64(1):53–7.
39. Burr RG, Nuseibeh IM. Urinary catheter blockage depends on urine pH, calcium and rate of flow. Spinal Cord 1997;35:521–5. 40. Stickler DJ. The role of antiseptics in the management of patients undergoing short-term indwelling catheterization. J Hosp Infect 1991;16:89–108. 41. Pratt RJ, Pellowe C, Loveday HP et al. The EPIC Project. Developing national evidence based guidelines for preventing healthcare associated infections. J Hosp Infect 2001;47(Suppl):S3–S4. 42. Hilton P, Stanton SL. Suprapubic catheterization. Br Med J 1980;281:1261–3. 43. O’Kelly JJ, Mathew A, Ross S, Munro A. Optimum method for urinary drainage in major abdominal surgery: a prospective trial of suprapubic versus urethral catheterization. Br J Surg 1995;82:1367–8. 44. Gott M, Hinchcliff S, Galena E. General practitioner attitudes to discussing sexual health issues with older people. Soc Sci Med. 2004;58(11):2093–103. 45. Gillespie WA, Lennon GG, Linton KB, Slacle NN. Prevention of urinary tract infection in gynaecology patients. Br Med J 1964;2:423–5. 46. Thornton GF, Andriole VT. Bacteriuria during indwelling catheter drainage: effect of a closed sterile drainage system. J Am Med Assoc 1970;214:339–42. 47. Mulhull A. Biofilms and urethral catheter infections. Nurs Stand 1991;5:26–8. 48. Rogers J, Norkett DI, Bracegirdle P et al. Examination of biofilm formation and risk of infection associated with the use of urinary catheters with leg bags. J Hosp Infect 1996;32:105–15. 49. Meers P (ed) Hospital Infection Control for Nurses. London: Chapman and Hall, 1992.
57. Walker L, Telanderm M, Sullivan L. The importance of osmolality in hydrophilic urethral catheters: a crossover study. Spinal Cord 1997;35:229–33. 58. White H. Continence products – the essentials. J Community Nurs 1997;11(12):10. 59. Newman DK, Fader M, Bliss DZ. Managing incontinence using technology, devices, and products: directions for research. Nurs Res 2004;53(6 Suppl):S42–8. 60. Fader M, Cottenden A, Brooks R. The CPE network: creating an evidence base for continence product selection. J Wound Ostomy Continence Nurs 2001;28(2):106–12. 61. Pomfret I. The use of continence products. In: Norton C (ed) Nursing for Continence, 2nd ed. Beaconsfield, UK: Beaconsfield Publishers, 1996; 335–64. 62. White H. Continence products – the essentials. J Community Nurs 1997;11(12):10. 63. Shepherd A, Blannin J. The role of the nurse. In: Mandelstam D (ed) Incontinence and its Management, 2nd ed. Beckenham, UK: Croom Helm, 1986; 60–184. 64. Norris C, Cottenden A, Ledger D. Underpad overview. Nurs Times 1993;89(21):68, 70, 72. 65. Clarke-O’Neill S, Petterson L, Fader M, Cottenden A, Brooks R. A multi-center comparative evaluation: disposable pads for women with light incontinence. J Wound Ostomy Continence Nurs 2004;31(1):32–42. 66. Macaulay M, Clarke-O’Neill S, Fader M, Pettersson L, Cottenden A. Are washable absorbents effective at containing urinary incontinence? Nurs Times 2004;100(12):58–62. 67. Norris C, Cottenden A, Ledger D. Underpad overview. Nurs Times 1993;89(21): 68, 70, 72.
50. Fader M, Pettersson L, Brooks R et al. A multi-centre comparative evaluation of catheter valves. Br J Nurs 1997;6:359, 362–4, 366–7.
68. Clarke-O’Neill S, Petterson L, Fader M, Dean G, Brooks R, Cottenden A. A multicentre comparative evaluation: washable pants with an integral pad for light incontinence. J Clin Nurs 2002;11(1):79–89.
51. Wison C, Sandhu SS, Kaisory AV. A prospective ran-
69. Le-Leivre S, Addison I. Incontinence and Skin Care: the
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Role of the Nurse. London: Royal College of Nursing, Continence Care Forum, 1996; 5:16. 70. Collier M. Pressure 1997;93(4):(Suppl):1–4.
area
care.
Nurs
Times
71. Watson R. Justifying your practice. Br J Nurs 1992;5(3): 11–2. 72. Fader M, Clarke-O’Neill S, Cook D, Dean G, Brooks R, Cottenden A, Malone-Lee J. Management of night-time urinary incontinence in residential settings for older people: an investigation into the effects of different pad changing regimes on skin health. J Clin Nurs 2003;12(3):374–86. 73. Fader M, Bain D, Cottenden A. Effects of absorbent incontinence pads on pressure management mattresses. J Adv Nurs 2004;48(6):569–74. 74. Cottenden A. Aids and appliances for incontinence. In: Roe B (ed) Clinical Nursing Practice. The Promotion and Management of Continence UK. London: Prentice Hall, 1992; 129–52. 75. Walker L, Telanderm M, Sullivan L. The importance of osmolality in hydrophilic urethral catheters: a crossover study. Spinal Cord 1997;35:229–33. 76. Continence Products Directory, 2nd ed. London: The Continence Foundation, 1996. 77. Bucknell A. When prevention fails, incontinence must be managed. Geriatric Medicine Supplement. Community Nurs (Suppl) 1998;(Sept):7. 78. Disabled Living Foundation. Notes on incontinence.
Information Service Handbook. Part II, Section 10. London: Disabled Living Foundation, 1989; 13. 79. Disabled Living Foundation. Continence. Hamilton Index. Part II, Section 10. London: Disabled Living Foundation, 1998; 9. 80. Association of Continence Advisers (ACA). Directory of Aids to Toileting, 1st ed. London: ACA, 1985. 81. Disability Equipment Assessment A9: A Comparative Evaluation. London: Medical Devices Agency, 1994. 82. McIntosh J. Realising the potential of urinals for women. J Community Nurs 1998;12:14. 83. Fader M, Pettersson L, Dean G, Brooks R, Cottenden A. The selection of female urinals: results of a multicentre evaluation. Br J Nurs 1999;8(14):918–20, 922–5. 84. Glazener CM, Evans JH, Peto RE. Alarm interventions for nocturnal enuresis in children. Cochrane Database Syst Rev 2003;(2):CD002911. 85. Taneli C, Ertan P, Taneli F et al. Effect of alarm treatment on bladder storage capacities in monosymptomatic nocturnal enuresis. San J Urol Nephrol 2004;38(3):207–10. 86. Cutner A, Haken J. Aids and appliances. In: Cardozo L (ed) Urogynaecology: ‘The King’s Approach’. London: Churchill Livingstone, 1997; 663–9. 87. Norton C. Nursing for Continence, 2nd ed. Beaconsfield, UK: Beaconsfield Publishers, 1996.
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36 Neurologic disorders Ricardo R Gonzalez, Renuka Tyagi, Alexis E Te
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INTRODUCTION Neural control of voiding involves complex interactions between the central and peripheral nervous systems and the bladder and sphincter. Neurologic disorders can affect this system in multiple locations, resulting in a disruption in the bladder’s ability to store or empty urine. This chapter will systematically review the characteristic voiding dysfunctions as they relate to the diseases from which they result.
VOIDING FUNCTION AND DYSFUNCTION The bladder’s ability to store and empty urine is under neurologic control. Therefore, any neurologic abnormality can result in voiding dysfunction. In general, neurologic lesions either cause loss of function (i.e. areflexia or denervation) or result in unopposed reflex ‘overactivity’, i.e. detrusor overactivity (DO) or hyperreflexia (DH), now called neurogenic detrusor overactivity.1 The effects of neurologic lesions can be broadly divided into two groups: those that cause areflexia (which usually results in failure to empty) and those that cause overactivity (which affects the ability to store urine). Neurologic lesions can also affect urinary sphincteric function, resulting in loss of the usual coordination with bladder function and consequently in detrusor–sphincter dyssynergia. To some extent, the anatomic level of neurologic injury can predict the type of dysfunction. The three gross anatomic distinctions that predict effect on voiding function are cerebral (suprapontine), spinal (suprasacral) or peripheral (infrasacral). These levels will serve as a structure by which to examine different neurologic disorders and their voiding effects later in this chapter. Table 36.1 summarizes characteristic dysfunctions that result from known levels of injury as adapted from Wein.2 Cerebral lesions above the pons usually result in detrusor overactivity (DO) with intact sphincter coordination. Suprasacral spinal (i.e. upper motor neuron) lesions result in DO with a variable effect on sphincter coordination. Injuries involving the sacral cord or cauda equina result in lower motor lesions and detrusor areflexia (DA), with or without sphincter denervation.1 However, neurologic lesions can be multiple or incomplete in nature, resulting in a mixed pattern of voiding dysfunction not predicted by anatomic location.3–5 Voiding dysfunction includes failure to store and/or empty urine, and can be categorized by the three broad urodynamic categories listed below.
Detrusor overactivity with synergistic external sphincteric function Incomplete and non-traumatic spinal lesions tend to result in DO with synergistic external sphincter function. Similarly, in patients with lesions above the pons, DO is not associated with loss of sphincteric coordination because the lesion is above the level where detrusor contraction is coordinated with reflex urethral relaxation. Typical causes of DO with preserved synergistic sphincteric function include cerebrovascular disease, Parkinson’s disease, and some cases of multiple sclerosis (MS).1,6 Exaggerated detrusor contractions that occur after suprasacral trauma may be explained by any of the following three mechanisms:
• loss of the inhibitory impulse transmission; • emergence of primitive alternative micturition •
pathways; from the collateral sprouting of new neural pathways.7
Medical management of the resulting DO can usually be achieved with anticholinergic therapy (see Chapter 41). However, when DO persists despite medical therapy, augmentation cystoplasty or neuromodulation may be used to manage DO resulting in urge incontinence.
Detrusor overactivity with detrusor–sphincter dyssynergia Complete thoracic and cervical level spinal cord injury (SCI), in which the coordination reflex occurs, may result in DO with simultaneous contraction of the striated urethral sphincter.8,9 This is known as detrusor–sphincter dyssynergia (DSD), typical causes of which are SCI and MS.10–12 The diagnosis of DSD is crucial because there is a 50% or greater chance of developing urologic complications within 5 years of the onset of DSD,13–15 particularly vesicoureteral reflux and upper tract damage due to the elevation in intravesical pressure (usually when the pressure is chronically above 40 cmH2O). The danger of unrecognized DO with DSD is the ensuing high pressure storage system that results in upper tract damage. Successful management of DH with DSD involves decreasing detrusor activity medically or surgically to allow low pressure urinary storage. As discussed elsewhere, this can be achieved with anticholinergics and clean intermittent catheterization (CIC), or by disruption of the
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Table 36.1.
Neuromuscular dysfunction of the lower urinary tract
Defect
Detrusor activity
Compliance
Smooth sphincter/ bladder neck
Striated sphincter
Notes
Cerebrovascular accident
DO
N
S
S, possible LOC
Possible decreased sensation of lower urinary tract events
Brain tumor
DO
N
S
S
Possible decreased sensation of lower urinary tract events
Cerebral palsy
DO
N
S
S, D (25%), LOC
Parkinson’s disease
DO, IDC
N
S
S, bradykinesia
Shy–Drager syndrome DO, IDC
N, D
O
S
Possible denervation of striated sphincter
Multiple sclerosis
DO, IDC
N
S
S, D (30–65%)
Dyssynergia figures refer to percentage of those with DO
Suprasacral injury
DO
N
S
D
Smooth sphincter may be dyssynergic if lesion above T7
Sacral injury
DA
N, possible D CNR, possible O F
Autonomic hyperreflexia
DO
N
Myelodysplasia
DA, DO
N, possible D O
F
Findings variable. Striated sphincter often denervated
Tabes dorsalis, pernicious anemia
IDC, DA
N, I
S
S
Primary problem is loss of sensation; detrusor may become decompensated from chronic overdistension.
Disk disease
DA
N
CNR
S
Striated sphincter may be denervated with fixed tone
Radical pelvic surgery
IDC, DA
D, N
O
F
Diabetes
IDC, DA, DO
N, I
S
S
Cerebral (suprapontine)
Spinal cord injury
Ds
D
Peripheral Sensory and motor neuropathy. DO predominates
CNR, competent, not relaxing; D, decreased; DA, detrusor areflexia; DO, detrusor overactivity; Ds, dyssynergic; F, fixed tone; I, increased; IDC, impaired detrusor contractility; LOC, loss of (voluntary) control; N, normal; O, open (incompetent at rest); S, synergic.
urinary sphincter (e.g. pharmacologically with botulinum toxin or mechanically with an intraurethral stent or surgical ablation)16,17 which may render the patient incontinent. Continuous drainage with an indwelling urethral catheter should be avoided, given the wellcharacterized complications of infection, urolithiasis, tissue erosion, and urothelial cancers. In addition, in those patients with normal sensation, the catheter may be uncomfortable, particularly where there is urethral spasm (DSD). If a long-term catheter is required, then a suprapubic approach is preferable as it reduces the risk of infection.
Detrusor areflexia In patients with lumbosacral or peripheral nerve lesions, such as myelodysplasia, cauda equina injury and diabetes mellitus, DA with high or low bladder compliance may develop.1 DA is characterized by the absence of a detrusor contraction, usually resulting in low pressure urinary storage with failure to empty. CIC is the standard treatment for DA. Impaired detrusor contraction and DA tend to result with sacral and low lumbar injuries. However, certain upper motor neuron lesions can also result in DA, especially if clinical or subclinical sacral 567
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lesions (e.g. coexistent traumatic injury) are present.18 Because upper tract damage varies directly with increasing time at or above the critical 40 cmH2O pressure, diminished compliance requires the use of anticholinergic agents or surgical bladder augmentation to establish urinary storage under acceptable pressure.19
CONDITIONS OF THE BRAIN AFFECTING THE URINARY TRACT Cerebrovascular accident Cerebrovascular accident (CVA) – stroke – is defined as the acute onset of a focal neurologic deficit, usually caused by an occlusive event such as an atherosclerotic thrombus, or hemorrhage. Over 500,000 CVAs occur annually in the United States. One-third are fatal, another third necessitate long-term nursing care, and a third allow patients to return home close to their prior level of functioning.20 The effects of CVA on the function of the lower urinary tract are variable, depending on the location of the neural injury, its size and etiology.21 Additionally, because CVAs occur predominantly in the elderly population, evaluation and management are often confounded by coexisting stress incontinence, dementia, and voiding dysfunction from impaired contractility attributable to aging and peripheral neuropathy.20
Clinical and urodynamic features Clinically, patients may experience a range of voiding complaints from urinary retention, urgency and frequency, and/or incontinence. Neural arcs above the pontine level – where most non-fatal CVAs occur – serve to inhibit micturition. Thus, injury in this area decreases inhibitory control over detrusor function, most often resulting in DO.22 While DO is the most common long-term problem following a CVA, a significant number of newly affected patients initially develop urinary retention. This retention occurs as a result of ‘cerebral shock’ and may last for a period of several weeks and is much like the classic acontractile bladder ‘spinal shock’ phase that immediately follows a SCI.23 As recovery ensues, patients most commonly experience urinary urgency, with the incidence of incontinence reported to be as high as 51% within a year of injury. Urinary incontinence may also result from limitations in cognitive function and mobility resulting from neural injury,24 known as functional incontinence. Although urethral sphincter function is usually preserved, urinary incontinence results from uninhibited
detrusor contractions.25 Patients with lesions above the level of the pons characteristically maintain synergetic activity of the sphincter with detrusor contractions.21 However, patients with suprapontine lesions may purposely increase sphincteric activity during an uninhibited detrusor contraction to avoid urge incontinence. This guarding reflex – or pseudodyssynergia – may be confused with true dyssynergia by those not familiar with the interpretation of urodynamic studies.26 As long as urethral sphincter activity remains coordinated with detrusor contraction, intravesical pressure should remain physiologic and therefore preserve the function of the urinary tracts. Evaluation of the stroke patient can be riddled with challenges. Difficulties include obtaining an adequate history, technical difficulty with performing studies, and interpreting urodynamic studies given coexisting findings incidental to aging or co-morbidities.20 However, careful neurologic examination and urodynamic evaluation are crucial when assessing the stroke patient who presents for evaluation of voiding dysfunction.
Parkinson’s disease Parkinson’s disease affects men and women equally, primarily in the sixth and seventh decades of life, and it increases in prevalence with advancing age.27 It occurs with a prevalence of 0.1% in the United States, making it one of the most frequent neurologic entities causing voiding dysfunction.28 Pathologically, the pigmented neurons in the substantia nigra and locus ceruleus in the brainstem degenerate. Systemic clinical features of tremor, bradykinesia, and muscular rigidity are probably due to focal dopamine deficiency in these areas, as well as the caudate nucleus, putamen, and globus pallidus.29 The typical urodynamic findings of patients with Parkinson’s disease include detrusor overactivity, sphincter bradykinesia, and impairment of relaxation of the striated muscle component of the urethral sphincter muscle.1,28
Clinical and urodynamic features Up to 75% of patients with Parkinson’s disease experience some degree of voiding dysfunction.30,31 Irritative symptoms of urinary frequency, urgency, and urge incontinence are reported by 57% of patients with Parkinson’s disease. Voiding disturbance may also be troublesome, with 23% of patients experiencing obstructive symptoms including hesitancy, incomplete emptying or urinary retention; 20% have mixed symptoms.29 However, voiding dysfunction associated with Parkinson’s disease in female patients is complex and not always congruent with symptoms.28
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Urodynamic evaluation reveals DO in up to 90% of patients, with sporadic electrical activity of the sphincter during uninhibited detrusor contractions in 61%.6 In a study of 17 women with Parkinson’s disease, stress urinary incontinence was identified in 50%.32 Impaired detrusor contractility is a much less frequent urodynamic finding in the patient with Parkinson’s.33 More recent attempts to correlate clinical disease states with urodynamic findings have revealed that increasing Parkinson’s disease stage results in worsening urge incontinence, DO, and decreasing bladder capacity.34 Holligar et al.34 studied 37 idiopathic parkinsonian patients with a mean age of 65 years. Symptoms were classified as mild, moderate or severe; mild symptoms were unilateral in nature, moderate involved exacerbated bilateral symptoms and deteriorating balance, and severe symptoms required the use of assistance with daily activities and/or ambulation. Table 36.2 summarizes the significant findings. As parkinsonian symptoms worsen, so do clinical and urodynamic parameters. This suggests that bladder function may worsen progressively with advancing disease. Neurologic evaluation is crucial to evaluate bladder function and to guide appropriate therapy. Urodynamics with simultaneous electromyography is the most sensitive available tool to investigate the nature of voiding dysfunction.28 The goals of proper management are to improve symptoms and protect the upper urinary tracts. Treatment of the patient with L-dopa can significantly improve symptoms; however, anticholinergic therapy can be added to suppress uninhibited detrusor contractions.
male predominance of 2 or 3:1.36 MSA results in the symmetrical degeneration of neurons and associated fibers of motor and extrapyramidal systems, including the cerebellum and brainstem.37 Disease progression usually results in death 7–20 years after the onset of neurologic symptoms.36 The difference in neuropathologic lesion location and number between patients explains the variance in urodynamic findings between Parkinson’s patients and those with MSA. Unlike Parkinson’s patients, MSA patients tend to have worse lower urinary tract dysfunction, characterized by poor bladder contractility and pelvic floor EMG findings, suggesting that almost 50% demonstrate peripheral denervation.28 The resulting incontinence is probably caused by DO and some element of paralysis of the external sphincter.38 Blaivas has demonstrated an open bladder neck during cystography, further indicative of peripheral sympathetic dysfunction.38 Thus, MSA affects sympathetic, parasympathetic, and the somatic nervous systems – compared to the relatively more defined idiopathic Parkinson’s disease – and thorough neurologic evaluation is invaluable in separating and characterizing these different disease entities.28 The combination of detrusor dysfunction and sphincter denervation does not support the surgical management of symptoms; currently recommended treatment is therefore that of a combination of intermittent catheterization and medical therapy, including anticholinergics and desmopressin.35,39
Shy–Drager syndrome (multiple system atrophy)
The majority of patients with intracranial neoplasms often maintain control over urinary tract function.1 Similar to cerebrovascular accidents, alterations in lower urinary tract function will tend to relate directly to the area of the brain affected, rather than the type of neoplasm. For example, compression by tumor or degeneration of neural arcs above the pontine level – such as the superior aspects of the frontal lobe40 and frontoparietal areas41 that inhibit detrusor activity – would induce DO with synergetic sphincter function.21,42
Shy and Drager described a neurologic syndrome of autonomic nervous system dysfunction characterized by orthostatic hypotension, anhydrosis, erectile dysfunction, extrapyramidal symptoms, and poor urinary and fecal control.35 Shy–Drager syndrome is also known as multiple system atrophy (MSA), and it is considered one of the ‘Parkinson Plus’ syndromes of movement disorders.28 The mean age of onset is 55 years, with a Table 36.2.
Brain neoplasms
Clinical and urodynamic features of Parkinson’s patients by severity of symptoms
Parkinson’s severity
Urge
Urge incontinence
Detrusor overactivity
Bladder capacity (ml)
Mild
5/14
0
6/14
380
Moderate
14/14
2
10/14
290
Severe
9/9
4
9/9
260
Data from ref. 34.
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Dementia Dementia is the loss of thought and reason that results from deterioration and atrophy of both gray and white matter in the brain, particularly of the frontal lobes.1 Although usually associated with conditions such as head injury, hydrocephalus, encephalitis, syphilis, Alzheimer’s, Pick’s and Creutzfeldt–Jakob diseases, the etiology of neuronal degeneration associated with dementia is poorly understood.29 The most common urinary symptom is incontinence, with a reported prevalence as high as 90%.43 However, the cause of incontinence remains unclear; it is not known whether detrusor dysfunction or, more likely, a defect in cognitive function (functional incontinence) is responsible for the lack of social continence in patients with dementia. In one report, 71% of elderly patients with cognitive impairment showed DO; however, 65% of those with no impairment demonstrated detrusor overactivity by the same criteria. Therefore, the incontinence associated with dementia is not likely due to detrusor overactivity.44
Multiple sclerosis Multiple sclerosis (MS) is the most common disabling neurologic disorder affecting people between 20 and 50 years of age.45 It is characterized by focal inflammatory and demyelinating lesions of the nervous system, affecting mainly those living in the temperate climates. Prevalence is estimated at 1/1000 in Americans, 2/1000 Northern Europeans, and 20 to 40/1000 in first-degree relatives of patients with MS.45–47 In approximately 60% of patients, the disease is initially manifested by exacerbations and remissions. The clinical course of MS can be acute, progressive, chronic and/ or benign.48 Neurologic dysfunction is caused by demyelinating plaques of the white matter of the brain and spinal cord, especially the posterior and lateral columns of the cervical cord, which serve as pathways for neurologic control over vesical and urethral function.49 These plaques are caused by an autoimmune response and attach to the central nervous system myelin, leading to a loss of salutatory conduction and conduction velocity in axonal pathways.45
Clinical and urodynamic features Voiding dysfunction is experienced by 90% of patients with MS.50 These include not only frequency, urgency and urge incontinence, but also urinary hesitancy, intermittency, and poor urinary stream. The nature of void-
ing dysfunction is most dependent on the location of the plaque formation, such as intracranial, suprasacral or sacral cord plaques. Urodynamically, the most frequent pattern seen is DO, which is observed in 50–99% of patients.45,50–52 DSD is also documented in up to 50% of patients with DO.12,53,54 Of patients with symptoms suggestive of obstruction, 73% had DA.55 DA is seen in 20–30% of patients, most of whom usually strain to void.56 Hypocontractility may be related to cerebellar plaque involvement, lack of cortical facilitatory input, or sacral cord involvement. Some evidence suggests that DA is a temporary condition that may progress to DO in 57–100%.55 Although these patients may be managed effectively with an intermittent catheterization program, periodic urodynamic re-evaluation is essential to ensure protection of the upper urinary tract.57 Given the waxing and waning nature of MS, re-evaluation is especially important because the neurourologic status of the patient with MS may change over time. Having said that, DSD revealed on urodynamic evaluation rarely remits.55 Optimal management of lower urinary tract dysfunction is based on the avoidance of indwelling catheters and minimizing intravesical storage pressure while assuring low pressure urinary drainage.57 Urinary storage pressure is minimized with anticholinergic medications, or augmentation cystoplasty if medical therapy is ineffective.58 Unfortunately, sphincterotomy is not an option for women, and many women with neuropathic bladder dysfunction are treated in the community with indwelling urethral or suprapubic catheters.1 However, early experience using botulinum toxin injections into the sphincter for the treatment of DSD is limited but growing, and may eventually prove to be a therapeutic option.59,60
CONDITIONS OF THE SPINAL CORD AFFECTING THE URINARY TRACT The degree of voiding dysfunction associated with spinal cord conditions is related to the process of the condition itself, the area of the spinal cord affected, the severity of neurologic impairment, and coexisting pelvic floor pathology. Neurologic injury, which can involve parasympathetic, sympathetic, and somatic nerve fibers, can result in a complex array of signs and symptoms. Urodynamic investigation of those with neurologic impairment is essential as it provides objective information regarding the nature and extent of the effect on lower urinary tract function. Such information is invaluable in adequate patient management.
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Spinal cord injury Neurogenic lower urinary tract dysfunction resulting from spinal cord injury (SCI) is an excellent model for understanding neurourologic dysfunction. The principles of urologic evaluation and management of traumatic SCI patients are applicable to those with other spinal cord pathology.16 The estimated annual incidence of SCI reaches 40 new injuries per million population in the United States, or approximately 11,000 new cases per year – with a prevalence of approximately 247,000 persons.61 With 85% of injuries occurring at or above the T12 level,62 the reported neurologic level and the extent of the lesion of SCI at hospital discharge reveal 34.3% of patients with incomplete quadriplegia and 25.1% with complete paraplegia; 22.1% of patients develop complete quadriplegia and 17.5% incomplete paraplegia.61 Historically, the most common cause of death in SCI patients had been secondary renal failure; however, improved medical assessment and management has led to dramatic shifts in the causes of death.1 Nonetheless, lower urinary tract dysfunction following SCI is frequent and may result in infection, urolithiasis, upper tract failure, and lower urinary tract symptoms.
Clinical and urodynamic features Characteristics of voiding dysfunction after SCI are dependent on the stage of recovery, i.e. spinal shock, recovery, and stable phases.1 Immediately following spinal cord trauma, spinal shock occurs. This phase characteristically presents with flaccid paralysis and absence of reflex activity below the level of the lesion. Voiding symptoms typically include urinary retention due to DA that may last for months. The DA usually resolves weeks to a few months following the SCI with resumption of reflex detrusor activity. While in acute retention, patients should be managed with a regime of intermittent catheterization. The recovery phase is marked by the return of reflex detrusor activity. The neurologic level of the SCI corresponds to the resulting type of lower urinary tract dysfunction (Figs 36.1, 36.2). With cervical or thoracic spinal cord lesions, the most common outcome will be DO with DSD. Sacral spinal cord injuries are commonly associated with DA, although this may also be seen with higher level lesions. Injuries of the lumbar spine are more difficult to predict, with lower urinary tract dysfunction ranging from DO with DSD, or DO with sphincter deficiency, to DA. The final phase following SCI is labeled the stable phase and by definition is the period characterized by the absence of additional neurologic recovery or change
in urodynamic pattern.1 During this phase it is critical to continue periodic evaluation of lower urinary tract function and surveillance of the upper urinary tract to avoid secondary insult to the upper urinary tracts. The level of spinal lesion and its relationship to lower urinary tract dysfunction has been documented and evaluated in 489 consecutive patients presenting with SCI.63 In 104 patients with cervical SCI, 15% (16 patients) had DA. In the remaining 85% (88 patients), involuntary detrusor contractions (IDC) were documented, with 65% (57 of 88) exhibiting concurrent DSD. All 87 thoracic SCI patients were found to have DO, and 90% of them exhibited concurrent DSD. Lumbar SCI was found to have the least predictable urodynamic patterns, with 40% having DA, 30% with DO, and 30% with DO with DSD. In the sacral SCI cohort, 12% of patients had normal urodynamic studies, while 64% of patients had DA.
Pontine micturition center
Pons T11–L2 sympathetic efferent (via hypogastric nerve) S2–S4 parasympathetic efferent (via pelvic nerve) Sympathetic chain ganglion S3–S4 somatic efferent (via pudendal nerve)
Hypogastric nerve
T11–L2 S2–S4
Pelvic nerve
Pudendal nerve Sacral micturition center
Figure 36.1. Innervation of the lower urinary tract. The control of micturition and continence arise at three levels: suprapontine (thin line box), spinal (thick line box) and peripheral/infrasacral (dashed box). Each level contains distinct nerve fibers with complex interplay between all levels. 571
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Pontine micturition center
Suprapontine (intracranial) lesions • detrusor overactivity with coordinated sphincter
Cervical/thoracic (spinal) lesions • Detruser overactivity with uncoordinated sphincter
Sacral micturition center
Suprasacral-lumbosacral (spinal) lesions • Detrusor overactivity with or without coordinated sphincter Infrasacral (peripheral; lower motor neuron) lesions • Detrusor areflexia with or without denervated sphincter
Figure 36.2. Urodynamic outcome following complete denervating injury. Outcomes are dependent on level and extent of injury. Incomplete or partial lesions may lead to variation in urodynamic findings.
Brown–Sequard syndrome Hemitransection of the spinal cord results in this rare, but well-documented condition with pathognomonic findings for a spinal cord injury.64,65 The classic presentation of this syndrome – provided that it results from a single spinal lesion – is ipsilateral hemiparesis (pyramidal tract) of the leg with contralateral loss of superficial sensation (spinothalamic tract) and ipsilateral loss of deep sensation (dorsal tract). The variable presentation that results in either motor or sensory symptoms depends upon the plane of the lesion.
Clinical and urodynamic features Voiding symptoms are variable among these patients. Those presenting with more severe motor deficits (i.e. intramedullary diseases) are more likely to have symptoms ranging from urinary retention to filling phase symptoms such as frequency and urge incontinence.66 However, there is no relationship between voiding symptoms and the laterality of the lesion or concurrent sensory disturbances.66–68 There is also a paucity of publications reporting urodynamic studies in these patients
with findings that are concordant with voiding symptom severity. The most frequent urodynamic findings in symptomatic patients tend to be detrusor overactivity and areflexia.66,69 Although the relationship between the spinal lesion and resulting voiding symptoms is variable, thorough neurologic examination paired with urodynamic evaluation are key in managing symptoms and protecting the upper tracts of each patient.
Autonomic dysreflexia Autonomic dysreflexia (AD) is a well-defined syndrome of acute excessive sympathetic output which occurs in patients with spinal cord injuries, most commonly above the T6 level. This condition is associated with an uncontrolled spinal reflex mechanism from afferent visceral (or other noxious) stimulus below the level of the lesion, resulting in, if not managed appropriately, a life-threatening hypertension. The most common cause is stimulation of the lower urinary tract, with 75–85% of cases precipitated by bladder distension.70 Other triggers including infection, urethral distension, instrumentation, stones, and testicular torsion. At presentation, the symptoms associated with AD generally include a bilateral pounding headache, with diaphoresis above the level of the spinal lesion, nasal congestion, malaise, nausea, and visual blurring. The signs observed commonly are flushed sweaty skin above the level of the lesion with cool, pale skin below that level. The main finding is elevation of the blood pressure with reflex bradycardia – which in a post-SCI patient may mean that readings of 120/80 mmHg are elevated, as base pressures in these patients are often in the 90/60 mmHg range.1 The labile hypertension associated with the AD response can result in intracranial hemorrhage and death.71 Early recognition of the syndrome is critical, with initiation of management immediately.72
Intervertebral disk disease Voiding dysfunction is a well-established complication of lumbar intervertebral disk herniation, resulting from displacement of any intervertebral disks into the spinal canal. Herniated disks occur in a variety of disease processes including degenerative disease and trauma. The symptoms resulting from the displacement will be dependent on the level of the lesion, the extent of the displacement, and the type of neural injury, which may involve parasympathetic, sympathetic and/or somatic nerve fibers (Table 36.3). The combination of these factors will result in a complex combination of signs and symptoms.
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Table 36.3.
Innervation of the lower urinary tract Spinal cord level
Function
Nociceptors
S2–S4
Initiation of micturition
Sensory
S2–S3
Perineal sensation
Sympathetic (hypogastric nerve)
T11–L2
Sphincter contraction, bladder relaxation
Parasympathetic (pelvic nerve)
S2–S4
Bladder contraction
Somatic (pudendal nerve)
S3–S4
External sphincter contraction
Afferent
Efferent (autonomic)
Nerve conduction will be compromised in cases of acute compression. At the level of the sacrum this can result in DA from impaired autonomic outflow to the detrusor. If there is additional interference of somatic outflow at the pudendal nerve, concomitant intrinsic sphincteric deficiency may occur.73 The most frequent site of lumbar disk herniation is the L4–L5 and L5–S1 intervertebral spaces, which can result in cauda equina syndrome.74,75 The characteristic symptoms and signs in this syndrome include lower back pain, obstructive voiding symptoms with or without incontinence, sensory loss at the perineum, sensory loss of the lateral foot (S1–S2 dermatome), and absence of the bulbocavernosus reflex.76 Disruption from gradual degenerative disk displacement may result in hyperexcitability of sensory and motor fibers, with symptoms including irritative urinary frequency and urgency with DO.77 Urodynamic testing should be an integral part of the evaluation of all patients with incomplete lumbosacral spinal injuries.1
Ankylosing spondylitis A rare inflammatory disease of the spine, ankylosing spondylitis results in fusion of the joints and ligamentous calcification. This disease predominantly affects men, with deleterious effects on neurologic function generally occurring following spinal cord compression, caused by either atlantoaxial subluxation or trauma to the rigid spine.78–80 The most common neurogenic lower urinary tract dysfunction caused by ankylosing spondylitis results in a cauda equina syndrome with impaired detrusor contractility.78 More severe cases may result in DA, and sphincteric activity may also be compromised as neuropathy progresses. Surgical decompression following neurologic impairment has met with varying success.81
Guillain–Barré syndrome Guillain–Barré syndrome is an inflammatory demyelinating polyneuropathy, usually arising following an infectious episode that primarily affects the peripheral nervous system, with some effect on the nerve roots.82–84 Although recovery is a hallmark of Guillain–Barré syndrome, 85% of patients sustain persistent neurologic deficits.85 In severe cases, progression continues to affect central nervous, respiratory and autonomic function, often including urinary retention.86 Lower urinary tract dysfunction is present in 6–40% of patients diagnosed with Guillain–Barré syndrome.87 Symptoms include detrusor and sphincter motor and sensory deficits consistent with variation in the combination of nerves affected during the course of Guillain–Barré syndrome.88,89 Urodynamic studies on Guillain–Barré patients have revealed DA, impaired bladder sensation, and occasionally DO; it is not known whether these findings are accounted for by either central nervous system involvement or the timing of the urodynamic study.89,90
Tabes dorsalis Tabes dorsalis (locomotor ataxia) is an uncommon form of neurosyphilis affecting less than 5% of the population worldwide. This condition results in a demyelination of the dorsal columns in the spinal cord.91–93 Progression of sacral root and dorsal column degeneration results in advancing stages of disease, and ultimately is manifested urologically with the development of urinary retention.94 Classic descriptions of the effects of tabes dorsalis on voiding discuss the prevalence of DA; however, more recent studies suggest that DO may occur.92 It is postulated that involvement of the conus medullaris or cauda equina predisposes to a poorly compliant areflexic blad573
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der, and that suprasacral lesions are responsible for the DO in these cases.95 These patients can be managed effectively with treatment of the primary infection with antibiotics and an intermittent catheterization program.96
Acquired immune deficiency syndrome Voiding dysfunction in patients with acquired immune deficiency syndrome (AIDS) of variable etiologies have been documented in recent studies.97–99 The most common cause of lower urinary tract dysfunction is simple cystitis, which is more likely to result from opportunistic organisms than in non-AIDS patients. This is because of the multiplicity of medical co-morbidities and the susceptibility of these patients to opportunistic infections. As a result, complete urologic assessment is critical in the evaluation of any complaints suggesting voiding dysfunction, especially as up to 40% of patients with AIDS have associated neurologic dysfunction.100,101 Neurologic pathologies in AIDS patients which can lead to voiding dysfunctions include toxoplasmosis (reported in 14% of AIDS patients with neurologic disease101), neoplasms of the central nervous system, lymphoma, systemic lymphoma with central nervous system involvement, and Kaposi’s sarcoma.102–104
Urodynamic evaluation Findings following urodynamic evaluation in patients with AIDS are variable and may include DA, DO, DO with DSD, or non-neurologic bladder outlet obstruction.101,105 In the study by Hermieu et al., the onset of lower urinary tract disturbance represented a poor prognostic indicator, as 44% of these patients died within 24 months of evaluation.105
Tropical spastic paraparesis Tropical spastic paraparesis is a condition of progressive paraparesis and back pain, most likely induced by infection with the retrovirus human T-cell lymphotrophic virus type 1.106 This clinical entity is caused by meningomyelitis with demyelinization and axonal loss, which can involve the corticospinal tracts.107 There is significant voiding dysfunction associated with this syndrome, with urinary hesitancy, urgency, and incontinence found in up to 60% of patients.106
Urodynamic evaluation Studies of affected patients have revealed a predominance of DO, often with impaired contractility at voiding, and less frequently DA.108,109 Despite variable
presentations, the lower urinary tract dysfunction can precipitate upper tract deterioration; therefore, urodynamic evaluation is recommended in all patients with acquired immune deficiency syndromes with voiding symptoms.100
Transverse myelitis Transverse myelitis is a rare inflammatory condition of the spinal cord which may affect children or adults in an acute or progressive fashion.110,111 The entire thickness of the cord is involved, including both the gray and white matter, with the diagnosis made following elimination of spinal cord compression and the absence of other neurologic disease.112 Affected individuals may suffer from residual neurologic deficits, most commonly urologic, although complete recovery may occur within 3–18 months.111,113
Urodynamic evaluation Lower urinary tract dysfunction in these patients usually presents as either urinary retention or incontinence. A recent study showed the outcomes with predominant DO, DO with DSD, and less frequently DA.114 These urodynamic findings often persisted despite complete neurologic recovery.
Lyme disease Lyme borreliosis is caused by the spirochete Borrelia burgdorferi, which has demonstrated the ability to invade numerous body tissues, including the central and peripheral nervous systems and the bladder.1 Although initially associated with urinary retention, symptoms of urinary urgency, urge incontinence, and nocturia may occur at any time during the disease process.115 Patients with Lyme disease may present with DA or DO.116 Although the disease may respond to a 2-week course of antimicrobial therapy,117 those with relapsing and remitting symptoms may require long-term administration of antimicrobials.118
Herpes zoster Reactivation of persistent varicella virus from a dorsal root ganglion will result in episodes of Herpes zoster.119 During such episodes, symptoms primarily include sensory disturbances such as pain and paresthesia, although paralytic complications do rarely occur.120 Infrequently, the virus reactivation includes the autonomic nerves of the bladder, with resultant irrita-
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tive voiding symptoms such as dysuria and frequency. In cases involving the afferent neurons of the sacral micturition reflex arc, somatic and visceral motor neuropathy can occur, and urinary retention may ensue.121,122 The course of the viral infection is usually self-limiting, with spontaneous recovery usually within several months.1,123
Poliomyelitis Following a World Health Organization resolution in 1988, great strides have been made in the eradication of poliomyelitis worldwide, with only 11 countries currently affected with endemic polio.124 Poliomyelitis results in destruction of the gray matter of the anterior horn cells and selective destruction of largediameter fast-conducting motor neurons.125 Polio is essentially a pure motor neuropathy, and sensory function is usually normal.126 Urinary retention may occur in up to 40% of patients, depending on disease severity. Patients with post-polio syndrome may manifest an increased incidence of irritative lower urinary tract symptoms, although studies on this issue are incomplete.1 Urodynamic evaluation reveals DA when testing affected individuals, with bladder sensation and anal sphincter function remaining intact.127
Tethered cord syndrome and short filum terminale The tethered cord syndrome results from impediment of the cephalad migration of the conus medullaris, and may result from a short filum terminale, intraspinal lipoma or fibrous adhesions resulting from the surgical repair of spinal dysraphism.128,129 The syndrome is classically diagnosed in children, especially during adolescence, but rarely the process may occur in adulthood.130,131 Lower urinary tract dysfunction is common in this syndrome and, in otherwise asymptomatic children, urodynamic abnormalities may be the basis for surgical intervention.132
Urodynamic evaluation Detrusor areflexia has been reported in 60% of patients, although recovery of lower tract function approached 60% with surgical release of the cord.130 Similarly, DO has also been reported.133 In another series, 22% of patients with tethered cords had DO; all improved following spinal surgery.134 Early and aggressive neurosurgical correction is therefore indicated.135
CONDITIONS OF THE PERIPHERAL NERVOUS SYSTEM AFFECTING THE URINARY TRACT Pelvic plexus injury The major sympathetic and parasympathetic innervation of the lower urinary tract follows the branching array of the pelvic plexus. These nerve fibers can be disrupted during complicated pelvic surgical procedures, or following pelvic fracture, with resultant lower urinary tract dysfunction. If the primary injury affects the parasympathetic nerve fibers, generally there is impaired detrusor contractility, although DA may occur in severe instances.1 Similarly, in cases involving predominately sympathetic innervation, the resultant symptoms usually include intrinsic sphincter deficiency with stress urinary incontinence. Study of patients with voiding dysfunction following major pelvic surgery has shown resolution of symptoms in 6 months for up to 80% of affected patients.136
Abdominoperineal resection Abdominoperineal resection (APR) for rectal cancer almost invariably results in the disruption of the pelvic plexus, with both cadaveric and operative dissection of the plexus pathway demonstrating its susceptible nature during rectal resection.137,138 As a result, this has been associated with significant lower urinary tract dysfunction as an operative complication.139 The reported rate of urinary retention following APR ranges from 25 to 90%, with urinary tract infection frequently being associated.140,141 The courses of the pelvic nerves are as follows: 1. from the inferior hypogastric plexus, it has multiple branches forming a web-like complex within the endopelvic fascial sleeve, some of which innervate the bladder detrusor; 2. a main branch traveling inferolateral to the rectum remains deep to the fascia of the levator ani muscle and courses to the external urinary sphincter; 3. at the level of the bladder neck in females, this pelvic nerve branch sends direct branches to the urinary sphincter.138 Prior studies reveal evidence of sympathetic denervation in 100%, parasympathetic denervation in 38%, and pudendal denervation in 54% of patients postoperatively.1 The postoperative voiding dysfunction is usually transitory, although sphincteric insufficiency may be 575
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permanent.142 Post-APR urinary retention is best managed by clean intermittent self-catheterization.
Radical hysterectomy A similar effect on the lower urinary tract is seen from radical hysterectomy as in APR due to the similar dissection necessitated during the operation and bilateral pelvic lymphadenectomy. However, the location of the plexus inferolateral to the rectum reduces the disruption of the parasympathetic nerve fibers during hysterectomy, and the extent of pericervical dissection (e.g. ‘nerve-sparing’ approach) does not appear to affect the postoperative urinary symptom complex.143 Persistent postoperative lower urinary tract dysfunction is best managed with a combination of anticholinergic therapy to decrease intravesical storage pressure and catheterization for retention, with most oncologists leaving the patients catheterized for a minimum of 1 week postoperatively. Effective control of intravesical pressure with the anticholinergic therapy can stabilize and even reverse upper tract dilation with detrusor overactivity.144
Diabetic cystopathy Diabetes mellitus is the most prevalent medical condition resulting in sensory neurogenic lower urinary tract dysfunction affecting 2% of the US population.1,145,146 Voiding symptoms generally develop at least 10 years after the onset of the disease, as a result of one of three types of neuropathy: peripheral neuropathy, mononeuritis multiplex, and autonomic neuropathy.38,147 Metabolic abnormalities of Schwann cell function result in segmental demyelinization and subsequent axonal degeneration, impairing nerve conduction.148,149
Clinical and urodynamic features Diabetes contributes significantly to voiding dysfunction in women.150 Gradual development of impaired bladder sensation is the first sign, usually associated with other sensory impairment consistent with peripheral neuropathy. Subsequently, symptoms associated with traditional ‘diabetic cystopathy’ may include urinary hesitancy, slowing of the urine stream, and decreasing urinary frequency.150,151 These symptoms may progress to include a sensation of incomplete emptying or even urinary dribbling from overflow incontinence.150,152 When questioned, up to 50% of unselected diabetes mellitus patients have subjective evidence of traditional
diabetic cystopathy. The urodynamic evaluation, however, suggests alterations in lower urinary tract function in only 27–85% of these patients.152,153 Urodynamic studies frequently reveal impaired bladder sensation, increased cystometric bladder capacity, decreased detrusor contractility, an impaired urine flow, and an elevated post-void residual urine volume.38 However, more recent studies suggest that the ‘traditional diabetic cystopathy’ may not be the most common observed voiding dysfunction in patients with diabetes. Kaplan and Te reported on another group of patients with diabetes referred because of voiding symptoms. Of this group, 55% were found to have involuntary bladder contractions, 23% impaired detrusor contractility, 10% detrusor areflexia, and 11% ‘indeterminate findings’. In the 42 patients in this group with sacral cord neurologic signs, 50% had impaired detrusor contractility and 24% had detrusor areflexia.154 In addition, poor diabetic control will contribute to urgency and frequency as a result of decreased warning time from impaired sensation and polyuria from the elevated glucose. Upper tract changes depend upon the duration and severity of the disease process, as well as the effect on intravesical pressure. The effect of diabetes-induced lower urinary tract dysfunction on the upper urinary tract is difficult to determine because of the other effects of diabetes on renal function.1 When managing patients with diabetic cystopathy, preservation of renal function is paramount. A direct effect of diabetes on renal microvasculature, combined with upper tract obstructive changes resulting from diabetic cystopathy, put the diabetic kidneys at great risk. A timed voiding schedule is effective in those with impaired contractility, while intermittent catheterization is reserved for those who experience greater difficulty with emptying. Anticholinergic therapy may be effective for those with DO or impaired bladder compliance.146
CONCLUSIONS While neurologic conditions are frequently associated with lower urinary tract dysfunction, neurologic etiologies are relatively rarely seen to the average clinician looking after lower urinary tract symptoms. A high index of suspicion should be maintained where the severity of symptoms is disproportionately high or in rapid onset of symptoms. A brief neurologic examination at the time of presentation of new patients or during urodynamics should be considered as a standard for good practice.
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The terminology utilized in this chapter is based on existing neurourology terms that may not conform to the latest ICS terminology. Autonomic Dysreflexia, also know as Hyperreflexia, is a condition where the blood pressure in a person with a spinal cord injury (SCI) above T5-6 becomes excessively high due to the over activity of the Autonomic Nervous System.
REFERENCES 1. Jung SY, Chancellor MB. Neurological disorders. In: Cardozo L, Staskin D (eds) Textbook of Female Urology and Urogynaecology. London: Martin Dunitz, 2001. 2. Wein AJ. Neuromuscular dysfunction of the lower urinary tract and its management. In: Walsh PC, Retik AB, Stamey TA, Vaughan ED (eds) Campbell’s Urology. Philadelphia: Saunders, 2003. 3. Weiss DJ, Fried GW, Chancellor MB et al. Spinal cord injury and bladder recovery. Arch Phys Med Rehabil 1996;77:1133–5. 4. Shenot PJ, Rivas DA, Watanabe T et al. Early predictors of bladder recovery and urodynamics after spinal cord injury. Neurourol Urodyn 1998;17:25–9. 5. Watanabe T, Vaccaro AR, Kumon H et al. High incidence of occult neurogenic bladder dysfunction in neurologically intact patients with thoracolumbar spinal injuries. J Urol 1998;159:965–8. 6. Berger Y, Blaivas JG, DeLaRocha ER, Salinas J. Urodynamic findings in Parkinson’s disease. J Urol 1987;138:836–8. 7. de Groat WC, Kawatani M. Neural control of the urinary bladder: possible relationship between peptidergic inhibitory mechanisms and detrusor instability. Neurourol Urodyn 1985;4:285–300. 8. Blaivas JG. The neurophysiology of micturition: a clinical study of 550 patients. J Urol 1982;127:958–63.
15. Lloyd K. New trends in urologic management of spinal cord injured patients. Central Nervous System Trauma 1986;3:3–11. 16. Chancellor MB, Rivas DA, Ackman D. Multicenter trials of Urolume™ endourethral Wallstent® prosthesis for the urinary sphincter in spinal cord injured men. J Urol 1994;152:924–30. 17. Phelan MW, Franks M, Somogyi GT et al. Botulinum toxin urethral sphincter injection to restore bladder emptying in men and women with voiding dysfunction. J Urol 2001;165(4):1107–10. 18. Tosi L, Righetti C, Terrini G, Zanette G. Atypical syndromes caudal to the injury site in patients following spinal cord injury. A clinical, neurophysiological and MRI study. Paraplegia 1993;31:751–6. 19. Staskin D, Nehra A, Siroky M. Hydroureteronephrosis after spinal cord injury: effects of lower urinary tract dysfunction on upper tract anatomy. Urol Clin North Am 1991;18:309–16. 20. Marinkovic SP, Badlani G. Voiding and sexual function after cerebrovascular accidents. J Urol 2001;165:359–70. 21. Tsuchida S, Noto H, Yamaguchi O, Itoh M. Urodynamic studies on hemiplegic patients after cerebrovascular accident. Urology 1983;21:315–8. 22. Redding MJ, Winter SW, Hochrein SA. Urinary incontinence after unilateral hemispheric stroke: a neurologic epidemiologic perspective. J Neurorehabil 1987;1:25–31. 23. Blaivas JG, Chancellor MB. Cerebrovascular accidents and other intracranial lesions. Practical Neurourology – Genitourinary Complications in Neurologic Disease. Boston: Butterworth-Heinemann, 1995; 119–25. 24. Borrie MJ, Campbell AJ, Caradoc-Davies TH, Spears GFS. Urinary incontinence after stroke: a prospective study. Age Aging 1986;15:177–81.
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10. Anderson RU. Urodynamic patterns after acute spinal cord injury: association with bladder trabeculation in male patients. J Urol 1983;129:777–9.
26. Siroky MB, Krane RJ. Neurologic aspects of detrusor– sphincter dyssynergia, with reference to the guarding reflex. J Urol 1982;127:953–7.
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27. Yahr MD. Parkinson’s disease – overview of its current status. Mt Sinai J Med 1977;44:183–91.
12. Goldstein I, Siroky MB, Sax DS, Krane RJ. Neurourologic abnormalities in multiple sclerosis. J Urol 1982;128:541–5. 13. Blaivas JG, Barbalias GA. Detrusor–external sphincter dyssynergia in men with multiple sclerosis: an ominous urologic condition. J Urol 1984;131:91–4. 14. Borges P, Hackler RH. The urologic status of the Vietnam War paraplegic: a 15-year prospective follow-up. J Urol 1982;127:710–11.
28. Dmochowski RR. Female voiding dysfunction and movement disorders. Int Urogynecol J 1999;10:144–51. 29. Staskin DR. Intracranial lesions that affect lower urinary tact function. In: Krane RJ, Siroky MB (eds) Clinical Neuro-urology, 2nd ed. Boston: Little, Brown, 1991; 345–51. 30. Antel JP, Arnason BW. Demyelinating diseases. In: Wilson JD, Braunwald EB, Isselbacher KJ (eds) Harrison’s Principles of Internal Medicine. New York: McGraw-Hill, 1991; 2038–65.
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50. McGuire EJ, Savastano JA. Urodynamic findings and long-term outcome management of patients with multiple sclerosis-induced lower urinary tract dysfunction. J Urol 1984;132:713–5.
33. Blaivas JG, Chancellor MB. Parkinson’s disease. Practical Neurourology – Genitourinary Complications in Neurologic Disease. Boston: Butterworth-Heinemann, 1995; 139–47. 34. Holligar S, Wenning GK, Kiss G, Ulmer H, Madersbacher H, Poewe W. The natural history of voiding dysfunction in patients with idiopathic Parkinson’s disease. J Urol 1997;157:1378. 35. Wulfsohn MA, Rubenstein A. The management of Shy–Drager syndrome with propantheline and intermittent self-catheterization: a case report. J Urol 1981;126:122–3. 36. Abyad A. Shy–Drager syndrome: recognition and management. J Am Board Fam Pract 1995;8:325–30. 37. Lockhart JL, Webster GD, Sheremata W et al. Neurogenic bladder dysfunction in the Shy–Drager syndrome. J Urol 1981;126:119–21. 38. Blaivas JG. Neurologic dysfunctions. In: Yalla SV, McGuire EJ, El-Badawi A, Blaivas JG (eds) Neurourology and Urodynamics: Principles and Practice. New York: Macmillan, 1988; 343–57. 39. Beck RO, Betts CD, Fowler CJ. Genitourinary dysfunction in multiple system atrophy: clinical features and treatment in 62 cases. J Urol 1994;151:1336–41. 40. Hald T, Bradley WE. The Urinary Bladder: Neurology and Dynamics. Baltimore: Williams and Wilkins, 1982; 48–50, 157–9. 41. Kahn Z, Hertanu J, Yang WC et al. Predictive correlation of urodynamic dysfunction and brain injury after cerebrovascular accident. J Urol 1981;126:86–8. 42. Yalla SV, Fam BA. Spinal cord injury. In: Krane RJ, Siroky MB (eds) Clinical Neuro-urology, 2nd ed. Boston: Little, Brown, 1991; 319–22. 43. Skelly J, Flint AJ. Urinary incontinence associated with dementia. J Am Geriatr Soc 1995;43:286–94. 44. Resnick NM, Yalla SV, Laurino E. The pathophysiology of urinary incontinence among institutionalized elderly persons. N Engl J Med 1989;320:1421–2. 45. Litwiller SE, Frohman EM, Zimmern PE. Multiple sclerosis and the urologist. J Urol 1999;161:743–57. 46. Ebers GC, Sandivick AD, Risch NJ, and the Canadian Collaborative Study Group. A genetic basis for familial aggregation in multiple sclerosis. Nature 1995;377:150–5.
51. Blaivas JG, Bhimani G, Labib KB. Vesicourethral dysfunction in multiple sclerosis. J Urol 1979;122:342–7. 52. Awad SA, Gajewski JB, Sogbein SK et al. Relationship between neurological and urological status in patients with multiple sclerosis. J Urol 1984;132:499–502. 53. Weinstein MS, Cardenas DD, O’Shaughnessy EJ, Catanzaro ML. Carbon dioxide cystometry and postural changes in patients with multiple sclerosis. Arch Phys Med Rehabil 1988;69:923–7. 54. Sirls LT, Zimmern PE, Leach GE. Role of limited evaluation and aggressive medical management in multiple sclerosis: a review of 113 patients. J Urol 1994;151:946–50. 55. Blaivas JG, Bhimani G, Labib KB. Vesicourethral dysfunction in multiple sclerosis. J Urol 1982;127:342–8. 56. Gonor SE, Carroll DJ, Metcalfe JB. Vesical dysfunction in multiple sclerosis. Urology 1985;25:429–31. 57. Chancellor MB, Blaivas JG. Multiple sclerosis. Practical Neurourology – Genitourinary Complications in Neurologic Disease. Boston: Butterworth-Heinemann, 1995; 127–37. 58. Fowler CJ, van Kerrebroeck PEV, Nordenbo A, van Poppel H. Treatment of lower urinary tract dysfunction in patients with multiple sclerosis. J Neurol Neurosurg Psychiatry 1992;55:986–9. 59. Dykstra DD, Sidi AA. Treatment of detrusor–sphincter dyssynergia with botulinum A toxin: a double-blind study. Arch Phys Med Rehabil 1990;71:24–6. 60. Smith CP, Chancellor MB. Emerging role of botulinum toxin in the management of voiding dysfunction. J Urol 2004;171:2128–37. 61. National Spinal Cord Injury Statistical Center. Online. Available: www.spinalcord.uab.edu. 62. Watanabe T, Rivas DA, Chancellor MB. Urodynamics of spinal cord injury. Urol Clin North Am 1996;23:459–73. 63. Kaplan SA, Chancellor MB, Blaivas JG. Bladder and sphincter behavior in patients with spinal cord lesions. J Urol 1991;146:113–7.
47. Poser CM. The epidemiology of multiple sclerosis: a general overview. Ann Neurol 1994;36:S180–S193.
64. Brown-Sequard CE. De la transmission des impressions sensitives par la moelle epiniere. Comptes Rendures des Seances et Memoires de la Societe de Biologie 1849;1:192–4.
48. McFarlin DE, McFarland HF. Multiple sclerosis. N Engl J Med 1982;307:1183–8.
65. Brown-Sequard CE. Lectures on the physiology and pathology of the central nervous system and on the treat-
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ment of organic nervous affections; lecture 1, on spinal hemiplegia. Lancet 1868;2:593–6, 659–62, 755–7, 821–3. 66. Sakakibara R, Hattori T, Uchiyama T, Yamanishi T. Urinary dysfunction in Brown–Sequard syndrome. Neurourol Urodyn 2001;20(6):661–7. 67. Inatomi Y, Itoh Y, Fujii N, Nakanishi K. The spinal cord descending pathway for micturition: analysis in patients with spinal cord infarction. J Neurol Sci 1998;157:154–7. 68. Koehler PJ, Endtz LJ. The Brown–Sequard syndrome: true or false? Arch Neurol 1986;43:921–4. 69. Kaplan SA, Chancellor MB, Blaivas JG. Bladder and sphincter behavior in patients with spinal cord injury. J Urol 1991;146:113–7.
83. Asbury AK, Arnason BG, Adams RD. The inflammatory lesion in idiopathic polyneuritis: its role in pathogenesis. Medicine 1969;48:173–215. 84. Haymaker W, Kernohan JW. The Landry–Guillain–Barré syndrome: clinicopathologic report of fifty fatal cases and a critique of the literature. Medicine 1949;28:59–65. 85. Ng KKP, Howard RS, Fish DR et al. Management and outcome of severe Guillain–Barré syndrome. Q J Med 1995;88:243–50. 86. Ropper AH. The Guillain–Barré syndrome. N Engl J Med 1992;326:1130–6. 87. Truax B. Autonomic disturbance in the Guillain–Barré syndrome. Semin Neurol 1984;4:462–8.
70. Lindan R, Joiner E, Freehafer A, Hazel C. Incidence and clinical features of autonomic dysreflexia in patients with spinal cord injury. Paraplegia 1980;18:285–92.
88. Kogan BA, Solomon MH, Diokno AC. Urinary retention secondary to Landry–Guillain–Barré syndrome. J Urol 1981;126:643–4.
71. Rivas DA, Chancellor MB, Huang B, Salzman SK. Autonomic dysreflexia in a rat model of spinal cord injury and the effect of pharmacologic agents. Neurourol Urodyn 1995;14:141–52.
89. Sakakibara R, Hattori T, Kuwabara S et al. Micturitional disturbance in patients with Guillain–Barré syndrome. J Neurol Neurosurg Psychiatry 1997;63:649–53.
72. Blackmer J. Rehabilitation medicine: autonomic dysreflexia. CMAJ 2003;169(9):931–5. 73. Malloch JD. Acute retention due to intervertebral disc prolapse. Br J Urol 1965;37:578–85. 74. O’Flynn KJ, Murphy R, Thomas DG. Neurogenic bladder dysfunction in lumbar intervertebral disc prolapse. Br J Urol 1992;69:38–40.
90. Wheeler JS, Siroky MB, Pavlakis A, Krane RJ. The urodynamic aspects of the Guillain–Barré syndrome. J Urol 1984;131:917–9. 91. Wheeler JS Jr, Culkin DJ, O’Hara RJ, Canning JR. Bladder dysfunction and neurosyphilis. J Urol 1986;136:903–5. 92. Berger JR, Sabet A. Infectious myelopathies. Semin Neurol 2002;22:133–42.
75. Scott PJ. Bladder paralysis in cauda equina syndrome from disc prolapse. J Bone Joint Surg 1965;47:224–7.
93. Garber SJ, Christmas TJ, Rickards D. Voiding dysfunction due to neurosyphilis. Br J Urol 1990;66(1):19–21.
76. Goldman HB, Appell RA. Voiding dysfunction in women with lumbar disc prolapse. Int Urogynecol J 1999;10:134–8.
94. Harper JM, Politano VA, Schwarcz B. The FTA–ABS test in the diagnosis of the neurogenic bladder. J Urol 1967;97:862–3.
77. Jones DL, Moore T. The types of neuropathic bladder dysfunction associated with prolapsed lumbar intervertebral discs. Br J Urol 1973;45:39–43.
95. Hattori T, Yasuda K, Kita K, Hirayama K. Disorders of micturition in tabes dorsalis. Br J Urol 1990;65:497–9.
78. Russell ML, Gordon DA, Ogryzlo MA, McPhedran RS. The cauda equina syndrome of ankylosing spondylitis. Ann Int Med 1973;78:551–4. 79. Haddad FS, Sachdev JS, Bellapravalu M. Neuropathic bladder in ankylosing spondylitis with spinal diverticula. Urology 1990;35(4):313–6. 80. Garza-Mercado R. Traumatic extradural hematoma of the cervical spine. Neurosurgery 1989;24(3):410–4. 81. Tyrrell PNM, Davies AM, Evans N. Neurological disturbances in ankylosing spondylitis. Ann Rheumatic Dis 1994;53:714–7. 82. Guillain G, Barré JA, Strohl A. Sur un syndrome de radiculo-névrite avec hyperalbuminose du liquode céphalo-rachidien sans réaction cellulaire: remarques sur les caractéres cliniques et graphiques des réflexes tendineux. Bulletins et Mémoires de la Société Médicale des Hôpitaux de Paris 1916;40:1462–70.
96. Chancellor MB, Blaivas JG. Infectious neurologic diseases. Practical Neurourology – Genitourinary Complications in Neurologic Disease. Boston: Butterworth-Heinemann, 1995; 179–85. 97. Khan Z, Singh VK, Yang WE. Neurogenic bladder in AIDS. Urology 1992;40:289–91. 98. Hermieu JF, Delmas V, Boccon-Gibod L. Micturition disturbances and human immunodeficiency virus infection. J Urol 1996;156:157–9. 99. Kane CJ, Bolton DM, Connolly JA, Tanagho EA. Voiding dysfunction in human immunodeficiency virus infections. J Urol 1996;155(2):523–6. 100. Lange DJ, Britton CB, Younger DS, Hays AP. The neuromuscular manifestations of human immunodeficiency infections. Arch Neurol 1988;45:1084–8. 101. Levy RM, Bredesen DE, Rosenblum ML. Neurological manifestations of acquired immunodeficiency syndrome:
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experiences at UCSF and review of the literature. J Neurosurg 1985;62:475–95.
120. Thomas JE, Howard FM. Segmental zoster paresis – a disease profile. Neurology 1972;22:459–66.
102. Snider WD, Simpson DM, Aronyk KE. Primary lymphoma of the nervous system associated with acquired immunodeficiency syndrome [letter]. N Engl J Med 1983;308:45.
121. Izumi AK, Dewards J Jr. Herpes zoster and neurogenic bladder dysfunction. J Am Med Assoc 1973;224:1748–9.
103. Levy RM, Pons VG, Rosenblum ML. Intracerebral-mass lesions in the acquired immunodeficiency syndrome (AIDS) [letter]. N Engl J Med 1983;309:1454. 104. Levy RM, Pons VG, Rosenblum ML. Central nervous system mass lesions in the acquired immunodeficiency syndrome (AIDS). J Neurosurg 1984;61:9–16. 105. Hermieu JF, Delmas V, Boccon-Gibod L. Micturition disturbances and human immunodeficiency virus infection. J Urol 1996;156:157–9. 106. Cruickshank JK, Rudge P, Dalgleish AG. Tropical spastic paraparesis and human T-cell lymphotrophic virus type 1 in the United Kingdom. Brain 1989;112:1057–90. 107. Montgomery RD, Cruickshank JK, Robertson WB. Clinical and pathological observations on Jamaican neuropathy. A report of 206 cases. Brain 1964;87:425–40. 108. Eardley I, Fowler CJ, Nagendran K et al. The neurourology of tropical spastic paraparesis. Br J Urol 1991;68:598–603. 109. Yamashita H, Kumazawa J. Voiding dysfunction: patients with human T-lymphotropic-virus-type-1-associated myelopathy. Urol Int 1991;47(Suppl 1):69–71. 110. Dunne K, Hopkins IJ, Shield LK. Acute transverse myelopathy in childhood. Dev Med Child Neurol 1986;28:198–204. 111. Lipton HL, Teasdall RD. Acute transverse myelopathy in adults. Arch Neurol 1973;28:252–7. 112. Adams RD, Victor M. Principles of Neurology, 3rd ed. New York: McGraw–Hill, 1985; 673–702. 113. Ropper AH, Poskanzer DC. The prognosis of acute and subacute transverse myelopathy based on early signs and symptoms. Ann Neurol 1978;4:51–9. 114. Kalita J, Shah S, Kapoor R, Misra UK. Bladder dysfunction in acute transverse myelitis: magnetic resonance imaging and neurophysiological and urodynamic correlations. J Neurol Neurosurg Psychiatry 2002;73:154–9. 115. Chancellor MB, Dato VM, Yang J. Lyme disease presenting as urinary retention. J Urol 1990;143:1223–4.
122. Straus SE, Ostrove JM, Inchauspe G. Varicella zoster virus infections. Biology, natural history, treatment, and prevention. Ann Intern Med 1988;109:438–9. 123. Rosenfeld T, Price MA. Paralysis in herpes zoster. Aust N Z J Med 1985;15:712–6. 124. Centers for Disease Control and Prevention (CDC). Progress toward poliomyelitis eradication – poliomyelitis outbreak in Sudan, 2004. MMWR Morb Mortal Wkly Rep 2005;54(4):97–9. 125. Hodes R. Selective destruction of large motor-neurons by poliomyelitis virus: I. Conduction velocity of motor nerve fibers of chronic poliomyelitis. J Neurophysiol 1949;12:257–66. 126. So YT, Olney RK. AAEM case report #23: acute paralytic poliomyelitis. Muscle Nerve 1991;14:1159–64. 127. Bors E, Comarr AE. Neurologic Urology. Baltimore: University Park Press, 1971. 128. Pang D, Wilberger JE Jr. Tethered cord syndrome in adults. J Neurosurg 1982;57:32–47. 129. Al-Mefty O, Kandzari S, Fox JL. Neurogenic bladder and the tethered spinal cord syndrome. J Urol 1979;179:112–5. 130. Kondo A, Kato K, Kanai S, Sakakibara T. Bladder dysfunction secondary to tethered cord syndrome in adults: is it curable? J Urol 1986;135:313–6. 131. Adamson AS, Gelister J, Hayward R, Snell ME. Tethered cord syndrome: an unusual case of adult bladder dysfunction. Br J Urol 1993;71:417–21. 132. Meyrat BJ, Tercier S, Lutz N, Rilliet B, Forcada-Guex M, Vernet O. Introduction of a urodynamic score to detect pre- and postoperative neurological deficits in children with a primary tethered cord. Childs Nerv Syst 2003;19(10–11):716–21. 133. Kondo A, Kato K, Sakakibar T et al. Tethered cord syndrome: cause for urge incontinence and pain in lower extremities. Urology 1992;40:143–6.
116. Chancellor MB, McGinnis D, Shenot PJ et al. Urinary dysfunction in Lyme disease. J Urol 1993;149:26–30.
134. Hellstrom WJG, Edwards MSB, Kogan BA. Urological aspects of the tethered cord syndrome. J Urol 1986;135:317–20.
117. Steere AC, Green J, Schoen RT et al. Successful penicillin therapy of Lyme arthritis. N Engl J Med 1985;312:869–74.
135. Fukui J, Kaizaki T. Urodynamic evaluation of tethered cord syndrome including tight filum terminale. Urology 1980;16:539–52.
118. Rahn DW, Malawista SE. Lyme disease: recommendations for diagnosis and treatment. Ann Intern Med 1991;114:472–81.
136. Blaivas JG, Chancellor MB. Cauda equina and pelvic plexus injury. Practical Neurourology – Genitourinary Complications in Neurologic Disease. Boston: Butterworth-Heinemann, 1995; 155–63.
119. Weller TH. Varicella and herpes zoster: a perspective and overview. J Infect Dis 1992;166(Suppl 1):S1–6.
137. Mundy AR. An anatomical explanation for bladder dys-
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function following rectal and uterine surgery. Br J Urol 1982;54:501–4. 138. Hollabaugh RS Jr, Steiner MS, Sellers KD, Samm BJ, Dmochowski RR. Neuroanatomy of the pelvis: implications for colonic and rectal resection. Dis Colon Rectum 2000;43(10):1390–7. 139. Marshal VF, Pollack RS, Miller C. Observations on urinary dysfunction after excision of the rectum. J Urol 1946;55:409–21. 140. Fowler JW, Bremner DN, Moffat LEF. The incidence and consequences of damage to the parasympathetic nerve supply to the bladder after abdominoperineal resection of the rectum for carcinoma. Br J Urol 1978;50:95–8. 141. Petrelli NJ, Nagel S, Rodriguez-Bigas M, Piedmonte M, Herrera L. Morbidity and mortality following abdominoperineal resection for rectal adenocarcinoma. Am Surg 1993;59(7):400–4. 142. Blaivas JG, Barbalias GA. Characteristics of neural injury after abdominoperineal resection. J Urol 1983;129:84–7. 143. Querleu D, Narducci F, Poulard V, Lacaze S, Occelli B, Leblanc E, Cosson M. Modified radical vaginal hysterectomy with or without laparoscopic nerve-sparing dissection: a comparative study. Gynecol Oncol 2002;85(1):154–8. 144. McGuire EJ. Urodynamic evaluation after abdominal– perineal resection and lumbar intervertebral disc herniation. Urology 1975;6:63–70. 145. Wetterhall SF, Olson DR, DeStefano F et al. Trends in diabetes and diabetic complications, 1980–1987. Diabetes Care 1992;15(8):960–7.
146. Chancellor MB, Blaivas JG. Diabetic neurogenic bladder. Practical Neurourology – Genitourinary Complications in Neurologic Disease. Boston: Butterworth-Heinemann, 1995; 149–54. 147. Frimodt-Moller C, Hald T. A new method for quantitative evaluation of bladder sensibility. Scand J Urol Nephrol 1972;15:134–5. 148. Faerman I. Autonomic nervous system and diabetes: histological and histochemical study of the autonomic nerve fibers of the urinary bladder in diabetic patients. Diabetes 1973;22:225–37. 149. Thomas PK, Lascelles RG. The pathology of diabetic neuropathy. Q J Med 1978;35:449–57. 150. Lee WC, Wu HP, Tai TY, Liu SP, Chen J, Yu HJ. Effects of diabetes on female voiding behavior. J Urol 2004;172 (3):989–92. 151. Clark CMJ, Lee DA. Prevention and treatment of the complications of diabetes mellitus. N Engl J Med 1995;332:1210–7. 152. Appel RA, Whiteside HV. Diabetes and other peripheral neuropathies affecting lower urinary tract function. In: Krane RJ, Siroky MB (eds) Clinical Neurourology, 2nd ed. Boston: Little, Brown, 1991; 365–73. 153. Ueda T, Yoshimura N, Yoshida O. Diabetic cystopathy: relationship to autonomic neuropathy detected by sympathetic skin responses. J Urol 1997;157:580–4. 154. Kaplan SA, Te AE, Blaivas JG. Urodynamic findings in patients with diabetic cystopathy. J Urol 1995;153:342–3.
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37 Non-neurogenic voiding difficulty and retention Amitabha Majumdar, Philip Toozs-Hobson
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IntroductIon Urinary continence and micturition are functions requiring both the integrity of organs involved (bladder, urethra, voluntary and involuntary sphincters) and the neural pathways responsible for micturition (parasympathetic), continence (sympathetic), and their control and coordination. Voiding difficulties can cause discomfort on urination, or retention (acute or chronic), and are a reflection of an imbalance between the power of bladder contraction and outlet resistance. The management of voiding disorder requires an understanding of the pathophysiologic mechanism involved as well as the underlying etiology (often multifactorial) to allow appropriate medical and/or surgical management to be selected. Normal voiding commences when the initiation of a bladder contraction is synchronized with the relaxation of the bladder neck and urethra. The act of micturition is coordinated by higher centers channeled through the pontine micturition center, sacral reflex arc, and the innervations of the bladder muscle and sphincter mechanism. Outflow resistance, the speed of contraction of the detrusor muscle fibers, and subsequent abnormalities of any of the above components of this interactive mechanism may result in voiding dysfunction. Failure of the bladder to empty results in voiding difficulties which may or may not progress to retention. These symptoms are poorly documented and are often misdiagnosed until additional symptoms (e.g. recurrent urinary infections, incontinence and retention) prevail. Since these symptoms rarely progress to upper tract dilation or renal failure, they are not associated with mortality; however, the morbidity may be significant.
defInItIons The standardization of terminology of lower urinary tract dysfunction, published by the International Continence Society, has recently defined lower urinary tract symptoms in relation to voiding difficulty and retention.1 This can be seen in Chapter 51b and needs to be noted in terms of how definitions have changed. There are usually two stages through which women pass before developing acute or chronic urinary retention: 1. The first stage is where the woman is unaware of impaired emptying and hence is asymptomatic. The urinary stream remains reduced, with peak flow rates <15 ml/s; the maximum voiding pressure in most cases is normal without any residual urine. 2. The second stage is characterized by symptoms of voiding difficulty such as hesitancy, weak or poor stream, straining to void, intermittent stream,
double voiding, and positional changes to start or complete voiding. The peak flow is <15ml/s with a reduced voiding pressure and the presence of residual urine. There is a paucity of data regarding the prevalence and incidence of voiding disorder in the absence of neuropathy. Various studies have sampled women attending clinics with symptoms of bladder dysfunction. Actual figures regarding the prevalence in the community are lacking.2,3
cAuses of non-neurogenIc voIdIng dIffIculty The causes of non-neurogenic voiding difficulty are listed in Table 37.1 and are described below.
Pharmacologic causes Epidural anesthesia is the most frequent pharmacologic cause of voiding dysfunction.4,5 If urinary retention is overlooked, long-term voiding difficulties may result from overdistension injury. Anticholinergic drugs (e.g. oxybutynin, tolterodine, etc.) used for overactive bladder symptoms can give rise to voiding difficulties, hence it is vital to exclude urinary residual before prescribing this class of medication. α-Adrenergic agents increase urethral resistance, whereas ganglion-blocking drugs have similar effects to anticholinergic agents. However, recent work suggests that the current dosages used for anticholinergics are such that the site of action is likely to be the bladder wall and are insufficient to cause total blockade at a motor neuron level. This would explain that while studies of anticholinergics have noted a modest rise in measured residual volumes, the clinical significance and incidence of retention is less.6
Inflammatory causes A vulvovaginal lesion may result in disturbance of normal micturition. Painful stimuli can cause voiding difficulty, either by urethral edema or by urine coming into contact with the inflamed mucosa of urethra in particular, but equally of the vagina as well. Anogenital herpes infection is a recognized cause of voiding difficulty.7,8
the hypersensitive female urethra Shah et al.9 described a group of women with symptoms of urgency, frequency and nocturia, who, when undergoing urodynamic testing, revealed an exquisitely
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table 37.1.
Causes of voiding dysfunction and retention
1. Pharmacological • Tricyclic antidepressants • Anticholinergic agents • Adrenergic agents • Ganglion blocking agents • Epidural anaesthesia 2. Inflammatory • Acute urethritis, cystitis, vulvovaginitis • Acute anogenital infections (including herpes) 3. The hypersensitive female urethra 4. Obstructive causes • Distal urethral stenosis • Acute urethral edema of surgery • Foreign body • Pelvic mass – retroverted gravid uterus, hematocolpos, uterine fibroid, ovarian cyst, fecal impaction • Cystocele • Uterine prolapse 5. Early post-partum voiding difficulty 6. Psychogenic • Anxiety or depressive illness • Hysteria 7. Endocrine • Hypothyroidism • Diabetic neuropathy 8. Detrusor myopathy 9. Urethral sphincter hypertrophy 10. Overdistension injury 11. Iatrogenic • After surgery for stress incontinence • After anal surgery • After hysterectomy • After transtrigonal phenol injection 12. Idiopathic
sensitive urethra during catheterization. Urodynamic testing in such patients usually reveals a high incidence of obstructed voiding and a lower incidence of detrusor overactivity.
obstructive causes Intrinsic causes of obstruction (e.g. urethral stenosis, urethral foreign bodies, calculi, scarring from instrumentation) are uncommon in women. Bladder neck surgery, tension-free vaginal tape (TVT), and collagen injection are recognized causes of compression and voiding difficulty.10 Extrinsic causes of obstruction include a retroverted gravid uterus, pelvic masses (uterine fibroids and ovarian cysts), fecal impaction and chronic constipation (people with severe constipation may have neuropathy affecting both the colonic and lower urinary tracts).11
Hematocolpos associated with cryptomenorrhea may present with retention and voiding difficulty. Similarly, distortion of the urethra following genital prolapse is also a recognized cause of voiding difficulty, with significant decline in urine flow rates in the presence of increasing grades of prolapse, particularly uterine prolapse, cystocele and enterocele (Fig. 37.1).12–15 Labial fusion, including the practice of female genital mutilation, may also lead to voiding difficulty.16
early post-partum voiding difficulty Significant prevalence of voiding difficulty has been noted in the early post-partum period, particularly after vacuum extraction rather than spontaneous vaginal delivery or cesarean section. The risk factors identified were prolonged first and second stages of labor and birth weight ≥3800 g.17,18
Psychogenic causes This diagnosis should only be made by a careful process of exclusion because of the social stigma attached to such a diagnosis. The majority of patients suffering from psychogenic retention of urine are women aged between 25 and 45 years. There is usually a relationship between the onset of symptoms and a stressful event such as childbirth, marital discord, surgical treatment or rape. Hysteria, depression, and schizophrenia may all be associated with this problem. Once a psychiatric assessment has been made, the treatment remains the same. Return to normal voiding function is expected in the majority of cases.19,20 Until this occurs, the use of clean intermittent self-catheterization is considered satisfactory management.
endocrine causes Individuals with hypothyroidism and diabetes mellitus can develop urinary retention as a result of peripheral neuropathy causing bladder atony.21
detrusor myopathy In 1985, the histologic features of this condition were described as chronic abacterial cystitis by Holm-Bentzen et al.22 They described detrusor muscle cell degeneration, fatty replacement, hydropic cytoplasmic changes, perinuclear vacuolization and other such changes. Electron microscopic studies revealed a decrease in myofibrillar mass along with formation of cytoplasmic vacuoles. More recently, Martin et al.23 described lipid 585
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Figure 37.1.
Flow cystometry showing a low flow rate with an abdominal strain pattern.
inclusion bodies in the detrusor as a possible cause of primary myopathy causing urinary retention.
urethral sphincter hypertrophy This is a primary disorder of the urethral sphincter in the absence of any other neurologic or urologic disorder. Bladder hypo- or acontractility appears to be secondary to the failure of the sphincter to relax. Fowler et al. described this entity and found it to be associated with polycystic ovaries.24 It is associated with characteristic EMG findings of complex repetitive discharges along with decelerating bursts, characteristically described as whale noises.25
overdistension injury Bladder overdistension is a major cause of voiding difficulty and should never be overlooked. A single episode of
urinary retention can result in a hypo- or acontractile bladder. Irreversible detrusor muscle damage due to laying down of collagen can occur as a result of overdistension. An increase in intravesical pressure leads to weakening of the bladder wall due to ischemic changes. Animal models suggest the urothelium is probably the initial site of the proliferative response to outlet obstruction.26–28
PresentIng syMPtoMs The majority of patients are symptomatic and present with hesitancy, straining to void, weak or prolonged stream, intermittent stream, double voiding, incomplete emptying, reduction, and positional changes to start or complete voiding.29 Acute retention most frequently presents with pain. Urodynamic studies show that objective evidence of voiding difficulty may be found in both asymptomatic and symptomatic patients and is usually due to impaired detrusor contractility. History taking,
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involving detailed drug, medical and surgical history, should be directed towards determination of a primary cause.
sIgns The importance of clinical examination cannot be overemphasized. A careful general abdominal, pelvic, and neurologic examination should be performed to exclude causes. A neurologic examination should include inspection of the lumbar region for underlying spinal disorder. Abdominopelvic examination should be undertaken after bladder emptying, and masses like ovarian cysts, fibroids, etc. should be sought. Vulvovaginal inflammation and genital prolapse need to be excluded. Finally, the patient’s general demeanor should be observed.
InvestIgAtIons The patient should be investigated according to the suspected abnormality. The simplest tests available are a flow rate, abdominal radiograph, and pelvic and (if appropriate) renal ultrasonography. Following demonstration of a reduced flow and residual urine on bladder ultrasound to confirm the diagnosis of voiding difficulty, the next step will be to perform urodynamic studies.
frequency volume chart Useful information will be obtained by asking the patient to keep a urinary diary for a minimum of 3 days (though preferably for a week) prior to their next outpatient appointment. Most patients will not find this task difficult.30
Infrequent voiding Normal voiding is generally considered as less than seven times a day. This is usually determined by fluid intake, habit, anxiety and stress, and the presence of abnormalities of bladder function (either motor or sensory). Patients who void infrequently should be investigated at the very least with a frequency volume chart and, based upon the information obtained, advised about normal requirements of intake and the frequency of voiding. Infrequent voiders should be advised to void every 3–4 hours during the day.
flow rate/uroflowmetry The free flow rate (uroflowmetry) is the most important initial screening tool and is simple and non-invasive. It
is best undertaken in a private area with a comfortably full bladder. Measurements may need to be repeated as a single measurement can be unreliable. A flow rate consistently below 15 ml/s for a volume greater than 150 ml indicates impaired voiding, which may be a precursor of retention.31 Obstructed voiding may occur in the presence of normal flowmetry. This is because the bladder has been able to compensate through an increase in the force of contraction associated with a rise in voiding pressure. Urodynamic evaluation is indicated in these patients.32,33 A peak flow <15 ml/s and/or residual urine >50 ml with a minimal total bladder volume of 150 ml before voiding, and the 10th centile curve of the Liverpool nomogram for the maximum urine flow rate, have been identified as useful discriminators when diagnosing voiding difficulties in women. Uroflowmetry has a good specificity, a high negative predictive value, and a good diagnostic capacity, making it a useful first diagnostic approach in urogynecologic patients.34
cystometry Filling and voiding cystometry may be all that is necessary for the majority of patients; however, combined synchronous videocystometry is preferable in those cases where radiologic examination of the voiding process is essential in providing information about the bladder appearance; for example, trabeculation, diverticula and reflux, behavior of the bladder neck and the urethral mechanism.35
Urodynamic features of voiding disorders
• First sensation may be greatly reduced or delayed; • •
•
this may be associated with early first sensation and urgency in upper motor neuron lesions. Capacity is greatly reduced with hyperreflexic bladder dysfunction; it is increased with acontractile bladders. End filling detrusor pressure and compliance are usually normal except in association with upper motor neuron hyperreflexic bladders or chronic bladder fibrosis. Isometric pressure (piso) is the additional detrusor pressure rise seen at the point of maximum detrusor pressure during voiding when voiding is stopped suddenly. Patients with low isometric pressures, low voiding pressures, and low preoperative maximum urethral closure pressure tend to be those who take longer to recover normal bladder emptying after surgery for stress incontinence. 587
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• Maximum voiding pressure is raised above the female upper limit of accepted normality (50 cmH2O) where obstruction is present. Voiding pressure may be low or non-existent where detrusor failure is present.
radiology A plain abdominal radiograph can demonstrate spina bifida and disk prolapse, although magnetic resonance imaging (MRI) or computed tomography (CT) scan would probably be the preferred investigation. Videocystourethrography can provide additional information at the time of cystometry (Fig. 37.2). An intravenous urogram (IVU) is not a dynamic investigation and its use is limited to delineating the anatomy of the urinary tract.
ultrasonography Abdominal ultrasound allows non-invasive measurement of urinary residual and assessment of the urinary tract.
cystourethroscopy Stenosis manifests with difficulty in instrumentation, and cystoscopy allows visualization of intravesical pathology such as trabeculation, sacculation and diverticula. However, they are more likely to be associated with detrusor instability than with obstruction.
Figure 37.2. Plain radiograph from a videourodynamic study demonstrating a significant cystocele with urinary residual.
electromyography Sphincter electromyography (EMG) requires special equipment and considerable experience in its use and interpretation. It is particularly useful in the diagnosis of unexplained acute retention of urine in which a neurologic abnormality may be present; for example, external sphincter dysfunction, where there is failure of relaxation of the sphincter, and multiple system atrophy (a condition which mimics Parkinson’s disease), characterized by atrophy of cells in the nucleus of Onuf in the spinal cord.36
treAtMent Prophylactic treatment Many voiding difficulties can be avoided by early recognition. If urinary retention is suspected or imminent after surgical procedures, the early use of bladder catheterization before bladder overdistension will prevent many long-term bladder problems. Difficulty with resuming normal micturition after surgical treatment may occur in over 60% of patients undergoing surgery for stress incontinence and in 45% of patients undergoing radical surgery for gynecologic malignancy.37,38 A clear explanation of the possibility of voiding difficulty should be given to all patients who are to undergo any surgery that carries this risk. Those who express dissatisfaction with surgical outcome are those who have not received an adequate preoperative explanation of the potential problems. In women with evidence of voiding difficulty prior to continence surgery (low flow rate and low maximum voiding pressure), it is reasonable to counsel appropriately and teach intermittent self-catheterization. Intermittent self-catheterization as a non-sterile procedure was first described by Gutmann and Frankel in 1966.39 Originally used in neurogenic conditions, it is now the principal treatment for chronic urinary retention. It allows women to lead independent lives with efficient bladder emptying and low rates of urinary tract infection when performed properly. Although patients are often initially hesitant at the idea of such a technique, if properly counseled by trained professional staff, most will easily master the technique and appreciate the consequent improvement in quality of life. There are two forms of intermittent self-catheterization: sterile and clean. The former is usually reserved for patients with neuropathic bladders in a hospital environment to prevent cross-infection.
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clean intermittent self-catheterization Clean intermittent self-catheterization (CISC)40,41 is usually performed by the patient but can be performed by a carer or relative. The technique is designed for everyday use. The patient has to be reasonably dextrous and is taught using a clean technique and a mirror: the patient lies down initially, and inserts a fine-bore catheter. When proficient with the mirror, she is taught to insert the catheter by feel in the sitting or standing position. Disposable catheters are available but reusable ones do not pose a significant risk of infection. A salt coating allows easier insertion with less urethral friction. The frequency of catheterization varies, with the aim being to avoid incontinence and filling beyond normal bladder capacity. The procedure has good long-term results and normal function often recovers with time, particularly if voiding difficulty has occurred postoperatively or after childbirth.
Pharmacotherapy Cholinergic agents – for example, bethanechol chloride and distigmine bromide (an anticholinesterase) – and intravesical prostaglandin E2 and F2 have been advocated but there is no real evidence of clinical benefit.42– 44 Although α-adrenergic blocking agents (e.g. phenoxybenzamine, prazocin and indoramine) have no proven benefit in women, they are useful in men with urodynamically proven bladder neck obstruction. Anxiolytic agents such as diazepam may help with postoperative voiding problems. In women with combined urge incontinence and retention, anticholinergic agents such as tolterodine may be used effectively in conjunction with CISC if required, but the incidence of this is reassuringly low due to the site of action of anticholinergics in their current doses.6
surgical management If voiding difficulty is due to urethral stenosis, urethral dilation using Hegar dilators or preferably the Otis urethrotome is an appropriate option.45 The place of bladder neck incision in patients with outflow obstruction is a contentious issue and should never be performed unless a diagnosis is confirmed by pressure/flow videourodynamics. Partial cystectomy has been performed for treating the myogenic decompensated bladder with excessive residual urine.46,47 However, the results are disappointing. Urinary diversion using appendix or fallopian tube, colocytoplasty, latissimus dorsi myoplasty, and vesical
cap operation with ileal seromuscular patch grafts have all been tried with variable success.48,49
Alternative methods and future trends Neuromodulation This two-stage procedure involves stimulation of the S3 nerve root through the S3 foramen. The first stage is that of percutaneous nerve evaluation using a temporary stimulation wire. If this has a beneficial effect then a permanent stimulator is implanted. Early results are encouraging but the mechanism of action is not understood.50,51
Turbine valve Monga et al. described a new replaceable intraurethral sphincter prosthesis with a self-contained urinary pump for chronic female urinary retention. The prosthesis consists of a valve and pump mounted inside a tube-shaped, catheter-like, soft polycarbonate casing. It is secured at the bladder neck by soft expandable silicone fins and at the external meatus by a flexible flange. Activation is achieved by turning on a small battery-operated remote control unit placed over the lower abdomen: the valve opens and the pump actively draws urine from the bladder and the patient ‘voids’. At the end of urination, the valve closes, restoring continence. Early results have been encouraging and a larger trial has confirmed this; however, it has yet to become established and crusting of the device has been a major problem.52,53
conclusIon • Failure of bladder emptying results in voiding difficul• • • • • • •
•
ties which may or may not progress to retention. There is a paucity of data regarding incidence and prevalence. Urinary retention can result from a variety of causes. Uroflowmetry is the most important initial screening tool. A frequency volume chart provides important information. Prevention or early recognition of retention may avoid long-term voiding difficulty. The case for routine urethral catheterization for 24 hours after all pelvic surgery remains unresolved. Intermittent self-catheterization allows women to lead independent lives with efficient bladder emptying and low rates of urinary tract infection, and is the mainstay of treatment. Pharmacotherapy and surgery currently have limited roles. 589
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references 1. Abrams P, Cardozo L, Fall M et al. The standardisation of terminology of lower urinary tract function: report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 2002;21(2):167–78. 2. Stanton SL, Ozsoy C, Hilton P. Voiding difficulties in the female: prevalence, clinical and urodynamic review. Obstet Gynecol 1983;61:144–7. 3. Dwyer PL, Desmedt E. Impaired bladder emptying. Aust N Z J Obstet Gynaecol 1994;34:73–8. 4. Jackson SR, Barry C, Davies G. Length of labour and epidural anaesthesia: long term effects on urinary symptoms. Int Urogynaecol J 1995;6:244. 5. Jackson S, Barry C, Davies G et al. Duration of second stage of labour and epidural anaesthesia: effect on subsequent urinary symptoms in primiparous women. Neurourol Urodyn 1995;14:498–9. 6. Andersson K-E, Yoshida M. Antimuscarinic and the overactive bladder – which is the main mechanism of action? Eur Urol 2003;1:1–5. 7. Oates J, Greenhouse PR. Retention of urine in anogenital herpetic infection. Lancet 1978;1:691–2. 8. Hemrika DJ, Schutte MF, Blecker OP. Elsberg syndrome: a neurological basis for acute urinary retention in patients with genital herpes. Obstet Gynecol 1986;68:37S–39S. 9. Shah PJR, Whiteside CG, Milroy EJG, Turner-Warwick RT. The hypersensitive female urethra – a catheter diagnosis? Proceedings of the XIIIth Annual Meeting of the International Continence Society, 1983: 202–3. 10. Smith RN, Cardozo L. Early voiding difficulty after colposuspension. Br J Urol 1997;80(6):911–4. 11. Lucanto C, Bauer SB, Hyman PE, Flores AF, Di-Lorenzo C. Function of hollow viscera in children with constipation and voiding difficulties. Dig Dis Sci 2000;45(7):1274–80. 12. Chaikin DC, Romanzi L, Rosenthal J. The effects of genital prolapse on micturition. Neurology Urodyn 1998;17:426–7. 13. Monga AK, Woodhouse C, Stanton SL. A case of simultaneous urethral and ureteric obstruction. Br J Urol 1995;77:606–7. 14. Marinkovic SP, Stuart SL. Incontinence and voiding difficulties associated with prolapse. J Urol 2004;171(3):1021–8. 15. Romanzi LJ, Chaikin DC, Blaivas JG. The effect of genital prolapse on voiding. J Urol 1999;161(2):581–6. 16. Ong NC, Dwyer PL. Labial fusion causing voiding difficulty and urinary incontinence. Aust N Z J Obstet Gynecol 1999;39(3):391–3. 17. Groutz A, Gordon D, Wolf Y et al. Early postpartum void-
ing dysfunction: incidence and correlation with obstetric parameters. J Reprod Med 2004;49(12):960–4. 18. Eustice S. Management of voiding difficulties associated with pregnancy. Nursing Times 2004;100(12):50–3. 19. Barrett DM. Evaluation of psychogenic urinary retention. J Urol 1978;120:191–2. 20. Krane R, Siroky M. Psychogenic voiding dysfunction. Clinical Neuro-urology. Boston: Little, Brown, 1978. 21. Yu HJ, Chia LW, Ping LS et al. Unrecognised voiding difficulty in female type 2 diabetic patients in the diabetic clinic: a prospective case-control study. Diabetes Care 2004;27(4):988–9. 22. Holm-Bentzen M, Larsen S, Hainau B, Hald T. Nonobstructive detrusor myopathy in a group of patients with chronic abacterial cystitis. Scand J Urol Nephrol 1985;124:1015–7. 23. Martin JE, Sobeh M, Swash C et al. Detrusor myopathy: a cause of detrusor weakness with retention. Br J Urol 1993;71:235–6. 24. Fowler CJ, Christmas TJ, Chapple CR et al. Abnormal electromyographic activity of the urethral sphincter, voiding dysfunction, and polycystic ovaries: a new syndrome? BMJ 1998;297:1436–8. 25. Fowler CJ, Kirby RS. Abnormal electromyographic activity in the striated muscle of the urethral sphincter in 5 women in urinary retention. Br J Urol 1985;57:67–70. 26. Hinman F. Postoperative overdistension of the bladder. Surg Gynaecol Obstet 1976;142:901–2. 27. Khan AU, Stern JM, Polasky Z. Vesical necrosis associated with acute bladder overdistension. Urology 1982;19:197–9. 28. Tong YC, Monson FC, Erika B, Levin RM. Effects of acute in vitro overdistension of the rabbit urinary bladder on DNA synthesis. J Urol 1992;148:1347–50. 29. Dorflinge A, Monga A. Voiding dysfunction. Curr Opin Obstet Gynaecol 2001;13(5):507–12. 30. Giesy JD. Voiding problems in women. Postgrad Med 1986;79:271–8. 31. Haylen BT, Law MG, Frazer M, Schulz S. Urine flow rates and residual urine volumes in urogynaecology patients. Int Urogynaecol J Pelvic Floor Dysfunct 1999;10(6):378–83. 32. Hilton P, Laor D. Voiding symptoms in the female: the correlation with urodynamic voiding characteristics. Neurourol Urodyn 1989;8:308–10. 33. Pauwels E, De Wachter S, Wyndale JJ. A normal flow pattern in women does not exclude voiding pathology. Int Urogynaecol J Pelvic Floor Dysfunct 2005;16(2):104–8. 34. Constantini E, Mearini E, Pajoncini C et al. Uroflowmetry in female voiding disturbances. Neurourol Urodyn 2003;22(6):569–73.
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35. Groutz A, Gordon D, Lessing JB, Wolman I, Jaffa A, David MP. Prevalence and characteristics of voiding difficulties in women: are subjective symptoms substantiated by objective urodynamic data? Urology 1999;54(2):268–72. 36. Fidas A, Galloway NTM, Varma J et al. Sacral reflex latency in acute retention in female patients. Br J Urol 1987;59:311–3. 37. Fraser AC. The late effects of Wertheim’s hysterectomy on the urinary tract. Br J Obstet Gynaecol 1966;73:1002–7. 38. Smith PH, Turnbull GA, Currie DW, Peel KR. The urological complications of Wertheim’s hysterectomy. Br J Urol 1969;41:685–8. 39. Gutmann L, Frankel H. The value of intermittent catheterisation in the early management of traumatic paraplegia and tetraplegia. Paraplegia 1966;4:63–84. 40. Lapides J, Diokno C, Silber SJ, Lowe BS. Clean intermittent self catheterization in the treatment of lower urinary tract disease. J Urol 1972;107:458–61. 41. Wyndaele J, Maes D. Clean intermittent self-catheterization: a 12-year follow up. J Urol 1990;143:906–8. 42. Cameron MD. Distigmine bromide in the prevention of post-operative retention of urine. J Obstet Gynaecol Br Commonw 1966;73:847–8. 43. Delaere KPJ, Thomas CMG, Moonen WA, Debbryune FMJ. The value of intravesical prostaglandin E2 and F2 in women with abnormalities of bladder emptying. Br J Urol 1981;53:306–9. 44. Bultitude MI, Hills NH, Shuttleworth KED. Clinical and experimental studies on the action of prostaglandins and their synthesis inhibitors on detrusor muscle in vitro and in vivo. Br J Urol 1976;48:631–63.
45. Worth PHL. Urethrotomy. In: Stanton SL, Tanagho EA (eds) Surgery for Female Incontinence, 2nd ed. Berlin: Springer-Verlag, 1986; 185–191. 46. Farrar D, Turner-Warwick RT. Outflow obstruction in the female. Symposium on Clinical Urodynamics. Urol Clin North Am 1979;6:217–25. 47. Klarskov P, Anderson JT, Asmussen CF et al. Acute urinary retention in women: a prospective study of 18 consecutive cases. Scand J Urol Nephrol 1987;21:29–31. 48. Toguchi Y. Augmentation and replacement sigmoid colocytoplasty. A review of 10 patients. Br J Urol 1987;60: 231–5. 49. Von Hayden B, Anthony J, Kaula N et al. The latissimus dorsi muscle for detrusor assistance: functional recovery after nerve division and repair. J Urol 1994;151: 1081–7. 50. Moore KN, Griffiths DJ, Metcalfe JB, McCracken PN. Electrostimulation of the bladder neck in acontractile bladder: two case reports. Urol Nursing 1993;13:113–5. 51. Scheepens WA, deBie RA, Weil EHJ, Van Kerrebroeck P. Unilateral versus bilateral sacral neuromodulation in patients with chronic voiding dysfunction. J Urol 2002;168(5):2046–50. 52. Monga AK, Madjar S, Stanton SL et al. A new intraurethral pump for urinary retention. Neurourol Urodyn 1996;4:363–4. 53. Madjar S, Sabo E, Halachmi S et al. Predictors of treatment success of the remote controlled intraurethral insert in women with voiding dysfunction. Neurourol Urodyn 1998;4:348–9.
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38 Painful bladder syndrome Deborah R Erickson
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IntroductIon: PaInful Bladder Syndrome and InterStItIal cyStItIS Painful bladder syndrome (PBS) is defined by the International Continence Society as the complaint of suprapubic pain related to bladder filling, accompanied by other symptoms such as increased daytime and night-time frequency, in the absence of proven urinary infection or other obvious pathology.1 PBS has similar symptoms and a likely overlap with interstitial cystitis (IC), but the two conditions are not identical. One important distinction is that PBS was a new definition in 2002, whereas IC has been recognized for generations. Therefore, almost all of the literature on this topic is written about IC. IC patients usually present with some combination of pelvic and/or perineal pain, urgency to urinate, frequent daytime voiding and nocturia. Approximately 90% of patients diagnosed with IC are women, which makes IC a relevant condition for gynecologists. Patients have often had problems for years by the time a diagnosis is made, and up to 85% have had a hysterectomy for pelvic pain prior to diagnosis. Outside of specialist centers, there has been little or no attention paid to IC as a diagnosis and as such, the services are predominantly fragmented, particularly with regard to pain management if treatments fail to cure or ameliorate symptoms. The definition and diagnostic criteria for IC are still being debated. In 1987, the National Institute of Arthritis, Digestive and Kidney Diseases (NIDDK) proposed a set of criteria to enroll IC patients in research studies.2 These criteria were revised a year later and continue to be used for research.3 The criteria were made strict to improve consistency among the research subjects, and it was understood that some patients with clinical IC would be excluded. Not surprisingly, a recent study showed that the NIDDK criteria excluded over half of the patients thought by expert urologists to ‘definitely’ or ‘very likely’ have IC.4 At this time, no criteria for the clinical definition of IC have been universally accepted. The NIDDK criteria did not include any bladder histologic findings. However, some investigators believe that histologic features are important for diagnosis. For example, Holm-Bentzen et al. defined IC as painful bladder disease with at least 28 mast cells/mm2 in the detrusor muscle.5 Surveys carried out by Dutch6 and Japanese7 urologists found that 79% and 24%, respectively, used detrusor mast cells as a diagnostic criterion for IC. Therefore, when reading IC literature, note should be taken of the diagnostic criteria used in each study.
A landmark study showed that IC patients formed two different groups.8 In one group, bladder ulcers were seen on cystoscopy, and bladder biopsies usually showed intense inflammation. The other group had no ulcers but had petechial bleeding on cystoscopy; they usually had scant or no inflammation. These two groups have several other clinical and pathologic differences,9–11 as well as different treatment responses,9 yet both could be included in the symptom definition of PBS. Therefore, any treatment trial should be read closely to determine the exact type of patients studied. Not all results can be generalized to the broad PBS population.
PoSSIBle etIologIeS of InterStItIal cyStItIS Many different etiologies have been proposed for IC. It is likely that PBS and IC have multiple etiologies, some of which may overlap. It is beyond the scope of this chapter to analyze the evidence for and against each theory. Instead, the major theories will be described briefly, since most treatments are based on them.
Bladder epithelial deficiency Most IC bladder biopsies have some degree of epithelial disruption.8,9,12 It is easy to understand how this could lead to painful symptoms, since urine could leak across the disrupted epithelium and irritate the underlying tissues. Some investigators also believe that the IC bladder epithelium is abnormally permeable, even if it appears intact on histology.13 If this theory is true, one possible explanation is that the glycoconjugate lining of the epithelium is deficient.13 This theory is the basis for treating IC with glycosaminoglycans (GAGs), which are thought to replace the deficient epithelial glycoconjugates. The urine of most IC patients contains a glycosylated 9-amino-acid peptide, which is named antiproliferative factor (APF) because it inhibits the proliferation of human bladder epithelial cells in culture.14 APF may be responsible for the disrupted or deficient epithelium in IC bladders. Future treatments may include strategies to neutralize the effects of APF.
Bladder mast cell activation Mast cells are found in some IC bladder biopsies.12,15,16 When mast cells are activated, they release various mediators that may be relevant to IC and PBS symptoms. These mediators include histamine, prostaglandins, leukotrienes, cytokines, and chemotactic factors.15,16 Bladder
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mast cell activation is a frequently proposed etiology for IC.15,16 With this rationale, antihistamines and mast cell stabilizers are used as treatments.
Inflammation Some IC bladder biopsies have an intense inflammatory infiltrate, which is an obvious explanation for symptoms of bladder pain and frequent voiding. The unknown question is: What causes the inflammation? Occult infection is an unlikely cause for IC.17–20 It has been reported that patients with irritative voiding symptoms may improve on antibiotics even though routine urine cultures are negative, and some of these patients have positive cultures for fastidious organisms.21,22 However, it could be argued that a patient whose symptoms resolve on antibiotics does not have IC or PBS as these entities are generally understood. A recent report showed that bacteria can persist within bladder epithelial cells after an acute infection, and it is proposed that these intraepithelial bacteria may cause symptoms but not be evident in urine culture.23 This hypothesis has not been tested directly in IC or PBS. Other causes of inflammation besides infection have also been proposed for IC. One possibility is neurogenic inflammation. When sensory nerves are stimulated, they can release inflammatory mediators. The inflammation leads to pain and continued sensory nerve stimulation, so the nerves continue to secrete inflammatory mediators in a ‘vicious cycle’.16,24 This process is thought to occur in some cases of IC.16 Another possibility is that some IC cases may be allergic or autoimmune in origin.25,26 This is the rationale for treating IC with anti-inflammatory or immunosuppressive agents.
neuropathic changes A more recent theory is that PBS involves changes in the sensitivity of bladder neurons and/or the relevant central neurons (neural plasticity).27 This is the basis for treatment with nerve-stabilizing drugs such as gabapentin. Another aspect of neural plasticity is that pain can develop in other areas that share innervation with the originally injured organ.27 For example, some patients with IC also have vulvar pain, irritable bowel symptoms and/or pelvic floor muscle dysfunction. These conditions may cause persistent pain, even if the bladder itself improves, and require other treatments besides those directed specifically to the bladder.27–29 Conversely, it is hypothesized that pelvic floor muscle dysfunction may lead to irritative voiding symptoms.30
clInIcal evaluatIon of Women WIth PaInful Bladder Syndrome Referring back to the definition at the start of the chapter, the diagnosis of PBS requires two steps: 1) elicit the history of ‘suprapubic pain related to bladder filling, accompanied by other symptoms such as increased daytime and night-time frequency’; and 2) rule out ‘urinary infection or other obvious pathology’.1 This leaves room for judgment on the part of the practitioner.
history The history defined for PBS is ‘suprapubic pain related to bladder filling, accompanied by other symptoms such as increased daytime and night-time frequency’. This is also the classic history for IC. Some patients with IC complain of urgency/frequency rather than pain.31,32 By definition, patients without pain would not be diagnosed with PBS. It is not known whether the main complaint (pain or urgency) affects what treatment is most likely to succeed. Incontinence is not a typical symptom of PBS or IC. If incontinence is present, it should prompt a more detailed investigation to determine whether PBS is truly the correct diagnosis. For example, involuntary detrusor contractions may cause frequency, urgency, and discomfort with holding urine. On the other hand, a patient may have PBS and incontinence as two coexisting problems. The symptoms of PBS or IC may be episodic. If so, the patient may attribute the symptom episodes to urinary tract infections, and present for evaluation of ‘recurrent infections’. Negative urine cultures during symptom episodes suggest PBS or IC. However, it is difficult to correlate dates of symptom episodes and urine cultures retrospectively. A more practical approach is to focus the initial history on the following:
• What symptoms occur during an episode? • Do these symptoms improve quickly on antibiotics? • Does the patient have any bladder complaints between episodes? A plan is then made to obtain a urine culture, before starting antibiotics, with the next symptom episode. The second part of the PBS evaluation is to rule out other causes for the symptoms. One clue is the relationship of the pain to voiding. Pain that is worse with bladder filling, and improved after voiding, is classic for PBS or IC. In contrast, pain that occurs during voiding is usually due to urinary tract infection, vulval/vaginal dis595
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orders, pelvic floor dysfunction, bladder neck dysfunction or urethral diverticulum. Other aspects of the history may also point to alternative causes for the symptoms, including hematuria or smoking (bladder cancer), neurologic symptoms (involuntary bladder contractions) or back, flank or lower abdominal pain (ureteral stone). Symptoms that are worse during the menstrual period may suggest endometriosis (although endometriosis pain can be out of synchronization with the menstrual cycle). Cystitis from known causes (e.g. cyclophosphamide, radiation) would not be included in the PBS or IC definitions.
Pelvic examination The pelvic examination in IC is usually normal except that the bladder is tender to palpate. The main goal of the examination is to exclude other possible causes for the symptoms, such as vulval disorders, vaginitis, urethral diverticulum or pelvic floor dysfunction. Inspection of the vulva and vagina should be performed to exclude skin lesions, atrophic changes, and discharge. Even if the vulva appears normal, lightly touch the posterior fourchette and introitus, asking if these areas are tender and if this pain reproduces the chief complaint. The classic sign of a urethral diverticulum is a suburethral mass which, when palpated, causes pus to appear at the urethral meatus. However, some patients have no palpable mass, so the clinician needs a high index of suspicion to avoid missing a diverticulum.33 Cystoscopy is not a good diagnostic test for urethral diverticulum because of its low sensitivity. Pelvic MRI has the highest sensitivity, and also provides useful anatomic details for surgical planning.33 Voiding cystourethrogram is not as sensitive for diverticulum as MRI, but it has the advantage of also evaluating for other causes of pain while voiding, such as bladder neck or pelvic floor dysfunction. To examine for pelvic floor dysfunction, palpate the levator muscles through the vagina. Tight or tender muscles suggest pelvic floor dysfunction, especially if palpating them reproduces the chief complaint.
urine studies Urinalysis and urine culture are important to exclude other causes for PBS symptoms. Urinalysis is usually normal in PBS and IC. Hematuria or pyuria may occur, but should not be attributed simply to PBS or IC. It should be evaluated according to usual practice. Urine cytology is recommended if the patient has hematuria, or is in a high-risk group for bladder can-
cer (e.g. smoking, older age, occupational exposure). However, for patients with no hematuria and no risk factors, the yield of cytology is low.34
voiding diary A voiding diary does not require special charts and does not need to be complex. Simply ask the patient, each time she voids, to write down the time of day and the volume of urine that she voids. A single 24-hour diary is sufficient.35 A voiding diary has several benefits. One is to rule out polyuria as a cause of frequency. In PBS or IC, the diary usually shows frequent voids with small volumes. The largest voided volume correlates with the maximal capacity on urodynamics.36 The pretreatment voiding diary is useful as a baseline, and subsequent diaries during treatment help to quantify improvement. The voiding diary is also useful as an adjunct to conservative treatment (see below).
urodynamics The main role of urodynamics is to rule out other causes for the symptoms, such as involuntary bladder contractions or obstructed voiding. The relationship of involuntary bladder contractions to IC or PBS is still not well defined. A reasonable working theory is that involuntary bladder contractions are a separate condition from PBS/IC, and a patient may have involuntary bladder contractions alone, PBS/IC alone, or both coexisting. The practical consequences are that:
• involuntary bladder contractions are likely to •
improve with anticholinergic therapy, while IC alone is not;3 dimethylsulfoxide (DMSO) treatment is less effective in IC patients who have involuntary bladder contractions.37
For clinical evaluation, it is debated whether urodynamics should be part of the routine evaluation or reserved for special cases.38 In the selective approach, urodynamics are used for patients who are thought to have alternate conditions causing their symptoms, such as obstructed voiding or involuntary bladder contractions. Advocates of the selective approach believe that these conditions can often be suspected based on history and examination, and patients at low risk can be spared the expense and discomfort of urodynamics. In addition, patients can be offered a trial of anticholinergic drugs without formally diagnosing involuntary bladder
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contractions. Currently, the decision for urodynamics is left to the clinician’s judgment. Urodynamics are required to enrol a patient in a research study that uses the NIDDK criteria, since these criteria include specific urodynamic findings. The NIDDK urodynamic criteria are as follows: 1) an intense urge to void at <150 ml fluid volume; 2) maximal capacity without anesthesia <350 ml fluid; and 3) no involuntary bladder contractions.3
Potassium sensitivity testing Briefly, potassium sensitivity testing (PST) involves the patient rating her symptoms of pain and urgency after having 40 ml water dwell in the bladder for 5 minutes, and again after instilling 40 ml 0.4M potassium chloride (KCl) into the bladder. If the KCl causes more pain or urgency than the water, the test is positive.13 Approximately 80% of IC patients have a positive test.39 A positive test is thought to reflect increased bladder epithelial permeability, but this has not been proven. An alternative explanation is that the bladder nerves are more sensitive to KCl (hyperesthesia). PST is not part of the standard PBS evaluation, for either clinical or research purposes. Some experts believe it is useful, whereas others believe that it does not give any additional diagnostic information beyond that obtained by the usual clinical evaluation.40,41 It may be most useful when the patient has non-specific pelvic pain, and the clinician is unsure which organ(s) may be contributing to the pain. A positive test points to the bladder as a source of the pain, especially if KCl instillation reproduces the chief complaint. In two IC treatment trials, the investigators analyzed whether PST results predicted which patients would achieve at least 50% symptom improvement. One trial was for pentosan polysulfate (PPS);13 the other for heparinoid (PPS or heparin) plus a tricyclic antidepressant.42 In both studies, patients with positive and negative PST were equally likely to improve. In contrast to these studies, the potassium sensitivity test was shown to be associated with good reponse to intravesical hyalvronic acid treatment.43
cystoscopy Office cystoscopy with local anesthesia is usually normal in PBS or IC. Its main value is to rule out other intravesical lesions that may cause symptoms. The decision for cystoscopy is based on the level of suspicion for an intravesical process. Indications include hematuria, smoking history, older age, occupational exposure, and
persistent symptoms. Tissot et al. reported that 1% of patients sent to a tertiary care center with the label of ‘IC’ actually had transitional cell carcinoma, most of which were high grade.44 For decades, cystoscopy under anesthesia with bladder distension was thought to be an important diagnostic test for IC. Briefly, the bladder is distended at 80 cm water pressure with the patient under general or spinal anesthesia. In typical cases of IC, multiple submucosal hemorrhages (glomerulations) or bladder ulcers are seen after distension. Recent findings have cast doubt on bladder distension as a diagnostic test for IC. First, glomerulations are seen in some normal women.45 Second, some patients with typical IC symptoms lack glomerulations or ulcer, yet their objective changes (e.g. urine abnormalities, bladder biopsy findings) are similar to the patients who do have glomerulations or ulcer.46 One exception is that patients with glomerulations have higher bladder expression of the angiogenic growth factor platelet-derived endothelial cell growth factor thymidine phosphorylase, compared to patients without glomerulations.47 Currently, the general consensus is that cystoscopy with bladder distension is not required to diagnose IC. By definition, bladder distension is not required to diagnose PBS. The decision for distension is based on the advantages and disadvantages to each patient. The main advantages are:
• psychological benefit of validation if glomerulations • • • • • •
or ulcers are seen; bladder ulcers, if present, can be treated at the same procedure; measuring the capacity under anesthesia helps with prognosis; some patients have an excellent (though temporary) symptom improvement after distension. The main disadvantages are: after the procedure, the symptoms often get worse temporarily (and occasionally long-term); expense; risks of anesthesia.
Bladder biopsy No specific bladder biopsy findings are required to diagnose IC or PBS. Furthermore, no bladder biopsy findings are pathognomonic for IC or PBS. At present, the main value of biopsy is to rule out other conditions (e.g. carcinoma in situ) that may cause symptoms. Some recent treatment trials required specific bladder biopsy findings for entry. For example, bladder 597
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inflammation was required for a cimetidine trial,48 and high mast cell counts were required for a montelukast trial.49 The treatments were beneficial (although only the cimetidine trial was placebo controlled). Since the same treatments were not given to patients who lacked the qualifying biopsy findings, it is not known what their treatment responses would have been. However, future research may identify bladder biopsy features that predict response to specific treatments. This would help to focus treatments more appropriately.
PaInful Bladder Syndrome treatmentS No single treatment is universally effective for IC or PBS. The usual practice is to try different treatments sequentially, starting with the most innocuous and progressing to the most risky. If one treatment is not effective, additional treatments may be either added or substituted, depending on the clinician’s judgment and the patient’s preference. If the new treatment has a different mechanism, then it is usually added rather than substituted, with the rationale that the two treatments may be synergistic. However, published evidence to support either choice (adding versus substituting) is virtually non-existent. This section will review the most commonly used treatments for IC or PBS. Pentosan polysulfate (PPS) and dimethylsulfoxide (DMSO) are approved by the United States Food and Drug Administration (FDA) for IC treatment. For all of the other oral and intravesical medications described below, treatment of PBS or IC is an off-label use.
conservative treatments Many PBS patients find that certain foods or drinks worsen their symptoms. However, not all patients are affected by the same foods, so one cannot prescribe the same diet to all patients. The most practical approach is to make a list of foods that are most commonly stated to increase PBS symptoms. (Many such lists are available on websites or published. The diet suggestions in Table 38.1 are reproduced with permission from the Interstitial Cystitis Association website.) Advise the patient to avoid all of the foods on the list for 1–2 weeks. The patient should then try different foods individually to see which specific food produces symptoms.28,29 For some patients, over-the-counter preparations such as Prelief or Coffee Tamer allow them to tolerate foods that would otherwise increase their symptoms. Another conservative treatment is a bladder holding protocol. This was reported to be effective by two differ-
ent investigators.29 Briefly, the patient starts by completing a voiding diary, and then is instructed to increase the voiding interval gradually. This obviously is not feasible for patients who have severe pain with even small volumes, but it can be beneficial for patients with urgency or milder discomfort with holding. Some patients with PBS have significant improvement after pelvic muscle physical therapy.28–30,50,51 The rationale is that pelvic muscle tension contributes to the symptoms, and tension relief by physical therapy improves symptoms. Although various techniques are available, there is no published evidence to indicate which technique is superior. The effects of other conservative treatments (e.g. heat, ice, specific exercises to do or avoid) vary among different patients. Patients can find advice on diet, exercise, and other self-help measures from the Interstitial Cystitis Association in the USA (www.ichelp.org), and from other national associations including the newly formed Multinational Interstitial Cystitis Association (www.multinationalica.org). The ICA email address is
[email protected] Several over-the-counter treatments are used for PBS, though none is reported to be effective in placebo-controlled trials. The most commonly used ones are quercetin, aloe vera, and chondroitin sulfate, alone or in various combinations. The ICA website gives information about these treatments, including links to order them.
oral medication Pentosan polysulfate PPS is a synthetic glycosaminoglycan that is thought to replace bladder epithelial glycoconjugates.52 However, it also has other effects that may improve IC, such as mast cell stabilization53 and various anti-inflammatory effects.54 PPS was effective in three of four placebocontrolled trials and in a meta-analysis of these trials.29 In contrast, a recent trial compared PPS, hydroxyzine, both or placebo, and showed no significant benefit of PPS.55 However, this trial occurred after PPS was already approved for IC, and it is difficult to enrol patients into a placebo-controlled trial of a drug already available. This problem may have skewed the enrolment, and certainly led to low sample size and low statistical power. A recent study comparing PPS with cyclosporine for IC showed much better symptom relief in the cyclosporine group.56 The usual dose of PPS is 100 mg three times daily, but some patients find this inconvenient because it must be taken on an empty stomach. Alternatives are 100 mg in the morning and 200 mg at bedtime, or 200 mg twice
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table 38.1.
Interstitial cystitis diet suggestions
Product
Avoid
OK to try
Milk/dairy products
Aged cheeses, sour cream, yogurt, chocolate
White chocolate, non-aged cheeses such as cottage or American, frozen yogurt, fresh milk
Vegetables
Fava beans, lima beans, onions, tofu, soy beans, tomatoes
Other vegetables and home-grown tomatoes (which may be less acidic)
Fruits
Apples, apricots, avocados, bananas, cantaloupes, citrus fruits (such as oranges, grapefruits, lemons, limes), cranberries, grapes, nectarines, peaches, pineapples, plums, pomegranates, rhubarb, strawberries and juices made from these fruits
Melons (other than cantaloupes), blueberries, pears
Carbohydrates and grains
Rye and sourdough bread
Other breads, pasta, potatoes, rice
Meats and fish
Aged, canned, cured, processed or smoked meats and fish, anchovies, caviar, chicken livers, corned beef, meats that contain nitrates or nitrites
Other poultry, fish and meat
Nuts
Most nuts
Almonds, cashews, pine nuts
Beverages
Alcoholic beverages (including beer and wine), carbonated drinks (such as sodas), coffee, tea, fruit juices (especially citrus or cranberry juice)
Non-carbonated bottled water, decaffeinated, acid-free coffee and tea, some herbal teas (call 1-800-TEALEAF for information on coffees and teas)
Seasonings
Mayonnaise, ketchup, mustard, salsa, spicy foods Garlic and other seasonings (especially such ethnic foods as Chinese, Indian, Mexican and Thai), soy sauce, miso, salad dressing, vinegar (including balsamic and flavored vinegars)
Preservatives and additives
Benzol alcohol, citric acid, monosodium glutamate (MSG), artificial sweeteners such as aspartame (Nutrasweet) and saccharine, foods containing preservatives and artificial ingredients and colors
–
Miscellaneous
Tobacco, caffeine, diet pills, junk foods, recreational drugs, cold and allergy medicines containing ephedrine or pseudoephedrine, certain vitamins
–
Reproduced with permission from the Interstitial Cystitis Association website, www.ichelp.org.
daily. A study of higher doses (200 or 300 mg three times daily) showed no increase in efficacy.57 It usually takes 3–6 months for symptom improvement to occur. The most common side effects are nausea and diarrhea. Other possible side effects include alopecia and elevated liver enzymes. PPS resembles heparin and has weak anticoagulant activity; however, significant bleeding or bruising is rare.52
Hydroxyzine Hydroxyzine is a H1 histamine receptor antagonist, and also inhibits mast cell activation.29 It was effective for IC in open-label studies, but not in a recent controlled trial.55 However, that trial had limitations as described above. Even without evidence from controlled studies, it is reasonable to try hydroxyzine for PBS. It is inexpensive and has few side effects except sedation. Sedation is
actually beneficial because the drug is given at bedtime, so the sedation helps with sleep difficulties and nocturia. The usual dose is 10 mg at bedtime, increasing as tolerated to 50–100 mg at bedtime. It can take up to 2 months for PBS symptom improvement to occur.
Amitriptyline Amitriptyline has many pharmacologic actions that may benefit PBS.29,52,58 These include H1 receptor blockade, stabilizing mast cells, and sedation (which improves sleep and nocturia). Amitriptyline also has generalized antinociceptive effects, and is used for several different types of chronic pain. Amitriptyline was effective for IC in uncontrolled trials and in a recent placebo-controlled trial.58 The main side effects are sedation, constipation, tachycardia, and weight gain. Some patients are unable to tolerate the sedation. This can be minimized by starting with 599
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a low dose (e.g. 10 mg at bedtime) and increasing gradually as tolerated. Another hint is to take it at dinnertime rather than at bedtime, so it has more time to be metabolized and the patient is not so sedated the next morning.28 The usual dose is 50–75 mg at bedtime, but some patients get significant improvement with lower doses.
Cimetidine The H2 blocker cimetidine was effective in three openlabel trials and one placebo-controlled trial.48 The placebo-controlled trial used a cimetidine dose of 400 mg twice daily, and specifically selected PBS patients who had inflammation on their bladder biopsies. It is not known whether cimetidine would be similarly effective for PBS patients without bladder inflammation. The mechanisms of action are unknown, but may include anti-inflammatory (since T cells have H2 receptors) and stabilization of mast cells (by binding to H2 receptors). By itself, cimetidine has few side effects. However, it has the potential for significant drug interactions. It alters microsomal enzyme systems and reduces hepatic metabolism of several drugs, including warfarin-type anticoagulants, phenytoin, propranolol, theophylline, and some benzodiazepines and tricyclic antidepressants. Patients taking these drugs need to be monitored more closely if they also take cimetidine. No published literature describes treating IC or PBS with other H2 blockers (nizatidine, famotidine, ranitidine), which have few or no drug interactions.
Other oral medications Several oral medications have been described in small open-label trials. These include montelukast,49 nifedipine59 and gabapentin.29 These drugs should not be used as first-line treatments, but may be considered if the usual treatments fail, especially if the patient has another indication for the same drug (e.g. asthma, hypertension, evidence of neuropathic pain). Various immunosuppressive drugs have also been described in small, open-label trials. These include cyclosporine, hydroxychloroquine, and methotrexate.25 In addition, a recent trial described oral prednisolone for the ulcer type of IC.60 These treatments can have significant side effects, but may be considered for patients with the inflammatory type of IC, especially before proceeding to major surgery such as urinary diversion. A second open-label trial of corticosteroids for ulcer-type IC was recently published.61 A recent study comparing PPS with cyclosporine for IC showed much better symptom relief in the cyclosporine group.56
Intravesical medication Intravesical DMSO DMSO has several effects that may improve IC, such as anti-inflammatory, free radical scavenging, and analgesic effects.28,29,62,63 The most common side effect is a garliclike odor after instillation. The usual practice is to instill 50 ml of 50% DMSO weekly for 6 weeks. If the patient has a good response, then biweekly or monthly maintenance is generally used. Patients on long-term DMSO need periodic ophthalmologic examination because DMSO can cause lens opacities. DMSO can be mixed with other ingredients including 5–10,000 units heparin and corticosteroids (either 100 mg hydrocortisone,62 10 mg triamcinolone,63 or 40 mg methylprednisolone64), with or without 44 mEq sodium bicarbonate.62–64 The theoretic advantage is that DMSO acts as a ‘carrier’ and facilitates penetration of the other ingredients into the bladder wall, which may improve their efficacy. However, no published studies have compared DMSO alone versus DMSO with other ingredients. Conversely, no studies have tested whether addition of DMSO improves the efficacy of other instillation treatments.
Intravesical glycosaminoglycans Heparin is thought to benefit IC by improving bladder epithelial glycoconjugates.52 However, it also has several anti-inflammatory actions.65 No placebo-controlled trials of heparin have been published, and no controlled trials regarding dose and frequency. A typical regimen is 10,000 units three times a week.52 Heparin is also a part of most intravesical ‘cocktails’ used to treat IC. One example is 80 mg gentamicin, 10,000 units heparin, 50 ml 0.5% bupivacaine, 50 ml 8.4% sodium bicarbonate, 100 mg hydrocortisone.29 Another is 10–20,000 units heparin, 3 ml 8.4% sodium bicarbonate, and either 10 ml 1% lidocaine or 16 ml 2% lidocaine.52 No published studies have compared different cocktail ingredients or frequencies of administration. The most recent recommendation is 40,000 units heparin, 3 ml 8.4% sodium bicarbonate and 8 ml 1% lidocaine (or 8 ml 2% lidocaine if 1% lidocaine is not effective).66 Hyaluronic acid is another glycosaminoglycan that has been used intravesically for IC.28,29 It also has antiinflammatory effects.29 It is usually given as 40 mg weekly for 4–6 weeks, then monthly for maintenance. It has been effective in small open-label trials, but no placebocontrolled trials have been published.
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Surgical treatments Sacral nerve stimulation Briefly, sacral nerve stimulation involves placing a small wire with stimulating electrodes into the S3 foramen. An external battery is used to stimulate the wire for a trial period, usually 5–10 days. If good symptom improvement occurs, the wire is connected to an internal pulse generator, similar to a pacemaker. The main risks are infection, pain, and migration of the wire with loss of efficacy. It is not feasible to do a placebo-controlled trial because the active wire causes a buzzing or tapping sensation, the location of which is used to confirm the correct wire position. In the United States, sacral nerve stimulation is approved for ‘urinary urge incontinence, urinary retention and significant symptoms of urgency–frequency’. Some patients with PBS or IC fit the latter indication. The published literature currently includes five studies specifically for the indication of IC based on the cystoscopic NIDDK criteria. Three studies were for the 3- to 7-day trial period.67 Rates of significant improvement during the trial were 52%, 73%, and 100% (six of six patients), respectively. Two studies had long-term follow-up (mean 14–15 months) after implanting the internal pulse generator.68,69 In these studies, good relief was maintained throughout the follow-up period for 16 of 17 and 20 of 21 patients, respectively.
Figure 38.1. Interstitial cystitis bladder ulcer (a) before and (b) after treatment with Nd:YAG laser. (Reprinted with permission from Rofeim O, Hom D, Fried RM et al. Use of the neodymium:YAG laser for interstitial cystitis: a prospective study. Journal of Urology 2001;166:134–6.) bladder augmentation without supratrigonal cystectomy has a high failure rate and is not recommended. No published evidence makes it clear which of the above procedures is best. Theoretical considerations include the following:
• If a toxic substance in the urine contributes to the
• •
Bladder ulcer treatment Some IC patients have bladder ulcers (approximately 10% in the USA;12 56% in a Swedish series9). Descriptions of an IC ulcer vary. A typical description is a patch of erythema, which cracks and bleeds after distension. In a recent report, 24 of 24 patients had good symptom relief after fulgurating the ulcer with a neodymium: YAG laser.70 Eleven of these patients had recurrent ulcer and symptoms, but they responded to repeat treatment. The main risk is that the laser energy may penetrate the bladder wall and injure the bowel. Figure 38.1 shows an ulcer before and after laser treatment. Good results have also been described after transurethral resection of the ulcer.71
Bladder substitution or urinary diversion In selected cases where all other options have failed, major surgery can be considered. The options include: 1) conduit diversion leaving the bladder in place; 2) conduit with cystectomy; 3) continent diversion with or without cystectomy; or 4) cystectomy with orthotopic bladder replacement (some authors advocate sparing the trigone and ureteral orifices for this procedure). Simple
•
pathophysiology of IC, then a continent diversion or orthotopic replacement has a higher risk of recurrent IC than a conduit. If the pain comes only from having urine in the bladder, then a simple diversion without cystectomy can give effective relief. In some cases, the pain may be neuropathic rather than from the bladder itself; if so, then pain may persist even after cystectomy. If an orthotopic bladder replacement is planned, opinions differ about preserving versus removing the trigone. If the trigone is removed, the patient is more likely to require intermittent catheterization;72 if the trigone is preserved, it may be a source of persisting pain.73,74
Published evidence does give advice regarding patient selection for these procedures. For example, if planning a cystectomy and orthotopic bladder substitution, better results are associated with the ulcer type of IC,75 smaller bladder capacity under anesthesia,72,75 and not having the urethra as the main site of pain.74 For urinary diversion, the best results occur in patients with a small bladder capacity under anesthesia,76,77 no neuropathic pain,76 and a favorable psychological profile.76
referenceS 1. Abrams P, Cardozo L, Fall M et al. The standardisation of terminology in lower urinary tract function: report from
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the standardisation sub-committee of the International Continence Society. Neurourol Urodyn 2002;21:167–78.
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20. Keay S, Zhang CO, Baldwin BR et al. Polymerase chain reaction amplification of bacterial 16s rRNA genes from cold-cup biopsy forceps. J Urol 1998;160:2229–31. 21. Burkhard FC, Blick N, Hochreiter WW et al. Urinary urgency and frequency, and chronic urethral and/or pelvic pain in females. Can doxycycline help? J Urol 2004;172:232–5. 22. Potts JM, Ward AM, Rackley RR. Association of chronic urinary symptoms in women and Ureaplasma urealyticum. Urology 2000;55:486–9. 23. Schilling JD, Mulvey MA, Hultgren SJ. Dynamic interactions between host and pathogen during acute urinary tract infections. Urology 2001;57(Suppl 6A):56–61. 24. Richardson JD, Vasko MR. Cellular mechanisms of neurogenic inflammation. J Pharm Exp Ther 2002;302:839–45. 25. Sairanen J, Forsell T, Ruutu M. Long-term outcome of patients with interstitial cystitis treated with low dose cyclosporine A. J Urol 2004;171:2138–41. 26. van de Merwe JP, Yamada T, Sakamoto Y. Systemic aspects of interstitial cystitis, immunology and linkage with autoimmune disorders. Int J Urol 2003;10:S35–8. 27. Butrick CW. Interstitial cystitis and chronic pelvic pain: new insights in neuropathology, diagnosis and treatment. Clin Obstet Gynecol 2003;46:811–23. 28. Moldwin RM. The Interstitial Cystitis Survival Guide. Oakland, CA: New Harbinger Publications, 2000. 29. Lukban JC, Whitmore KE, Sant GR. Current management of interstitial cystitis. Urol Clin North Am 2002;29:649–60. 30. Weiss JM. Pelvic floor myofascial trigger points: manual therapy for interstitial cystitis and the urgency–frequency syndrome. J Urol 2001;166:2226–31. 31. Driscoll A, Teichman JMH. How do patients with interstitial cystitis present? J Urol 2001;166:2118–20. 32. Porru D, Politano R, Gerardini M et al. Different clinical presentation of interstitial cystitis syndrome. Int Urogynecol J 2004;15:198–202.
15. Theoharides TC, Kempuraj D, Sant GR. Mast cell involvement in interstitial cystitis: a review of human and experimental evidence. Urology 2001;57(Suppl 6A):47–55.
33. Aspera AM, Rackley RR, Vasavada SP. Contemporary evaluation and management of the female urethral diverticulum. Urol Clin North Am 2002;29:617–24.
16. Elbadawi A. Interstitial cystitis: a critique of current concepts with a new proposal for pathologic diagnosis and pathogenesis. Urology 1997;49(Suppl 5A):14–40.
34. Duldulao KE, Diokno AC, Mitchell B. Value of urinary cytology in women presenting with urge incontinence and/or irritative voiding symptoms. J Urol 1997;157:113–16.
17. Warren JW, Horne LM, Hebel JR et al. Pilot study of sequential oral antibiotics for the treatment of interstitial cystitis. J Urol 2000;163:1685–8.
35. Mazurick CA, Landis JR. The Interstitial Cystitis Data Base Study Group. Evaluation of repeat daily voiding measures
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in the national Interstitial Cystitis Data Base study. J Urol 2000;163:1208–11. 36. Kirkemo A, Peabody M, Diokno AC et al. Associations among urodynamic findings and symptoms in women enrolled in the Interstitial Cystitis Data Base (ICDB) study. Urology 1997;49(Suppl 5A):76–80. 37. Perez-Marrero R, Emerson L, Juma S. Urodynamic studies in interstitial cystitis. Urology 1987;29(Suppl 4):27–30. 38. Irwin PP, Takei M, Sugino Y. Summary of the urodynamics workshops on IC, Kyoto, Japan. Int J Urol 2003;10: S19–23.
51. Doggweiler-Wiygul R, Wiygul JP. Interstitial cystitis, pelvic pain, and the relationship to myofascial pain and dysfunction: a report on four patients. World J Urol 2002;20:310–14. 52. Dell JR, Parsons CL. Multimodal therapy for interstitial cystitis. J Reprod Med 2004;49(Suppl 3):243–52. 53. Chiang G, Patra P, Letourneau R et al. Pentosan polysulfate inhibits mast cell histamine secretion and intracellular calcium ion levels: an alternative explanation of its beneficial effect in interstitial cystitis. J Urol 2000;164:2119–25.
39. Parsons CL, Greenberger M, Gabal L et al. The role of urinary potassium in the pathogenesis and diagnosis of interstitial cystitis. J Urol 1998;159:1862–7.
54. Elliot SJ, Zorn BH, Mcleod DG et al. Pentosan polysulfate decreases prostate smooth muscle proliferation and extracellular matrix turnover. Prostate Cancer Prostatic Dis 2003;6:138–42.
40. Chambers GK, Fenster HN, Cripps S et al. An assessment of the use of intravesical potassium in the diagnosis of interstitial cystitis. J Urol 1999;162:699–701.
55. Sant GR, Propert KJ, Hanno PM et al. A pilot clinical trial of oral pentosan polysulfate and oral hydroxyzine in patients with interstitial cystitis. J Urol 2003;170:810–15.
41. Gregorie M, Liandier F, Naud A et al. Does the potassium stimulation test predict cystometric, cystoscopic outcome in interstitial cystitis? J Urol 2002;168:556–7.
56. Sairanen J, Tammela TL, Leppilahti M et al. Cyclosporine A and pentosan polysulfate sodium for the treatment of interstitial cystitis: a randomized comparative study. J Urol 2005;174:2235–8.
42. Teichman JMH, Nielsen-Omeis BJ. Potassium leak test predicts outcome in interstitial cystitis. J Urol 1999;161:1791–6. 43. Gupta SK, Pidock L, Parr NJ. The potassium sensitivity test: a predictor of treatment response in interstitial cystitis. BJU Int 2005;96:1063–6. 44. Tissot WD, Diokno AC, Peters KM. A referral center’s experience with transitional cell carcinoma misdiagnosed as interstitial cystitis. J Urol 2004;172:478–80. 45. Waxman JA, Sulak PJ, Kuehl TJ. Cystoscopic findings consistent with interstitial cystitis in normal women undergoing tubal ligation. J Urol 1998;160:1663–7. 46. Erickson DR, Tomaszewski JE, Kunselman AR et al. Do the National Institute of Diabetes and Digestive and Kidney Diseases cystoscopic criteria associate with other clinical and objective features of interstitial cystitis? J Urol 2005;173:93–7. 47. Tamaki M, Saito R, Ogawa O et al. Possible mechanisms inducing glomerulations in interstitial cystitis: relationship between endoscopic findings and expression of angiogenic growth factors. J Urol 2004;172:945–8. 48. Thilagarah R, Witherow R O’N, Walker MM. Oral cimetidine gives effective symptom relief in painful bladder disease: a prospective, randomized, double-blind placebocontrolled trial. BJU Int 2001;87:207–12.
57. Nickel JC, Barkin J, Forrest J et al. Randomized, doubleblind, dose-ranging study of pentosan polysulfate sodium (PPS) for interstitial cystitis. Urol 2005;65:654–8. 58. van Ophoven A, Pokupic S, Heinecke A et al. A prospective, randomized, placebo controlled, double-blind study of amitriptyline for the treatment of interstitial cystitis. J Urol 2004;172:533–6. 59. Fleischmann JD, Huntley HN, Shingleton WB et al. Clinical and immunological response to nifedipine for the treatment of interstitial cystitis. J Urol 1991;146:1235–9. 60. Hosseini A, Ehren I, Wikllund NP. Nitric oxide as an objective marker for evaluation of treatment response in patients with classic interstitial cystitis. J Urol 2004;172:2261–5. 61. Soucy F, Gregoire M. Efficacy of prednisone for severe, refractory ulcerative interstitial cystitis. J Urol 2005;173:841–3. 62. Parkin J, Shea C, Sant GR. Intravesical dimethyl sulfoxide (DMSO) for interstitial cystitis – a practical approach. Urology 1997;49(Suppl 5A):105–7. 63. Pontari MA, Hanno PM, Wein AJ. Logical and systematic approach to the evaluation and management of patients suspected of having interstitial cystitis. Urology 1997;49(Suppl 5A):114–20.
49. Bouchelouche K, Nordling J, Hald T et al. The cysteinyl leukotriene D4 receptor antagonist montelukast for the treatment of interstitial cystitis. J Urol 2001;166:1734–7.
64. Ghoniem GM, McBride D, Sood OP et al. Clinical experience with multi-agent intravesical therapy in interstitial cystitis patients unresponsive to single-agent therapy. World J Urol 1993;11:178–82.
50. Oyama IA, Rejba A, Lukban JC et al. Modified Thiele massage as therapeutic intervention for female patients with interstitial cystitis and high-tone pelvic floor dysfunction. Urology 2004;64:862–5.
65. Elsayed E, Becker RC. The impact of heparin compounds on cellular inflammatory responses: a construct for future investigation and pharmaceutical development. J Thromb Thrombolysis 2003;15:11–18.
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66. Parsons CL. Successful downregulation of bladder sensory nerves with combination of heparin and alkalinized lidocaine in patients with interstitial cystitis. Urology 2005;65:45–8. 67. Whitmore KE, Payne CK, Diokno AC et al. Sacral neuromodulation in patients with interstitial cystitis: a multicenter clinical trial. Int Urogynecol J 2003;14:305–9. 68. Comiter CV. Sacral neuromodulation for the symptomatic treatment of refractory interstitial cystitis: a prospective study. J Urol 2003;169:1369–73. 69. Peters KM, Konstandt D. Sacral neuromodulation decreases narcotic requirements in refractory interstitial cystitis. BJU Int 2004;93:777–9. 70. Rofeim O, Hom D, Fried RM et al. Use of the neodymium: YAG laser for interstitial cystitis: a prospective study. J Urol 2001;166:134–6. 71. Peeker R, Aldenborg F, Fall M. Complete transurethral resection of ulcers in classic interstitial cystitis. Int Urogynecol J 2000;11:290–5. 72. Linn JF, Hohenfeller M, Roth S et al. Treatment of intersti-
tial cystitis: comparison of subtrigonal and supratrigonal cystectomy combined with orthotopic bladder substitution. J Urol 1998;159:774–8. 73. Christmas TJ, Holmes SAV, Hendry WF. Bladder replacement by ileocystoplasty: the final treatment for interstitial cystitis. Br J Urol 1996;78:69–73. 74. van Ophoven A, Oberpenning F, Hertle L. Long-term results of trigone-preserving orthotopic substitution enterocystoplasty for interstitial cystitis. J Urol 2002;167:603–7. 75. Peeker R, Aldenborg F, Fall M. The treatment of interstitial cystitis with supratrigonal cystectomy and ileocystoplasty: difference in outcome between classic and nonulcer disease. J Urol 1998;159:1479–82. 76. Lotenfoe RR, Christie J, Parsons A et al. Absence of neuropathic pelvic pain and favorable psychological profile in the surgical selection of patients with disabling interstitial cystitis. J Urol 1995;154:2039–42. 77. Hohenfeller M, Linn J, Hampel C et al. Surgical treatment of interstitial cystitis. In: Sant GR (ed) Interstitial Cystitis. Philadelphia: Lippincott-Raven, 1997; 223–33.
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39 The neuropathology of chronic pelvic pain Ursula Wesselmann
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INTRODUCTION Chronic pelvic pain syndromes belong to the category of visceral pain. Pelvic pain is a debilitating problem that can significantly impair the quality of life of a woman. Patients with chronic pelvic pain are usually evaluated and treated by gynecologists, urologists, gastroenterologists, and internists. Although these patients seek medical care because they are looking for help to alleviate their pelvic discomfort and pain, in clinical practice much emphasis has been placed on finding a specific etiology and specific pathologic markers for pelvic disease. These patients typically undergo many diagnostic tests and procedures. However, often the examination and workup remain unrevealing and no specific cause of the pain can be identified. In these cases, it is important to recognize that pain is not only a symptom of pelvic disease, but that the patient is suffering from a chronic pelvic pain syndrome, where ‘pain’ is the prominent symptom of the chronic visceral pain syndrome. This chapter will focus on the neuropathology of chronic non-malignant pelvic pain, a chronic visceral pain syndrome. Knowledge of the neurophysiologic characteristics of visceral pain will guide the physician in making a diagnosis of chronic pelvic pain and in differentiating it from the lump diagnosis of idiopathic pain.1 A basic understanding of neurobiology is paramount to gain further insights into the mechanisms of the pelvic pain disorders and to develop effective clinical management strategies for patients presenting with these syndromes.
ogy, which might not necessarily be the case, and it also excludes cases where pathology is present although not necessarily the cause of pain. In fact, the relationship of pain to the presence of pathology is often unclear in women with chronic pelvic pain. More recently, several medical societies have taken a lead in revising the definition of chronic pelvic pain. The International Continence Society has defined ‘pelvic pain syndrome’ as the occurrence of persistent or recurrent episodic pelvic pain associated with symptoms suggestive of lower urinary tract, sexual, bowel or gynecologic dysfunction in the absence of proven infection or other obvious pathology.4 The European Association of Urology has suggested extending this definition by considering two subgroups based on the presence or absence of well-defined conditions that produce pain.5 In the gynecologic literature, chronic pelvic pain is often referred to as pelvic pain in the same location for at least 6 months. The American College of Obstetricians and Gynecologists has proposed the following definition:6 Chronic pelvic pain is non-cyclic pelvic pain of 6 or more months’ duration that localizes to the anatomic pelvis, anterior abdominal wall at or below the umbilicus, the lumbosacral back, or the buttocks and is of sufficient severity to cause functional disability or lead to medical care. A lack of physical findings does not negate the significance of a patient’s pain, and normal examination results do not preclude the possibility of finding pelvic pathology.
DefINITIONs Of ChRONIC PelvIC PaIN
ePIDemIOlOgy Of ChRONIC PelvIC PaIN
Definitions are important, if a body of reliable information is to be built up in the scientific literature, which will eventually lead to a better understanding of the pathophysiology of chronic pelvic pain. At present, one of the major problems of research into chronic pelvic pain is the lack of agreed definitions, which would allow comparison between studies. On the other hand, the lack of understanding of the pathophysiologic mechanisms of the pelvic pain syndromes makes it difficult to decide on criteria to define chronic pelvic pain conditions. There is no generally accepted definition of chronic pelvic pain. The International Association for the Study of Pain (IASP) defines chronic pelvic pain without obvious pathology as chronic or recurrent pelvic pain that apparently has a gynecologic origin but for which no definitive lesion or cause is found.2 However, the IASP definition for pelvic pain has not been widely used in the literature.3 This definition implies absence of pathol-
Chronic pelvic pain is a common condition. Epidemiologic data from the USA showed that 14.7% of women in their reproductive years reported chronic pelvic pain.7 Extrapolating to the total female population gave an estimated 9.2 million chronic pelvic pain sufferers in the United States alone. Analysis of a large primary care database from the United Kingdom demonstrated that the annual prevalence rate of chronic pelvic pain in women is 38/1000, which is comparable to the prevalence rate of asthma.8 Diagnoses related to the urinary or gastrointestinal tracts were more common than gynecologic causes.9 Despite a high prevalence of pain, many women never had the condition diagnosed.10 Populations at risk of having chronic pelvic pain seem to be women with a history of pelvic inflammatory disease, endometriosis, interstitial cystitis, irritable bowel syndrome, obstetric history, previous abdominopelvic surgery, musculoskeletal disorders and physical and sexual abuse.6
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T10 - L2 CEL
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G
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HG P
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G
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C SA
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Figure 39.1. Innervation of the pelvic area in females. Although this diagram attempts to show the innervation in humans, much of the anatomic information is derived from animal data. (CEL, celiac plexus; DRG, dorsal root ganglion; HGP, hypogastric plexus; IHP, inferior hypogastric plexus; PSN, pelvic splanchnic nerve; PUD, pudendal nerve; SA, short adrenergic projections; SAC, sacral plexus; SCG, sympathetic chain ganglion; SHP, superior hypogastric plexus; Vag, vagina.) (Reproduced from ref. 38 with permission of the International Association for the Study of Pain.)
INNeRvaTION Of The PelvIs Over the last 20 years, the basic neurobiology of the pelvis, despite the complexity of this region of the body, has come to be a reasonably well-developed discipline.11 This section provides an overview of the innervation of the pelvis, which is a prerequisite to understanding the functional mechanisms that might
play a role in the neuropathology of chronic pelvic pain. It is important to note that this summary attempts to derive as much information as possible from investigations involving humans although some generalizations are necessarily taken from animal studies, recognizing that much research in this field is in its infancy. 607
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In general, the pelvis and the pelvic floor are innervated by both divisions of the autonomic nervous system (the sympathetic and parasympathetic), as well as by the somatic and sensory nervous systems. In a broad anatomic view, dual projections from the thoracolumbar and sacral segments of the spinal cord carry out this innervation, converging primarily into discrete peripheral neuronal plexuses before distributing nerve fibers throughout the pelvis (Fig. 39.1). Interactive neuronal pathways routing from higher origins in the brain through the spinal cord add to the complexity of neuronal regulation in the pelvis. The nomenclature of the various plexuses, ganglia and nerves in the pelvic cavity12 is varied and sometimes confusing, presenting designations from both Nomina Anatomica (1977) and clinical usage.13 In this chapter the anatomic nomenclature is provided, and the clinical usage is given in brackets: superior hypogastric plexus (presacral nerve), hypogastric plexus (hypogastric nerve), inferior hypogastric plexus (pelvic plexus), and pelvic splanchnic nerve (pelvic nerve). Within the pelvis, the inferior hypogastric plexus (pelvic plexus) is regarded as the major neuronal integrative center. This plexus is located retroperitoneally adjacent to each lateral aspect of the rectum, with interconnections between the left and right inferior hypogastric plexuses at the posterior aspect of the rectum. It innervates multiple pelvic organs, including the urinary bladder, proximal urethra, distal ureter, rectum, and internal anal sphincter, as well as genital and reproductive tract structures.14 The anterior part of the inferior hypogastric plexus, associated with the distal extent of the hypogastric plexus (hypogastric nerve), is referred to as the paracervical ganglia in females.15 The inferior hypogastric plexus receives sympathetic and parasympathetic input. Sympathetic nerves originate in the thoracolumbar segments of the spinal cord (T10–L2) and condense into the superior hypogastric plexus (presacral nerve) located just inferior to the aortic bifurcation. Preganglionic efferents originate largely in the intermediolateral cell column whereas afferents have their cell bodies located in dorsal root ganglia of these segments. Nerve fibers project from the superior hypogastric plexus as paired hypogastric plexuses (hypogastric nerves) and fuse distally before diverging bilaterally into branches destined for the inferior hypogastric plexuses. Additional sympathetic innervation to pelvic organs may involve preganglionic nerves, which synapse on postganglionic nerves originating in sympathetic chain ganglia; these postganglionic nerves join sacral nerves and course to their destinations via pelvic somatic neuronal pathways.16 Parasympathetic preganglionic
nerve efferents are thought to arise from cell bodies of the sacral parasympathetic nucleus located in the sacral spinal cord (S2–S4) and fuse as the pelvic splanchnic nerve (pelvic nerve) before entering the inferior hypogastric plexus.17 Parasympathetic afferents have cell bodies located in the S2–S4 dorsal root ganglia and course also within the pelvic splanchnic nerve. In addition to its parasympathetic efferent and afferent component, the pelvic splanchnic nerve also receives postganglionic axons from the caudal sympathetic chain ganglia.18 Somatic efferent and afferent innervation to the pelvis is generally understood to involve the sacral nerve roots (S2–S4) and their ramifications. Somatic efferents arise within Onuf’s nucleus situated in the ventral horn of the S2–S4 spinal cord, and afferents reach the dorsal horn with their cell bodies in dorsal root ganglia of these segments.19 Central projections of somatic afferents overlap with pelvic nerve afferents within the spinal cord, which theoretically allows coordination of somatic and visceral motor activity.16 The sacral nerve roots emerge from the spinal cord forming the sacral plexus, from which the pudendal nerve diverges (S2–S3). The pudendal nerve also receives postganglionic axons from the caudal sympathetic chain ganglia. Nociception and pain arising from within the pelvis and pelvic floor involve diverse neuronal mechanisms. In general, sensations from the pelvic viscera are conveyed within the sacral afferent parasympathetic system, with a far lesser afferent supply from thoracolumbar sympathetic origins.20 Receptive fields in the perineum are understood to be carried out primarily by sensory–motor discharges associated with pudendal nerve afferents.20,21 While the interactions of sensory afferents are quite complex, likely possibilities by which these pathways exert effects on autonomic efferent function include mediatory effects on spinal cord reflexes and modulatory effects on efferent release in peripheral autonomic ganglia and in peripheral organs. These neural structures in the periphery comprise the first of numerous relays of sensory neurons, which transmit painful sensations from the abdominal/pelvic cavity to the brain. Traditionally it was thought that ascending pathways for visceral and other types of pain were mainly the spinothalamic and spinoreticular tracts. However, three previously undescribed pathways that carry visceral nociceptive information have been discovered: the dorsal column pathway, the spino(trigemino)-parabrachio-amygdaloid pathway, and the spino-hypothalamic pathway (reviewed in ref. 22). Specifically, the dorsal column pathways play a key role in the processing of pelvic pain, and neurosurgeons have successfully used punctate midline myelotomy to relieve pelvic pain due to
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cancer.23 In addition, descending facilitatory influences may contribute to the development of maintenance of hyperalgesia, thus contributing to the development of chronic pelvic pain.24
DIffeReNCes beTweeN vIsCeRal aND sOmaTIC PaIN Persistent pain of visceral origin is a much greater clinical problem than that from skin, but the overwhelming focus of experimental work on pain mechanisms relates to cutaneous sensation. Until relatively recently, it was often assumed that concepts derived from cutaneous studies could be transferred to the visceral domain. However, there are several reasons to believe that the neural mechanisms involved in pain and hyperalgesia of the skin are different from the mechanisms involved in painful sensations from the viscera.25,26 In contrast to somatic pain, visceral pain cannot be evoked from all viscera and is not always linked to visceral tissue injury (see ‘Visceral nociceptors’, below). In addition, visceral pain tends to be diffuse and poorly localized, whereas somatic pain can be localized exactly. This is due to the fact that the visceral innervation is not as dense as the somatic innervation and that there is an extensive divergence in the central nervous system. Further, visceral pain can be referred to other visceral structures and somatic structures of the same segmental level (see ‘Referred visceral pain mechanisms’, below).
visceral nociceptors and sensitization The existence of visceral nociceptors has been debated for a long time. This is partially due to the difficulty of defining and applying physiologically relevant noxious stimuli to the viscera. Research in animal models of visceral pain has shown that several types of sensory receptor exist in most internal organs, and that different pain states are mediated by different neurophysiologic mechanisms.27 Acute, brief visceral pain appears to be triggered initially by the activation of high-threshold visceral afferents and by the high-frequency bursts that these stimuli evoke in intensity coding afferent fibers, which are afferents with a range of responsiveness in the innocuous and noxious ranges. However, more prolonged forms of visceral stimulation, including those leading to hypoxia and inflammation of the tissue, result in sensitization of high-threshold receptors and the bringing into play of previously unresponsive afferent fibers (silent nociceptors; see below). This increased afferent activity enhances the excitability of central neurons and leads to the development of persistent pain
states. In addition, a special class of C-fiber nociceptors – mechano-insensitive or ‘silent’ nociceptors – has been found in nearly all tissues. They were first described in an animal model of experimental arthritis28 and subsequently in animal models of visceral pain.29 Silent afferents are activated only in the presence of tissue damage or inflammation. Following release of injury products, these previously silent receptors are activated by a wide range of thermal and mechanical stimuli and may also have a background discharge. There are two potential molecular substrates that may play a key role in the peripheral sensitization of nociceptor terminals in viscera: TTX-resistant sodium channels and TRPV1 receptors. Sensory fibers expressing TRPV1 have been demonstrated in patients with rectal hypersensitivity,30 and the TRPV1 expression was correlated positively with the degree of hypersensitivity. In addition, urothelial cells (non-neuronal tissue) have also been shown to express TRPV1 receptors;31 these can be activated by vanilloids to produce the release of ATP, which can then activate P2X3 receptors in sensory afferent fibers.32 This mechanism might account for the enhanced bladder sensitivity observed in interstitial cystitis.
Referred visceral pain mechanisms There are two components of visceral pain, both of which were described more than 100 years ago;33 ‘true visceral pain’ (deep visceral pain arising from inside the body) and ‘referred visceral pain’ (pain that is referred to segmentally related somatic and also other visceral structures). Secondary hyperalgesia usually develops at the referred site.34 A number of explanations have been offered for the existence of referred pain (reviewed in ref. 26). An initial model for interpreting referred pain was based on the idea of viscerosomatic convergence occurring in primary afferent fibers, with multiple branches innervating both viscera and somatic structures. This hypothesis is unlikely, since few branching axons have been found in animal studies. In addition, the hypothesis does not explain the time delay in the evolution of referred pain. Another suggested mechanism for referred pain is that visceral and somatic primary neurons converge onto common spinal neurons. This is the convergence– projection theory. There is considerable experimental evidence for this hypothesis. It offers a ready explanation for the segmental nature of referred pain, but does not address explicitly the issue of hyperalgesia in the referred zone. To interpret ‘referred pain with hyperalgesia’, two main theories have been proposed, which are 609
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not mutually exclusive. The first is known as the convergence–facilitation theory. It proposes that the abnormal visceral input would produce an irritable focus in the relative spinal cord segment, thus facilitating messages from somatic structures. The second theory postulates that the visceral afferent barrage induces the activation of a reflex arc whose afferent branch is presented by visceral afferent fibers and the efferent branch by somatic efferents and sympathetic efferents toward the somatic structures (muscle, subcutis, and skin). The efferent impulses towards the periphery would then sensitize nociceptors in the parietal tissues of the referred area, thus resulting in the phenomenon of hyperalgesia. When examining and treating a woman with chronic pelvic pain it is important to consider both aspects of the pain syndrome (true and referred pain), including the pain deep in the pelvic cavity and pain referred to somatic structures (lower back and legs) and other visceral organs. The mechanisms of referred viscero-visceral pain might explain the substantial overlap observed in epidemiologic studies between chronic pelvic pain and other abdominal symptoms.10,35 Considering the concept of referred visceral pain will allow the physician to look at the global picture of visceral dysfunction, rather than ‘chasing’ one aspect of the visceral pain syndrome out of context.
PhaRmaCOlOgIC asPeCTs Despite the fact that it is a very common chronic pain syndrome, very little is known about effective pharmacologic treatment for chronic pelvic pain.36 Controlled clinical trials are desperately needed to design improved pharmacologic treatment strategies. Since epidemiologic data have confirmed the widespread existence of chronic pelvic pain in the female population in the last 10 years, there is growing interest in the pharmaceutical industry to expand basic science and clinical research efforts for this underserved patient population. Despite these limitations and the need for improvement, currently available pharmacologic treatment strategies, which have mainly been evaluated for other chronic pain syndromes (but not specifically for chronic pelvic pain), can be successfully applied to patients with chronic pelvic pain. Several different pharmacologic classes of medication have been demonstrated to be effective in alleviating pain in patients with chronic pain syndromes: non-steroidal anti-inflammatory drugs (NSAIDs), antidepressants, anticonvulsants, local anesthetic antiarrhythmics, and opioids.36,37
The principal guidelines for pharmacologic pain management for chronic pelvic pain are similar to the pharmacologic treatment of other chronic pain states. Although clinical trials and case reports on the pharmacologic management of chronic pain syndromes provide general guidelines as to which drug to choose, currently we have no method to predict which drug is most likely to alleviate pain in a given patient. The goal of pharmacotherapy is to find a medication that provides significant pain relief with minimal side effects. It is important that the patient understands the limitations of this ‘trial and error’ method of prescribing drugs. Adequate trials should be performed for each drug prescribed and only one drug should be titrated at a time, otherwise it is not possible to assess the effects of a certain drug on pain scores. The starting dose should always be the smallest available and titration should occur at frequent intervals, guided by pain scores and side effects. This requires frequent contact between the patient and the pain clinic during the titration period. It is important for the patient and the physician to understand that some side effects actually improve as the patient continues to take the drug for several weeks. If these side effects are not intolerable, the patient should be guided through this period.
ClINICal ImPlICaTIONs As the pathophysiologic mechanisms of visceral pain explored in basic science research provide an explanation for some of the clinical phenomena observed in patients, additional, revived and new concepts of chronic pelvic pain have emerged: 1. a spectrum of different insults might lead to chronic pelvic pain; 2. different underlying pathogenic pain mechanisms may require different pain treatment strategies for patients presenting with pelvic pain; 3. multiple different pathogenic pain mechanisms may coexist in the same patient presenting with chronic pelvic pain, requiring several different pain treatment strategies (perhaps concomitantly) to treat visceral pain successfully.37
aCkNOwleDgmeNTs Ursula Wesselmann is supported by NIH grants DK57315 (NIDDK), DK066641 (NIDDK), HD39699 (NICHD, Office of Research for Women’s Health) and the National Vulvodynia Association.
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RefeReNCes 1. Wesselmann U. Guest Editorial: Pain – the neglected aspect of visceral disease. Eur J Pain 1999;3:189–91. 2. Merskey H, Bogduk N. Classification of chronic pain. Seattle: IASP Press, 1994. 3. Campbell F, Collett BJ. Chronic pelvic pain. Br J Anaesth 1994;73:571–3. 4. Abrams P, Cardozo L, Fall M et al. The standardisation of terminology of lower urinary tract function: report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 2002;21(2):167–78. 5. Fall M, Baranowski AP, Fowler CJ et al. EAU guidelines on chronic pelvic pain. Eur Urol 2004;46(6):681–9. 6. ACOG Practice Bulletin No. 51. Chronic pelvic pain. Obstet Gynecol 2004;103(3):589–605. 7. Mathias SD, Kuppermann M, Liberman RF et al. Chronic pelvic pain: prevalence, health-related quality of life, and economic correlates. Obstet Gynecol 1996;87:321–7. 8. Zondervan KT, Yudkin PL, Vessey MP et al. Prevalence and incidence of chronic pelvic pain in primary care: evidence from a national general practice database. Br J Obstet Gynaecol 1999;106(11):1149–55.
18. de Groat WC. Neurophysiology of the pelvic organs. In: Rushton DN (ed) Handbook of Neuro-urology. New York: Marcel Dekker, 1994; 55–93. 19. Lincoln J, Burnstock G. Autonomic innervation of the urinary bladder and urethra. In: Maggi CA (ed) Nervous Control of the Urogenital System. Chur, Switzerland: Harwood Academic, 1993; 33–68. 20. Jänig W, Koltzenburg M. Pain arising from the urogenital tract. In: Maggi CA (ed) Nervous Control of the Urogenital System. Chur, Switzerland: Harwood Academic, 1993; 525–78. 21. de Groat WC, Booth AM, Yoshimura N. Neurophysiology of micturition and its modification in animal models of human disease. In: Maggi CA (ed) Nervous Control of the Urogenital System. Chur, Switzerland: Harwood Academic, 1993; 227–90. 22. Cervero F, Laird 1999;353:2145–8.
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9. Zondervan KT, Yudkin PL, Vessey MP et al. Patterns of diagnosis and referral in women consulting for chronic pelvic pain in UK primary care. Br J Obstet Gynaecol 1999;106:1156–61.
25. Gebhart GF. Visceral nociception: consequences, modulation and the future. Eur J Anesthesiol 1995;12:24–7.
10. Zondervan KT, Yudkin PL, Vessey MP et al. Chronic pelvic pain in the community – symptoms, investigations, and diagnoses. Am J Obstet Gynecol 2001;184(6):1149–55.
27. Cervero F, Jänig W. Visceral nociceptors: a new world order? Trends Neurosci 1992;15:374–8.
11. Burnett AL, Wesselmann U. History of the neurobiology of the pelvis. Urology 1999;53(6):1082–9. 12. Dail WG. Autonomic innervation of male reproductive genitalia. In: Maggi CA (ed) Nervous Control of the Urogenital System. Chur, Switzerland: Harwood Academic, 1993; 69–101. 13. Baljet B, Drukker J. The extrinsic innervation of the pelvic organs in the female rat. Acta Anat (Basel) 1980;107(3):241–67. 14. Burnstock G. Innervation of bladder and bowel. In: Bock G, Whelan J (eds) Neurobiology of Incontinence, Ciba Foundation Symposium. Chichester: Wiley, 1990; 2–26. 15. Janig W, McLachlan EM. Organization of lumbar spinal outflow to distal colon and pelvic organs. Physiol Rev 1987;67(4):1332–404. 16. McKenna KE, Nadelhaft I. The organization of the pudendal nerve in the male and female rat. J Comp Neurol 1986;248(4):532–49. 17. Nadelhaft I, Booth AM. The location and morphology of preganglionic neurons and the distribution of visceral afferents from the rat pelvic nerve: a horseradish peroxidase study. J Comp Neurol 1984;226(2):238–45.
26. McMahon SB, Dmitrieva N, Koltzenburg M. Visceral pain. Br J Anaesth 1995;75:132–44.
28. Schaible HG, Grubb BD. Afferent and spinal mechanisms of joint pain. Pain 1993;55:5–54. 29. Häbler HJ, Jänig W, Koltzenburg M. A novel type of unmyelinated chemosensitive nociceptor in the acutely inflamed urinary bladder. Agents Actions 1988;25:219–21. 30. Chan CL, Facer P, Davis JB et al. Sensory fibers expressing capsaicin receptor TRPV1 in patients with rectal hypersensitivity and faecal urgency. Lancet 2003;361:385–91. 31. Birder LA, Kanai AJ, DeGroat WC et al. Vanilloid receptor expression suggests a sensory role for urinary bladder epithelial cells. Proc Natl Acad Sci USA 2001;98:13396–401. 32. Caterina MJ. Vanilloid receptors take a TRP beyond the sensory afferent. Pain 2003;105:5–9. 33. Head H. On disturbances of sensation with special reference to the pain of visceral disease. Brain 1893;16:1–113. 34. Giamberardino MA, Vecchiet L. Experimental studies on pelvic pain. Pain Reviews 1994;1:102–15. 35. Alagiri M, Chottiner S, Ratner V et al. Interstitial cystitis: unexplained associations with other chronic disease and pain. Urology 1997;49(Suppl 5A):52–7.
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36. Wesselmann U. Chronic pelvic pain. In: Turk DC, Melzack R (eds) Handbook of Pain Assessment. New York: Guilford Press, 2001; 567–78. 37. Wesselmann U. A call for recognizing, legitimizing and
treating chronic visceral pain syndromes. Pain Forum 1999;8:146–50. 38. Wesselmann U, Burnett AL, Heinberg LJ. The urogenital and rectal pain syndromes. Pain 1997;73:269–94.
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40 Lower urinary tract infections – simple and complex James Gray, Dudley Robinson
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IntroductIon Cystitis is the clinical term used to describe inflammation of the urinary bladder, which occurs in response to lower urinary tract infection. It describes the inflammatory response to microbiologic invasion of the lower urinary tract and includes the clinical symptoms of urinary frequency, urgency, and dysuria. Lower urinary tract infection may be acute, chronic or recurrent as well as being simple or complex. Infection is characterized by large numbers of microorganisms and leukocytes in the urine. The natural history is dependent on the type and virulence of the urinary pathogen, resistance to antimicrobial agents, and host defences. Diagnosis in the majority of simple cases is based on clinical symptoms, preferably together with laboratory confirmation through urine dipstick testing, microscopy, and/or culture. Recurrent or complex lower urinary tract infections may require additional investigations such as imaging of the upper urinary tracts and testing for fastidious microorganisms. Overall, the principles of management are to identify the causative organism and, based on the results of urine culture and sensitivity, to administer an appropriate antimicrobial agent for an appropriate length of time. In those women with recurrent or complex infections, specific strategies may need to be developed to treat the infection adequately. An understanding of the natural history and pathogenesis of lower urinary tract infection can facilitate both primary prevention, through reduction or modification of associated risk factors, and secondary prevention by directing cost-effective screening of women who have an increased susceptibility to urinary tract infection. This chapter examines the epidemiology, etiology, and pathogenesis of urinary tract infections, and reviews the management of women presenting with both simple and complex lower urinary tract infection.
Prevalence Lower urinary tract infection is one of the most common clinical diagnoses in developed countries, accounting for six million consultations a year in the United States1,2 and between 1 and 6% of visits to general practitioners in the UK. Other than in the elderly, urinary tract infection is more common in women than in men. Approximately 50% of women will develop a urinary infection during their lifetime,3 the prevalence being 5% per year.
defInItIons Bacteriuria This has previously been described as less than 10,000 colony forming units (cfu) per milliliter in a clean-catch, freshly voided sample. However, ‘asymptomatic bacteriuria’ (ASB) may be a better term, merely describing the presence of bacteria in the bladder.
Significant bacteriuria The concept of significant bacteriuria was developed by Kass and colleagues in the mid-1950s, on the basis that quantitative culture could help distinguish between the presence of bacteria multiplying in the urine and bacteria introduced as contaminants from the urethra or introitus during voiding of a midstream sample of urine (MSU). Based on the fact that most urinary tract infections are caused by Escherichia coli and related Gram-negative bacteria that multiply rapidly in urine, significant bacteriuria was defined as a microbial count of greater than 100,000 cfu/ml,4 although even using this criterion a single culture has up to a 20% chance of representing contamination only.5 Following the widespread adoption of quantitative urine cultures, it was noted that 20–40% of women with symptoms of acute urinary tract infection (UTI) have bacterial counts of less than 100,000 cfu/ml. Further evidence that UTI can be associated with bacterial counts of less than 100,000 cfu/ml stems from observations that the species of bacteria isolated from these women are the same as those from women with higher bacterial counts; bacteria can be isolated from urine samples collected directly from the bladder (e.g. by catheterization or suprapubic aspiration), and symptoms often respond to antimicrobial therapy. Some studies have reported that bacterial counts as low as 100 cfu/ml can be associated with symptoms. However, up to 10% of asymptomatic women have bacterial counts of this magnitude in urine. As the bacterial count increases within the range 100– 100,000 cfu/ml, the greater the association with symptoms and in the magnitude of pyuria.6,7 Thus there is no reliable cut-off for bacteriuria to be considered significant, but the importance of bacterial counts of less than 100,000 cfu/ml should be assessed in the light of symptoms and pyuria. There are various possible explanations for the finding of low level bacteriuria in symptomatic UTI, including concurrent use of antimicrobials or the representation of an early phase of the infection.8
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Asymptomatic bacteriuria This is the term used to describe the condition when there is confirmed bacteriuria but the patient remains asymptomatic. It is found in approximately 5% of young women and increases with age, reaching a prevalence of 22–43% in elderly women. In general, it is not thought to be of clinical significance except in certain clinical circumstances such as pregnancy, instrumentation of the lower urinary tract, and renal transplant patients. It is more likely to be present in those patients with a chronic indwelling catheter.9
recurrent urinary tract infection This is the term used to describe a symptomatic infection which follows the resolution of a previous UTI, generally after treatment. It occurs in up to 26% of women within 6 months of their first UTI6 and in 48% of women who have had a previous infection.7 The ratio of recurrent lower UTI to pyelonephritis has been estimated to range between 18:18 to 28:1.10 Overall, approximately 20–40% of women who experience a UTI develop recurrent infections11 and 10–15% of women over the age of 60 complain of frequent recurrences.12 Recurrent infection may be due to relapse of the original organism or to reinfection with the same or a different organism. Relapse is defined as recurrence of bacteriuria with the same organism within 7 days of treatment and implies failure to eradicate the infection. In contrast, if bacteriuria is absent after treatment for 14 days or longer, and it is then followed by recurrence of infection with the same or a different organism, this is considered to represent reinfection. Risk factors for recurrent infection are shown in Table 40.1. Around 80–90% of recurrent infections are due to reinfections, with one-third being with the same organism.10 While recurrent infections are relatively common in adult women, they are rarely accompanied by upper tract dysfunction such as reflux, renal scarring or renal hypertension.
complicated lower urinary tract infections This describes infections that are related to other conditions (Table 40.2). One of the most common forms of complicated UTI is related to the use of catheterization. The incidence of bacteriuria associated with an indwelling urinary catheter is 3–10% per day, duration of catheterization being the most important risk factor for infection. While fewer than 5% of catheter-associated UTIs result in bacteremia, they are nevertheless a significant cause of morbidity, and are increasingly
table 40.1.
• • • • • • • • • •
Risk factors for recurrent urinary tract infection
Lower urinary tract obstruction and chronic retention of urine Bladder stones or intravesical foreign bodies Trauma Enterovesical and vesicovaginal fistulae Urethral diverticulae Malformations of the urinary tract Cystocele Vesicoureteric reflux Infected paraurethral glands Contraceptive diaphragm use
table 40.2.
Conditions associated with complicated lower urinary tract infection
1. Structural • Urolithiasis • Malignancy • Ureteric stricture • Urethral stricture • Bladder diverticulae • Renal cysts • Fistulae • Urinary diversions 2. Functional • Neurogenic bladder • Vesicoureteric reflux • Voiding difficulties (incomplete bladder emptying) 3. Foreign bodies • Indwelling catheter • Ureteric stent • Nephrostomy tube 4. Other • Diabetes mellitus • Pregnancy • Renal failure • Renal transplant • Immunosuppression • Multidrug resistance • Hospital-acquired (nosocomial) infection
being seen as an important reservoir of antibiotic-resistant bacteria in hospitals and nursing homes. Although pregnant women are not at greater risk of ASB, unless such women are treated, there is an increased risk of perinatal complications such as premature delivery and developing a symptomatic infection and pyelonephritis in later pregnancy.
PathogenesIs The urinary tract is usually sterile above the level of the distal urethra although bacteria do gain access to the bladder, generally from neighboring sites. The 615
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fecal–perineal–urethral route of infection is well documented. E. coli is the main causative organism, with the rectal flora serving as the main reservoir.13 Other sites include the bowel, perineum, vaginal vestibule, urethra, and paraurethral tissues. Ascending infection along the urethra is the most commonly occurring symptom, and may be spontaneous or facilitated by sexual intercourse or catheterization. Meatal colonization occurs, mediated by fimbriae and specific receptor proteins in the epithelial cells in the region of the external meatus. The periurethral area is heavily colonized with bacteria, and these ascend the urethra to enter the bladder and adhere to the urothelium.14 The method of entry is not fully understood although it has been proposed that bacteria may reflux into the bladder following a void, may ascend against the urinary stream because of turbulent flow, or may milk back into the bladder.15 However, these factors alone do not necessarily stimulate infection within the bladder and it has been demonstrated that even virulent organisms require some degree of host susceptibility.16 Consequently, it would appear that there is a relationship between host factors (determining susceptibility) and the characteristics of urinary pathogens to invade and colonize the bladder, which affect the course and severity of the disease.17 In addition, infection may also be via lymphatic spread or blood-borne on rare occasions.
host defences The bladder has a number of mechanisms to resist infection. The most important is the hydrokinetic or ‘washout’ effect in which diuresis and voiding dilute the bacterial load and wash away infecting organisms. In one study, 40% of women with bacteriuria became free of infection spontaneously within 12 months18 while a further study demonstrated that the urine of 80% of women with simple infections became sterile on placebo alone.19 Consequently, the risk of infection will depend on the size and multiplication rate of the organism in addition to the urinary residual, urine flow rate, and frequency of voiding.
Microbiologic factors The mechanism by which uroepithelial cells of the bladder resist ascending infection remains poorly understood although it has been demonstrated that activation of uroepithelial cell defense and suppression of bacterial growth depend on direct contact between the two. The composition of urine within the bladder may also have
an effect on bacterial growth with extremes of urine pH, high osmolality, and high urea concentration tending to be protective, which is why historically urine has been used as an antiseptic. Urea is the principal antibacterial electrolyte in urine, and its effect is also modulated by concentration and the pH.20
epithelial factors The bladder mucosa is also thought to have a bactericidal action although the cells themselves are not phagocytic. In addition, it has been postulated that nitric oxide may have a role in bladder wall inflammation and host defense. Nitric oxide produced locally in the bladder has a cytotoxic effect and may contribute as a host defense mechanism within the bladder. Levels of nitric oxide have been found to be 30–50 times higher in all types of cystitis when compared to controls.21 In addition, natural killer cells have been shown to be activated in inflamed urothelium, with increased cytolytic activity enhancing the immunologic defense mechanisms of the bladder.22 The bladder also produces a surface secretion of mucus preventing bacterial adhesion to the bladder wall.23
Immunologic factors Secretory IgA is synthesized by plasma cells within the lamina propria of the bladder wall and hence provides a degree of humoral immunity. In addition, a significant proportion of IgA originates in the urethra and this may help prevent ascending infection.24 Secretory IgA has also been shown to prevent microbial invasion by disrupting bacterial adherence25 and that production of IgA may be deficient in women with recurrent urinary tract infection.26
tamm–horsfall protein Tamm–Horsfall protein, a mucoprotein shed from the renal tubular cells and excreted in the urine, has been demonstrated in concentrated urine by electrophoresis.27 This uromucoid protein can bind and trap E. coli, thus providing a natural defense mechanism.28 Levels of antibodies to this protein have been shown to be significantly higher in women with pyelonephritis and vesicoureteric reflux although less is known about the response in uncomplicated lower urinary tract infection.29,30
role of the organIsM Uropathogens have the ability to survive and multiply in the bladder as well as being able to adhere to the blad-
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der epithelium. These unique qualities make them particularly virulent in the lower urinary tract.
terms of congenital anomalies (Table 40.3) and acquired causes (Table 40.4).
adherence
age
The ability of bacteria to adhere to the urothelium of the lower urinary tract is an important initial step in the pathogenesis of lower urinary tract infection. This is supported by the findings of one study in which those women with recurrent urinary tract infections had increased receptivity of urothelial cells for bacteria and increased frequency of vaginal colonization and subsequent infection when compared to a control population.31 Adherence of the organism to the bladder wall triggers an acute inflammatory response by the activation of cytokines. These in turn stimulate the production of an intracellular adhesion molecule, which, by leukocyte adhesion, causes migration of cells to the point of infection.32 These events inadvertently prevent the organism from being ‘washed out’ and, by increasing their nutrient supply, they divide more efficiently.
Among children the incidence of UTI is highest in the first year of life, with a gradual decrease to the lowest rate at 11–15 years of age. In children there is a strong association between recurrent infection and non-neurogenic bladder dysfunction, with one study of urodynamic studies revealing a 44% incidence of detrusor overactivity.36
uropathogen structure The structure of bacteria is also known to be important when considering virulence and pathogenicity. Members of the family Enterobacteriaceae possess an antigenic structure which promotes an antibody immune response and this contributes to the invasiveness and virulence of these bacteria. The outer cell membrane contains O antigens which, together with endotoxins, initiate the immune response in the bladder wall by stimulating cytokine production.33 Capsular (K) antigens on the surface of the bacteria help to inhibit phagocytosis and the actions of IgA and IgG in the urothelium. Pili and fimbriae are found on the outer membrane of uropathogenic bacteria and promote binding using an adhesion molecule on their tip. This is responsible for the binding of the bacterium to the surface of the epithelial cells within the bladder wall. P-fimbriae mediate adherence to the glycolipids in the urothelium34 while Type I fimbriae confer the ability to adhere to the mucus layer within the bladder. In addition, some uropathogens are able to break down bladder mucin and invade the urothelium beneath, and this has been associated with the development of recurrent infections.35
rIsK factors for urInarY tract InfectIon In general, host factors rather than bacterial virulence are probably the most important contributors to lower UTI. These predisposing factors can be considered in
table 40.3.
Congenital risk factors for urinary tract infection
1. Bladder • Vesicoureteric reflux • Ectopic ureters • Obstructive megaureter 2. Pelvis • Pelvic–ureteric junction obstruction 3. CNS • Meningomyelocele • Tethered cord syndrome
table 40.4.
Acquired risk factors for urinary tract infection
1. Traumatic • Surgery (urinary diversion, clam cystoplasty) • Sexual intercourse • Sexual abuse • Foreign bodies (catheters, stents) • Contraceptive diaphragm 2. Inflammatory • Vulvourethritis • Chronic inflammation (TB, syphilis, schistosomiasis) • Interstitial cystitis • Radiotherapy • Fistula 3. Metabolic • Calculi • Diabetes mellitus 4. Drugs • Cyclophosphamide • Tiaprofenic acid 5. Anatomic • Cystocele • Urethral diverticulum 6. Functional • Detrusor hypotonia • Detrusor dyssynergia • Constipation 7. Malignancy • Bladder tumors • Other pelvic tumors (cervix, uterus, ovary)
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The incidence of UTI increases in young adult women, where sexual activity is an important contributory factor, and increases again in old age. The increasing prevalence of lower UTI in old age is most likely to be multifactorial in nature, and is associated with the presence of concomitant systemic disease, increasing immobility, fecal and urinary dysfunction, and instrumentation of the urinary tract. Acute cystitis has been found to be one of the most commonly acquired infections in nursing home residents and is often the most frequent cause for admission to hospital.37
obesity At present there is little evidence to suggest a link between obesity and lower urinary tract infection. In a large study assessing the factors influencing the rate of first referral for urinary infection in 17,032 women, the risk of first infection declined with age, was higher in nulliparous than in parous women, and was higher in the non-obese compared to the obese.38
Behavioral factors There is considerable evidence to suggest that behavioral factors such as voiding habits, diet, clothing, and use of soaps and bubble baths may be associated with the development of urinary tract infections. The use of tampons as opposed to sanitary towels has been associated with an increased risk of infection.39 There is also a strong association with sexual intercourse, with 75–90% of women relating infections to sexual intercourse.40,41 Furthermore, the frequency of intercourse has also been shown to be a significant risk factor42 and certain strains of E. coli may be transmitted between partners.43 Contraceptive usage has also been implicated in the development of urinary tract infections. The contraceptive diaphragm and spermicide creams have been found to be positively associated with the risk of developing urinary tract infections.44 This may be due to the effect of intermittent urethral obstruction for 6–8 hours following intercourse or, alternatively, due to changes in the vaginal flora. In one large study, the main increase in risk in current diaphragm users occurred during the first 24 months when overall rates were two to three times higher in users than non-users.42
Instrumentation of the urinary tract The incidence of lower urinary tract infection following urethral catheterization is approximately 5%, and
a patient has only a 50% probability of remaining free of infection for 4 days following catheterization.45 Following catheter removal the bacteriuria will resolve spontaneously in around a third of cases.46 Suprapubic catheterization provides an alternative method of longor short-term bladder drainage and is associated with lower infection rates. In a meta-analysis of studies comparing suprapubic to urethral catheterization following vaginal surgery, the incidence of bacteriuria ranged from 12.5 to 44.5% in the suprapubic group compared to 37.2–50.7% in the urethral group.47 The suprapubic route also has the advantage that it allows women to void with the catheter in situ and have post-void residuals checked without the need for repeated catheterization. Finally, the rate of urinary tract infection following cystoscopy is approximately 7.5% without interventions.48 As a result, clinicians are increasingly being encouraged to use a single dose of antibiotic prophylaxis such as gentamicin.
voiding dysfunction Incomplete emptying of the bladder is an important cause of UTI in women.49 Voiding dysfunction in women is predominantly secondary to detrusor failure although in a minority of cases it may be associated with outflow obstruction secondary to a pelvic mass, significant urogenital prolapse or surgery. In addition, urodynamic studies have shown that, with increasing age, there is a significant increase in post-void residual and a decrease in urinary flow rates, voided volume, and bladder capacity.50 This would suggest that voiding function deteriorates with age and may be partly responsible for the increased incidence of UTI in the elderly. Voiding dysfunction may also be associated with detrusor hypotonia, detrusor–sphincter dyssynergia, and outflow obstruction secondary to a urethral stricture or previous surgery.
vesicoureteric reflux During a detrusor contraction, if the vesicoureteric valves are incompetent, vesicoureteric reflux may occur. When the detrusor relaxes again, stagnant urine drains back from the upper renal tracts into the bladder which predisposes to infection. In a review of 200 girls with recurrent lower UTI, 43% demonstrated vesicoureteric reflux, whereas in those with only one episode of infection the corresponding rate was 36%.51 These findings would suggest that failure to institute appropriate investigations in children may mean that potentially severe urinary tract abnormalities remain undetected.
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causatIve organIsMs Gram-negative coliform bacilli of the family Enterobacteriaceae are the most common cause of UTI, accounting for over 80% of cases. E. coli is the predominant species in both community and hospital infections, but more antibiotic-resistant species such as Klebsiella and Enterobacter are more common in the latter. Antibiotic-resistant non-coliform Gram-negative bacilli such as Pseudomonas aeruginosa and Acinetobacter species occur almost exclusively in hospital-acquired infections. Among Gram-positive bacteria, Staphylococcus saprophyticus is an important cause of UTI in sexually active women. Other coagulase-negative staphylococci, and S. aureus, are more commonly hospital associated. Fastidious bacteria that can only be isolated on enriched culture media, including Streptococcus pneumoniae and Haemophilus influenzae, are an occasional cause of UTI in primary care. Bacteria that require special detection techniques, such as the cell wall deficient mycoplasma (including Ureaplasma urealyticum) and the obligate intracellular pathogen Chlamydia trachomatis, are also recognized causes of lower urinary tract symptoms. Urinary tract infection can also be caused by microorganisms other than bacteria. Lower UTI due to Candida species is most common in patients with urinary catheters. Cystitis due to viruses such as polyoma and adenoviruses occasionally occurs in immunocompromised patients, especially those who have undergone renal or bone marrow transplantation.
hospital- versus community-acquired infections Community-acquired infections differ from those originating from within the hospital environment52 (Table 40.5) where Klebsiella, Staphylococcus and Pseudomonas are more prevalent.
clInIcal sYMPtoMs Women with lower urinary tract infections typically complain of symptoms of cystitis, these being dysuria, suprapubic discomfort, frequency, and nocturia. There may also be associated microscopic or macroscopic hematuria. Of these women, approximately 30% will also have an upper urinary tract infection which may present as loin pain and tenderness.53 However, only around half of patients in general practice with the typical symptoms of frequency, dysuria, and suprapubic pain are found to have bacteriuria.52 In the elderly, urinary tract infections may present with atypical symptoms such as confusion and falls,54 whereas young children may present with general malaise and pyrexia. Consequently, symptoms
table 40.5.
Common uropathogens in primary care and hospital practice Percentage of isolates in UTI in:
Species
Primary care
Hospital practice
Escherichia coli
70–90
30–60
Proteus mirabilis
5–10
5–10
Klebsiella–Enterobacter spp.
1–5
10–20
Enterococcus spp.
1–5
5–10
Staphylococcus spp.
5–15
5–10
Pseudomonas aeruginosa <1
5–10
Candida spp.
<1
1–10
Other
7.4
1–10
and signs may be unreliable, and in complicated cases or in recurrent infections, it may be necessary to perform investigations to localize the site of infection within the urinary tract.55
InvestIgatIons In primary care the diagnosis of UTI is often made on clinical grounds alone, with or without point-of-care dipstick urinalysis (see below). This approach is reasonable for women with uncomplicated non-recurrent UTIs in whom the etiologic agents and local antibiotic sensitivity patterns can be predicted with reasonable accuracy. There are several reasons why primary care physicians may elect not to send samples to the laboratory, including the advantages of completing the consultation at a single visit, and the fact that urine samples deteriorate during transport to the laboratory. Urine examination in suspected UTI can include tests of urine for nonspecific markers of urinary infection, as well as tests to establish the microbial etiology and antimicrobial susceptibilities.
Point-of-care diagnosis It is now common practice to investigate urine samples by dipstick testing using test strips that detect leukocyte esterase (produced by segmented neutrophils) and nitrite (produced by most uropathogens by reduction of urinary nitrates). In some primary care settings a positive result is used to confirm UTI, and samples are not sent to the laboratory. In other settings, a negative dipstick test may be used to exclude UTI, avoiding the need to send urine samples to the 619
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laboratory. Dipstick testing performs less well for specific patient groups. In screening pregnant women for asymptomatic bacteriuria (ASB), the sensitivity may be as low as 33.3%,42,43 probably because women with ASB often have low level or absent pyuria. In patients with urinary symptoms associated with low bacterial counts, nitrite testing is of little value, meaning that the sensitivity of combined leukocyte esterase (LE) and nitrite testing may be as low as 25%.39 Although dipstick testing has been reported to be useful in a urodynamics clinic,47 it is probably inadvisable to use it as a replacement for culture in specialist urology or urogynecology clinics.
Microbiologic investigation In the laboratory, urine samples are conventionally investigated by microscopy and culture. Microscopy is mainly used to detect and quantify leukocytes. Gram staining is sometimes useful where there is a clinical need to establish the diagnosis urgently, because the presence of bacteria can be confirmed, and it may be possible to presumptively identify the causative microorganisms on the basis of the Gram stain appearance. Different species of bacteria have differing growth requirements. Media used to culture urine routinely (e.g. CLED, blood and MacConkey agars) are designed to optimize growth of common uropathogens. Figure 40.1 illustrates E. coli, the most common uropathogen, growing on blood agar. Standard culture media do not support the growth of fastidious microorganisms that are occasional causes of UTI. Consideration should be given to further investigation of culture-negative urine samples from women with significant pyuria, especially if this is confirmed on a second sample. However, in the authors’ experience there is little value in further investigating such samples unless the white cell count exceeds 100 per high powered field and antibacterial substances are absent from the urine. There is a wide table 40.6.
range of potential pathogens that require different detection methods (Table 40.6) and have different epidemiologic and clinical risk factors. Liaison between the requesting clinician and the laboratory is essential to ensure optimal investigation.
further investigations In the majority of women with simple acute cystitis there is no need for further investigation. However, some cases (Table 40.7) warrant further investigation in order to exclude an underlying cause. In those women who have recurrent or complicated urinary infections, renal function should be assessed with serum creatinine, urea, and electrolytes. In specific cases it may be helpful to investigate or exclude atypical infections (Mycoplasma hominis,
Figure 40.1.
Escherichia coli growing on blood agar.
Laboratory investigations of sterile pyuria
Sample required
Microorganisms
Test method
MSU
Fastidious bacteria (e.g. S. pneumoniae, Culture on enriched media, e.g. H. influenzae) chocolate agar
MSU
Mycoplasmas, Ureaplasmas
Mycoplasma culture system
Three early morning urine samples
Mycobacterium tuberculosis
Mycobacterial culture
First pass urine or urethral, vaginal or endocervical swab
C. trachomatis
Nucleic acid amplification technique
MSU
Adenoviruses Polyomaviruses
Specialist virologic investigations
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table 40.7.
• • • • • •
Indications for investigation of lower urinary tract infection
Children Proven recurrent urinary tract infection Adults with a childhood history of urinary tract infection Hematuria Persistent infection Failure to respond to antibiotic therapy
Ureaplasma urolyticum and Chlamydia trachomatis). The usual history is of a woman suffering repeated cystitis episodes which improve with antibiotics, but symptoms return as soon as antibiotics are stopped. Often there have been repeated MSUs which demonstrate a sterile pyuria which is interpreted as clear as there is no growth on culture. Women with a history suggestive of voiding dysfunction should be investigated using non-invasive tests to determine urinary flow rate and residual urine. Those who also complain of other lower urinary tract symptoms should be investigated using videocystourethrography in order to exclude underling detrusor overactivity, bladder or urethral diverticulae, and vesicoureteric reflux. While it is generally accepted that assessment of the upper urinary tract is not mandatory in all women with urinary tract infection,56 consideration should be given to further investigation in those patients with a history of recurrent or complex infections. Ultrasound of the upper urinary tract will exclude renal causes such as hydronephrosis or calculi; a postmicturition scan will rule out a significant urinary residual. An alternative is radiologic imaging using an intravenous urogram (IVU), although this involves exposure to ionizing radiation and has not been shown to influence treatment in the majority of cases.57 In addition, a transvaginal ultrasound should be performed to exclude the possibility of a pelvic mass which may be affecting voiding function and therefore predisposes to urinary tract infection. Renal imaging may be useful in women with demonstrated upper urinary tract abnormalities in order to detect or confirm obstructed drainage from the kidney and also to determine differential function between the left and right kidneys or upper and lower poles unilaterally. Dimercaptosuccinic acid (DMSA) scans are generally not indicated in women with acute pyelonephritis where there is a rapid response to antimicrobial therapy, but may be considered when the course of the infection is complicated or protracted.58 Mercaptoacetyl triglycine (MAG3) and technetium-labeled diethyltriaminepentaacetic acid (DTPA) may also be considered in order to
exclude both upper urinary tract obstruction and renal scaring. In those women complaining of recurrent UTI, cystoscopy should be considered to exclude an intravesical lesion and a bladder biopsy to exclude a chronic or follicular cystitis. Microscopic or frank hematuria should also be considered as an indication for cystoscopy. Cystourethroscopy and bladder biopsy will exclude an intravesical lesion such as a bladder tumor and also anomalies such as diverticulae and calculi. A bladder biopsy may show evidence of chronic follicular or interstitial cystitis.
treatMent Management of lower urinary tract infection is aimed at treating the current infection and preventing further recurrences (Table 40.8).
general measures – prophylaxis Primary prevention consists of general advice regarding hygiene, fluid intake, and frequency of voiding. In women complaining of recurrent infections related to sexual intercourse, postcoital voiding should be encouraged. They should also be advised to avoid using a diaphragm or condoms with nonoxynol-9 as both of these may increase the risk of recurrent infection. Appropriate advice regarding bladder emptying such as timed voiding or double voiding may also help those with mild voiding difficulties. Should these not be successful, then self-catheterization or a long-term suprapubic catheter may be the only option. Anecdotal support of the use of α-blockers or calcium channel blockers helping in isolated cases could be mentioned.
general measures – treatment Patients with cystitis should be encouraged to increase their fluid intake in order to achieve a short voiding interval and a high flow rate which will help to dilute and flush out the infecting organism. Symptomatic
table 40.8.
• • • • • • •
Aims of treatment
Symptomatic relief Clinical cure Microbiologic cure Detection of predisposing factors Prevention of upper urinary tract involvement Management of recurrence Prevention of recurrence
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relief may be provided by using potassium citrate preparations. With such measures spontaneous remission of symptoms may occur in up to 40% of women.59 Cranberry juice has also been shown to be preventive for lower urinary tract infections. Regular intake of at least 300 ml/day has been associated with a reduced risk of urinary tract infections. The incidence of bacteriuria in those taking cranberry juice was 42% of that in the control group; they were also found to be four times more likely to clear bacteria spontaneously.60 Cranberry juice is thought to act by reducing bacterial adherence to the bladder wall.
antIMIcroBIals When treating urinary tract infections, an antimicrobial that has an appropriate spectrum of activity, a low risk of promoting the emergence or spread of antibiotic resistance, and achieves a high concentration within the urinary tract, should be selected (Table 40.9). Where the pathogen is known, narrow spectrum therapy can be used. Broader spectrum therapy may be necessary for empiric treatment, especially for hospital-associated infections, but in such cases consideration should be given to switching to a narrower spectrum agent once the pathogen has been identified. Ideally, drugs should be reliably absorbed after oral administration, safe and well-tolerated. Undue emphasis is often placed on the distinction between bactericidal and bacteriostatic antibiotics. In most cases it makes no difference to outcome. However, bactericidal antibiotics are preferred on theoretical grounds for patients with immunodeficiencies. Of the antibiotics commonly used to treat UTIs, the β-lactam antibiotics and fluoroquinolones are the most reliably bactericidal.
Individual antibiotics Amoxicillin Amoxicillin is a derivative of ampicillin that has a similar antibacterial spectrum, but is better and more reliably
table 40.9.
• • • • • • •
Choice of antimicrobial agent
Specificity for the urinary tract High levels of drug in the urine Broad spectrum of activity Safe and efficacious Rapid and complete absorption Minimal effect on normal bowel reservoir and vaginal flora Bactericidal for known pathogens
absorbed. These drugs are no longer recommended as first line empiric therapy for UTIs because of the high prevalence of resistance amongst Enterobacteriaceae. Co-amoxiclav is a mixture of amoxicillin and clavulanic acid that inhibits the β-lactamase enzymes produced by many amoxicillin-resistant bacteria. Coamoxiclav has a spectrum of antibacterial activity that is often unnecessarily broad for treating UTIs, and is notoriously associated with pseudomembranous enterocolitis in the elderly.
Cephalosporins First generation cephalosporins have a spectrum of activity that encompasses most community-associated uropathogens. However, they are not active against enterococci, Enterobacter and Pseudomonas, and therefore may be less suitable for use in complex UTIs. Although serum levels of first generation cephalosporins are poor after oral administration, they appear in high concentrations in urine. For treating UTIs the newer and more expensive second generation oral cephalosporins offer little or no benefits over the earlier (and cheaper) cephalosporins.
Trimethoprim Trimethoprim is now widely used as first line empiric therapy for UTIs; however, resistance is increasing, even in the community. Trimethoprim is best avoided in pregnancy (especially first trimester), because of the theoretical risk of teratogenicity. Co-trimoxazole is a mixture of trimethoprim and sulfamethoxazole, which rarely offers any benefits over trimethoprim but has a higher risk of side effects. The UK Committee for Safety of Medicines recommends that co-trimoxazole should be used only where there is good bacteriologic evidence of benefit over trimethoprim.
Tetracyclines Tetracyclines have a spectrum of activity that covers most uropathogens, including atypical microorganisms. Other than doxycycline and minocycline, they are excreted mainly in the urine. However, they are little used for treating UTIs because widespread use of tetracyclines in the past was associated with rapid emergence of resistance. Tetracyclines are deposited in growing bones and teeth, and are contraindicated in pregnancy, breastfeeding women, and children aged less than 12 years.
Fluoroquinolones Fluoroquinolones such as ciprofloxacin, ofloxacin, and norfloxacin are predominantly active against Gram-neg-
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ative bacteria. They are the only orally available drugs with activity against P. aeruginosa. Because high drug concentrations occur in urine, they may be effective in UTIs due to Gram-positive bacteria, although they are not the recommended first line therapy for these infections. They are contraindicated in pregnancy, and recommended for use in children only where there is no alternative. Nalidixic acid is an older quinolone antibiotic that is inactive against P. aeruginosa, and is now little used.
transferred between species and are frequently associated with genes conferring resistance to other antibiotic classes, such as quinolones and aminoglycosides. Community-acquired UTIs with ESBL-producing bacteria that are resistant to all oral antibiotics are already being encountered. There may be some local variation in antibiotic resistance patterns amongst uropathogens. Table 40.10 summarizes the activity of oral antibiotics against common uropathogens.
Nitrofurantoin
duration
Nitrofurantoin appears in high concentrations in urine, but serum and tissue levels are subtherapeutic. It is therefore only useful for treating lower urinary tract infections. Because it has a complex mode of action, acquired resistance to nitrofurantoin is uncommon. Nitrofurantoin is notoriously associated with nausea, but this can often be contained by taking the drug with food. Nitrofurantoin is safe during pregnancy, but is contraindicated at term because of the risk of causing neonatal hemolysis.
Azithromycin Azithromycin is a macrolide-like antibiotic that is not excreted in the urine, nor does its spectrum of activity encompass most common uropathogens. However, it is effective in treating genital chlamydial infections after single dose therapy, and there are anecdotal reports that longer courses of treatment have been successful in treating refractory urogenital mycoplasma infections.
antIBIotIc resIstance Patterns antibiotic sensitivities Antibiotic resistance in bacteria causing UTI is a growing problem both in hospitals and in the community. Amoxicillin resistance is now prevalent in E. coli and other Enterobacteriaceae, and resistance to trimethoprim is increasing. Most isolates in the community remain susceptible to cephalosporins and co-amoxiclav, although this is not the case in hospitals where cephalosporinase-producing species such as Enterobacter are more common. The recent emergence and spread of plasmid-borne extended-spectrum β-lactamases (ESBLs) that confer resistance to penicillins and cephalosporins in Enterobacteriaceae and other Gram-negative bacteria represent a considerable threat for the future. The genes encoding these enzymes are readily
Compliance with therapy may be improved by using shorter courses of antimicrobial therapy or ideally by using a single dose regimen. This also has the advantage of reducing the effect on fecal and vaginal flora, and may help in reducing the emergence of resistant organisms. A large number of studies have assessed the use of single dose therapy61 and found it to be as effective as a short-term (3 day) regimen.62 Trimethoprim or a fluoroquinolone (ciprofloxacin, norfloxacin or ofloxacin) is the preferred single dose agent; amoxicillin has been shown to be less effective. There is no evidence to show that protracted courses are more effective in uncomplicated lower UTIs in adult women.
estrogens Estrogen therapy has been shown to increase vaginal pH and reverse the microbiologic changes that occur in the vagina following the menopause.63 Initial small uncontrolled studies using oral or vaginal estrogens in the treatment of recurrent urinary tract infection appeared to give promising results;64,65 unfortunately, this has not been supported by larger randomized trials. Several studies have been performed examining the use of oral and vaginal estrogens although these have had mixed results. Kjaergaard and colleagues66 compared vaginal estriol tablets with placebo in 21 postmenopausal women over a 5-month period and found no significant difference between the two groups. However, a subsequent randomized, double-blind, placebo-controlled study assessing the use of estriol vaginal cream in 93 postmenopausal women during an 8-month period did reveal a significant effect.67 Kirkengen et al. randomized 40 postmenopausal women to receive either placebo or oral estriol and found that although initially both groups had a significantly decreased incidence of recurrent infections, after 12 weeks estriol was shown to be significantly 623
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++
++
–
–
–
+++
++
++
+
–
–
–
–
E. coli
Proteus
Klebsiella
Enterobacter
P. aeruginosa
Streptococci
Enterococci
S. saprophyticus
Other coagulasenegative staphylococci
S. aureus (meticillin-sensitive; MSSA)
S. aureus (meticillin-resistant; MRSA)
Mycoplasmas
C. trachomatis –
–
–
+++
+
+++
–
+++
–
–
++
+++
+++
First generation cephalosporins
–
–
–
+++
+
+++
–
+++
–
–
+++
+++
+++
Second generation cephalosporins
–
–
–
+++
+++
++
+++
–
–
+++
+++
+++
Co-amoxiclav
–
–
++
+++
+
++
++
++
–
++
++
++
++
Trimethoprim
++
++
+
++
+
++
–
–
+++
+++
+++
+++
+++
Fluoroquinolones
+++, >90% isolates sensitive; ++, 51–90% isolates sensitive; +, 10–50% isolates sensitive; –, <10% isolates sensitive.
Amoxicillin
Expected antibiotic susceptibilities of common uropathogens
Species
table 40.10.
–
–
+++
+++
++
+++
++
+++
–
+++
+++
–
+++
Nitrofurantoin
+++
++
++
+++
++
+++
++
+++
–
++
++
++
++
Tetracyclines
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more effective.68 These findings, however, were not confirmed subsequently in a trial of 72 postmenopausal women with recurrent urinary tract infections randomized to oral estriol or placebo. Following a 6-month treatment period and a further 6-month follow-up, estriol was found to be no different from placebo.69 More recently, a randomized, open, parallel-group study assessing the use of an estradiol-releasing silicone vaginal ring (Estring) in postmenopausal women with recurrent infections has been performed which showed the cumulative likelihood of remaining infection free was 45% in the active group and 20% in the placebo group.70 Estring was also shown to decrease the number of recurrences per year and to prolong the interval between infection episodes.
Prophylaxis Antimicrobials may be used as prophylaxis for recurrent urinary tract infections. Short- and long-term lowdose prophylaxis as well as intermittent and postcoital therapy may be used depending on the clinical situation. The most effective drugs include norfloxacin, nitrofurantoin, and trimethoprim. In addition, cephalexin may be used as effective prophylaxis against recurrent infections in sexually active women. Overall prophylactic therapy has been shown to reduce recurrence rates by up to 95% when compared to placebo, with reinfection rates being reduced from 2 to 3 per patient year to 0.1–0.4 per patient year.71 The idea of single dose treatment of simple (recurrent) infections in susceptible women at a time of increased risk has given rise to some clinicians now using ‘PRN’ antibiotics in women with recurrent infections rather than low dose continual therapy.
coMPleX loWer urInarY tract InfectIon lower urinary tract infections in pregnancy ASB occurs in 4–7% of pregnancies. It is associated with the development of acute cystitis, pyelonephritis, preterm labor, and low birth weight. The prevalence of bacteriuria in the first trimester of pregnancy is 5–6%, similar to that in non-pregnant women.72 If untreated, up to 30% of women will develop acute cystitis although this can be reduced to 3% with effective treatment.73 Recurrent infections may also be a problem following delivery in women who have had
bacteriuria in pregnancy, occurring in up to 25% of cases.74 The increased susceptibility to lower urinary tract infection in pregnancy may be due to the effects of incomplete bladder emptying and chronic residual urine secondary to the weight of the gravid uterus. Progesterone is also known to increase stasis in the urinary tract by causing ureteric relaxation which will also increase the risk of ascending infections. In addition, bacterial growth is also increased in pregnancy, the bacterial count of E. coli being twice that in non-pregnant women.75 During pregnancy, more serious urinary tract infections follow untreated silent bacteriuria in 25% of women.76 There is also an increased risk of developing pyelonephritis in pregnancy and, of these women, up to 20% may develop serious complications such as septic shock.77 Several authorities have suggested that there may be an association between positive urine cultures for group B streptococci and preterm delivery although this remains unproven. However, an association has been reported between elevated levels of urinary antibacterial antibodies and bacterial antigens and preterm delivery, suggesting that a local inflammatory response to urogenital infection may be important in stimulating preterm labor.78 Treatment of ASB has been shown to reduce preterm delivery.
Treatment The treatment of ASB in pregnancy will lead to a decrease in the risk of cystitis and pyelonephritis, and has been shown to be cost effective.79 Treatment of bacteriuria prevents up to 80% of cases of pyelonephritis and has been shown to be effective in the reduction of preterm labor.80 When treating lower urinary tract infections in pregnancy, penicillins and cephalosporins have been shown to be safe in the first and second trimesters.81 Trimethoprim, since it is a folate antagonist, should be avoided in the first trimester although may be used safely in late pregnancy.82 Conversely, nitrofurantoin is safe in early pregnancy but should be avoided around term when it may cause neonatal hemolytic anemia.83 There is little agreement on the duration of therapy for ASB in pregnancy. Although single dose regimens have been investigated, the shortest course of therapy that appears promising is 3 days, and even here it is recommended that a follow-up culture be undertaken after around 10 days to ensure microbial clearance. Many clinicians still prefer to use conventional treatment courses of 7–10 days. 625
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lower urinary tract infections in the elderly Following the menopause there is a fall in endogenous estrogen levels, resulting in a decrease in lactobacilli colonization of the vagina, a rise in vaginal pH, and a subsequent increase in colonization with uropathogenic bacteria. Bacteriuria has a low predictive value for identifying febrile urinary tract infections in the elderly.84 Persistent bacteriuria has been shown to be common in non-catheterized nursing home residents, with little evidence that it is associated with significant morbidity.85 In part this is because bacteriuria with low virulence Gram-positive bacteria such as enterococci, coagulasenegative staphylococci, and group B streptococci is more common in this age group.86 Consequently, ASB, although very common in the elderly, need not be treated.87 However, it is important to recognize that UTI in the elderly can be associated with systemic symptoms and signs such as fever, confusion, nausea, and vomiting without localizing urinary tract symptoms. With regard to symptomatic infection, the aim of antimicrobial treatment is the relief of symptoms rather than achieving long-term sterility of urine, and it should be noted that the elderly are less likely to be cured by shorter courses of therapy.88
lower urinary tract infections in children Lower urinary tract infection in children should always be investigated in view of the potential for subsequent renal scarring and other sequelae.89 In addition, low bacterial counts, the absence of pyuria or a finding of sterile pyuria are common in the course of acute or chronic cystitis and should not be regarded as insignificant.90 In a large follow-up study of 57,432 children under the age of 15 years and 7143 children under 2 years, it was found that infection is often underdiagnosed and, after a confirmed infection, only a minority of children received imaging for complications and microbiology follow-up to assess cure.91 Vesicoureteric reflux is not usually diagnosed in children until it is complicated by an ascending urinary tract infection. The peak incidence is in early infancy and thus it may be possible to prevent infections by screening newborn babies for familial reflux, the frequency of vesicoureteric reflux in babies of women with a similar history being significantly higher than in the general population.92
Treatment Much of the risk of developing complications following lower urinary tract infections in children is related to
the delay in diagnosis and treatment, and also the lack of suitable imaging. When first diagnosed, 70–80% of girls with bacteriuria have no radiologic evidence of renal scarring,93 whereas children who have a history of acute cystitis but unscarred kidneys after their third birthday have a 1 in 40 risk of developing a scar subsequently. However, after the fourth birthday the risk is almost zero.94 Consequently, efforts to reduce the incidence and severity of renal scarring following cystitis in infancy and childhood should be directed towards rapid diagnosis and early effective treatment. When considering the treatment of children with lower urinary tract infections the choice of antimicrobial should be based on results of urine culture and sensitivity. There is less experience of the efficacy of short course therapy in children, and most pediatricians prefer to use a 7–10 day course of treatment. Where investigation of the urinary tract is undertaken after UTI in childhood, it is normal practice to commence antibiotic prophylaxis until the results of the investigations are known. If vesicoureteric reflux is diagnosed, antibiotic prophylaxis is continued.
catheterization The frequency of catheter-acquired infection increases with the duration of catheterization and the failure to maintain a closed drainage system. Consequently, it is not uncommon that infections with multiple organisms occur in women with long-term indwelling catheters.95 Using interventions such as topical antimicrobials, disinfectants added to the urinary drainage bag, antimicrobial coatings for catheters, or antimicrobial irrigation does not decrease the incidence of catheter-associated infections.96 UK evidence-based guidelines for preventing infections associated with short-term urethral catheters have been published.97 Bacteriuria should be expected in women with longterm catheterization and, if asymptomatic, treatment is generally not justified as it may result in the development of resistant organisms. It is common practice to collect a urine sample for culture at the time of catheter removal, and to treat any infection documented at that time. However, the value of this approach has been questioned. Given that bacteriuria will be common at the time of catheter removal, it is probably more rational to collect a urine sample 24 hours or more after catheter removal if there is clinical suspicion of infection at that time. As an alternative to long-term catheterization, the technique of clean intermittent self-catheterization (CISC) may be considered in women who are able to
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learn the technique. Bacteriuria occurs in up to 61% of women performing long-term CISC although the incidence of significant cystitis is approximately 6%.98 Overall, the incidence of infection was 10.3 per 1000 patient days of CISC during early follow-up and 13.6 per 1000 patient days of CISC over an average of 22 months.99 Evidence, however, would suggest that the use of prophylactic antibiotics does not improve the outcome in women performing CISC and should not be used.
conclusIon Lower urinary tract infection is common in women of all ages. Rigid adherence to Kass’s criteria and the use of standard urine culture techniques lead to significant underdiagnosis of UTI. The continuing emergence and spread of antibiotic-resistant bacteria presents a growing challenge in treating UTI, with options for oral therapy in particular becoming more limited. Liaison between clinicians and their microbiology laboratory is essential to facilitate the diagnosis and management of UTI.
references 1. Griebling TL. Urologic diseases in America project: trends in resource use for urinary tract infections in women. J Urol 2005;173:1281–7. 2. National Centre for Health Statistics: 1985 Summary. National ambulatory medical survey. Adv Data 1985;128:1–8. 3. Asscher AW. Urinary tract infections. J R Coll Physicians Lond 1981;15:232–8. 4. Kass EH. Asymptomatic infections of the urinary tract. Trans Assoc Am Phys 1956;69:56–64. 5. Kass EH. The role of asymptomatic bacteriuria in the pathogenesis of pyelonephritis. In: Quinn EL, Kass EH (eds) Biology of Pyelonephritis. Boston: Little, Brown, 1960; 399–406. 6. Foxman B. Recurring urinary tract infection: incidence and risk factors. Am J Public Health 1990;80:331–3. 7. Ikaheimo R, Siitonen A, Heiskanen T et al. Recurrence of urinary tract infection in a primary care setting: analysis of a 1 year follow up of 179 women. Clin Infect Dis 1996;22:91–9. 8. Stamm WE, McKevitt M, Roberts PL, White NJ. Natural history of recurrent urinary tract infections in women. Rev Infect Dis 1991;13:77–84.
causing recurrent infections – a prospective follow-up of biochemical phenotypes. Clin Nephrol 1992;38:318–23. 11. Mabeck CE. Treatment of uncomplicated urinary tract infection in non-pregnant women. Postgrad Med J 1972;48:69–75. 12. Romano JM, Kaye D. UTI in the elderly: common yet atypical. Geriatrics 1981;36:113–5. 13. Yamamoto S, Tsukamato T, Terai A et al. Genetic evidence supporting the faecal–perineal–urethral hypothesis in cystitis caused by Escherichia coli. J Urol 1997;157:1127–9. 14. Kallenius G, Svenson S, Hulberg H et al. P-fimbriae of pyelonephrogenic Escherichia coli: significance for reflux and renal scarring – a hypothesis. Infections 1983;11:73–6. 15. O’Grady F, Cattell WR. Kinetics of urinary tract infection II. The bladder. Br J Urol 1966;38:156–62. 16. Schlager TA, Whittam TS, Hendley JO et al. Comparison of expression of virulence factors by Escherichia coli causing cystitis and Escherichia coli colonising the periurethra of healthy girls. J Infect Dis 1995;172:772–7. 17. Wisinger DB. Urinary tract infection. Current management strategies. Postgrad Med 1996;100:229–36. 18. Asscher A, Sussman M, Waters W et al. The clinical significance of asymptomatic bacteriuria in the non-pregnant woman. J Infect Dis 1969;120:17–21. 19. Mabeck CE. Uncomplicated urinary tract infections in women. Proc R Soc Med 1971;3:31–5. 20. Schegel J, Cuellar J, O’Dell R. Bactericidal effects of urea. J Urol 1961;86:819–21. 21. Lundberg JO, Ehern I, Jansson O et al. Elevated nitric oxide in the urinary bladder in infectious and noninfectious cystitis. Urology 1996;48:700–2. 22. Natsis K, Toliou T, Stravoravdi P et al. Natural killer cell assay within bladder mucosa of patients bearing transitional cell carcinoma after interferon therapy: an immunohistochemical and ultrastructural study. Int J Clin Pharmacol Res 1997;17(1):31–6. 23. Parsons C, Pollen J, Anwar H et al. Antibacterial activity of bladder surface mucin duplicated in the rabbit bladder by exogenous glycosaminoglycans (sodium pentosampolysulphate). Infect Immun 1980;27:876–81. 24. Burdon D. Immunoglobulins of the urinary tract: discussion on a possible role in urinary tract infection. In: Brumfitt W, Asscher A (eds) Urinary Tract Infection. London: Oxford University Press, 1973; 148–58. 25. Tomasi TB. Mechanisms of immune regulation at mucosal surfaces. Dev Infect Dis 1983;5:5784–92.
9. Raz R. Asymptomatic bacteriuria. Clinical significance and management. Int J Antimicrob Agents 2003;22(Suppl 2):45–7.
26. Riedasch G, Heck P, Rauterberg E et al. Does low urinary IgA predispose to urinary tract infection? Kidney Int 1983;23:759–63.
10. Brauner A, Jacobson SH, Kuhn I. Urinary Escherichia coli
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resis to unconcentrated human urine proteins. Electrophoresis 1997;18:1842–6. 28. Tamm I, Horsfall F. Mucoprotein derived from human protein which reacts with influenza, mumps and Newcastle disease viruses. J Exp Med 1952;95:71–97. 29. Jelakovic B, Benkovic J, Cikes N et al. Antibodies to TammHorsfall protein subunit prepared in vitro in patients with acute pyelonephritis. Eur J Clin Chem Clin Biochem 1996;34:315–7. 30. Hanson LA, Fasth A, Jodal U. Autoantibodies to TammHorsfall protein, a tool for diagnosing the level of urinary tract infection. Lancet 1976;1:226–8. 31. Kozody NL, Harding GK, Nicolle LE et al. Adherence of Escherichia coli to epithelial cells in the pathogenesis of urinary tract infection. Clin Invest Med 1985;8:121–5. 32. Roberts JA. Factors predisposing to urinary tract infections in children. Pediatr Nephrol 1996;10:517–22. 33. Svanborg-Eden C, Korhonen T, Lettler R, Marild S. Pathogenic aspects of bacterial adherence in urinary tract infections. In: Losse H, Asscher A, Lison A (eds) Pyelonephritis, vol IV: Urinary Tract Infection. Stuttgart: Thieme, 1980; 54–9. 34. Domisgue G, Roberts H, Laucirica R et al. Pathogenic significance of P-fimbriated Escherichia coli in urinary tract infections. J Urol 1985;133:983–9. 35. Brooks H, O’Grady F, McSherry M, Cattell W. Uropathogenic properties of Escherichia coli in recurrent urinary tract infection. J Med Microbiol 1980;13:57–68. 36. Qvist N, Neilsn KK, Kristensen ES et al. Detrusor instability in children with recurrent urinary tract infections and/or enuresis. II. Treatment. Urol Int 1986;41:199–201. 37. Yoshikawa TT, Norman DC. Approach to fever and infection in the nursing home. J Am Geriatr Soc 1996;44:74–82. 38. Vessey MP, Metcalf M, McPhersen K, Yeates D. Urinary tract infection in relation to diaphragm use and obesity. Int J Epidemiol 1987;16:441–4. 39. Foxman B, Frerichs R. Epidemiology of urinary tract infection: II. Diet, clothing and urination habits. Am J Public Health 1985;75:1314–7. 40. Nicolle LE, Harding GM, Preiksatis J, Ronald AR. The association of urinary infection with sexual intercourse. J Infect Dis 1982;146:579–83. 41. Leibovici L, Alpert G, Laor A et al. Urinary tract infection and sexual activity in young women. Arch Int Med 1987;147:345–7. 42. Hooton T, Scholes D, Hughes J. A prospective study of risk factors for symptomatic urinary infection in young women. N Engl J Med 1996;335:468–74. 43. Foxman B, Zhang L, Tallman P et al. Transmission of uropathogens between sex partners. J Infect Dis 1997;175:989–92.
44. Foxman B, Chi J. Health behaviour and urinary tract infections in college-aged women. J Clin Epidemiol 1990;43:329–37. 45. Maizels M, Schaeffer A. Decreased incidence of bacteriuria associated with periodic instillations of hydrogen peroxide into the urethral catheter drainage bag. J Urol 1980;123:841–5. 46. Harding GKM, Nicolle LE, Ronald AR et al. How long should catheter acquired urinary tract infection in women be treated? A randomised controlled study. Ann Intern Med 1991;114:713–9. 47. Schiotz HA. Urinary tract infection after vaginal repair surgery. Int Urogynecol J 1992;3:185–90. 48. Clark KR, Higgs MJ. Urinary infection following outpatient flexible cystoscopy. Br J Urol 1990;66:503–5. 49. Hansoon S, Hyalmas K, Jodal V, Sixt R. Lower urinary tract dysfunction in girls with untreated asymptomatic or covert bacteriuria. J Urol 1990;143:313–5. 50. Madersbacher S, Pycha A, Schatzl G et al. The ageing lower urinary tract: a comparative urodynamic study of men and women. Urology 1998;51:206–12. 51. Baker R, Barbaris HT. Comparative results of urological evaluation of children with initial and recurrent urinary tract infections. J Urol 1976;116:503–5. 52. Mond NC, Percival A, Williams JD, Brumfitt W. Presentation, diagnosis and treatment of urinary tract infections in general practice. Lancet 1965;1:514–6. 53. Kurowski K. The women with dysuria. Am Fam Phys 1998;57:2155–64; 2169–70. 54. Yoshikawa TT, Norman DC. Approach to fever and infection in the nursing home. J Am Geriatr Soc 1996;44:74–82. 55. Pollock H. Laboratory techniques for detection of urinary tract infections and assessment of value. Am J Med 1983;75:79–84. 56. Fowler J, Pulaski E. Excretory urography cystography and cystoscopy in the evaluation of women with urinary tract infections. N Engl J Med 1981;304:462–5. 57. Mogensen P, Hansen LK. Do intravenous urography and cystoscopy provide important information in otherwise healthy women with recurrent urinary tract infection? Br J Urol 1983;55:261–3. 58. Bailey RR, Lynn KL, Robson RA, Smith AH, Maling TMJ, Turner JG. DMSA renal scans in adults with acute pyelonephritis. Clin Nephrol 1996;46:99–104. 59. Froom J. The spectrum of urinary tract infections in family practice. J Fam Pract 1980;11:385–91. 60. Foxman B, Geiger AM, Palin K, Gillespie B, Koopman JS. First time urinary tract infection and sexual behaviour. Epidemiology 1995;6:162–8. 61. Bailey RR. Single oral dose treatment of uncompli-
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cated urinary tract infections in women. Chemotherapy 1996;42(Suppl):10–6. 62. Delrio G, Dalet E, Aguilar L et al. Single dose rufloxacin versus 3 day norfloxacin treatment of uncomplicated cystitis. Clinical evaluation and pharmacodynamic considerations. Antimicrob Agents Chemother 1996;40:408–12. 63. Brandberg A, Mellstrom D, Samsioe G. Low dose oral oestriol treatment in elderly women with urogenital infections. Acta Obstet Gynaecol Scand 1987;140:33–8. 64. Parsons CL, Schmidt JD. Control of recurrent urinary tract infections in postmenopausal women. J Urol 1982;128:1224–6. 65. Privette M, Cade R, Peterson J et al. Prevention of recurrent urinary tract infections in postmenopausal women. Nephron 1988;50:24–7. 66. Kjaergaard B, Walter S, Knudsen A et al. Treatment with low dose vaginal oestradiol in postmenopausal women. A double blind controlled trial. Ugeskr Laeger 1990;152:658–9.
78. McKenzie H, Donnet ML, Howice PW et al. Risk of preterm delivery in pregnant women with group B streptococcal urinary infections or urinary antibodies to group B and E coli antigens. Br J Obstet Gynaecol 1994;101:107–13. 79. Villar J, Bergsjo P. Scientific basis for the content of routine antenatal care. I. Philosophy, recent studies and power to eliminate or alleviate adverse maternal outcomes. Acta Obstet Gynaecol Scand 1997;76:1–14. 80. Kiningham RB. Asymptomatic bacteriuria in pregnancy. Am Fam Phys 1997;47:1232–8. 81. Gerstner G, Muller G, Nahler G. Amoxicillin in the treatment of asymptomatic bacteriuria in pregnancy. A single dose of 3g amoxicillin versus a 4 day course of 3 doses 750mg amoxicillin. Gynecol Obstet Invest 1989;27:84–7. 82. Locksmith G, Duff P. Preventing neural tube defects: the importance of periconceptual folic acid supplements. Obstet Gynaecol 1998;91:1027–34. 83. Harris RE. Antibiotic therapy of antepartum urinary tract infections. J Int Med Res 1980;8(Suppl. 1):40–4.
67. Az R, Stamm WE. A controlled trial of intravaginal oestriol in postmenopausal women with recurrent urinary tract infections. N Engl J Med 1993;329:753–6.
84. Nicolle LE, Orr P, Duckworth H et al. Gross hematuria in residents of long term care facilities. Am J Med 1993;94:611–8.
68. Kirkengen AL, Anderson P, Gjersoe E et al. Oestriol in the prophylactic treatment of recurrent urinary tract infections in postmenopausal women. Scand J Primary Health Care 1992;10:139–42.
85. Eberle CM, Winsemius D, Garibaldi RA. Risk factors and consequences of bacteriuria in non-catheterised nursing home residents. J Gerontol 1993;48:M266–71.
69. Cardozo LD, Benness C, Abbott D. Low dose oestrogen prophylaxis for recurrent urinary tract infections in elderly women. Br J Obstet Gynaecol 1998;105:403–7. 70. Eriksen B. A randomised, open, parallel-group study on the preventative effect of an oestradiol-releasing vaginal ring (Estring) on recurrent urinary tract infections in postmenopausal women. Am J Obstet Gynecol 1999;180:1072–9.
86. Nicolle LE. Topics in long term care: urinary tract infection in long term care facilities. Infect Control Hosp Epidemiol 1993;14:220–5. 87. Wood CA, Abrutyn E. Optimal treatment of urinary tract infections in elderly patients. Drugs Aging 1996;9:352–62. 88. Nicolle LE. Urinary tract infections in the elderly. J Antimicrob Chemother 1994;33(Suppl. A):99–109.
71. Nicolle LE, Ronald AR. Recurrent urinary tract infections in adult women: diagnosis and treatment. Infect Dis Clin North Am 1987;1:793–806.
89. Preston AA. Imaging strategies and discussion of vesicoureteric reflux as a risk factor in the evaluation of urinary tract infection in children. Curr Opin Paediatr 1994;6:178–82.
72. Kass EH. Bacteriuria and pyelonephritis of pregnancy. Arch Intern Med 1960;105:194–8.
90. Pead L, Maskell R. Study of urinary tract infection in children in one health district. Br Med J 1994;309:631–4.
73. Whalley PJ. Bacteriuria of pregnancy. Am J Obstet Gynecol 1967;97:723–38.
91. Jadresic L, Cartwright K, Cowie N et al. Investigation of urinary tract infection in children. Br Med J 1993;307:761–4.
74. Gower P, Haswell B, Sidaway M et al. Follow–up of 164 patients with bacteriuria of pregnancy. Lancet 1968;1:990–4. 75. Roberts A, Beard R. Some factors affecting bacterial invasion of the bladder during pregnancy. Lancet 1965;1:1133–6. 76. Cunningham FG, Lucas MJ. Urinary tract infections complicating pregnancy. Baillières Clin Obstet Gynaecol 1994;8:353–73. 77. Millar LK, Cox SM. Urinary tract infections complicating pregnancy. Infect Dis Clin North Am 1997;11:13–26.
92. Scott JE, Swallow V, Coulthard MG et al. Screening of newborn babies for familial ureteric reflux. Lancet 1997;350:396–400. 93. Asscher A, McLachlan M, Jones R et al. Screening for asymptomatic urinary tract infection in schoolgirls. A two centre feasibility study. Lancet 1973;2:1–4. 94. Vernon SJ, Coulthard MG, Lambery HJ et al. New renal scarring in children who at age 3 and 4 years had had normal scans with dimercaptosuccinic acid: follow up study. Br Med J 1997;315:905–8.
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95. Grahn D, Normal DC, White ML et al. Validity of urinary catheter specimen for diagnosis of urinary tract infection in the elderly. Arch Intern Med 1985;145:1858–60. 96. Nicolle LE. Prevention and treatment of urinary catheter related infections in older patients. Drugs Aging 1994;4:379–91. 97. Pratt RJ, Pellowe C, Loveday HP et al. The EPIC project: developing national evidence-based guidelines for preventing healthcare associated infections. Phase 1 guidelines for preventing hospital-acquired infections. J Hosp Infect 2001;47:S3–S82.
98. National Institute on Disability and Rehabilitation Research Consensus Statement, Jan 27–29 1992. The prevention and management of urinary tract infections among people with spinal cord injuries. J Am Paraplegia Soc 1992;15:194–204. 99. Rhame F, Perkash I. Urinary tract infections occurring in recent spinal cord injury patients on intermittent catheterisation. J Urol 1979;122:669–73.
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41 The overactive bladder syndrome Philip Toozs-Hobson, Matthew Parsons
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IntroductIon Urinary incontinence (UI) is a common, distressing condition, affecting millions of men and women worldwide, and is defined by the International Continence Society (ICS) as ‘any involuntary leakage of urine’.1 In population estimates the range for urinary leakage varies, but only a minority perceive it as a problem (encompassing the original ICS definition of ‘involuntary urinary leakage that is a social or hygienic problem’). UI may be the endpoint of multiple pathologic processes. Urge urinary incontinence (UUI) is one of the most common chronic conditions in those aged over 60 years2 and the elderly3 with significant impact on the physical and psychological well-being of individuals. The economic burden on the state (and often on the individual) has been highlighted4,5 but is often ignored by managers and politicians as incontinence is a low priority in healthcare terms. As with many conditions, understanding and research may be hampered by the use of a variety of different terms to describe the same, or similar, conditions. These terms vary depending on whether they are used to describe symptoms or the results of a diagnostic test.
HIstory and termInology Incontinence has probably been a problem since prehistoric times but there was little interest in investigating the etiology and potential treatment of UI until the 18th century. Cystometry, the measurement of the pressure/volume relationship of the bladder, was pioneered in 1882 by Mosso and Pellicani6 using a smoke drum and water manometer. Along with air cystoscopy, developed by Kelly in 1893,6 they formed the beginnings of a classification system for incontinence. As technology improved further, the appreciation of the potential mechanisms of incontinence became better understood. Hodgkinson described ‘dyssynergic detrusor dysfunction’ in 1963, recognizing the importance of diagnosing it prior to incontinence surgery. Bates and Turner-Warwick developed the understanding of abnormal detrusor activity and coined the term ‘detrusor instability’ (DI), so that the role of abnormal detrusor activity as a cause of incontinence was fully appreciated and treatment became more coordinated.7 DI has subsequently been defined by the ICS as ‘a condition in which the bladder is shown to contract either spontaneously or with provocation, during bladder filling whilst the subject is attempting to inhibit micturition’. The latest terminology from the Standardization Sub-committee of the ICS in 20021 (www.icsoffice.org) has redefined DI as detrusor overactivity (DO) – a ‘urodynamic observation characterized by involuntary detru-
sor contractions during the filling phase which may be spontaneous or provoked’. Phasic DO is defined by a characteristic waveform, which may or may not lead to urinary incontinence. Terminal DO is a single involuntary detrusor contraction occurring at cystometric capacity, which cannot be suppressed, and may be associated with DO incontinence. Neuropathic DO is the term used to describe DO as part of a relevant neurologic condition. Idiopathic DO has no defined cause, and may be considered a diagnosis of exclusion. Subjectively urgency, with or without urge incontinence, usually with frequency and nocturia, can be described as the overactive bladder syndrome, urge syndrome, or urgency-frequency syndrome. This group is frequently further subdivided on the basis of urinary leakage into ‘OAB wet’ and ‘OAB dry’. Despite the strict definitions, symptomatic and urodynamic terms are often used interchangeably in common usage, and to a degree in the scientific literature, which further adds to confusion.
PHysIology and PatHoPHysIology Conventionally, the motor nerve supply to the bladder is described as via the parasympathetic nervous system (S2–S4) with sympathetic innervations from the hypogastric nerve acting predominantly on β-receptors, causing relaxation of the detrusor muscle. A detrusor contraction is initiated by acetylcholine release at the neuromuscular junction and acting on muscarinic receptors. However, there is increasing recognition of other innervation with different chemical transmitters contributing to bladder muscle contractility, including adenosine triphosphate in purinergic receptors, and vasoactive intestinal polypeptide. In those cases where a neurologic cause is identified, the term neuropathic DO is used to confer an idea of etiology. Such conditions include multiple sclerosis, cerebrovascular accidents, and diabetes. The pathophysiology of idiopathic DO remains a mystery and there is frequent debate on the ‘level’ of the lesion associated with the development of symptoms. In vitro studies have shown that the ‘overactive’ detrusor muscle contracts more than normal detrusor muscle. These contractions may not be nerve mediated and can be inhibited by the neuropeptide vasoactive intestinal polypeptide.8,9 Other studies10 have shown that increased α-adrenergic activity causes increased detrusor contractility. However, in obstructive DO animal and human studies the detrusor develops postjunctional supersensitivity, possibly due to partial denervation,11,12 with reduced sensitivity to electrical stimulation of its nerve supply but a greater sensitivity to stimulation with acetylcholine. If
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outflow obstruction is relieved, the detrusor can return to normal although a recent study that followed patients for 10 years after transurethral resection of the prostate challenges this.13 Relaxation of the urethra is known to precede contraction of the detrusor in a proportion of women with DO. This may represent primary pathology in the urethra which triggers a detrusor contraction, or may merely be part of a complex sequence of events which originate elsewhere. It has been postulated that incompetence of the bladder neck, allowing passage of urine into the proximal urethra, may precipitate an uninhibited contraction of the detrusor. However, the bladder neck is open at rest in up to 50% of normal parous women. It has recently been suggested12–14 that the common feature in all cases of DO is a change in the properties of the smooth muscle of the detrusor which predispose to unstable contractions. Partial denervation of the detrusor may be responsible for altering the properties of the smooth muscle, leading to increased excitability and increased ability of activity to spread between cells, resulting in coordinated myogenic contractions of the whole detrusor. This theory would add weight to suggestions that DO increases after any type of surgery where the bladder is reflected (e.g. cesarean section and hysterectomy). In addition, there may be a fundamental abnormality in the bladder wall with evidence of altered spontaneous contractile activity consistent with increased electrical coupling of cells, a patchy denervation of the detrusor and supersensitivity to potassium. Other authorities15 suggest that the primary defect in idiopathic and neuropathic bladders might be a loss of nerves accompanied by hypertrophy of the cells and an increased production of elastin and collagen within the muscle fascicles. Studies looking at the elderly have demonstrated a shift in the innervation of the bladder from parasympathetic towards increased purinergic nerves. This is also found in DO and interstitial cystitis.
clInIcal PresentatIon Lower urinary tract symptoms ‘are the subjective indicator of a disease or change in condition as perceived by the patient, carer or partner and may lead him/her to seek help from the healthcare professional’.1
• Increased daytime frequency is the complaint by the
•
patient who considers that they void too often by day (equivalent to pollakisuria, which is used in many countries); Nocturia is the complaint that the individual has to wake at night one or more times to void;
• Urgency is the complaint of a sudden compelling desire to pass urine that is difficult to defer;
• Urge urinary incontinence is the complaint of involuntary leakage accompanied by, or immediately preceded by, a strong desire to void. DO usually presents with a multiplicity of symptoms, the most common being urgency and frequency of micturition, which occurs in about 80% of patients, and nocturia occurring in almost 70%. The terms urge and urgency are currently under scrutiny and it is likely that urge will be reclassified as a normal sensation and urgency as an abnormal desire, hence the term urgency incontinence is increasingly being used to replace urge incontinence.16 There also appears to be a strong correlation between nocturnal enuresis (either childhood or current) and idiopathic DO. Some women complain of incontinence during sexual intercourse and can be broadly divided into two groups: those who leak during penetration and those who leak at orgasm; however, there is as yet no proof of a specific association with either urodynamic stress incontinence or DO, and indeed the literature on this is confusing and inconclusive. In addition to clinical presentation, there is frequent misinterpretation of urodynamics leading to an underreporting of DO. This occurs because urodynamics can demonstrate only two things: leakage and pressure change. Over-reliance on these, without referring back to the patient’s history or reproduction of symptoms during the test, results in a failure of the diagnostic capabilities of the test. In particular, failure of the test to demonstrate a pressure change (relying on the isometric principle that if the muscle contracts and the volume is constant, then the pressure will rise) does not mean that the detrusor muscle did not contract. This was acknowledged, to a degree, when the diagnostic criterion for DO was changed from a pressure rise of 15 cmH2O to any pressure rise associated with urgency. To extrapolate further, if the urethral resistance is reduced by intrinsic urethral sphincter deficiency, or by a (patho)physiologic relaxation of the urethra, then an isotonic contraction occurs and results in a decrease in volume rather than an increase in pressure (Fig. 41.1).
Prevalence The exact prevalence of OAB is unknown. Most epidemiologic studies estimate the prevalence of OAB wet but not frequency or urgency (OAB dry), so prevalence is likely to be underestimated. The prevalence of urge incontinence (OAB wet) has mostly been reported as being between 7 and 12% of the total population stud633
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Figure 41.1. ied. Brocklehurst17 estimated the prevalence of urgency, frequency, and nocturia in elderly women (UK) to be as high as 60%. Using stricter criteria, Yarnell et al.18 found that 3–7% of women in the general population complained of significant urinary incontinence. There is a relationship, although not a strong one, between symptom severity and the perception of the degree of bothersomeness of incontinence: 14% of women with mild incontinence have been found to be worried by their condition, compared with 24% with moderate and 29% with severe incontinence.19 The prevalence of DO also increases with advancing age.20 Although urinary symptoms are common in the population, discussions about them are often avoided. There appears to be a clear relationship between the severity of symptoms and the likelihood of reporting these to a healthcare provider. Reasons for delay in seeking advice include acceptance of symptoms as normal and the inherent fear that surgery is the only treatment. Embarrassment and reluctance to discuss the problem with the general practitioner are very common, more so if the general practitioner is male. One-fifth of women consult a doctor within 1 year of symptoms becoming troublesome, a third delay for 1–5 years, and a quarter wait for more than 5 years. Delay is significantly associated with age.21
treatment Historically, a variety of surgical treatments have been described for incontinence, including creating a vesicoabdominal fistula, closing the vagina and creating a rectovaginal fistula, compression of the urethra with
Urodynamic trace.
an anterior colporrhaphy, periurethral injection of paraffin, and advancement of the urethral meatus to the clitoris. These treatment options were designed before urodynamic diagnosis of DO or stress incontinence was available, and all have now fallen into disuse. For the last 20 years, with the understanding of detrusor contractions as the mechanism for irritative symptoms and the widespread adoption of urodynamics, treatment has centered on behavioral therapy and lifestyle modification, in combination with pharmacotherapy to modulate the cholinergic control of detrusor contractions.
Behavioral therapy All women with overactive bladder benefit from simple advice regarding fluid balance and to avoid tea, coffee, and alcohol. Many drugs affect bladder function, and often review of coexistent pharmacotherapy alone may lead to dramatic improvement or cure of symptoms (Table 41.1). In women with mixed incontinence, pelvic floor exercises and/or duloxetine (licensed in Europe for moderate to severe stress incontinence) may be helpful. Treatment of the urge component with pharmacotherapy and behavioral therapy may obviate the need for surgery (there is a risk that an incontinence operation may exacerbate the symptoms of DO which, due to their unpredictability, often have a greater impact on quality of life). Bladder retraining involves voluntary repetitive efforts to rediscover central control using the operant learning model. In simple terms, this is allowing the various centers of the brain which feed into the pontine micturition center to suppress the dominant stimuli that precipitate detrusor contraction. The pathway may vary as the pre-
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table 41.1.
Types of drugs affecting bladder function
1. Antihypertensives • Diuretics • Calcium channel antagonists • α-Adrenoreceptor agonists 2. Anticholinergics • Antihistamines • Antipychotics • Antispasmodics • Antiparkinsonian agents 3. Non-steroidal anti-inflammatory drugs 4. Lithium
cise trigger to contraction may vary (sensory stimuli, central lesions, local ‘leakage’ of acetylcholine within the bladder wall or increased purinergic interaction). There are four different schedules for bladder retraining: prompted voiding, timed voiding, habit retraining, and bladder drill. There appears to be Level 1b evidence to suggest that, for women with all forms of urinary incontinence, bladder retraining is more effective than no treatment. Evidence is inconsistent about expected cure rates, which may be dependent on when and how the outcome was measured or reflect differences in the bladder retraining protocol. Findings on objective (cystometric) changes do not always correspond to successful subjective change. One randomized controlled trial (RCT) has indicated that bladder retraining and pelvic floor muscle training have similar efficacy, and this requires further investigation. Bladder retraining appears to have benefits similar to those of drug therapy to date, and may have greater long-term benefit. Similarly, the effectiveness of bladder retraining in combination with pelvic floor muscle training in comparison to either bladder or pelvic floor training alone is as yet unclear and further investigation is warranted. The one RCT available suggests that the long-term benefit of bladder retraining alone may be similar to bladder retraining combined with pelvic floor muscle training. Further RCTs could help to compare bladder retraining alone and in combination with drugs and physical therapies.22,23
drug therapy Most women with DO will require drug therapy, as this remains the mainstay of treatment. Many drugs have been tried over the years in the treatment of DO – none is completely satisfactory, and many have had to be abandoned due to lack of efficacy or dangerous, or unpleasant, side effects. For many of the drugs, their clinical use is based on weak, open studies rather than randomized
controlled trials. Even then, the placebo response is so large that clinical effect is difficult to distinguish.24 Drug effects in individuals, however, can vary markedly. Even those drugs presently in use are not without their problems. Most of these drugs exert their effect by acting on the acetylcholine receptors within the detrusor muscle; other drugs have central effects, act to reduce urine production, or raise the sensory threshold of the bladder. As they are not without side effects, therapy is seldom continued indefinitely, and so must be considered as an adjunct to behavioral therapy. The use of drugs in the frail, elderly and infirm is contentious, and lower doses of drugs may be preferable in these patients. Alcohol and medication use are major causes of acute incontinence in the elderly (see Table 41.1). Polypharmacy and the use of psychotropic medication are most prevalent in those aged 85 years or over with women predominating, and appear to be increasing,25 compounding the problem. The main transmitter in the parasympathetic nervous system is acetylcholine. Voluntary and involuntary bladder contractions are mediated via muscarinic receptors in the bladder smooth muscle. Antimuscarinic agents act by competitive inhibition at the postganglionic receptor sites and therefore suppress both types of contraction, irrespective of the activation of the efferent part of the reflex.
oxybutynin and tolterodine Oxybutynin has well-documented efficacy in the treatment of detrusor overactivity, and is becoming more widely available with new and novel delivery systems. Oxybutynin or tolterodine is currently the first line medication for patients with this condition.26 Tolterodine is a potent and competitive antagonist of muscarinic receptors. However, it has no selectivity for the subtypes of muscarinic receptor, but appears to show selectivity for the bladder over the salivary glands.27 The therapeutic effect of tolterodine is bolstered by the similar activity of its metabolite.28,29 Although tolterodine and oxybutynin immediate release preparations have similar benefit in reducing incontinence episodes and urinary frequency,30 the side effect profile appears to favor tolterodine. In a large, double-blind, multicenter, randomized study, a once-daily preparation of tolterodine extendedrelease (ER) 4 mg was compared with immediate-release (IR) tolterodine 2 mg bd and placebo. Both preparations were significantly better than placebo in treating the symptoms of DO; however, tolterodine ER was 18% more effective than the immediate release preparation, 635
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with a 23% lower rate of dry mouth.31 In an open-label study comparing oxybutynin ER and oxybutynin IR in a community setting over 12 months, significant improvements were seen in quality of life measures. The majority of withdrawals occurred in the first 3 months (25.5%). Of those who continued after 3 months, 62% remained on oxybutynin ER for 1 year. The majority of discontinuations were for adverse events; dry mouth was the most frequently cited event leading to discontinuation (8.4%).32 Transdermal oxybutynin has been investigated in a general population of subjects with overactive bladder and urge or mixed UI.33 A 12-week double-blind placebo-controlled trial of oxybutynin transdermal delivery system (TDS) was undertaken. This study administered patches twice weekly, followed by a 12-week open-label, dose titration period. Doses of 2.6 and 3.9 mg oxybutynin daily improved overactive bladder symptoms and quality of life, and were well tolerated. The most common adverse event was application site pruritus (oxybutynin 10.8–16.8%, placebo 6.1%). Dry mouth incidence was similar in both groups (7.0% versus 8.3%). The oxybutynin patch has also been compared with tolterodine ER and placebo.34 Oxybutynin patches and tolterodine ER were found to be effective and comparable treatments for urge and mixed incontinence, when compared with placebo. Patients in the tolterodine ER and placebo groups applied placebo patches – application site reactions were most common in the oxybutynin group (14% versus 4.3% with placebo). However, only 4.1% of patients taking oxybutynin reported dry mouth (versus 1.7% on placebo) compared with 7.3% of patients in the tolterodine ER group (p=0.0379 when compared with placebo). Transdermal oxybutynin has the lowest reported incidence of adverse anticholinergics side effects from large multicenter trials.34 Anticholinergic therapy is typically limited by patient complaints of dry mouth,35 and the extended release preparations described above have significantly helped in reducing this. However, the development of newer highly selective antimuscarinic drugs (e.g. solifenacin and darifenacin) has also offered advantages in the efficacy/side effect balance. The development of bladderselective M3 specific antagonists offers the possibility of increasing efficacy while minimizing adverse effects. Solifenacin has recently been marketed, and darifenacin will soon be available.
ble-blind, parallel group, placebo and active controlled multicenter study in Europe and South Africa.36 The primary aim of the study was to assess the efficacy of solifenacin 5 and 10 mg; secondary aims were to compare the safety and efficacy with that of tolterodine. There was a statistically significant reduction of micturition frequency with both solifenacin 5 and 10 mg when compared with placebo, the former equating to a reduction of 2.2 micturitions per 24 hours and the latter 2.6. Tolterodine showed a smaller reduction of 1.9 micturitions. In addition, solifenacin was statistically superior to placebo with respect to the secondary outcome variables. In those patients who were incontinent, 37.3% of the placebo group were continent at the end of study compared to 51.1%, 50.6%, and 48.4% in the 5 and 10 mg solifenacin and the tolterodine groups, respectively (Table 41.2). When considering safety, the incidence of one or more adverse event was 45.3% in the placebo group compared to 48.4%, 51.9%, and 48.3% in the 5 and 10 mg solifenacin and the tolterodine groups, respectively. Most adverse events were anticholinergic and mild or moderate in severity (Table 41.3). This study provides further evidence that solifenacin is effective in patients with overactive bladder, and improvement in quality of life scores shows that this is clinically meaningful as well as being statistically significant. In addition, solifenacin would appear to be as effective as tolterodine, the current market leader, although unfortunately the study was performed before the slow release, once daily preparation was available for comparison. Again, adverse events were shown to be dose related and suggest that solifenacin 5 mg once daily may offer the best compromise between efficacy and tolerability. More recently, the comparative study (designed to demonstrate equivalence) against ER tolterodine has confirmed equal effect on frequency of the two drugs, but superiority of solifenacin in a number of parameters including urge incontinence episode frequency and all incontinence episode frequency. However, superiority was not demonstrated at the first assessment in most parameters when all patients were on 5 mg of solifenacin. Significance was demonstrated subsequently when 48% of patients had elected to increase to 10 mg (51% of the tolterodine group requested dose increase but a placebo was given as tolterodine is only licensed at a 4 mg dose)
solifenacin
trospium chloride
Solifenacin has also been directly compared to tolterodine 2 mg twice daily in a phase III randomized, dou-
Trospium chloride is a quaternary ammonium compound which is non-selective for muscarinic receptor
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table 41.2.
Efficacy of solifenacin 5 mg and 10 mg od when compared to tolterodine in the treatment of overactive bladder Placebo
Solifenacin 5 mg od
Solifenacin 10 mg od
Tolterodine 2 mg bd
n=253
n=266
n=264
n=250
Baseline mean
12.20
12.08
12.32
12.08
Change from baseline
–1.20
–2.19
–2.61
–1.88
–0.98 (0.0003)
–1.41 (0.0001)
–0.67 (0.0145)
Micturitions/24 hours
Difference from placebo (p) Urge incontinence/24 hours Baseline mean Change from baseline
n=127
n=113
n=127
n=119
2.02
2.33
2.14
1.86
–0.62
–1.41
–1.36
–0.91
–0.78 (0.0020)
–0.73 (0.0028)
–0.29 (0.2390)
Difference from placebo (p) Incontinence episodes/24 hours Baseline mean Change from baseline
n=153
n=141
n=158
n=119
2.71
2.64
2.59
2.32
–0.76
–1.42
–1.45
–1.14
–0.66 (0.0080)
–0.70 (0.0038)
–0.38 (0.1122)
Difference from placebo (p) Mean volume voided/24 hours Baseline mean Change from baseline
n=253
n=266
n=264
n=250
143.8
149.6
147.2
147.0
7.4
32.9
39.2
24.4
25.4 (0.0001)
31.8 (0.0001)
17.0 (0.0001)
Difference from placebo (p)
table 41.3.
Antimuscarinic adverse effects of solifenacin and tolterodine Placebo (n=267)
Solifenacin 5 mg od (n=279)
Solifenacin 10 mg (n=268)
Tolterodine 2 mg bd (n=263)
Dry mouth
4.9%
14.0%
21.3%
18.6%
Constipation
1.9%
7.2%
7.8%
2.7%
Blurred vision
2.6%
3.6%
5.6%
1.5%
subtypes and shows low biologic availability.37 In a recent placebo-controlled, randomized, double-blind, multicenter trial, trospium chloride produced significant improvements in maximum cystometric capacity and bladder volume at first unstable contraction. Clinical improvement was significantly greater in the group receiving trospium, and the frequency of adverse events was similar in both groups.38 Trospium chloride has also been compared to oxybutynin in a randomized, double-blind, multicenter trial. With both agents there was a significant increase in bladder capacity, a decrease in maximum voiding detrusor pressure, and a significant increase in compliance although there were no statistically significant differences between the two treatment groups. Those taking trospium had a lower incidence of dry mouth
(4% versus 23%) and were also less likely to withdraw (6% versus 16%) when compared to the group receiving oxybutynin.39
Propiverine Propiverine has been shown to combine anticholinergic and calcium channel blocking actions40 and is the most popular drug for detrusor overactivity in Germany, Austria and Japan. Open studies in patients with detrusor overactivity have demonstrated a beneficial effect,41 and in a double-blind placebo-controlled trial of its use in neurogenic detrusor overactivity, it has been shown to significantly increase bladder capacity and compliance in comparison to placebo. 637
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Dry mouth was experienced by 37% in the treatment group as opposed to 8% in the placebo group with dropout rates being 7% and 4.5%, respectively.42
Imipramine Imipramine has been shown to have systemic anticholinergic effects43 and blocks the reuptake of serotonin. Some authorities have found a significant effect in the treatment of patients with detrusor overactivity44 although others report little effect.45 In light of this evidence and the serious adverse effects associated with tricyclic antidepressants, their role in detrusor overactivity remains of uncertain benefit although they are often useful in patients complaining of nocturia or bladder pain. In the authors’ own practice it is often added as a second agent to a ‘conventional’ anticholinergic. table 41.4
desmopressin Desmopressin (DDAVP) – synthetic vasopressin – has been shown to be effective in reducing nocturia in patients with multiple sclerosis;46 recent studies have also demonstrated benefit in daytime urinary frequency and urinary incontinence.47
capsaicin Intravesical instillations of capsaicin, a neurotoxin extracted from red chili peppers,48 have significant effect over placebo in the treatment of neurogenic DO. Its analog resiniferatoxin49 has been shown to have fewer side effects, with an increase in bladder capacity. Table 41.4 compares the strengths and weaknesses of these drugs in the treatment of detrusor overactivity.
Comparison of different drugs used in the treatment of detrusor overactivity
Drug
Strengths
Weaknesses
Comments
Generic oxybutynin
Cheap Well established Safe in pregnancy Dosing versatility
Side effects
Still the most commonly prescribed drug Often not continued when prescribed because of imbalance of side effects versus efficacy
Slow release oxybutynin
Has good efficacy Is M3 predominant
While side effects are reduced and therefore more acceptable still limits use
Single day dosing is easier for many patients and use at night may improve further but may need to increase dose if taken in the evening
Oxybutynin patches
Avoids many of the ‘conventional’ side effects while maintaining efficacy
Patch irritation in around 15% Single dose
Offers a new option in the most established medication Many patients prefer patches to tablets
Tolterodine
Available as bd or ER preparations Tends towards bladder specificity
While probably has a reduced side effect profile compared to oxybutynin may not be quite as effective Often prescribed off license as 8 mg dose
Developed from terodoline which was very effective but associated with torsades de pointes and voluntarily withdrawn in the early 1990s
Trospium chloride
Quaternary ammonium compound Very inert and therefore unlikely to interact with other medications Minimal crossing of blood– brain barrier and therefore less likely to have CNS effects
Broad spectrum anticholinergic effects giving rise to side effects in many patients
Long established as a treatment in Germany, Poland and Spain Has good safety profile and can be used as a second agent with tertiary compounds
Solifenacin
M3 selectivity Recent STAR study suggests some advantages over detrusitol Has variable dosing regimen
Most common side effect is Place in practice changing from currently constipation, but this can second line to increasingly first line for be useful in treating patients many secondary care clinicians with concurrent IBS which may cause diarrhea
Darifenacin
Most M3 selective medication
Not currently launched
Delay in phase III studies postponed launch
ER, extended release; IBS, irritable bowel syndrome.
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surgery Many different surgical treatments have been tried over the years in the management of DO, but few are still in regular use today. Abandoned procedures include bladder distension, vaginal denervation, bladder transection, and sacral neurectomy. Their demise was caused by an unacceptably high rate of complications and limited efficacy. Surgical solutions for DO include botulinum toxin-A (Botox), sacral neuromodulation, detrusor myectomy, augmentation cystoplasty, or urinary diversion.
Botulinum toxin The discovery that botulinum toxin blocks neuromuscular transmission, and thereby causes weakness, laid the foundations for its therapeutic development. In 1981, Alan Scott, an ophthalmologist, pioneered botulinum toxin therapy by using it to treat strabismus.50 The bacterium produces its effect by production of a neurotoxin; different strains produce seven distinct serotypes designated A–G. All seven have a similar structure and molecular weight, consisting of a heavy (H) and a light (L) chain, joined by a disulphide bond.51 They interfere with neural transmission by blocking the calcium-dependent release of neurotransmitter (acetylcholine), causing the affected muscle to become weak and atrophic. The affected nerves do not degenerate, as the blockage is irreversible. Only the development of new nerve terminals and synaptic contacts allows recovery of function which usually takes 3 months or so. In urogynecology, botulinum toxin has been used successfully to overcome outflow obstruction in women with voiding difficulty52 and to overcome detrusor– sphincter dyssynergia after spinal cord injury,53,54 despite the expense of repeated injections. It is currently the subject of research to assess its efficacy in the suppression of DO, although the long-term effects of repeated cystoscopic injections are not known. Since 2002 there have been an increasing number of abstracts and articles presenting promising data on the use of botulinum toxin-A. To date this has not been subjected to any placebo or therapeutic comparisons.55
neuromodulation Stimulation of the S3 nerve root by an implanted electrical pulse generator can provide effective relief from frequency–urgency symptoms. In a prospective randomized trial of sacral neuromodulation versus delay, incontinence episode frequency (IEF), severity, and
pad use were all reduced in the active arm (p<0.0001): 47% were dry and 29% reported a reduction in IEF of more than 50% at 6 months.56 Neuromodulation is, however, very expensive, as the implant alone costs around £6000. Patients need expert assessment and management; although it is not suitable for routine use, sacral neuromodulation appears to be useful for a selected minority. The stimulator is a small electrical pulse generator, approximately the same size as a cardiac pacemaker, and is commonly implanted in the upper outer quadrant of the buttock. Complications most commonly reported are generator site pain (15.9%) and implant site pain (19.1%). Lead migration may occur in up to 7%. The surgical revision of technical failures and complications was 32.5%.57 This may be expected to reduce in the future as the technological development of generators and implant leads progresses.
augmentation cystoplasty This is used to increase the size of the urinary reservoir. It is indicated in patients:
• who lack adequate bladder capacity or detrusor compliance;
• who manifest debilitating frequency–urgency • • •
symptoms, with urge incontinence, recurrent urinary tract infections or renal insufficiency; who have failed to derive benefit from medical therapy; whose lifestyle is severely limited; have high pressure urine storage endangering the upper renal tracts.
The operation most frequently performed is the ‘clam’ cystoplasty. A cure rate up to 90% has been reported, which compares very favorably with alternatives, such as Ingelman-Sundberg bladder denervation (54% complete response at 44 months) and detrusor myectomy (63% showed improvement of compliance and/or resolution of detrusor contractions).58 Postoperative complications include a significant risk of postoperative voiding difficulty, presumably secondary to a failure to generate adequate voiding pressures. This may be overcome by teaching the patient clean intermittent self-catheterization. Mucus production by the ileal segment may cause distress, especially when it is passed per urethram. This may be ameliorated by the ingestion of cranberry juice, which decreases mucus viscosity.59 Additionally there is an increased risk of urolithiasis. Of those who develop 639
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stones, there is a 30% risk of further stone formation within 2 years.60 Electrolyte and acid–base balance may become disturbed, resulting in a metabolic acidosis. Malignant change occasionally occurs within the ileal segment. The bowel segment used for the cystoplasty does not seem relevant, and the mortality, where it occurs, is significant – as high as 30%. Of the 16 cases reported, 13 had tuberculosis or chronic cystitis as the primary indication for cystoplasty.61 Urinary nitrites, produced by recurrent bacterial infection, may also contribute to the malignant risk. The carcinogenic effects of this and nitrosamines have been implicated in tumors of urinary conduits and those with ureterosigmoidostomy.62
urinary diversion In some patients, the bladder becomes severely contracted due to severe long-term detrusor overactivity. In these cases, drug therapy and behavior modification are of little or no benefit, and augmentation cystoplasty is inappropriate and technically difficult. The only relief for intractable detrusor overactivity, especially of neurogenic origin, may be from a urinary diversion procedure with an ileal conduit. The management of a stoma may be easier than constantly changing incontinence pads and washing wet underwear.
tHe Future There are a variety of potential central and peripheral targets for pharmacotherapy. Central targets include:
• γ-aminobutyric acid (GABA) – an inhibitory
• • •
neurotransmitter in the CNS (e.g. baclofen – a GABA agonist that has been used in the past for idiopathic DO); serotonin – has an effect on the urethral sphincter; this is mainly used in stress incontinence; noradrenaline (NA) – tricyclic antidepressants work partly by peripheral blockade of NA; dopamine – possibly related with incontinence associated with parkinsonism, although the exact mechanism and response to dopamine agonists is less predictable.
The peripheral targets are aimed at mainly muscarinic receptors, β-adrenoceptors, ion channels such as the calcium channel (blockers) and potassium channel (openers), sensory nerves (capsaicin interferes with afferent signals from the bladder by interacting with vanilloid receptors), and prostanoids.
conclusIon DO is a common disorder affecting millions of women worldwide. It is often easier to diagnose than to treat. Treatment remains unsatisfactory as behavioral modification is often ignored and drug therapy with anticholinergic medication is often associated with side effects. Highly selective compounds are under development, which will increase the therapeutic options available. Only when these have failed, and as a last resort, is surgical intervention considered. Increasing general awareness and decreased tolerance of urinary incontinence over the last 10–15 years has helped to raise the profile of OAB. With this there has been a quiet revolution in the treatment options available and an improvement in the quality of research in this disease area. The next 10 years promise to be as exciting as the last, with a real opportunity to improve symptoms consistently for patients.
reFerences 1. Abrams P, Cardozo L, Fall M et al. The standardisation of terminology of lower urinary tract function: report from the Standardisation Sub-Committee of the International Continence Society. Neurourol Urodyn 2002;21:167–78. 2. Brown JS. OAB: broadening our understanding and impact. Key Issues in the Treatment of Overactive Bladder. Seminar Session, 27th August 2002. 32nd Annual Meeting of the ICS. 3. Castleden CM, Duffin HM, Asher MJ. Clinical and urodynamic studies in 100 elderly women. Br Med J Clin Res 1981;282(6270):1103–5. 4. Department of Health. Modernising health and social services: national priorities guidance. 1999/00-2001/02. London: Department of Health, 1998. 5. The Continence Foundation. The cost of incontinence to the NHS. Online. Available: www.continence-foundation. org.uk/in-depth/integrated-continence-service.php#13. 6. Bidmead J, Cardozo L. Short cuts. In: Sturdee D, Oláh K, Purdie D, Keane D (eds) Yearbook of Obstetrics and Gynaecology, vol. 10. London: RCOG Press, 2002. 7. Drutz HP, Schulz JA. History of urogynaecology. In: Staskin D, Cardozo LD (eds) Textbook of Female Urology and Urogynaecology. London: Martin Dunitz, 2001; 215–26. 8 Levin RM, Wein AJ. Effect of vasoactive intestinal peptide on the contractility of the rabbit urinary bladder. Urology 1981;9:217–8. 9 Gu J, Blank MA, Huang WM et al. Peptide containing nerves in human urinary bladder. Urology 1984;24:353–7. 10. Smet PJ, Moore KH, Johavicus J. Distribution and localization of calcitonin-related peptide, tachykinin and VIP in
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11. Marcus DJ, Hedland P, Mills W et al. Structural and functional denervation of human detrusor after spinal cord injury. Lab Invest 2000;80:1491–9.
26. Andersson K-E, Appell R, Cardozo LD et al. Pharmacological treatment of urinary incontinence. In: Abrams P, Cardozo LD, Khoury S, Wein A (eds) Incontinence. Second International Consultation on Incontinence, July 1–3, 2001. Plymouth: Health Publication, 2002; 479–511.
12. Wagatoni J, Gloeckner DC, Chancellor MB, de Groat WC, Sacks MS. Changes in the bioaxial viscoelastic response of the urinary bladder following spinal cord injury. Ann Biomed Eng 2004(10);32:1409–19.
27. Stahl MMS, Ekström B, Sparf B et al. Urodynamic and other effects of tolterodine: a novel antimuscarinic drug for the treatment of detrusor overactivity. Neurourol Urodyn 1995;14:647–55.
13. Thomas AW, Cannon A, Bartlett E, Ellis-Jones J, Abrams P. The natural history of voiding dysfunction in men: the long term follow up of TURP. Br J Urol 1998;81(Suppl 4):22.
28. Brynne N, Stahl MMS, Hallén B. Pharmacokinetics and pharmacodynamics of tolterodine in man: a new drug for the treatment of urinary bladder overactivity. Int J Clin Pharmacol Ther 1997; 35:287–95.
14. Gilpin SA, Gosling JA, Barnard RJ. Morphological and morphometric studies of the human obstructed trabeculated urinary bladder. Br J Urol 1985;57:525–9.
29. Brynne N, Dalen P, Alvan G. Influence of CYP2D6 polymorphism on the pharmacokinetics and pharmacodynamics of tolterodine. Clin Pharmacol Ther 1998;63:529–39.
15. Gosling JA, Gilpin SA, Dixon JS, Gilpin CJ. Decrease in the autonomic innervation of human detrusor muscle in outflow obstruction. J Urol 1986;136:501–3.
30. Abrams P, Freeman R, Anderstrom C et al. Tolterodine, a new anti-muscarinic agent: as effective but better tolerated than oxybutynin in patients with an overactive bladder. Br J Urol 1998;81:801–10.
normal and idiopathic unstable human urinary bladder. Lab Invest 1997;77:37–49.
16. Cortivo R, Pagano F, Passeri G, Abatangelo G, Castellani I. Elastin and collagen in the normal and obstructed urinary bladder. Br J Urol 1981;53:134–7. 17. Brocklehurst J. Aging of the human bladder. Geriatrics 1972;27:154–61. 18. Yarnell J, Voyle G, Richards C, Stephenson T. The prevalence and severity of urinary incontinence in women. J Epidemiol Community Health 1981;35:71–4. 19. Lagro-Janssen TLM, Suits AJA, Van Weel C. Women with urinary incontinence: self-perceived worries and general practitioners’ knowledge of the problem. Br J Gen Pract 1990;40:331–4. 20. Milsom I, Abrams P, Cardozo L, Roberts G, Thüroff J, Wein A. How widespread are the symptoms of overactive bladder and how are they managed? A population-based prevalence study. BJU Int 2001;87:760–6. 21. Norton PA, MacDonald LD, Sedgwick PM, Stanton SL. Distress and delay associated with urinary incontinence, frequency, and urgency in women. BMJ 1988;297:1187–9. 22. Jarvis GJ, Millar DR. Controlled trial of bladder drill for detrusor instability. BMJ 1980;281:1322–3. 23. Frantl JA, Wyman JF, McClish DK et al. Efficacy of bladder training in older women with urinary incontinence. J Am Med Assoc 1991;265:609–13. 24. Thuroff JW, Bunke B, Ebner A et al. Randomized, double-blind, multicenter trial on treatment of frequency, urgency and incontinence related to detrusor hyperactivity: oxybutynin versus propantheline versus placebo. J Urol 1991;145:813–7. 25. Linjakumpu T, Hartikainen S, Klaukka T, Koponen H, Kivela SL, Isoaho R. Psychotropics among the home-dwelling elderly – increasing trends. Int J Geriatr Psychiatry 2002;17(9):874–83.
31. Van Kerrebroeck P, Kreder K, Jonas U, Zinner N, Wein A. Tolterodine Study Group. Tolterodine once-daily: superior efficacy and tolerability in the treatment of the overactive bladder. Urology 2001;57(3):414–21. 32. Diokno A, Sand P, Labasky R et al. Long-term safety of extended-release oxybutynin chloride in a communitydwelling population of participants with overactive bladder: a one-year study. Int Urol Nephrol 2002;34(1):43–9. 33. Dmochowski RR, Davila GW, Zinner NR et al for the Transdermal Oxybutynin Study Group. Efficacy and safety of transdermal oxybutynin in women with urge and mixed urinary incontinence. J Urol 2002;68(2):580–6. 34. Dmochowski RR, Sand PK, Zinner NR, Gittelman MC, Davila GW, Sanders SW. Transdermal Oxybutynin Study Group. Comparative efficacy and safety of transdermal oxybutynin and oral tolterodine versus placebo in previously treated patients with urge and mixed urinary incontinence. Urology 2003;62(2):237–42. 35. Gleason DM, Susset J, White C, Munoz DR, Sand PK. Evaluation of a new once-daily formulation of oxybutynin for the treatment of urinary urge incontinence. Ditropan XL Study Group. Urology 1999;54(3):420–3. 36. Chapple CR, Rechberger T, Al-Shukri S et al. Randomized, double-blind placebo- and tolterodine-controlled trial of the once-daily anti-muscarinic agent solifenacin in patients with symptomatic overactive bladder. BJU Int 2004;93(3):303–10. 37. Schladitz-Keil G, Spahn H, Mutschler E. Determination of bioavailability of the quaternary ammonium compound trospium chloride in man from urinary excretion data. Arzneimittel Forsch/Drug Res 1986;36:984–7. 38. Cardozo LD, Chapple CR, Toozs-Hobson P et al. Efficacy of trospium chloride in patients with detrusor instability: a
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placebo-controlled, randomized, double-blind, multicentre clinical trial. BJU Int 2000;85(6):659–64.
nary results in stable and unstable detrusor. J Urol 1997;158(6):2093–7.
39. Madersbacher H, Stoher M, Richter R, Burgdorfer H, Hachen HJ, Murtz G. Trospium chloride versus oxybutynin: a randomized, double-blind, multicentre trial in the treatment of detrusor hyperreflexia. Br J Urol 1995;75(4):452–6.
50. Scott AB. Botulinum toxin injection of eye muscles to correct strabismus. Trans Am Ophthalmol Soc 1981;79:734–70.
40. Haruno A, Yamasaki Y, Miyoshi K et al. Effects of propiverine hydrochloride and its metabolites on isolated guinea pig urinary bladder. Folia Pharmacol Japon 1989;94:145–50.
52. Phelan MW, Franks M, Somogyi GT et al. Botulinum toxin urethral sphincter injection to restore bladder emptying in men and women with voiding dysfunction. J Urol 2001;165(4):1107–10.
41. Mazur D, Wehnert J, Dorschner W, Schubert G, Herfurth G, Alken RG. Clinical and urodynamic effects of propiverine in patients suffering from urgency and urge incontinence. Scand J Urol Nephrol 1995;29:289–94. 42. Stoher M, Madersbacher H, Richter R, Wehnert J, Dreikorn K. Efficacy and safety of propiverine in SCI-patients suffering from detrusor hyperreflexia: a double-blind, placebocontrolled clinical trial. Spinal Cord 1999;37(3):196–200. 43. Baldessarini KJ. Drugs in the treatment of psychiatric disorders. In: Gilman AG, Goodman LS, Rall TW et al (eds) Goodman and Gilman’s The Pharmacological Basis of Therapeutics, 7th ed. New York: Macmillan, 1985; 387– 445. 44. Castleden CM, Duffin HM, Gulati RS. Double-blind study of imipramine and placebo for incontinence due to bladder instability. Age Aging 1986;15:299–303. 45. Diokno AC, Hyndman CW, Hardy DA, Lapides J. Comparison of action of imipramine (Tofranil) and propantheline (Probanthine) on detrusor contraction. J Urol 1972;107:42–3. 46. Hilton P, Hertogs K, Stanton SL. The use of desmopressin (DDAVP) for nocturia in women with multiple sclerosis. J Neurol Neurosurg Psychiatry 1983;46:854–5. 47. Robinson D, Cardozo L, Akeson M et al. Women take control; desmopressin – a drug for daytime urinary incontinence. Neurourol Urodyn 2002;21:385–6.
51. Dolly JO. Therapeutic and research exploitation of botulinum neurotoxins. Eur J Neurol 1997;4(Suppl 2):S5–10.
53. Gallien P, Robineau S, Verin M, Le Bot MP, Nicolas B, Brissot R. Treatment of detrusor sphincter dyssynergia by transperineal injection of botulinum toxin. Arch Phys Med Rehabil 1998;79(6):715–7. 54. Schurch B, Hauri D, Rodic B, Curt A, Meyer M, Rossier AB. Botulinum-A toxin as a treatment of detrusor–sphincter dyssynergia: a prospective study in 24 spinal cord injury women. J Urol 1996;155(3):1023–9. 55. Sahai A, Khan M, Fowler C et al. Botulinum toxin for treatment of lower urinary tract symptoms: a review. Neurourol Urodyn 2005;24(1):2–12. 56. Schmidt RA, Jonas U, Oleson KA et al. Sacral nerve stimulation for treatment of refractory urinary urge incontinence. Sacral Nerve Stimulation Study Group. J Urol 1999;162(2):352–7. 57. Mark SD, McRae CU, Arnold EP, Gowland SP. Clam cystoplasty for the overactive bladder: a review of 23 cases. Aust N Z J Surg 1994;64(2):88–90. 58. Westney OL, McGuire EJ. Surgical procedures for the treatment of urge incontinence. Tech Urol 2001;7(2):126–32. 59. Avorn J, Monane M, Gurnitz JH, Glynn RJ, Choodnovsky I, Lipsitz LA. Reduction of bacteriuria and pyuria after ingestion of cranberry juice. JAMA 1994;271(10):751–4. 60. Gough DCS. Enterocystoplasty. BJU Int 2001;88:739–43.
48. de Seze M, Wiart L, Joseph PA et al. Capsaicin and neurogenic detrusor hyperreflexia: a double-blind placebocontrolled study in 20 patients with spinal cord lesions. Neurourol Urodyn 1998;17(5):513–23.
61. Fernandez-Arjona M, Herrerro L, Romera J et al. Synchronous signet ring cell carcinoma and squamous cell carcinoma arising in an augmented ileocystoplasty. Case report and review of the literature. Eur Urol 1996;29: 125–8.
49. Lazzeri M, Beneforti P, Turini D. Urodynamic effects of intra-vesical resiniferatoxin in humans: prelimi-
62. Westney OL, McGuire EJ. Surgical procedures for the treatment of urge incontinence. Tech Urol 2001;7(2):126–32.
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42 Vaginitis Brian G Wise, Gopalan Vijaya
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INTRODUCTION Vaginitis is a condition that represents a spectrum of vulvovaginal symptoms including vaginal discharge, pruritus, vaginal soreness, dysuria, and dyspareunia. Most women and their doctors use the term vaginitis synonymously with infection and they assume that all vulvovaginal irritation or itching, especially when accompanied by abnormal secretions, is caused by infection.1 Although infection is the commonest cause of vaginitis, noninflammatory processes can produce similar symptoms. Acute symptoms are often due to infection; however, chronic vaginitis may have a different etiology.1 Diagnosis can be difficult because symptoms are non-specific, patients often self-diagnose their condition, and their symptoms may have more than one cause. A thorough evaluation of the patient’s symptoms and use of appropriate investigations will allow accurate diagnosis and effective treatment.
VAGINAL ECOSYSTEM An understanding of the normal environment is helpful in identifying abnormal conditions and directing appropriate therapy. The normal vaginal flora is complex and many of the normally commensal microorganisms are potential pathogens.2 The vaginal flora consists of aerobic, facultative, and obligate anaerobic bacteria. Vaginitis occurs when there is an alteration in the normal vaginal flora, either by introduction of pathogens or changes in the environment that allow existing organisms to proliferate.3 The estrogen status of the vagina has an important role in determining the vaginal flora. In the prepubertal state (from 6 weeks postpartum), the vagina is thin and hypoestrogenic. The pH of the vagina is more than 4.7, and culture shows a variety of organisms as shown in Table 42.1. From puberty to the menopause, increased levels of estrogen stimulate and thicken the vaginal epithelium. The glycogen content of the epithelial cells increases and the pH decreases to less than 4.5. This encourages the growth of lactobacilli, which comprise more than 95% of the bacteria in the normal vagina.5 This is achieved by the lactobacilli interfering with other bacterial adherence mechanisms and competition for available energy sources. Several mechanisms have been proposed as to why lactobacilli have a protective effect against infective vaginitis, including the production of lactic acid, hydrogen peroxide, and bacterial toxins. Patients with vaginitis often complain of vaginal discharge. It is important to understand the characteristics of a healthy vaginal discharge in order to differentiate
Table 42.1.
• • • • • • • • • • • • • • •
Normal vaginal flora
Lactobacillus Staphylococcus Streptococcus Escherichia Enterococcus Corynebacterium Diphtheroids Klebsiella Bacteroides Proteus Peptostreptococcus Prevotella Eubacterium Fusobacterium Clostridium
it from the abnormal. Healthy vaginal discharge is slate gray to white in color. It is homogenous, may be thick or thin, and is odorless. The pH varies from 3.8 to 4.6.5 On microscopy, the squamous epithelial cells are mature and clear, white blood cells (WBCs) are absent, and the dominant bacterial morphotype is the lactobacilli.6 The physiologic discharge does not adhere to the vaginal walls and is not usually associated with other symptoms.7 Vaginal discharge varies over the menstrual cycle. Stress increases the rate of vaginal desquamation and thus the amount of discharge.8 Hormonal contraception and pregnancy are associated with increased vaginal discharge.9 Hence the ‘normal’ discharge may vary and it is important to reassure the patient that a discharge, while troublesome, may not be abnormal.
EPIDEMIOLOGY It is difficult to obtain accurate figures since vaginitis is not a notifiable disease and many women will selfdiagnose and receive over-the-counter (OTC) treatment. Vaginitis is said to be the most common reason for gynecologic consultation in the United States and accounts for approximately 10 million visits annually.10 Ninety percent of vaginitis cases are secondary to bacterial vaginosis, candidiasis, and trichomonas vaginalis.3 National figures in the US show that 40–50% of patients with vaginal symptoms have bacterial vaginosis, 20–25% have vulvovaginal candidiasis, and 15–20% have trichomonas vaginalis.11 Thirty percent of women with vaginal symptoms go without a diagnosis.12 The incidence of vaginitis is greater in the more humid, subtropical countries. Vaginal discharge is an extremely common reason for women to seek care, with an estimated one woman in 10 presenting to her general practitioner.13
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CAUSES OF VAGINITIS 1. Infection (common) • Bacterial vaginosis • Candidiasis • Trichomonas vaginalis 2. Infection (less common) • Gonorrhea • Chlamydia • Herpes simplex • Human papilloma virus • Entamoeba histolytica • Enterobius vermicularis • Giardia lamblia 3. Atrophic vaginitis 4. Desquamative inflammatory vaginitis 5. Lactobaccillosis 6. Allergic vulvovaginitis 7. Psychosomatic (may have history of sexual abuse14) 8. Poor hygiene 9. Foreign body (e.g. retained tampon) 10. Idiopathic The differential diagnosis in vaginitis includes:
• • • • • •
vulval ulcers/erosions; vulval pain syndromes; fistula; cervicitis; endometrial polyp; cervical carcinoma.
EVALUATION OF VAGINAL SYMPTOMS When a patient presents with vaginal symptoms, a complete history is often not obtained due to embarrassment on the part of the patient or the healthcare provider. A detailed history is essential in order to arrive at a proper diagnosis and adequately address any associated concerns.4 Many women with vaginitis have vulvar or vestibular symptoms rather than vaginal symptoms, and so questioning the patient about the location of symptoms is important. Sexually active women are at an increased risk of vaginitis because the presence of semen in the vagina may increase the pH and thereby allow proliferation of pathogenic anaerobic bacteria.10 It is well known that the risk of vaginitis and all sexually transmitted diseases (STDs) is increased in women with multiple sexual partners. A thorough history of the patient’s sexual activity is essential. A sexual history may indicate the need to investigate for STDs or to highlight domestic violence issues. It will
provide a better understanding of the chronicity of a patient’s symptoms, their relationship with sexual activity, and their impact on sexual self-image.4 A checklist for history-taking is provided in Table 42.2.
PELVIC EXAMINATION Vaginitis is frequently, but not invariably, accompanied by inflammatory changes in the vulva, vestibule, and cervix.15 Pelvic examination should be undertaken systematically, starting from the vulva. The vagina should be examined for signs of edema, erythema, excoriation, fissures, scaling, peripheral satellite pustules, ulcers, atrophic signs, etc. The cervix should be visualized for
Table 42.2.
History-taking checklist in the evaluation of vaginal symptoms
1. Vaginal discharge • Quantity • Color: clear, white, gray, green, yellow • Consistency: thin, thick, curd-like • Purulent or not • Presence of odor 2. Duration and mode of onset of these symptoms 3. Associated symptoms and location of these symptoms (e.g. vulva, deep vagina or introitus) • Pruritus • Soreness • Irritation • Pain • Burning • Bleeding • Superficial dysuria • Superficial dyspareunia • Lower abdominal pain • Vulvar symptoms 4. Past treatment and response (e.g. any use of over-thecounter medication?) 5. History of chemicals that have come into contact with the perineum 6. History of douching 7. Menstrual history and variation of symptoms with menstrual cycle 8. Obstetric history 9. Sexual history • Number of sexual partners • Frequency of sexual practice 10. Contraception (e.g. use of condoms, spermicides, intrauterine contraceptive device, etc.) 11. Cervical smear history 12. Medical history • History of diabetes, lupus, AIDS • Thyroid disorder 13. Drug history (e.g. systemic antibiotics, steroids) 14. History of allergies 15. History of smoking
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abnormal features such as a ‘strawberry cervix’ and it should be noted whether discharge is from the cervix or the vagina. The presence of discrete, punctuate, bright red hemorrhagic macules and papules on the cervix produces the classic but non-specific strawberry cervix in trichomoniasis. Retained tampons may be found on examination. Bimanual examination for adnexal tenderness and masses should be part of the evaluation.
INVESTIGATIONS
the anterior fornix or lateral vaginal wall. On microscopy, the normal vaginal superficial cell is large with a small nucleus. At times of hypoestrogenism (postmenopausally or postnatally) or infection, parabasal cells are found which are smaller and oval shaped with a large nucleus. The ratio of WBCs and epithelial cells of more than 1:1 is suggestive of an infection.4 Clue cells are squamous epithelial cells with a fine granular cytoplasm and indistinct borders due to coccobacilli (Fig. 42.1). Clue cells are seen in more than 90% of patients with bacterial vaginosis.5
Symptoms and signs are non-specific; therefore a diagnosis made by history and examination alone is unreliable. With a standardized approach to the evaluation of vaginal symptoms, a cause can be identified in most cases. Bacterial vaginosis, candidiasis, and trichomoniasis can be diagnosed by microscopy if typical findings are present; however, as negative findings cannot rule out the diagnosis, culture is needed in recurrent or resistant cases. Although simple tests such as checking the vaginal pH can be used as a guide to diagnose the type of infection, these are not always accurate. Causes of increased pH are trichomoniasis, bacterial vaginosis, a foreign body with secondary infection, and streptococcal vaginitis. Other causes include desquamative inflammatory vaginitis, hypoestrogenism, menses, heavy cervical mucus, and pregnancy with ruptured membranes. Semen, vaginal douches, and intravaginal medication can increase the pH; gel used on the speculum can alter the pH. Swabbing the vagina from the posterior fornix may not be representative of true vaginal pH and microscopic findings may also be difficult to interpret.4 Sampling should be taken from the middle third of the vagina or
Figure 42.1. Bacterial vaginosis is typified by the presence of coccoid bacteria which adhere in large numbers to squamous cells. These are known as ‘clue cells’. Magnification 600 ×. (Courtesy of Mr Malcolm Mackie, Clinical Cytologist, William Harvey Hospital, Ashford, UK).
Table 42.3.
Investigations to diagnose the different types of vaginitis
Investigation
Description
Vaginal pH
Normal 3.5–4.6
Whiff test
Release of a fishy odor after a drop of 10% potassium hydroxide (KOH) is placed on the secretion is a positive ‘whiff test’, diagnostic of bacterial vaginosis
Microscopy
Wet mount: epithelial cells, WBCs, lactobacilli, yeasts, trichomonads, clue cells KOH slide: KOH lyses epithelial cells, WBCs and yeast cells; hyphae are seen more easily
Gram stain
Can be used to diagnose bacterial vaginosis and candidiasis; trichomonads are more difficult to identify
Culture and polymerase chain reaction (PCR) based tests
Performed when microscopy is negative, or in recurrent or resistant cases
Endocervical swabs
Obtained for Chlamydia and Gonococcus in all sexually active women since the presence of vaginal discharge is poorly correlated with the presence of infection9
Other specific tests
Herpes cultures should be obtained in the presence of ulceration Tests to rule out allergens (see ‘Allergic vulvovaginitis’) Blood tests to detect antibodies when HIV or syphilis is suspected
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The investigations outlined in Table 42.3 may be used to diagnose different types of vaginitis but their use will vary, depending on the availability of resources, staffing, equipment, expertise, time, etc.
SPECIFIC CAUSES OF VAGINITIS Bacterial vaginosis Bacterial vaginosis is the most common cause of abnormal discharge in women of childbearing age,16 but is often underdiagnosed and incorrectly managed as thrush. It was reported in 12% of pregnant women in the United Kingdom17 and 30% of women undergoing termination of pregnancy.18 The prevalence is apprecia-
Table 42.4.
ble in lesbians,19 among whom other STDs are relatively uncommon. Bacterial vaginosis represents a disruption in the vaginal ecosystem. There is an overgrowth of organisms often present as part of normal vaginal flora (predominantly anaerobes) leading to replacement of hydrogen peroxide-producing lactobacilli. On microscopy there is a shift from normal bacillary flora (scant or no lactobacilli) and the finding of normal levels of WBCs. Contributory factors and management of bacterial vaginosis are outlined in Table 42.4.
Vulvovaginal candidiasis The most common cause of vulvovaginal candidiasis is Candida albicans. This accounts for 80–90% of cases
Contributory factors and management of bacterial vaginosis
Factor
Description
Causes
Gardenerella vaginalis, Mycoplasma hominis, Mobilincus sp., Prevotella sp., Peptostreptococcus sp., Bacteroides sp., etc.
Transmission
Not sexually transmitted but increases the susceptibility of HIV transmission
Risk factors
Smoking Intrauterine contraceptive device Vaginal douching Orogenital sex
Signs and symptoms
Increased vaginal discharge which presents as a thin white, homogenous coating on the walls of the vagina Itching and irritation may be present but dysuria and dyspareunia are rare Offensive fishy odor due to volatilization of bacterial amines (produced by anaerobic metabolism following exposure to alkaline substances such as KOH and semen) Fifty percent are asymptomatic4 Inflammatory signs are absent
Diagnosis
By Amsel’s criteria: at least three out of four of the following criteria should be present for the diagnosis to be confirmed: 1) thin, white, homogenous discharge; 2) clue cells on microscopy; 3) pH >4.5; 4) fishy odor on addition of 10% KOH Gram stain vaginal smears using Hay, Ison or Nugent’s criteria:16 Gram stain has a sensitivity and specificity of 89% and 83%, respectively;20 Gram-variable coccobacilli overlie the surface of the epithelial cells Cultures are not useful because they are positive in 50% of asymptomatic women Cervical cytology has a sensitivity and specificity of 55% and 98%, respectively21
Treatment
Recommended regimens: Metronidazole 400–500 mg PO bd for 5–7 days or metronidazole 2 g PO single dose Alternatives: intravaginal metronidazole gel (0.75%) od for 5 days; intravaginal clindamycin cream (2%) od for 7 days; clindamycin 300 mg bd for 7 days Lactobacillus recolonization (via yoghurt or capsules) shows promise for the treatment of bacterial vaginosis with little potential for harm22
Complications
Obstetric: Premature labor (40% elevated risk of having preterm infants with low birth weight23), premature rupture of membranes, chorioamnionitis, postpartum endometritis Gynecologic:* Post-termination infections, post-hysterectomy vaginal cuff infections, pelvic inflammatory disease, urinary tract infection, postoperative infections, mucopurulent cervicitis
* Screening and treatment with metronidazole results in a significant reduction in these morbidities.
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women with recurrent candidiasis will be recolonized with Candida within 1 month of a short-term treatment.33 Drug resistance is less of a factor than with recurrent bacterial infections.34 Risk factors need to be addressed where identified; for example, women who develop post-antibiotic candidiasis should be treated with prophylactic antifungals. Treatment comprises induction therapy followed by a maintenance regimen using fluconazole 100–200 mg or a clotrimazole 500 mg pessary weekly for 6 months. Boric acid capsules, flucytosine capsules, and amphotericin suppositories have been used with good effect.
Trichomoniasis Figure 42.2. Candida albicans. Often seen as branching septate hyphae or yeast bodies. Appearance likened to a bamboo cane. Inflammatory changes are variable and frequently show intense eosinophilic staining of fungus and epithelial cells. Magnification 100 ×. (Courtesy of Mr Malcolm Mackie, Clinical Cytologist, William Harvey Hospital, Ashford, UK). (Fig. 42.2); non-albicans Candida accounts for the other 20%.24 The relative incidence of vaginitis caused by fungi other than C. albicans is increasing and is more difficult to eradicate. Between 20 and 40% of women who have positive cultures are asymptomatic.9 It is estimated that 75% of adult women will suffer at least one episode of vulvovaginal candidiasis during their lifetime.25 However, accurate figures are difficult to obtain, firstly due to the availability of OTC medication, and secondly to the assumption of candidiasis by clinicians prescribing without microbiologic confirmation (prospectively or retrospectively). In addition, the frequent use of OTC preparations has increased the likelihood that women will come to medical attention with inadequately treated infections.7 This, along with the widespread use of oral agents (especially in patients with HIV disease), are possible explanations for the increasing emergence of antifungal resistance.5 The contribution of sexual transmission to vulvovaginal candidiasis is currently poorly defined. Contributory factors and management of vulvovaginal candidiasis are outlined in Table 42.5.
Recurrent candidiasis Recurrent candidiasis is defined as four or more episodes of symptomatic candidiasis in a year; its prevalence is <5% of healthy women of reproductive years.30 The most common cause is incomplete eradication as demonstrated by strain typing.32 In addition, 30–50% of
Trichomoniasis is caused by the protozoan Trichomonas vaginalis. It is a relatively unusual cause of vaginal discharge in the United Kingdom.9 T. vaginalis is a flagellated protozoan which causes multifocal infection (Fig. 42.3). Apart from vaginitis, it also affects the paraurethral ducts, urethra, Bartholin’s glands, and Skene’s glands. Trichomoniasis is associated with a shift in the vaginal flora away from the normal lactobacillus-predominant flora in a majority of cases, and approximately a third meets the diagnostic criteria for frank bacterial vaginosis.35
Figure 42.3. Cervical cytology specimen. Magnification 100 ×. Unicellular pear-shaped organism 8–20 mm in diameter. Appears pale green–gray, often with eosinophilic granules and contains an oval vesicular nucleus. Inflammatory changes are usually pronounced. The single flagellum is not observed in cervical smears. (Courtesy of Mr Malcolm Mackie, Clinical Cytologist, William Harvey Hospital, Ashford, UK).
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Table 42.5.
Contributory factors and management of vulvovaginal candidiasis
Factor
Description
Risk factors
Immunocompromise (e.g. diabetes, AIDS) Medications (e.g. topical steroids, immunosuppressants, systemic antibiotics, oral contraceptives) Pregnancy – increased hormone levels affect the glycogen content which favors the growth of yeast A warm, moist environment and local maceration favor the growth of yeast (e.g. obesity, incontinence, tightfitting clothing, synthetic underwear) Use of diaphragm, spermicide or intrauterine contraceptive device Orogenital sex and frequency of sexual activity26 Any condition causing pruritus – scratching, lichenification, hyperkeratosis and maceration create a favorable environment for Candida so candidiasis and dermatosis coexist
Symptoms
Pruritus (present in 70–90%12) Cheesy discharge Soreness Superficial dysuria Superficial dyspareunia
Signs
Edema Erythema Cheesy discharge which is adherent to vaginal walls Excoriation Fissuring Satellite lesions
Diagnosis
Clinical, but symptoms and signs are non-specific Investigations: pH is 4.0–4.5; saline microscopy (sensitivity to detect pseudohyphae ranges from 40 to 60%27); increased polymorphonuclear neutrophils are present; KOH slide (sensitivity is 70%27); Gram stain may detect 65–68% of symptomatic cases28,29 Culture: Sabouraud’s media should be considered where microscopy is inconclusive, or in recurrent cases Latex agglutination tests show no advantage over microscopy30
Treatment
Both vulva and vagina should be treated simultaneously All topical and oral azole (e.g. clotrimazole vaginal cream and pessary) therapies give a 80–90% cure rate in acute cases; nystatin gives a 70–90% cure rate31 Topical therapies: Clotrimazole pessary 500 mg stat/200 mg for three nights/100 mg for six nights; nystatin pessary (100,000 units) 1–2 for 14 nights Oral therapy: Fluconazole 150 mg given as a single dose Lactobacillus recolonization (via yoghurt or capsules) shows promise for the treatment of yeast vaginitis with little potential for harm22
Pregnant women should be treated with topical agents for at least 7 days. Oral azole antifungal therapy should not be used.5
Contributory factors and management of trichomoniasis are outlined in Table 42.6.
Allergic vulvovaginitis Allergic causes of vulvovaginitis are often overlooked. The vaginal mucosa is able to show an allergic response similar to that seen in the skin, nose, eyes, and lungs. A type 1 IgEmediated allergic reaction is caused by house dust, latex, foods, semen, C. albicans, spermicides, condoms, etc. Type 4 contact and or irritant dermatitis can occur due to KY jelly, pads, tampons, deodorants, soaps, vaginal sprays, bubble bath, laundry detergents, textile dyes, etc.41 Contributory factors and management of allergic vulvovaginitis are outlined in Table 42.7.
Atrophic vaginitis Vaginal atrophy is due to hypoestrogenism and can cause abnormal vaginal discharge, dryness, burning, and introital dyspareunia among other symptoms. The atrophic process also affects the lower urinary tract and causes urinary symptoms including dysuria, frequency, nocturia, urgency, and incontinence. On examination, there are signs of atrophy which include vaginal pallor, occasional ecchymosis, petechiae, and loss of rugal folds. Lack of estrogen gives rise to thin vaginal epithelium which lacks glycogen. This change encourages overgrowth of non-acidophilic coliform organisms and loss of lactobacillus species. The vaginal pH is >5.5. Saline microscopy shows the presence of 649
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Table 42.6.
Contributory factors and management of trichomoniasis
Factor
Description
Other manifestations
Urinary tract infection, pelvic inflammatory disease, Bartholin’s gland infection
Transmission
Usually sexually transmitted Screening for other sexually transmitted infections, and notification and treatment of all other sexual partners is important It is occasionally acquired non-venerally5
Risk factors
Multiple sexual partners Smoking Intrauterine contraceptive device History of other STDs Non-use of barrier or oral contraception
Complications
Associated with preterm delivery and low birth weight infants5 May enhance HIV transmission Vaginitis emphysematosa is an uncommon condition in which gas-filled blebs occur in vaginal wall36 Vaginal cuff cellulitis can occur after hysterectomy5 Post-abortal infection is less common5 Infection of the upper genital tract is rare5
Symptoms
Frothy yellow/green discharge Pruritus, vaginal irritation, burning and soreness Lower abdominal pain Bleeding Superficial and internal dysuria5 Superficial dyspareunia Offensive odor Between 10 and 50% are asymptomatic37 Men are usually asymptomatic but can present with urethral discharge and symptoms of urethritis
Signs
Frothy yellow discharge Vulvitis Vaginitis Strawberry cervix (present in 2%37)
Diagnosis
Microscopy (wet mount) will diagnose 60% of cases36 Flagellate motile protozoans and increased levels of WBCs are seen Culture will diagnose 95% of cases37 Cervical cytology: Trichomonads have sometimes been reported; sensitivity is between 50 and 60%5 In PCR-based diagnostic tests, sensitivity and specificity levels approaching 100% have been reported38,39 With a pH >4.5, a positive whiff test is not unusual
Treatment
Oral treatment is required because topical treatment does not reach paraurethral ducts and organisms sequestered within the urethra40 Recommended regimens: Metronidazole 2 g PO single dose or metronidazole 400–500 mg PO bd for 5–7 days
Resistant cases
Diagnosis should be reconfirmed by wet preparation or culture Dose and duration of metronidazole therapy is increased23 Vaginal cream (e.g. 0.75% metronidazole cream) should be given in combination to improve response Alternative agents such as tinidazole can be tried in metronidazole-resistant cases
parabasal or intermediate cells (immature cells) with or without leukocytes (Fig. 42.4). Treatment with estrogen cream is often better than oral hormone replacement (HRT). The condition can occur in women on systemic HRT and the addition of a topical estrogen is often necessary to reverse the changes. Treatment regimens vary from daily treatments for up to 3 months to weekly treatments. Often
a long-term maintenance regimen is used to prevent recurrence.
Vaginal disease due to increased levels of lactobacilli7 Increased levels of lactobacilli can cause a thick discharge (similar to Candida) and inflammatory symp-
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Table 42.7.
Contributory factors and management of allergic vulvovaginitis
Factor
Description
Risk factors
Sexual intercourse: IgE mediated disease caused by semen, change in pH, microscopic abrasions due to inadequate lubrication, etc. are all risk factors Psychological disturbances including depression, stress, low self-esteem, and sexual dissatisfaction have all been implicated Exaggerated personal hygiene: cleansing agents or vaginal douching are significant risk factors Styles of clothing such as tight jeans or lycra underwear
Symptoms
Pruritus Burning Non-odorous vaginal discharge Dyspareunia
Signs
Often localized to mucocutaneous margins of vaginal introitus and fourchette but can also affect labia, perineum and clitoris Erythema Excoriation Lichenification Fissuring
Diagnosis
Infection, systemic disease and vulvar dermatosis should be excluded:41 • Prick and or intradermal skin test using common allergens • Total and specific IgE antibodies to these allergens • Specific IgE antibodies in vaginal secretions • Total eosinophil counts in vaginal secretions • Patch test in cases of contact dermatitis • Vaginal provocation tests
Treatment
Avoid risk factors Avoid allergens Oral antihistamines may be effective Local cromolyn sodium (a mast cell stabilizer) can improve symptoms Oral corticosteroids may be effective Immunotherapy and desensitization can be effective
toms such as burning, pruritus, superficial dysuria, and dyspareunia. Inflammatory signs are absent on examination and pH is <4.5 (more acidic). On microscopy, there is an abundance of lactobacilli but no increased levels of WBCs. Two types of vaginosis are described: cytolytic vaginosis and lactobacillus vaginosis.
Cytolytic vaginosis This represents an abnormal increase in lactobacilli and is associated with desquamation of squamous epithelial cells42 as a result of the increased acidity. Treatment aims to bring the pH to 3.8–4.5. Alkalinization with sodium bicarbonate can relieve symptoms, and therapy is continued until symptoms resolve.
Lactobacillus vaginosis Figure 42.4. A postmenopausal smear which shows parabasal squamous cells. Magnification 200 ×. (Courtesy of Mr Malcolm Mackie, Clinical Cytologist, William Harvey Hospital, Ashford, UK).
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Desquamative inflammatory vaginitis Desquamative inflammatory vaginitis (DIV) is an uncommon but disabling condition whose causation and natural history remain largely unknown. It is not a diagnosis in itself and may be associated with a range of blistering disorders such as lichen planus, pemphigus vulgaris, and pemphigoid.44 It can be a local manifestation of a systemic illness such as systemic lupus erythematosus.5 It can present at any stage of reproductive life, but may be found in an increased incidence in the perimenopausal phase.45 Patients complain of increased purulent vaginal discharge, severe dyspareunia, discomfort and irritation. On examination, the vulva appears normal but the vagina shows erythematous areas. There may be superficial erosions of the mucosa, which are characteristic of this condition.5 The vaginal pH is often elevated to greater than 4.6. There is no odor when the vaginal secretions are mixed with 10% KOH. The secretion shows increased numbers of WBCs and immature squamous epithelial cells. It has been described as a sterile inflammatory vaginitis.44 No microorganism has been clearly associated with this disease.45 Treatment is difficult though there is some response to topical steroids and 2% clindamycin cream.5,15,44
Chronic vaginitis It is important that the clinician understands the emotional state of the patient suffering with chronic vaginitis. She is often frustrated, depressed, and develops a sense of despair. There is often strain in personal relationships. Thorough evaluation is needed, and the clinician must reassess the diagnosis before proceeding with further therapy. Further investigations such as culture are needed and other differential diagnoses should be considered. Sometimes stopping treatment may even be helpful to ascertain if any remaining symptoms are iatrogenic.
social well-being of a patient. This is particularly true in patients with chronic vaginitis. Trichomoniasis is a sexually transmitted infection and therefore has important implications. Diagnosis and treatment of bacterial vaginosis prevents complications such as pelvic inflammatory disease and premature labor. Although infection is the commonest cause of vaginitis, other non-infectious, inflammatory causes should not be forgotten.
REFERENCES 1. Edwards L. The diagnosis and treatment of infectious vaginitis. Dermatol Ther 2004;17(1):102–10. 2. Hammill HA. Normal vaginal flora in relation to vaginitis. Obstet Gynecol Clin North Am 1989;16(2):329–36. 3. Egan M, Lipsky MS. Vaginitis: case reports and brief review. AIDS Patient Care STDS 2002;16(8):367–73. 4. Nyirjesy P. Vaginitis in the adolescent patient. Pediatr Clin North Am 1999;46(4):733–45. 5. McCormack WM. Vulvovaginitis and cervicitis. In: Mandell G, Bennett J, Dolin R (eds) Principles and Practice of Infectious Diseases. Amsterdam: Elsevier, 2005; 357–69. 6. Faro S. Vaginitis: diagnosis and management. Int J Fertil Menopausal Stud 1996;41(2):115–23. 7. Carr PL, Felsenstein D, Freidman RH. Evaluation and management of vaginitis. J Gen Intern Med 1998;13(5):335–46. 8. Friedrich EG. Vaginitis. 1985;152:247–51.
Am
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9. French P. Sorting out vaginal discharge. Trends Urol Gynaecol Sexual Health 2004;9(6):22–7. 10. Kent HL. Epidemiology of vaginitis. Am J Obstet Gynecol 1991;165(4 Pt 2):1168–76. 11. Mulley AG. Approach to the patient with vaginal discharge. In: Goroll AH, Mulley AG (eds) Primary Care Medicine: Office Evaluation and Management of the Adult Patient. Philadelphia: Lippincott Williams and Wilkins, 2000; 702–7. 12. Anderson MR, Klink K, Cohrssen A. Evaluation of vaginal complaints. JAMA 2004;291(11):1368–79. 13. O’Dowd TC, Bourne N. Inventing a new diagnostic test for vaginal infection. Br Med J 1994;309:40–2.
CONCLUSION Vaginitis is the most common cause for gynecologic consultation but has too often been ignored by the medical community or regarded as a minor annoyance to women. Patients who present with vaginitis deserve a thorough evaluation of their symptoms. Vaginitis can have an impact on the physical, emotional, sexual, and
14. Hammill HA. Unusual causes of vaginitis (excluding trichomonas, bacterial vaginosis, Candida albicans). Obstet Gynecol Clin North Am 1989;16(2):337–45. 15. Sobel JD. Vulvo-vaginitis in healthy women. Compr Ther 1999;25(6–7):335–46. 16. Clinical Effectiveness Group. National Guideline for the management of bacterial vaginosis. Association for
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Genitourinary Medicine and the Medical Society for the Study of Venereal Diseases, 2001. Online. Available: www.bashh.org/guidelines/2002/bv_0601.pdf. 17. Hay PE, Lamont RF, Taylor-Robinson D, Morgan DJ, Ison C, Pearson J. Abnormal colonisation of the genital tract and subsequent preterm delivery and late miscarriage. Br Med J 1994;308:295–8. 18. Blackwell AL, Thomas PD, Wareham K, Emery SJ. Health gains from screening for infection of the lower genital tract in women attending for termination of pregnancy. Lancet 1993;342:206–10. 19. Marrazzo JM, Koutsky LA, Eschenbach DA et al. Characterization of vaginal flora and bacterial vaginosis in women who have sex with women. J Infect Dis 2002;185:1307–13. 20. Schwebke J, Hillier S, Sobel J et al. Validity of the vaginal gram stain for the diagnosis of bacterial vaginosis. Obstet Gynecol 1996;88:573–6. 21. Davis J, Connor E, Clarke P et al. Correlation between cervical cytologic results and Gram stain as diagnostic tests for bacterial vaginosis. Am J Obstet Gynecol 1997;177: 532–5. 22. Van Kessal K, Assefi N, Marrazzo J, Eckert L. Common complementary and alternative therapies for yeast vaginitis and bacterial vaginosis: A systematic review. Obstet Gynecol Survey 2003;58(5):351–8. 23. Haefner HK. Current evaluation and management of vulvo-vaginitis. Clin Obstet Gynaecol 1999;42(2):184–95. 24. Spinillo A, Capuzzo E, Gulminetti R, et al. Prevalence of and risk factors for fungal vaginitis caused by non-albicans species. Am J Obstet Gynecol 1997;176:138–41. 25. Sobel JD. Epidemiology and pathogenesis of recurrent vulvovaginal candidiasis. Am J Obstet Gynecol 1985;1523:924–35. 26. Geiger AM, Foxman B. Risk factors for vulvovaginal candidiasis: a case-control study among university students. Epidemiology 1996;7:182–7.
Online. Available: candida_0601.pdf.
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31. Reef SE, Levine WC, McNeil MM et al. Treatment options for vulvovaginal candidiasis: 1993. Clin Infect Dis 1995;20(Suppl 1):S80–S90. 32. Vazquez JA, Sobel JD, Demetriou R, Vaishampayan J, Lynch M, Zervos MJ. Karyotyping of Candida albicans isolates obtained longitudinally in women with recurrent vulvovaginal candidiasis. J Infect Dis 1994;170:1566–9. 33. Horowitz BJ, Glaquinta D, Ito S. Evolving pathogens in vulvovaginal candidiasis: implications for patient care. J Clin Pharmacol 1992;32:248–55. 34. Fong TW, Bannatyne RM, Wong P. Lack of in vitro resistance of Candidiasis albicans to ketoconazole, itraconazole and clotrimazole in women treated for recurrent vaginal candidiasis. Genitourin Med 1993;69:44–6. 35. Hillier SL, Krohn MA, Nugent RP et al. Characteristics of three vaginal flora patterns assessed by Gram stain among pregnant women. Am J Obstet Gynecol 1992;166:938–44. 36. Josey WE, Campbell WG Jr. Vaginitis emphysematosa. A report of four cases. J Reprod Med 1990;35:974–977. 37. Wolner-Hanssen P, Krieger JN, Stevens CE, et al. Clinical manifestations of vaginal trichomoniasis. JAMA 1989;264:571–6. 38. Madico G, Quinn TC, Rompalo A, McKee KT Jr, Gaydos CA. Diagnosis of trichomonas vaginalis infection by PCR using vaginal swab samples. J Clin Micobiol 1998;36:3205–10. 39. Mayto H, Gilman RH, Calderon MM et al. 18S ribosomal DNA-based PCR for the diagnosis of trichomonas vaginalis. J Clin Microbiol 2000;38:2683–7. 40. Clinical Effectiveness Group. National guideline on the management of trichomonas vaginalis. 2001. Online. Available: www.bashh.org/guidelines/2002/tv_0601.pdf. 41. Moraes PS, Taketomi EA. Allergic vulvo-vaginitis. Ann Allergy Asthma Immunol 2000;85(4):253–65.
27. Sobel JD. Vaginitis. N Engl J Med 1997;337:1896–1903.
42. Cibley LJ. Cytolytic vaginosis. Am J Obstet Gynecol 1991;165:1245–9.
28. Emmerson J, Gunputrao A, Hawkswell J et al. Sampling for vaginal candidiasis: how good is it? Int J STD AIDS 1994;5:356–8.
43. Horowitz BJ, Mardh PA, Nagy E, Rank EL. Vaginal lactobacillosis. Am J Obstet Gynecol 1994;170:857–61.
29. Sonnex C, Lefort W. Microscopic features of vaginal candidiasis and their relation to symptomatology. Sex Transm Infect 1999;75:417–9. 30. Clinical Effectiveness Group. National guidelines on the management of vulvo-vaginal candidiasis. 2001.
44. Murphy R. Desquamative inflammatory vaginitis. Dermatol Ther 2004;17(1):47–9. 45. Sobel JD. Desquamative inflammatory vaginitis: a new subgroup of purulent vaginitis responsive to topical 2% clindamycin therapy. Am J Obstet Gynecol 1994;171:1215–20.
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INTRODUCTION Urinary incontinence is often regarded as a problem affecting older, postmenopausal, multiparous women.1 However, several epidemiologic studies have demonstrated that symptoms of stress urinary incontinence (SUI) is also frequent in populations of nulliparous young females.1–10 Prevalence data vary between 12 and 52%, and may be explained by differences in definitions, study design, and populations. Typically, for prevalence studies the percentage tends to drop when the former International Continence Society (ICS) definition of symptoms being socially and hygienically problematic is used.6,11 The most common type of urinary incontinence in women is SUI,12 defined as involuntary leakage on effort, exertion, on sneezing or coughing.13 Urodynamic assessment, however, is necessary to be able to separate between different diagnostic subtypes of urinary incontinence.13,14
Kulseng-Hanssen and Klevmark19 improved the methodology by placing bladder and urethral transducer catheters in a silicon cuff and sutured it to the external urethral opening to keep it stable during activity. Figure 43.1 demonstrates measurements of a patient with SUI during jumping and coughing. In 16 of the patients, 115 leakage episodes were seen in 45 minutes. In 92 of these episodes, the maximum urethral pressure decrease was larger than the detrusor pressure increase. However, some patients complained of urinary leakage during strenuous exercise (running and jumping for longer periods), although leakage was undetected even in this test. Similar results were seen in the study of Bø et al.20 where the test did not detect leakage in four subjects with convincing history of urinary leakage. As SUI may occur due to fatigue of the striated urethral wall and pelvic floor muscles, some women may need even more vigorous and continuous activities to provoke the leakage they experience outside the laboratory.
AssessmeNT Of INCONTINeNCe DURINg physICAl ACTIvITy Cough 100
RP
Jump
10 s
0 100
BP
0 Pressure (cmH2O)
Usually the diagnosis of urodynamic SUI is made during assessment in a half sitting, lithotomy position. The validity of this evaluation can be questioned, as most women only leak in a standing position. The original ICS pad test did not involve physical activity at all. However, a subsequent test involved activities such as stair climbing and jumping.15 Hennalla et al.16 and Hagen et al.17 designed tests based on physical activities. These latter tests, which involved running, jumping jacks, standing up and lying down, and abdominal curls, were found to be nine times as provocative as the ICS test involving physical activity. The authors concluded that assessment of the degree of SUI has to be physically provocative to detect SUI. Nygaard et al. reported that 7% of women admitted to urine loss only during sports, and that 40% and 17% first noted urinary incontinence during sport while in high school or junior high school, respectively.1 Methodologic problems in study design have meant that there is a lack of studies describing bladder and urethral function during physical activity. James18 has argued that assessment of SUI should be performed in standing and working positions and during physical activity. He used ambulatory bladder pressure measurements to demonstrate peaks of bladder pressure rise during running and jumping which occurred when the feet touched the ground. Although pressure rise was higher during coughing, some women were leaking only during exercise.
100
MUP
0 100
CP
0 100
DP
0
ML
Figure 43.1. Trace from a stress incontinent patient during jumping and coughing. CP, closure pressure; DP, detrusor pressure; ML, leakage; MUP, maximum urethral pressure; RP, rectal pressure. (Reproduced from ref. 19 with permission.)
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Comparing change in foot arch flexibility in 47 continent and incontinent varsity athletes, Nygaard et al.21 demonstrated a significant decreased foot flexibility in incontinent women (p<0.03). They suggested that how impact forces are absorbed may be one etiologic factor for stress incontinence, and that more research is required to understand how impact forces are transmitted to the pelvic floor. The high prevalence of urine loss in gymnasts may be explained by the extremely high impact during landing and takeoff and the transmission of this pressure to the pelvic floor.
pRevAleNCe Of URINARy INCONTINeNCe AmONg pARTICIpANTs IN spORT AND fITNess ACTIvITIes SUI implies that urine loss occurs during an increase in abdominal pressure. Therefore, one may expect that women with this condition are likely to experience urine loss during participation in most forms of physical activity. Sedentary women are less exposed to physical exertions and therefore may prevent leakage from occurring, despite the underlying condition potentially being present. The literature on urine loss associated with sport and fitness activities is mostly based on epidemiologic studies. It is therefore difficult to separate between different incontinence types, and the term SUI will be used. Studies have demonstrated that SUI is common both among physical education/sport students, women who exercise for fitness, and female elite athletes.22 Bø et al.7 demonstrated (in a study with an 84% response rate) that 26% of young physical education students reported having urinary leakage during different forms of physical activity. This study also showed a difference between a group exercising three times a week in addition to daytime physical activities at the university, and a group of sedentary nutrition students. The respective prevalences were 31% and 10%, which reached statistical significance (p=0.02). A subsequent study of first year female students (n=37) with a mean age 20.2 years demonstrated a prevalence of 38% of SUI symptoms. Eight of 13 women (61.5%) considered the leakage a social or hygienic problem,20 giving a prevalence using the former ICS definition of 21.6% for this population of physically fit, young, exercising nulliparous women. In this latter study, ambulatory urodynamic testing was used to verify urodynamic SUI. Seven women with symptoms were evaluated by urodynamics, and in six of seven urethral sphincter incompetence was confirmed. Mean leakage measured
by pad test with standardized bladder volume was 12 g (range 0–46). Nygaard et al.9 studied incontinence and exercise in a group of 326 women presenting to private gynecology offices (response rate 50%). Eighty-nine percent were exercising at least once per week, with an average of three times per week for 30–60 minutes per session. Forty-seven percent reported some degree of urinary incontinence. There is a lack of information about incontinence in female elite athletes. Bø22 performed a systematic review of the prevalence studies up to 2004, and found a variation in prevalence between sports, from zero in golfers1 up to 80% in high impact sports.23 Nygaard et al.1 surveyed all 156 women participating in varsity athletics at a large state university. The response rate was 92%. Mean age was 19.9 ± 3.3 years and all were nulliparous. The women were asked whether they had ever experienced urinary leakage during participation in sports and during coughing, sneezing, heavy lifting, walking to the bathroom, sleeping, and upon hearing the sound of running water. They rated frequency of leakage in a five-point scale. Twenty-eight percent reported urine loss while participating in their sports. There was a tendency in two-thirds of these women to be incontinent frequently rather than rarely. Sixteen percent were incontinent during practice sessions and 14% during competition.1 Forty-two percent reported urine loss during at least one of the activities of daily life, 18% more often than rarely. Twenty-one percent reported urine loss only during daily life and not during sports, and 7% noted incontinence only during sports. Bø and Sundgot-Borgen24 compared prevalence of symptoms of urinary incontinence in Norwegian elite athletes and age-matched controls and found a prevalence of 41% and 39% of SUI, and 16% and 19% of urge incontinence in athletes and controls, respectively. In order to ascertain whether high impact activity contributes to later urinary incontinence, Nygaard25 compared former female Olympians who had competed in swimming (low impact) and gymnastics or track and field (high impact). One hundred and four women participated (response rate 51%). When doing their sport as Olympians, high impact athletes had higher prevalence (36%) compared to low impact athletes (4.5%). However, when studied more than 20 years after cessation of the sport, there was no significant difference in prevalence of incontinence between the groups. It was concluded that participation in regular, strenuous, high impact activity when younger did not predispose to significant urinary leakage later in life. 657
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CONseqUeNCes Of sUI DURINg physICAl ACTIvITy Urinary incontinence may lead to withdrawal from social activities and reduction of well-being.26 Norton et al.27 reported that urinary leakage frequently interfered with daily life in more than 50% of their study group. Additionally, Fall et al.28 reported that, in their study of women with incontinence, 42% had problems during sport and physical activities. Bø et al.29 showed that two-thirds of sedentary women with urodynamic SUI reported urinary leakage to be the cause of inactivity. Of 52 women participating in specific sport and fitness activities, 27 had withdrawn from one or more activities because of leakage. Of these 27 women, 19 had withdrawn from aerobic and dance activities, despite these being among the most popular fitness activities for women. They all reported that the major leakage occurred during high impact activities during the aerobics session, especially when performing ‘jumping jacks’ (jumping with legs in subsequent abduction and adduction), which is one of the most commonly used high impact exercises in aerobic dance and general fitness programs. This corresponds with the results of Nygaard et al.9 where women reported leakage with running and high impact aerobics. Thirty percent of the exercisers noted incontinence during at least one type of exercise. Twenty percent of these women stopped doing the activity solely because of incontinence, 18% changed the way they performed an exercise, and 55% wore a pad during exercise. Frequency, time spent per session, and duration of a particular exercise had no significant impact on the prevalence.9 Brown and Miller10 concluded that urinary incontinence was an important barrier to women’s participation in physical activities. Regular physical activity is an important factor for women’s health at all ages. Moderate physical activity can be one important factor in prevention of coronary heart disease, high blood pressure, osteoporosis, musculoskeletal diseases, obesity, breast and colon cancer, anxiety, and depression.30 If one consequence of incontinence is withdrawal from physical activity, the impact on women’s health is potentially huge.
CAN physICAl ACTIvITy CAUse URINARy INCONTINeNCe? Several risk factors have been suggested for development of female urinary incontinence; hereditary weak connective tissue, weak or non-functional pelvic floor muscles, hormonal factors, dyssynergia between detrusor and
urethral smooth and striated muscle activity, pregnancy, vaginal delivery, heavy physical exertion, inactivity, obesity, cigarette smoking, menopause, and old age are suggested as being etiologic factors.31,32 To date there is little evidence supporting a strong causal effect for many of these factors. The reality is that urinary incontinence has a multifactorial etiology in women, including failure of one or more factors to compensate for another weak factor. The speed and strength of the pelvic floor muscle contraction may be one such important factor.33 Optimal pelvic floor muscle function implies a localization of the pelvic floor in an adequate anatomic position, with sufficient cross-sectional area to give structural support for the vagina, bladder, and the urethra in order to prevent descent during an increase in the abdominal pressure.34 The muscles have to be in a neurologic state of ‘readiness for action’, allowing an appropriate quick and strong response, or be a part of a feed forward loop, contracting automatically simultaneously with, or before, the intra-abdominal pressure increase.
pelvic floor muscles and female athletes Typically, there are two hypotheses about female athletes and pelvic floor muscles strength, with these hypotheses going in opposite directions.22 The first hypothesis is that general physical activity may lead to strengthening of the pelvic floor, thus making the pelvic floor muscles in female athletes stronger. To date, no research has verified this hypothesis. The fact that so many female athletes report SUI22 actually contradicts this view. No studies have yet focused on measuring pelvic floor muscle strength in female elite athletes and matched controls. However, Bø et al.20 did not find any significant difference between incontinent female sport students and a comparable continent group. However, the sample was small, and other studies have demonstrated significantly stronger pelvic floor muscles in continent than in incontinent women.33,35,36 Further studies are needed to answer this question. The second hypothesis is that heavy exercise (e.g. marathon running with repetitive bouncing towards the pelvic floor or weight lifting) may overload the pelvic floor and weaken the muscles over time. Nichols and Randall37 proposed that women exposed to chronic straining may have increased prevalence of genital prolapse because of connective tissue damage as a result of persistent intra-abdominal pressure increase. Nichols and Milley38 suggested that the cardinal and uterosacral ligaments, pelvic floor muscles, and the connective tissue of the perineum may be damaged chronically because of repeatedly increased abdominal pressure
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due to, for example, manual work and chronic cough. According to this theory, strenuous exercise raising the abdominal pressure may contribute to development of SUI in women with a predisposition to incontinence. Davis and Goodman39 studied 512 of 2651 female soldiers who entered the airborne infantry and found that nine developed urinary incontinence during the training period. Urodynamic investigation demonstrated detrusor instability in three, and urodynamic SUI in six of the women. All six with SUI demonstrated a definite cystourethrocele, a hypermobile vesical neck with loss of the posterior ureterovesical angle, and visible urine loss with Valsalva after the training period. Four of the women reported feeling a tearing pain in their lower quadrant on impact during a parachute jump, and one subject related a similar event during heavy lifting and doing sit-ups. Parachute jumping is an extreme high impact activity, and from the data available today, it is not possible to conclude whether moderate to high impact activities can cause connective tissue or pelvic floor muscle damage. It is likely that there is a self-selection of continent women who undertake high impact sports and fitness activities. Another contributing factor for SUI in female elite athletes may be hypothalamic amenorrhea due to either intensive exercise or eating disorders (or a combination of both), with resultant low estrogen levels.1 However, the association between low estrogen levels and prevalence of SUI is not clear.40 Most women in the studies of Nygaard et al. and Bø et al. who reported and demonstrated SUI had regular menstrual cycles.1,20 However, in the study by Bø and Sundgot-Borgen,24 a higher prevalence of SUI was found in those with eating disorders. Eating disorders may be associated with low estrogen levels. Nygaard et al.1 argue that some athletes (e.g. gymnasts) may have been selected for their sport because of hypermobility, and that changes in collagen concentration may be one factor in the higher prevalence of incontinence in gymnasts. However, although some studies have shown reduction in collagen tissue in women with incontinence compared to continent women,41 the links between collagen, hypermobility, and SUI is not clear. There are no studies comparing the collagen structure in gymnasts and athletes with or without SUI with that of matched controls.
leakage. However, they can be advised about choosing low impact activities; for example, walking, Nordic walking, dancing, low impact aerobics, step training, cycling, swimming, cross-country skiing, etc. If an incontinent woman wishes to participate in high impact aerobics, she may use low impact alternatives; for example, walking while the others are running, doing ‘step touch’ while others are doing jumping jacks, etc. In addition, if she leaks or feels downward pressure during sit-ups she should be advised to make an attempt to contract the pelvic floor muscles before doing abdominal curls/sit-ups. A good alternative, and an important abdominal muscle to train, is to exercise the transversus abdominis muscle. This internal abdominal muscle is most easily contracted in a crawling position with one hand on the lower abdominal wall (Fig. 43.2). The exercise is performed by lifting the abdominal wall away from the hand, and holding the contraction for 6–8 seconds. This contraction should always be combined with simultaneous pelvic floor muscle contraction, and can be done in the prone, supine, sitting and standing position. During exercise the woman should be encouraged to use specially designed protection. Fortunately, some of the best protecting pads are now manufactured in small sizes, making active women more comfortable when wearing them while exercising. In addition, women may use urethral or vaginal devices to prevent leakage during physical activity.42,43 In the study of Glavind,44 six women with stress incontinence demonstrated total dryness when using a vaginal device during 30 minutes of aerobic exercise.
protection during exercise to prevent leakage Because of the health benefits of regular moderate exercise, it is important to emphasize that women should be encouraged to continue exercising despite their urinary
Figure 43.2. Training the transversus abdominis muscle. Hold one hand under the lower abdomen and lift the navel towards the spine without curving the back. 659
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TReATmeNT No studies have been found that evaluate any treatment methods for urinary incontinence in a defined subgroup of athletes. Generally, the least invasive treatment should be tried first,45,46 with pelvic floor muscle training being the method recommended as first line treatment.46 In addition, as female elite athletes are mostly young and nulliparous, surgery is not recommended. Several randomized controlled trials have demonstrated a positive effect of pelvic floor muscle training on SUI in the general population.46–48 Bø et al.29 demonstrated that after specific strength training of the pelvic floor muscles, 17 of 23 women had improved during jumping and running, and 15 during lifting. In addition, significant improvement was obtained while dancing, hiking, during general group exercise, and in an overall score on ability to participate in different activities.29 Measured with a pad test with a standardized bladder volume, tests comprising running, jumping jacks, and sit-ups showed a significant reduction in urine loss from a mean of 27 g (95% CI: 8.8–45.1, range 0–168) to 7.1 g (95% CI: 0.8–13.4, range 0–58.3), p<0.01.49 There appear to be no published data on the effect of pelvic floor muscle training in treatment of female elite athletes. However, as these women are accustomed to conducting regular training and are highly motivated for exercise, one would expect that the effect would be equally effective or even more effective in this specific group of women. Pelvic floor muscle training should be the first choice of treatment for several reasons:
• When conducted intensively with a close follow up, it has proved to be effective.
• It is a functional and physiologic, non-invasive
•
treatment with no known side effects that can be very cost effective compared to other treatment modalities. The woman herself is given the opportunity to take control over her health: she learns body awareness and, if successful, the training may enhance selfesteem and coping strategies.
CONClUsIONs Stress urinary incontinence is prevalent in exercising women at all levels. This may well be because the activity ‘unmasks’ a predisposition to leak as it is yet not possible to conclude whether strenuous physical activity may cause SUI or pelvic organ prolapse. Current understanding certainly suggests that more vigorous exercise is associated with higher rates of leakage and that women with such problems restrict their physical
activities. More research is needed to understand how impact from different exercises may affect pelvic organs, connective tissue, and pelvic floor muscles. The effect of pelvic floor muscle training on elite athletes has not yet been evaluated. However, from current knowledge on the effect of pelvic floor muscle training, this is suggested as the first choice of treatment.
RefeReNCes 1. Nygaard I, Thompson FL, Svengalis SL, Albright JP. Urinary incontinence in elite nulliparous athletes. Obstet Gynecol 1994;84:183–7. 2. Nemir A, Middleton RP. Stress incontinence in young nulliparous women. Am J Obstet Gynecol 1954;68(4):1166–8. 3. Wolin LH. Stress incontinence in young, healthy nulliparous female subjects. J Urol 1969;101:545–9. 4. Hørding U, Pedersen KH, Sidenius K, Hedegaard L. Urinary incontinence in 45-year-old women. Scand J Urol Nephrol 1986;20:183–6. 5. Jolleys J. Reported prevalence of urinary incontinence in women in a general practice. BMJ 1988;296:1300–2. 6. Sommer P, Bauer T, Nielsen KK et al. Voiding patterns and prevalence of incontinence in women: a questionnaire survey. Br J Urol 1990;66:12–5. 7. Bø K, Mæhlum S, Oseid S, Larsen S. Prevalence of stress urinary incontinence among physically active and sedentary female students. Scand J Sports Sci 1989;11(3):113–16. 8. Simeonova Z, Bengtsson C. Prevalence of urinary incontinence among women at a Swedish primary health care centre. Scand J Prim Health Care 1990;8:203–6. 9. Nygaard I, DeLancey JOL, Arnsdorf L, Murphy E. Exercise and incontinence. Obstet Gynecol 1990;75:848–51. 10. Brown W, Miller Y. Too wet to exercise? Leaking urine as a barrier to physical activity in women. J Sci Med Sport 2001;4(4):373–8. 11. Elving LB, Foldsprang A, Lam GW, Mommsen S. Descriptive epidemiology of urinary incontinence in 3,100 women age 30–59. Scand J Urol Nephrol Suppl 1989;125:37–43. 12. Hunskaar S, Burgio K, Diokno A, Herzog A, Hjaelmås K, Lapitan M. Epidemiology and natural history of urinary incontinence in women. Urology 2003;62(Suppl 4A):16–23. 13. Abrams P, Cardozo L, Fall M et al. The standardization of terminology of lower urinary tract function: report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 2002;21:167–78. 14. Cundiff GW, Harris RL, Coates KW, Bump RC. Clinical predictors of urinary incontinence in women. Am J Obstet Gynecol 1997;177:262–7.
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15. Abrams P, Blaivas JG, Stanton SL, Andersen JT. The standardisation of terminology of lower urinary tract function. Scand J Urol Nephrol Suppl 1988;114:5–19.
Bouchard C, Shephard RJ, Stephens T (eds) Physical Activity, Fitness and Health. Champaign, IL: Human Kinetics, 1994; 774–95.
16. Henalla SM, Kirwan P, Castleden DM, Hutchins CJ, Breeson AJ. The effect of pelvic floor muscle exercises in the treatment of genuine stress incontinence in women at two hospitals. Br J Obstet Gynaecol 1988;95:81–92.
32. Bø K. Risk factors for development and recurrence of urinary incontinence. Curr Opin Urol 1997;7:193–6.
17. Hagen RH, Kvarstein B, Bø K, Larsen S. A simple pad test with fixed bladder volume to measure urine loss during physical activity. International Continence Society Annual Meeting, Oslo. 1988; 88–9. 18. James ED. The behaviour of the bladder during physical activity. Br J Urol 1978;50:387–94. 19. Kulseng-Hanssen S, Klevmark B. Ambulatory urethrocystorectometry: a new technique. Neurourol Urodyn 1988;7:119–30. 20. Bø K, Stien R, Kulseng-Hanssen S, Kristoffersen M. Clinical and urodynamic assessment of nulliparous young women with and without stress incontinence symptoms: a case control study. Obstet Gynecol 1994;84:1028–32. 21. Nygaard IE, Glowacki C, Saltzman L. Relationship between foot flexibility and urinary incontinence in nulliparous varsity athletes. Obstet Gynecol 1996;87:1049–51. 22. Bø K. Urinary incontinence, pelvic floor dysfunction, exercise and sport. Sports Med 2004;34(7):451–64. 23. Eliasson K, Larsson T, Mattson E. Prevalence of stress incontinence in nulliparous elite trampolinists. Scand J Med Sci Sports 2002;12:106–10. 24. Bø K, Sundgot-Borgen J. Prevalence of stress and urge urinary incontinence in elite athletes and controls. Med Sci Sports Exer 2001;33:1797–1802. 25. Nygaard IE. Does prolonged high-impact activity contribute to later urinary incontinence? A retrospective cohort study of female Olympians. Obstet Gynecol 1997;90:718–22. 26. Hunskaar S, Vinsnes A. The quality of life in women with urinary incontinence as measured by the sickness impact profile. JAGS 1991;39:378–82. 27. Norton P, MacDonald LD, Sedgwick PM, Stanton SL. Distress and delay associated with urinary incontinence, frequency, and urgency in women. BMJ 1988;297:1187–9. 28. Fall M, Frankenberg S, Frisen M, Larsson B, Petren M. 456 000 svenskar kan ha urininkontinens. Endast var fjærde søker hjelp før besværen. Laekartidningen 1985;82(22):2054–6. 29. Bø K, Hagen R, Kvarstein B, Larsen S. Female stress urinary incontinence and participation in different sport and social activities. Scand J Sports Sci 1989;11(3):117–21.
33. Lose G. Simultaneous recording of pressure and crosssectional area in the female urethra: a study of urethral closure function in healthy and stress incontinent women. Neurourol Urodyn 1992;11(2):54–89. 34. Bø K. Pelvic floor muscle training is effective in treatment of stress urinary incontinence, but how does it work? Int Urogynecol J 2004;15:76–84. 35. Hahn I. Pelvic floor training for genuine stress urinary incontinence. University of Gothenburg, 1993. 36. Mørkved S, Salvesen K, Bø K, Eik-Nes S. Pelvic floor muscle strength and thickness in continent and incontinent nulliparous pregnant women. Int Urogynecol J 2004;15:384–90. 37. Nichols DH, Randall CL 3rd (eds) Vaginal Surgery. Baltimore: Williams and Wilkins, 1989. 38. Nichols DH, Milley PS. Functional Pelvic Anatomy: The Soft Tissue Supports and Spaces of the Female Pelvic Organs. The Human Vagina. Amsterdam: Elsevier/NorthHolland Biomedical Press, 1978; 21–37. 39. Davis GD, Goodman M. Stress urinary incontinence in nulliparous female soldiers in airborne infantry training. J Pelvic Surg 1996;2(2):68–71. 40. Fantl JA, Cardozo L, McClish DK. Estrogen therapy in the management of urinary incontinence in postmenopausal women: a meta analysis. First report of the hormones and urogenital therapy committee. Obstet Gynecol 1994;83:12–18. 41. Ulmsten U, Ekman G, Giertz G, Malmstrøm A. Different biochemical composition of connective tissue in continent and stress incontinent women. Acta Obstet Gynecol Scand 1987;66:455–7. 42. Thyssen HH, Lose G. Long-term efficacy and safety of a disposable vaginal device (Continence Guard) in the treatment of female stress incontinence. Int Urogynecol J 1997;8:130–3. 43. Staskin D, Bavendam T, Miller J. Effectiveness of a urinary control insert in the management of stress urinary incontinence; results of a multicenter study. Urology 1996;47:629–36. 44. Glavind K. Use of a vaginal sponge during aerobic exercises in patients with stress urinary incontinence. Int Urogynecol J 1997;8:351–3.
30. Bouchard C, Shephard RJ, Stephens T. Physical activity, fitness, and health. Consensus Statement. Champaign, IL: Human Kinetics, 1993.
45. Fantl JA, Newman DK, Colling J et al. Urinary incontinence in adults: acute and chronic management. 2, update [96-0682]. Rockville, MD: U.S. Department of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research, 1996; 1–154.
31. Bø K. Physical activity, fitness and bladder control. In:
46. Wilson PD, Bø KH-SJ, Nygaard I, Staskin D, Wyman J, Bour-
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chier A. Conservative treatment in women. In: Abrams P, Cardozo L, Khoury S, Wein A (eds) Incontinence. Plymouth, UK: Health Publication, 2002; 571–624. 47. Hay-Smith E, Bø K, Berghmans L et al. Pelvic floor muscle training for urinary incontinence in women (Cochrane Review). Oxford: The Cochrane Library, 2001. 48. Bø K. Is there still a place for physiotherapy in the
treatment of female incontinence? EAU Update Series 2003;1:145–53. 49. Bø K, Hagen RH, Kvarstein B, Jørgensen J, Larsen S. Pelvic floor muscle exercise for the treatment of female stress urinary incontinence: III. Effects of two different degrees of pelvic floor muscle exercise. Neurourol Urodyn 1990;9:489–502.
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44 Problems associated with sexual activity Andrew Hextall, Nicholas Christofi
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INTRODUCTION Urinary incontinence may have an adverse effect on almost every aspect of a woman’s life, including sexual relations with her partner.1 A woman’s sexuality is concerned not only with her sexual activity, but also with the perception of her own image and the formation of relationships with others.2 Nearly 50% of women presenting with incontinence, frequency or urgency report feeling odd or different from other people because of their bladder problems and 40% feel less attractive.3 Poor self-esteem is a frequent problem and difficulties with personal relationships may contribute to the depression and social isolation often felt by women with bladder dysfunction.4,5 Sexual intercourse may have an impact on the bladder in several important ways:
• Coital incontinence may give rise to sexual problems • •
for the woman, her partner or both where none had previously existed. Incontinence during intercourse may be blamed for problems within a relationship, although a degree of sexual dysfunction may have already existed. Sexual activity can give rise to urogenital problems – for example, dysuria and urinary tract infection (UTI).
In this chapter we review the impact of urinary incontinence and gynecologic interventions in the sexually active woman and examine the role of sexual intercourse in the pathophysiology of a UTI.
PREVALENCE OF COITAL INCONTINENCE Despite increasing media attention and public awareness, 40% of women with incontinence delay seeking treatment because of embarrassment about their condition.3 Discussing their urinary problem with a doctor or nurse is very difficult for many women, and this may explain why symptoms of coital incontinence are not always volunteered immediately. For example, in a survey of 400 incontinent women, of whom 324 were sexually Table 44.1.
active, only two women mentioned the problem except in response to direct enquiry.6 Clinicians may also feel uncomfortable or concerned about their ability to take an adequate history regarding what may be considered a private problem. Some hospitals use a preconsultation questionnaire, and while this may be time saving and give valuable information, further enquiry is often necessary. As with other history taking, it is important to put the patient at ease,7 perhaps by asking about other urinary symptoms or medical complaints first. Open questions such as ‘Is there anything else you would like to discuss?’ or ‘Many women with incontinence leak during sex. Is this a problem for you?’ are then a good way forward. It may also be appropriate to ascertain if the coital incontinence has had any impact on the patient’s relationship with her partner, although it should be noted that for some couples leakage during intercourse may not necessarily give rise to any sexual dysfunction. A systematic review of the literature suggests that coital incontinence occurs in 2% of the female population in the community, but data on the subject are very limited as only two studies met the criteria for inclusion in the review.8 However, several studies have attempted to determine the frequency of coital incontinence among women presenting with a variety of urinary complaints (Table 44.1). The retrospective nature of some of the studies, variations in questionnaire design and sensitivity, and type of study population may account for some of the observed differences. The four largest reports suggest a prevalence of between 24 and 34%.6,9–11 Walters et al12 reported a figure of 62%, which should be interpreted with caution because of the small number of patients studied. A much larger study looked at 2153 consecutive women attending for urodynamic investigation: 228 women complained of coital incontinence on direct questioning, with only 22 women (10%) volunteering this symptom prior to direct enquiry.13 There were no data, however, as to the number of women from the total sample who were sexually active. It is clear that coital incontinence may occur in women with many types of lower urinary tract dysfunction. Most studies do not show any significant differ-
The prevalence of coital incontinence among women presenting with lower urinary tract symptoms
Reference
Number of sexually active women
Sexually active women with coital incontinence (%)
324
24
839
23
Thiede & Thiede
235
27
Vierhout & Gianotten11
254
34
42
62
6
Hilton
9
Korda et al.
10
Walters et al.
12
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ences in the overall prevalence of coital incontinence between women with (former nomenclature) genuine stress incontinence (GSI) or detrusor instability (DI). In addition, urodynamic studies usually fail to discriminate between those women likely to leak during sexual activity and those who do not. Some reports have attempted to assess if the timing of the incontinence occurring during sexual activity differed in women with GSI or DI. Hilton6 found that in two-thirds of affected women the incontinence occurred during penile penetration whereas in the remaining third it was restricted to orgasm. In the group who experienced leakage on penetration, 70% had GSI and only 4% had DI, whereas in the group that experienced leakage during orgasm, 42% had GSI and 35% had DI. It was concluded that incontinence occurring during penetration was frequently associated with GSI, and women who experienced leakage during orgasm alone were more likely to have DI. However, others have found that 77–93% of women with GSI and coital incontinence experience urine loss at orgasm.11,13
PATHOPHYSIOLOGY OF COITAL INCONTINENCE There are a number of theoretical reasons why women may develop coital incontinence but practical difficulties have limited attempts at clarification. Riley and co-workers14 used ultrasonography to show that penetrative intercourse in humans is associated with considerable displacement of the female pelvic anatomy. A high degree of indentation and stretching of the anterior vaginal wall and bladder base occurs in both the missionary and female-superior positions, and illustrates how the lower urinary tract may become traumatized during intercourse and give rise to postcoital urinary symptoms.15 The presence of the erect penis in the vagina may therefore displace the bladder neck and disturb the continence mechanism.11 Women with a degree of urethral sphincteric incompetence may be expected to be at particular risk of coital incontinence. However, urodynamic studies have failed to show that women who leak during penetration have lower urethral pressures than continent controls.6 Penile stimulation of the trigone and bladder base may provoke abnormal detrusor contractions during intercourse, resulting in raised intravesical pressures and incontinence. A similar effect may also occur at orgasm,16 particularly given the increased prevalence of DI in women who leak only at climax. However, cystometry has not been performed in asymptomatic women during sexual intercourse to confirm or refute this hypothesis.
The phenomenon of female ejaculation has a long and often disputed history, with considerable debate still occurring between gynecologists and sex therapists as to its existence and possible origin. Grafenberg17 reported the expulsion of large quantities of clear fluid at the peak of orgasmic response, which was thought to originate from the urethral glands. However, other authors have suggested that urinary leakage is a more likely, but less socially acceptable, explanation.18 It does seem clear, however, that many women report having fluid release at the time of orgasm. Anderson Darling and co-workers19 performed an anonymous survey of 2350 professional women in the United States and Canada. Of the 1172 (50%) women whose responses were used in the analysis, 40% reported having experienced ejaculation at the moment of orgasm, with almost 10% admitting that they ‘frequently’ urinated at climax.
INCONTINENCE AND SEXUAL DYSFUNCTION Several studies have examined the prevalence of sexual dysfunction among middle-aged women, the group most likely to be affected by coital incontinence. Osborn and co-workers20 interviewed 436 women aged 35–59 years, with a male partner, who were identified from a general practitioner database. One-third of women had at least one operationally defined sexual problem (impaired interest 17%, vaginal dryness 17%, infrequent orgasm 16%, dyspareunia 8%), but only 10% of women regarded themselves as having sexual dysfunction. Sexual difficulties were also found in 45% of 40-year-old Danish women surveyed by Garde and Lunde21 and 49% of 1219 randomly selected Latin American women with a mean age of 35.6 years.22 In the study by Osborn and co-workers,20 the only gynecologic factor that was associated with sexual dysfunction was the presence of stress incontinence occurring once or more a week, regardless of age. Sexual problems are certainly more frequent among women with incontinence than the background community rates; this may be explained in part by the presence of a number of physical and psychological factors (Table 44.2). Sutherst23 reported that 46% of incontinent patients felt that their sex life had been adversely affected by their bladder problem: 35% said that intercourse took place less frequently; 12% had ceased to have any sexual activity. It is possible that psychosexual abnormalities may be related to urinary symptoms in general, rather than specific diseases of the lower urinary tract.12,24 However, Field and Hilton25 found that significantly more women with DI had sexual dysfunction (71%) than had those with GSI (29%). An interest665
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Table 44.2.
Reasons why incontinence may lead to sexual dysfunction
Reduced sexuality • Poor self-esteem • Depression • Decreased libido • Presence of pads/pants • Reduced spontaneity Performance anxiety • Concerns about odor • Fear of leaking occurring during penetration or at orgasm Pain • Urinary dermatitis • Dyspareunia from previous prolapse or continence surgery Adverse reaction from partner • Reduced attraction • Erectile dysfunction
ing finding was that in women in whom no urodynamic abnormality was detected, 54% reported sexual problems. This may be related to the fact that women in this group tend to have higher anxiety and neuroticism scores than do women with DI or GSI.26 Urinary incontinence and urogenital prolapse have similar etiologies and the two conditions frequently coexist.27 Weber and co-workers28 compared the sexual function of 80 women complaining of prolapse, with or without incontinence, with 30 continent controls. Only 45 (56%) of the women with prolapse and 17 (57%) of the women without prolapse were currently sexually active. Of the sexually active women with prolapse, 70% said that their prolapse or incontinence had not led to a change in interest in sexual activity or intercourse. Indeed, anecdotal evidence suggests that many women with severe prolapse, and even those with a pessary in situ, can continue having relatively normal intercourse. One of the main findings of this study and others20,25 is that, in women with urinary symptoms, sexual dysfunction and inactivity become increasingly common with age. Several epidemiologic studies have reported a tendency towards a gradual decline in sexual activity in both men and women with aging.29,30 Impaired mobility, psychological disturbance, chronic illness and the use of medication, particularly sedatives, are also important factors associated with a decline in sexual activity,31,32 and each becomes more prevalent with advancing age. Most population studies also show that sexual difficulty is related to continence status. Sexual dysfunction has also been reported in about 70% of women with multiple sclerosis, with a significant correlation between bladder
and sexual dysfunction (p<0.0001).33 This is a particular problem for women over the age of 50 years, and is strongly associated with bladder and bowel dysfunction. In some women, the onset of incontinence may coincide with the menopause,34 which is itself a significant risk factor for sexual problems. During the climacteric, many women and their partners experience a decline in sexual interest, activity, and responsiveness.35 The problem is not restricted to women; approximately one in five women attending a menopause clinic had a partner suffering from medical, psychiatric or sexual problems that contributed to the deterioration in the couple’s sex life.36 In a recent study of 2465 communitydwelling Swedish women aged over 55 years, the most frequent reason for cessation of sexual activity was lack of a partner.37 The prevalence of male sexual dysfunction among the partners of women having treatment for urogynecologic problems is unknown. Hysterectomy is the most frequently performed major gynecologic operation but whether the procedure has a major impact on urinary or sexual function has been a controversial issue.38 A number of physical and psychological factors – including cultural beliefs, preconceived views on the role of the uterus, and knowledge of reproductive anatomy – are important but are difficult to quantify. In general, gynecologists tend to reassure women that hysterectomy is unlikely to have a significant effect on their sex life and may even enhance it, particularly if concerns about troublesome vaginal bleeding and pelvic pain are eradicated. Recent evidence supports this view and also sheds light onto the other controversial issue of whether subtotal hysterectomy – where the cervix is preserved – confers any psychosexual benefit compared to total hysterectomy. Thakar and co-workers conducted a randomized, double-blind trial comparing total (TAH) and subtotal (SAH) abdominal hysterectomy in 279 women for benign disease.39 The main outcome measures were bladder, bowel, and sexual function at 12 months. There was no detrimental effect on bowel or bladder function in either group. In fact, they observed a non-statistically significant improvement in urinary frequency, nocturia, stress incontinence, and bladder capacity equally in both arms of the study. Measures of sexual function (including frequency of intercourse, frequency of orgasm, and rating of sexual relationship with partner) did not change significantly with either intervention. In another large multicenter trial, 319 Danish women were randomized to TAH and SAH as above.40 Women were followed up to 12 months with regard to desire for sex; frequency of intercourse; frequency, quality, and localization of orgasm; satisfac-
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tion with sexual life and dyspareunia. None of these variables changed significantly between entry and the 1-year follow-up except dyspareunia, which was significantly reduced equally in both intervention groups (p=0.009). Perhaps not surprisingly, however, it is clear that women undergoing hysterectomy and radiotherapy for gynecologic malignancy experience more sexual dysfunction than those undergoing hysterectomy for benign disease.41 A number of factors may therefore contribute to sexual dysfunction in women with urinary incontinence. The psychological consequences of this distressing condition, once established, can become incorporated into an individual’s lifestyle and personality. Sexual dysfunction often becomes worse over time because of the development of performance anxiety, where the goal of sexuality is no longer enjoyment, but ‘getting it right’. Such factors, described by Masters and Johnson as ‘spectating’, are important in perpetuating sexual difficulties.42 This may have major implications for the treatment of these women, as the successful management of lower urinary tract symptoms may not necessarily improve their sexual dysfunction.
TREATMENT OF INCONTINENCE AND SEXUAL DYSFUNCTION Treatments for urinary incontinence are almost always assessed in terms of objective changes in urodynamic results and subjective improvement in urinary symptoms. More recently, this limited approach has been extended and now quality-of-life measures are becoming much more important, particularly in the evaluation of new techniques. Conservative therapies such as pelvic floor exercises or electrical stimulation carry virtually no reported long-term sequelae. However, for women with incontinence or prolapse opting for surgical treatment, the type of operation and subsequent risks of dyspareunia are important considerations. For some patients, simple measures such as emptying the bladder before sex or a change of position are effective in reducing the risk of coital leakage. However, few studies have assessed the effect of treatment on coital incontinence, despite the fact that urinary incontinence and sexual dysfunction are so closely related; most have considered it only as a secondary outcome measure after results of therapy for stress or urge incontinence have been presented. Hilton43 reported that the cure rate for coital incontinence following treatment for stress incontinence may be lower when compared to that of other symptoms, with only 66% of women reporting a cure compared with 88% in other circumstances. Other
authors reported cure rates of 70% for coital incontinence and 77% for stress incontinence following Burch colposuspension.44 There is very little information about the benefits of non-surgical treatments on sexual activity in women with urinary symptoms. One study of 42 women undergoing intensive pelvic floor physiotherapy found improvement in the ability to achieve orgasm and a reduced incidence of dyspareunia compared to the beginning of the program, but there is clearly a need for larger studies on the subject.45 There are no randomized trials comparing surgical and non-surgical treatments. Haase and Skibsted46 performed a prospective study of 55 women undergoing a primary surgical procedure for stress incontinence or prolapse. Postoperatively, 13 women experienced an improvement in their sex life, 35 no change, and 5 a deterioration. Improvement resulted from a cure of coital incontinence; deterioration resulted from dyspareunia secondary to a posterior vaginal wall repair. Although colposuspension alters the vaginal axis, none of the 14 patients who underwent this procedure alone, or the six women who underwent this procedure in combination with a vaginal repair, reported any dyspareunia. A more recent study looked at 118 women undergoing vaginal surgery for urinary incontinence or genital prolapse with follow-up to 1 year.47 Women in the prolapse group reported increase in dyspareunia and of stress incontinence by 13% and 14%, respectively. Although dyspareunia did not seem to increase significantly in women in the incontinence group, they reported reduced frequency of sexual intercourse 1 year postoperatively. The total score of all sexual variables deteriorated in both groups. Two other studies have addressed the same issue and found that 8% (3 out of 36)48 and 18% (7 out of 39)49 of women complained of postoperative dyspareunia, although in the latter series no attempt was made to exclude the effects of previous surgery. The use of synthetic mesh for the repair of urogenital prolapse seems to reduce the risk of recurrence, at least in the short term. In a recent prospective study, Milani and colleagues recruited 63 women for vaginal repair with a prolene mesh (32 for anterior repair and 31 for posterior repair) with a mean follow-up of 17 months.50 The mesh was placed just beneath the vaginal mucosa, which was dissected superficially so that all the fascial tissue was left attached to the bladder or rectum. The fascial tissue was then plicated anteriorly or posteriorly with interrupted sutures prior to inserting the mesh. Despite the fact that anatomic success was achieved in 94% of cases, in the anterior repair arm dyspareunia increased by 20%, and 13% had vaginal erosion of the 667
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mesh. In the posterior repair arm, 63% complained of increased dyspareunia, and erosion occurred in 6.5%. One mesh had to be removed due to pelvic abscess. The authors felt that routine use of the prolene mesh for vaginal repair should be abandoned and only considered in exceptional cases. However, pain on intercourse following vaginal surgery has been known to be a problem for many years51,52 and remains a significant cause of sexual morbidity, even after standard operations not using synthetic materials.53 Insertion of tension-free vaginal tape (TVT) is becoming the most common operation for stress incontinence. Two retrospective questionnaire studies looked at the impact of the procedure on women’s sexual function. They found an overall improvement in sexual activity and satisfaction in 26%54 and 50%55 of women, mainly due to cure of stress and/or coital incontinence. Deterioration in sexual function was observed in 1% and 4%, respectively. The results of larger prospective studies on the subject are awaited with interest. Women with DI usually present with more than the symptom of urinary leakage during intercourse. Bladder retraining and anticholinergic therapy are the treatments of choice but their cure rate in this situation remains unclear. Imipramine has been advocated as a particularly useful treatment.18 Women who have a urinary diversion for intractable incontinence may find an improvement in their sex life following surgery. Nordstrom and Nyman56 investigated the effect of ileal-conduit urinary diversion on the sexual function of 15 women who were undergoing the procedure for incontinence, mainly because of spinal cord injury or radiotherapy for gynecologic malignancy. Seven women (47%), four of whom were sexually inactive before surgery, reported increased sexual desire and activity, and found their overall sex life to be more satisfying following surgery. In a larger series of 126 men and 47 women, 56% of patients had reduced sexual desire following ileal loop urostomy.57 Schover and von Eschenbach58 interviewed nine sexually active women before and after radical cystectomy (six of the women also received preoperative irradiation). All seven of the women who resumed sexual activity experienced initial dyspareunia but this eventually improved. Catheterization may be indicated for women with acute or chronic urinary retention or a neuropathic bladder, or sometimes for incontinence. Clean intermittent self-catheterization is of particular benefit to women who remain sexually active.59 Long-term urethral catheterization has the drawback of discomfort, urethral trauma, and a high incidence of contamination from perineal flora, which may lead to symptomatic infection.
Suprapubic catheterization is often more comfortable, and should always be considered if the patient wants to continue with sexual relations. Even when the physical aspects of coital incontinence have been treated, there may well be psychological sequelae. Thus, overall management must take account of both aspects.60 A sympathetic approach is required, with the aim of helping the couple come to terms with their disability, which will hopefully allow them to have a mutually enjoyable sex life despite their problem.43
URINARY TRACT INFECTION AND SEXUAL INTERCOURSE Generations of women have recognized the association between sexual intercourse and the development of urinary symptoms. Nulliparity and a rigid perineum contribute to the development of postcoital dysuria, also known as ‘honeymoon cystitis’. Kunin and McCormac61 showed that nuns have a lower prevalence of bacteriuria than other populations of women in early adult life. Organisms are massaged into the urethra and bladder during intercourse and, if they are not voided soon after, they multiply and may cause infection. Buckley et al.62 found an increase in the urinary bacterial count after coitus in 30% of women, and Nicolle et al.63 reported that both symptomatic and asymptomatic bacteriuria was more frequent the day after intercourse. Several behavioral factors have been shown to enhance the risk of UTI following sexual intercourse. These include deferred voiding after intercourse,64 frequent intercourse,65 low fluid intake,66 and deferred voiding after the initial urge to micturate.67 A large prospective study by Hooton and co-workers examined the risk factors for UTI in young women.68 A total of 796 healthy, sexually active women were included on the basis that they were starting a new contraceptive method and were willing to participate in the study. Two cohorts of women were investigated for a total of 323 person-years of follow-up. The annual incidence of acute cystitis was 0.7 episodes per person-year among university students (90% were confirmed infections on culture) and 0.5 episodes per person-year among women enrolled in a health maintenance program. Using multivariate analysis, the authors were able to identify the contraceptive diaphragm and spermicide use, recent sexual intercourse, and a history of recurrent UTI as independent risk factors for UTI among women at each study site. The relative risk of UTI increased from 1.0 for unmarried women who had not been sexually active in the previous week to 9.0 for women who had had intercourse seven times during that period.
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Some women are particularly sensitive to postcoital urinary tract dysfunction due to the development of a relatively high urethral pressure following intercourse. Contraceptive diaphragms may also reduce urinary flow, and research has shown that the risk of referral to hospital for UTI is two to three times higher amongst diaphragm users than among well-matched controls.69 Spermicidal cream and the use of spermicidal-lubricated condoms can sometimes result in vaginal and urethral irritation. Several simple measures may be effective in reducing the risk of postcoital UTI. Close attention to perineal hygiene, change of coital technique, use of a vaginal lubricant, and avoidance of the contraceptive diaphragm may all be successful first-line measures. Women should be encouraged to drink fluid before anticipated sex to facilitate postcoital voiding. Ingestion of products containing cranberry (as juice or a supplement) has long been thought to afford protection against UTIs.70 Cranberries contain two substances (proanthocyanidines and fructose) which are thought to inhibit adhesion of infecting bacteria, particularly type 1 and type P fimbriated Escherichia coli, to the uroepithelium.71,72 A systematic review of the literature considered the role of cranberry in the setting of recurrent UTIs and found the relative risk of developing a UTI over 6 months while taking cranberry to be reduced to 0.61 (CI 0.4–0.91) compared to 1.0 for placebo or no treatment.73 The role of cranberry in prophylaxis against infection following intercourse, however, has yet to be established. For women who do not respond to simple measures, regular or intermittent antibiotic prophylaxis is usually effective.74,75 A recent systematic review of the literature found evidence that in women with recurrent UTIs associated with sexual activity, postcoital ciprofloxacin is equally as effective as a continuous daily prescription and should be considered in this setting.76 There is evidence that local application of estrogen could be protective against infection in the context of recurrent UTIs in young women who are on oral contraceptives. Pinggera et al. administered a 4-week course of vaginal estrogen cream to 30 women with proven recurrent UTIs and followed them up to 11 months.77 Of these 30 women, 24 reported no symptoms of cystitis over the duration of the study. Improvement was also observed in the cystoscopic appearances of the bladder epithelium and the arterial perfusion of the bladder base as quantified by Doppler studies (p<0.001) at 11 months. The role of estrogen therapy for postmenopausal women with recurrent UTIs is controversial and is discussed further in Chapter 47. Those women who continue to have postcoital symptoms should undergo further investigation. Mid-stream
urine analysis is mandatory and culture for fastidious organisms, including Mycoplasma hominis and Ureaplasma urealyticum, is often worthwhile. Acute urethritis may also be caused by Chlamydia, which, although difficult to isolate, responds well to a 7–14 day course of doxycycline or single dose of azithromycin. Underlying abnormalities such as voiding difficulties and vesicoureteric reflux should always be considered, and imaging of the renal tract with ultrasonography, intravenous urography or videocystourethrography may be necessary. It is also sometimes appropriate to perform a cystourethroscopy and or magnetic resonance imaging to exclude a urethral diverticulum or an intravesical foreign body such as a calculus. Our policy is also to take a bladder biopsy, even if the cystoscopic appearance is normal, because 50% of women will have histologic evidence of underlying chronic cystitis in this situation.78
CONCLUSIONS Urinary symptoms may have a profound effect on the sexual health of women. Coital incontinence is a relatively frequent problem encountered in the urogynecology clinic but few women admit to this symptom unless asked directly. The pathogenesis is not entirely understood but it is clear that urinary leakage during intercourse can occur on penetration, orgasm, or both, in women with a variety of different urinary problems. Uterovaginal prolapse frequently coexists with incontinence as the two conditions have similar etiologies; it can also interfere with sexual function. Hysterectomy is the most frequently performed major gynecologic operation. There is no evidence that abdominal hysterectomy for benign disease, whether total or subtotal, has a detrimental effect on sexual function. It might, in fact, relieve dyspareunia in some cases. Vaginal surgery for prolapse can cause significant dyspareunia postoperatively and even more so if synthetic materials in the form of a mesh are inserted. Initial reports on sexual function after TVT insertion for stress incontinence are encouraging, but further research on the subject is underway. Sexual dysfunction may continue even when other urinary symptoms have been treated successfully and objective urodynamic evaluation fails to detect any residual abnormality. Sexual intercourse is an important risk factor for many symptoms, but particularly for UTI. For many women, simple measures such as maintaining good perineal hygiene, passing urine after sex, and avoiding the contraceptive diaphragm are all that is necessary. There is limited evidence that ingestion of cranberry juice and local application of estrogen can reduce the incidence 669
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of recurrent UTIs, but their role in preventing postcoital infection is controversial. Prophylactic antibiotics, taken either after intercourse or on a regular basis, are effective second-line measures. However, some women with persistent problems require investigation to exclude an underlying urogenital abnormality.
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16. Khan Z, Bhola A, Starer P. Urinary incontinence during orgasm. Urology 1988;31:279–82. 17. Grafenberg E. The role of the urethra in female orgasm. Int J Sexol 1950;3:145–8. 18. Cardozo LD. Sex and the bladder. Br Med J (Clin Res Ed) 1988;296:587–8. 19. Anderson Darling C, Davidson JK, Conway-Welch C. Female ejaculation: perceived origins, the Grafenberg spot/area and sexual responsiveness. Arch Sex Behav 1990;19:29–47. 20. Osborn M, Hawton K, Gath D. Sexual dysfunction among middle aged women in the community. Br Med J 1988;296:959–62. 21. Garde K, Lunde I. Female sexual behaviour: a study in a random sample of 40-year-old Danish women. Maturitas 1980;2:225–40. 22. Abdo CHN, Oliveira WM Jr, Moreira ED Jr et al. Prevalence of sexual dysfunctions and correlated conditions in a sample of Brazilian women – results of the Brazilian study on sexual behavior (BSSB). Int J Impot Res 2004;16:160–6. 23. Sutherst JR. Sexual dysfunction and urinary incontinence. Br J Obstet Gynaecol 1979;86:387–8. 24. Clark A, Romm J. Effect of urinary incontinence on sexual activity in women. J Reprod Med 1993;38:679–83.
6. Hilton P. Urinary incontinence during sexual intercourse: a common, but rarely volunteered, symptom. Br J Obstet Gynaecol 1988;95:377–81.
25. Field SM, Hilton P. The prevalence of sexual problems in women attending for urodynamic investigation. Int Urogynecol J 1993;4:212–15.
7. Tomlinson J. ABC of sexual health. Taking a sexual history. Br Med J 1998;317:1573–6.
26. Norton KRW, Bhat AV, Stanton SL. Psychiatric aspects of urinary incontinence in women attending an outpatient urodynamic clinic. Br Med J 1990;301:271–2.
8. Shaw C. A systematic review of the literature on the prevalence of sexual impairment in women with urinary incontinence and the prevalence of urinary leakage during sexual activity. Eur Urol 2002;42:432–40.
27. Stanton SL. Vaginal prolapse. In: Shaw R, Soutter P, Stanton SL (eds) Gynaecology. Edinburgh: Churchill Livingstone, 1992; 437–47.
9. Korda A, Cooper M, Hunter P. Coital incontinence in an Australian Population. Asia Oceania J Obstet Gynaecol 1989;15:313–15.
28. Weber AM, Walters MD, Schover LR et al. Sexual function in women with uterovaginal prolapse and urinary incontinence. Obstet Gynecol 1996;85:483–7.
10. Thiede HA, Thiede FK. A glance at the urodynamic database. J Reprod Med 1990;35:925–31.
29. Verwoert A, Pfeiffer E, Wang H. Sexual behaviour in senescence: changes in sexual activity and interest in aging men and women. J Geriatr Psychiatry 1969;2:163–80.
11. Vierhout ME, Gianotten WL. Mechanisms of urine loss during sexual activity. Eur J Obstet Gynecol Reprod Biol 1993;52:45–7. 12. Walters MD, Taylor S, Schoenfeld LS. Psychosexual study of women with detrusor instability. Obstet Gynecol 1990;75:22–6. 13. Moran PL, Dwyer SP, Ziccone P. Urinary leakage during coitus in women. J Obstet Gynaecol 1999;19:286–8. 14. Riley AJ, Lees WR, Riley EJ. An ultrasound study of human coitus. In: Bezemer W (ed) Sex Matters. Amsterdam: Elsevier Science, 1992; 29–32. 15. Kelleher CJ, Cardozo LD. Sex and the bladder. Sexual Marital Ther 1993;8:231–41.
30. Diokno AC, Brown MB, Herzog R. Sexual function in the elderly. Arch Intern Med 1990;150:197–200. 31. Nilsson L. Sexuality in the elderly. Acta Obstet Gynecol Scand 1987;140:52–8. 32. Mooradian AD, Greiff V. Sexuality in older women. Arch Intern Med 1990;150:1033–8. 33. Zorzon M, Zivadinov R, Monti-Bragadin L et al. Sexual dysfunction in multiple sclerosis: a 2-year follow-up study. J Neurol Sci 2001;187:1–5. 34. Hextall A, Cardozo LD. The menopause and lower urinary tract dysfunction. Urogynecol Int J 1997;11:103–7. 35. Graziottin A. Sexuality and the menopause. In: Studd
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JW (ed). The Modern Management of the Menopause. Annual review 1998. Carnforth, Lancashire: Parthenon, 1998; 49–58.
53. Kahn M, Stanton SL. Posterior colporrhaphy: its effects on bowel and sexual function. Br J Obstet Gynaecol 1997;104:82–6.
36. Sarrel PM, Whitehead MI. Sex and menopause: defining the issues. Maturitas 1985;7:217–24.
54. Elzevier-Hendrik W, Venema-Pieter L, Lycklama-aNijeholt-August AB. Sexual function after tension free vaginal tape (TVT) for stress incontinence: results of a mailed questionnaire. Int Urogynecol J Pelvic Floor Dysfunct 2004;15:313–18.
37. Lindgren R, Berg G, Hammar M et al. Hormone replacement therapy and sexuality in a population of Swedish postmenopausal women. Acta Obstet Gynecol Scand 1993;72:292–7. 38. Thakar R, Mayonda I, Stanton SL et al. Bladder, bowel and sexual function after hysterectomy for benign conditions. Br J Obstet Gynaecol 1997;104:983–7.
55. Glavind K, Tetsche-Mette S. Sexual function in women before and after suburethral sling operation for stress urinary incontinence: a retrospective questionnaire study. Acta Obstet Gynecol Scand 2004;83:965–8.
39. Thakar R, Ayers S, Clarkson P et al. Outcomes after total versus subtotal hysterectomy. N Engl J Med 2002;347:1318–25.
56. Nordstrom GM, Nyman CR. Male and female sexual function and activity following ileal conduit urinary diversion. Br J Urol 1992;70:33–9.
40. Zobbe V, Gimbel H, Anderson-Birthe M et al. Sexuality after total vs subtotal hysterectomy. Acta Obstet Gynecol Scand 2004;83:191–6.
57. Boyd SD, Feinberg SM, Skinner DG et al. Quality of life survey of urinary diversion patients: comparison of ileal conduits versus continent Kock ileal reservoirs. J Urol 1987;138:1387–9.
41. Lalos O, Lalos A. Urinary, climacteric and sexual symptoms one year after treatment of endometrial and cervical cancer. Eur J Gynaecol Oncol 1996;17:128–36. 42. Masters WH, Johnson VE. Human Sexual Inadequacy. London: Churchill Livingstone, 1970. 43. Hilton P. Sexuality and urinary incontinence. Br J Sex Med 1989;6:230–3. 44. Baessler K, Stanton SL. Does Burch colposuspension cure coital incontinence? Am J Obstet Gynecol 2004;190:1030–3. 45. Beji NK, Yalcin O, Erkan HA. The effect of pelvic floor training on sexual function of treated patients. Int Urogynecol J Pelvic Floor Dysfunct 2003;14:234–8. 46. Haase P, Skibsted L. Influence of operations for stress incontinence and/or genital descensus on sexual life. Acta Obstet Gynecol Scand 1988;67:659–61. 47. Helstrom L, Nilsson B. Impact of vaginal surgery on sexuality and quality of life in women with urinary incontinence or genital descensus. Acta Obstet Gynecol Scand 2005;84:79–84. 48. Walter S, Olsen KP, Frimodt-Moller C et al. [Urinary incontinence in women treated with colposuspension. Clinical urodynamic and radiological assessment.] Ugeskr Laeger 1975;137:2979–81.
58. Schover LR, von Eschenbach AC. Sexual function and female radical cystectomy: a case series. J Urol 1985;134:465–8. 59. Roe BH, Brocklehurst JC. Study of patients with indwelling catheters. J Adv Nurs 1987;12:713–19. 60. Ramage M. ABC of sexual health. Management of sexual problems. Br Med J 1998;317:1509–12. 61. Kunin CM, McCormack RC. An epidemiology study of bacteriuria and blood pressure among nuns and working women. N Engl J Med 1968;278:635–42. 62. Buckley RM, McGuckin M, MacGregor RR. Urine bacterial counts after sexual intercourse. N Engl J Med 1978;298:321–4. 63. Nicolle LE, Harding GK, Preiksaitis J et al. The association of urinary tract infection with sexual intercourse. J Infect Dis 1982;146:579–83. 64. Strom BL, Collins M, West SL. Sexual activity, contraception use, and other risk factors for symptomatic and asymptomatic bacteriuria. Ann Intern Med 1987;107:816–23. 65. Foxman B, Frerichs RR. Epidemiology of urinary tract infection 1. Diaphragm use and sexual intercourse. Am J Pub Health 1985;75:1308–13.
49. Kampar AL, Tikjob G, Bay-Nielsen A. Kolposuspension a. M. Burch. Ugeskr Laeger 1982;144:1921.
66. Ervine C, Komaroff AL, Pass TM. Behavioural factors and urinary incontinence. J Am Med Assoc 1980;243:330–1.
50. Milani R, Salvatore S, Soligo M et al. Functional and anatomical outcome of anterior and posterior vaginal prolapse repair with prolene mesh. BJOG 2005;112:107–11.
67. Adatto K, Doebele KG, Galland L, Granowetter L. Behavioural factors and urinary tract infection. J Am Med Assoc 1979;241:2525–6.
51. Jeffcoate TNA. Posterior colpoperineorrhaphy. Am J Obstet Gynecol 1959;77:490–502.
68. Hooton TM, Scholes D, Hughes JP et al. A prospective study of risk factors for symptomatic urinary tract infection in young women. N Engl J Med 1996;335:468–74.
52. Francis WJA, Jeffcoate TNA. Dyspareunia following vaginal operations. J Obstet Gynaecol Br Commonw 1961;68:1–10.
69. Gillespie L. The diaphragm: an accomplice in recurrent urinary tract infections. Urology 1984;254:240–5.
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70. Ronald AR. Sex and urinary tract infections [editorial]. N Engl J Med 1996;335:511–12. 71. Zafriri D, Ofek I, Adar R et al. Inhibitory activity of cranberry juice on adherence of type 1 and type P fimbriated Escherichia coli to eukaryotic cells. Antimicrob Agents Chemother 1989;33:92–8. 72. Ofek I, Goldhar J, Zafriri D et al. Anti-Escherichia coli adhesion activity of cranberry and blueberry juices. N Engl J Med 1991;324:1599. 73. Jepson RG, Michaljevic L, Craig J. Cranberries for preventing urinary tract infections. Cochrane Database Syst Rev 2004;2:CD001321. 74. Pfau A, Sacks T, Engelstein D. Recurrent urinary tract infections in premenopausal women: prophylaxis based on an understanding of the pathogenesis. J Urol 1983;129:1153–7.
75. Stapleton A, Latham RH, Johnson C et al. Postcoital antimicrobial prophylaxis for recurrent urinary tract infection. J Am Med Assoc 1990;264:703–6. 76. Albert X, Huertas I, Pereiro II et al. Antibiotics for preventing recurrent urinary tract infections in non-pregnant women. Cochrane Database Syst Rev 2004;3:CD001209. 77. Pinggera GM, Feuchtner G, Frauscher F et al. Effects of local estrogen therapy on recurrent urinary tract infections in young females under oral contraceptives. Eur Urol 2005;47(2):243–9. 78. Hextall A, Boos K, Aslam N et al. The value of a cystoscopy for diagnosing chronic cystitis in women with irritative urinary symptoms or recurrent urinary tract infections. Int Urogynecol J 1997;8:62.
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IntroductIon Pelvic floor dysfunction encompasses urinary incontinence, anal incontinence, and symptomatic prolapse, as well as previous bladder or vaginal surgical repair, and is present in up to 11.1% of men and 46.2% of women.1 While urogynecologic complaints are undoubtedly more common in older multiparous women, nulliparous women can also be significantly troubled by these conditions. The odds ratios for urinary incontinence in comparison with nulliparas were 1.3 for para one, 1.9 for para two, and 2.2 for women of para three and over.2 In addition, 12% of women aged 18–30 years (regardless of parity) have been shown to complain of urinary incontinence.3 This chapter is dedicated to exploring the lower urinary tract problems of nulliparas in more detail, and will be looked at in the following sections:
• • • • • • •
Prevalence; Significance of symptoms; Urinary tract infections; Giggle incontinence; Etiologic factors; Management; Prevention.
Prevalence of urInary IncontInence and PelvIc organ ProlaPse In nullIParous women Prevalence is difficult to quantify for the following reasons: 1. Patients fail to present due to various reasons4 • A hope that symptoms would get better on their own; • Feeling too embarrassed to discuss their problems; • Fear that symptoms are normal; • Fear of surgery. 2. Changing definitions of urinary incontinence The current standardized International Continence Society definition of urinary incontinence is ‘the complaint of any involuntary leakage of urine’.5 There are many studies describing the presence of urinary incontinence prior to the current definition. The previous definition of urinary incontinence was ‘involuntary loss of urine which is objectively demonstrable and a social or hygienic problem’.6 3. Methods of data collection These will influence the number of cases that are picked up. Methods that count the number of
patients presenting will show far fewer patients than methods that ask the general population about urinary symptoms. 4. Population differences Different populations may have different rates due to differences in lifestyle or even possible racial differences in connective tissue strength or anatomy.7–9 Attitudes towards incontinence vary between different migrant groups. Work from focus groups has shown that some ethnic groups are very concerned about being incontinent, but do not tell their family or seek help, whereas others actively seek treatment. Additionally, some ethnic groups accept incontinence and others felt ashamed.10 5. Bothersomeness of symptoms This will vary for each individual and may influence who is included as a ‘case’.10 Measuring the prevalence of pelvic floor dysfunction in nulliparous women is as challenging. A primary care questionnaire found that 17% of nulliparous women had urinary incontinence compared with an overall prevalence rate of 41%.11 A New York study on a cohort of 149 nuns found that 50% had urinary incontinence. According to their symptoms, 35% had mixed incontinence, 30% had stress incontinence, 24% had urge incontinence, and 11% had incontinence unrelated to stress or urge. Of the respondents who admitted to leakage, 52% wore sanitary protection because of it.12 A survey of 34 nulliparous physical education students found that 38% had symptoms suggestive of stress incontinence13 (this is explored in more detail in Chapter 43). Interviews with community-dwelling people over the age of 15 revealed stress incontinence in 10.9% of nulliparous women and 2.5% of men. After the first pregnancy, the prevalence rose to 37.4%. Various complaints were uncovered in this study1 (Table 45.1).
table 45.1.
Prevalence of pelvic floor dysfunction in nulliparous women
Feature
Prevalence in nulliparas* (%)
Stress
10.9
Urge
4.4
Flatus
5.3
Fecal
1.6
Bladder repairs
0.5
Vaginal hysterectomy
12.4
* n=433. Data from ref. 1.
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A study into American University nulliparous female athletes found that 28% of the 156 eligible respondents reported urine loss while participating in sport. Among the same sample, whose average age was 19.9 years, 42% reported urine loss during at least one activity of daily life. The most common activity associated with urinary leakage was walking to the bathroom, followed by coughing and upon hearing running water.14 The issue of urinary leakage experiences since childhood was discussed with 725 Swedish women in their first pregnancy. Pre-pregnancy, 39% of the women had experienced occasional urinary leakage. Of these, 79% were predominantly stress-type symptoms and 21% urge symptoms. In many of these women the leakage was described as small and occasional.15 Another study of women in their first pregnancy found that 3.5% of their sample had urinary incontinence pre-pregnancy, 35.6% antenatally, 13.7% postpartum and 13% postnatally.16 Pregnancy itself has an effect on the pelvic floor. Nulliparous women in their first pregnancy have been shown to have a greater degree of vaginal prolapse, measured using the pelvic organ prolapse quantification (POPQ), than those who have not embarked on a pregnancy.17
sIgnIfIcance of symPtoms While the relative frequency with which urinary incontinence occurs has been highlighted, only a proportion of women find this bothersome. In a United States study, this has been quantified in women suffering from stress incontinence:18 22.5% were not bothered, 48.8% were slightly bothered, and 28.8% were moderately to extremely bothered. Of women who were moderately to extremely bothered, only 48.8% had talked to a physician about incontinence.18 In the UK, a postal survey of over 15,000 people found that while 34% of the population reported clinically significant symptoms, only 2.4% found them bothersome and socially disabling.19 This translates to approximately 50 patients per general practice of 2000 patients. Various measures have been developed to measure the impact of incontinence on people’s lives. The Incontinence Impact Questionnaire was applied to a cohort of nuns and found that of those with urinary incontinence, 21.9% reported that their incontinence affected church attendance, 66.2% stated that it had an impact on their ability to go places in public, and 46% stated that it affected their sleep.12 The Sickness Impact Profile was used to show that the categories which contributed most to overall sickness impact were sleep and
rest, emotional behavior, mobility, social interaction, recreation, and pastimes.20
urInary tract InfectIons The risk of first referral to hospital for urinary tract infection (UTI) has been found to be higher in nulliparous than in parous women.21 Increasing age, obesity, and use of the contraceptive diaphragm were also found to increase the risk of first referral with UTI.21 It is not clear why women with obesity may have a reduced risk but it has been postulated that adipose tissue may protect against genital trauma during sexual intercourse.21 Another possibility is that peripheral conversion in adipose tissue of androstenedione to estrone has a possible beneficial effect on the bladder and urethra.21 Lower urinary tract symptoms have been positively associated with parity, body mass index (BMI), prior hysterectomy, straining at stool, and constipation.22 Recent intercourse is a risk factor for developing urinary tract infections. The relative risk of urinary tract infection among unmarried university women increases dramatically from 1.0 for women who were not sexually active during the preceding week to 9.0 for women who had intercourse seven times during that period.23 Subjects with recurrent UTIs are more likely to have a distance from urethra to anus of less than 4.5 cm than controls. This suggests that the distance that uropathogens have to travel may be related to the risk of recurrent UTI in some women.24
gIggle IncontInence Giggle incontinence is particularly common in children. This probably results from detrusor overactivity induced by laughter; however, it is difficult to reproduce during investigation. A positive family history is present in 13% of sufferers. Treatment for detrusor overactivity results in an improvement in all patients and complete resolution in 89% of sufferers.25 It rarely occurs after 25 years of age.26 It is important to provide strong reassurance that this condition is often self-limiting and sufferers grow out of it.
etIologIc factors Risk factors for and associations with nulliparous incontinent women vary between different studies. This may be due to differences in methodology and the population selected for study. Statistically significant risk factors for urinary incontinence in nulliparous women appear 675
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to be current hormone replacement therapy (HRT) use, multiple UTIs, hypertension, arthritis, depression, hysterectomy, and previous spinal surgery. Age, years after the menopause, prior HRT use, and diuretic use were not found to be statistically significant.12 The significance of BMI appears to vary between different studies.12,13,15 A case-control study did not find significant differences between symptomatic and asymptomatic nulliparous women with regard to pelvic floor muscle strength, menstrual cycle, and electromyographic patterns. More than half of the women in the symptomatic group had benign hypermobility joint syndrome; however, none in the control group was similarly affected.13 Urethral sphincter incompetence was found to be present in six out of the seven young physical education students with stress leakage.13 A comparison of nulliparous and multiparous women referred with urinary incontinence and pelvic organ prolapse unsurprisingly showed that the nulliparas were less likely to have pelvic organ prolapse. Among incontinent women who did not have prolapse, nulliparas were significantly more likely to have solely detrusor overactivity (DO). Of those patients who had pure urodynamic stress incontinence (USI), nulliparas were older, had less anterior vaginal wall descent, less bladder neck mobility, narrower genital hiatus and perineal body measurements, and lower maximum urethral closure pressures compared to parous sufferers of USI. Of those with DO only, the only difference was that the nulliparas were significantly younger.27 Inability to interrupt urinary flow, age, and high impact physical activity have also been found to be independent risk factors for urinary leakage. Interestingly, urinary incontinence was reported more often in women who graduated from university than in those who did not. This may be related to their levels of physical exercise or ability to articulate their problems and seek medical help. It was also more common in women with concomitant chronic diseases. Hard work, contraceptive pills, abdominal surgery, constipation or pre-pregnancy smoking were not found to differ between women with and without urinary leakage in this particular study.15 The development of pelvic organ prolapse may have a congenital component, and a wide number of normal values relating to urethral rotation on Valsalva maneuver and cervical descent are found in asymptomatic subjects.28
micturition habits Two micturition habits are significantly associated with urinary leakage: straining with micturition and preven-
tative micturition. Preventative micturition is a common behavior, reported in 71% of a sample of women in their first pregnancy, and is therefore not just a behavior learned by those who suffer from incontinence. This may result in bladder dysfunction with reduced capacity. There is an association between reporting of straining and preventative micturition. Women who practice preventative micturition may need to strain to empty their bladders (when they do not need to void). An alternative explanation is that women who tend to strain will frequently be increasing their intra-abdominal pressure and this may contribute to their problems in the same way as high impact physical activity.15 Sometimes it can be difficult to achieve a normal flow when the bladder has become very full. This may result from distortion of the usual ergonomic spherical shape achieved at functional capacity, which is the most effective shape for efficient bladder emptying due to the surface area to volume ratio.29
exercise A significantly increased incidence of urinary leakage was seen in those women who undertook exercise regimes incorporating one or more activities with a high impact on the pelvic floor (Table 45.2). Such activities include jogging, gymnastics, and ball sports.15 Many women who exercise regularly experience episodes of incontinence, and 30% of exercisers noted incontinence during at least one type of exercise. This was also associated with parity. The highest incidences were in activities with repetitive bouncing. Twenty percent stopped an exercise because of incontinence, 18% changed the way they did a specific exercise, and 55% wore a pad during exercise. Thirty-five percent had consulted a healthcare professional about their incontinence.30
table 45.2.
Urinary leakage related to type of sport
Type of sport
Proportion of urinary leakage (%)
Gymnastics
56
Ballet
43
Aerobics
40
Badminton
31
Volleyball
30
Athletics
25
Handball
21
Basketball
17
Data from ref. 51.
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The relationship between exercise and pelvic floor dysfunction is explored in more detail in Chapter 43.
connective tissue Differences in connective tissue are associated with pelvic floor symptoms.31,32 Biopsies from continent and incontinent women show alterations in collagen fibril morphology.31 An association has also been found between decreased foot flexibility and urinary incontinence in nulliparous athletes.33 Periurethral biopsies in nulliparous women with and without urodynamic stress incontinence have shown significantly less collagen in the tissues of those without USI. There are several different subtypes of collagen with different properties. In women with USI there is a decreased ratio of type I to type III collagen, and the cross-link content is also significantly reduced. Type I collagen is found in skin, tendon, and bone, whereas type III is found in skin, muscles, and blood vessels. There is, therefore, both a qualitative and quantitative reduction in their collagen. Associations have been found between osteoporosis, arthritis, and the major types of pelvic floor disorder. The reason for this is unknown but may be related to a genetic predisposition to connective tissue and structural disorders and/or estrogen deficiency.1 The racial differences that are observed in prevalence and type of urinary incontinence9 may be explained, at least in part, by variations in connective tissue in addition to previously discussed issues of attitudes towards incontinence between different ethnic groups.10
muscle Biopsies of pubococcygeus muscle show differences between women with and without USI or genital tract prolapse. Symptomatic women showed a significant increase in the number of muscle fibers showing pathologic damage in the posterior part of the pelvic floor. The range of diameters of type I and type II fibers obtained from this region was significantly different between symptomatic and asymptomatic women. This may be attributable to partial denervation of the pelvic floor. There was an association between histologic features, not only with parity but also with age, with pathology of muscle fibers more likely in older parous women.34 Cadaveric research has shown considerable variation in the quality of neural tissue among individuals. Reduced nerve density correlates significantly with reduced muscle fibers and advancing age.35,36
Innervation Electromyographic studies have shown that, compared with nulliparous controls, patients with USI and pelvic organ prolapse have changes in the levator ani and external anal sphincter consistent with either motor unit loss or failure of central activation, or both.37 Women with USI were shown to have delayed conduction to both the striated urethral muscle and pelvic floor muscle, indicative of denervation injury. In women whose urinary control was normal but who had genitourinary prolapse, conduction times to the urethral sphincter were normal but there was evidence of denervation damage to the pelvic floor.38 There is a gradual increase in the denervation of the striated muscle of the pelvic floor with age in nulliparous women,39 and there are fewer nerves in parous women than in nulliparous women.35
smoking Smoking has been shown to have an association with stress and urge incontinence. Women who previously smoked had a 2.2-fold increase and women who currently smoke had a 2.5-fold increase in the risk of USI.40 A two- to three-fold increase was also seen for urge incontinence. This may be due to several different mechanisms (Table 45.3). Smokers with pure USI have been shown to have stronger urethral sphincters, manifested by significantly greater functional urethral length, than non-smokers with USI.41 They still have USI because they also generate significantly greater increases in abdominal pressure with coughing. Smokers seen for evaluation of USI are significantly younger than non-smokers.41
table 45.3.
• • • • • • • •
Mechanisms by which smoking may cause incontinence
Coughing may damage components of the urethral sphincter mechanism Products of tobacco smoke Antiestrogenic hormonal effects of smoking General conditions associated with smoking (vascular and respiratory disease) Disruption of collagen synthesis Decreased smooth muscle tone Bulging down of pelvic floor due to coughing Nicotine has been shown in vitro and in animal studies to cause large spontaneous bladder contractions
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management An awareness and acknowledgement that pelvic floor dysfunction occurs in nulliparous women is essential. Steps to improve education and services both in primary and secondary care are outlined in the UK Department of Health’s document Good Practice in Continence Services.42 It has been shown that socioeconomic status may influence urinary incontinence knowledge, and consideration of this may improve the effectiveness of educational programs.43
pelvic floor. There are several different options available in the UK to help individuals to stop smoking:
• There is a National Health Service telephone helpline;
• Some general practices have smoking cessation help •
groups; Nicotine replacement is available on prescription.
Firstly, women should be encouraged to present with their complaints. Lower urinary tract symptoms and allied complaints should be explored and investigated in nulliparous women in the same way as in other women. In adolescents, this may be the first occasion that requires an intimate examination, particularly as the recommended age for first routine cervical smear increases. Practitioners need to be sensitive to this. An initial unpleasant assessment may reduce compliance with recommended management plans that could include a further intimate examination such as urodynamics or physiotherapy.
Some measures have been taken to discourage the population as a whole from smoking, including health warnings on cigarette packets and hard-hitting advertisements on television, radio, and posters. A ban on smoking in public places is being considered in the UK and this has already been successfully implemented in the Republic of Ireland. Whether or not this will result in reduced smoking rates is yet to be seen. Despite these incentives, smoking continues to increase in young women in the UK. Other conservative treatment measures are available, including pelvic floor exercises, electrical stimulation, and bladder retraining. While vaginal ring pessaries may not be thought of as an ideal solution for young women with uterovaginal prolapse, they have been shown to be well tolerated by sexually active women.46
conservative management
Pharmacotherapy
Women who are grossly overweight may benefit from weight loss.44 Care should be taken about what is suggested regarding weight loss and how it is to be approached. Surgically induced weight loss (following gastric bypass surgery) in women whose weight was greater than 120% of their average weight for their height and age resulted in significant improvements in lower urinary tract function, including stress and urge incontinence. Statistically significant changes were seen in measures of vesical pressure, cough-induced bladder pressure increases, bladder-to-urethra pressure transmission with cough, urethral axial mobility, number of incontinence episodes, and pad use.44 Moderately obese women (BMI between 25 and 45) who lost weight found a 40% decrease in the number of weekly incontinence episodes. Seventy percent of women were either dry or experienced a greater than 50% reduction in weekly incontinent episodes.45 While smoking has been shown to be associated with pelvic floor dysfunction,40 it is not clear whether stopping smoking will reverse pathology. As prevalence of urinary incontinence is less in ex-smokers than in current smokers, this would appear logical. Stopping smoking may reduce the risk of further deterioration of the
Pharmacotherapy is available for both USI and overactive bladder (OAB). Caution should be exercised in those actively trying to become pregnant and the manufacturer’s advice should be sought in such cases, as many agents are not recommended during pregnancy or breastfeeding. Pharmacotherapy is discussed in Chapters 33 and 41.
Identification of cases
surgery While it appears prudent to wait until a woman’s family is complete before contemplating a surgical solution to a pelvic floor dysfunction, this does not mean that necessary treatment should be withheld. There are case studies of successful pregnancies following continence surgery and preservation of continence does seem possible;47–49 however, mode of delivery remains controversial.
PreventIon It has been suggested1 that the prevalence of pelvic floor morbidity may be reduced by avoidance of excess body weight and of factors that exacerbate coughing (e.g. smoking) and possibly treating estrogen deficiency.
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Management of the first pregnancy could influence the natural history of pelvic floor dysfunction.1 The first pregnancy and delivery probably does the most damage to the pelvic floor; therefore, as parity increases, the effects of subsequent pregnancies accumulate. Pregnancy (certainly in higher order multiparas), more than delivery, appears to contribute to long-term pelvic floor dysfunction. Cesarean section is not associated with a significant reduction in the risk of pelvic floor morbidity compared with spontaneous vaginal delivery. Offering elective cesarean section does not therefore guarantee prevention of pelvic floor damage. Performing pelvic floor exercises during the first pregnancy may help to prevent the risk of postpartum USI in those who have a mobile bladder neck.50 Age of more than 35 years at first birth is associated with increased urinary leakage compared with first birth between the ages of 21 and 25 years. It is also more frequent if the first birth is before 21 years.8 Smoking cessation prior to the onset of symptoms is likely to be beneficial for both the pelvic floor and for general health.
references 1. MacLennan AH, Taylor AW, Wilson DH et al. The prevalence of pelvic floor disorders and their relationship to gender, age, parity and mode of delivery. Br J Obstet Gynaecol 2000;107:1460–70. 2. Borlotti A, Bernardini B, Colli E et al. Prevalence and risk factors for urinary incontinence in Italy. Eur Urol 2000;37:30–5. 3. Hagglund D, Olsson H, Leppert J. Urinary incontinence: an unexpected large problem among young females. Results from a population-based study. Fam Pract 1999;16(5):506–9. 4. Norton PA, MacDonald LD, Sedgwick PM et al. Distress and delay associated with urinary incontinence, frequency, and urgency in women. BMJ 1988;297:1187–9. 5. Abrams P, Cardozo L, Fall M et al. The standardisation of terminology in lower urinary tract function. Neurourol Urodyn 2002;21:167–78. 6. Abrams P, Blaivas JG, Stanton S et al. The standardisation of terminology of lower urinary tract function. Neurourol Urodyn 1988;7:403–26. 7. Baragi RV, DeLancey JOL, Caspari R et al. Differences in pelvic floor area between African American and European American women. Am J Obstet Gynecol 2002;187(1):111–15. 8. Grodstein F, Fretts R, Lifford K et al. Association of age, race, and obstetric history with urinary symptoms among
women in the Nurses’ Health Study. Am J Obstet Gynecol 2003;189(2):428–34. 9. Duong TH, Korn AP. A comparison of urinary incontinence among African American, Asian, Hispanic, and white women. Am J Obstet Gynecol 2002;184(6):1083–6. 10. Burton G, Mathie L. An assessment of attitudes to incontinence in different migrant groups. Neurourol Urodyn 1995;14(5):554. 11. Jolleys J. Reported prevalence of urinary incontinence in women in a general practice. BMJ 1988;296(6632):1300–2. 12. Buchsbaum GM, Chin M, Glantz C et al. Prevalence of urinary incontinence and associated risk factors in a cohort of nuns. Obstet Gynecol 2002;100(2):226–9. 13. Bo K, Stein R, Kulseng-Hanssen S et al. Clinical and urodynamic assessment of nulliparous young women with and without stress incontinence symptoms: a case-control study. Obstet Gynecol 1994;84(6):1028–32. 14. Nygaard IE, Thompson FL, Svengalis SL et al. Urinary incontinence in elite nulliparous athletes. Obstet Gynecol 1994;84(2):183–7. 15. Eliasson K, Nordlander I, Matteson E et al. Prevalence of urinary leakage in nulliparous women with respect to physical activity and micturition habits. Int Urogynecol J 2004;15:149–53. 16. Dolan LM, Walsh D, Hamilton S et al. A study of quality of life in primigravidae with urinary incontinence. Int Urogynecol J 2004;15:160–4. 17. O’Boyle AL, Woodman PJ, O’Boyle JD et al. Pelvic organ support in nulliparous pregnant and non-pregnant women: a case control study. Am J Obstet Gynecol 2002;187(1):99–102. 18. Fultz NH, Burgio K, Diokno AC et al. Burden of stress urinary incontinence for community-dwelling women. Am J Obstet Gynecol 2003;189:1275–82. 19. Perry S, Shaw C, Assassa P et al. An epidemiologic study to establish the prevalence of urinary symptoms and felt need in the community: the Leicestershire MRC Incontinence Study. J Public Health Medicine 2000;22(3):427–34. 20. Hunskaar S, Vinsnes A. The quality of life in women with urinary incontinence as measured by the sickness impact profile. JAGS 1991;39(4):378–82. 21. Vessey MP, Metcalfe MA, McPherson K et al. Urinary tract infection in relation to diaphragm use and obesity. Int J Epidemiol 1987;16(3):441–4. 22. Moller LA, Lose G, Jorgensen T. Risk factors for lower urinary tract symptoms in women 40 to 60 years of age. Obstet Gynecol 2000;96(3):446–50. 23. Ronald A. Sex and urinary tract infections. N Engl J Med 1996;335(7):510–12. 24. Hooton TM, Stapleton AE, Roberts PL et al. Perineal anatomy and urine-voiding characteristics of young women
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with and without recurrent urinary tract infections. Clin Infect Dis 1999;29:1600–1. 25. Chandra M, Saharia R, Shi Q et al. Giggle incontinence in children: a manifestation of detrusor instability. J Urol 2002;168(5):2184–7.
38. Smith ARB, Hosker GL, Warrell DW. The role of pudendal nerve damage in the aetiology of genuine stress incontinence in women. Br J Obstet Gynaecol 1989;96:29–32.
26. Cardozo L. Urogynaecology. Edinburgh: Churchill Livingstone 1997; 91.
39. Smith ARB, Hosker GL, Warrell DW. The role of partial denervation of the pelvic floor in the aetiology of genitourinary prolapse and stress incontinence of urine. A neurophysiologic study. Br J Obstet Gynaecol 1989;96:24–8.
27. Harris RL, Cundiff GW, Coates KW et al. Urinary incontinence and pelvic organ prolapse in nulliparous women. Obstet Gynecol 1998;92(6):951–4.
40. Bump RC, McClish DK. Cigarette smoking and urinary incontinence in women. Am J Obstet Gynecol 1992;167(5):1213–18.
28. Dietz HP, Eldridge A, Grace M et al. Pelvic organ descent in young nulligravid women. Am J Obstet Gynecol 2004;191(1):95–9.
41. Bump RC, McGlish DM. Cigarette smoking and pure genuine stress incontinence of urine: a comparison of risk factors and determinants between smokers and nonsmokers. Am J Obstet Gynecol 1994;170(2):579–82.
29. Simmons A, Williams S, Craggs MD et al. Dynamic multiplanar EPI of the urinary bladder during voiding with simultaneous detrusor pressure measurement. J Mag Res Imaging 1997;15:295–300.
42. Department of Health. Good practice in continence services. London: Department of Health, 2000.
30. Nygaard I, DeLancy JOL, Arnsdorf L et al. Exercise and incontinence. Obstet Gynecol 1990;75(5):848–51.
43. Kubik K, Blackwell L, Heit M. Does socio-economic status explain racial differences in urinary incontinence knowledge? Am J Obstet Gynecol 2004;191(1):188–93.
31. FitzGerald MP, Mollenhauer J, Hale DS et al. Urethral collagen morphologic characteristics among women with genuine stress incontinence. Am J Obstet Gynecol 2000;182(6):1565–74.
44. Bump RC, Sugarman HJ, Fantl A et al. Obesity and lower urinary tract function in women: Effect of surgically induced weight loss. Am J Obstet Gynecol 1992;167:392–9.
32. Keane DP, Sims TJ, Abrams P et al. Analysis of collagen status in premenopausal nulliparous women with genuine stress incontinence. Br J Obstet Gynaecol 1997;104:994–8.
45. Subak LL, Johnson C, Whitcomb E et al. Does weight loss improve incontinence in moderately obese women? Int Urogynecol J 2002;13:40–3.
33. Nygaard IE, Glowacki C, Saltzman CL. Relationship between foot flexibility and urinary incontinence in nulliparous varsity athletes. Obstet Gynecol 1996;87(6):1049– 51. 34. Gilpen SA, Gosling JA, Smith ARB et al. The pathogenesis of genitourinary prolapse and stress incontinence of urine. A histologic and histochemical study. Br J Obstet Gynaecol 1989;96:15–23. 35. Pandit M, DeLancey JOL, Iyengar J et al. Variation in quantity and distribution of neural tissue in the striated urogenital sphincter muscle. Int Urogynecol J 1999;10(Suppl 1):36. 36. Perucchini D, DeLancey JOL, Patane L et al. Age associated striated muscle loss in the female urethral sphincter. Int Urogynecol J 1997;8(1):85. 37. Weidner AC, Barber MD, Visco AG et al. Pelvic muscle electromyography of levator ani and external anal sphincter in nulliparous women and women with pelvic floor dysfunction. Am J Obstet Gynecol 2000;183(6):1390–1401.
46. Brincat C, Kenton K, Fitzgerald MP et al. Sexual activity predicts continued pessary use. Am J Obstet Gynecol 2004;191(1):198–200. 47. Gauruder-Burmester A, Tunn R. Pregnancy and labour after TVT-plasty. Acta Obstet Gynecol Scand 2001;80:283–4. 48. Toh K, Diokno AC. Management of intrinsic sphincter deficiency in adolescent females with normal bladder emptying function. J Urol 2002;186:1150–3. 49. Lynch CM, Powers AK, Keating AB. Pregnancy complicated by a suburethral sling: a case report. Int Urogynecol J 2001;12:218–19. 50. Reilly ETC, Freeman RM, Waterfield MR et al. Prevention of postpartum stress incontinence in primigravidae with increased bladder neck mobility: a randomised controlled trial of antenatal pelvic floor exercises. BJOG 2002;109:68–76. 51. Thyssen HH, Clevin L, Olesen S et al. Urinary incontinence in elite female athletes and dancers. Int Urogynecol J 2002;13:15–17.
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46 Pregnancy and childbirth and the effect on the pelvic floor Charlotte Chaliha
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IntroductIon There has been increasing recognition over the past few decades of the consequences of childbirth on the physical and psychological well-being of a woman. MacArthur et al.,1 in a postal survey of 11,701 women 13 months to 9 years after delivery, found that 47% experienced at least one or more health problems within 3 months of delivery. These included backache, headache, hemorrhoids, depression and bowel and bladder symptoms that persisted for a minimum of 6 weeks. Glazener et al.2 questioned 1249 women about their postnatal symptoms on three occasions after childbirth; 85% of women experienced one new symptom during the first 8 weeks and 76% reported one or more health problems persisting for up to 18 months. Sleep and Grant3 reported that 15% of women experience dyspareunia up to 3 years after a normal vaginal delivery and up to 8% experience perineal pain 12 weeks after a normal vaginal delivery.4 However, although health problems seem to be common after childbirth, it appears women often do not seek medical attention.1 Urinary and/or fecal incontinence and genital prolapse are considered to be inevitable sequelae of a vaginal birth. One in every three women will have incontinence during her lifetime and, of these, up to 65% will recall that it began either during pregnancy or after childbirth.5 Clinical and epidemiologic studies strongly indicate that women who undergo vaginal delivery are at higher risk of subsequent incontinence than nulliparas and those who undergo cesarean section. This is most likely related to the detrimental impact of vaginal delivery on the pelvic floor.6–12 Furthermore, it appears that the first vaginal delivery is the time when women sustain this damage.10,13, Supporting these findings are several studies showing a relationship between vaginal delivery and mechanical
Dorsal border of pubic bone
and neurologic damage to the pelvic floor which are related to the development of urinary or anal incontinence or both.13–16 There may also be women at increased predisposition to pelvic floor trauma, and thus incontinence and prolapse, due to an inherent weakness of collagen within the pelvic floor fascia.17–19 This chapter focuses on the effect of pregnancy and childbirth on the pelvic floor and discusses the possible mechanisms by which pelvic floor damage may occur and its long-term sequelae.
MechanIsMs of Injury to the pelvIc floor There are several mechanisms of pelvic floor injury: direct muscle trauma, nerve injury, and connective tissue damage disrupting the urethral and anal sphincters and their support (Fig. 46.1).
direct perineal trauma Direct perineal trauma from perineal laceration and episiotomy is a well-known complication of vaginal delivery. The long-term sequelae of perineal injuries include pain, dyspareunia, fistulae, and anal incontinence.13,20–23 The incidence of lacerations involving the anal sphincter has been reported as 0–6.4% when an episiotomy has not been performed, 0.2–23.9% after a midline episiotomy, and 0–9% after a mediolateral episiotomy.23 Severity and frequency of postpartum dyspareunia has been related to perineal trauma and obstetric instrumentation, with a quicker resumption of sexual activity in those with an intact perineum versus those women who have a spontaneous laceration or trauma.21,24
Hypoechogenic horseshoe of rhabdosphincter
Ventral border of pubic bone
Right anterior vaginal sulci
Probe artifact
Rectum
Hyperechogenic core of urethra Pubococcygeus
Figure 46.1. pelvic floor.
Ultrasound of the
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Muscle trauma Anatomic and functional changes to the pelvic floor may occur secondary to pelvic floor distension during descent of the fetal head and maternal expulsive efforts during the active second stage of labor. Peschers et al.25 evaluated pelvic floor strength by means of palpation, perineometry and perineal ultrasound, and found that pelvic floor muscle strength was significantly decreased after vaginal delivery compared to cesarean section at 3–8 days postpartum. However, at 6–10 weeks postpartum there was no significant difference from antenatal values except for a lower intravaginal pressure in nulliparous women. Therefore, although pelvic strength is impaired shortly after vaginal birth, it recovers in most women within 2 months after the first pregnancy.
nerve damage The pudendal nerve is particularly susceptible to compression and damage at the point where it curves round the ischial spine and enters the pudendal canal enclosed in a tight fibrous sheath. Nerve damage has been shown to occur in patients with a history chronic of straining on defecation who show increased pudendal nerve terminal motor latencies.26 Childbirth-induced denervation injuries of the pubococcygeus and external sphincter muscles may occur by a similar mechanism and have been reported after 42–80% of vaginal deliveries.14,15
the lower urInary tract In pregnancy and after delIvery Lower urinary tract symptoms are very common in pregnancy. Several large epidemiologic studies have assessed the prevalence of urinary symptoms in pregnancy, most focusing on the symptom of stress incontinence. Most of these symptoms may be a consequence of the normal anatomic and physiologic changes that occur in pregnancy; however, superimposed on these changes may be further pathologic changes as a consequence of tissue damage, either from pregnancy or labor, resulting in persistent symptoms. The distinction between normal physiologic changes and transient or permanent pathophysiology is often not clear and may be a continuum.
anatomic and physiologic changes The urinary tract undergoes both structural and functional changes during pregnancy and after delivery. These changes may be specific in response to pregnancy
and in some women may be compounded by pathologic changes that persist after delivery. In normal pregnancy, the kidneys increase by 1 cm in length due to an increase in vascular volume and interstitial space. Dilation of the ureters is a well-known phenomenon in pregnancy and hydroureter is noted in approximately 90% of pregnant women by the third trimester. This dilation is more marked on the right compared to the left side, probably related to the relative dextrorotation of the uterus. There is a 40–50% increase in glomerular filtration rate and a 60–80% increase in the effective renal plasma flow.27 As a result, plasma creatinine, urea, and urate values are lower than the normal range for non-pregnant women. The bladder is passively drawn upwards and anteriorly as the uterus enlarges, resulting in lengthening of the urethra.28 The urethral mucosa becomes more hyperaemic and congested in pregnancy in response to the increase in circulating estrogen levels. The detrusor muscle also hypertrophies in response to estrogen. After delivery, cystoscopy of the bladder shows changes such as mucosal congestion, submucosal hemorrhage, and capillary oozing, especially around the bladder neck, trigone, and ureteric orifices. These changes have been seen in association with a decrease in bladder sensation and tone,29 and are most marked in those who underwent vaginal delivery.30 Studies assessing bladder capacity have revealed conflicting results, with most early studies using simple cystometry only. Muellner31 reported an increase in bladder capacity to an average of 1300 ml in the third trimester due to bladder hypotonia, with a return to normal values postpartum. However, other investigators found no change in bladder capacity in the first trimester and a reduced bladder capacity in the third trimester in association with increased detrusor irritability rather than bladder hypotonia.32 Dual channel cystometry studies have found that all urodynamic variables, such as first sensation and maximum bladder capacity, are lower in pregnancy and postpartum compared to a non-pregnant population and this may account for symptoms of frequency, nocturia, and urgency.33,34
pregnancy and urInary syMptoMs frequency and nocturia These are among the commonest and earliest symptoms to develop in pregnancy. Normal non-pregnant women void between four to six times per day, and rarely at night. 683
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Using a definition of frequency as at least seven daytime voids and one night-time void, Francis32 studied the voiding habits in 400 healthy women during and after an uncomplicated pregnancy and compared them with 50 healthy non-pregnant patients of a similar age. Frequency was reported by 59% in early pregnancy, 61% in mid-pregnancy, and 81% in late pregnancy. Parboosingh & Doig,35 defining nocturia as at least three night-time voids, questioned 873 healthy antenatal patients and found that nearly 66% experienced nocturia by the third trimester. Cutner et al.36 assessed lower urinary tract symptoms in 47 women undergoing termination of pregnancy at 6–15 weeks’ gestation, and found that 40% complained of frequency and 23% of nocturia. The cause of frequency was not related to bladder capacity or the effect of posture, but due to the polydypsia and polyuria of pregnancy.32 Both fluid intake and output rise rapidly in the first trimester, remaining constant until the third trimester, when a decrease in sodium excretion leads to a decrease in output. Despite this, frequency persists related to the pressure on the bladder by the uterus. Cutner37 found that there was a correlation between the maximum voided volumes and first sensation to void and maximum bladder capacity, which was in turn related to the presence of low compliance. There was no correlation between the maximum voided volumes and diurnal frequency and nocturia. Parboosingh and Doig38 measured mean urine flow and solute excretion in 24-hour and overnight collections in 100 normal and non-pregnant women. An increase in sodium excretion was the major reason for increased night-time voiding as well as the mobilization of dependent edema at night in the recumbent position.
voiding difficulties Urinary hesitancy may be found in up to 27% of patients in the first two trimesters.38 Fischer and Kittel39 assessed flow rates in 290 women during pregnancy and found that there was a significant increase in peak flow rates in the second and third trimesters compared to controls and early pregnancy, but these higher flow rates were associated with larger voided volumes. Cutner37 assessed flow rates in pregnancy, adjusting for volume voided, and found no difference in women complaining of hesitancy, or incomplete emptying, compared to pregnant women with normal voiding. Urinary retention can occur in pregnancy associated with the enlargement of a retroverted uterus with subsequent entrapment of the fundus below the sacral promontory.40 Other causes include an enlarging
fibroid or a pelvic mass. This retention usually resolves by 16 weeks’ gestation as the uterus grows out of the pelvis, and can be managed in the interim with either bladder drainage or intermittent self-catheterization. Alternatively, manual reduction of the uterus can be performed or a Hodge pessary may be inserted to maintain uterine position and relieve the obstruction on the bladder neck. Postpartum urinary retention is common, with a reported incidence of 1.7–17.9%.41 Risk factors include a first labor, instrumental delivery epidural analgesia, and a longer duration of labor (>800 minutes).42–44 Khullar and Cardozo45 found that the bladder can take up to 8 hours to regain sensation after the last topup of an epidural. Overdistension of the bladder may occur during this period, leading to permanent detrusor dysfunction.
urinary incontinence Incontinence is a common symptom associated with pregnancy and has been reported in up to 85% of women.32,46–48 Francis32 found that in the first trimester of pregnancy 16% of women complained of stress incontinence and 34% in the second half of pregnancy. Stanton et al.49 assessed the prevalence of both stress and urge incontinence at 32 weeks’ gestation and found an incidence of 36% and 13%, respectively. Viktrup and Lose50 interviewed 305 primiparae and found that 39% had stress incontinence before, during or after pregnancy, and 7% developed de novo stress incontinence after delivery. The association with these obstetric risk factors was lost by 3 months postpartum. Only 3% had incontinence at 1 year. However, in a subsequent follow-up study of the original cohort of 278 women, they reported a prevalence of stress incontinence of 30% at 5 years. In those without symptoms after the first delivery the incidence was 19%; however, in those who reported stress incontinence 3 months after first delivery there was a 92% risk of having stress incontinence 5 years later.50 This pattern of development of incontinence during pregnancy, with rapid postpartum recovery followed by a steady decline of continence over time, suggests a dual mechanism of nerve and tissue damage. The presence of antenatal stress incontinence seems to increase the risk of future stress incontinence.51,52 The contribution of obstetric risk factors to the development of stress incontinence is conflicting. Some investigators have found a relationship with the duration of the second stage of labor53–55 and birth weight.1 Conversely, other investigators have not found a signifi-
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cant correlation between stress incontinence and fetal head circumference,56,57 second stage of labor1,46,54,58 or birth weight.56–59 However, these studies differ widely in their questioning techniques and definition of stress incontinence. The effect of epidural analgesia is unclear. Epidural analgesia has been reported to be more protective than pudendal block against postpartum stress incontinence;56 however, this was not established by other authors who have found a higher incidence of stress incontinence in those who received epidural analgesia than those who did not.58 Jackson et al.55 found that the incidence of stress incontinence increased in women delivered with epidural analgesia, especially if the second stage of labor was longer than 120 minutes.
changes in the lower urinary tract and pelvic floor related to the development of incontinence The exact etiologic mechanism of stress incontinence is unclear and probably multifactorial, related to nerve damage and/or physiologic and structural changes of the lower urinary tract.
Functional changes Iosif and Ulmsten60 compared urethral pressure profile measurements in pregnant women with stress incontinence with continent healthy women from an earlier study.3 They found that the absolute urethral length increased by an average of 6.7 mm and the functional urethral length by 4.8 mm. The maximum urethral closure pressure increased to 93 cmH2O at 38 weeks and table 46.1.
then dropped to pre-pregnancy values of 69 cmH2O postpartum. These changes were not seen in women complaining of incontinence, and are postulated to be a mechanism whereby continence is maintained despite an increase in intravesical pressure in pregnancy. This corresponds with other studies that have shown evidence of low urethral pressure in non-pregnant women with stress incontinence.61,62 This increase in urethral closure pressure may be the result of an increase in urethral sphincter volume from increased blood flow. There is also an increase in the amplitude of vascular pulsations recorded from the urethral wall, especially in the first 16 weeks of pregnancy, which may be related to an increase in blood volume in pregnancy. Pregnant women with urodynamic stress incontinence showed a decrease in the amplitude of vascular pulsations in the periurethral plexus compared to continent women, suggesting that this affects urethral closure pressure.63 Three-dimensional imaging of the urethral sphincter after vaginal delivery shows a reduction in sphincter volume which has been implicated in the development of stress incontinence.4,65 Cystometry in pregnancy has been performed by several workers. Chaliha et al.34 found a high prevalence of urodynamic stress incontinence and detrusor overactivity. This was 8.7% and 8.1% respectively in the antenatal period and 5.0% and 6.8% respectively postpartum. The mean values for urodynamic variables in the third trimester and postpartum were lower than values defined in a non-pregnant population and not related to obstetric or neonatal variables (Table 46.1). However, despite the high prevalence of symptoms in
Urodynamic values (sitting and standing cystometry) and urodynamic diagnoses before and after delivery
Urodynamic variable
Antenatal values*
Postnatal values*
Sit FDV (ml)
111 (70)
148 (83)
Sit SDV (ml)
188 (91)
217 (94)
Sit MXCC (ml)
301 (146)
299 (114)
Stand FDV (ml)
96 (69)
139 (90)
Stand SDV (ml)
167 (102)
209 (105)
Stand MXCC (ml)
239 (136) (n=125)
271 (123) (n=118)
MVP (cmH2O)
38 (22) (n=153)
32 (17) (n=157)
Peak flow rate (ml/s)
28 (16.3)
23 (14)
Urodynamic stress incontinence
14 (9%)
8 (5%)
Detrusor overactivity
13 (8%)
11 (7%)
* n=161. Data from ref. 34. FDV, first desire to void; MVP, maximum voiding pressure; MXCC, maximum cystometric capacity; SDV, strong desire to void.
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this study, there was poor correlation between symptoms and urodynamic findings, which agrees with data in nonpregnant women.66 Therefore these observed changes in bladder function were consistent with a pressure effect of a gravid uterus and not related to mode of delivery or neonatal factors.
Nerve damage Patients with urodynamic stress incontinence have been shown to have abnormal conduction in the perineal branch of the pudendal nerve which innervates the periurethral striated muscle and pubococcygeus muscle.67,68 Several workers have also demonstrated injury to the nerve supply after childbirth. However, these studies often do not relate objective damage to symptoms. Snooks et al.14 found prolongation of pudendal nerve terminal motor latencies 48–72 hours after delivery in 42% of those delivered vaginally but not those delivered by cesarean section. The degree of pudendal nerve damage was greater in multiparous women and correlated with the use of forceps and a longer second stage of labor. In 60% of these women, pudendal nerve latency had returned to normal at 2 months postpartum. The authors suggested that vaginal delivery results in pudendal nerve damage, probably through a combination of direct trauma and traction injury during delivery, and this may be involved in the development of stress incontinence. However, this study was not prospective and included multiparous women who may have sustained prior nerve damage. Furthermore, it looked at innervation of the striated anal sphincter which may not actually reflect striated urethral sphincter innervation, and there was a poor correlation between abnormal latencies and symptoms. Using concentric needle electromyography and pudendal nerve conduction tests, Allen et al.15 found evidence of denervation injury in 80% of women after delivery. Those women with a long (active) second stage of labor (>56.7 minutes) and a large baby (>3.41 kg) showed a greater degree of nerve damage. Electromyography of the right and left pubococcygeus muscle has shown that childbirth induces both qualitative as well as quantitative changes such that sphincter weakness was due not only to loss of motor units but also asynchronous activity in those that remained.69
Structural changes Peschers et al.70 evaluated bladder neck position and mobility using perineal ultrasound at 8 weeks postpartum. Bladder neck position was significantly lower and bladder neck mobility increased after vaginal delivery compared with women who had an elective cesarean sec-
tion and nulligravid controls. Meyer et al.71 noted a significant increase in bladder neck mobility after vaginal delivery in primiparae; however, bladder neck position was only lowered after forceps delivery. It has been suggested that there may be a group of women at an inherent increased risk of developing incontinence due to abnormalities in collagen,72 as the collagenous component of the connective tissue contributes to structural support of the bladder neck. In pregnancy, the tensile properties of the connective tissue are reduced, with a reduction in total collagen content and increase in glycosaminoglycans.73 Changes in collagen may result in greater mobility of the bladder neck resulting in stress incontinence. In a study of 116 primigravidae, perineal ultrasound was used to assess bladder neck mobility. Women with antenatal bladder neck mobility >5 mm on linear movement (equivalent to >10-degree rotation) were found to be at higher risk of developing postpartum stress incontinence. Approximately 50% of this group reported stress incontinence at 3 months postpartum.74
anal sphIncter Morphology durIng pregnancy and after delIvery Sultan et al.75 examined 20 women before and after a cesarean section and found that pregnancy did not have any significant effect on anal sphincter morphology and function.
fecal IncontInence Fecal incontinence is a distressing social handicap and vaginal delivery is a major etiologic factor.13,76,77 MacArthur et al.16 investigated the prevalence of postnatal fecal symptoms in a postal questionnaire study of 906 women 10 months after delivery and reported that 36 women (4%) developed de novo fecal incontinence. Six of these women became incontinent after an emergency cesarean section but none after an elective cesarean section. This estimate for fecal incontinence is conservative, as it did not enquire about incontinence of flatus that is probably more common and has been reported to be as high as 29% at 9 months after delivery in one study of 349 primiparous women.78 Fecal incontinence is especially common after anal sphincter rupture, with a reported prevalence of 16– 47%.79–82 Tetzschner et al.57 assessed the long-term impact of obstetric anal sphincter rupture on the frequency of urinary and anal incontinence. At 2–4 years postpartum, 42% of the 94 women in their study had anal incontinence, 32% had urinary incontinence, and 18% had
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both urinary and anal incontinence. Despite the high number of women with incontinence, only a few had sought medical advice.
changes in the anal canal and pelvic floor related to anal incontinence The etiology of postpartum anal incontinence is complex and both nerve and mechanical trauma have been implicated.
Nerve damage Denervation injury of the pelvic floor may occur from traction and straining during vaginal delivery, similar to the mechanism of nerve damage reported in patients with chronic constipation which may result in anorectal incontinence.83 In 80% of women with idiopathic anorectal incontinence there is histologic evidence of denervation of the striated pelvic floor muscle, particularly the puborectalis and external anal sphincter muscles.84–86 Serial measurements of pudendal nerve terminal motor latencies in patients with idiopathic anorectal incontinence show progressive damage from recurrent stretch injury during straining at stool.87 This mechanism of strain-induced damage may occur during vaginal delivery. Denervation injuries of the pubococcygeus and external sphincter muscles have been reported after 42–80% of vaginal deliveries.14,15 The presence of neuropathy has been found to be related to the length of the second stage of labor, size of the baby, and instrumental delivery.88 Sultan et al.89 investigated pudendal nerve function before and after delivery, and found that pudendal nerve terminal motor latencies were significantly prolonged, especially on the left side, which the authors postulated could be due to the unequal traction from the fetal head on the two sides of the pelvic floor during descent down the birth canal. However, no relationship between abnormal neurophysiology and symptoms of anal incontinence was shown. Sensory nerve function may also be affected by nerve damage. The anal canal has a greater variety of afferent nerve endings than the rectum. These allow the detection of differences in touch, temperature, and pain in the anal canal. The rectum has a configuration of nerve plexuses that serve as specialized sensory receptors for distension for perception of fullness, urgency to defecate, and pain.90,91 It is believed that sensory information is critical to the preservation of continence and in patients with fecal incontinence there is a significant reduction in the ability to perceive electrical and other forms of stimulation.92–95 In pregnancy, however, the role of anal sensation is unclear
as deficits in anal canal sensation appear to be transient and unrelated to the development of incontinence.96–98
Anal sphincter trauma The incidence of anal sphincter damage varies between 0.5 and 2.5% in centers where mediolateral episiotomy is practiced and 7% in units performing midline episiotomies.57,99,100 The use of anal endosonography has enabled accurate visualization of the sphincters, thus providing strong direct evidence of the much higher incidence of previously unrecognized occult anal sphincter trauma after delivery and its importance in the pathophysiology of anal incontinence13,101,102 (Figs 46.2–46.4).
Figure 46.2. Two-dimensional image of the anal sphincter, demonstrating an external sphincter defect (arrows). The external sphincter appears hyperechoic surrounding the hypoechoic external sphincter.
Figure 46.3. sphincter.
Three-dimensional image of an intact anal 687
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Figure 46.4. Three-dimensional image of internal and external sphincter trauma. Sultan et al.13 investigated 202 pregnant women 6 weeks before delivery using anal endosonography, manometry, perineometry, and pudendal nerve terminal motor latencies. These tests were repeated in 150 of these women 6 weeks after delivery and then in the 32 women with abnormal findings (defects on endosonography or prolonged pudendal nerve terminal motor latencies) at 6 months after delivery. Ten of the 79 primiparous women (13%) and 11 of the 48 multiparous women (23%) who delivered vaginally had anal incontinence or fecal urgency when studied 6 weeks after delivery. Twenty-eight of the 79 primiparous women (35%) had a sphincter defect on endosonography at 6 weeks; the defect persisted in all 22 women studied at 6 months. Of the 48 multiparous women, 19 (40%) had a sphincter defect before delivery and 21 (44%) afterward. None of the 23 women who underwent cesarean section had table 46.2.
a new sphincter defect after delivery. The use of forceps was the single independent factor associated with anal sphincter damage and there was a strong correlation with the presence of defects and the development of symptoms. This suggests that it is the first vaginal delivery that is the most important factor for damage to the anal sphincters. Forceps delivery results in more trauma to the anal sphincters and is associated with a higher incidence of defecatory symptoms than a ventouse delivery. Anal sphincter defects were seen in 81% of those who had a forceps delivery compared to 24% of those who had a ventouse delivery and 36% of controls.102 Subsequent studies have looked at the incidence of anal sphincter injury using endoanal ultrasound and meta-analysis of five of these studies reveals a 26.9% incidence of anal sphincter injury in primiparous women and an 8.5% incidence of new sphincter defects in multiparous women. Overall, 29.7% of women with anal sphincter defects were symptomatic though 3.4% of women experienced postpartum fecal incontinence without a sphincter defect103 (Table 46.2). The use of episiotomy and its relationship to anal sphincter injury is unclear. Poen et al.108 reported that the use of a mediolateral episiotomy was associated with fewer third-degree tears. Sultan et al.,99 in a retrospective study of women who had sustained thirddegree tears, reported that almost half of these women had undergone an episiotomy. The use of midline episiotomies, favored in the United States, has been strongly associated with third-degree tears, with those women having midline episiotomies 50 times more likely to sustain a third-degree tear.109 This is reflected
Sphincter defects and symptoms: meta-analysis of studies reporting obstetric sphincter damage
Reference
Total
Sultan et al.13
No. of women for metaanalysis
No. with sphincter defect
Primip Multip
Primip Multip
Symptomatic defect (%)
Postpartum fecal incontinence but no new sphincter tear (%)
Follow-up rate (%)
127
79
48
28
2 new (19 old)
20.4 (10 of 49)
1.3 (1 of 78)
100
202
96
106
25
14 new
23.1 (9 of 39)
6.7 (11 of 163)
100
120
78
42
9
6 old and new
0
0
71.6
118
59
59
20
2 new
68.2 (15 of 22)
0 (0 of 96)
100
Faltin et al.
150
150
0
42
0
36.6 (15 of 41)
6.8 (7 of 103)
96
Overall
717
167 new and old, all women
32.5 (49 of 151)
4.3 (19 of 440)
104
Abramovitz et al. Varma et al.
105
106
Fynes et al.
107
Data from ref. 103. Multip, multiparae; Primip, primiparae.
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in the three-fold increased risk of fecal incontinence following midline episiotomy versus a spontaneous perineal laceration.110 Despite obvious injury to the anal sphincters, symptoms of anal incontinence may not occur for some time after delivery. Bek et al.111 found that in women who experienced transient anal incontinence after a complete tear, 39% had a relapse of symptoms after the next vaginal delivery. The major long-term problem seen in these women was incontinence of flatus. Fynes et al.,106 in a study of women undergoing a second vaginal delivery, with a history of occult sphincter injury or transient fecal incontinence after their first delivery, found that there was a significant risk of these women having persistent fecal incontinence. Full thickness anal sphincter disruption was the most significant risk factor in the development of fecal incontinence after a second vaginal delivery.
chIldbIrth and prolapse Genital prolapse occurs as a consequence of weakness of the fibromuscular supports of the pelvic organs. The etiology is multifactorial but childbirth has been implicated as a major factor. It is far commoner in parous women, with 50% of parous women having some degree of genital prolapse, of which 10–20% are symptomatic. In contrast, only 2% of symptomatic prolapse is found to occur in nulliparous women. The risk of prolapse is higher with increasing parity.112 The mechanism of prolapse is unclear. Pathologic and electrophysiologic studies have shown that significant pelvic nerve denervation and reinnervation are associated with stress incontinence and prolapse. However, there are also collagenous changes in the pelvic floor which are related to ageing, childbirth, and endogenous hormone changes which may also predispose to prolapse and stress incontinence.113–116 During vaginal delivery the combination of distension by the fetal head and pressure of maternal expulsive efforts stretching the pelvic floor may lead to functional and anatomic alterations in the muscles, nerves, and the connective tissue of the pelvic floor and anal canal. Trauma to the pelvic floor may also lead to repair with weaker collagen and so predispose to incontinence and prolapse. Prolapse is noted to be more common in women after a vaginal delivery compared to after a cesarean section.117,118 Using the pelvic organ prolapse quantification (POPQ) examination, O’Boyle et al. found that the 23 nulliparous pregnant women had an increased POPQ stage compared to 21 non-pregnant controls.119 An increase in POPQ stage is
also seen after vaginal delivery and this correlates well with increased mobility of the bladder base and neck.120 These studies suggest that both pregnancy and delivery are important etiologic factors for the development of pelvic organ prolapse.
conclusIons The development of pelvic floor disorders such as urinary and fecal incontinence and genital prolapse have been associated with pregnancy and vaginal delivery. Mechanisms include direct muscle trauma, disruption of connective tissue support and denervation injury. The time of greatest risk of damage would appear to be the first vaginal delivery. In recent years, there has been increasing interest in the elective cesarean section to reduce the risk of pelvic floor disorders. Less pelvic floor damage may occur after elective but not necessarily emergency cesarean section.15,89,121,122 Elective cesarean section appears to prevent against mechanical trauma to the anal sphincter but not necessarily the urethral sphincter.123 However, before considering these potential benefits of cesarean delivery, they must be weighed against the potential risks for mother and child, including increased risk of postpartum hysterectomy, adhesions, ileus, placental implantation, problems in future pregnancies, and increased respiratory distress syndrome in the newborn.124,125 Further research is required to clarify the long-term risks, cost-benefits of cesarean section. Ideally, women should be offered strategies to reduce pelvic floor injury and incontinence such as pelvic floor exercises which have been shown to reduce urinary incontinence and increase pelvic floor strength.126,127 Adequate training is required in effective labor ward management, postpartum bladder care, and perineal suturing. For those women in whom postpartum incontinence and prolapse develops, treatment strategies and follow-up should be readily available and standardized protocols developed.
references 1. MacArthur C, Lewis D, Bick D. Stress incontinence after childbirth. Br J Midwifery 1991;1:207–14. 2. Glazener CMA, Abdalla M, Stroud P et al. Postnatal maternal morbidity: extent, causes, prevention and treatment. Br J Obstet Gynaecol 1995;102:282–7. 3. Sleep J, Grant A. West Berkshire perineal management trial: three year follow-up. BMJ 1987;295:749–51. 4. Sleep J, Grant A, Garcia J et al. West Berkshire perineal management trial. BMJ 1984;289:587–90.
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5. Handa VL, Harris TA, Ostergard MD. Protecting the pelvic floor: obstetric management to prevent incontinence and pelvic organ prolapse. Obstet Gynecol 1996;88:470–8. 6. Nicholls C, Randall C. Vaginal Surgery. Baltimore: Williams and Wilkins, 1976. 7. Foldspang A, Lam GW, Elving L. Parity as a correlate of adult female urinary incontinence prevalence. J Epidemiol Comm Health 1992;46:595–600. 8. Milsom I, Ekelund P, Molander U, Arvidsson L, Areskoug B. The influence of age, parity, oral contraception, hysterectomy and menopause on the prevalence of urinary incontinence in women. J Urol 1993;149:1459–62. 9. Wilson PD, Herbison RM, Herbison GP. Obstetric practice and the prevalence of urinary incontinence three months after delivery. Br J Obstet Gynaecol 1996;103:154–61. 10. Viktrup L, Lose G. The risk of stress incontinence 5 years after first delivery. Am J Obstet Gynecol 2001;185:52–87. 11. Rortveit G, Daltveit AK, Hannestad YS, Hunskaar S. Urinary incontinence after vaginal delivery or caesarean section. N Engl J Med 2003;348:900–7. 12. Chaliha C, Digesu A, Hutchings A, Soligo M, Khullar V. Caesarean section is protective against stress urinary incontinence: an analysis of women with multiple deliveries. Br J Obstet Gynaecol 2004;111:754–5. 13. Sultan AH, Kamm MA, Hudson CN, Thomas JM, Bartram CI. Anal sphincter disruption during vaginal delivery. N Engl J Med 1993;329:1905–11. 14. Snooks SJ, Swash M, Setchell M, Henry MM. Injury to the innervation of pelvic floor sphincter musculature in childbirth. Lancet 1984;ii:546–50. 15. Allen RE, Hosker GL, Smith ARB, Warrell DW. Pelvic floor damage and childbirth: a neurophysiological study. Br J Obstet Gynaecol 1990;97:770–9. 16. MacArthur C, Bick D, Keighley MRB. Faecal incontinence after childbirth. Br J Obstet Gynaecol 1997;104:46–50. 17. Ulmsten U, Ekman G, Giertz G, Malmstrom A. Different biochemical composition of connective tissue in continent and stress incontinent women. Acta Obstet Gynecol Scand 1987;66:455–7. 18. King J, Freeman R. Can we predict antenatally those patients at risk of postpartum stress incontinence. Neurourol Urodyn 1996;15:330–1. 19. Skoner M, Thompson WD, Caron VA. Factors associated with risk of stress urinary incontinence in women. Nurs Res 1994;43:301–6. 20. Madoff RD, Williams JG, Caushaj PF. Current concepts: fecal incontinence. N Engl J Med 1992;362:1002–7. 21. Klein MC, Gauthier RJ, Robbins JG et al. Relationship of episiotomy to perineal trauma and morbidity, sexual dysfunction, and pelvic floor relaxation. Am J Obstet Gynecol 1994;171:591–8.
22. Woolley RJ. Benefits and risks of episiotomy: a review of the English language literature since 1980. Obstet Gynecol Surv 1995;50:806–35. 23. Thacker SB, Banta DH. Benefits and risks of episiotomy: an interpretative review of the English language literature, 1860–1890. Obstet Gynecol Surv 1983;38(6):322–338. 24. Signorello LB, Harlow BL, Chekos A, Repke JT. Postpartum sexual functioning and its relationship to perineal trauma: a retrospective cohort study of primiparous women. Am J Obstet Gynecol 2001;184:881–90. 25. Peschers UM, Schaer GN, DeLancey JOL, Schuessler B. Levator ani function before and after childbirth. Br J Obstet Gynaecol 1997;104:1004–8. 26. Kiff ES, Barnes RPH, Swash M. Evidence of pudendal neuropathy in patients with perineal descent and chronic constipation. Gut 1984;5:1279–82. 27. Dafnis E, Sabatini S. The effect of pregnancy on renal function: physiology and pathophysiology. Am J Med Sci 1992;303:184–205. 28. Lobel RW, Sand PK, Bowen LW. The urinary tract in pregnancy. In: Ostergard DR, Bent AE (eds) Urogynaecology and Urodynamics, 4th ed. Baltimore: Williams and Wilkins, 1996; 323. 29. Bennetts FA, Judd GE. Studies of the postpartum bladder. Am J Obstet Gynaecol 1941;42:419–27. 30. Seski AG, Duprey WM. Postpartum intravesical photography. Obstet Gynecol 1961;18:548–56. 31. Muellner SR. Physiological bladder changes during pregnancy and the puerperium. J Urol 1939;41:691–2. 32. Francis WJA. Disturbances of bladder function in relation to pregnancy. J Obstet Gynaecol Br Emp 1960;67:353–66. 33. Kerr-Wilson RHJ, Thompson SW, Orr JW, Davis RO, Cloud GA. Effect of labor on the postpartum bladder. Obstet Gynecol 1984;64:115–8. 34. Chaliha C, Kalia V, Monga A, Sultan AH, Stanton SL. Pregnancy, childbirth and delivery: a urodynamic viewpoint. Br J Obstet Gynaecol 2000;107:1354–9. 35. Parboosingh J, Doig A. Studies of nocturia in normal pregnancy. Obstet Gynecol Br Emp 1973;80:888–95. 36. Cutner A, Carey A, Cardozo LD. Lower urinary tract symptoms in early pregnancy. Br J Obstet Gynaecol 1992;12:75–8. 37. Cutner A. The lower urinary tract in pregnancy. MD Thesis, University of London, 1993. 38. Parboosingh A, Doig A. Renal nyctohemeral excretory patterns of water and solutes in normal human pregnancy. Am J Obstet Gynecol 116; 609–15. 39. Fischer W, Kittel K. Urine flow measurement in pregnancy and the puerperium. Zentralbl Gynakol 1990;112:593–9. 40. Myers DL, Scott RJ. Acute urinary retention and
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incarcerated retroverted gravid uterus. J Reprod Med 1995;40:487–90.
incontinence in women with obstetric anal sphincter rupture. Br J Obstet Gynaecol 1996;103:1034–40.
41. Saultz JW, Toffler WL, Shackles JY. Postpartum urinary retention. J Am Board Fam Pract 1991;4(5):341–4.
58. Viktrup L, Lose G. Epidural analgesia during labour and stress incontinence after delivery. Obstet Gynecol 1993;82:984–6.
42. Andolf E, Iosif CS, Jorgensen C, Rydstrom H. Insidious urinary retention after vaginal delivery: prevalence and symptoms at follow-up in a population based study. Gynecol Obstet Invest 1994;38:51–3. 43. Yip S-K, Hin L-K, Chung TKH. Effect of duration of labor on postpartum postvoid residual bladder volume. Gynecol Obstet Invest 1998;45:177–80. 44. Carley ME, Carley JM, Vasdev G et al. Factors that are associated with clinically overt postpartum urinary retention after vagina delivery. Am J Obstet Gynecol 2002;187:430–3. 45. Khullar V, Cardozo LD. Bladder sensation after epidural analgesia. Neurourol Urodyn 1993;12:424–5.
59. Röckner G. Urinary incontinence after perineal trauma at childbirth. Scand J Caring Sci 1990;4:169–72. 60. Iosif S, Ulmsten U. Comparative urodynamic studies of continent and stress incontinent women in pregnancy and the puerperium. Am J Obstet Gynecol 1981;140:645–50. 61. Toews H. Intraurethral pressure in normal and stress incontinent women. Obstet Gynecol 1967;29:613–24. 62. Bunne G, Obrink A. Urethral closure pressure in stress: a comparison between stress incontinent and continent women. Urol Res 1977;6:127–34.
46. Francis WJA. The onset of stress incontinence. J Obstet Gynaecol Br Emp 1960;67:899–903.
63. Schultze H, Wolansky D. Urethral wall pulsation in pregnant patients, continent and stress incontinent females. Zentralbl Gynakol 1990;112:19–22.
47. Viktrup L, Lose G, Rolff M, Barfoed K. The symptom of stress incontinence caused by pregnancy or delivery in primiparas. Obstet Gynecol 1992;79:945–9.
64. Perucchini D, DeLancey JOL, Ashton-Miller JA. Regional striated muscle loss in the female urethra: where is striated muscle vulnerable? Neurourol Urodyn 1997;16:407–8.
48. Chaliha C, Khullar V, Stanton SL, Monga AK, Sultan AHS. Urinary symptoms in pregnancy: are they useful for diagnosis? Br J Obstet Gynaecol 2002;109:1181–3.
65. Toozs-Hobson P, Athanasiou PS, Khullar V et al. Why do women develop incontinence after childbirth? Neurourol Urodyn 1997;16:384–5.
49. Stanton SL, Kerr-Wilson R, Harris GV. The incidence of urological symptoms in normal pregnancy. Br J Obstet Gynaecol 1980;87:897–900.
66. Benness CJ, Barnick CG, Cardozo L. Normal urodynamic findings in symptomatic women: who to believe, the patient or the test? Int Urogynecol J 1990;1:173–4.
50. Viktrup L, Lose G. The risk of stress incontinence 5 years after first delivery. Am J Obstet Gynecol 2001;185:82–7.
67. Smith ARB, Hosker G, Warrell DW. The role of partial denervation of the pelvic floor in the aetiology of genitourinary prolapse and stress incontinence of urine: a neurophysiological study. Br J Obstet Gynaecol 1989;96:24–8.
51. Foldspang A, Hvidman L, Momssen S, Nielsen JB. Risk of postpartum urinary incontinence associated with pregnancy and mode of delivery. Acta Obstet Gynecol Scand 2004;83:923–7. 52. Dolan LM, Hosker G, Mallett VT, Allen RE, Smith ARB. Stress incontinence and pelvic floor neurophysiology 15 years after first delivery. Br J Obstet Gynaecol 2003;110:1107–14. 53. Chaliha C, Kalia V, Stanton SL et al. Antenatal prediction of postpartum urinary and fecal incontinence. Obstet Gynecol 1992;79:945–9. 54. Wilson PD, Herbison RM, Herbison GP. Obstetric practice and the prevalence of urinary incontinence three months after delivery. Br J Obstet Gynaecol 1996;103:154–61. 55. Jackson S, Barry C, Davies G et al. Duration of the second stage of labour and epidural analgesia: effect on subsequent urinary symptoms in primiparous women. Neurourol Urodyn 1995;14:498–9.
68. Smith ARB, Hosker GL, Warrell DW. The role of pudendal nerve damage in the etiology of genuine stress incontinence in women. Br J Obstet Gynaecol 1989;96:29–32. 69. Deindl FM, Vodusek DB, Hesse U, Schussler B. Pelvic floor activity patterns: comparison of nulliparous continent and parous urinary stress incontinent women. Br J Urol 1994;73:413–7. 70. Peschers U, Schaer G, Anthuber C, DeLancey JOL, Schuessler B. Changes in vesical neck mobility following vaginal delivery. Obstet Gynecol 1996;88:1001–6. 71. Meyer S, Schreyer A, De Grandi P, Hohlfeld P. The effects of birth on urinary continence mechanisms and other pelvic floor characteristics. Obstet Gynecol 1998;92:613–8.
56. Dimpfl T, Hesse U, Schussler B. Incidence and cause of postpartum urinary stress incontinence. Eur J Obstet Gynecol Reprod Biol 1992;43:29–33.
72. Keane DP, Sims TJ, Bailey AJ, Abrams P. Analysis of the pelvic floor electromyography and collagen status in premenopausal nulliparous females with genuine stress incontinence. Neurourol Urodyn 1992;11:308–9.
57. Tezschner T, Sorensen M, Lose G et al. Anal and urinary
73. Lavin JM, Smith ARB, Anderson J, Grant M, Buckley
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H, Critchley H, Hosker GL. The effect of pregnancy on the connective tissue rectus sheath. Neurourol Urodyn 1997;16:381–2.
90. Miller R, Bartolo DCC, Roe A, Cervero F, Mortensen NJ. Anal sensation and the continence mechanism. Dis Colon Rectum 1988;31:433–8.
74. King J, Freeman R. Is antenatal bladder neck mobility a risk factor for postpartum stress incontinence? Br J Obstet Gynaecol 1998;105:1300–7.
91. Rogers J. Testing for and the role of anal rectal sensation. Baillières Clin Gastroenterol 1992;6:179–91.
75. Sultan AH, Kamm MA, Hudson CN, Bartram CI. Effect of pregnancy on anal sphincter morphology and function. Int J Colorect Dis 1993;8:206–9.
92. Aitchinson M, Fisher BM, Carter K, McKee R, MacCuish AC, Finlay IG. Impaired anal sensation and early diabetic faecal incontinence. Diabet Med 1991;8:960–3.
76. Kamm MA. Obstetric damage and faecal incontinence. Lancet 1994;344:730–3.
93. Ferguson GH, Redford J, Barrett JA, Kiff ES. The appreciation of rectal distension in fecal incontinence. Dis Colon Rectum 1989;32:964–7.
77. Law PJ, Kamm MA, Bartram CI. Anal endosonography in the investigation of faecal incontinence. Br J Surg 1991;78:312–4.
94. Miller R, Bartolo DCC, Mortensen NJ. Anorectal temperature sensation: a comparison of normal and continent patients. Br J Surg 1987;74:511–5.
78. Zetterstrom JP, Lopez A, Anzen B et al. Anal incontinence after vaginal delivery: a prospective study in primiparous women. Br J Obstet Gynaecol 1999;106:324–30.
95. Barrett JA, Brocklehurst JC, Kiff ES, Ferguson G, Faragher EB. Anal function in geriatric patients with faecal incontinence. Gut 1989;30:1224–51.
79. Combs CA, Robertson PA, Laros RK. Risk factors for third-degree and fourth-degree perineal lacerations in forceps and vacuum deliveries. Am J Obstet Gynecol 1990;163:100–4.
96. Small KA, Wynne JM. Evaluating the pelvic floor in obstetric patients. Aust N Z J Obstet Gynaecol 1990;30:41–5. 97. Cornes H, Bartolo DCC, Stirrat GM. Changes in anal canal sensation after childbirth. Br J Surg 1991;78:74–7.
80. Walker M, Farine D, Robin S, Ritchie J. Epidural analgesia, episiotomy and obstetric laceration. Obstet Gynecol 1991;77:668–71.
98. Chaliha C, Bland JM, Monga A, Sultan AHS, Stanton SL. Anal function: effect of pregnancy and delivery. Am J Obstet Gynecol 2001;185:427–32.
81. Henriksen TB, Bek KM, Hedegaard M, Secher NJ. Episiotomy and perineal lesions in spontaneous vaginal deliveries. Br J Obstet Gynaecol 1992;99:950–4.
99. Sultan AH, Kamm MA, Hudson CN, Bartram CL. Third degree obstetric anal sphincter tears: risk factors and outcome of primary repair. Br Med J 1994;308:887–91.
82. Crawford LA, Quint EH, Pearl ML, DeLancey JO. Incontinence following rupture of the anal sphincter during delivery. Obstet Gynecol 1993;82:527–31.
100. Klein MC, Gauthier RJ, Robbins JM et al. Relationship of episiotomy to perineal trauma and morbidity, sexual dysfunction and pelvic floor relaxation. Am J Obstet Gynecol 1994;171:591–8.
83. Snooks SJ, Barnes PRH, Swash M, Henry MM. Damage to the innervation of the pelvic floor musculature in chronic constipation. Gastroenterology 1985;89:977–81. 84. Parks AG, Swash M, Urich H. Sphincter denervation in anorectal incontinence and rectal prolapse. Gut 1977;18:656–65. 85. Parks AG, Swash M. Denervation of the anal sphincter causing idiopathic ano-rectal incontinence. J R Coll Surg Edinb 1979;24:94–6. 86. Beersiek F, Parks AG, Swash AM. Pathogenesis of anorectal incontinence: a histometric study of anal sphincter musculature. J Neurol Sci 1979;42:111–27.
101. Sultan AH, Kamm MA, Talbot IC, Nicholls RJ, Bartram CI. Anal endosonography for identifying external sphincter defects confirmed histologically. Br J Surg 1994;81:463–5. 102. Sultan AH, Kamm MA, Bartram CI, Hudson CN. Anal sphincter trauma during instrumental delivery. A comparison between forceps and vacuum extraction. Int J Gynecol Obstet 1993;43:263–70. 103. Oberwalder M, Connor J, Wexner SD. Meta-analysis to determine the incidence of obstetric anal sphincter damage. Br J Surg 2003;90:1333–7.
87. Lubowski DZ, Swash M, Nicholls RJ, Henry MM. Increase in pudendal nerve terminal motor latency with defaecation straining. Br J Surg 1988;75:786–8.
104. Abramowitz L, Sobhani I, Ganansia R et al. Are sphincter defects the cause of anal incontinence after vaginal delivery? Results of a prospective study. Dis Colon Rectum 2000;43:590–6.
88. Snooks SJ, Swash M, Mathers SE, Henry MM. Effect of vaginal delivery on the pelvic floor: 5 year follow-up. Br J Surg 1990;77:1358–60.
105. Varma A, Gunn J, Gardiner A, Lindow SW, Duthie GS. Obstetric anal sphincter injury: prospective evaluation of incidence. Dis Colon Rectum 1999;42:1537–43.
89. Sultan AH, Kamm MA, Bartram CI, Hudson CN. Pudendal nerve damage during labour: prospective study before and after childbirth. Br J Obstet Gynaecol 1994;101:22–8.
106. Fynes M, Donnelly V, Behan M, O’Connell PR, O’Herlihy C. Effect of second vaginal delivery on anorectal physiology and faecal continence: a prospective study. Lancet 1999;354:983–6.
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107. Faltin DL, Boulvain M, Irion O, Bretones S, Stan C, Weil A. Diagnosis of anal sphincter tears by postpartum endosonography to predict fecal incontinence. Obstet Gynecol 2000;95:643–7.
119. O’Boyle AL, Woodman PJ, O’Boyle JD, Davis GD, Swift SE. Pelvic organ support in nulliparous pregnant and non-pregnant women: a case control study. Am J Obstet Gynecol 2002;187:99–102.
108. Poen AC, Felt-Bersma RJF, Dekker GA, Deville W, Cuesta MA, Muewissen SGM. Third degree obstetric perineal tears: risk factors and the preventative role of mediolateral episiotomy. Br J Obstet Gynaecol 1997;104:563–6. 109. Shiono P, Klebanoff MA, Carey JC. Midline episiotomies: more harm then good? Obstet Gynecol 1990;75:765–70.
120. Dannecker C, Lienemann A, Fischer T, Anthuber C. Influence of spontaneous instrumental vaginal delivery on objective measures of pelvic organ support: assessment with pelvic organ prolapse quantification (POPQ) technique and functional cine magnetic resonance imaging. Eur J Obstet Gynecol 2004;115:32–8.
110. Signorello L, Harlo LB, Chekos AK, Repke JT. Midline episiotomy and anal incontinence: a retrospective cohort study. BMJ 2000;320:86–90.
121. Fynes M, Donnelly V, O’Connell PR, O’Herlihy C. Caesarean delivery and anal sphincter injury. Obstet Gynecol 1998;92;496–500.
111. Bek KM, Laurberg S. Risks of anal incontinence from subsequent vaginal delivery after a complete obstetric anal sphincter tear. Br J Obstet Gynaecol 1992;99:724–6. 112. WHO Population Report. Healthier mothers and children through family planning programmes. Geneva: WHO, 1984;27:J677. 113. Hayflick L. Theories of biological aging. Exp Gerontol 1985;20:145–59. 114. Yamauchi M, Woodley DT, Mechanic GL. Aging and crosslinking of skin collagen. Biochem Biophys Res Commun 1988;152:898–903. 115. Norton PA. Pelvic floor disorders: the role of fascia and ligaments. Clin Obstet Gynecol 1993;36:926–38.
122. MacArthur C, Bick DE, Keighley MRB. Faecal incontinence after childbirth. Br J Obstet Gynaecol 1997;104:46–50. 123. Fitzpatrick M, O’Herlihy C. The effects of labour and delivery on the pelvic floor. Clin Obstet Gynecol 2001;15:63–79. 124. Jackson N, Paterson-Brown S. Physical sequelae of caesarean section. Clin Obstet Gynecol 2001;14:49–61. 125. Bowers SK, Macdonald HM, Shapiro ED. Prevention of iatrogenic neonatal respiratory distress syndrome: elective repeat cesarean section and spontaneous labor. Am J Obstet Gynecol 1982;143:186–9.
117. De Gregorio G, Hillemans HG, Quaas L, Mentzel J. Late morbidity following caesarean section: a neglected factor. Geburtshilfe Frauenheilkd 1988;48:16–9.
126. Reilly ETC, Freeman RM, Waterfield MR, Waterfield AE, Steggles P, Pedlar F. Prevention of postpartum stress incontinence in primigravidae with increased bladder neck mobility: a randomised controlled trial of antenatal pelvic floor exercises. Br J Obstet Gynaecol 2002;1109:68–76.
118. Chiaffarino F, Chatenoud L, Dindelli M et al. Reproductive factors, family history, occupation and risk of urogenital prolapse. Eur J Obstet Gynecol Reprod Biol 1999;82:63–7.
127. Harvey MA. Pelvic floor exercises during and after pregnancy: a systematic review of their role in preventing pelvic floor dysfunction. J Obstet Gynaecol Can 2003;25:487–98.
116. Morley R, Cumming J, Weller R. Morphology and neuropathology of the pelvic floor in patients with stress incontinence. Int Urogynecol J 1966;7:3–12.
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47 Menopause Andrew Hextall, Dudley Robinson
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INTRODUCTION
including frequency, nocturia, incontinence, urinary tract infections (UTIs), and the ‘urge syndrome’. These may coexist with vaginal symptoms of dryness, itching, burning, and dyspareunia.
HORMONAL INFLUENCES ON THE FEMALE LOWER URINARY TRACT The female lower urinary and genital tracts both arise from the primitive urogenital sinus and develop in close anatomic proximity from early in the first trimester of pregnancy (Fig. 47.2). Estrogen receptors are consis tently expressed in the squamous epithelium of the proximal and distal urethra and vagina, and in areas of the trigone of the bladder that have undergone squa mous metaplasia5,6 (Fig. 47.3). However, they are not present in the transitional epithelium of the bladder dome, reflecting the different embryologic origin of this tissue. The pubococcygeus muscle of the pelvic floor is also estrogen sensitive.7,8 Alpha and βestrogen recep tor subtypes are both present in the urogenital tract but their precise role remains unclear.9 Estrogen increases cell cycle activity in the female lower urinary tract,10 dem onstrated by an increase in the number of intermediate and superficial cells in the urethra and bladder,11 with similar changes occurring in the vagina in postmeno pausal women.12 Alterations in urinary cytology during the menstrual cycle are comparable with those seen in vaginal cytology,13 changes that also occur in the urinary sediment following treatment with estrogens.14 Progesterone receptors are expressed inconsistently in the lower urinary tract and may be dependent on the
300 250 200 150 100
Market economies
Former socialist Europe
World region
Middleeastern crescent
Latin America
Other Asia and Islands
China
0
India
50
Sub-saharan Africa
Number of women aged 50 and over (millions)
Ovarian function starts to decline from as early as the 20th week of embryologic life, and estrogen produc tion falls to a critical level during a period known as the climacteric. De Gardanne coined the term ‘la mene spausie’ from the Greek men (month) and pausis (ces sation).1 The menopause is diagnosed when a woman has not had a period for 12 months. Aristotle (384–322 BC)2 recognized that menstruation normally stopped at about the age of 40 years but that some women con tinued to have periods until their 50th year. In the 17th century, less than a third of women lived to experience the menopause. However, increased life expectancy dur ing the last century means that many women will spend a significant part of their life in the postmenopausal years and will therefore be at risk of the effects of estrogen deficiency. The average age at the menopause is now generally accepted to be 50 years, but some variation is thought to exist between different countries and geographical regions.3 In 1990 there were approximately 467 million women aged 50 years and above throughout the world; this number is expected to have increased to 1200 million by the year 20304 (Fig. 47.1). Postmenopausal women make up over 15% of the population in indus trialized countries, with a growth rate of 1.5% predicted until the 2020s. Hormonal changes occurring at the time of the menopause have an impact on all estrogensensitive tissues, and the female urogenital tract is no excep tion. Estrogen deficiency, particularly when prolonged, is associated with a wide range of urinary symptoms
Figure 47.1. Summary statistics for number of menopausal women by world region, 1990–2030: 1990; 2000; 2010; 2020; 2030.
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Menopause
Bladder
Allantois Ureter Urogenital sinus
Perineum
Figure 47.2.
Anorectal canal
a
Embryology of the female lower urinary tract.
estrogen status of the woman.7,15,16 Androgen receptors are found in the female bladder and urethra, but their role is unclear at present.17 Cyclical variations in the levels of sex steroids during the menstrual cycle may lead to both symptomatic and urodynamic changes. In a survey of 133 women with a regular menstrual cycle, 55 (41%) complained that their urinary symptoms were cyclical, with the premenstrual period/luteal phase appearing to be the most bother some.18 The prevalence of abnormal detrusor overactiv ity on cystometry increased significantly with time from the last menstrual period and might reflect increases in the circulating level of progesterone following ovu lation. Van Geelen and coworkers19 measured the ure thral pressure profiles of 27 nulliparous women with normal ovulatory cycles and found an increase in the functional urethral length midcycle and early in the luteal phase. The data suggested a causal relationship between changes in serum estradiol and alterations in urethral length. During pregnancy, many women com plain of urinary symptoms that are due only in part to an increase in urine output and pressure effects from the gravid uterus.20–22 However, the prevalence of detru sor overactivity is significantly greater antenatally than postnatally,23 suggesting a hormonal effect thought to be mediated through progesterone.
PREVALENCE OF POSTMENOPAUSAL URINARY SYMPTOMS Urinary symptoms secondary to estrogen deficiency may develop many years after the menopause and may, therefore, be underreported by both patient and doctor. Epidemiologic studies have shown that the incidence
b
c
Figure 47.3. Estrogen receptors are expressed in the squamous epithelium of the vagina (a) and urethra (b) but not in the transitional epithelium of the bladder dome (c). Estrogen receptor-positive cell nuclei appear brown; estrogen receptor-negative nuclei appear blue. (Provided by Blakeman et al. based on the data in ref. 6.) of urogenital problems increases with age, with many women delaying the seeking of treatment for several years. In a study of 2045 British women aged between 55 and 85 years, Barlow and coworkers24 showed that 48.5% of postmenopausal women had been affected by urogen ital symptoms at some time and that 11% were currently affected by individual symptoms (Table 47.1). At least twothirds of women did not relate their vaginal or uri 697
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Table 47.1.
Prevalence of urogenital symptoms by age in the preceding 2 years
Age group (years)
All
55–64
65–74
75–84
>85
TOTAL
2011 [2011]
662 [706]
697 [678]
539 [517]
113 [109]
Urgency, dysuria, frequency
312 (16)
101 (14)
96 (14)
95 (18)
19 (18)
Urinary incontinence
172 (9)
46 (7)
45 (7)
65 (13)
16 (14)
Vaginal itching
217 (11)
68 (10)
72 (11)
65 (12)
15 (13)
Vaginal dryness
156 (8)
75 (11)
4 (7)
34 (7)
3 (2)
33 (2)
23 (3)
8 (1)
Painful intercourse
2 (0–4)
0
Values are given as n with weighted totals in square brackets or percentages in parentheses. Reproduced from ref. 24 with permission.
nary complaint to the menopause. Iosif and Bekassey,25 in their study of 2200 women aged 61 years, also found a high prevalence of lower urinary tract disorders, 49% of women having some symptoms. In addition, 70% of the women with incontinence related the onset of their uri nary leakage to the time of their final menstrual period. Urinary tract symptoms are certainly frequent following the menopause: of women who attend a menopause clinic, one in five complains of severe urgency and nearly half complain of stress incontinence.26 The prevalence of postmenopausal incontinence in the community is thought to be between 16 and 29%.27–29 While the aging process is clearly a significant etiologic factor in the pathogenesis of urinary inconti nence, there is conflicting evidence as to whether the menopause and estrogen deficiency are also implicated. Thomas and coworkers30 found that the peak preva lence of occasional or regular incontinence occurred in the 45 to 54yearold age group, a period that coincides with the menopause in most women (Fig. 47.4). Jolleys27
surveyed 937 women registered with a rural general practice and detected similar changes in the prevalence of incontinence with age (Fig. 47.5). A similar pattern appears to occur in hospital practice: Hilton31 reported that the mean age of women referred to a urogynecol ogy unit was almost identical to the age of the natural menopause. Urge incontinence in particular occurs more frequently after the menopause32 (Fig. 47.6). Most studies, however, show that many women develop incontinence at least 10 years before the menopause; Jolleys27 found that significantly more premenopausal women than postmenopausal women were affected. In addition, the prevalence of stress incontinence in the community actually starts to fall after the meno pause, particularly in age groups that are most likely to be affected by relative estrogen deficiency. These data probably simply confirm that the development of uri nary incontinence is a multifactorial process, and that the menopause is just one of a number of etiologic factors.
40 35 30
Prevalence (%)
25 20 15 10 5 0
5–14
15–24
25–34
35–44 45–54 55–64 Age group (years)
65–74
75–84
>85
Figure 47.4. Prevalence of occasional or regular incontinence in women. (Data from ref. 30.)
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70 60
Prevalence (%)
50 40 30 20 10 0
<25
25–34
35–44
45–54 55–64 Age group (years)
65–74
75–84
>85
Figure 47.5. Prevalence of stress urinary incontinence with increasing age. (Data from ref. 27.)
8
Figure 47.6. Changes in prevalence of symptoms of stress incontinence ( ) and urge incontinence ( ) with increasing age. (Data from ref. 32.)
50
Prevalence (%)
40
30
20
10
0
1
2
3
4 5 Age (decade)
6
MENOPAUSE AND THE CONTINENCE MECHANISM Effects of aging Many women consider the development of urinary symp toms as they get older to be a normal phenomenon rather than the manifestation of a disease.33 In a study by Gjorup and coworkers,34 over 50% of women aged more than 75 years thought that their symptoms were normal for elderly people. The aging population is at risk for a num ber of systemic illnesses and transient problems that may present with lower urinary tract symptoms, including dia betes mellitus, congestive cardiac failure, and renal dis ease (Table 47.2). A patient with impaired mobility may
7
develop urinary incontinence if suitable access to a toilet is not available, a situation which may be exacerbated if medications such as diuretics or hypnotics are being taken. However, symptomatic and functional changes certainly do occur in the lower urinary tract as a result of the aging process itself; these changes are difficult to differentiate from those due to estrogen deficiency. The prevalence of nocturia increases with age from 10.5% (50–59 years) to 50% (>80 years).35 In addition, the proportion of women with nocturia secondary to nocturnal polyuria also rises after the menopause. Younger women tend to excrete most of their fluid intake during the day, whereas in the elderly this pattern may be reversed. Postural effects may lead to daytime 699
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Table 47.2.
• • • • • • •
Transitional causes of urinary incontinence in the elderly
Urinary tract infection Fecal impaction Estrogen deficiency Restricted mobility Drug therapy Depression Confusional state
pooling of extracellular fluid, particularly in the ankles. This fluid returns to the systemic circulation during the night, leading to an increase in urine output. This, com bined with abnormal sleep patterns, may lead to noc turia. Impaired secretion of antidiuretic hormone may also be a factor in some women. Urodynamic studies have shown that the bladder becomes less efficient with age.36–38 Elderly women have a reduced urine flow rate, increased urinary residual, higher first sensation to void and increased bladder capacity, although bladder capacity may decrease in the eighth and ninth decades. Detrusor pressures at ure thral opening and closure during voiding decrease in absolute terms as women become older.39 Histologically, there is an agerelated increase in fibrosis in the bladder neck40 and in collagen content41 of the female bladder. In a study of the female urethral sphincter postmortem, Perucchini and coworkers42 demonstrated reductions in the number of striated muscle fibers and their density with increasing age, although the size of individual fibers remained unchanged. The number and diameter of the fibers in the muscles of the pelvic floor does appear to decrease with age,43 although neuronal damage second ary to childbirth may be a confounding factor.44,45
Sex hormones and the continence mechanism For a woman to remain continent, urethral pressure must exceed the intravesical pressure at all times except during micturition.46 Sex steroids appear to influence the neuronal control of the continence mechanism, and evidence is emerging that hormones may have a direct (nongenomic) effect on detrusor smooth muscle function. In addition, the functional layers of the ure thra, which help to maintain a positive urethral closure pressure (epithelium, vasculature, connective tissue and muscle), all appear to be targets for estrogens.
Neuronal control of micturition During a woman’s reproductive life, gonadal steroids interact with neurotransmitters/neuropeptides at the
hypothalamic level, modifying the synthesis and release of gonadotrophinreleasing hormone. It is now clear that estrogens are also important in a number of other cere bral functions including pain control, thermoregulation, hunger and thirst mechanisms, and psychological well being. Estrogen receptors are found throughout the brain cortex, limbic system, hippocampus, and cerebel lum.47,48 In these regions estrogens can alter the synthe sis, release, and metabolism of neurotransmitters such as dopamine, acetylcholine, serotonin, and melatonin. This may explain why estrogen supplementation can improve cognitive function and enhance mood and psy chological wellbeing in the peri and postmenopausal periods.49–52 Recent animal studies have shown that androgen receptors are present in the pontine micturition center.53 They are also present in the preoptic area of the hypo thalamus, an area of the forebrain which may play an important role in the initiation of micturition. Further work is required to establish the exact type and distribu tion of sexsteroid receptors in the human micturition pathways and their importance in the control of the con tinence mechanism.
Detrusor function Estrogen appears to have a direct effect on detrusor function by modifying muscarinic receptors54,55 and inhibiting the influx of extracellular calcium ions into muscle cells.56 Studies of female rats have shown that oophorectomy alters the pressure–flow characteristics of micturition.57 This effect may be only partly reversed by estrogen supplementation and is possibly age dependent. Further animal studies of ovariectomy in the rabbit show that estrogen deficiency leads to decreased blood flow to bladder smooth muscle and bladder mucosa.58 The resulting mucosal hypoxia leads to significant mucosal thinning and an increase in permeability. It is not clear if similar effects occur in humans. Estrogen may theoretically play a role in the treat ment of sensory and motor urge incontinence. Estradiol reduces the amplitude and frequency of spontaneous rhythmic contractions, which has been associated with detrusor overactivity.59 In addition, pretreatment of rats with estrogen in vivo reduces the contractile response of isolated detrusor muscle.60 There is also evidence to suggest that the sensory threshold of the bladder may be raised by estrogen supplementation.61 In general, progestogens have an adverse effect on the continence mechanism. Elliott and Castleden62 have shown that progesterone blocks the inhibitory effect of estradiol on detrusor muscle contractions in the rat. The effect of estrogen on the responsiveness of muscarinic
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receptors therefore appears to be modified by proges terone. Clinically, progestogens are associated with an increase in irritative bladder symptoms63,64 and urinary leakage in those women with incontinence taking hor mone replacement therapy (HRT).65 However, proges togens do not appear to alter significantly the urethral pressure profile of continent women.66
Urethral function Estrogen improves the ‘maturation index’ of urethral squamous epithelium,67 increases urethral closure pressure, and improves pressure transmission to the proximal urethra.68–70 There is evidence to suggest that the vasodilatory effects of estrogens that occur in the systemic and cerebral circulations71–73 may also occur in the urogenital tract. Using urethral pressure profilom etry, Versi and Cardozo74 showed that vascular pulsations seen secondary to blood flow in the urethral submucosa and urethral sphincter increase in size in response to estrogen. Attempts have been made to quantify changes in ure thral blood flow in response to estrogen therapy using Doppler ultrasonography.75 Unfortunately, the repro ducibility of this technique is limited by difficulties in imaging the same vessel repeatedly and natural variation in the blood flow through pelvic vessels. Alphaadrenoceptors in the urethral sphincter are sensitized by estrogens, helping to maintain muscular tone.76 Finally, connective tissue metabolism is stimu lated by estrogens, increasing production of collagen in periurethral tissues and, therefore, possibly reversing the changes that occur as a result of aging.77 The estrogen status of the patient can therefore have a significant effect on urethral pressure,78 and this may be particularly important when there is already some impairment of urethral function.
ESTROGEN TREATMENT FOR INCONTINENCE Estrogens may be useful for the treatment of urinary incontinence for a number of reasons (Table 47.3). Salmon and coworkers79 first reported the success ful use of estrogens to treat urinary incontinence over 50 years ago. It is now well recognized that there is a poor correlation between a woman’s symptoms and the diagnosis made following appropriate investigation.80 Unfortunately, early trials took place before the wide spread introduction of urodynamic studies and, there fore, almost certainly included a heterogeneous group of individuals with a number of different pathologies. Lack of objective outcome measures also limits inter
Table 47.3.
Mechanisms by which estrogens may improve female urinary incontinence
1. Increased urethral closure pressure • Increased urethral cell maturation • Increased urethral blood flow • Increased α-adrenergic receptor sensitivity in urethral smooth muscle 2. Improved abdominal pressure transmission to proximal urethra 3. Stimulation of periurethral collagen production 4. Improved neuronal control of micturition 5. Increased sensory threshold of the bladder 6. Improved mood and quality of life 7. Reduced incidence of urinary tract infection
pretation of these studies. Despite a number of recent papers and reviews,81–86 the benefits of estrogen given in this situation are far from clear.
Estrogen treatment for stress incontinence The role of estrogen in the treatment of stress inconti nence is controversial, even though a number of stud ies have been reported. Some studies gave promising results but this may be because they were observational, and were not randomized, blinded or controlled. The situation is further complicated by the fact that a num ber of different types of estrogen have been used, with various doses, routes of administration, and durations of treatment. The concurrent use of progestogens in women with a uterus to prevent endometrial hyperplasia may also be a confounding factor. A metaanalysis from the Hormones and Urogenital Therapy (HUT) Committee81 included six reported controlled trials and 17 reported uncontrolled series published in English between 1969 and 1992. The results showed a significant subjective improvement for all patients, including those with urodynamic stress incontinence (USI), possibly because estrogens improve feelings of wellbeing and quality of life. However, assess ment of the objective parameters revealed that there was no change in the volume of urine lost. Maximum urethral closure pressure did increase significantly, but this result was influenced by only one study showing a large effect. A recently reported metaanalysis has helped deter mine the role of estrogen replacement in women with stress incontinence.86 Of the papers reviewed, 14 were nonrandomized studies, 6 were randomized trials (of which 4 were placebo controlled) and 2 were metaanal yses. Interestingly, there was only a symptomatic or clini cal improvement noted in the nonrandomized studies, 701
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whereas there was no such effect noted in the random ized trials. The authors conclude that currently the evidence would not support the use of estrogen replace ment alone in the management of stress incontinence. In a Cochrane Review of estrogens for incontinence in women, 28 trials were identified, including 15 trials, which compared estrogen with a placebo.87 Objective outcome data were not reported consistently and were available only for a minority of trials. When subjective cure and improvement were considered together, there was a statistically higher cure and improvement rate for both stress (46/107 [43%] on estrogen versus 29/109 [27%] on placebo) and urge (35/61 [57%] versus 16/58 [28%]) incontinence. There were few data about the effect of estrogen after treatment had finished and none about longterm effects. Several studies have assessed the role of estrogen in combination with other therapies. Beisland and cowork ers88 treated 24 women with USI using phenylpropanol amine (50 mg twice daily) and estriol (1 mg per day vaginally), separately or in combination. Symptoms were cured in eight women receiving the combination treat ment and were improved in a further nine women; the combination was more effective than either drug alone. Hilton and coworkers89 used estrogen (vaginal or oral) alone or in combination with phenylpropanolamine to treat 60 postmenopausal women with USI in a double blind, placebocontrolled study. The symptoms of stress incontinence improved subjectively in all groups but objectively only in the women taking the combination therapy. However, concerns about side effects limit clini cal usefulness and many, more effective treatments are now available.
Estrogen treatment for urge incontinence Estrogen has been used for many years to treat post menopausal urgency and urge incontinence but few con trolled trials have been performed to confirm that it is of benefit.11,90–93 These studies should also be interpreted with caution because of the small patient numbers and lack of objective outcome measures, despite the known large placebo effect that occurs in the treatment of this condition. In some it is possible that the wrong type of estrogen was used for too short a period or the estro gen may have been given via the wrong route. Estriol is a naturally occurring estrogen but has little effect on the endometrium and does not prevent osteoporosis. It is therefore questionable whether the low dose used in these studies is sufficient to treat urinary symptoms. However, it is possible that some benefit may have been gained by a reversal of atrophic changes in the lower uri
nary/genital tract. 17βEstradiol is absorbed well from sustainedrelease vaginal tablets and this has been shown to induce maturation of the vaginal epithelium within 14 days;93 however, higher systemic levels may be needed for therapy to be effective. A doubleblind, placebocontrolled trial of the effects of estrogen implants on the urge syndrome has recently been reported.94 Forty postmenopausal women with the ‘urge syndrome’ were randomly allocated to receive a 25 mg estradiol implant or placebo. Subjectively, there was a significant improvement in urgency in both groups, although the differences were not statistically significant. Despite using numerous outcome measures, there were no apparent objective benefits of the active treatment, although this did produce much higher sys temic estrogen levels and a higher complication rate (mainly by inducing vaginal bleeding). In a systematic review of the effects of estrogen on symptoms suggestive of overactive bladder, 11 random ized trials were identified which included a total of 430 subjects.95 Overall, estrogen therapies were asso ciated with statistically significant improvements in all outcome variables including frequency, urgency, and incontinence episodes. Local therapy appeared to be the most beneficial route of administration. A Cochrane Review of estrogen for incontinence reported similar conclusions.87 Estrogen was found to be of particular benefit for women with urge inconti nence, with the chance of cure or improvement being approximately 25% higher than in women with stress incontinence.
Hormone replacement therapy as prophylaxis against the development of incontinence It is unclear if estrogen supplementation is beneficial or harmful when used prophylactically against the develop ment of urinary incontinence in peri/postmenopausal women, and if the effects last beyond the treatment period.96 Data from the Heart and Estrogen/Progestin Replacement Study (HERS) suggested that combined hormone replacement therapy was associated with wors ening stress and urge urinary incontinence.97 However, there was no significant difference in daytime fre quency or nocturia. Although these findings can only be applied to women with ischemic heart disease, other studies in apparently healthy postmenopausal women have reached similar conclusions, even when estrogen is given unopposed.98–100 These findings have also been confirmed in the Nurses’ Health Study which followed 39,436 postmeno pausal women aged 50–75 years over a 4year period.
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The risk of incontinence was found to be elevated in those women taking HRT when compared to those who had never taken HRT. There was an increase in risk in women taking oral estrogen (relative risk [RR] 1.54; 95% CI: 1.44–1.65), transdermal estrogen (RR 1.68; 95% CI: 1.41–2.00), oral estrogen and progesterone (RR 1.34; 95% CI: 1.24–1.34), and transdermal estrogen and progesterone (RR 1.46; 95% CI: 1.16–1.84). In addition, while there remained a small risk after the cessation of HRT (RR 1.14; 95% CI: 1.06–1.23), by 10 years the risk was identical (RR 1.02; 95% CI: 0.91–1.41) to those women who had never taken HRT. More recently, the effects of oral estrogens and progestogens on the lower urinary tract have been assessed in 32 female nursing home residents101 with an average age of 88 years. Subjects were randomized to oral estrogen and progesterone or placebo for 6 months. At followup there was no difference between severity of incontinence, prevalence of bacteriuria and the results of vaginal cultures, although there was an improvement in atrophic vaginitis in the group.
ESTROGENS AND INCONTINENCE – POST WHI The most recent paper to be reported by the Women’s Health Initiative (WHI) writing group has studied the effect of estrogens with and without progestogens on urinary incontinence.98 This paper represents another subanalysis of the data from the large WHI study and it should be borne in mind that the study was not designed to assess urinary incontinence and thus may lack the appropriate power to do so conclusively. Overall, 27,347 postmenopausal women aged 50–79 years were assessed in a multicenter, doubleblind, pla cebocontrolled trial. Of these, 23,296 were known to complain of lower urinary tract symptoms at baseline and at 1year followup. Women were randomized based on hysterectomy status to active treatment or placebo in either the estrogen and progestogen or estrogenonly tri als. The estrogen was conjugated equine estrogen (CEE) and the progestogen was medroxyprogesterone acetate (MPA). The main outcome measure was the incidence of urinary incontinence at 1 year among women who were continent at baseline and the severity of urinary incontinence at 1 year in those who were incontinent at baseline. In general, HRT was found to increase the incidence of all types of urinary incontinence at 1 year in those women continent at baseline. The risk was highest for stress incontinence (CEE+MPA; RR 1.87 [1.61–2.18]; CEE alone; RR 2.15 [1.77–2.62]), followed by mixed incontinence (CEE+MPA; RR 1.49 [1.10–2.01]; CEE
alone; RR 1.79 [1.26–2.53]). However, the effect on urge urinary incontinence was not uniform (CEE+MPA; RR 1.15 [0.99–1.34]; CEE alone; RR 1.32 [1.10–1.58]). When considering those women who were symptom atic at baseline, urinary frequency was found to increase in both arms (CEE+MPA; RR 1.38 [1.28–1.49]; CEE alone; RR 1.47 [1.35–1.61]) and the incidence of urinary incontinence was seen to increase at 1 year (CEE+MPA; RR 1.20 [1.06–1.36]; CEE alone; RR 1.59 [1.39–1.82]). In addition, while no formal quality of life (QoL) assess ment was reported, women receiving HRT were more likely to report that urinary incontinence limited their daily activities and bothered and disturbed them. These results, while supportive of the previously reported HERS study and the Nurses’ Health Study, would certainly seem to contradict much of the previous work in assessing the use of estrogens in the manage ment of lower urinary tract symptoms. There are several possible explanations as why these findings may differ. 1. This trial was not designed specifically to assess urinary symptoms and the questionnaires used may have lacked the sensitivity to correctly identify incontinence. 2. The actual prevalence of urinary incontinence in this population was probably overestimated and this is supported by the finding that over 45% of 60 to 69yearold women in the study were found to be incontinent. 3. In addition to a possible overestimation of the population, the relatively large age range of this trial (50–79 years), and considerable comorbidities of participants, may not accurately reflect the current clinical use of HRT. Since the majority of women receive HRT for symptomatic relief in the perimenopausal period, it may be more appropriate to stratify the results with respect to age as this may more accurately reflect current clinical practice. 4. It should also be borne in mind that this trial only examined the use of oral systemic replacement therapy, whereas local topical estrogens have been shown to be effective in the management of troublesome lower urinary tract symptoms and to have minimal systemic effects. 5. Finally, perhaps the strongest evidence to negate the somewhat controversial findings of this study is that, based on our current knowledge, there is no plausible physiologic explanation for these findings regarding the use of estrogenonly HRT on the lower urinary tract, although there is some evidence to suggest that progestogens may increase the irritative urinary symptoms of urgency and frequency. 703
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ESTROGEN DEFICIENCY AND RECURRENT URINARY TRACT INFECTION
Proportion of samples positive
UTIs occur in women of all ages. They are a particu lar problem in the elderly, with a reported incidence of 20% in communitydwelling women and sometimes over 50% in institutionalized patients.102,103 Pathophysiologic changes that may account for this increase in risk include impairment of bladder emptying, poor peri neal hygiene, and both fecal and urinary incontinence. At present there is no conclusive evidence that impair ment of immune function as a result of aging per se is an independent risk factor for the development of UTI.104 However, once an infection is acquired, the elderly are usually sicker and at considerably greater risk of dying than the young. Alterations in the vaginal flora after the menopause are also thought to place women at an increased risk of UTI, particularly if they are sexually active. There is an increase in the vaginal pH and a decrease in the number of lactobacilli, allowing colonization with Gramnegative bacteria which act as uropathogens. However, the exact role of the menopause as an etiologic factor in the devel opment of UTI may have been overstated. Analysis of midstream urine (MSU) specimens sent to the microbi ology department of a teaching hospital from the com munity indicate that the proportion of positive results increases with age in both men and women, with no specific changes in the rate of infection occurring at or after the menopause105 (Fig. 47.7).
0.50 0.45 0.40 0.35 0.30 0.25 0.20 0.15 0.10 0.05 0
0 5 10 15 20 25 30 35 40 45 50 55 60 65 70 75 80 85 90 95 Age (years)
Figure 47.7. Proportion of mid-stream urine (MSU) samples that were positive, by subject’s age. Analysis of all MSU samples sent to the Department of Microbiology at King’s College Hospital, London, from the community in 1997. The proportions for females (—) are calculated and plotted at each year of age. For males (—), from whom there were fewer samples, the proportion plotted at a given age is calculated over a 3-year age interval around that age.
Estrogen reverses the microbiologic changes in the vaginal flora that occur after the menopause, an effect which enables it to be used for treatment or prophylaxis. Early small uncontrolled studies106,107 using oral or vaginal estrogen appeared to give prom ising results. For example, Brandberg and cowork ers108 used oral estriol to treat 41 elderly women with recurrent UTI and showed that their vaginal flora was restored to the premenopausal type and that they required fewer antibiotics. Subsequent randomized trials have shown rather mixed and largely disappoint ing benefits109–112 (Table 47.4). Kirkengen and cowork ers110 randomized 40 elderly women with recurrent UTIs to receive either oral estriol (3 mg per day for 4 weeks followed by 1 mg per day for 8 weeks) or matching placebo. There was no difference between estriol and placebo after the first treatment period; however, after the second treatment period, estriol was significantly better than placebo in reducing the incidence of UTIs. A randomized, doubleblind, placebocontrolled study of 93 postmenopausal women also showed that intravaginal estriol cream prevented recurrent UTIs in women presenting with this problem.111 MSU cultures were obtained at enrolment, monthly for 8 months and whenever urinary symptoms occurred. Changes in the vaginal pH and colonization with lactobacilli occurred within 1 month of the start of treatment in the estriol group only, and the incidence of UTI in this group was significantly reduced compared with that in the placebo group (0.5 versus 5.9 episodes per patient per year). Unfortunately, these results were not repeated in a doubleblind, placebocontrolled, study of oral estriol in the prevention of recurrent UTI in elderly women.112 Although both estriol and placebo improved urinary symptoms during the trial, the inci dence of UTI did not differ significantly between the two groups. In the largest report to date, Eriksen113 conducted a multicenter, randomized, open, parallelgroup trial of 108 postmenopausal women with recurrent, symp tomatic, bacteriologically confirmed UTIs. The women were randomly assigned to receive either Estring (7.5 mg estradiol/24 hours) or no estrogen treatment. After 36 weeks of study the cumulative likelihood of remaining free of infection was 45% in the women with the vaginal estrogen compared to 20% in the placebo group. This finding is also supported by the HUT Committee who concluded in their third report that estrogen seemed to be of benefit when used in women with this problem, particularly when used locally.114
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Table 47.4.
Summary of randomized controlled trials of estrogen for UTI
Study
Study group
Kjaergaard et al. (1990)108
Kirkengen et al. (1992)109
Type of estrogen
Route of delivery
Duration of therapy
Results
21 postmenopausal Estradiol women with recurrent cystitis; 10 active treatment 11 placebo
Vaginal tablets
5 months
No statistical difference in number of positive cultures between the two groups
40 postmenopausal Estriol women with recurrent UTIs; 20 active treatment 20 placebo
Oral
12 weeks
Both estriol and placebo significantly reduced the incidence of UtIs (p<0.05)
Raz & Stamm (1993)110
93 postmenopausal Estriol women with recurrent UTIs; 50 active treatment 36 placebo
Vaginal cream
8 months
Significant reduction in the incidence of UTIs in treatment group compared with placebo group (p<0.001)
Cardozo et al. (1998)111
72 postmenopausal Estriol women with recurrent UTIs; 36 active treatment 36 placebo
Oral
6 months’ treatment further 6 months’ followup
Urinary symptoms and incidence of UTIs reduced in both groups; estriol no better than placebo
Eriksen (1999)112
108 women with recurrent UTIs 53 active group 55 no treatment
Estring (vaginal ring)
36 weeks for the active group; 36 weeks or until first recurrence for the controls
Cumulative likelihood of remaining free of infection was 45% in active treatment group and 20% in control group (p=0.008)
Estradiol
Estriol was significantly more effective than placebo after 12 weeks (p<0.05)
UTI, urinary tract infection.
UROGENITAL ATROPHY Urogenital atrophy is a manifestation of estrogen with drawal following the menopause and symptoms may appear for the first time more than 10 years after the last menstrual period.115 It has been estimated that 10–40% of all postmeno pausal women are symptomatic116 although only 25% are thought to seek medical help. In addition, two out of three women report vaginal symptoms associated with urogenital atrophy by the age of 75 years.117 The prevalence of urogenital atrophy and urogenital prolapse has also been examined in a population of 285 women attending a menopause clinic.118 Overall, 51% of women were found to have anterior vaginal wall pro lapse, 27% posterior vaginal prolapse and 20% apical prolapse. In addition, 34% of women were noted to have urogenital atrophy, 40% complaining of dyspareunia. While urogenital atrophy and symptoms of dyspareunia were related to menopausal age, the prevalence of pro lapse showed no association.
Estrogens in the management of urogenital atrophy Symptoms of urogenital atrophy do not occur until the levels of endogenous estrogen are lower than those required to promote endometrial proliferation.119 Consequently, it is possible to use a low dose of estro gen replacement therapy in order to alleviate urogenital symptoms while avoiding the risk of endometrial prolif eration and removing the necessity of providing endo metrial protection with progestogens.120 The dose of estradiol commonly used in systemic estrogen replace ment is usually 25–100 µg, although studies investigating the use of estrogens in the management of urogenital symptoms have shown that 8–10 µg of vaginal estradiol is effective.121 Thus only 10–30% of the dose used to treat vasomotor symptoms may be effective in the manage ment of urogenital symptoms. Since 10–25% of women receiving systemic hormone replacement therapy still experience the symptoms of urogenital atrophy,122 low 705
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dose local preparations may have an additional benefi cial effect. A recent review of estrogen therapy in the manage ment of urogenital atrophy has been performed by the Hormones and Urogenital Therapy Committee.123 Ten randomized trials and 54 uncontrolled series were exam ined from 1969 to 1995, assessing 24 different treatment regimens. Metaanalysis of ten placebocontrolled trials confirmed the significant effect of estrogens in the man agement of urogenital atrophy. The route of administration was assessed, and oral, vaginal and parenteral (transcutaneous patches and subcutaneous implants) routes were compared. Overall, the vaginal route of administration was found to corre late with better symptom relief, greater improvement in cytological findings, and higher serum estradiol levels. With regard to the type of estrogen preparation, estra diol was found to be most effective in reducing patient symptoms, although conjugated estrogens produced the most cytological change and the greatest increase in serum levels of estradiol and estrone. Finally, the effect of different dosages was examined. Low dose vaginal estradiol was found to be the most efficacious according to symptom relief, although oral estriol was also effective. Estriol had no effect on the serum levels of estradiol or estrone, whereas vaginal estriol had minimal effect. Vaginal estradiol was found to have a small effect on serum estrogen although not as great as systemic preparations. In conclusion, it would appear that estrogen is efficacious in the treatment of urogenital atrophy and low dose vaginal preparations are as effective as systemic therapy. More recently, the use of a continuous low dose estra diolreleasing silicone vaginal ring (Estring), releasing estradiol 5–10 µg/24 hours, has been investigated in postmenopausal women with symptomatic urogenital atrophy.112 There was a significant effect on symptoms of vaginal dryness, pruritus vulvae, dyspareunia and uri nary urgency, with improvement being reported in over 90% of women in an uncontrolled study. The patient acceptability was high, and while the maturation of vagi nal epithelium was significantly improved, there was no effect on endometrial proliferation. Longterm safety has been confirmed by a 10year review of the use of the estradiol ring delivery system which found its safety, efficacy, and acceptability to be comparable to other forms of vaginal administration.124
CONCLUSIONS Estrogen has important physiologic effects on the female lower urinary tract throughout adult life; fluc
tuations in its level produce symptomatic, histologic, and functional changes. The menopause and subse quent estrogen deficiency have been implicated in the pathogenesis of a number of urogenital problems including incontinence, the urge syndrome, and recur rent UTIs. Estrogens do subjectively improve urinary leakage when used alone to treat urinary incontinence but are more effective when given in combination with other treatments. HRT appears to be particularly useful for irritative urinary symptoms of frequency and urgency, but the effect may be secondary to reversing urogenital atrophy. Treatment for several weeks or even months may be needed for maximum efficacy but the optimal route of delivery and dura tion of therapy remain to be determined. It is unclear if prophylactic estrogen replacement therapy around the time of the menopause is of benefit, and recent evidence suggests that it may in fact increase the risk of incontinence. There is conflicting evidence regard ing the effectiveness of estrogen to prevent recurrent UTIs but it does seem to be useful, particularly when given vaginally.
REFERENCES 1. Wilbush J. La Menespausie – the birth of a syndrome. Maturitas 1979;1:145–51. 2. Aristotle. Historia Animalium, book VII c.350 BC. Creswell R (translator), London: George Bell and Sons, 1897. 3. Research on the menopause in the 1990s. Report of a WHO Scientific Group. In: WHO Technical Report Series 866. Geneva: WHO, 1994. 4. Hill K. The demography of the menopause. Maturitas 1996;23:113–27. 5. Iosif CS, Batra S, Ek A. Estrogen receptors in the human female lower urinary tract. Am J Obstet Gynecol 1981;41:817–20. 6. Blakeman PJ, Hilton P, Bulmer JN. Oestrogen and progestin receptor expression in the female lower uri nary tract, with reference to oestrogen status. BJU Int 2000;86(1):32–8. 7. IngelmanSundberg A, Rosen J, Gustafsson SA. Cytosol oestrogen receptors in urogenital tissues in stress inconti nent women. Acta Obstet Gynecol Scand 1981;60:585–6. 8. Smith P. Estrogens and the urogenital tract. Acta Obstet Gynecol Scand 1993;72(Suppl):1–26. 9. Fu X, Rezapour M, Wu X et al. Expression of estrogen receptoralpha and beta in anterior vaginal walls of gen uine stress incontinent women. Int Urogynecol J Pelvic Floor Dysfunct 2003;14(4):276–81.
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10. Blakeman PJ, Hilton P, Bulmer JN. Cellular proliferation in the female lower urinary tract with reference to oes trogen status. BJOG 2001;108(8):813–6.
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11. Samsioe G, Jansson I, Meelstrom D et al. Occurrence, nature and treatment of urinary incontinence in a 70 year old female population. Maturitas 1985;7:335–42.
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12. Smith PJB. The effect of oestrogens on bladder func tion. In: Campbell S (ed) Management of the Meno pause and Postmenopausal years. Lancaster: MTP Press, 1976; 291–8. 13. McCallin PF, Taylor ES, Whitehead RW. A study of the changes in the urinary sediment during the menstrual cycle. Am J Obstet Gynecol 1950;60:64–74. 14. Soloman C, Panagotopoulos P, Oppenheim A. The use of urinary sediment as an aid in endocrinological disor ders in the female. Am J Obstet Gynecol 1958;76:56–60.
28. Rekers H, Drogendijk AC, Valkenburg H et al. Urinary incontinence in women from 35 to 79 years of age: preva lence and consequences. Eur J Obstet Gynecol Reprod Biol 1992;43:229–34. 29. Vetter NJ, Jones DA, Victor CR. Urinary incontinence in the elderly at home. Lancet 1981;2:1275–7. 30. Thomas TM, Plymat KR, Blannin J et al. Prevalence of urinary incontinence. Br Med J 1980;281:1243–5.
15. Batra SC, Iosif CS. Progesterone receptors in the female lower urinary tract. J Urol 1987;138:1301–4.
31. Hilton P. Urethral Pressure Measurement by Micro Transducer: Observations on the Methodology, the Pathophysiology of Stress Incontinence and the Effects of Treatment in the Female. MD thesis, University of Newcastle upon Tyne, 1981.
16. Risk DE, Raaschou T, Mason N, Berg B. Evidence of pro gesterone receptors in the mucosa of urinary bladder. Scand J Urol Nephrol 2001;35(4):35–9.
32. Kondo A, Kato K, Saito M et al. Prevalence of hand wash ing incontinence in females in comparison with stress and urge incontinence. Neurourol Urodyn 1990;9:330–1.
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18. Hextall A, Bidmead B, Cardozo L, Hooper R. The impact of the menstrual cycle on urinary symptoms and the results of urodynamic investigation. BJOG 2001;108(11):1193–6. 19. Van Geelen JM, Doesburg WH, Thomas CMG. Uro dynamic studies in the normal menstrual cycle: the relationship between hormonal changes during the menstrual cycle and the urethral pressure profile. Am J Obstet Gynecol 1981;141:384–92.
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39. Wagg AS, Lieu PK, Ding YY. A urodynamic evalua tion of age associated changes in urethral function in women with lower urinary tract symptoms. J Urol 1996;156:1984–8.
23. Cutner A. The Lower Urinary Tract in Pregnancy. MD thesis, University of London, 1993. 24. Barlow DH, Cardozo LD, Francis RM et al. Urogenital ageing and its effect on sexual health in older British women. Br J Obstet Gynaecol 1997;104:87–91.
40. Brocklehurst JC. Ageing of the human bladder. Geriat rics 1972;27:154. 41. Susset JG, ServotViguier D, Lamy F et al. Collagen in 155 human bladders. Invest Urol 1978;16:204–6.
25. Iosif CS, Bekassey Z. Prevalence of genitourinary symp toms in the late menopause. Acta Obstet Gynecol Scand 1984;63:257–60.
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vic relaxation and genuine stress incontinence. Obstet Gynecol 1989;74:789–95. 44. Smith ARB, Hosker GL, Warrell DW. The role of partial denervation of the pelvic floor in the etiology of genito urinary prolapse and stress incontinence of urine. Br J Obstet Gynaecol 1989;96:24–8. 45. Allen RE, Warrell DW. The role of pregnancy and child birth in the partial denervation of the pelvic floor. Neur ourol Urodyn 1992;6:183–4. 46. Abrams P, Blaivas JG, Stanton SL et al. The standardisa tion of terminology of lower urinary tract dysfunction. Br J Obstet Gynaecol 1990;97:1–16. 47. Maggi A, Perez J. Role of female gonadal hormones in the CNS. Life Sci 1985;37:893–906. 48. Smith SS. Hormones, mood and neurobiology – a summary. In: Berg G, Hammar M (eds) The Modern Management of the Menopause. Carnforth: Parthenon, 1993; 204. 49. Schneider MA, Brotherton PL, Hailes J. The effect of exogenous oestrogens on depression in menopausal women. Med J Aust 1977;2:162–3.
59. Shenfield OZ, Blackmore PF, Morgan CW et al. Rapid effects of estradiol and progesterone on tone and spon taneous rhythmic contractions of the rabbit bladder. Neurourol Urodyn 1998;17:408–9. 60. Elliott RA, Castleden CM, Miodrag A. The effect of in vivo oestrogen pretreatment on the contractile response of rat isolated detrusor muscle. Br J Pharmacol 1992;107:766–70. 61. Fantl JA, Wyman JF, Anderson RL et al. Postmenopausal urinary incontinence: comparison between nonestro gen and estrogen supplemented women. Obstet Gynecol 1988;71:823–8. 62. Elliott RA, Castleden CM. Effect of progestogens and oes trogens on the contractile response of rat detrusor muscle to electrical field stimulation. Clin Sci 1994;87:337–42. 63. Burton G, Cardozo LD, Abdalla H et al. The hormo nal effects on the lower urinary tract in 282 women with premature ovarian failure. Neurourol Urodyn 1992;10:318–9. 64. Cutner A, Burton G, Cardozo LD et al. Does progesterone cause an irritable bladder? Int Urogynecol J 1993;4:261.
50. Sherwin BB. Affective changes with estrogen and andro gen replacement therapy in surgically menopausal women. J Affect Disord 1988;14:177–87.
65. Benness C, Gangar K, Cardozo LD et al. Do progestogens exacerbate urinary incontinence in women on HRT? Neurourol Urodyn 1991;10:316–8.
51. Ditkoff EC, Crary WG, Cristo M. Estrogen improves psy chological function in asymptomatic postmenopausal women. Obstet Gynecol 1991;78:991–5.
66. Raz S, Ziegler M, Laine M. The effect of progesterone on the adrenergic receptors of the urethra. Br J Urol 1973;45:131–5.
52. Best NR, Rees MP, Barlow DH et al. Effect of estra diol implant on noradrenergic function and mood in menopausal subjects. Psychoneuroendocrinology 1992;17:87–93.
67. Bergman A, Karram MM, Bhatia NN. Changes in ure thral cytology following estrogen administration. Gyne col Obstet Invest 1990;29:211–3.
53. Blok BFM, Holstege G. Androgen receptor immunoreac tive neurons in the hypothalamic preoptic area project to the pontine micturition center in the male cat. Neur ourol Urodyn 1998;17:404–5. 54. Shapiro E. Effect of oestrogens on the weight and mus carinic receptor density of the rabbit bladder and ure thra. J Urol 1986;135:1084–7. 55. Batra S, Anderson KE. Oestrogeninduced changes in muscarinic receptor density and contractile responses in the female rat urinary bladder. Acta Physiol Scand 1989;137:135–41. 56. Elliott RA, Castleden CM, Miodrag A et al. The direct effects of diethylstilboestrol and nifedipine on the con tractile responses of isolated human and rat detrusor muscles. Eur J Clin Pharmacol 1992;43:149–55. 57. Diep N, Yokota T, Soo Choo M et al. Effect of estrogen supplementation of ovariectomized rats on micturition. Neurourol Urodyn 1998;17:405–6. 58. Parekh MH, Chicester P, Lobel RW et al. Effects of castra tion on female rabbit bladder physiology and morphol ogy. Urology 2004;64(5):1048–51.
68. Hilton P, Stanton SL. The use of intravaginal oestrogen cream in genuine stress incontinence. Br J Obstet Gynae col 1983;90:940–4. 69. Bhatia NN, Bergman A, Karram MM et al. Effects of oestrogen on urethral function in women with urinary incontinence. Am J Obstet Gynecol 1989;160:176–81. 70. Karram MM, Yeko TR, Sauer MV et al. Urodynamic changes following hormone replacement therapy in women with premature ovarian failure. Obstet Gynecol 1989;74:208–11. 71. Ganger KF, Vyas S, Whitehead RW et al. Pulsatility index in the internal carotid artery in relation to transder mal oestradiol and time since the menopause. Lancet 1991;338:839–42. 72. Jackson S, Vyas S. A doubleblind, placebo controlled study of postmenopausal oestrogen replacement therapy and carotid artery pulsatility index. Br J Obstet Gynaecol 1998;105:408–12. 73. Penotti M, Farina M, Sironi L et al. Long term effects of postmenopausal hormone replacement therapy on pulsatility index of internal carotid and middle cerebral arteries. Menopause 1997;4:101–4.
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74. Versi E, Cardozo LD. Urethral instability: diagnosis based on variations in the maximum urethral pres sure in normal climacteric women. Neurourol Urodyn 1986;5:535–41.
89. Hilton P, Tweddel AL, Mayne C. Oral and intravaginal estrogens alone and in combination with alpha adren ergic stimulation in genuine stress incontinence. Int Urogynecol J 1990;12:80–6.
75. Jackson S, McDonnell C, James M et al. Is postmenopau sal urethral blood flow affected by hormone replacement therapy? A placebo controlled pilot study. Neurourol Urodyn 1997;16:352–3.
90. Walter S, Wolf H, Barlebo H et al. Urinary incontinence in postmenopausal women treated with oestrogen. Urol Int 1978;33:135–43.
76. Screiter F, Fuchs P, Stockamp K. Estrogenic sensitivity of alpha receptors in the urethral musculature. Urol Int 1976;31:13–9. 77. Jackson S, James M, Abrams P. The effect of oestradiol on vaginal collagen metabolism in postmenopau sal women with genuine stress incontinence. BJOG 2002;109(3):339–44. 78. Rud T. The effects of estrogens and gestogens on the urethral pressure profile in urinary continent and stress incontinent women. Acta Obstet Gynecol Scand 1980;59:265–70. 79. Salmon UL, Walter RI, Gast SH. The use of estrogen in the treatment of dysuria and incontinence in postmeno pausal women. Am J Obstet Gynecol 1941;14:23–31. 80. Jarvis GJ, Hall S, Stamp S et al. An assessment of urody namic investigation in incontinent women. Br J Obstet Gynaecol 1980;87:184–90. 81. Fantl JA, Cardozo LD, McClish DK et al. Estrogen ther apy in the management of urinary incontinence in post menopausal women: a metaanalysis. Obstet Gynecol 1994;83:12–8.
91. Cardozo L, Rekers H, Tapp A et al. Oestriol in the treat ment of postmenopausal urgency: a multicentre study. Maturitas 1993;18:47–53. 92. Benness C, Wise BG, Cutner A et al. Does low dose vaginal estradiol improve frequency and urgency in post menopausal women? Int Urogynecol J 1992;3:281. 93. Nilsson K, Heimer G. Low dose oestradiol in the treatment of urogenital oestrogen deficiency – a pharmacokinetic and pharmacodynamic study. Maturitas 1992;15:121–7. 94. Rufford J, Hextall A, Cardozo L, Khullar K. A double blind placebo controlled trial on the effects of 25 mg oestradiol implants on the urge syndrome in postmeno pausal women. Int Urogynecol J 2003;14:78–83. 95. Cardozo L, Lose G, McClish D, Versi E. A systematic review of the effects of estrogens for symptoms sugges tive of overactive bladder. Acta Obstet Gynecol Scand 2004;83:892–7. 96. DuBeau CE. Estrogen treatment for urinary incontinence. Never, now or in the future? JAMA 2005;293(8):998–1001.
82. Sultana CJ, Walters MD. Estrogen and urinary inconti nence in women. Maturitas 1995;20:129–38.
97. Grady D, Brown JS, Vittinghoff E et al. Postmenopau sal hormones and incontinence: the heart and estro gen/progestin replacement study. Obstet Gynecol 2001;97:116–20.
83. Fantl JA, Bump RC, Robinson D et al. Efficacy of estro gen supplementation in the treatment of urinary incon tinence. Obstet Gynecol 1996;88:745–9.
98. Grodstein F, Lifford K, Resnick NM, Curhan GG. Post menopausal hormone therapy and risk of developing uri nary incontinence. Obstet Gynecol 2004;103(2):254–60.
84. Zullo MA, Olivia C, Falconi G et al. Efficacy of oestrogen therapy in urinary incontinence. A metaanalytic study. Minerva Ginecol 1998;50:199–205.
99. Goldstein SR, Johnson S, Walls NB. Incidence of urinary incontinence in postmenopausal women treated with raloxifene or estrogen. Menopause 2005;12(2):160–4.
85. Jackson S, Shepherd A, Brookes S, Abrams P. The effect of oestrogen supplementation on postmenopausal stress incontinence: a double blind placebo controlled trial. BJOG 2000;107(3):433–4.
100. Hendrix SL, Cochrane BB, Nygaard IE et al. Effects of estrogen with or without progestin on urinary inconti nence. JAMA 2005;293(8):935–48.
86. AlBadr A, Ross S, Soroka D, Drutz HP. What is the avail able evidence for hormone replacement therapy for women with stress urinary incontinence? J Obstet Gyne col Can 2003;25:567–74. 87. Moehrer B, Hextall A, Jackson S. Oestrogens for uri nary stress incontinence in women (Cochrane Review). Cochrane Database Syst Rev 2003;2:CD001405. 88. Beisland HO, Fossberg E, Moer A et al. Urethral insuf ficiency in postmenopausal females: treatment with phenylpropanolamine and estriol separately and in com bination. Urol Int 1984;39:211–6.
101. Ouslander JG, Greendale GA, Uman G, Lee C, Paul W, Schnelle J. Effects of oral oestrogen and progestin on the lower urinary tract among female nursing home resi dents. Am Geriatr Soc 2001;49(6): 803–7. 102. Sandford JP. Urinary tract symptoms and infection. Ann Rev Med 1975;26:485–505. 103. Boscia JA, Kaye D. Asymptomatic bacteria in the elderly. Infect Dis Clin North Am 1987;1:893–903. 104. Horan MA, Parker SG. Infections, aging and host response. In: Horan MA, Little RA (eds) Injury in the Aging. Cambridge: Cambridge University Press, 1998; 126–46.
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105. Hextall A, Hooper R, Cardozo LD et al. Does the meno pause influence the risk of bacteriuria? Int J Urogynecol J Pelvic Floor Dysfunct 2001;12(5):332–6. 106. Parsons CL, Schmidt JD. Control of recurrent lower uri nary tract infections in postmenopausal women. J Urol 1982;128:1224–6. 107. Privette M, Cade R, Peterson J et al. Prevention of recur rent urinary tract infections in postmenopausal women. Nephron 1988;50:24–7.
committee. Int Urogynecol J Pelvic Floor Dysfunction 2001;12(1):15–20. 115. Iosif CS. Effects of protracted administration of oestriol on the lower genitourinary tract in postmenopausal women. Acta Obstet Gynaecol Scand 1992;251:115–20. 116. Greendale GA, Judd JL. The menopause: health impli cations and clinical management. J Am Geriatr Soc 1993;41:426–36.
108. Brandberg A, Mellstrom D, Samsioe G. Low dose oral oestriol treatment in elderly women with urogenital infections. Acta Obstet Gynecol Scand 1987;140:33–8.
117. Samsioe G, Jansson I, Mellstrom D, Svanborg A. The occurrence, nature and treatment of urinary inconti nence in a 70 year old population. Maturitas 1985;7:335– 43.
109. Kjaergaard B, Walter S, Knudsen A et al. Treatment with low dose vaginal estradiol in postmenopausal women. A double blind controlled trial. Ugeskr Laeger 1990;152:658–9.
118. Versi E, Harvey MA, Cardozo L, Brincat M, Studd JW. Urogenital prolapse and atrophy at menopause: a prevalence study. Int Urogynecol J Pelvic Floor Dysfunct 2001;12(2):107–10.
110. Kirkengen AL, Anderson P, Gjersoe E et al. Oestriol in the prophylactic treatment of recurrent urinary tract infections in postmenopausal women. Scand J Prim Health Care 1992;10:139–42.
119. Samsioe G. Urogenital ageing – a hidden problem. Am J Obstet Gynecol 1998;178(5):S245–S249.
111. Raz R, Stamm WE. A controlled trial of intravaginal estriol in postmenopausal women with recurrent urinary tract infections. N Engl J Med 1993;329:753–6. 112. Cardozo L, Benness C, Abbott D. Low dose oestrogen prophylaxis for recurrent urinary tract infections in eld erly women. Br J Obstet Gynaecol 1998;105:403–7.
120. Mettler L, Olsen PG. Long term treatment of atrophic vaginitis with low dose oestradiol vaginal tablets. Maturi tas 1991;14:23–31. 121. Smith P, Heimer G, Lindskog M, Ulmsten U. Oestradiol releasing vaginal ring for treatment of postmenopausal urogenital atrophy. Maturitas 1993;16:145–54. 122. Smith RJN, Studd JWW. Recent advances in hormone replacement therapy. Br J Hosp Med 1993;49:799–809.
113. Eriksen B. A randomized, open, parallel groupstudy on the preventive effect of an estradiolreleasing vaginal ring (Estring) on recurrent urinary tract infec tions in postmenopausal women. Am J Obstet Gynecol 1999;180:1072–9.
123. Cardozo LD, Bachmann G, McClish D, Fonda D, Birger son L. Metaanalysis of oestrogen therapy in the manage ment of urogenital atrophy in postmenopausal women: Second report of the Hormones and Urogenital Therapy Committee. Obstet Gynecol 1998;92:722–7.
114. Cardozo L, Lose G, McClish D et al. A systematic review of oestrogens for recurrent urinary tract infections: third report of the hormones and urogenital therapy
124. Bachmann G. Oestradiolreleasing vaginal ring delivery system for urogenital atrophy. Experience over the last decade. J Reprod Med 1998;43:991–8.
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IntroductIon Anal incontinence is the involuntary loss of solid or liquid stool per rectum. It is personally and socially incapacitating and only a half of sufferers will volunteer their symptoms spontaneously if not asked directly.1 Although it affects men and women of all ages, incontinence is eight times more common in women than in men at the age of 45, implicating obstetric factors in the etiology. A study from Birmingham found that 4% of women develop fecal incontinence following childbirth2. The focus of this chapter is on obstetric injuries, which are the underlying cause of anal incontinence in most women, but other causes must be considered (Table 48.1). The principles of management are broadly similar whatever the etiology. Vaginal delivery is the most important etiologic factor in postobstetric anal incontinence. Two principal mechanisms are responsible for the development of fecal incontinence following vaginal delivery:
• direct injury to the sphincter muscle itself; • damage to the nerves supplying the pelvic floor or anal sphincter. Less frequently, new symptomatic anal incontinence may occur in women following cesarean delivery.
table 48.1.
Etiology of fecal incontinence
Traumatic • Obstetric • Accident/injury • Surgical Colorectal disease • Rectal prolapse • Inflammatory bowel disease • Hemorrhoids • Neoplasia • Fistulae Congenital • Anal atresia Neurological • Cerebral • Spinal • Peripheral Miscellaneous • Impaction • Behavioral • Immobility
PathogenesIs sphincter injury Direct damage to the sphincter muscles is responsible for anal incontinence in most of the women who present early after childbirth. Sphincter injuries are more common in primiparous women; new sphincter injuries are less common with subsequent deliveries.3 Other risk factors or associations for sphincter injury include large babies, forceps delivery, a prolonged second stage of labor, and occipitoposterior presentation.4 It has become clear that following vaginal delivery anal sphincter injuries are frequently unrecognized or misclassified as a less severe injury. When perineal examination is undertaken by a trained clinician immediately following delivery, the incidence of detected sphincter injury may be significantly increased.5 Some sphincter defects may be truly occult, occurring with minimal or no perineal injury, where the mechanism is likely to be tissue shearing during delivery. However, there is a notable variation in incidence of recognized third-degree tears between centers publishing their data,6 and the observation that women with seconddegree tears are the group most likely to develop anal incontinence postpartum7 further suggests that a proportion of anal sphincter injury remains undetected following delivery. Even when sphincter damage is recognized and repaired at the time of delivery, up to 85% of women still have identifiable sphincter defects and around 50% of women have some symptoms of anal incontinence.4 The development of incontinence later in life is more likely to be multifactorial in origin, resulting from a combination of one or more factors including sphincter damage, progressive neuropathy, muscle atrophy, hormonal changes,8 and alteration in bowel function.9
neurologic damage Prolonged pudendal nerve motor terminal latencies (PNMTL) have been demonstrated in a third of primigravidae following vaginal delivery.10 These usually revert back to normal, but up to a third remain prolonged at 6 months. Prolonged PNMTL is not necessarily associated with incontinence. After emergency cesarean section late in labor, pudendal nerve latencies may be increased, implicating damage to the nerves supplying the pelvic floor or sphincter.11 In some women, electromyographic studies revealed increased fiber density in the external sphincter consistent with damage to sphincter innerva-
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tion. Pudendal nerve damage and increased fiber density were seen more frequently in multiparae, suggesting that nerve damage may be cumulative with subsequent deliveries. The development of neurogenic incontinence is likely to be a progressive process, rather than an acute event at the time of delivery, and therefore may be exacerbated by subsequent deliveries or prolonged straining.
of defecation with no call to stool, or the involuntary passage of flatus, indicates a poor anal canal resting tone and suggests damage or degeneration of the internal sphincter muscle. Inability to discriminate solid stool from flatus suggests damage to anorectal sensory pathways. Seepage or perineal soiling may be seen in situations where there is distortion of the anal canal by scarring or in the presence of a fistula. A careful medical history should be taken with specific attention to colonic function, previous anorectal surgery and any potential causes of anal incontinence. An obstetric history should include details of birth weight, mode of delivery, length of labor, instrumental delivery, and details of any perineal trauma. Scoring systems, such as the St Marks score (Table 48.2), may be used to quantify anal incontinence and for audit or research.14 Its role may also include assessing the outcome in terms of cure or improvement in symptoms.
PatIent assessment The maintenance of continence is a complex process involving an interrelationship between intestinal function, rectal sensitivity and compliance, and anal sphincter function. This in turn depends upon the integrity of sensory and motor neural pathways and the sphincter musculature itself. The anal sphincter complex comprises two muscles – an inner circular smooth muscle maintaining constant tone and largely responsible for resting anal canal tone,12 and an outer striated muscle under voluntary control which can be contracted to defer defecation when appropriate.13
examination Physical examination should include inspection of the perineum, noting scarring from previous surgery or obstetric trauma. Voluntary contraction of the external sphincter can be seen and defects in the sphincter may be observed. Gaping of the anus at rest or on gentle perineal traction suggests a low resting tone and impaired internal anal sphincter function. Descent of the perineum at rest with accentuation on straining suggests pelvic floor weakness, pudendal neuropathy, or both. Straining may also reveal an unsuspected rectal prolapse. Perineal sensation can be tested by light touch and pinprick. Digital examination will allow crude assessment of resting anal tone and voluntary squeeze pressure, and any sphincter defects may be palpable.
history Careful questioning can give a clue to the etiology of incontinence. A change in bowel habit to increased frequency and looseness may precipitate anal incontinence and could be suggestive of underlying colorectal disease. Urgency of defecation with reduced warning time (sometimes to only a few minutes) indicates loss of voluntary muscle control and suggests damage to the striated external anal sphincter or its nerve supply. Similarly, incontinence associated with vigorous activity or coughing suggests a deficiency of external sphincter function. Incontinence occurring between episodes table 48.2.
St Mark’s incontinence scoring system Never
Rarely (<1/month)
Sometimes (<1/week)
Usually (<1/day)
Always (daily)
Solid
0
1
2
3
4
Liquid
0
1
2
3
4
Gas
0
1
2
3
4
Lifestyle
0
1
2
3
4
No
Yes
Need to wear plug/pad/change underwear for soiling
0
2
Taking constipating medicine
0
2
Lack of ability to defer defecation for 15 minutes
0
2
Total score = /24
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Investigation Special investigations can provide useful information in the management of women with incontinence (Table 48.3). Presentation with new anal incontinence, particularly in middle age, may be precipitated by a change in frequency or consistency of stool. Routine examination of the colon by barium enema or colonoscopy should be carried out to detect the presence of colonic pathology such as neoplasia or colitis. Clinical assessment of the pelvic floor and anal sphincters should be combined with anorectal physiologic studies. Manometry allows measurement of functional anal canal length and of the resting and squeeze pressures. These provide objective evidence of internal and external anal sphincter function, respectively.15 Anal canal sensation can be tested using a stimulating electrode and may be transiently impaired by vaginal delivery. Rectal sensation and compliance are usually measured by balloon distension. Measurement of PNMTL assesses pudendal nerve function by stimulating the pudendal nerve on each side and measuring the evoked response in the external anal sphincter.16 Normal latencies do not necessarily exclude pudendal nerve damage. Endoanal ultrasonography (EAUS) has revolutionized the understanding of anal canal anatomy (Figs 48.1, 48.2). Both the internal and external anal sphincters can be visualized and EAUS is the investigation of choice for detection of defects in these sphincters.17 The detection of sphincter defects enables clinicians to select women to undergo surgical sphincter repair, and the accuracy of EAUS for detecting sphincter disruption has been validated by correlation with operative findings.18 Abnormal table 48.3.
thinning of the internal sphincter can be measured accurately using EAUS; this may be indicative of idiopathic degeneration, whereas thickening of the muscle may be associated with prolapse syndrome. Magnetic resonance imaging (MRI) using an endoanal coil provides excellent multiplanar views of the sphincter complex and can demonstrate defects in both the internal and external anal sphincters. It is probably most useful in identifying abnormalities in the external anal sphincter, the outer border of which may be difficult to visualize using EAUS. Expertise in MRI of the sphincters is not widely available and most clinicians continue to rely on EAUS. Where both imaging facilities are available, one or both may be used for diagnosis since they are complementary.
management early recognition of obstetric injuries Evidence of sphincter injury should be sought by careful bimanual examination in all women who have a perineal tear or who have had an instrumental delivery. This should be carried out by someone trained in the recognition of sphincter injury. In the UK, there are a number of courses specifically for training obstetricians in this maneuver. An adjunct to bimanual examination is the use of EAUS in the delivery suite immediately postpartum. This is acceptable to women and can be used to diagnose sphincter injury and to assess the integrity of any repair.19 Once recognized, repair of a sphincter injury should be carried out by someone adequately
Investigations for anal incontinence
Investigation
Information
Imaging/structural Colonoscopy/barium enema/sigmoidoscopy
Underlying colorectal pathology precipitating or contributing to incontinence
Endoanal ultrasound (EAUS)
Integrity of internal and external anal sphincter Thickness of internal anal sphincter Fistulae
Magnetic resonance imaging (MRI)
Integrity of internal and external anal sphincter
Functional Manometry
Resting anal canal pressure Voluntary squeeze pressure Involuntary squeeze pressure Functional anal canal length
Rectal sensation and compliance
Rectal hypo/hypersensitivity Normal or reduced compliance
Pudendal nerve motor terminal latency (PNMTL)
Damage to pudendal nerves
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cedures being reserved for those women with severe symptoms or in whom conservative measures fail.
Drugs
Figure 48.1. postpartum.
Normal endoanal ultrasound immediately
Attention to diet or the addition of a bulking agent such as ispaghula husk can improve symptoms in some individuals. Antidiarrheal agents such as codeine phosphate or loperamide reduce colonic motility and increase fluid absorption, producing more manageable formed stools. The use of enemas or rectal washouts may help some women. The enema induces a bowel action and keeps the rectum empty between bowel movements. There has been some reports of duloxetine hydrochloride helping women with fecal incontinence. Whether in the future this represents a viable treatment option remains to be seen.
Biofeedback
Figure 48.2. sphincters.
Defects in internal and external anal
trained to do so, in an operating theatre under regional or general anesthetic. Training in repair of sphincter injury should be part of any basic obstetric training program as the adequacy of sphincter repair is related to the experience of the operator. At postnatal follow-up visits, women should be asked directly about anal incontinence as they are about other postpartum symptoms. Increased general awareness of the risk of postobstetric sphincter injury among midwifery and obstetric staff will also aid in the early diagnosis and treatment of anal incontinence. Early follow-up in a multidisciplinary clinic of women who have sustained obstetric trauma further increases the recognition of residual sphincter injury and enables effective early intervention where necessary.20
conservative therapy
Biofeedback therapy can be helpful for some women with anal incontinence. It is a behavioral technique using equipment which provides auditory or visual feedback to alter physiologic events.21 The technique uses electromyography (EMG), where a sensing device monitoring external sphincter contraction is connected to a transducer producing an audio or visual response for the woman. The audiovisual record of sphincter activity assists the woman in recognizing strength and length of contraction. Using a balloon to distend the rectum, women are encouraged to improve sphincter contraction in response to decreasing rectal distension, so that over a period of time their response becomes automatic. These techniques are most useful for women who are well motivated, have some rectal sensation, and are able to contract the external sphincter voluntarily. In a series of 100 patients treated with biofeedback, 43 regarded themselves as cured and 24 symptomatically improved.22 Interestingly, 27 of the 46 patients in this series with structural sphincter damage also reported cure or improvement. Biofeedback is initially labor intensive requiring a dedicated therapist but can be carried out at home after training. It has the advantage of being painless, safe, and complementary to other interventions. Biofeedback training has been shown to improve functional outcome for women with persistent symptoms following sphincter repair.23 However, a more recent study has suggested that it is the therapist rather than the technique that is important to the outcome.24
Anal plug For most women, symptoms are relatively minor and should be managed conservatively, interventional pro-
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device expands after insertion and is removed to allow evacuation. Use of the anal tampon has been shown to improve continence scores and quality of life but only about half of patients found it comfortable to use on a regular basis.25 It has a role for those with severe symptoms who are awaiting (or are unsuitable for) surgery.
surgery For some women conservative therapies will fail and surgical options need to be considered. Two categories of patient may be identified:
• women with evidence of a sphincter defect; • women where the sphincters are intact but weak, secondary to denervation or muscle atrophy. In the first group, direct repair of the sphincter defect should be considered; in the second group, decision-making is more difficult, the surgical options more varied, and outcome less predictable.
sphincter repair Sphincter repair is the operation of choice where there is a single defect of the external anal sphincter, either alone or in combination with a defect of the internal anal sphincter. Two different surgical techniques have been used: direct apposition and overlapping repair. Sphincter repair by mobilization of the sphincter muscle, scar excision and direct apposition resulted in a failure rate of around 40%,26 these poor results being attributed to the cutting out of sutures or retraction of the muscle ends. Parks and McPartlin subsequently modified this technique by mobilizing the sphincter muscle and employing an overlapping repair of the muscle.27 This overlapping technique has become the gold standard for anal sphincter repair. The need for a defunctioning stoma following sphincter repair has been studied and is only necessary where there is significant perineal sepsis. A temporary stoma confers no benefit in terms of functional outcome and is associated with higher morbidity and longer hospital stay related to the stoma closure.28 Medical bowel confinement confers no benefit in terms of septic complications or functional outcome.29 Prophylactic broad spectrum antibiotics are used to prevent infection which may be linked to breakdown of the repair. Review of published series shows that excellent or good results, with continence to solid and liquid stool, can be achieved in between 47 and 79% of patients
undergoing sphincter repair.30–32 The outcome data for overlapping sphincter repair should, however, be interpreted with caution for a number of reasons. Many of the reported series are small, with patients recruited over several years, often involving several different operating surgeons and follow-up tends to be short. The groups of patients reported are often heterogeneous in terms of age, sex, and indication for repair. The frequent absence of standardized scoring systems or physiologic measurements to evaluate continence pre- and postoperatively does not allow series to be readily compared. Outcome where there has also been damage to the internal sphincter is less certain. Internal sphincter defects are far more difficult to identify surgically and repair adequately, and soiling – together with incontinence to flatus – will remain a problem for some women.
Factors predicting outcome from anal sphincter repair A number of factors have been identified as predictive of outcome following anal sphincter repair. Age and body habitus Some authors have reported an adverse influence of age on outcome.33 Although older age is not a contraindication to surgery,31,32 it should certainly be considered in preoperative counseling when discussing outcome. Pudendal neuropathy Prolonged PNMTL (unilateral or bilateral) have been shown by some to be predictive of a poorer outcome after sphincter repair.34 Although this finding may be useful in counseling women preoperatively, it should not necessarily be used to deny a woman operative correction of an obvious sphincter defect. External sphincter atrophy The detection by MRI scanning of atrophy of the external anal sphincter, which is characterized by thinning and fatty replacement, has been shown to adversely affect outcome following sphincter repair.35
Failure of sphincter repair Up to 10% of repairs may break down, resulting in persistent defects and poor functional results. Where such defects are identified, repeated sphincter repair may be successful.36 Since the operation may be technically more difficult and tissue quality poor, the outcome following repeated sphincter repair is less certain. Where failure has resulted from significant perineal sepsis, a temporary defunctioning colostomy may be required.
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Long-term outcomes after sphincter repair Most series report only short-term follow-up and interest has recently focused upon the long-term outcomes of sphincter repair. In a 5-year follow-up study of incontinent women who had a overlapping repair for obstetric trauma, only four out of 38 were totally continent of solid and liquid stool and none was fully continent of stool and flatus.37 The overall success of the overlap method deteriorated with time. Whether the deterioration was due to progressive denervation of mobilized muscle or failure to repair internal sphincter defects adequately is uncertain. While sphincter repair remains the standard first approach for isolated defects, women should be made aware that initial good results may not be permanent and that deterioration in continence may occur in the future.
alternative surgical techniques For women with symptomatic anal incontinence but an intact sphincter confirmed by imaging, other surgical options can be considered.
Postanal repair and total pelvic floor repair The operation of postanal repair (PAR) aims to restore an adequate anorectal angle, which is of theoretical importance in maintaining continence. The long-term results from PAR are poor, with only a third of women maintaining continence at 5-year follow-up. Total pelvic floor repair (TPFR) combines PAR with anterior sphincter plication and anterior levatoroplasty. Long-term follow-up indicates that TPFR rarely renders women fully continent, but around half have substantially improved continence and lifestyle.38 The poor long-term success rates reflect progressive neuropathy or atrophy of the muscles and have led to a move away from PAR and TPFR as surgical options. These operations are, however, associated with low morbidity and thus may still have a role for women with significant symptoms who are unsuitable for more complex reconstructive procedures or who refuse a stoma.
neosphincters
muscle wrap being tight enough to keep the anal canal closed, as coordinated voluntary contraction of the muscle itself is difficult. Gluteus transposition is a technically more demanding procedure but has the advantage that the muscles are easier to contract since the glutei are natural synergists of the anal sphincter. Results of unstimulated muscle transposition vary widely and it is now a rarely used technique. Bilateral graciloplasty may be useful where lack of local technical expertise or financial resources do not allow stimulated transposition.
Stimulated muscle transposition The observation that by chronic stimulation muscle fibers could be converted from type II fast twitch to fatigue-resistant slow twitch fibers led to the development of the stimulated graciloplasty.40 The mobilization of the gracilis muscle and wrap are similar to that for unstimulated graciloplasty but involve identification of the nerve to gracilis and implantation of a stimulating electrode around the nerve trunk or its branches. The stimulator is placed in a subcutaneous pocket in the abdominal wall and the electrode wires tunneled to it. After satisfactory healing, a period of muscle stimulation is commenced until continuous stimulation results in sustained muscle contraction. The patient switches off the stimulator to allow the muscle to relax and enable defecation.41 Contraindications to stimulated graciloplasty include a history of perianal sepsis or Crohn’s disease. In addition, as the stimulator may interfere with pacemakers and implanted defibrillators, the technique may not be appropriate in these patients. In a study of 52 patients undergoing stimulated graciloplasty, 73% were continent after a median followup of 2 years and success was associated with improved quality of life.41 Others have reported far less favorable results. Septic complications, hardware problems, and physiologic imbalance have led to the high failure rates reported in some series.39 Case selection is important; patients need to be well motivated and require careful preoperative assessment and counseling. The procedure has a recognized failure rate and may be associated with significant morbidity and scarring. In addition, patients may require significant input in terms of support for fine-tuning the stimulator.
Muscle transposition It is possible to augment the anal sphincter with another striated muscle. The muscles most commonly used are gracilis or gluteus but others such as obturator internus have also been employed.39 Graciloplasty involves mobilization of the muscle from the inner thigh, which is wrapped around the anal canal and fixed to the contralateral ischial tuberosity. Continence is reliant upon the
Artificial bowel sphincter When the sphincter muscles are irretrievably damaged or previous attempts at reconstruction have failed, the use of an artificial bowel sphincter may provide a simpler and less invasive approach than stimulated muscle transposition. The artificial sphincter prosthesis was developed from use in the treatment of urinary inconti717
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nence. It comprises a cuff which is implanted around the anus and a pressure-regulating balloon which is placed behind the rectus muscles and connected to a pump placed in the subcutaneous tissues of the labia. A temporary colostomy is not normally required. Cuff opening is controlled by squeezing the labial pump which empties the cuff to enable evacuation; the cuff then slowly refills from the pressure-regulating balloon over a number of minutes to close the anal canal. Early reports of the purpose-designed artificial bowel sphincter indicated that excellent functional results can be achieved both in terms of improving continence scores and improving anal canal resting pressures without adversely affecting rectal function.42 An audit of the United Kingdom experience, however, showed that two-thirds of the sphincters implanted had required removal.43 Infection was the predominant cause and meticillin-resistant Staphylococcus aureus (MRSA) a common pathogen. Despite good functional outcomes in a proportion of patients, the future for the artificial sphincter remains uncertain. Early septic complications necessitate removal of the device in some patients and improvements in care directed at preventing infection are required.
Sacral nerve modulation A novel approach to women with incontinence and weak but intact internal and external sphincters is to modulate the neurologic control of the anorectum. Sacral nerve modulation (SNM) was initially used in patients with urinary incontinence. The observation that bowel symptoms improved in some of these led to its use in patients with anal incontinence. SNM involves continuous electrostimulation of one of the sacral spinal nerves (S2, S3 or S4). A major advantage of this technique is that it involves placement of a temporary electrode, which can be used over a 1–3 week test period to measure response prior to embarking on surgical implantation of the permanent device. Where costs are important, the value of such a trial period is evident. There is little morbidity associated with the procedure, which does not involve any risk of direct surgical trauma to the sphincter mechanism itself. A systematic review of the early results of SNM showed an improvement in anal incontinence in patients resistant to conservative treatment.44 The mechanism of action of SNM is uncertain: there appears to be an effect on rectal and internal sphincter smooth muscle activity, rectal sensitivity, and facilitation of the striated muscle of the external anal sphincter. This is thought to be due to neuromodulation of sacral reflexes, which regulate rectal sensitivity and anorectal motility. The application
of sacral nerve stimulation to patients with anal incontinence remains in its infancy and the long-term outcome is uncertain. Encouragingly, SNM appears to be effective long term for patients with urinary incontinence but only continued evaluation will determine whether the same is true for women with anal incontinence.
Stomas Reconstruction may be impossible in some women and a colostomy is the only alternative to managing intolerable symptoms. In these individuals, a stoma should not be seen as a treatment failure and may allow many women to return to a near normal lifestyle. Colostomy irrigation is possible and may further improve their quality of life. Unfortunately, for a few women with a colostomy, persistent incontinence of mucus from the defunctioned rectum remains a problem and a proctectomy may be required.
summary Careful assessment and investigation of anal incontinence can usually determine the underlying cause. Most women can be managed conservatively by a combination of dietary modification, medication, and biofeedback. Where conservative treatment fails, surgery may be considered. Women with sphincter defects may benefit from overlapping sphincter repair which offers good short-term functional results. They should be counselled that longer-term results are less certain. When sphincter repair fails or where the sphincter itself is intact but weak, other surgical options are available. Postanal repair, total pelvic floor repair, and unstimulated muscle transposition offer short-term improvement for many women. Stimulated muscle transposition and artificial sphincters may provide a more satisfactory solution, but may be associated with significant morbidity. Sacral nerve modulation is promising, although longer-term outcomes and indications for its application need to be determined.
reFerences 1. Leigh RJ, Turnbull LA. Faecal incontinence: the unvoiced symptom. Lancet 1982;1:1349–51. 2. MacArthur C, Bick DE, Keighley MRB. Faecal incontinence after childbirth. Br J Obstet Gynaecol 1997;104:46–50. 3. Fynnes M, Donnelly V, Behan M et al. Effect of second vaginal delivery on anorectal physiology and faecal continence: a prospective study. Lancet 1999;354:983–6. 4. Sultan AH, Kamm MA, Hudson CN et al. Third degree
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obstetric anal sphincter tears: risk factors and outcome of primary repair. BMJ 1994;308:887–91.
21. Macleod JH. Management of anal incontinence by biofeedback. Gastroenterology 1987;93:291–4.
5. Groom KM, Paterson-Brown S. Can we improve on the diagnosis of third degree tears? Eur J Obstet Gynecol Reproduc Biol 2002;101:19–20.
22. Norton C, Kamm MA. Outcome of biofeedback for faecal incontinence. Br J Surg 1999;86:1159–63.
6. Johanson RB, Fernando RJ, Kettle C et al. The ‘REPAIR’ survey of the incidence of 3rd degree perineal tears in UK hospitals. 2001, unpublished data. 7. Lal M, Mann CH, Callender R et al. Does caesarean delivery prevent anal incontinence? Obstet Gynecol 2003;101:19–20. 8. Donnelly VS, Fynes M, O’Connell PR et al. The influence of oestrogen replacement on faecal incontinence in post menopausal women. Br J Obstet Gynaecol 1997;104:311–5. 9. Donnelly VS, O’Herlihy C, Campbell DM et al. Post partum faecal incontinence is more common in women with irritable bowel syndrome. Dis Colon Rectum 1998;41:586–9. 10. Snooks SJ, Setchell M, Swash M et al. Injury to the innervation of the pelvic floor sphincter musculature in childbirth. Lancet 1984;1:546–50. 11. Fynes M, Donnelly VS, O’Connell PR et al. Cesarean delivery and anal sphincter injury. Obstet Gynecol 1998;92:496–500. 12. Bennet RC, Duthie HL. The functional importance of the internal sphincter. Br J Surg 1964;51:355–7. 13. Henry MM, Thompson JP. The anal sphincter. Scand J Gastroenterol 1989;19:53–7. 14. Vaizey CJ, Carapeti E, Cahill J et al. Prospective comparison of faecal incontinence grading systems. Gut 1999;44:77–80. 15. Coller JA. Clinical application of anorectal manometry. Gastroenterol Clin North Am 1987;16:17–33. 16. Snooks SJ, Swash M. Nerve stimulation techniques. In: Henry MM, Swash M (eds) Coloproctology and the pelvic floor. London: Butterworths, 1985; 112–28. 17. Tjandra JJ, Milsom JW, Schroeder T et al. Endoluminal ultrasound is preferable to electromyography in mapping anal sphincter defects. Dis Colon Rectum 1993;36:689–92. 18. Deen KI, Kumar D, Williams JG et al. Anal sphincter defects: correlation between endoanal ultrasound and surgery. Ann Surg 1993;218:201–5. 19. Pretlove SJ, Thompson P, Guest P et al. Detecting anal sphincter injury: acceptability and feasibility of endoanal ultrasound immediately postpartum. Ultrasound Obstet Gynecol 2003;22:214–7. 20. Pretlove SJ, Thompson PJ, Toozs-Hobson PM et al. The first 18 months of a new perineal trauma clinic. J Obstet Gynecol 2004;24:399–402.
23. Jensen LL, Lowry AC. Biofeedback improves functional outcome after sphincteroplasty. Dis Colon Rectum 1996;40:197–200. 24. Norton C, Chelvanagam S, Kamm M. Randomised controlled trial of biofeedback for fecal incontinence. Neurourol Urodyn 2002;21(4):295–6. 25. Mylonakis E, Radley S, Payton N et al. The role of an intraanal tampon for faecal incontinence; preliminary results of a prospective study. Colorectal Dis 2001;3(Suppl 1):82. 26. Blaisdell PC. Repair of the incontinent sphincter ani. Surg Gynecol Obstet 1940;70:692–7. 27. Parks AC, McPartlin JF. Late repair of injuries of the anal sphincter. Proc R Soc Med 1971;64:1187–9. 28. Hasegawa H, Yoshioka K, Keighley MRB. Randomised trial of faecal diversion for sphincter repair. Dis Colon Rectum 2000;43:961–5. 29. Nessim A, Wexner SD, Agachan F et al. Is bowel confinement necessary after anorectal reconstructive surgery? Dis Colon Rectum 1999;42:16–23. 30. Laurberg S, Swash M, Henry MM. Delayed external sphincter repair for obstetric tear. Br J Surg 1988;75:786–8. 31. Engel AF, Kamm MA, Sultan AH et al. Anterior anal sphincter repair in patients with obstetric trauma. Br J Surg 1994;81:1231–4. 32. Oliveira L, Pfeifer J, Wexner SD. Physiological and clinical outcome of anterior sphincteroplasty. Br J Surg 1996;83:502–5. 33. Nikiteas N, Korgsen S, Kumar D et al. Audit of sphincter repair. Factors associated with poor outcome. Dis Colon Rectum 1996;39:1164–70. 34. Baig MK, Wexner SD. Factors predictive of outcome after surgery for anal incontinence. Br J Surgery 2000;87:1316–30. 35. Briel JW, Stoker J, Rociu E et al. External sphincter atrophy on magnetic resonance imaging adversely affects continence after sphincteroplasty. Br J Surg 1999;86:1322–7. 36. Pinedo G, Vaizey CJ, Nicholls RJ et al. Results of repeat anal sphincter repair. Br J Surg 1999;86:66–9. 37. Malouf AJ, Norton CS, Engel AF et al. Long-term results of overlapping anal-sphincter repair for obstetric trauma. Lancet 2000;355:260–5. 38. Korsgen S, Deen KI, Keighley MRB. Long-term results of total pelvic floor repair for postobstetric fecal incontinence. Dis Colon Rectum 1997;40:835–9. 39. Niriella DA, Deen KI. Neosphincters in the management of faecal incontinence. Br J Surg 2000; 87:1617–28.
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40. Williams NS, Patel J, George BD et al. Development of an electrically stimulated neoanal sphincter. Lancet 1991;338:1166–9. 41. Baeten CG, Geerdes BP, Adang EMM et al. Anal dynamic graciloplasty in the treatment of intractable fecal incontinence. N Engl J Med 1995;332:1600–5. 42. Vaizey CJ, Kamm MA, Gold DM et al. Clinical, physiologi-
cal, and radiological study of a purpose-designed artificial bowel sphincter. Lancet 1998;352:105–9. 43. Malouf AJ, Vaizey CJ, Kamm MA et al. Reassessing artificial bowel sphincters. Lancet 2000;355:2219–20. 44. Jarrett MED, Mowatt G, Glazener CMA et al. Systematic review of sacral nerve stimulation for faecal incontinence and constipation. Br J Surg 2004;91:1559–69.
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IntroductIon Constipation affects 3–15% of the general population.1,2 The majority of the clinical scenarios of chronic constipation are treated by general practitioners. These include simple dietary fiber and fluid deficiency, irritable bowel syndrome, systemic causes of slow transit (endocrine, drug-induced, metabolic), immobility, neurologic conditions, fecal impaction and overflow, and pseudo-obstruction, and are summarized in Table 49.1. There remains a minority subgroup with complex, intractable symptomatology that can be broadly classified into idiopathic slow transit constipation (STC), obstructed defecation, or a combination syndrome of both. This latter group, with its female preponderance, presents a major diagnostic and therapeutic challenge to a multidisciplinary team that may include a urologist and a gynecologist. A population-based study in 1965 found that 99% of healthy subjects in the United Kingdom have bowel frequency of between three times a day and three times a week.3 More recently, the lower limit of ‘normal’ bowel frequency has been defined as twice a week by the Rome consensus group. It is important to appreciate that reduced frequency alone does not constitute constipation. While the oft-quoted Rome criteria (Table 49.2)4 have more application in the clinical trial and research setting, they serve to reinforce the other symptoms that afflict the constipated patient, namely straining, passage of hard stool, sensation of incomplete evacuation, sensation of anorectal blockage, and the need to use manual maneuvers to facilitate defecation. This chapter reviews the mechanics of normal defection, the pathophysiology of STC and obstructed defecation, history-taking and clinical examination, investigations and treatment. table 49.1.
• • • • • • • • • • • •
Different scenarios of constipation encountered in clinical practice
Dietary fiber and fluid deficiency Irritable bowel syndrome Endocrine and metabolic causes (e.g. hypercalcemia, diabetes mellitus, hypothyroidism) Drugs (e.g. opiates, calcium channel antagonists, etc.) Spinal cord lesions Neurologic disease (e.g. Parkinson’s disease, stroke, nerve injury) Elderly or poorly mobile patients Colorectal cancer Pseudo-obstruction or pan-gut dysmotility disorders Posthysterectomy constipation Idiopathic slow transit constipation Obstructed defecation (e.g. structural anorectal disorders and pelvic floor dysfunction)
table 49.2.
Rome II criteria for constipation
Adults Two or more of the following for at least 12 weeks (not necessarily consecutive) in the preceding 12 months: • Straining during >25% of bowel movements • Lumpy or hard stools for >25% of bowel movements • Sensation of incomplete evacuation for >25% of bowel movements • Sensation of anorectal blockage for >25% of bowel movements • Manual maneuvers to facilitate >25% of bowel movements (e.g. digital evacuation or support of the pelvic floor) • Less than three bowel movements per week • Loose stools not present, and insufficient criteria for irritable bowel syndrome Infants and children • Pebble-like, hard stools for a majority of bowel movements for at least 2 weeks • Firm stools ≤2 times per week for at least 2 weeks • No evidence of structural, endocrine, or metabolic disease Data from ref. 4.
PhysIology of normal colonIc transIt and defecatIon Orocecal transit time in Caucasian subjects has been estimated at 4–6 hours, and colonic transit per se at 54 hours.5 Mean mouth-to-anus transit time is 72 hours in women and 55 hours in men.5,6 Gut transit is clearly influenced by genetic, racial, hormonal and dietary factors, as well as age. Women suffer far more with constipation than men, and referrals to secondary and tertiary specialty clinics are almost exclusively female. Higher stool bulk and water content promote transit time and ease of evacuation. Undigested carbohydrate presenting to the colon contributes to stool volume in two ways: 1. Some of this resistant carbohydrate is fermented by bacteria, which in turn favors bacterial proliferation, with the latter contributing to nearly a third of the stool biomass. 2. The unfermented fiber holds onto water and adds further to stool mass. The increased bulk stimulates colonic peristaltic propulsion to speed its transit to the rectal reservoir. Defecation/evacuation is an intricate process that requires the coordination of an intact spinal and enteric neuronal network, anal sphincter complex, pelvic floor and abdominal wall musculature, with major influence from the consistency of the luminal content. In the resting position, continence is maintained by rectal compli-
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ance, tonic contraction of the anal sphincter complex, and an acute anorectal angle maintained by a sling of puborectalis. The sensory and motor innervation of the anal sphincter complex and pelvic floor musculature is provided by the pudendal nerve, lumbar colonic nerves, and the L2–S4 nerve roots. When rectal compliance is exceeded, the critical stool volume can trigger off the rectoanal inhibitory reflex (RAIR) which inhibits the tonically contracted internal anal sphincter. The squatting position is more effective than the sitting position in facilitating evacuation. Hip flexion aids in straightening of the anorectal angle, which requires relaxation of the puborectalis muscle (Fig. 49.1). ‘Straining’ of the diaphragm and abdominal wall musculature increases the intrapelvic pressure, which, along with the minor contribution of colonic propulsive contractions, is coupled with relaxation of the pelvic floor musculature and sphincter complex, resulting in successful evacuation. One of the most important recent advances in this area is the concept of classifying chronic constipation into slow transit constipation and obstructed defecation.7,8 The two have different pathophysiology, clinical presentations, and treatment algorithms, and may coexist in a combination syndrome.
PathoPhysIology slow transit constipation It is not difficult to envisage that colonic transit can be delayed by a variety of factors including unfavorable size and consistency of the stool, hormonal fluctuations, drugs, and neuromuscular pathology affecting the
a
smooth muscle or the myenteric plexus of nerves. This is broadly referred to as slow transit constipation (STC). The clinical problem is often a lack of urge to defecate. In pure STC, the evacuation process itself is relatively effortless. The subgroup of women with idiopathic or primary STC is particularly difficult to treat.9 The human gut is richly innervated by its intrinsic neuronal network known as the enteric nervous system (ENS) and extrinsic nerves from the autonomic nervous system. The intrinsic nerve ganglia, along with glial cells, form the myenteric and submucosal plexus that together constitute the ENS. Richly interspersed among the myenteric plexus and circular muscle in the colon are the interstitial cells of Cajal. These non-neuronal cells of mesenchymal origin provide pacemaker function. Collectively, the ENS provides the baseline tonic and rhythmic ring contractions throughout the colon.10 This is further modulated by the extrinsic (autonomic) nerves from the vagus nerve and the sacral (pelvic) plexus. The pathophysiology of idiopathic STC is unknown.8 Morphologic studies of the colectomy specimens reveal reduced c-KIT immunohistochemical staining for the interstitial cells of Cajal but it is unclear if this is a pathogenetic mechanism or secondary to chronic constipation and/or laxative use.11 Dysfunction of the secretory enterochromaffin cells and/or 5-hydroxytryptophan (5-HT) signaling has also been implicated in the pathogenesis of STC.12 Endocrine features such as reduced levels of serum estradiol, urinary estrogen excretion and increased serum prolactin have been found in female subjects with STC. It is noteworthy that a large proportion of patients with STC have chronic pain syndromes and a long history of opioid analgesic use.
b
Figure 49.1. The female pelvis (a) at rest and (b) on straining/defecation. Note the descent of the pelvic floor and the increase in the anorectal angle on straining. (Courtesy of Mr David Gourevitch, Consultant Surgeon, University Hospital Birmingham, UK.) 723
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STC can coexist with obstructed defecation – this is known as combination syndrome. In this setting, however, it is often thought to be a phenomenon secondary to the chronic obstruction. Clinically, it is important to differentiate STC from constipation-predominant irritable bowel syndrome (IBS) although this can be difficult in practice. Abdominal, not rectal, pain is a predominant feature in IBS and is often associated with a change in bowel habit and consistency of the stool at the time of pain (as defined in the Rome II criteria for IBS). Delayed colonic transit is less consistently objectively demonstrated in IBS. Visceral hypersensitivity is not a feature in idiopathic STC although these patients may still describe profound pain associated with stimulant laxative use or severe fecal loading. This differentiation is important as therapeutic colectomy should not be performed for constipation-predominant IBS but may benefit a subset of patients with intractable idiopathic STC.
obstructed defecation Obstructed defecation, also referred to as evacuatory failure or dyschezia, is a descriptive term for a heterogeneous group of structural and functional disorders of the anorectum characterized by an obstruction to the process of defecation. This has been used interchangeably, and wrongly, with the terms ‘pelvic floor dysfunction’ and ‘anismus’. In pure obstructed defecation, proximal colonic motility is intact, or at worst, secondarily affected.7,13
Structural disorders of the anorectum The classic disorder causing obstructed defecation is Hirschsprung’s disease. The congenital aganglionic colonic segment leads to failure of relaxation of the internal anal sphincter and megarectum. While the problem usually starts in infancy or childhood, an ‘ultrashort’ segment of Hirschsprung’s may not manifest itself until well into the teens or even early twenties. In Chagas disease, trypanosomal infection leads to a very similar clinicopathologic picture. Bulging of the anterior rectal wall through a weakness in the rectovaginal septum into the vagina gives rise to a rectocele. While the majority of rectoceles are ‘physiological’ and asymptomatic, two features help set this apart: 1) the sensation of a bulging lump in the vagina and the need to self-digitate the vagina or rectum to facilitate successful evacuation; and 2) the trapping of barium paste seen at the end of a defecating proctogram (see ‘Investigations’, below). Under these circumstances, surgical repair may abolish obstructed
defecation. Occasionally, an enterocele in the posthysterectomy state can cause similar problems. There is also a group where the enterocele comes down and displaces the rectum posteriorly. This group may have little to see on vaginal examination and the diagnosis is made on a combined vaginal–rectal examination and asking the patient to bear down. In this group, the rectum is displaced backwards as the enterocele descends. Full-thickness rectal prolapse can be subtle enough to evade diagnosis on history or clinical examination alone. Subtler still is intussusception of the rectal mucosa which may or may not protrude past the anal canal. Both can be associated with the solitary rectal ulcer syndrome. It is debatable whether rectal prolapse is a primary pathologic event or secondary to chronic straining. While obstetric trauma is more likely to cause fecal incontinence, weakness of the pelvic floor musculature and the perineal body may give rise to the ‘descending perineum syndrome’. In this setting, straining at the time of defecation leads to greater than normal descent of the perineum. This ‘shifting of goalpost’ leads to supranormal widening of the anorectal angle and often renders the evacuation process fruitless and frustrating. It may also lead to chronic damage to the pudendal nerve through repeated stretching. The rare conditions of protalgia fugax and levator ani syndrome are not well understood and are not major considerations in the diagnostic workup of obstructed defecation.
Functional causes of obstructed defecation Failure of relaxation, or even paradoxical contraction of the puborectalis during attempted defecation, leads to evacuatory failure. This subconscious behavior may also involve the anal sphincter and gluteal muscles. This has been variably referred to as ‘anismus’ or ‘pelvic floor dyssynergia’, and should to be distinguished from structural abnormalities causing obstructed defecation. The pathopsychophysiologic basis of this behavior differs from that encountered in IBS. In contrast to IBS, visceral hypersensitivity and gut dysmotility are not prominent features in pelvic floor dysfunction. A past history of sexual abuse is common in pelvic floor dysfunction. The existence of pelvic floor dysfunction or anismus as a distinct disease entity still invites debate. Poor correlation of symptoms with objective electromyographic (EMG) findings, and the observation of ‘physiologic’ contraction of the anal sphincter complex during defecation in normal subjects, lead some authorities to question its diagnosis.7,8,13 Nevertheless, the term ‘pelvic floor dysfunction’ is best used to describe a group of young
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females with clinical features of obstructed defecation, who may have a history of abuse, with demonstrable failure of relaxation or paradoxical contraction of the pelvic floor musculature during defecation.
Posthysterectomy constIPatIon A small proportion of women develop constipation posthysterectomy. Some even time the onset of symptoms to the immediate postoperative period. Despite a plethora of observational studies, the subject continues to divide opinion. Symptoms reported range from reduced urge and frequency, to features of obstructed defecation. Neurologic, anatomic, hormonal and other factors have been implicated in its pathogenesis.14 While surgical damage to the autonomic innervation of the hindgut and bladder may be incurred during a radical hysterectomy, the same does not hold true for a simple hysterectomy.15 Disruption to the autonomic supply to the gut and bladder should be minimal in a simple hysterectomy unless the cardinal ligaments or an unusually long cuff of the vagina are resected.16 The external anal sphincter is largely unaffected by hysterectomy. Most posterior vaginal hernias or hernias of the pouch of Douglas (enteroceles and sigmoidoceles) develop following abdominal or vaginal hysterectomy. Wiersma et al.17 found a five-fold rise in incidence of enteroceles and sigmoidoceles in women who had undergone hysterectomy. These can cause the classic symptoms of obstructed defecation and can be demonstrated by a defecating proctogram combined with fluoroscopy of the small bowel and vagina. However, not all enteroceles are symptomatic and in themselves can be a consequence of chronic constipation! It is important to appreciate that IBS and psychological symptoms are very prevalent among attendees at a gynecologic clinic. It is plausible that addressing gynecologic symptoms with a hysterectomy may unmask preexisting IBS. Drugs such as iron supplements, hormonal treatment, and analgesics may also contribute to constipation following hysterectomy. There are still no prospective studies comparing bowel habit pre- and posthysterectomy. Studies linking constipation to hysterectomy do not distinguish between STC and obstructed defecation.14,18 To complicate matters, a questionnaire study identified onset of mild to moderate fecal incontinence but not constipation after abdominal hysterectomy in 120 women.19 For now, patients presenting with constipation following hysterectomy are best evaluated individually using the general principles outlined here and elsewhere.7,13,17
clInIcal hIstory The symptoms listed in Table 49.2 are not always freely volunteered by the patient and should be actively sought. Symptom diaries and scores are probably of more value in assessing fecal incontinence than constipation. Graphic description of stool consistency and shape in the mode of the Bristol stool chart is of limited value. The clinician should distinguish between a presentation of a change in bowel habit and chronic constipation at the outset. The former follows a completely different diagnostic algorithm which aims to exclude cancer and other systemic diseases. A predominance of abdominal pain, bloating, and psychological co-morbidity are more indicative, although not always, of the visceral hypersensitivity seen in IBS. A detailed history of the patient’s dietary habit, fluid, fiber and caffeine intake may provide insight to remediable causes of delayed transit (see ‘Treatment’, below). Certain symptom cluster may help categorize the patient into STC and/or obstructed defecation although there is a considerable overlap: 1. STC • A lack of urge • Relative ease of evacuation with laxatives 2. Obstructed defecation • Sensation of anorectal obstruction • A grossly prolonged time to defecation (can be up to 1 hour) • Rectal fullness • Tenesmus • Recourse to manual maneuvers such as support of the perineum and digitation of the rectum or vagina Rectal prolapse, mucosal intussusception, and the solitary rectal ulcer syndrome may cause pain and rectal bleeding. More severe cases may result in bizarre urologic and neurologic symptoms as a consequence of compression from a megarectum. On assessing the etiology, specific questioning may reveal a drug, neurologic, endocrine or other systemic causes. Concurrent symptoms of vomiting or a history of pseudo-obstruction and malnutrition may suggest that delayed colonic transit is only part of a spectrum of pangut dysmotility disorder secondary to a neuropathy or visceral myopathy. A history of prolonged labor, obstetric trauma to the pelvic floor, and parity are of equal relevance in constipation and fecal incontinence. Some patients often date their onset of symptoms to the time of 725
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hysterectomy (see ‘Posthysterectomy constipation’, above). Many patients with STC frequently have a long history of dependence on opioid analgesics. Primary psychiatric or psychological disorders are less relevant to the types of constipation under consideration here than to constipation-predominant IBS. A history of sexual abuse is common in STC and pelvic floor dysfunction. It is important to elicit this sensitive aspect of the history as any treatment of constipation should be accompanied by appropriate psychotherapy in these patients.
InvestIgatIons
clInIcal examInatIon
Blood tests
Frequently, general examination of these patients is unremarkable. Obvious features of hypothyroidism or spinal stenosis may be apparent. Abdominal examination may reveal poor muscle tone of the abdominal wall or distension with feces. In the left lateral position, visual inspection of the perineum may give an idea of the integrity of the perineal body. Fair or excessive perineal descent can be assessed by asking the patient to bear down in this position. Rectal prolapse is not easily demonstrated in the left lateral position except when irreducible. Asking the patient to bear down in the squatting position may demonstrate a prolapse but is hardly dignifying. Digital rectal examination (DRE) can give some idea of the resting and squeeze pressure of the anal sphincter. Excessive mucosa may suggest intussusception. The finger expulsion test is performed by asking the patient to attempt to expel the finger. This is a simple means of assessing perineal descent but is not reliable and often not reproducible. Paradoxical tightening of the anal sphincter complex and puckering of the perineum during attempts to bear down is indicative but not diagnostic of anismus or pelvic floor dysfunction. DRE can be supplemented by proctoscopy or a rigid or flexible sigmoidoscopy in the outpatient suite. Sensory testing of the perianal skin and lower limbs may reveal saddle anesthesia or a sensory level indicative of spinal cord disease. Where the history is suggestive of a rectocele or enterocele, bimanual examination of the vagina may be appropriate. The information derived from clinical examination alone may be limited and misleading. A patient ill at ease on the examination couch may be misinterpreted as a case of pelvic floor dysfunction. Evaluation of these patients continues with radiologic and endoscopic investigations.
Generally, if patients are thought to have a normal transit constipation and respond to empirical medical therapy, further investigations are not necessary. However, when STC or pelvic floor dysfunction is suspected, or when constipation is thought to be secondary to a medical problem, further investigations become necessary to orchestrate an appropriate management strategy. Figure 49.2 shows a diagnostic algorithm based on one proposed by the American Gastroenterological Association7 which can be adopted to investigate patients with refractory constipation.
Serum calcium and thyroid function testing (TFT) are mandatory in all patients with constipation to exclude hypercalcemia and hypothyroidism. A full blood count, inflammatory markers (ESR and CRP), urea and electrolytes are usually easy to obtain and are particularly useful if an underlying neoplastic or metabolic cause for the constipation is suspected. Diabetic neuropathy leads to an increase in whole gut transit time; in diabetic patients, glycemic control can be assessed by measuring serum glucose and glycosylated hemoglobin levels.
colonoscopy and barium enema studies Endoscopy is necessary only in patients where there is a suspicion that the constipation has developed secondary to organic pathology or an obstructive lesion such as bowel cancer. Either full preparation colonoscopy or a flexible sigmoidoscopy in conjunction with a barium enema study can be performed. In addition, the barium enema can also show evidence of a megarectum (diameter of the rectum at the pelvic brim greater than 6.5 cm) and the characteristic denervated bowel segment with proximal dilation of the colon in Hirschsprung’s disease.
colonic transit testing Fecal colonic transit time testing is a means of obtaining objective evidence on whether the patient is indeed constipated as evidenced by a delayed transit time. Objective documentation of colonic transit time is useful to:
• support or refute patients’ description of decreased bowel frequency;
• support a diagnosis of ‘normal transit constipation’ or IBS.
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Clinical history and examination Blood tests (FBC, TFT, Ca)
Trial of laxative Organic pathology unlikely
Normal CTT, abnormal ARM, BET or DP: Pelvic floor dysfunction
Abnormal CTT and abnormal ARM, BET or DP: Pelvic floor dysfunction and slow flow constipation
Discharge
Evidence of organic pathology Colonoscopy or barium enema
CTT, ARM, BET, DP
Normal CTT, ARM, BET, DP: Normal transit constipation, ?IBS
Improves
Abnormal CTT and normal ARM, BET and DP: Slow transit and constipation
The test is an essential prelude to colectomy as a treatment for STC. Two methods used to assess this are as follows.
Transit testing using radiopaque markers (‘shapes’ test) This is an indirect but also the simplest and the most inexpensive method to measure colonic transit time.6 Essentially, radiopaque markers (these are commercially available, contained in gelatin capsules) are swallowed and subsequently an abdominal radiograph is taken (Fig. 49.3).20 Radiographs can be performed at 12 and 120 hours after ingestion. Normal subjects retain more than 20% of markers at 12 hours and less than 80% at 120 hours. If required, markers of different shapes (hence the term ‘shapes’ test) can be given on successive days, so that several transit studies providing intermediate values can be obtained from a single abdominal radiograph taken at 12 hours. The transit time can be calculated by counting the number of retained markers. It is important to bear in mind that this test actually measures whole gut transit time, the largest component of which is colonic transit. However, if surgical intervention such as colectomy is being considered, then it is important to measure the rates of gastric emptying and small bowel transit (radionucleotide and manometric study). Abstinence from laxative medication is mandatory for the test.
Colonic scintigraphy This is a useful alternative to the radiopaque marker
Figure 49.2. Diagnostic algorithm for investigating constipation. ARM, anorectal manometry; BET, balloon expulsion test; Ca, calcium; CTT, colonic transit test; DP, defecation proctogram; FBC, full blood count; IBS, irritable bowel syndrome; TFT, thyroid function test. (Based on the American Gastroenterological Association guidelines on constipation, ref. 7.)
technique. However, it has the drawbacks of being expensive, requiring expert personnel, special equipment, and patient exposure to radiation. Radionuclides such as indium 111-diethylenetriamine pentaacetic acid (111In-DTPA) or iodine 131 (technetium 99m can be added to measure gastric and small bowel transit) are delivered to the colon by dissolving the isotope (111InDTPA) in water or by the use of activated charcoal or a pH-sensitive methacrylate-coated capsule that dissolves and releases the isotope at alkaline pH in the distal ileum. The progress of the isotope can then be followed with a large field-view gamma camera. This technique can be used to measure transit through different segments of the colon.
anorectal manometry While this test is strongly indicated in patients with fecal incontinence, the indication in constipated patients is less robust. The main role of anorectal manometry (ARM) in the evaluation of refractory constipation is to exclude Hirschsprung’s disease to assess pelvic floor dysfunction.13 ARM provides some important measurements, which include:
• resting (predominately internal anal sphincter) and •
squeeze (predominately external anal sphincter) anal sphincter pressure; the ability of the anal sphincter to relax during straining and coughing; 727
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Figure 49.3. The ‘shapes’ test used to evaluate colonic transit. Six gelatin capsules, each containing 10 radiopaque polyurethane markers, are taken two at a time on three consecutive days. The marker shapes are as follows: day 1 – spheres; day 2 – small rods; day 3 – rings. The patient then returns to hospital on day 6 to have an abdominal X-ray, which is used to calculate the global and segmental transit times. These are based on the number and types of markers retained. (Reproduced from ref. 20 with permission.)
• the rectoanal inhibitory reflex (RAIR): reflex •
inhibition of the anal sphincter in response to simulated defecation by rectal distension; rectal sensitivity to balloon distension.
Water-perfused catheters attached to transducers or solid-state microtransducers can be used to perform ARM.13 Hirschsprung’s disease is effectively excluded if the internal anal sphincter relaxes in response to rectal distension, i.e. a positive RAIR. It is important to appreciate that a false-negative RAIR may be secondary to a megarectum from non-Hirschsprung’s causes. In this respect, a positive RAIR excludes Hirschsprung’s disease. A negative RAIR is suggestive of Hirschsprung’s disease (Fig. 49.4) and confirmatory histology needs to be obtained via full thickness rectal biopsy. Pressures recorded within an inflated balloon in the rectum reflect intra-abdominal pressure, particularly during an expulsion effort. In
Figure 49.4. An example of a negative rectoanal inhibitory response (RAIR) in Hirschsprung’s disease. Inflation of a balloon in the rectum (start of inflation is shown by the arrow) fails to cause a corresponding relaxation of the anal canal. The manometric ports are positioned as follows: P1, rectum; P2, upper anal canal; P3, mid-anal canal; P4, low anal canal. (Courtesy of Ms Joanne Hayes, GI Physiologist, University Hospital Birmingham, UK.) the context of the clinical history, a diagnosis of pelvic floor dysfunction can be inferred if there is a paradoxical rise in the external anal sphincter pressure while there is a raised pressure within a rectal balloon. Further diagnostic evidence can be obtained from concomitant EMG recordings of the external anal sphincter muscle using adhesive or anal plug electrodes.
defecation proctogram (defecography) Defecography may be of value in patients who give a history of manipulation of the rectal wall per vagina (may have an anterior rectocele) or those that have previously had a hysterectomy and may have an enterocele (Fig. 49.5). It may also be useful in patients suspected of having pelvic floor dysfunction. Various materials such as oatmeal have been used as the vehicles for the barium which can be visualized by the use of fluoroscopy. It gives an objective measure of the rate of rectal emptying and information on structural abnormalities such as rectal prolapse, rectoceles, and enteroceles. In addition, it shows the width of the anal canal, the rectoanal angle, and movement of the pelvic floor during the process of defecation. The technique has been criticized on a number of grounds, not least of which is poor correlation of the rectoanal angle between independent observers. This measure is critical to the interpretation of the results.
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Posterior
latency (PNTML). The technique is very much operator dependent and patients with chronic constipation are frequently diagnosed with bilateral pudendal neuropathy, which may be a secondary phenomenon or a falsepositive result. This test is now not recommended for routine investigation of chronic constipation under the guidelines issued by the American Gastroenterological Association.13
treatment Femur
Contrast in vagina
general principles Enterocele
Rectocele
Figure 49.5. Defecating proctogram. The figure shows a ‘sideview’ of the female pelvis with the rectum and sigmoid colon outlined by barium paste. Both a rectocele and an enterocele are clearly demonstrated. The investigations can be enhanced by estimating percentage contrast retention by the rectocele and by performing a simultaneous vaginogram. (Courtesy of Dr Peter Guest, Consultant Radiologist, University Hospital Birmingham, UK.) Moreover, some of the findings of this test (e.g. pelvic floor descent, internal intussusception, rectoceles) are often found in many non-constipated individuals. Close clinical correlation is essential for the interpretation of a defecation proctogram.
Balloon expulsion test This is a simple screening test that can be carried out in the clinic. A latex balloon filled with 50 ml of water is inserted into the rectum and the patient is asked to expel this. Inability to do this within 2 minutes suggests a defecatory disorder.
Pudendal nerve latency studies This test is more useful in incontinent patients,6 but has a role where constipation is thought to be secondary to pudendal nerve injury. An electrode placed on the operator’s finger is used to measure the conduction of the pudendal nerves – the pudendal nerve terminal motor
Treatment of severe constipation requires a multidisciplinary approach that may involve any combination of the family physician, gastroenterologist, dietitian, gastrointestinal physiologist, pelvic floor physiotherapist, nurse specialist, colorectal and gynecologic surgeon. Treatment options can be broadly categorized into lifestyle and dietary modification, pharmacologic, behavioral and surgical treatment. Once systemic, neoplastic or neurologic disorders and IBS have been excluded, it is important to derive from the clinical evaluation and diagnostic algorithms if the patient is suffering from STC, obstructed defecation, or a combination syndrome of both (see Fig. 49.2). Conceptually, patients with STC respond better to laxative treatment and patients with obstructed defecation respond poorly. Within the subgroup of obstructed defecation, the functional group of disorders (pelvic floor disorder, anismus) may respond to appropriate behavioral therapy, whereas some structural diseases of the anorectum are more amenable to surgery. However, the reality of treatment outcome may veer disappointingly away from these principles. Treatment of constipation suffers from a dearth of evidence base. Paucity of double-blind, placebocontrolled trials for non-pharmacologic therapy, heterogeneity of study subjects, and a lack of uniform diagnostic criteria had led to a wide variation in treatment approach and outcome. It may be useful to advise the patient from the outset that no miracle cure is being promised. Realistic treatment goals should be set in conjunction with the patient, such as improving bowel frequency from once a week to three times a week rather than aiming for daily bowel action. Others may include reduction in or freedom from laxative use, reduction in hospital admissions for bowel evacuation, and improvement in the process and mechanics of defecation. 729
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dietary and lifestyle modification Irregular eating habits and a diet poor in fluid and fiber and rich in ‘junk food’ set the scene for reduced bowel transit. Eating breakfast followed by attempted bowel opening to take advantage of the gastrocolic reflex can form part of the ‘bowel retraining’ program. The patient often ascribes her irregular mealtimes to satiety secondary to bloating from constipation or a busy daily routine. This mindset must be undone to revert to the ‘healthyeating’ norm of three to four meals a day. A patient’s perception of oral fiber and fluid intake often falls short of the daily recommended intake. Not all fruits and vegetables have equal efficacy on promoting bowel transit. Practical advice on increasing intake of leafy vegetables and whole fruits rather than juice should be offered. Description of hard, ‘rabbit droppings’ type stool is an indication of inadequate oral fluid intake. Caffeine intake in the form of soft drinks, coffee and tea should be reduced. Objectively ensuring a daily intake of 1.52 liters of fluids may be achieved reliably and pragmatically by drinking from an appropriately sized bottle. This advice must take into consideration patients who are also suffering from urinary frequency and incontinence. A record of fluid and fiber intake may be helpful for follow-up in certain cases.
Pharmacologic treatment Attitude to pharmacologic treatment varies from center to center, ranging from the provision of a mutually agreed supervised laxative regimen, to complete prohibition of laxatives. The patient and clinician can embark jointly on a regimen of oral laxative (bulking, stimulant, osmotic) or rectal treatment (suppository or enema). In general, bulking agents are simple, effective and make up for dietary fiber deficiency. Natural fiber supplements (ispaghula, sterculia) are widely prescribed and well tolerated. Lactulose is also widely used but may exacerbate bloating due to fermentation. For patients who develop excessive bloating from fermentation, switching to a synthetic preparation such as methylcellulose may be helpful.21 The methylation process confers resistance of the fiber to degradation by colonic bacteria. Polyethylene glycol preparations are gaining in popularity and have proven efficacy over placebo in both constipation and fecal impaction.22 Stimulant laxatives such as senna and bisacodyl are favored by some patients; in others, they produce unpleasant abdominal cramps and unpredictable bowel urgency. Initial fears of increased apoptosis of the enterocytes with long-term use have not been substan-
tiated. Pulsed usage (e.g. three times a week) may be more effective than daily use. Hard stool may be softened by enemas of arachis oil. Some patients prefer twice or thrice weekly self-administered enemas or suppositories to achieve evacuation. This should not be encouraged as a long-term solution. Many patients take over-the-counter medicines and alternative preparations from health food shops. Some even attend regular colonic irrigation sessions. These approaches are not subject to the rigors of clinical trials and most clinicians adopt a neutral attitude. Prokinetic drugs such as domperidone, metoclopramide and erythromycin are more effective for upper gastrointestinal dysmotility than promoting colonic transit. Tegaserod, a 5-HT4 agonist, has been shown to be safe and effective for constipation-predominant IBS and chronic constipation, and is widely used in the United States.23,24 A European license may see its use in STC in the near future and it appears to be the most promising colonic prokinetic drug to date. A summary of laxatives is shown in Table 49.3. A subgroup of patients with long-term dependence on opioid analgesics may be referred to specialist ‘pain clinics’ for rationalization of the analgesic regimen. Alternative non-pharmacologic approaches such as nerve block or TENS may be helpful. However, delayed transit often persists long after opioids have been withdrawn. The use of laxatives may be counterproductive and is inappropriate in patients with suspected obstructed defecation.
Patient education, bowel retraining and biofeedback Due to time constraint in a clinic, the role of patient education – including teaching the patient normal and abnormal physiology, advice on diet and lifestyle, and pelvic floor exercise – can be assumed by a nurse specialist, a trained gastrointestinal physiologist or a physiotherapist. However, there is little evidence to support favorable long-term outcome of patient education in the treatment of constipation other than improving patient satisfaction. Biofeedback is widely used for the treatment of fecal incontinence and pelvic floor dysfunction. This can take the form of sensory training, EMG and manometric feedback.25 Patients with demonstrable paradoxical contraction of pelvic floor muscles are asked to expel a rectal balloon (simulated defecation) in sensory training. Using one of three modalities, training can take the form of sensory training alone or in combination with EMG (surface electrodes on perianal skin or intrarec-
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table 49.3.
Laxative classification
Bulk laxative (these increase fecal bulk and stimulate peristalsis) • Psyllium (Fybogel, Metamucil, Perdiem) • Methylcellulose (Citrucel) • Polycarbophil (Fibercon, Equalactin, Konsyl) Osmotic laxative (draws water into the intestines along osmotic gradient) • Saline laxatives • Magnesium hydroxide (Phillips’ Milk of Magnesia) • Magnesium citrate (Evac-Q-Mag) • Sodium phosphate (Fleet Enema, Fleet Phospho-soda, Visicol) Poorly absorbed sugar • Lactulose (Cephulac, Chronulac, Duphalac) • Sugar alcohols • Sorbitol (Cystosol) • Polyethylene glycol and electrolytes (Colyte, Golytely, MiraLax, Nulytely) Stimulant laxative (stimulates intestinal motility or secretion) • Senna (Ex-Lax, Senokot) • Anthraquinones • Cascara sagrada (Colamin, Sagrada-lax) • Bisacodyl (Correctol, Dulcolax) • Sodium picosulfate (Lubrilax, Sur-lax) Stool softener • Docusate sodium (Colace, Regulax, Surfak) • Mineral oil (Fleet Mineral Oil) Rectal enema or suppository • Phosphate enema (Fleet Enema) • Mineral oil retention enema (Fleet Enema) • Tap water enema • Soapsuds enema • Arachis oil enema • Glycerin bisacodyl suppository Cholinergic agent • Bethanechol (Urecholine) • Colchicine (Colsalide) • Misoprostol (Cytotec) Prokinetic agent • 5-HT4 receptor agonists • Tegaserod (Zelnorm)
tal probes) or manometric means. Failure of relaxation or paradoxical increase in EMG or manometric activity during simulated defecation is explained to the patient, who then ‘learns’ appropriate relaxation of the pelvic floor. This behavior is ‘rewarded’ and reinforced by successful expulsion of the balloon. In parallel, effective contraction of the abdominal wall muscle is taught to overcome ineffective rise in intra-abdominal pressure. The patient learns to effectively couple contraction of abdominal wall muscles with relaxation of the pelvic floor and anal sphincter complex to achieve successful
evacuation. Treatment can continue at home or at the hospital. Various studies have reported 70–100% short-tomedium improvement in clinical and physiologic parameters.25,26 Meta-analysis of 38 published studies on biofeedback for pelvic floor dysfunction (of which only 20% were controlled trials) concluded an average probability of successful treatment outcome in 62.4% of patients.26 Data on long-term efficacy are few and disappointing,27,28 but reported 50% patient satisfaction up to 12–44 months of follow-up. There is no uniform biofeedback protocol (single versus combination techniques, home versus hospital follow-up treatment, duration and follow-up, treatment objectives, etc.) and provision of service depends on local expertise and experience. Patients with descending perineum syndrome are thought to have sustained injury to the sacral nerves from childbirth or chronic straining. Treatment here comprises an intensive program of physiotherapy to strengthen the pelvic floor. It has been suggested that more unselected cases of STC and obstructed defecation may benefit equally from biofeedback although data on its efficacy in these heterogeneous groups of disorders are lacking. In practice, it may be worthwhile referring all patients with STC and obstructed defecation for education, physiotherapy and/or biofeedback (where appropriate) as an adjunct to pharmacologic treatment or before more radical treatment is offered.
surgical treatment STC Despite optimal treatment, it is estimated that 5% of patients with intractable STC seen at tertiary care will require surgical treatment.29,30 A subtotal colectomy and ileorectal anastomosis (IRA) with preservation of the presacral sympathetic nerves is the procedure of choice. Preoperative counseling is crucial to set clear and realistic treatment objectives. For example, patients with complex symptoms of pain, bloating, and depression in addition to severe STC must be counseled that not all their symptoms can be ‘cured’ by surgery. There are data to suggest poor outcome in patients with significant psychological co-morbidity and a preoperative psychological evaluation is standard in many units.31 Preoperative workup should also aim to exclude dysmotility in the proximal gastrointestinal tract (scintillography, manometry or barium studies) and demonstrate 731
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integrity of the anal sphincter. Prerequisites of colectomy for STC are objective documentation of delayed colonic transit and effective evacuation. Although not evidence based, some surgeons may perform a defunctioning ileostomy or a colostomy in the first instance to assess resolution of symptoms as a predictor of outcome following colectomy. Preservation of the colon (e.g. cecum and sigmoid colon) is associated with poorer outcome than an IRA.32 Unfortunately, colectomy for STC is associated with unpredictable short- and longterm outcomes. Factors contributing to poor outcome include significant psychological co-morbidity, superimposed IBS, undiagnosed obstructed defecation or pan-gut dysmotility disorder. Variable and disappointing long-term outcomes from colectomy for STC were reported in some early series.29,30 Encouragingly, a recent series of 74 patients undergoing colectomy and IRA for STC or STC/pelvic floor dysfunction reported 97% patient satisfaction and 90% long-term improvement in quality of life, probably reflecting careful patient selection.33 Others report an increase in bowel frequency associated with significant postoperative diarrhea and fecal incontinence.34,35 Colectomy remains a treatment option for patients with intractable STC but must only be undertaken after comprehensive investigations and counseling.
Obstructed defecation Hirschsprung’s disease generally presents in childhood and is treated accordingly. Rectal prolapse requires surgical correction. There are many surgical techniques described for the treatment of rectal prolapse. These may take the form of abdominal or perineal procedures. Generally, abdominal procedures are associated with lower recurrence rates but have a potential for higher morbidity, whereas perineal procedures are associated with a lower morbidity but higher recurrence.36 Abdominal approaches undertaken by open or laparoscopic techniques may include suture or mesh fixation of the rectum, with or without a resection of the redundant sigmoid colon. Resection appears to be more effective than rectopexy alone in improving the element of symptoms related to obstructed defecation secondary to a rectocele.36 Perineal approaches include Delormes procedure or perineal rectosigmoidectomy (Altemeier procedure). Both remain a popular choice for elderly patients with significant co-morbidity. Delormes procedure involves mucosal stripping and muscle plication; perineal rectosigmoidectomy involves resection of the prolapsing rectum and sigmoid colon with a coloanal anastomosis. Associated morbidity is low and improvement of
obstructed defecation and fecal incontinence may be achieved in many patients.36,37 Rectoceles can produce symptoms of bulging and obstructed defecation. Approaches to repair of a rectocele include a transvaginal or posterior repair. Traditionally, rectoceles are repaired transvaginally by gynecologists. This approach is thought to be associated with significant sexual dysfunction although there are conflicting data in the literature.38–41 Furthermore, anorectal symptoms often persist despite correction of the anatomic defect transvaginally.40,41 The transanal approach is comparable to vaginal colporrhaphy in improving the symptoms of vaginal bulging and obstructed defecation.41–43 It has been proposed that the transanal approach may be preferable to the transvaginal in addressing anorectal symptoms produced by rectoceles.44,45 Heriot et al.46 reported significant improvement in functional and physiologic parameters without sexual dysfunction or dyspareunia at 24 months follow-up in a series of 45 women who underwent transanal repair of symptomatic rectoceles. Strict selection criteria may account in part for the favorable outcome. The authors were satisfied that symptoms of obstructed defecation were directly attributable to a clinical rectocele and a contrast retention of ≥15% on isotope defecography was a prerequisite. The transanal technique involves making a transverse mucosal incision in the anterior rectal wall just above the dentate line. A vertical mucosal flap is then made and elevated from the anterior rectal wall to reveal the underlying rectal circular muscle. This is followed by suture plication of the rectovaginal septum done longitudinally. Any excess mucosa is then excised and the mucosal flap sutured back into place.46 Surgical treatment is not recommended for pelvic floor dysfunction. Division of the posterior fibers of the puborectalis muscle in which paradoxical contraction is objectively documented has been disappointing and not routinely practised. Fashioning a colostomy to circumvent functional obstructed defecation is equally disappointing. There is little or no role for surgery in functional causes of obstructed defecation.
Sacral nerve modulation Sacral nerve modulation (SNM) represents an exciting and promising treatment modality for fecal and urinary incontinence. The technical details can be found in the relevant chapters. Paradoxical as it may seem, SNS may equally benefit patients with constipation from varying etiology such as spinal cord injury and idiopathic STC. The mechanisms are unclear but most likely involve neuromodulation of the sacral nerve plexus characterized by its rapid onset and offset of effect.
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To date, there are a total of four open-label patient series44–50 and one cross-over study.51 The numbers remain small and follow-up short, but a systematic review52 concluded that encouraging improvements in bowel frequency, obstructed defecation, associated abdominal pain and bloating, quality of life, and rectal sensation have been demonstrated for a very heterogeneous cohort with STC, IBS, and obstructed defecation. Further data are required to refine patient selection, mechanisms of action, and long-term outcome. It is likely that SNS will have a greater role to play in the management of constipation in the future.
13. Diamant NE, Kamm MA, Wald A et al. AGA technical review on anorectal testing techniques. Gastroenterology 1999;116:735–60.
references
18. Martinelli E, Altomare DF, Rinaldi M, Portincasa P. Constipation after hysterectomy: fact or fiction? Eur J Surg 2000;166:356–60.
1. Thompson WG, Keaton KW. Functional bowel disorders in apparently healthy people. Gastroenterology 1980;79:283–8. 2. Drossman DA, Li Z, Andruzzi E et al. US householder survey of functional gastrointestinal disorders. Prevalence, sociodemography, and health impact. Dig Dis Sci 1993;38:1569–80. 3. Connell AM, Hilton C, Irvine G et al. Variation of bowel habit in two population samples. BMJ 1965;2:1095–9. 4. Thompson WG, Longstreth GF, Drossman DA, Heaton KW, Irvine EJ, Muller-Lissner SA. Functional bowel disorders and functional abdominal pain. Gut 1999;45(Suppl 2):II43–7. 5. Cummings JH, Bingham SA, Heaton KW, Eastwood MA. Faecal weight, colon cancer risk and dietary intake of nonstarch polysaccharides (dietary fibre). Gastroenterology 1992;103:1783–9. 6. Evans RC, Kamm MA, Hinton JM, Lennard-Jones JE. The normal range and a simple diagram for recording whole gut transit time. Int J Colorectal Dis 1992;7:15–7.
14. Radley S, Radley SC, Mann CH, Keighley MRB. Bowel dysfunction after hysterectomy. Br J Obstet Gynaecol 1999;106:1120–5. 15. Stanhope CR. Chronic constipation following simple hysterectomy is rare. Gynaecol Oncol 1991:42:114–5. 16. Mundy AR. An anatomical explanation for bladder dysfunction following rectal and uterine surgery. Br J Urol 1982;54:501–4. 17. Wiersma TG, Werre AJ, Den Hartog G et al. Hysterectomy: the anorectal pitfall. A guideline for evaluation. Scand J Gastroenterol 1997;223(Suppl):3–7.
19. Altman D, Zetterstrom J, Lopez A et al. Effect of hysterectomy on bowel function. Dis Colon Rectum 2004;47:502–8. 20. Chaussade S, Roche H, Khyari A, Couturier D, Guerre J. [Measurement of colonic transit time: description and validation of a new method.] Gastroenterol Clin Biol 1986;10(5):385–9. 21. Levitt MD, Furne J, Olsson S. The relation of passage of gas and abdominal bloating to colonic gas production. Ann Intern Med 1996;124:422–4. 22. Wald A. Slow transit constipation. Curr Treat Options Gastroenterol 2002;5:279–83. 23. Kamm MA, Muller-Lissner S, Talley NJ et al. Tegaserod for the treatment of chronic constipation: a randomised, double-blind, placebo-controlled multinational study. Am J Gastroenterol 2005;100:362–72. 24. Chey WD. Review article: Tegaserod – the global experience. Aliment Pharmacol Ther 2004;20(Suppl 7):15–9.
7. Locke GR III, Pemberton JH, Phillips SF. American Gastroenterological Association technical review on constipation. Gastroenterology 2000;119:1766–78.
25. Bassotti G, Chistolini F, Sietchiping-Nzepa F et al. Biofeedback for pelvic floor dysfunction in constipation. BMJ 2004;328:393–6.
8. Crowell MD. Pathogenesis of slow transit and pelvic floor dysfunction: from bench to bedside. Rev Gastroenterol Disord 2004;4(Suppl 2):S17–S27.
26. Palsson OS, Heymen S, Whitehead WE. Biofeedback treatment for functional anorectal disorders: a comprehensive efficacy review. Appl Psychophysiol Biofeedback 2004;29:153–74.
9. Preston DM, Lennard-Jones JE. Severe chronic constipation of young female: ‘idiopathic slow transit constipation’. Gut 1986;27:41–8. 10. Schermann M, Neunlist M. The human enteric nervous system. Neurogastroenterol Motil 2004;16(S1):55–9. 11. Tong WD, Liu BH, Zhang LY et al. Deceased interstitial cells of Cajal in the sigmoid colon of patients with slow transit constipation. Int J Colorectal Dis 2004;19:467–73. 12. Crowell MD, Schetzline MA, Moses PL et al. Enterochromaffin cells and 5-HT signalling in the pathophysiology of disorders of gastrointestinal function. Curr Opin Investig Drugs 2004;5:55–60.
27. Battaglia E, Serra AM, Buonafede G et al. Long-term study on the effects of visual biofeedback and muscle training as a therapeutic modality in pelvic floor dyssynergia and slow transit constipation. Dis Colon Rectum 2004;47:90–5. 28. Wang J, Luo MH, Hui Q et al. Prospective study of biofeedback retraining in patients with chronic idiopathic functional constipation. World J Gastroenterol 2003;9:2109–13. 29. Leon SH, Krishnamurthy S, Schuffler MD. Subtotal colectomy for severe idiopathic constipation: a follow up study of 13 patients. Dig Dis Sci 1987;32:1249–54.
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30. Kamm MA, Hawley PR, Lennard-Jones JE. Outcome of colectomy for severe idiopathic constipation. Gut 1988;29:969–73.
41. Zhar AP, Lienemann A, Fritsch H et al. Rectocele: pathogenesis and surgical management. Int J Colorectal Dis 2003;18:369–84.
31. Fisher SE, Breckon K, Andrews HA et al. Psychiatric screening for patients with faecal incontinence or chronic constipation referred for surgical treatment. Br J Surg 1989;76:352–5.
42. Sarles JC, Arnaud A, Selezneff I, Oliver S. Endo-rectal repair of rectocele. Int J Colorectal Dis 1989;4:167–71.
32. Pemberton JH, Rath DM, Ilstrup DM. Evaluation and surgical treatment of severe chronic constipation. Ann Surg 1991;214:403–11. 33. Nyam DC, Pemberton JH, Ilstrup DM, Rath DM. Long term results of surgery for chronic constipation. Dis Colon Rectum 1997;40:273–9. 34. Nylund G, Oresland T, Fasth S, Nordgren S. Long-term outcome after colectomy in severe idiopathic constipation. Colorectal Dis 2001;3:253–8.
43. Murthy VK, Orkin BA, Smith LE, Glassman LM. Excellent outcome using selective criteria for rectocele repair. Dis Colon Rectum 1996;39:374–8. 44. Segal JL, Karram MM. Evaluation and management of rectoceles. Curr Opin Urol 2002;12:345–52. 45. Marks MM. The rectal side of the rectocele. Dis Colon Rectum 1967;10:387–8. 46. Heriot AG, Skull A, Kumar D. Functional and physiological outcome following transanal repair of rectocele. Br J Surg 2004;91:1340–4.
35. FitzHarris GP, Garcia-Aguilar J, Parker SC et al. Quality of life after subtotal colectomy for slow transit constipation: both quality and quantity count. Dis Colon Rectum 2003;46:433–40.
47. Ganio F, Masin A, Ratto C et al. Short-term sacral nerve stimulation for functional anorectal and urinary disturbances: results in 40 patients. Dis Colon Rectum 2001;44:1261–7.
36. Madiba TE, Baig MK, Wexner SD. Surgical treatment of rectal prolapse. Arch Surg 2005;140:63–73.
48. Kenefick NJ, Nicholls JR, Cohen RG, Kamm MA. Permanent sacral nerve stimulation for the treatment of idiopathic constipation. Br J Surg 2002;89:882–8.
37. Lieberman H, Hughes C, Dippolito A. Evaluation and outcome of the Delorme procedure in the treatment of rectal outlet obstruction. Dis Colon Rectum 2000;43:188–92. 38. Kahn M, Stanton SL. Posterior colporrhaphy: its effects on bowel and sexual function. Br J Obstet Gynaecol 1997;104:82–6. 39. Kahn MA, Kumar D, Stanton SL. A prospective randomised trial of posterior colporrhaphy vs transanal repair of rectocele: an interim analysis. Gut 1997;40(3S)(Suppl 1):54A. 40. Mellgren A, Anzen B, Nilsson BY et al. Results of rectocele repair. a prospective study. Dis Colon Rectum 1995;38:7–13.
49. Malouf AJ, Wiesel PH, Nicholls T et al. Short term effects of sacral nerve stimulation for idiopathic slow transit constipation. World J Surg 2002;26:166–70. 50. Ganio F, Masin A, Ratto C et al. Sacral nerve modulation for chronic outlet constipation. Online. Available: www. colorep.it. 51. Kenefick NJ, Vaizey CJ, Cohen CR et al. Double-blind placebo-controlled crossover study of sacral nerve stimulation for idiopathic constipation. Br J Surg 2002;89:1570–1. 52. Jarrett MED, Mowatt G, Glazener CMA et al. Systematic review of sacral nerve stimulation for faecal incontinence and constipation. Br J Surg 2004;91:1559–69.
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50 The purpose of standardization of terminology and methods in patients with lower urinary tract dysfunction Anders Mattiasson
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INTRODUCTION The standardization of terminology and methods used to characterize the lower urinary tract (LUT) is motivated first and foremost by the need for communication and documentation. As in other contexts, to achieve satisfactory communication it is vital that people speak the same language and that the terms used have the same meaning for everyone who uses them. This is not simply a matter of characterizing and classifying different types of dysfunction, but also of applying methods and quantifying different findings in terms of measurements. We also need to ensure that the methods we use are well defined and characterized with regard to suitability, sensitivity, and reproducibility. In short, we need a common language with definitions of what is normal and what is abnormal. In the case of abnormalities, it is assumed that we can measure how large the abnormality is in relation to what is normal, to an earlier situation or to another chosen definition of the desirable state. The measurements and the measures we choose also need to be standardized so that we know that our measurements and investigations are comparable over time and between different places. In addition, our definitions and classification of LUT disorders should ideally rest on a firm biologic foundation, and also include consequences on an organism ± individual ± patient level such as symptoms, bother, quality of life, and health economic factors.
WHAT IS A STANDARD? Standardization is a tool for quality assurance, and the production of standards is itself a part of such work. Standards are needed in all three principal sections of quality-assurance work:
• in the structure; • in the process; • for describing the result. The procedure of standardization is one of writing down terms, descriptions of methods and measures which, at present and for the foreseeable future, are judged to best reflect the pathologic condition/function/dysfunction in both qualitative and quantitative terms. It is, therefore, an intraprofessional agreement, which sometimes has to be a compromise since practicability is important – the methods and terms must be perceived as being adequate and reflecting everyday reality. Sometimes the demand for precision has to be combined with demands for practicability. A standard – whether it concerns a term or a measure – must be
practical, simple, and perceived as meaningful to use; it must have a high degree of acceptance. Describing and measuring the functions of the LUT is not as easy as one might think. In biologic systems with superimposed functional disorders, it is difficult to capture the overall picture purely statistically using simple means. Standardization is based on what is common to patients with a certain type of complaint, even if there are significant differences in other respects when the pathologic picture is described more precisely at an individual level. We often know more about the manifestations of a disease than about its true intrinsic nature. Standardization will therefore be designed primarily to describe secondary manifestations – the consequences (e.g. a detrusor contraction) instead of the primary cause (e.g. a lesion in the nervous system). One problem with standardization of the LUT is that often the symptoms do not go hand in hand with urodynamic findings, which is what we usually measure. There is, therefore, a lack of correlation between subjective and objective measurements. It is clear from the above argument that a standard in itself does not have to express what is true. Standards can be said to express what we believe to be correct, but are not, therefore, necessarily synonymous with what is correct. We endeavor to bridge this discrepancy so that the standard we agree to use is as true as possible.
Application and acceptance of standards Standardization is just as important for day-to-day practice as for scientific studies. Ideally, this should be common ground for researchers, clinicians and others, i.e. all those who need to communicate within the subject area. Information and knowledge are vital tools if agreed standards are to be used by everyone. Quick, effective dissemination guaranteed by established scientific journals with a wide circulation in the target group is one of the prerequisites. Another is that each and every one of us must take standards on board, and adjust our terminology and shape our work to correspond with what has been agreed. A very important link, and one which must not be neglected, is to create understanding through education and training of colleagues in different areas and the staff with whom one is working in this context. It may seem obvious to use (correspondingly) accepted designations for conditions and methods in one’s own laboratory, and to be familiar with, for example, the test–retest variations in one’s analyses for different sexes of different ages. However, most of us need to take a very
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large step in this direction before we can be sure that this really is the case. Current standards must be accepted and used if it is to be possible to compare data from different researchers both within and between studies. Because this is so often not the case, the conclusions from meta-analyses, for example, are often regarded with a touch of skepticism.
Creation and institution of standards First, it is important to create standards around the most frequent diseases/disorders and examination methods. That is why the Standardization Committee of the International Continence Society (ICS) has chosen to work with the major diagnosis groups of women, men, children, the old and frail, and patients with neurogenic functional disorders of the LUT. The most significant methods for diagnosis and followup, both in quantitative and qualitative terms, are, of course, the first to be considered for standardization. Traditional urodynamic investigations can be mentioned in this context, but newer examination methods such as ambulatory urodynamics, imaging, etc. are also relevant. General recommendations under the heading ‘good urodynamic practice’ and signal processing are also important. When we take our clinical diagnostic work into account, it is probably relatively easy to explain why we have ended up with the system as it appears today. Our current definitions and classification originate from clinical practice, and after systematic standardization work and renewal of terms, definitions, classes, methods, and acronyms, they have returned as standards, guidelines, and recommendations to clinical practice and research. If the recommendations or, in some cases, guidelines produced are to be received with respect and used, those doing the work must be experts who are well grounded in their respective fields.
Updating and revising standards There are no set rules or recommendations stating how long a standard should be regarded as valid. Some wellestablished standards are impossible to question (e.g. the length of a meter). In dynamic areas that develop quickly (e.g. computer technology) increased understanding may mean that previously agreed standards need to be replaced relatively often with new ones that are up to date. The demand for change must always be weighed against the need for continuity. To some extent one is, of course, dependent on respecting traditions that have become established within certain fields over a number
of years. This has turned out to be particularly true of our terminology. It also has to be remembered that the introduction of a new standard may make it impossible to make comparisons with historical data. At the same time, it is important that current standards are not perceived as either an expression of rules that are too rigid or a desperate insistence on the old for its own sake. When it comes to setting a standard for the first time, one has greater freedom than when an existing standard needs updating. It is also important that standardization is kept up to date and is considered when new fields are developed, when new technology becomes available, and as the understanding of the causes and manifestations of diseases increases. Renewal always means a simultaneous and recurrent rejuvenation process in the groups working on these questions. Many more people than those who currently take an active interest in standardization will have to do so in the future if we are to have the best possible tools to work with. Involving both young people, who we already know will be responsible for formulating the problems of the future, and more experienced colleagues in this work is the best we can do.
Methods, measurements and terms Ideally, the methods we use should reflect pathologic activity and degree of damage etc., and the findings should agree with the patient’s perception of the whole thing (i.e. symptomatology, level of discomfort and quality-of-life factors). There is often a discrepancy between these measurements, which is why each observation we make must be considered on its own merits, and why we should be careful with regard to making assumptions about correlations that are not proven. Choosing structure and function as the primary basis for a new system of definition and classification of LUT disorders is no different from what is done in other areas of medicine. The analysis of the patient’s situation should ideally not only reflect structure and function in a static way, but also have a dynamic dimension, which in turn refers to changes in both space and time. This is valid for the whole micturition cycle. However, if it is impossible to reflect all pathologic activity with one method, which is usually the case, it is reasonable to demand that what is examined is representative of the disease/disorder or, from the point of view of the method used, really hits the target picture. Regardless of which perspective is preferred – that of the examined or the examiner – the next major problem is whether the methods used block the view between the examiner and the object. We often ascribe a greater 739
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degree of sensitivity and specificity to methods than we have reason to. In reality, however, we often do not know the reproducibility of a method at our own clinic, in our own laboratory or in our own hands. Since we cannot readily establish whether there is a significant change over time unless the observed difference lies outside the test–retest interval, most of us have no way of establishing whether there is a small difference between two instances of measurement. As well as making intraindividual comparisons, interindividual comparisons are also needed, usually with reference to what is normal for the age and sex of the patient in question. Unfortunately, normative data are lacking and, with a few exceptions, we have no validated nomograms for urodynamic investigations.
Normality We know all too little about what is normal when it comes to the LUT. This may seem strange; however, consider the bladder and urethra as an example. We would like to know what is normal from both a quantitative and a qualitative point of view. However, normality can only be described almost solely in qualitative terms such as ‘not leaking’ and ‘emptying completely without difficulty’. As soon as we come to individual measurements in the normal population of both sexes and for different ages we have very few studies to use as a basis. This makes it difficult to draw a boundary between normal and abnormal; the problem becomes particularly difficult when it comes to differentiating between the results of aging and the consequences of disease.
OUTCOME RESEARCH Outcome refers to the result of intervention in a patient or group of patients. Usually the same type of measurement is performed before and after a particular period of a particular treatment; the treatment outcome is compared with the accepted standard treatment for the disease in question and, if possible, a placebo as well. There are variations on this theme. It is now recommended that when performing outcome research on patients with LUT dysfunction, measurements from as many as possible of the following five domains be considered:
• • • • •
the patient’s medical history; quantification of symptoms; anatomic and functional data; quality of life; socioeconomic factors.
Well-developed measurements are not available for all these areas; intensive work is being done to produce good measurements of quality of life for different groups and of the social and economic consequences of LUT dysfunction. The patient’s medical history and experience of the situation have come to control treatment more and more, and our previously rather one-sided focus on anatomic and functional measurements is now being supplemented by consideration of the patient’s symptoms and level of discomfort, as well as quality of life and socioeconomic factors. Our ability to describe what we can offer patients and society in such terms will be vital in determining how well we succeed in maintaining awareness of these disease groups in comparison with other types of disease and dysfunction. In the first three areas listed above there should be plenty of good appropriate measurements that could be recommended and, where appropriate, combined in different indices to capture a pathologic picture. A comprehensive examination of work in the area of incontinence research on men, women, children, the old and frail, and patients with neurogenic disorders has instead revealed an apparent large-scale lack of knowledge in this field. There is a particular lack of knowledge in the pathophysiologic area, i.e. the actual reasons for LUT dysfunction. We also have difficulty differentiating between dysfunction that is due to disease and that which is a consequence of the aging process. In some cases we may come to the conclusion that they are the same and that our present approach is in need of adjustment. We should also acknowledge that we are never, or rarely, able to reverse the course of a disease with our interventions, but are able merely to slow down and, at best, stop its development. Some consequences, such as thickening of the bladder wall if outflow is obstructed, are reversible in many cases, but we never achieve an entirely normal situation. We can provide a partial or complete symptomatic recovery and a partial but incomplete pathophysiologic recovery. We really need to establish a new balance between the organs involved and their control systems, i.e. balance at a point that is different from that if the individual were counted as normal. This approach makes it much easier to see the outcome of treatment in relation to what is possible and reasonable. One should also ask oneself, perhaps first and foremost, what the patient wishes to achieve. For the reasons given above, cure and normalization are not realistic goals for treatment, whereas improvement towards a situation that is perceived as normal by the patient is more achievable. At best, this will be a large improvement; however, in other cases we are looking at small steps forward.
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CLINICAL RESEARCH ASSESSMENT GROUPS On the basis of the arguments above with regard to outcome, it is easy to conclude that we have large gaps in our knowledge. Once we have agreed on how best to conduct outcome research in principle, we need to formulate a plan as to how the missing knowledge is best acquired. This task has been assigned within the ICS to the Clinical Research Assessment groups; these groups correspond to the structure of the outcome groups: one each for women, men, children, the old and frail, and patients with neurogenic LUT dysfunction. There are great opportunities to make an international, multidisciplinary contribution to this area in a logical, structured, and meaningful way. We seem to have had a tendency over the years to contribute pieces to a jigsaw, each of which is nicely shaped and colored, but where the different pieces do not fit together to provide a single, coherent picture. It is for this reason that we should now work together to plan the future picture and the size and shape of the pieces of the LUT puzzle.
Specific questions for each diagnostic group Current recommendations and guidelines are best read in the relevant reports from the Standardization Committee of the ICS, listed at the end of the chapter. The following describes some of the questions with which the Standardization Committee is currently grappling, illustrating some of the issues already raised about drawing boundaries and replacing standards. It is of central importance to characterization of a dysfunctional state in the LUT that both the internal and external characteristics of the disorder/disease are encompassed in the terms we decide to use, and that the methods applied to measurement reflect the same things. Precision requires complete understanding of the nature of the disease in terms of both its pathophysiology and how advanced the disease is. However, we do not have complete information for any of the major diagnostic groups – incontinence, obstruction, and neurogenic disorders – so we cannot be certain that we have used terms which exactly describe the internal and external characteristics of these disorders. In order to throw light on our difficulties and sometimes, failures, examples from each of the three main areas are presented below.
Incontinence Incontinence as a symptom, a sign, and a condition As well as defining urinary incontinence as a social and hygienic problem, we were in the habit of defining
incontinence as a symptom, a sign, and a condition. The first two definitions do not in themselves present a problem but we need to discuss what is meant by incontinence as a condition. Hitherto we meant the underlying pathologic condition or disorder. This way of looking at it was probably incorrect since, from a medical point of view, incontinence is a consequence and not a cause. The condition in itself means, of course, the involuntary passing of urine through the urethra – such a definition by no means refers to the pathologic condition. This means that we needed to redefine the condition of incontinence. Motor and sensory urge incontinence According to the past definition, motor urge incontinence existed when we could detect motor activity urodynamically, usually in the bladder in the form of hyperactivity, combined with the patient’s experiences of the urge to pass urine and urine leakage. If such hyperactivity cannot be detected, we talked about sensory urge incontinence. This was an inappropriate term, however, since urine cannot reasonably pass through the urethra unless motor activity – an increase in pressure in the bladder and/or a decrease in pressure in the urethra – occurs. Logically speaking, urge incontinence should therefore be regarded as motor incontinence in all cases. There are several explanations for this, including the fact that hyperactivity in the bladder does not always occur during cystometric examination, and that we usually measure the pressure ratios in the urethra. A reduction in pressure in the urethra can, of course, be combined with a feeling of the urge to pass urine, but also with incontinence.
Obstruction We have adopted a definition of obstruction in pressure– flow terms, the recommended nomogram being based on the original diagram of Abrams–Griffiths.1 There are other similar classifications that are essentially the same, for example Schäfer’s nomogram.2 These nomograms are probably a simplification of a more complex reality; none of them takes into account the significance of the temporal component, for example. If a patient with symptoms has two consecutive measurements approaching the obstructed range, and we assume that these two observations in the form of plots on the pressure–flow nomogram are significantly different but still within the normal range, this might very well be an indication of an obstruction. The obstruction may not yet be particularly pronounced or developed, but an obstructive process is nevertheless involved. This patient still ends up inside the so-called normal range in the current nomogram. 741
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This is, of course, because our present definition does not take into account a temporal component in the dynamic process of obstruction. What we have at the moment is a static, physical classification of obstruction and non-obstruction. What we need is a biologic and dynamic definition, i.e. a biodynamic definition.
Neurogenic dysfunction We now know that primarily non-neurogenic pathologic conditions in experimental models give rise to neurogenic changes, and neural plasticity is thought to be an important factor in coping with the situation that arises in the case of infravesical obstruction. We suspect that these secondary neurogenic changes are important in terms of pathologic development, but are not sure what role they play. It may be appropriate to consider both primary and secondary neurogenic disorders, primary disorders being diseases of the nervous system that affect the functioning of the LUT, and secondary disorders being those that begin in other organs (e.g. the bladder, urethra or prostate). It also follows that LUT disorders might be regarded as primary or secondary in nature. Future research may provide answers to these questions. For these reasons, the term ‘hyperreflexia’ may be best described more generically as ‘detrusor overactivity’ of neurogenic etiology.
THE FUTURE The importance of broad-based commitment and the pursuit of standardization as a continuous process, with repeated questioning of the terminology used and the methods available, cannot be stressed enough. The more people who contribute to the work on standardization, the better it will be. It does, after all, concern our common use of language and our common methods, i.e. our ability to communicate with each other. To describe LUT disorders and their consequences, we should ideally have a system of definitions, classification, and terminology that is as precise as possible, i.e. a system that reflects the real nature of the disorders in terms of structure and function, and a system that allows quantification of the induced amount of change away from normality. Equally important is that we can characterize the consequences of the disorders in terms of symptoms, behavior, bother, and quality of life, and then also include socioeconomic data. In relation to the pathophysiologic and/or aging processes, however, these factors must be considered as secondary. Our current system for standardization of definitions, classification, and terminology does not fulfill all of the above-mentioned criteria. Some of the difficul-
ties have been highlighted in a series of reports from the Standardisation Committee of the International Continence Society on methodology and terminology, and also in reports on outcome research in patients with LUT dysfunction: Bates et al. (1976, 1977, 1980, 1981), Abrams et al. (1986, 1988, 2002), Rowan et al. (1987), Andersen et al. (1992), Bump et al. (1996), Thuroff et al. (1996), Blaivas et al. (1997a,b), Griffiths et al. (1997), Fonda et al. (1998), Lose et al. (1998, 2002), Mattiasson et al. (1998), Nordling et al. (1998), Stöhrer et al. (1999), van Waalwijk van Door et al. (2000), Sand et al. (2002), Schafer et al. (2002), van Kerrebroeck et al. (2002), van Mastrigt & Griffiths (2004). We need to continually update our thinking and opportunely and carefully revise our standards for characterization of LUT disorders (Table 50.1). Our definitions and classification should be allowed to rest on a firm biologic and pathophysiologic foundation, taking both structure and function into account as well as all parts of the LUT, incorporating the whole micturition cycle:
• A structure/function map should be created. • Measurements of structure and function should be performed, and expressed quantitatively.
• Normality for different age groups of both sexes • • • •
•
should be defined. Correlations between different measures should be made. Patterns of recognition should be used for definition and classification on both an individual and a group level. Temporal and spatial static and dynamic factors should be considered. The patient's history should be matched with the structural/functional findings and taken together with consequences such as symptoms, behavior, bother, quality of life, and socioeconomic factors. Physicians and other certified healthcare professionals should make risk–benefit and cost– benefit analyses on behalf of their patients.
The current system has a historical and traditional basis and has served us well in spite of obvious and not so obvious shortcomings. There is significant basis for adoption of the proposed parameters, and the methods suggested for the integration of definitions, measurements, and disease impact into a more dynamic description in the institution of standards. This may be interpreted as being tantamount to suggesting a new way of characterizing LUT disorders3,4 which would have far-reaching consequences and eventually lead to a new
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Table 50.1.
Considerations for standardization
Baseline data • Age • Gender • General well-being, lifestyle • History of disorder/disease • Physical examination • Pregnancies/deliveries; pelvic surgery • Intercurrent disorders/diseases; metabolic status Structure and function of the lower urinary tract (LUT) (at the cell ± tissue ± structure ± organ ± organ system levels) • All parts of the LUT with support • Innervation and blood supply of the LUT • The whole micturition cycle • Static and dynamic factors • Primary and secondary changes • Quantity (degree) of change Consequences of LUT disease/disorder (at the organism ± individual ± patient ± group ± society levels) • Symptoms • Behavior • Bother • Quality of life • Health economy Diagnosis of the condition • Ability • Accuracy • Methods and techniques • Diagnostic resources • Contribution to therapy (see below) Effect of therapy • Structure and function (see above) • Consequences of disease (see above) • Quality of life • Socioeconomic factors
way to define and classify LUT function. This interpretation would be correct.
REFERENCES 1.
Abrams P, Griffiths DJ. The assessment of prostatic obstruction from urodynamic measurements and from residual urine. Br J Urol 1979;51:129–34.
2.
Schäfer W. The contribution of the bladder outlet to the relation between pressure and flow rate during micturition. In: Hinman F Jr (ed) Benign Prostatic Hypertrophy. New York: Springer-Verlag, 1983; 470–96.
3.
Mattiasson A. Characterisation of lower urinary tract disorders: a new view. Neurourol Urodyn 2001;20:601–21.
4.
Mattiasson A. Classification of lower urinary tract dysfunction. In: Corcos J, Schick E (eds) Textbook of the Neurogenic Bladder. Adults and Children. London: Martin Dunitz, 2004; 469–80.
BIBLIOGRAPHY: REPORTS FROM THE STANDARDIZATION COMMITTEE OF THE ICS 1. Bates P, Bradley WE, Glen E et al. First report on the standardisation of terminology of lower urinary tract function. Urinary incontinence. Procedures related to the evaluation of urine storage: cystometry, urethral closure pressure profile, units of measurements. Br J Urol 1976;48:39–42; Eur Urol 1976;2:274–6; Scand J Urol Nephrol 1976;11:193–6; Urol Int 1976;32:81–7. 2. Bates P, Glen E, Griffiths D et al. Second report on the standardisation of terminology of lower urinary tract function. Procedures related to the evaluation of micturition: flow rate, pressure measurement, symbols. Acta Urol Jpn 1977;27:1563–6; Br J Urol 1977;49:207–10; Eur Urol 1977;3:168–70; Scand J Urol Nephrol 1977;11:197–9. 3. Bates P, Bradley WE, Glen E et al. Third report on the standardisation of terminology of lower urinary tract function. Procedures related to the evaluation of micturition: pressure flow relationships, residual urine. Br J Urol 1980;52:348–59; Eur Urol 1980;6:170–1; Acta Urol Jpn 1980;27:1566–8; Scand J Urol Nephrol 1980;12:191–3. 4. Bates P, Bradley WE, Glen E et al. Fourth report on the standardisation of terminology of lower urinary tract function. Terminology related to neuromuscular dysfunction of the lower urinary tract. Br J Urol 1981;52:333–5; Urology 1981;17:618–20; Scand J Urol Nephrol 1981;15:169– 71; Acta Urol Jpn 1981;27:1568–71. 5. Abrams P, Blaivas JG, Stanton SL et al. Sixth report on the standardisation of terminology of lower urinary tract function. Procedures related to neurophysiological investigations: electromyography, nerve conduction studies, reflex latencies, evoked potentials and sensory testing. World J Urol 1986;4:2–5; Scand J Urol Nephrol 1986;20:161–4. 6. Rowan D, James ED, Kramer AEJL et al. (ICS working party on urodynamic equipment) Urodynamic equipment: technical aspects. J Med Eng Technol 1987;11:57–64. 7.* Abrams P, Blaivas JG, Stanton SL, Andersen JT. The standardisation of terminology of lower urinary tract function. Scand J Urol Nephrol Suppl 1988;114:5–19. 8. Abrams P, Cardozo L, Fall M et al. The standardisation of terminology in lower urinary tract dysfunction. Report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 2002;21:167–78. 9. Andersen JT, Blaivas JG, Cardozo L, Thüroff J. Lower urinary tract rehabilitation techniques: seventh report on the standardization of terminology of lower urinary tract function. Int Urogynecol J 1992;3:75–80. 10.* Bump RC, Mattiasson A, Bø K et al. The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 1996;175:10–7. 11. Thüroff J, Mattiasson A, Andersen JT et al. Standardization of terminology and assessment of functional charac-
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teristics of intestinal urinary reservoirs. Neurourol Urodyn 1996;15:499–511; Br J Urol 1996;78:516–23; Scand J Urol Nephrol 1996;30:349–56. 12. Blaivas JG, Appell RA, Fantl JA et al. Standards of efficacy for evaluation of treatment outcomes in urinary incontinence: recommendations of the Urodynamic Society. Neurourol Urodyn 1997a;16(3):145–7. 13. Blaivas JG, Appell RA, Fantl JA et al. Definition and classification of urinary incontinence: recommendations of the Urodynamic Society. Neurourol Urodyn 1997b;16(3):149–51. 14. Griffiths D, Höfner K, van Mastrigt R et al. Standardization of terminology of lower urinary tract function: pressure–flow studies of voiding, urethral resistance, and urethral obstruction. Neurourol Urodyn 1997;16:1–18.
19. Nordling J, Abrams P, Ameda K et al. Outcome measures for research in treatment of adult males with symptoms of lower urinary tract dysfunction. Neurourol Urodyn 1998,17:263–71. 20. Stöhrer M, Goepel M, Kondo A et al. The standardisation of terminology in neurogenic lower urinary tract dysfunction with suggestions for diagnostic procedures. Neurourol Urodyn 1999;18:139–58. 21. van Waalwijk van Doorn E, Anders K, Khullar V et al. Standardisation of ambulatory urodynamic monitoring: report from the Standardisation Sub-committee of the ICS for ambulatory urodynamic studies. Neurourol Urodyn 2000;19:113–25.
15. Fonda D, Resnick NM, Colling J et al. Outcome measures for research of lower urinary tract dysfunction in frail older people. Neurourol Urodyn 1998;17:273–81.
22. Sand PK, Dmochowski R. Analysis of the standardisation of terminology of lower urinary tract dysfunction: report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 2002;21:167–78.
16. Lose G, Fantl SA, Victor A et al. Outcome measures for research in adult women with symptoms of lower urinary tract dysfunction. Neurourol Urodyn 1998;17:255–62.
23. Schafer W, Abrams P, Liao L et al. Good urodynamic practices: uroflowmetry, filling cystometry, and pressure–flow studies. Neurourol Urodyn 2002;21:261–74.
17. Lose G, Griffiths D, Hosker G et al. Standardisation of urethral pressure measurement: report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 2002;21(3):258–60.
24. van Kerrebroeck P, Abrams P, Chaikin D et al. The standardisation of terminology in nocturia: report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 2002;21:179–83.
18. Mattiasson A, Djurhuus JC, Fonda D et al. Standardization of outcome studies in patients with lower urinary tract dysfunction: a report on general principles from the Standardisation Committee of the International Continence Society. Neurourol Urodyn 1998;17:249–53.
25. van Mastrigt R, Griffiths DJ. ICS standard for digital exchange of urodynamic study data. Neurourol Urodyn 2004;23:280–1. * Reports 7 and 10 are reproduced in Chapters 51 and 52, respectively, of this volume.
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51a The standardization of terminology of lower urinary tract function: Report from the Standardization Subcommittee of the International Continence Society (ICS) Paul Abrams, Linda Cardozo, Magnus Fall, Derek Griffiths, Peter Rosier, Ulf Ulmsten, Philip van Kerrebroeck, Arne Victor, Alan J Wein
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Introduction
LOWER URINARY TRACT SYMPTOMS (LUTS)
This report presents definitions of the symptoms, signs, urodynamic observations, and conditions associated with lower urinary tract dysfunction (LUTD) and urodynamic studies (UDS), for use in all patient groups from children to the elderly. The definitions restate or update those presented in previous International Continence Society Standardisation of Terminology reports (see references) and those recently published on urethral function (Lose et al. 2002) and nocturia (van Kerrebroeck et al. 2002). The published ICS report on the technical aspects of urodynamic equipment (Rowan et al. 1987) is complemented by the new ICS report on urodynamic practice (Schäfer et al. 2002). In addition, there are four published ICS outcome reports (Fonda et al. 1998, Lose et al. 1998, Mattiasson et al. 1998, Nordling et al. 1998). New or changed definitions are all indicated; however, recommendations concerning technique are not included in the main text of this report. The definitions have been written to be compatible with the WHO publication ICIDH-2 (International Classification of Functioning, Disability and Health) published in 2001, and ICD10, the International Classification of Diseases. As far as possible, the definitions are descriptive of observations, without implying underlying assumptions that may later prove to be incorrect or incomplete. By following this principle the International Continence Society (ICS) aims to facilitate comparison of results and enable effective communication by investigators who use urodynamic methods. This report restates the ICS principle that symptoms, signs and conditions are separate categories, and adds a category of urodynamic observations. In addition, terminology related to therapies is included (Andersen et al. 1992). When a reference is made to the whole anatomic organ the vesica urinaria, the correct term is the bladder. When the smooth muscle structure known as the m.detrusor urinae is being discussed, then the correct term is detrusor. It is suggested that acknowledgement of these standards in written publications be indicated by a footnote to the section ‘Methods and Materials’ or its equivalent, to read as follows:
Symptoms are the subjective indicator of a disease or change in condition as perceived by the patient, carer or partner and may lead him/her to seek help from health care professionals. (NEW) Symptoms may either be volunteered or described during the patient interview. They are usually qualitative. In general, lower urinary tract symptoms cannot be used to make a definitive diagnosis. Lower urinary tract symptoms can also indicate pathologies other than lower urinary tract dysfunction, such as urinary infection.
SIGNS SUGGESTIVE OF LOWER URINARY TRACT DYSFUNCTION (LUTD) Signs are observed by the physician, including simple means to verify symptoms and quantify them. (NEW) For example, a classic sign is the observation of leakage on coughing. Observations from frequency volume charts, pad tests, and validated symptom and quality of life questionnaires are examples of other instruments that can be used to verify and quantify symptoms.
URODYNAMIC OBSERVATIONS Urodynamic observations are observations made during urodynamic studies. (NEW) For example, an involuntary detrusor contraction (detrusor overactivity) is a urodynamic observation. In general, an urodynamic observation may have a number of possible underlying causes and does not represent a definitive diagnosis of a disease or condition, and may occur with a variety of symptoms and signs, or in the absence of any symptoms or signs.
CONDITIONS Conditions are defined by the presence of urodynamic observations associated with characteristic symptoms or signs and/or non-urodynamic evidence of relevant pathologic processes. (NEW)
TREATMENT Treatment for lower urinary tract dysfunction: these definitions are from the 7th ICS report on lower urinary tract rehabilitation techniques (Andersen et al. 1992).
Methods, definitions and units conform to the standards recommended by the International Continence Society, except where specifically noted.
1. Lower URINARY TRACT SYMPTOMS (LUTS)
The report covers the following areas:
Lower urinary tract symptoms are defined from the individual’s perspective, who is usually, but not
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necessarily, a patient within the healthcare system. Symptoms are either volunteered by, or elicited from, the individual or may be described by the individual’s caregiver. Lower urinary tract symptoms are divided into three groups: storage, voiding, and postmicturition symptoms.
1.1 Storage symptoms
• Stress urinary incontinence is the complaint of • •
Storage symptoms are experienced during the storage phase of the bladder, and include daytime frequency and nocturia. (NEW)
•
• Increased daytime frequency is the complaint by the
•
• • •
patient who considers that he/she voids too often by day. (NEW) This term is equivalent to pollakisuria used in many countries. Nocturia is the complaint that the individual has to wake at night one or more times to void. (NEW) Urgency is the complaint of a sudden compelling desire to pass urine, which is difficult to defer. (CHANGED) Urinary incontinence is the complaint of any involuntary leakage of urine. (NEW)
In each specific circumstance, urinary incontinence should be further described by specifying relevant factors such as type, frequency, severity, precipitating factors, social impact, effect on hygiene and quality of life, the measures used to contain the leakage, and whether or not the individual seeks or desires help because of urinary incontinence. Urinary leakage may need to be distinguished from sweating or vaginal discharge.
The term night-time frequency differs from that for nocturia, as it includes voids that occur after the individual has gone to bed, but before he/she has gone to sleep; and voids which occur in the early morning which prevent the individual from getting back to sleep as he/she wishes. These voids before and after sleep may need to be considered in research studies, for example, in nocturnal polyuria. If this definition were used, then an adapted definition of daytime frequency would need to be used with it. In infants and small children the definition of urinary incontinence is not applicable. In scientific communications the definition of incontinence in children would need further explanation. The original ICS definition of incontinence, ‘Urinary incontinence is the involuntary loss of urine that is a social or hygienic problem’, relates the complaint to quality of life (QoL) issues. Some QoL instruments have been, and are being, developed in order to assess the impact of both incontinence and other LUTS on QoL.
• • •
involuntary leakage on effort or exertion, or on sneezing or coughing. (CHANGED) Urge urinary incontinence is the complaint of involuntary leakage accompanied by or immediately preceded by urgency. (CHANGED) Mixed urinary incontinence is the complaint of involuntary leakage associated with urgency and also with exertion, effort, sneezing or coughing. (NEW) Enuresis means any involuntary loss of urine. (ORIGINAL) If it is used to denote incontinence during sleep, it should always be qualified with the adjective ‘nocturnal’. Nocturnal enuresis is the complaint of loss of urine occurring during sleep. (NEW) Continuous urinary incontinence is the complaint of continuous leakage. (NEW) Other types of urinary incontinence may be situational, for example the report of incontinence during sexual intercourse, or giggle incontinence. Bladder sensation can be defined, during history taking, by five categories. Normal: the individual is aware of bladder filling and increasing sensation up to a strong desire to void. (NEW) Increased: the individual feels an early and persistent desire to void. (NEW) Reduced: the individual is aware of bladder filling but does not feel a definite desire to void. (NEW) Absent: the individual reports no sensation of bladder filling or desire to void. (NEW) Non-specific: the individual reports no specific bladder sensation, but may perceive bladder filling as abdominal fullness, vegetative symptoms, or spasticity. (NEW)
1.2 Voiding symptoms Voiding symptoms are experienced during the voiding phase. (NEW)
The committee considers the term ‘stress incontinence’ to be unsatisfactory in the English language because of its mental connotations. The Swedish, French and Italian expression ‘effort incontinence’ is preferable; however, words such as ‘effort’ or ‘exertion’ still do not capture some of the common precipitating factors for stress incontinence such as coughing or sneezing. For this reason the term is left unchanged. Urge incontinence can present in different symptomatic forms, for example, as frequent small losses between micturitions, or as a catastrophic leak with complete bladder emptying. These non-specific symptoms are most frequently seen in neurologic patients, particularly those with spinal cord trauma, and in children and adults with malformations of the spinal cord.
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• Slow stream is reported by the individual as his or her
• •
•
• •
perception of reduced urine flow, usually compared to previous performance or in comparison to others. (NEW) Splitting or spraying of the urine stream may be reported. (NEW) Intermittent stream (intermittency) is the term used when the individual describes urine flow which stops and starts, on one or more occasions, during micturition. (NEW) Hesitancy is the term used when an individual describes difficulty in initiating micturition resulting in a delay in the onset of voiding after the individual is ready to pass urine. (NEW) Straining to void describes the muscular effort used to initiate, maintain or improve the urinary stream. (NEW) Terminal dribble is the term used when an individual describes a prolonged final part of micturition, when the flow has slowed to a trickle/dribble. (NEW)
1.3 Postmicturition symptoms
1.6 Genital and lower urinary tract pain Pain, discomfort and pressure are part of a spectrum of abnormal sensations felt by the individual. Pain produces the greatest impact on the patient and may be related to bladder filling or voiding, may be felt after micturition, or be continuous. Pain should also be characterized by type, frequency, duration, precipitating and relieving factors, and by location as defined below:
• Bladder pain is felt suprapubically or retropubically, • • • • •
Postmicturition symptoms are experienced immediately after micturition. (NEW)
• Feeling of incomplete emptying is a self-explanatory term •
for a feeling experienced by the individual after passing urine. (NEW) Postmicturition dribble is the term used when an individual describes the involuntary loss of urine immediately after he or she has finished passing urine, usually after leaving the toilet in men, or after rising from the toilet in women. (NEW)
1.4 Symptoms associated with sexual intercourse Dyspareunia, vaginal dryness, and incontinence are among the symptoms women may describe during or after intercourse. These symptoms should be described as fully as possible. It is helpful to define urine leakage as: during penetration, during intercourse, or at orgasm.
1.5 S ymptoms associated with pelvic organ prolapse The feeling of a lump (‘something coming down’), low backache, heaviness, dragging sensation, or the need to digitally replace the prolapse in order to defecate or micturate, are among the symptoms that women with a prolapse may describe. Suprapubic pressure may be used to initiate or maintain urine flow. The Cred3 maneuver is used by some spinal cord injury patients, and girls with detrusor underactivity sometimes press suprapubically to help empty the bladder.
•
usually increases with bladder filling, and may persist after voiding. (NEW) Urethral pain is felt in the urethra and the individual indicates the urethra as the site. (NEW) Vulval pain is felt in and around the external genitalia. (NEW) Vaginal pain is felt internally, above the introitus. (NEW) Scrotal pain may or may not be localized, for example to the testis, epididymis, cord structures or scrotal skin. (NEW) Perineal pain is felt: in the female, between the posterior fourchette (posterior lip of the introitus) and the anus; and in the male, between the scrotum and the anus. (NEW) Pelvic pain is less well defined than, for example, bladder, urethral or perineal pain, and is less clearly related to the micturition cycle or to bowel function, and is not localized to any single pelvic organ. (NEW)
1.7 G enitourinary pain syndromes and symptom syndromes suggestive of LUTD Syndromes describe constellations, or varying combinations of symptoms, but cannot be used for precise diagnosis. The use of the word syndrome can only be justified if there is at least one other symptom in addition to the symptom used to describe the syndrome. In scientific communications the incidence of individual symptoms within the syndrome should be stated, in addition to the number or individuals with the syndrome. The syndromes described are functional abnormalities for which a precise cause has not been defined. It is presumed that routine assessment (history taking, physical examination, and other appropriate investigations) The terms ‘strangury’, ‘bladder spasm’, and ‘dysuria’ are difficult to define and of uncertain meaning and should not be used in relation to lower urinary tract dysfunction, unless a precise meaning is stated. Dysuria literally means ‘abnormal urination’, and is used correctly in some European countries. However, it is often used to describe the stinging/burning sensation characteristic of urinary infection. It is suggested that these descriptive words should not be used in future.
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has excluded obvious local pathologies, such as those that are infective, neoplastic, metabolic or hormonal in nature. 1.7.1 Genitourinary pain syndromes These syndromes are all chronic in their nature. Pain is the major complaint but concomitant complaints are of lower urinary tract, bowel, sexual or gynecologic nature.
• Painful bladder syndrome is the complaint of
•
•
•
•
•
suprapubic pain related to bladder filling, accompanied by other symptoms such as increased daytime and night-time frequency, in the absence of proven urinary infection or other obvious pathology. (NEW) Urethral pain syndrome is the occurrence of recurrent episodic urethral pain, usually on voiding, with daytime frequency and nocturia, in the absence of proven infection or other obvious pathology. (NEW) Vulval pain syndrome is the occurrence of persistent or recurrent episodic vaginal pain, which is either related to the micturition cycle or associated with symptoms suggestive of urinary tract or sexual dysfunction. There is no proven infection or other obvious pathology. (NEW)10 Vaginal pain syndrome is the occurrence of persistent or recurrent episodic vaginal pain which is associated with symptoms suggestive of urinary tract or sexual dysfunction. There is no proven vaginal infection or other obvious pathology. Scrotal pain syndrome is the occurrence of persistent or recurrent episodic scrotal pain which is associated with symptoms suggestive of urinary tract or sexual dysfunction. There is no proven epididimo-orchitis or other obvious pathology. Perineal pain syndrome is the occurrence of persistent or recurrent episodic perineal pain, which is either related to the micturition cycle or associated with symptoms suggestive of urinary tract or sexual dysfunction. There is no proven infection or other obvious pathology. (NEW)11
The ICS believes this to be a preferable term to ‘interstitial cystitis’. Interstitial cystitis is a specific diagnosis and requires confirmation by typical cystoscopic and histologic features. In the investigation of bladder pain it may be necessary to exclude conditions such as carcinoma in situ and endometriosis.
• Pelvic pain syndrome is the occurrence of persistent or recurrent episodic pelvic pain associated with symptoms suggestive of lower urinary tract, sexual, bowel or gynecologic dysfunction. There is no proven infection or other obvious pathology. (NEW) 1.7.2 S ymptom syndromes suggestive of lower urinary tract dysfunction In clinical practice, empirical diagnoses are often used as the basis for initial management after assessing the individual’s lower urinary tract symptoms, physical findings and the results of urinalysis and other indicated investigations.
• Urgency, with or without urge incontinence, usually with frequency and nocturia, can be described as the overactive bladder syndrome, urge syndrome or urgency– frequency syndrome. (NEW) These symptom combinations are suggestive of urodynamically demonstrable detrusor overactivity, but can be due to other forms of urethrovesical dysfunction. These terms can be used if there is no proven infection or other obvious pathology.
• Lower urinary symptoms suggestive of bladder outlet obstruction is a term used when a man complains predominantly of voiding symptoms in the absence of infection or obvious pathology other than possible causes of outlet obstruction. (NEW)12
2. S IGNS SUGGESTIVE OF LOWER URINARY TRACT DYSFUNCTION (LUTD) 2.1 M easuring the frequency, severity and impact of lower urinary tract symptoms Asking the patient to record micturitions and symptoms13 for a period of days provides invaluable information. The recording of micturition events can be in three main forms:
• Micturition time chart: this records only the times of •
micturitions, day and night, for at least 24 hours. (NEW) Frequency volume chart (FVC): this records the volumes voided as well as the time of each micturition, day and night, for at least 24 hours. (CHANGED)
10 The ICS suggests that the term vulvodynia (vulva-pain) should not be used, as it leads to confusion between single symptom and a syndrome.
12 In women, voiding symptoms are usually thought to suggest detrusor underactivity rather than bladder outlet obstruction.
11 The ICS suggests that, in men, the term prostatodynia (prostatepain) should not be used as it leads to confusion between a single symptom and a syndrome.
13 Validated questionnaires are useful for recording symptoms, their frequency, severity, and both, and the impact of LUTS on QoL. The instrument used should be specified.
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• Bladder diary: this records the times of micturitions and voided volumes, incontinence episodes, pad usage and other information such as fluid intake, the degree of urgency, and the degree of incontinence. (NEW)14 The following measurements can be abstracted from frequency volume charts and bladder diaries:
• Daytime frequency is the number of voids recorded
• • •
during waking hours and includes the last void before sleep and the first void after waking and rising in the morning. (NEW) Nocturia is the number of voids recorded during a night’s sleep: each void is preceded and followed by sleep. (NEW) 24-hour frequency is the total number of daytime voids and episodes of nocturia during a specified 24-hour period. (NEW) 24-hour production is measured by collecting all urine for 24 hours. (NEW)
This is usually commenced after the first void produced after rising in the morning, and is completed by including the first void on rising the following morning.
• Polyuria is defined as the measured production of
•
•
more than 2.8 liters of urine in 24 hours in adults. It may be useful to look at output over shorter time frames (van Kerrebroeck et al., 2002). (NEW)15 Nocturnal urine volume is defined as the total volume of urine passed between the times the individual goes to bed with the intention of sleeping and the time of waking with the intention of rising. (NEW) Therefore, it excludes the last void before going to bed but includes the first void after rising in the morning. Nocturnal polyuria is present when an increased proportion of the 24-hour output occurs at night (normally during the 8 hours while the patient is in bed). (NEW) The night-time urine output excludes
14 It is useful to ask the individual to make an estimate of liquid intake. This may be done precisely by measuring the volume of each drink or crudely by asking how many drinks are taken in a 24-hour period. If the individual eats significant quantities of water-containing foods (vegetables, fruit, salads) then an appreciable effect on urine production will result. The time that diuretic therapy is taken should be marked on a chart or diary. 15 The causes of polyuria are various and reviewed elsewhere but include habitual excess fluid intake. The figure of 2.8 is based on a 70 kg person voiding >40 ml/kg.
•
the last void before sleep but includes the first void in the morning.16 Maximum voided volume is the largest volume of urine voided during a single micturition and is determined either from the frequency/volume chart or bladder diary. (NEW)
The maximum, mean and minimum voided volumes over the period of recording may be stated.17
2.2 Physical examination Physical examination is essential in the assessment of all patients with lower urinary tract dysfunction. It should include abdominal, pelvic, perineal and a focused neurologic examination. For patients with possible neurogenic lower urinary tract dysfunction, a more extensive neurologic examination is needed. 2.2.1 Abdominal The bladder may be felt by abdominal palpation or by suprapubic percussion. Pressure suprapubically or during bimanual vaginal examination may induce a desire to pass urine. 2.2.2 Perineal/genital inspection This allows the description of the skin (e.g. the presence of atrophy or excoriation), any abnormal anatomic features, and the observation of incontinence.
• Urinary incontinence (the sign) is defined as urine •
leakage seen during examination: this may be urethral or extraurethral. Stress urinary incontinence is the observation of involuntary leakage from the urethra, synchronous with exertion/effort, or sneezing or coughing. (CHANGED)18
16 The normal range of nocturnal urine production differs with age and the normal ranges remain to be defined. Therefore, nocturnal polyuria is present when greater than 20% (young adults) to 33% (over 65 years) is produced at night. Hence the precise definition is dependent on age. 17 The term ‘functional bladder capacity’ is no longer recommended as ‘voided volume’ is a clearer and less confusing term, particularly if qualified (e.g. ‘maximum voided volume’). If the term bladder capacity is used, in any situation, it implies that this has been measured in some way, if only by abdominal ultrasound. In adults, voided volumes vary considerably. In children, the ‘expected volume’ may be calculated from the formula (30 + (age in years × 30) in ml). Assuming no residual urine, this will be equal to the ‘expected bladder capacity’. 18 Coughing may induce a detrusor contraction, hence the sign of stress incontinence is only a reliable indication of urodynamic stress incontinence when leakage occurs synchronously with the first proper cough and stops at the end of that cough.
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Stress leakage is presumed to be due to raised abdominal pressure.
• Extraurethral incontinence is defined as the observation •
of urine leakage through channels other than the urethra. (ORIGINAL) Uncategorized incontinence is the observation of involuntary leakage that cannot be classified into one of the above categories on the basis of signs and symptoms. (NEW)
2.2.3 Vaginal examination Vaginal examination allows the description of observed and palpable anatomic abnormalities and the assessment of pelvic floor muscle function, as described in the ICS report on pelvic organ prolapse. The definitions given are simplified versions of the definitions in that report. (Bump et al. 1996)
• Pelvic organ prolapse is defined as the descent of one or more of: the anterior vaginal wall, the posterior vaginal wall, and the apex of the vagina (cervix/ uterus) or vault (cuff) after hysterectomy. Absence of prolapse is defined as stage 0 support; prolapse can be staged from stage I to stage IV. (NEW) Pelvic organ prolapse can occur in association with urinary incontinence and other lower urinary tract dysfunction, and may on occasion mask incontinence.
• Anterior vaginal wall prolapse is defined as descent
•
•
of the anterior vagina so that the urethrovesical junction (a point 3 cm proximal to the external urinary meatus) or any anterior point proximal to this is less than 3 cm above the plane of the hymen. (CHANGED) Prolapse of the apical segment of the vagina is defined as any descent of the vaginal cuff scar (after hysterectomy) or cervix below a point which is 2 cm less than the total vaginal length above the plane of the hymen. (CHANGED) Posterior vaginal wall prolapse is defined as any descent of the posterior vaginal wall so that a midline point on the posterior vaginal wall 3 cm above the level of the hymen, or any posterior point proximal to this, is less than 3 cm above the plane of the hymen. (CHANGED)
2.2.4 Pelvic floor muscle function This can be qualitatively defined by the tone at rest and the strength of a voluntary or reflex contraction as strong, weak or absent, or by a validated grading system
(e.g. Oxford 1–5). A pelvic muscle contraction may be assessed by visual inspection, by palpation, electromyography or perineometry. Factors to be assessed include strength, duration, displacement, and repeatability. 2.2.5 Rectal examination Rectal examination allows the description of observed and palpable anatomic abnormalities and is the easiest method of assessing pelvic floor muscle function in children and men. In addition, rectal examination is essential in children with urinary incontinence to rule out fecal impaction.
• Pelvic floor muscle function can be qualitatively defined, during rectal examination, by the tone at rest and the strength of a voluntary contraction, as strong, weak or absent. (NEW)
2.3 Pad testing Pad testing may be used to quantify the amount of urine lost during incontinence episodes, and methods range from a short provocative test to a 24-hour pad test.
3. UROD YNAMIC OBSERVATIONS AND CONDITIONS 3.1 Urodynamic techniques There are two principal methods of urodynamic investigation:
• Conventional urodynamic studies normally take place
•
in the urodynamic laboratory and usually involve artificial bladder filling. (NEW) − artificial bladder filling is defined as filling the bladder, via a catheter, with a specified liquid at a specified rate. (NEW) Ambulatory urodynamic studies are defined as a functional test of the lower urinary tract, utilizing natural filling, and reproducing the subject’s everyday activities.19 − natural filling means that the bladder is filled by the production of urine rather than by an artificial medium.
Both filling cystometry and pressure flow studies of voiding require the following measurements:
19 The term ambulatory urodynamics is used to indicate that monitoring usually takes place outside the urodynamic laboratory, rather than the subject’s mobility using natural filling.
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• Intravesical pressure is the pressure within the bladder. •
•
(ORIGINAL) Abdominal pressure is taken to be the pressure surrounding the bladder. In current practice it is estimated from rectal, vaginal or, less commonly, from extraperitoneal pressure or a bowel stoma. The simultaneous measurement of abdominal pressure is essential for the interpretation of the intravesical pressure trace. (ORIGINAL) Detrusor pressure is that component of intravesical pressure that is created by forces in the bladder wall (passive and active). It is estimated by subtracting abdominal pressure from intravesical pressure. (ORIGINAL)
3.2 Filling cystometry The word ‘cystometry’ is commonly used to describe the urodynamic investigation of the filling phase of the micturition cycle. To eliminate confusion the following definitions are proposed:
3.2.1 Bladder sensation during filling cystometry
• Normal bladder sensation can be judged by three
•
•
• •
• Filling cystometry is the method by which the pressure/ volume relationship of the bladder is measured during bladder filling. (ORIGINAL) The filling phase starts when filling commences and ends when the patient and urodynamicist decide that ‘permission to void’ has been given.20 Bladder and urethral function, during filling, need to be defined separately. The rate at which the bladder is filled is divided into:
• Physiologic filling rate is defined as a filling rate less
•
than the predicted maximum – predicted maximum body weight in kg divided by 4, expressed as ml/min (17). (CHANGED) Non-physiologic filling rate is defined as a filling rate greater than the predicted maximum – predicted maximum body weight in kg divided by 4 expressed as ml/min (Klevmark 1999). (CHANGED)
Bladder storage function should be described according to bladder sensation, detrusor activity, bladder compliance, and bladder capacity.21 20 The ICS no longer wishes to divide filling rates into slow, medium, and fast. In practice, almost all investigations are performed using medium filling rates, which have a wide range. It may be more important during investigations to consider whether or not the filling rate used during conventional urodynamic studies can be considered physiologic. 21 While bladder sensation is assessed during filling cystometry, the assumption that it is sensation from the bladder alone, without urethral or pelvic components, may be false.
• • •
• • •
defined points noted during filling cystometry and evaluated in relation to the bladder volume at that moment and in relation to the patient’s symptomatic complaints. First sensation of bladder filling is the feeling the patient has, during filling cystometry, when he/she first becomes aware of the bladder filling. (NEW) First desire to void is defined as the feeling, during filling cystometry, that would lead the patient to pass urine at the next convenient moment, but voiding can be delayed if necessary. (CHANGED) Strong desire to void is defined, during filling cystometry, as a persistent desire to void without the fear of leakage. (ORIGINAL) Increased bladder sensation is defined, during filling cystometry, as an early first sensation of bladder filling (or an early desire to void) and/or an early strong desire to void, which occurs at low bladder volume and which persists. (NEW)22 Reduced bladder sensation is defined, during filling cystometry, as diminished sensation throughout bladder filling. (NEW) Absent bladder sensation means that, during filling cystometry, the individual has no bladder sensation. (NEW) Non-specific bladder sensations, during filling cystometry, may make the individual aware of bladder filling, for example, abdominal fullness or vegetative symptoms. (NEW) Bladder pain, during filling cystometry, is a selfexplanatory term, and is an abnormal finding. (NEW) Urgency, during filling cystometry, is a sudden compelling desire to void. (NEW)23 The vesical/urethral sensory threshold is defined as the least current that consistently produces a sensation, perceived by the subject during stimulation at the site under investigation (Andersen et al. 1992). (ORIGINAL)
22 The assessment of the subject’s bladder sensation is subjective, and it is not, for example, possible to quantify ‘low bladder volume’ in the definition of ‘increased bladder sensation’. 23 The ICS no longer recommends the terms ‘motor urgency’ and ‘sensory urgency’. These terms are often misused and have little intuitive meaning. Furthermore, it may be simplistic to relate urgency just to the presence or absence of detrusor overactivity when there is usually a concomitant fall in urethral pressure.
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3.2.2 Detrusor function during filling cystometry In everyday life the individual attempts to inhibit detrusor activity until he or she is in a position to void. Therefore, when the aims of the filling study have been achieved, and when the patient has a desire to void, normally the ‘permission to void’ is given (see ‘Filling cystometry’, above). That moment is indicated on the urodynamic trace and all detrusor activity before this ‘permission’ is defined as ‘involuntary detrusor activity’.
• Normal detrusor function: allows bladder filling with
•
• •
•
little or no change in pressure. No involuntary phasic contractions occur despite provocation. (ORIGINAL) Detrusor overactivity is an urodynamic observation characterized by involuntary detrusor contractions during the filling phase, which may be spontaneous or provoked. (CHANGED)24 There are certain patterns of detrusor overactivity: Phasic detrusor overactivity is defined by a characteristic waveform, and may or may not lead to urinary incontinence. (NEW)25 Terminal detrusor overactivity is defined as a single involuntary detrusor contraction occurring at cystometric capacity, which cannot be suppressed, and results in incontinence, usually resulting in bladder emptying (voiding). (NEW)26 Detrusor overactivity incontinence is incontinence due to an involuntary detrusor contraction. (NEW)
In a patient with normal sensation, urgency is likely to be experienced just before the leakage episode.27 Detrusor overactivity may also be qualified, when possible, according to cause; for example:
• Neurogenic detrusor overactivity when there is a relevant neurologic condition.
24 There is no lower limit for the amplitude of an involuntary detrusor contraction but confident interpretation of low pressure waves (amplitude smaller than 5 cmH2O) depends on ‘high quality’ urodynamic technique. The phrase ‘which the patient cannot completely suppress’ has been deleted from the old definition. 25 Phasic detrusor contractions are not always accompanied by any sensation, or may be interpreted as a first sensation of bladder filling, or as a normal desire to void. 26 ‘Terminal detrusor overactivity’ is a new ICS term: it is typically associated with reduced bladder sensation, for example in the elderly stroke patient when urgency may be felt as the voiding contraction occurs. However, in complete spinal cord injury patients there may be no sensation whatsoever. 27 ICS recommends that the terms ‘motor urge incontinence’ and ‘reflex incontinence’ should no longer be used as they have no intuitive meaning and are often misused.
This term replaces the term ‘detrusor hyperreflexia’. (NEW)
• Idiopathic detrusor overactivity when there is no defined cause. (NEW) This term replaces ‘detrusor instability’.28 In clinical and research practice, the extent of neurologic examination/investigation varies. It is likely that the proportion of neurogenic:idiopathic detrusor overactivity will increase if a more complete neurologic assessment is carried out. Other patterns of detrusor overactivity are seen; for example, the combination of phasic and terminal detrusor overactivity, and the sustained high-pressure detrusor contractions seen in spinal cord injury patients when attempted voiding occurs against a dyssynergic sphincter.
• Provocative maneuvers are defined as techniques used during urodynamics in an effort to provoke detrusor overactivity; for example, rapid filling, use of cooled or acid medium, postural changes, and hand washing. (NEW) 3.2.3 Bladder compliance during filling cystometry
• Bladder compliance describes the relationship between change in bladder volume and change in detrusor pressure. (CHANGED)29 Compliance is calculated by dividing the volume change (∆V) by the change in detrusor pressure (∆pdet) during that change in bladder volume (C = V.∆pdet). It is expressed in ml/cmH2O. A variety of means of calculating bladder compliance has been described. The ICS recommends that two standard points should be used for compliance calculations: the investigator may wish to define additional points. The standards points are: 1. The detrusor pressure at the start of bladder filling and the corresponding bladder volume (usually zero), and
28 The terms ‘detrusor instability’ and ‘detrusor hyperreflexia’ were both used as generic terms, in the English speaking world and in Scandinavia, prior to the first ICS report in 1976. As a compromise, they were allocated to idiopathic and neurogenic overactivity, respectively. As there is no real logic or intuitive meaning to the terms, the ICS believes they should be abandoned. 29 The observation of reduced bladder compliance during conventional filling cystometry is often related to relatively fast bladder filling: the incidence of reduced compliance is markedly lower if the bladder is filled at physiologic rates, as in ambulatory urodynamics.
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2. The detrusor pressure (and corresponding bladder volume) at cystometric capacity or immediately before the start of any detrusor contraction that causes significant leakage (and therefore causes the bladder volume to decrease, affecting compliance calculation). Both points are measured excluding any detrusor contraction. 3.2.4 Bladder capacity: during filling cystometry • Cystometric capacity is the bladder volume at the end of the filling cystometrogram, when ‘permission to void’ is usually given. The end point should be specified, for example, if filling is stopped when the patient has a normal desire to void. The cystometric capacity is the volume voided together with any residual urine. (CHANGED)30 • Maximum cystometric capacity, in patients with normal sensation, is the volume at which the patient feels he/she can no longer delay micturition (has a strong desire to void). (ORIGINAL) • Maximum anesthetic bladder capacity is the volume to which the bladder can be filled under deep general or spinal anesthetic, and should be qualified according to the type of anesthesia used, the speed of filling, the length of time of filling, and the pressure at which the bladder is filled. (CHANGED) 3.2.5 Urethral function during filling cystometry The urethral closure mechanism during storage may be competent or incompetent.
• Normal urethral closure mechanism maintains a positive
• •
urethral closure pressure during bladder filling even in the presence of increased abdominal pressure, although it may be overcome by detrusor overactivity. (CHANGED) Incompetent urethral closure mechanism is defined as one which allows leakage of urine in the absence of a detrusor contraction (ORIGINAL) Urethral relaxation incontinence is defined as leakage due to urethral relaxation in the absence of
30 In certain types of dysfunction, the cystometric capacity cannot be defined in the same terms. In the absence of sensation, the cystometric capacity is the volume at which the clinician decides to terminate filling. The reason(s) for terminating filling should be defined, e.g. high detrusor filling pressure, large infused volume or pain. If there is uncontrollable voiding, it is the volume at which this begins. In the presence of sphincter incompetence the cystometric capacity may be significantly increased by occlusion of the urethra, e.g. by Foley catheter.
•
raised abdominal pressure or detrusor overactivity. (NEW)31 Urodynamic stress incontinence is noted during filling cystometry, and is defined as the involuntary leakage of urine during increased abdominal pressure, in the absence of a detrusor contraction. (CHANGED)
Urodynamic stress incontinence is now the preferred term to ‘genuine stress incontinence’.32 3.2.6 Assessment of urethral function during filling cystometry • Urethral pressure measurement − Urethral pressure is defined as the fluid pressure needed to just open a closed urethra. (ORIGINAL) − The urethral pressure profile is a graph indicating the intraluminal pressure along the length of the urethra. (ORIGINAL) − The urethral closure pressure profile is given by the subtraction of intravesical pressure from urethral pressure. (ORIGINAL) − Maximum urethral pressure is the maximum pressure of the measured profile. (ORIGINAL) − Maximum urethral closure pressure (MUCP) is the maximum difference between the urethral pressure and the intravesical pressure. (ORIGINAL) − Functional profile length is the length of the urethra along which the urethral pressure exceeds intravesical pressure in women. − Pressure ‘transmission’ ratio is the increment in urethral pressure on stress as a percentage of the simultaneously recorded increment in intravesical pressure. • Abdominal leak point pressure is the intravesical pressure at which urine leakage occurs due to
31 Fluctuations in urethral pressure have been defined as the ‘unstable urethra’. However, the significance of the fluctuations and the term itself lack clarity and the term is not recommended by the ICS. If symptoms are seen in association with a decrease in urethral pressure, a full description should be given. 32 In patients with stress incontinence, there is a spectrum of urethral characteristics ranging from a highly mobile urethra with good intrinsic function to an immobile urethra with poor intrinsic function. Any delineation into categories such as ‘urethral hypermobility’ and ‘intrinsic sphincter deficiency’ may be simplistic and arbitrary, and requires further research.
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•
increased abdominal pressure in the absence of a detrusor contraction. (NEW)33 Detrusor leak point pressure is defined as the lowest detrusor pressure at which urine leakage occurs in the absence of either a detrusor contraction or increased abdominal pressure. (NEW)34
• Maximum flow rate is the maximum measured •
3.3 Pressure flow studies
•
Voiding is described in terms of detrusor and urethral function and assessed by measuring urine flow rate and voiding pressures.
•
• Pressure flow studies of voiding are the method by which the relationship between pressure in the bladder and urine flow rate is measured during bladder emptying. (ORIGINAL) The voiding phase starts when ‘permission to void’ is given or when uncontrollable voiding begins, and ends when the patient considers voiding has finished. 3.3.1 Measurement of urine flow Urine flow is defined either as continuous, that is without interruption, or as intermittent, when an individual states that the flow stops and starts during a single visit to the bathroom in order to void. The continuous flow curve is defined as a smooth, arc-shaped curve or fluctuating when there are multiple peaks during a period of continuous urine flow.35
• Flow rate is defined as the volume of fluid expelled •
via the urethra per unit time. It is expressed in ml/s. (ORIGINAL) Voided volume is the total volume expelled via the urethra. (ORIGINAL)
•
value of the flow rate after correction for artifacts. (CHANGED) Voiding time is total duration of micturition, i.e. includes interruptions. When voiding is completed without interruption, voiding time is equal to flow time. (ORIGINAL). Flow time is the time over which measurable flow actually occurs. (ORIGINAL) Average flow rate is voided volume divided by flow time. The average flow should be interpreted with caution if flow is interrupted or there is a terminal dribble. (CHANGED) Time to maximum flow is the elapsed time from onset of flow to maximum flow. (ORIGINAL)
3.3.2 P ressure measurements during pressure flow studies (PFS) The following measurements are applicable to each of the pressure curves: intravesical, abdominal, and detrusor pressure.
• Premicturition pressure is the pressure recorded • •
immediately before the initial isovolumetric contraction. (ORIGINAL) Opening pressure is the pressure recorded at the onset of urine flow (consider time delay). (ORIGINAL) Opening time is the elapsed time from initial rise in detrusor pressure to onset of flow. (ORIGINAL)
This is the initial isovolumetric contraction period of micturition. Flow measurement delay should be taken into account when measuring opening time.
• Maximum pressure is the maximum value of the measured pressure. (ORIGINAL)
• Pressure at maximum flow rate is the lowest pressure 33 The leak pressure point should be qualified according to the site of pressure measurement (rectal, vaginal or intravesical) and the method by which pressure is generated (cough or Valsalva). Leak point pressures may be calculated in three ways from the three different baseline values which are in common use: zero (the true zero of intravesical pressure), the value of pves measured at zero bladder volume, or the value of pves immediately before the cough or Valsalva (usually at 200 or 300 ml bladder capacity). The baseline used and the baseline pressure should be specified. 34 Detrusor leak point pressure has been used most frequently to predict upper tract problems in neurologic patients with reduced bladder compliance. ICS has defined it ‘in the absence of a detrusor contraction’ although others will measure DLPP during involuntary detrusor contractions. 35 The precise shape of the flow curve is decided by detrusor contractility, the presence of any abdominal straining, and by the bladder outlet. (11).
• • •
recorded at maximum measured flow rate. (ORIGINAL) Closing pressure is the pressure measured at the end of measured flow. (ORIGINAL) Minimum voiding pressure is the minimum pressure during measurable flow. This is not necessarily equal to either the opening or closing pressures. Flow delay is the time delay between a change in bladder pressure and the corresponding change in measured flow rate.
3.3.3 Detrusor function during voiding
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Normal voiding is achieved by a voluntarily initiated continuous detrusor contraction that leads to complete bladder emptying within a normal time span, and in the absence of obstruction. For a given detrusor contraction, the magnitude of the recorded pressure rise will depend on the degree of outlet resistance. (ORIGINAL)
• Abnormal detrusor activity can be subdivided: − Detrusor underactivity is defined as a contraction
− −
of reduced strength and/or duration, resulting in prolonged bladder emptying and/or a failure to achieve complete bladder emptying within a normal time span. (ORIGINAL) Acontractile detrusor is one that cannot be demonstrated to contract during urodynamic studies. (ORIGINAL)36 Post-void residual (PVR) is defined as the volume of urine left in the bladder at the end of micturition. (ORIGINAL)37
3.3.4 Urethral function during voiding Normal urethral function during voiding is defined as a urethra that opens, and is continuously relaxed to allow the bladder to be emptied at a normal pressure. (CHANGED) Abnormal urethral function may be due to either obstruction to urethral overactivity, or a urethra that cannot open due to anatomic abnormality, such as an enlarged prostate or a urethral stricture.
• Bladder outlet obstruction is the generic term for
•
obstruction during voiding and is characterized by increased detrusor pressure and reduced urine flow rate. It is usually diagnosed by studying the synchronous values of flow rate and detrusor pressure. (CHANGED)38 Dysfunctional voiding is defined as an intermittent and/or fluctuating flow rate due to involuntary intermittent contractions of the periurethral striated
36 A normal detrusor contraction will be recorded as: a high-pressure if there is high outlet resistance, normal pressure if there is normal outlet resistance, or low pressure if urethral resistance is low. 37 If after repeated free flowmetry no residual urine is demonstrated, then the finding of residual urine during urodynamic studies should be considered an artifact, due to the circumstances of the test. 38 Bladder outlet obstruction has been defined for men but, as yet, not adequately in women and children.
•
•
muscle during voiding, in neurologically normal individuals. (CHANGED)39 Detrusor sphincter dyssynergia is defined as a detrusor contraction concurrent with an involuntary contraction of the urethral and/or periurethral striated muscle. Occasionally flow may be prevented altogether. (ORIGINAL)40 Non-relaxing urethral sphincter obstruction usually occurs in individuals with a neurologic lesion and is characterized by a non-relaxing, obstructing urethra, resulting in reduced urine flow. (NEW)41
4. CONDITIONS • Acute retention of urine is defined as a painful, •
palpable or percussable bladder, when the patient is unable to pass any urine. (NEW)42 Chronic retention of urine is defined as a non-painful bladder, which remains palpable or percussable after the patient has passed urine. Such patients may be incontinent. (NEW)43
39 Although dysfunctional voiding is not a very specific term, it is preferred to terms such as ‘non-neurogenic neurogenic bladder’. Other terms such as ‘idiopathic detrusor sphincter dyssynergia’, or ‘sphincter overactivity voiding dysfunction’, may be preferable. However, the term dysfunctional voiding is very well established. The condition occurs most frequently in children. While it is felt that pelvic floor contractions are responsible, it is possible that the intraurethral striated muscle may be important. 40 Detrusor sphincter dyssynergia typically occurs in patients with a suprasacral lesion, for example after high spinal cord injury, and is uncommon in lesions of the lower cord. Although the urethral and periurethral striated muscles are usually held responsible, the smooth muscle of the bladder neck or urethra may also be responsible. 41 Non-relaxing sphincter obstruction is found in sacral and infrasacral lesions such as meningomyelocele, and after radical pelvic surgery. In addition. there is often urodynamic stress incontinence during bladder filling. This term replaces ‘isolated distal sphincter obstruction’. 42 Although acute retention is usually thought of as painful, in certain circumstances pain may not be a presenting feature, for example when due to prolapsed intervertebral disk, postpartum, or after regional anesthesia such as an epidural anesthetic. The retention volume should be significantly greater than the expected normal bladder capacity. In patients after surgery, due to bandaging of the lower abdomen or abdominal wall pain, it may be difficult to detect a painful, palpable or percussable bladder. 43 The ICS no longer recommends the term ‘overflow incontinence’. This term is considered confusing and lacking a convincing definition. If used, a precise definition and any associated pathophysiology, such as reduced urethral function, or detrusor overactivity/low bladder compliance, should be stated. The term chronic retention excludes transient voiding difficulty, for example after surgery for stress incontinence, and implies significant residual urine; a minimum figure of 300 ml has been previously mentioned.
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• Benign prostatic obstruction is a form of bladder outlet
• •
obstruction; it may be diagnosed when the cause of outlet obstruction is known to be benign prostatic enlargement, due to histologic benign prostatic hyperplasia. (NEW) Benign prostatic hyperplasia is a term used (and reserved for) the typical histologic pattern, which defines the disease. (NEW) Benign prostatic enlargement is defined as prostatic enlargement due to histologic benign prostatic hyperplasia. The term ‘prostatic enlargement’ should be used in the absence of prostatic histology. (NEW)
5. TREATMENT The following definitions were published in the 7th ICS report on lower urinary tract rehabilitation techniques (3) and remain in their original form.
5.1 Lower urinary tract rehabilitation This is defined as non-surgical, non-pharmacologic treatment for lower urinary tract function and includes:
• Pelvic floor training is defined as repetitive selective •
•
voluntary contraction and relaxation of specific pelvic floor muscles. Biofeedback is the technique by which information about a normally unconscious physiologic process is presented to the patient and/or the therapist as a visual, auditory or tactile signal. Behavioral modification is defined as the analysis and alteration of the relationship between the patient’s symptoms and his or her environment for the treatment of maladaptive voiding patterns.
This may be achieved by modification of the behavior and/or environment of the patient.
5.3.1 Intermittent (in/out) catheterization This is defined as drainage or aspiration of the bladder or a urinary reservoir with subsequent removal of the catheter. The following types of intermittent catheterization are defined:
• Intermittent self-catheterization is performed by the patient himself/herself.
• Intermittent catheterization is performed by an • •
attendant (e.g. doctor, nurse or relative). Clean intermittent catheterization: use of a clean technique. This implies ordinary washing techniques and use of disposable or cleansed reusable catheters. Aseptic intermittent catheterization: use of a sterile technique. This implies genital disinfection and the use of sterile catheters and instruments/gloves.
5.3.2 Indwelling catheterization This describes an indwelling catheter that remains in the bladder, urinary reservoir or urinary conduit for a period of time longer than one emptying.
5.4 Bladder reflex triggering This comprises various maneuvers performed by the patient or the therapist in order to elicit reflex detrusor contraction by exteroceptive stimuli. The most commonly used maneuvers are suprapubic tapping, thigh scratching, and anal/rectal manipulation.
5.5 Bladder expression This comprises various maneuvers aimed at increasing intravesical pressure in order to facilitate bladder emptying. The most commonly used maneuvers are abdominal straining, Valsalva maneuver, and Credé maneuver.
5.2 Electrical stimulation
ACKNOWLEDGMENTS
This is the application of electrical current to stimulate the pelvic viscera or their nerve supply. The aim of electrical stimulation may be to directly induce a therapeutic response or to modulate lower urinary tract, bowel or sexual dysfunction.
The authors of this report are very grateful to Vicky Rees, Administrator of the ICS, for her typing and editing of numerous drafts of this document.
5.3 Catheterization Catheterization is a technique for bladder emptying employing a catheter to drain the bladder or a urinary reservoir.
ADDENDUM Formation of the ICS Terminology Committee The Terminology Committee was announced at the ICS meeting in Denver in 1999 and expressions of interest 757
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were invited from those who wished to be active members of the committee, and they were asked to comment in detail on the preliminary draft (the discussion paper published in Neurourology and Urodynamics). The nine authors replied with a detailed critique by 1st April 2000 and constitute the committee: Paul Abrams, Linda Cardozo, Magnus Fall, Derek Griffiths, Peter Rosier, Ulf Ulmsten, Philip van Kerrebroeck, Arne Victor, and Alan Wein. We thank other individuals who later offered their written comments: Jens Thorup Andersen, Walter Artibani, Jerry Blaivas, Linda Brubaker, Rick Bump, Emmanuel Chartier-Kastler, Grace Dorey, Clare Fowler, Kelm Hjalmas, Gordon Hosker, Vik Khullar, Guus Kramer, Gunnar Lose, Joseph Macaluso, Anders Mattiasson, Richard Millard, Rien Nijman, Arwin Ridder, Werner Schäfer, David Vodusek, and Jean Jacques Wyndaele. A half-day workshop was held at the ICS Annual Meeting in Tampere (August 2000) and a 2-day meeting in London (January 2001), which produced draft 5 of the report which was then placed on the ICS website (www.icsoffice.org). Discussions on draft 6 took place at the ICS meeting in Korea (September 2001), and draft 7 then remained on the ICS website until final submission to journals in November 2001.
REFERENCES 1. Abrams P (Chair), Blaivas JG, Stanton S, Andersen JT. ICS standardisation of terminology of lower urinary tract function. Neurourol Urodyn 1988;7:403–26. 2. Abrams P, Blaivas JG, Stanton SL, Andersen J. ICS 6th report on the standardisation of terminology of lower urinary tract function. Neurourol Urodyn 1992;11:593–603. 3. Andersen JT, Blaivas JG, Cardozo L, Thuroff J. ICS 7th report on the standardisation of terminology of lower urinary tract function: lower urinary tract rehabilitation techniques. Neurourol Urodyn 1992;11:593–603. 4. Bump RC, Mattiasson A, Bo K et al. The standardisation of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 1996;175:10–1.
flow studies of voiding, urethral resistance and urethral obstruction. Neurourol Urodyn 1997;16:1–18. 7. International Classification of Functioning, Disability and Health. ICIDH-2 website www.who.int/icidh. 8. Klevmark B. Natural pressure: volume curves and conventional cystometry. Scand J Urol Nephrol Suppl 1999;201:1–4. 9. Lose G, Fantl JA, Victor A, Walter S, Wells TL, Wyman J, Mattiasson A. Outcome measures for research in adult women with symptoms of lower urinary tract dysfunction. Neurourol Urodyn 1998;17:255–62. 10. Lose G, Griffiths D, Hosker G et al. Standardisation of urethral pressure measurement: report from the standardisation sub-committee of the International Continence Society. Neurourol Urodyn 2002;21:167–78. 11. Mattiasson A, Djurhuus JC, Fonda D, Lose G, Nordling J, Stöhrer M. Standardisation of outcome studies in patients with lower urinary dysfunction: a report on general principles from the standardisation committee of the International Continence Society. Neurourol Urodyn 1988;17:249–53. 12. Nordling J, Abrams P, Ameda K et al. Outcome measures for research in treatment of adult males with symptoms of lower urinary tract dysfunction. Neurourol Urodyn 1998;17:263–71. 13. Rowan D, James ED, Kramer AEJL et al. (ICS working party on urodynamic equipment) Urodynamic equipment: technical aspects. J Med Eng Technol 1987;11:57–64. 14. Stöhrer M, Goepel M, Kondo A et al. ICS report on the standardisation of terminology in neurogenic lower urinary tract dysfunction. Neurourol Urodyn 1999;18:139– 58. 15. Schäfer W, Abrams P, Liao L et al. Good urodynamic practice: report from the standardisation sub-committee of the International Continence Society. Neurourol Urodyn 2002;21:261–74. 16. Van Kerrebroeck P, Abrams P, Chaikin D et al. ICS standardisation report on nocturia: report from the standardisation sub-committee of the International Continence Society. Neurourol Urodyn 2002;21:193–99.
5. Fonda D, Resnick NM, Colling J et al. Outcome measures for research of lower urinary tract dysfunction in frail and older people. Neurourol Urodyn 1998;17:273–81.
17. Van Waalwijk van Doorn E, Anders K, Khullar V et al. Standardisation of ambulatory urodynamic monitoring: report of the standardisation sub-committee of the International Continence Society for ambulatory urodynamic studies. Neurourol Urodyn 2000;19:113–25.
6. Griffiths D, Hofner K, van Mastrigt R, Rollema HJ, Spangberg A, Gleason D. ICS report on the standardisation of terminology of lower urinary tract function: pressure–
18. Wan D, James ED, Kramer AEJL, Sterling AM, Suhel PF. ICS report on urodynamic equipment: technical aspects. J Med Eng Technol 1987;11(2):57–64.
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51b The standardization of terminology of lower urinary tract function recommended by the ICS 2002 Samih Al-Hayek, Paul Abrams
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IntrodUctIon The International Continence Society (ICS) established a committee for the standardization of terminology of lower urinary tract function in 1973 because until that time there were no internationally accepted terms and definitions that could be used to describe different aspects of lower urinary tract function and dysfunction. As a result, published studies could not be compared or their outcomes pooled. Since 1973, the ICS has published a series of reports, the last of which was issued in 2002.1–29 The new 2002 definitions and terminology agreed by the ICS will facilitate comparison of results and enable effective communication by investigators. The definitions are compatible with the World Health Organization (WHO) publication ICIDH-2 (International Classification of Functioning, Disability and Health) published in 2001 and ICD10, the International Classification of Diseases. It is suggested that acknowledgement of these ICS standards in written publications be indicated by a footnote to the section ‘Methods and Materials’ or its equivalent, to read as follows: ‘Methods, definitions and descriptions conform to the standards recommended by the International Continence Society, except where specifically noted’. The lower urinary tract is composed of the bladder and the urethra. When a reference is made to the whole anatomic organ – the ‘vesica urinaria’ – the correct term is the bladder. When the smooth muscle structure known as the ‘m. detrusor urinae’ is being discussed, then the correct term is detrusor. In 2002, the ICS subcommittee restated the principle of describing any lower urinary tract dysfunction from four aspects: as a symptom (taken by detailed history), a sign (physical examination and bedside tests), a condition, and as a urodynamic observation in addition to the terminology related to therapies.1
PatIent’s HIstory or Lower UrInary tract symPtoms Lower urinary tract symptoms (LUTS) are the subjective indicator of a disease or change in condition as perceived by the patient, carer or partner, and may lead the patient to seek help from healthcare professionals. Symptoms are either volunteered by, or elicited from, the individual or may be described by the individual’s caregiver. They are usually qualitative. In general, LUTS cannot be used to make a definitive diagnosis; they may also indicate pathologies other than lower urinary tract dysfunction (LUTD), such as urinary infection. The general history should include information relevant to neurologic and congenital abnormalities,
bowel function, and gynecologic and obstetric history, as well as relevant surgery and medication. The urinary history must include questions related to storage, voiding, and postmicturition symptoms. In addition, there are symptoms associated with sexual intercourse, pelvic organ prolapse, lower urinary tract pain and LUTD syndromes.
storage symptoms Storage symptoms are experienced during the storage phase of the bladder and include daytime frequency and nocturia.
• Increased daytime frequency is the complaint by the
•
• •
• •
•
patient who considers that she voids too often by day. This term is equivalent to ‘pollakisuria’ used in many countries. Nocturia is the complaint that the individual has to wake up at night one or more times to void. The term night-time frequency differs from that for nocturia, as it includes voids that occur after the individual has gone to bed, but before she has gone to sleep, and voids which occur in the early morning which prevent the individual from getting back to sleep as she wishes. Urgency is the complaint of a sudden compelling desire to pass urine which is difficult to defer. Urinary incontinence is the complaint of any involuntary leakage of urine. Urinary leakage may need to be distinguished from sweating or vaginal discharge. In each specific circumstance, urinary incontinence should be further described by specifying relevant factors such as type, frequency, severity, precipitating factors, social impact, effect on hygiene and quality of life, the measures used to contain the leakage, and whether or not the individual seeks or desires help because of urinary incontinence. Stress urinary incontinence is the complaint of involuntary leakage on effort or exertion, or on sneezing or coughing. Urge urinary incontinence is the complaint of involuntary leakage accompanied by or immediately preceded by urgency. Urge incontinence can present in different symptomatic forms; for example, as frequent small losses between micturitions or as a catastrophic leak with complete bladder emptying. Mixed urinary incontinence is the complaint of involuntary leakage associated with urgency and also with exertion, effort, sneezing or coughing.
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• Enuresis means any involuntary loss of urine. If
• • • •
it is used to denote incontinence during sleep, it should always be qualified with the adjective ‘nocturnal’. Nocturnal enuresis is the complaint of loss of urine occurring during sleep. Continuous urinary incontinence is the complaint of continuous leakage, both day and night. Other types of urinary incontinence may be situational, for example the report of incontinence during sexual intercourse, or giggle incontinence. Bladder sensation can be defined during history taking as normal, increased, reduced, absent or nonspecific.
Voiding symptoms
Genitourinary pain syndromes and symptom syndromes suggestive of LUtd Syndromes describe constellations, or varying combinations of symptoms, but cannot be used for precise diagnosis. The use of the word ‘syndrome’ can only be justified if there is at least one other symptom in addition to the symptom used to describe the syndrome. The syndromes described are functional abnormalities for which a precise cause has not been defined. It is presumed that routine assessment (history taking, physical examination, and other appropriate investigations) has excluded obvious local pathologies such as those that are infective, neoplastic, metabolic or hormonal in nature.
Genitourinary pain syndromes These are experienced during the voiding phase.
• Slow stream is reported by the individual as her • •
•
•
•
perception of reduced urine flow, usually compared to previous performance or in comparison to others. Splitting or spraying of the urine stream may be reported. Intermittent stream (intermittency) is the term used when the individual describes urine flow which stops and starts, on one or more occasions, during micturition. Hesitancy is the term used when an individual describes difficulty in initiating micturition resulting in a delay in the onset of voiding after the individual is ready to pass urine. Straining to void describes the muscular effort used to initiate, maintain or improve the urinary stream. Suprapubic pressure may be used to initiate or maintain urine flow. The Credé maneuver is used by some spinal cord injury patients, and women with detrusor underactivity sometimes press suprapubically to help empty the bladder. Terminal dribble is the term used when an individual describes a prolonged final part of micturition, when the flow has slowed to a trickle or dribble.
Postmicturition symptoms These are experienced immediately after micturition.
• Feeling of incomplete emptying. • Postmicturition dribble is the term used when an individual describes the involuntary loss of urine immediately after she has finished passing urine, usually after rising from the toilet in women.
All such syndromes are chronic in their nature. Pain is the major complaint but concomitant complaints relate to the lower urinary tract or bowel, or are sexual or gynecologic in nature. The terms ‘strangury’, ‘bladder spasm’, and ‘dysuria’ are difficult to define and of uncertain meaning and should not be used in relation to LUTD, unless a precise meaning is stated. Painful bladder syndrome is the complaint of suprapubic pain related to bladder filling, accompanied by other symptoms such as increased daytime and nighttime frequency, in the absence of proven urinary infection or other obvious pathology. The ICS believes this to be a preferable term to ‘interstitial cystitis’. Interstitial cystitis is a specific diagnosis and requires confirmation by typical cystoscopic and histologic features. In the investigation of bladder pain, it may be necessary to exclude conditions such as carcinoma in situ and endometriosis. Urethral pain syndrome is the occurrence of recurrent episodic urethral pain usually on voiding, with daytime frequency and nocturia, in the absence of proven infection or other obvious pathology.
Symptom syndromes suggestive of LUT dysfunction Overactive bladder syndrome presents with urgency, with or without urge incontinence, usually with frequency and nocturia; it has also been described as urge syndrome or urgency–frequency syndrome. These symptom combinations are suggestive of urodynamically demonstrable detrusor overactivity but can be due to other forms of urethrovesical dysfunction. These terms can be used if there is no proven infection or other obvious pathology. Lower urinary tract symptoms suggestive of bladder outlet obstruction is a term used when the individual complains 761
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predominately of voiding symptoms in the absence of infection or obvious pathology other than possible causes of outlet obstruction. In women, voiding symptoms are usually thought to suggest detrusor underactivity rather than bladder outlet obstruction.
• Frequency volume chart (FVC): this records the volumes •
cLInIcaL assessment of sIGns sUGGestIVe of LUtd Signs are observed by the physician to verify symptoms and quantify them.
Physical examination Physical examination is essential in the assessment of all patients with LUTD. It should include abdominal, pelvic (vaginal and pelvic floor muscles), perineal/genital, and rectal examination, in addition to a focused neurologic assessment. For patients with possible neurogenic LUTD, a more extensive neurologic examination is needed. Urinary incontinence (the sign) is defined as urine leakage seen during examination; this may be urethral or extraurethral.
• Stress urinary incontinence is the observation of
• •
involuntary leakage from the urethra, synchronous with exertion/effort, or sneezing or coughing. Stress leakage is presumed to be due to raised abdominal pressure. Coughing may induce a detrusor contraction, hence the sign of stress incontinence is a reliable indication of urodynamic stress incontinence only when leakage occurs synchronously with the first proper cough and stops at the end of that cough. Extraurethral incontinence is defined as the observation of urine leakage through channels other than the urethra. Uncategorized incontinence is the observation of involuntary leakage that cannot be classified into one of the above categories on the basis of signs and symptoms.
measuring the frequency, severity and impact of LUts Asking the patient to record micturitions and symptoms for a period of days provides invaluable information. The recording of micturition events can be in three main forms:
• Micturition time chart: this records only the times of micturitions, day and night, for at least 24 hours.
voided as well as the time of each micturition, day and night, for at least 24 hours. Bladder diary: this records the times of micturitions and voided volumes, incontinence episodes, pad usage, and other information such as fluid intake, the degree of urgency, and the degree of incontinence. It is useful to ask the individual to make an estimate of liquid intake. The time that diuretic therapy is taken should be marked on a chart or diary.
The following measurements can be abstracted from frequency volume charts and bladder diaries:
• Daytime frequency is the number of voids recorded
• • •
• •
•
during waking hours and includes the last void before sleep and the first void after waking and rising in the morning. Nocturia is the number of voids recorded during a night’s sleep: each void is preceded and followed by sleep. 24-hour frequency is the total number of daytime voids and episodes of nocturia during a specified 24-hour period. 24-hour production is measured by collecting all urine for 24 hours. This is usually commenced after the first void produced after rising in the morning and is completed by including the first void on rising the following morning. Polyuria is defined as the measured production of more than 2.8 liters (based on a 70 kg person voiding >40 ml/kg) of urine in 24 hours in adults. Nocturnal urine volume is defined as the total volume of urine passed between the time the individual goes to bed with the intention of sleeping and the time of waking with the intention of rising. Therefore, it excludes the last void before going to bed but includes the first void after rising in the morning. Nocturnal polyuria is present when an increased proportion of the 24-hour output occurs at night (normally during the 8 hours while the individual is in bed). The night-time urine output excludes the last void before sleep but includes the first void of the morning. The normal range of nocturnal urine production differs with age and the normal ranges remain to be defined. Nocturnal polyuria is present when greater than 20% (young adults) to 33% (over 65 years) is produced at night, hence the precise definition is dependent on age.
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• Maximum voided volume is the largest volume of urine voided during a single micturition and is determined either from the frequency/volume chart or bladder diary. The term ‘functional bladder capacity’ is no longer recommended.
Pad testing Pad testing may be used to quantify the amount of urine lost during incontinence episodes; methods range from a short provocative test to a 24-hour pad test.
ProcedUres reLated to eVaLUatIon of LUtd or UrodynamIc obserVatIons Urodynamic observations are observations made during urodynamic studies. In general, a urodynamic observation may have a number of possible underlying causes and does not represent a definitive diagnosis of a disease or condition; it may occur with a variety of symptoms and signs, or in the absence of any symptoms or signs.
Urodynamic techniques There are two principal methods of urodynamic investigation: conventional and ambulatory. Conventional urodynamic studies normally take place in the urodynamic laboratory and usually involve artificial bladder filling, defined as filling the bladder, via a catheter, with a specified liquid at a specified rate. Ambulatory urodynamic studies are defined as a functional test of the lower urinary tract, utilizing natural filling, and reproducing the subject’s everyday activities. The term ‘ambulatory’ is used to indicate that monitoring usually takes place outside of the urodynamic laboratory, rather than the subject’s mobility. The natural filling means that the bladder is filled by the production of urine rather than by an artificial medium. Both filling cystometry and pressure flow studies of voiding require the following measurements:
• Intravesical pressure is the pressure within the bladder. • Abdominal pressure is taken to be the pressure
•
surrounding the bladder. In current practice it is estimated from rectal, vaginal or, less commonly, from extraperitoneal pressure or a bowel stoma. The simultaneous measurement of abdominal pressure is essential for the interpretation of the intravesical pressure trace. Detrusor pressure is that component of intravesical pressure that is created by forces in the bladder wall
(passive and active). It is estimated by subtracting abdominal pressure from intravesical pressure.
Procedures related to the evaluation of urine storage (filling cystometry) The word ‘cystometry’ is commonly used to describe the urodynamic investigation of the filling phase of the micturition cycle. To eliminate confusion, the term ‘filling cystometry’ is proposed. Filling cystometry is defined as the method by which the pressure/volume relationship of the bladder is measured during bladder filling. The filling phase starts when filling commences and ends when the patient and urodynamicist decide that ‘permission to void’ has been given. Bladder and urethral function, during filling, need to be defined separately. The rate at which the bladder is filled is divided into physiologic and non-physiologic:
• Physiologic filling rate is defined as a filling rate
•
less than the predicted maximum. The predicted maximum is calculated by body weight in kilograms divided by 4, expressed as ml/min. Non-physiologic filling rate is defined as a filling rate greater than the predicted maximum filling rate. The ICS no longer wishes to divide filling rates into slow, medium, and fast.
Bladder storage function should be described according to bladder sensation, detrusor activity, bladder compliance, and bladder capacity.
Bladder sensation during filling cystometry While bladder sensation is assessed during filling cystometry, the assumption that it is sensation from the bladder alone, without urethral or pelvic components, may be false. • Normal bladder sensation can be judged by three defined points noted during filling cystometry and evaluated in relation to the bladder volume at that moment and to the patient’s symptomatic complaints. 1. First sensation of bladder filling is the feeling the patient has, during filling cystometry, when she first becomes aware of the bladder filling. 2. First desire to void is the feeling that would lead the patient to pass urine at the next convenient moment, but voiding can be delayed if necessary. 3. Strong desire to void is defined as a persistent desire to void without the fear of leakage. • Increased bladder sensation is an early first sensation of bladder filling (or an early desire to void) and/or 763
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• • • • •
•
an early strong desire to void, which occurs at low bladder volume and which persists. Reduced bladder sensation is a diminished sensation throughout bladder filling. Absent bladder sensation means that the individual has no bladder sensation. Non-specific bladder sensations may make the individual aware of bladder filling, for example, abdominal fullness or vegetative symptoms. Bladder pain is an abnormal finding. Urgency during filling cystometry is a sudden compelling desire to void. The ICS no longer recommends the terms ‘motor urgency’ and ‘sensory urgency’. These terms are often misused and have little intuitive meaning. The vesical/urethral sensory threshold is defined as the least current which consistently produces a sensation perceived by the subject during stimulation at the site under investigation.
Detrusor function during filling cystometry In everyday life, the individual attempts to inhibit detrusor activity until in a position to void. Therefore, when the aims of the filling study have been achieved, and when the patient has a desire to void, normally the ‘permission to void’ is given. That moment is indicated on the urodynamic trace and all detrusor activity before this ‘permission’ is defined as ‘involuntary detrusor activity’. Normal detrusor function allows bladder filling with little or no change in pressure. No involuntary phasic contractions occur despite provocation. Detrusor overactivity is a urodynamic observation characterized by involuntary detrusor contractions during the filling phase which may be spontaneous or provoked. There is no lower limit for the amplitude of an involuntary detrusor contraction but confident interpretation of low pressure waves (amplitude smaller than 5 cmH2O) depends on ‘high quality’ urodynamic technique. The phrase ‘which the patient cannot completely suppress’ has been deleted from the old definition. There are certain patterns of detrusor overactivity:
• Phasic detrusor overactivity is defined by a
•
characteristic waveform, and may or may not lead to urinary incontinence. Phasic detrusor contractions are not always accompanied by any sensation or may be interpreted as a first sensation of bladder filling or as a normal desire to void. Terminal detrusor overactivity is defined as a single, involuntary detrusor contraction, occurring at cystometric capacity, which cannot be suppressed
•
and results in incontinence, usually with bladder emptying (voiding). Detrusor overactivity incontinence is incontinence due to an involuntary detrusor contraction. In a patient with normal sensation, urgency is likely to be experienced just before the leakage episode. ICS recommends that the terms ‘motor urge incontinence’ and ‘reflex incontinence’ should no longer be used as they have no intuitive meaning and are often misused.
Other patterns of detrusor overactivity are seen; for example, the combination of phasic and terminal detrusor overactivity, and the sustained high pressure detrusor contractions seen in spinal cord injury patients when attempted voiding occurs against a dyssynergic sphincter. Detrusor overactivity may also be qualified, when possible, according to cause, for example:
• Neurogenic detrusor overactivity when there is a relevant •
neurologic condition. This term replaces the term ‘detrusor hyperreflexia’. Idiopathic detrusor overactivity when there is no defined cause. This term replaces ‘detrusor instability’.
Bladder compliance during filling cystometry Bladder compliance describes the relationship between change in bladder volume and change in detrusor pressure. The observation of reduced bladder compliance during conventional filling cystometry is often related to relatively fast bladder filling Compliance (C) is calculated by dividing the volume change (∆V) by the change in detrusor pressure (∆pdet) during that change in bladder volume (C = V/∆pdet). It is expressed in ml/cmH2O. A variety of methods of calculating bladder compliance have been described. The ICS recommends that two standard points should be used for compliance calculations: 1. The detrusor pressure at the start of bladder filling and the corresponding bladder volume (usually zero). 2. The detrusor pressure (and corresponding bladder volume) at cystometric capacity or immediately before the start of any detrusor contraction that causes significant leakage (and therefore causes the bladder volume to decrease, affecting compliance calculation). Both points are measured excluding any detrusor contraction.
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Cystometric capacity is the bladder volume at the end of the filling cystometrogram, when ‘permission to void’ is usually given. The endpoint should be specified; for example, if filling is stopped when the patient has a normal desire to void, then the cystometric capacity is the volume voided together with any residual urine. In certain types of dysfunction, the cystometric capacity cannot be defined in the same terms. In the absence of sensation, the cystometric capacity is the volume at which the clinician decides to terminate filling. The reason(s) for terminating filling should be defined; for example, high detrusor filling pressure, large infused volume, or pain. If there is uncontrollable voiding, it is the volume at which this begins. In the presence of sphincter incompetence, the cystometric capacity may be significantly increased by occlusion of the urethra (e.g. by Foley catheter). Maximum cystometric capacity, in patients with normal sensation, is the volume at which the patient can no longer delay micturition (has a strong desire to void). Maximum anesthetic bladder capacity is the volume to which the bladder can be filled under deep general or spinal anesthetic and should be qualified according to the type of anesthesia used and the speed, the length of time, and the pressure at which the bladder is filled.
Urethral function during filling cystometry The urethral closure mechanism during storage may be competent or incompetent.
• Normal urethral closure mechanism maintains a positive
• •
•
urethral closure pressure during bladder filling even in the presence of increased abdominal pressure, although it may be overcome by detrusor overactivity. Incompetent urethral closure mechanism is defined as one which allows leakage of urine in the absence of a detrusor contraction. Urethral relaxation incontinence is defined as leakage due to urethral relaxation in the absence of raised abdominal pressure or detrusor overactivity. Fluctuations in urethral pressure have been defined as the ‘unstable urethra’. However, the significance of the fluctuations and the term itself lack clarity and the term is not recommended by the ICS. If symptoms are seen in association with a decrease in urethral pressure, a full description should be given. Urodynamic stress incontinence is noted during filling cystometry and is defined as the involuntary leakage of urine during increased abdominal pressure, in the absence of a detrusor contraction. Urodynamic
stress incontinence is now the preferred term to ‘genuine stress incontinence’. In patients with stress incontinence, there is a spectrum of urethral characteristics ranging from a highly mobile urethra with good intrinsic function to an immobile urethra with poor intrinsic function. Any delineation into categories such as ‘urethral hypermobility’ and ‘intrinsic sphincter deficiency’ may be simplistic and arbitrary, and requires further research.
Assessment of urethral function during filling cystometry Urethral pressure measurement • Urethral pressure is defined as the fluid pressure needed to just open a closed urethra. • The urethral pressure profile is a graph indicating the intraluminal pressure along the length of the urethra (Fig. 51b.1). • The urethral closure pressure profile is given by the subtraction of intravesical pressure from urethral pressure. • Maximum urethral pressure (MUP) is the maximum pressure of the measured profile. • Maximum urethral closure pressure (MUCP) is the maximum difference between the urethral pressure and the intravesical pressure. • Functional profile length is the length of the urethra along which the urethral pressure exceeds intravesical pressure in women. • Pressure ‘transmission’ ratio is the increment in urethral pressure on stress as a percentage of the simultaneously recorded increment in intravesical pressure.
120 Intraurethral pressure (cmH2O)
Bladder capacity during filling cystometry
100 Maximum urethral closure pressure
80 60
Maximum urethral pressure
40
Bladder pressure
20
Functional profile length Total profile length
0 0
1
2
3 4 Distance (cm)
5
6
Figure 51b.1. Diagram of a female urethral pressure profile with ICS recommended nomenclature. 765
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Leak point pressure Abdominal leak point pressure is the intravesical pressure at which urine leakage occurs due to increased abdominal pressure in the absence of a detrusor contraction. The leak pressure point should be qualified according to the site of pressure measurement (rectal, vaginal or intravesical) and the method by which pressure is generated (cough or Valsalva). Leak point pressures may be calculated in three ways from the three different baseline values which are in common use: zero (the true zero of intravesical pressure), the value of pves measured at zero bladder volume, or the value of pves immediately before the cough or Valsalva (usually at 200 or 300 ml bladder capacity). The baseline used, and the baseline pressure, should be specified. Detrusor leak point pressure (DLPP) is defined as the lowest detrusor pressure at which urine leakage occurs in the absence of either a detrusor contraction or increased abdominal pressure. DLPP has been used most frequently to predict upper tract problems in neurologic patients with reduced bladder compliance. The ICS has defined it ‘in the absence of a detrusor contraction’ although others will measure DLPP during involuntary detrusor contractions.
Procedures related to the evaluation of micturition (pressure–flow studies) Voiding is described in terms of detrusor and urethral function and assessed by measuring urine flow rate and voiding pressures. Pressure–flow studies of voiding are the method by which the relationship between pressure in the bladder and urine flow rate is measured during bladder emptying. The voiding phase starts when ‘permission to void’ is given, or when uncontrollable voiding begins, and ends when the patient considers voiding has finished.
Flow rate (ml/s) Maximum flow rate Voided volume
Time (s)
Time to maximum flow Flow time
Figure 51b.2. Diagram of a continuous urine flow recording with ICS recommended nomenclature.
• Voided volume is the total volume expelled via the • •
• • •
urethra. Maximum flow rate is the maximum measured value of the flow rate after correction for artifacts. Voiding time is total duration of micturition, i.e. includes interruptions. When voiding is completed without interruption, voiding time is equal to flow time (Fig. 51b.3). Flow time is the time over which measurable flow actually occurs. Average flow rate is voided volume divided by flow time. The average flow should be interpreted with caution if flow is interrupted or there is a terminal dribble. Time to maximum flow is the elapsed time from onset of flow to maximum flow.
Pressure measurements during pressure–flow studies (PFS) The following measurements are applicable to each of the pressure curves: intravesical, abdominal, and detrusor pressure (Fig. 51b.4).
Measurement of urine flow Urine flow is defined as either continuous (i.e. without interruption) or intermittent (i.e. when an individual states that the flow stops and starts during a single visit to the bathroom in order to void). The continuous flow curve is defined as a smooth, arc-shaped curve, or fluctuating when there are multiple peaks during a period of continuous urine flow. The precise shape of the flow curve is governed by detrusor contractility, the presence of any abdominal straining, and by the bladder outlet (Fig. 51b.2).
• Flow rate is the volume of fluid expelled via the urethra per unit time. It is expressed in ml/s.
Flow rate (ml/s)
Voiding time
Time (s)
Figure 51b.3. Diagram of an interrupted urine flow recording with ICS recommended nomenclature.
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• Premicturition pressure is the pressure recorded • •
• • • • •
immediately before the initial isovolumetric contraction. Opening pressure is the pressure recorded at the onset of urine flow (consider time delay). Opening time is the elapsed time from initial rise in detrusor pressure to onset of flow. This is the initial isovolumetric contraction period of micturition. Flow measurement delay should be taken into account when measuring opening time. Maximum pressure is the maximum value of the measured pressure. Pressure at maximum flow is the lowest pressure recorded at maximum measured flow rate. Closing pressure is the pressure measured at the end of measured flow. Minimum voiding pressure is the minimum pressure during measurable flow but is not necessarily equal to either the opening or closing pressures. Flow delay is the time delay between a change in bladder pressure and the corresponding change in measured flow rate.
Detrusor function during voiding With normal detrusor function, normal voiding is achieved by a voluntarily initiated continuous detru-
Abdominal pressure at maximum flow
Abdominal opening pressure
Abdominal pressure (cmH 2 O)
Detrusor pressure (cmH 2 O)
• detrusor underactivity, which is defined as a
•
contraction of reduced strength and/or duration, resulting in prolonged bladder emptying and/or a failure to achieve complete bladder emptying within a normal time span; acontractile detrusor, which is defined as one that cannot be demonstrated to contract during urodynamic studies.
Post-void residual (PVR) is defined as the volume of urine left in the bladder at the end of micturition. If no residual urine is demonstrated after repeated free flowmetry, then the finding of residual urine during urodynamic studies should be considered an artifact, due to the circumstances of the test.
Maximum abdominal pressure
Abdominal premicturition pressure pabd cont. max. flow Intravesical opening pressure
Intravesical pressure (cmH 2 O)
sor contraction that leads to complete bladder emptying within a normal time span, and in the absence of obstruction. For a given detrusor contraction, the magnitude of the recorded pressure rise will depend on the degree of outlet resistance. A normal detrusor contraction will be recorded as high pressure if there is high outlet resistance, normal pressure if there is normal outlet resistance, or low pressure if urethral resistance is low. Abnormal detrusor activity can be subdivided into:
Intravesical pressure at maximum flow
Intravesical contraction pressure at Maximum maximum intravesical flow pressure
Intravesical premicturition pressure
Detrusor opening pressure Detrusor premicturition pressure
Detrusor pressure at maximum flow
Maximum detrusor pressure
Flow rate (ml/s)
Detrusor contraction pressure at maximum flow
Maximum flow
Opening time
Figure 51b.4. Diagram of a pressure–flow recording of micturition with ICS recommended nomenclature. pabd, abdominal pressure. 767
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Urethral function during voiding Normal urethral function is defined as a urethra that opens and is continuously relaxed to allow the bladder to be emptied at a normal pressure; abnormal urethral function may be due to either obstruction because of urethral overactivity or the urethra cannot open due to anatomic abnormality (e.g. a urethral stricture). Bladder outlet obstruction is the generic term for obstruction during voiding and is characterized by increased detrusor pressure and reduced urine flow rate. It is usually diagnosed by studying the synchronous values of flow rate and detrusor pressure. Bladder outlet obstruction has been defined for men but, as yet, not adequately in women and children. Dysfunctional voiding is characterized by an intermittent and/or fluctuating flow rate due to involuntary intermittent contractions of the periurethral striated muscle during voiding in neurologically normal individuals. Although dysfunctional voiding is not a very specific term, it is preferred to terms such as ‘non-neurogenic neurogenic bladder’. Other terms such as ‘idiopathic detrusor sphincter dyssynergia’, or ‘sphincter overactivity voiding dysfunction’, may be preferable. However, the term dysfunctional voiding is well established. The condition occurs most frequently in children. While it is felt that pelvic floor contractions are responsible, it is possible that the intraurethral striated muscle may be important. Detrusor sphincter dyssynergia is defined as a detrusor contraction concurrent with an involuntary contraction of the urethral and/or periurethral striated muscle. Occasionally, flow may be prevented altogether. Detrusor sphincter dyssynergia typically occurs in patients with a suprasacral lesion. Non-relaxing urethral sphincter obstruction usually occurs in individuals with a neurologic lesion and is characterized by a non-relaxing, obstructing urethra resulting in reduced urine flow. It is found in sacral and infrasacral lesions (e.g. meningomyelocele) and after radical pelvic surgery. In addition, there is often urodynamic stress incontinence during bladder filling. This term replaces ‘isolated distal sphincter obstruction’.
condItIons Conditions are defined by the presence of urodynamic observations associated with characteristic symptoms or signs and/or non-urodynamic evidence of relevant pathologic processes.
Although acute retention is usually thought of as painful, in certain circumstances pain may not be a presenting feature; for example when due to prolapsed intervertebral disk, postpartum, or after regional anesthesia such as an epidural anesthetic. The retention volume should be significantly greater than the expected normal bladder capacity. In patients after surgery, due to bandaging of the lower abdomen or to abdominal wall pain, it may be difficult to detect a painful, palpable or percussable bladder.
Chronic retention of urine This is defined as a non-painful bladder, which remains palpable or percussable after the patient has passed urine. Such patients may be incontinent. The ICS no longer recommends the term ‘overflow incontinence’. This term is considered confusing and lacking a convincing definition. If used, a precise definition and any associated pathophysiology such as reduced urethral function or detrusor overactivity/low bladder compliance should be stated. The term chronic retention excludes transient voiding difficulty (e.g. after surgery for stress incontinence) and implies significant residual urine; a minimum volume of 300 ml has been previously mentioned.
UnIts of measUrements and symboLs Results of urodynamic studies should be reported in SI units to avoid confusion and to facilitate communication. Table 51b.1 includes the units commonly used during urodynamics. Likewise, symbols should be used only if they conform to the international usage. Table 51b.2 lists the symbols frequently used in urodynamics.
table 51b.1.
Recommended units of measurement
Quantity
Acceptiable unit
Symbol
Volume
millilter
ml
Time
second
s
Flow rate
millilters/second
ml/s a
Pressure
centimeters of water
cmH2O
Length
meters or submultiples
m, cm, mm
Velocity
meters/second or submultiples
m/s, cm/s
Temperature
degress Celsius
°C
a
Acute retention of urine This is defined as a painful, palpable or percussable bladder, when the patient is unable to pass any urine.
The SI unit is the pascal (Pa), but it is only practical at present to calibrate our instruments in cmH2O. One centimetre of water pressure is approximately equal to 100 pascals (1 cmH2O = 98.07Pa = 0.098 kPa).
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table 51b.2.
List of symbols
Basic symbols
Urologic qualifiers
Value
Pressure
p
Bladder
ves
Maximum
max
Volume
V
Urethra
ura
Minimum
min
Flow rate
Q
Ureter
ure
Average
ave
Velocity
v
Detrusor
det
Isovolumetric
Time
t
Abdomen
abd
Isotonic
ist
Temperature
T
External stream
ext
Isobaric
isb
Isometric
ism
Length
l
Area
A
Diameter
d
Force
F
Energy
E
Power
P
Compliance
C
Work
W
Energy per unit volume
isv
e
pdet/max = maximum detrusor pressure. eext = kinetic energy per unit volume in the external stream.
acknowLedGements The authors are grateful to the International Continence Society for their permission to reproduce information from the 2002 ICS terminology report.
references 1. [Standardisation of the terminology of function of the lower urinary tract. Incontinence, cystometry, ureteral profile, units of measurement (author’s translation)]. J Urol Nephrol (Paris) 1976;82(6):429–36. 2. First report on the standardisation of terminology of lower urinary tract function. Br J Urol 1976;48(1):39–42. 3. Second report on the standardisation of terminology of lower urinary tract function. Br J Urol 1977; 49(3):207–10. 4. Second report on the standardisation of terminology of lower urinary tract function. International Continence Society Committee on Standardisation of Terminology, Copenhagen, August 1976. Eur Urol 1977;3(3):168–70. 5. Second report on the standardisation of terminology of lower urinary tract function. Procedures related to the evaluation of micturition: flow rate, pressure measurement, symbols. Scand J Urol Nephrol 1977;11(3):197–9. 6. First report on the standardisation of terminology of lower urinary tract function. Incontinence, cystometry, urethral closure pressure profile, and units of measurement. Scand J Urol Nephrol 1977;11(3):193–6.
7. Third report on the standardisation of terminology of lower urinary tract function procedures related to the evaluation of micturition: pressure–flow relationships, residual urine. Produced by the International Continence Society, February 1977. Br J Urol 1980;52(5):348–50. 8. Third report on the standardisation of terminology of lower urinary tract function. Procedures related to the evaluation of micturition, pressure–flow relationships, residual urine. Produced by the International Continence Society Committee on Standardisation of Terminology, Nottingham, February 1977. Eur Urol 1980;6(3):170–1. 9. Fourth report on the standardisation of terminology of lower urinary tract function. Terminology related to neuromuscular dysfunction of the lower urinary tract. Produced by the International Continence Society. Br J Urol 1981;53(4):333–5. 10. Fourth report on the standardisation of terminology of lower urinary tract function. Terminology related to neuromuscular dysfunction of the lower urinary tract. The International Continence Society Committee on Standardisation of Terminology. Scand J Urol Nephrol 1981;15(3):169–71. 11. Sixth report on the standardisation of terminology of lower urinary tract function. Procedures related to neurophysiological investigations: electromyography, nerve conduction studies, reflex latencies, evoked potentials and sensory testing. The International Continence Society Committee on Standardisation of Terminology, New York, May 1985. Int Urol Nephrol 1986;18(3):349–56.
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12. Seventh report on the standardisation of terminology of lower urinary tract function: lower urinary tract rehabilitation techniques. Scand J Urol Nephrol 1992;26(2):99– 106. 13. Abrams P, Blaivas JG, Stanton SL et al. Sixth report on the standardisation of terminology of lower urinary tract function. Procedures related to neurophysiological investigations: electromyography, nerve conduction studies, reflex latencies, evoked potentials and sensory testing. The International Continence Society Committee on Standardisation of Terminology, New York, May 1985. Scand J Urol Nephrol 1986;20(3):161–4. 14. Abrams P, Blaivas JG, Stanton SL et al. Sixth report on the standardisation of terminology of lower urinary tract function. Procedures related to neurophysiological investigations: electromyography, nerve conduction studies, reflex latencies, evoked potentials and sensory testing. The International Continence Society. Br J Urol 1987;59(4):300–4. 15. Abrams P, Blaivas JG, Stanton SL, Andersen JT. The standardisation of terminology of lower urinary tract function. The International Continence Society Committee on Standardisation of Terminology. Scand J Urol Nephrol Suppl 1988;114:5–19.
20. Klevmark B. Natural pressure–volume curves and conventional cystometry. Scand J Urol Nephrol Suppl 1999;201:1–4. 21. Lose G, Fantl JA, Victor A et al. Outcome measures for research in adult women with symptoms of lower urinary tract dysfunction. Neurourol Urodyn 1998;17(3):255–62. 22. Lose G, Griffiths D, Hosker G et al. Standardisation of urethral pressure measurement: report from the Standardisation Sub-Committee of the International Continence Society. Neurourol Urodyn 2002;21(3):258–60. 23. Mattiasson A, Djurhuus JC, Fonda D, Lose G, Nordling J, Stohrer M. Standardization of outcome studies in patients with lower urinary tract dysfunction: a report on general principles from the Standardisation Committee of the International Continence Society. Neurourol Urodyn 1998;17(3):249–53. 24. Rowan D, James ED, Kramer AE, Sterling AM, Suhel PF. Urodynamic equipment: technical aspects. Produced by the International Continence Society Working Party on Urodynamic Equipment. J Med Eng Technol 1987;11(2):57–64. 25. Schafer W, Abrams P, Liao L et al. Good urodynamic practices: uroflowmetry, filling cystometry, and pressure–flow studies. Neurourol Urodyn 2002;21(3):261–74.
16. Abrams P, Cardozo L, Fall M et al. The standardisation of terminology of lower urinary tract function: report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 2002;21(2):167–78.
26. Stohrer M, Goepel M, Kondo A et al. The standardization of terminology in neurogenic lower urinary tract dysfunction: with suggestions for diagnostic procedures. International Continence Society Standardization Committee. Neurourol Urodyn 1999;18(2):139–58.
17. Bump RC, Mattiasson A, Bo K et al. The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 1996;175(1):10–7.
27. van Waalwijk van DE, Anders K, Khullar V et al. Standardisation of ambulatory urodynamic monitoring: Report of the Standardisation Sub-Committee of the International Continence Society for Ambulatory Urodynamic Studies. Neurourol Urodyn 2000;19(2):113–25.
18. Fonda D, Resnick NM, Colling J et al. Outcome measures for research of lower urinary tract dysfunction in frail older people. Neurourol Urodyn 1998;17(3):273–81. 19. Griffiths D, Hofner K, von Mastrigt R, Rollema HJ, Spangberg A, Gleason D. Standardization of terminology of lower urinary tract function: pressure–flow studies of voiding, urethral resistance, and urethral obstruction. International Continence Society Subcommittee on Standardization of Terminology of Pressure–Flow Studies. Neurourol Urodyn 1997;16(1):1–18.
28. Van KP, Abrams P, Chaikin D et al. The standardisation of terminology in nocturia: report from the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 2002;21(2):179–83. 29. Andersen JT, Blaivas JG, Cardozo L, Thuroff J. Seventh report on the standardisation of terminology of lower urinary tract function: lower urinary tract rehabilitation techniques. International Continence Society. Neurourol Urodyn 1992;11:593–603.
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52 The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction Richard C Bump, Anders Mattiasson, Kari Bø, Linda P Brubaker, John O L DeLancey, Peter Klarskov, Bob L Shull, Anthony R B Smith
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INTRODUCTION The International Continence Society (ICS) has been at the forefront in the standardization of terminology of lower urinary tract function since the establishment of the Committee on Standardization of Terminology in 973. This committee’s efforts over the past two decades have resulted in the worldwide acceptance of terminology standards that allow clinicians and researchers interested in the lower urinary tract to communicate efficiently and precisely. While female pelvic organ prolapse and pelvic floor dysfunction are intimately related to lower urinary tract function, such accurate communication using standard terminology has not been possible for these conditions. There is no universally accepted system for describing the anatomic position of the pelvic organs. Many reports use terms for the description of pelvic organ prolapse which are undefined; none of the many aspiring grading systems has been adequately validated with respect either to reproducibility or to the clinical significance of different grades. The absence of standard, validated definitions prevents comparisons of published series from different institutions and longitudinal evaluation of an individual patient. A primary goal of this report is to introduce a system that will allow the accurate, quantitative description of pelvic support findings in individual patients. This document is a first effort toward the establishment of standard, reliable, and validated descriptions of female pelvic anatomy and function. The subcommittee acknowledges a need for well-designed reliability studies to evaluate and validate various descriptions and definitions. We have tried to develop guidelines that will promote new insights rather than existing biases. Acknowledgement of these standards in written publications and scientific presentations should be indicated in the Methods section with the following statement: ‘Methods, definitions, and descriptions conform to the standards recommended by the International Continence Society, except where specifically noted’.
DESCRIPTION OF PELVIC ORGAN PROLAPSE The clinical description of pelvic floor anatomy is determined during the physical examination of the external genitalia and vaginal canal. Although the specifics of the examination technique are not dictated by this document, authors should describe their specific technique precisely. Segments of the lower reproductive tract will Article reprinted with permission of the International Continence Society.
replace such terms as ‘cystocele, rectocele, enterocele, or urethrovesical junction’ because these terms may imply an unrealistic certainty as to the structures on the other side of the reproductive tract bulge, particularly in women who have had previous prolapse surgery.
Conditions of the examination Many variables of examination technique may influence findings in patients with pelvic organ prolapse. It is critical that the examiner sees and describes the maximum protrusion noted by the individual subject during her daily activities. Therefore, the criteria for the endpoint of the examination and the full development of the prolapse must be specified in any report. Suggested criteria for demonstration of maximum prolapse should include one or all of the following: a. Any protrusion of the vaginal wall has become tight during straining by the patient. b. Traction on the prolapse causes no further descent. c. The subject confirms that the size of the prolapse and extent of the protrusion seen by the examiner is as extensive as the most severe protrusion that she has experienced. The means of this confirmation should be specified. For example, the subject may use a small handheld mirror to visualize the protrusion. d. A standing, straining examination confirms that the full extent of the prolapse was observed in other positions used. Other variables of technique that should be specified during the quantitative description and the ordinal staging of pelvic organ prolapse include the following: a. the position of the subject (e.g. supine lithotomy, lateral Sims’ position, specified degrees of upright, erect sitting, standing, etc.); b. the type of examination table or chair used; c. the type of standard vaginal specula, retractors, or tractors used; d. diagrams of any customized retraction, traction, or measuring devices used; e. the type (e.g. Valsalva maneuver, cough) and, if measured, intensity (e.g. vesical or rectal pressure rise) of straining used to develop the prolapse maximally; f. fullness of bladder, and, if the bladder was empty, whether this was by spontaneous voiding or by catheterization; g. content of rectum;
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h. the method by which any quantitative measurements were made (e.g. estimation by visualization or palpation, direct measurement with a calibrated device, etc.). There is a critical need to define the importance of all variables of technique as they relate to the ease of assessment and reproducibility of measurements. Researchers should determine the intra- and interobserver reliability of measurements made with their assessment techniques before utilizing them as baseline and outcome variables. Manuscript descriptions of assessment techniques should include sufficient detail to ensure that other researchers can replicate them precisely.
Quantitative description of pelvic organ position This description system is a tandem profile in that it contains a series of component measurements grouped together in combination, but listed separately in tandem, without being fused into a distinctive new expression or ‘grade’. It allows for the precise description of an individual woman’s pelvic support without assigning a ‘severity value’. Second, it allows accurate site-specific observations of the stability or progression of prolapse over time by the same or different observers. Finally, it allows similar judgments as to the outcome of surgical repair of prolapse. For example, noting that a surgical procedure moved the vaginal apex from 0.5 cm beyond the hymeneal ring to 0.5 cm above the hymeneal ring denotes more meager improvement than stating that the prolapse was reduced from Grade 3 to Grade as would be the case using some current grading systems.
The anatomic position of the six defined points for measurement (see ‘Defined points for measurement’ below) should be centimeters above or proximal to the hymen (negative number) or centimeters below or distal to the hymen (positive number) with the plane of the hymen being defined as zero (0). For example, a cervix that protruded 3 cm distal to the hymen would be +3 cm. Palpably, the ischial spines provide precisely identifiable landmarks. In the sitting or standing position, or in situations with limited viability due to obesity or limited ability for hip abduction, the position of the cervix or the leading point of the prolapse relative to the ischial spines may be measured by palpation. Measurements so obtained should be normalized to the level of the hymen by noting the distance between the ischial spines and the plane of the hymen. For example, a cervix that is 3 cm distal to the ischial spines would be at –2 cm if the spines were 5 cm above the plane of the hymen. Defined points for measurement Anterior Vaginal Wall Because the only structure directly visible to the examiner is the surface of the vagina, anterior prolapse should be discussed in terms of a segment of the vaginal wall rather than the organs which lie behind it. Thus, the term ‘anterior vaginal wall prolapse’ is preferable to ‘cystocele’ or ‘anterior enterocele’ unless the organs involved are identified by ancillary tests. Point Aa
Definition of anatomic landmarks Prolapse should be evaluated by a standard system relative to clearly defined anatomic points of reference. These are of two types: fixed reference points and defined points for measurement. Point Ba Fixed point of reference Prolapse should be evaluated relative to a fixed anatomic landmark which can be consistently and precisely identified. The hymen will be the fixed point of reference used throughout this system of quantitative prolapse description. Visually, the hymen provides a precisely identifiable landmark for reference. Although it is recognized that the plane of the hymen is somewhat variable depending upon the degree of levator ani dysfunction, it remains the best landmark available. ‘Hymen’ is preferable to the ill-defined and imprecise term ‘introitus’.
A point located in the midline of the anterior vaginal wall 3 cm proximal to the external urethral meatus. This corresponds to the approximate location of the ‘urethrovesical crease’, a visible landmark of variable prominence that is obliterated in many patients. By definition, the range of position of Point Aa relative to the hymen is –3 to +3 cm. A point that represents the most distal (i.e. most dependent) position of the upper portion of the anterior vaginal wall from the vaginal cuff or anterior vaginal fornix to Point Aa. By definition, Point Ba is at –3 cm in the absence of prolapse and would have a positive value equal to the position of the cuff in women with total posthysterectomy vaginal eversion.
Vaginal Apex These points represent the most proximal locations of the normally positioned lower reproductive tract. 773
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Point C
Point D
A point that represents either the most distal (i.e. most dependent) edge of the cervix or the leading edge of the vaginal cuff scar in a woman who has undergone total hysterectomy. A point that represents the location of the posterior fornix (or pouch of Douglas) in a woman who still has a cervix. It represents the level of uterosacral ligament attachment to the proximal posterior cervix. It is included as a point of measurement to differentiate suspensory failure of the uterosacral–cardinal ligament complex from cervical elongation. When the location of Point C is significantly more positive than the location of Point D, this is indicative of cervical elongation which may be symmetrical or eccentric (e.g. involving only the anterior lip of the cervix due to a prior laceration). Point D is omitted as a point for measurement in the absence of the cervix.
Other landmarks and measurements The genital hiatus is measured from the middle of the external urethral meatus to the posterior midline hymen. If the location of the hymen is distorted by a loose band of skin without underlying muscle or connective tissue, the firm palpable tissue of the perineal body should be substituted as the posterior margin for this measurement. The perineal body is measured from the posterior margin of the genital hiatus (as just described) to the midanal opening. Measurement of the genital hiatus and perineal body is expressed in centimeters. The total vaginal length is the greatest depth of the vagina in centimeters when Point C or D is reduced to its full normal position. Note: Eccentric elongation of a prolapsed anterior or posterior vaginal wall should not be included in the measurement of total vaginal length (see Fig. 52.4a and accompanying discussion). The points and measurements discussed in this section are presented in Figure 52..
Making and recording measurements
Point Bp A point that represents the most distal (i.e. most dependent) position of the upper portion of the posterior vaginal wall from the vaginal cuff or posterior vaginal fornix to Point Ap. By definition, Point Bp is at –3 cm in the absence of prolapse and would have a positive value equal to the position of the cuff in a woman with total posthysterectomy vaginal eversion. Point Ap A point located in the midline of the posterior vaginal wall 3 cm proximal to the hymen. By definition, the range of position of Point Ap relative to the hymen is –3 to +3 cm.
The position of Points Aa, Ba, Ap, Bp, C, and (if applicable) D with reference to the hymen should be measured and recorded. Positions are expressed as centimeters above or proximal to the hymen (negative number) or centimeters below or distal to the hymen (positive number) with the plane of the hymen being defined as zero (0). While an examiner may be able to make measure-
C D 3 cm
Ba
Aa Bp Ap tvl
Posterior Vaginal Wall Analogous to anterior prolapse, posterior prolapse should be discussed in terms of segments of the vaginal wall rather than the organs which lie behind it. Thus, the term ‘posterior vaginal wall prolapse’ is preferable to ‘rectocele’ or ‘enterocele’ unless the organs involved are identified by ancillary tests. If small bowel appears to be present in the rectovaginal space, the examiner should comment on this fact and should clearly describe the basis for this clinical impression (e.g. by observation of peristaltic activity in the distended posterior vagina, by palpation of loops of small bowel between an examining finger in the rectum and one in the vagina, etc.). In such cases, a ‘pulsion’ addendum to the point Bp position should be noted (e.g. Bp = +5[pulsion]) (see ‘Supplementary physical examination techniques’, points a and b, below).
gh
pb
Figure 52.1. Six points, genital hiatus (gh), perineal body (pb), and total vaginal length (tvl) used for prolapse quantitation.
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ments to the nearest half (0.5) cm, it is doubtful that further precision is possible. All reports should clearly specify how measurements were derived. For example, were direct measurements made using a probe, ruler, glove, speculum or other device marked in centimeters, were indirect measurements made with the examiner’s fingers and then measured off a centimeter tape, were measurements estimated by the examiner without using a graduated device, or were combinations of techniques used? If customized measuring devices were used, diagrams of such should be included in any manuscript or presentation. Measurements may be recorded as a simple line of numbers (e.g. –3, –3, –7, –9, –3, –3, 9, 2, 2 for Points Aa, Ba, C, D, Bp, Ap, total vaginal length, genital hiatus, and perineal body, respectively). Note that the last three numbers have no sign (i.e. – or +) attached to them because they denote lengths and not positions relative to the hymen. Alternatively, a three-by-three ‘tic-tac-toe’ grid can be used to organize concisely the measurements as noted in Figure 52.2. If point D is not applicable due to a prior hysterectomy, this should be noted as such with ‘NA’ or ‘—’ in either the line of numbers or in the grid. Figure 52.3 is a line diagram contrasting measurements indicating normal support to those of posthysterectomy vaginal eversion. In the example of normal support (Fig. 52.3a), Points Aa and Ba and Points Ap and Bp are all –3 since there is no anterior or posterior wall descent. The lowest point of the cervix is 8 cm above the hymen (–8) and the posterior fornix is 2 cm above this (–0). The vaginal length is 0 cm and the genital hiatus and perineal body measure 2 and 3 cm, respectively. In the example of complete eversion (Fig. 52.3b), the most distal point of the anterior wall (Point Ba), the vaginal cuff scar (Point C), and the most distal point of the posterior wall (Point Bp) are all at the same position (+8) and Points Aa and Ap are maximally distal (both at +3). The fact that the total vaginal length equals the maximum protrusion reflects the fact that the eversion is total. Figure 52.4 is a line diagram representing predominant anterior and posterior vaginal wall prolapse with partial vault descent. In the example of a predominant anterior support defect (Fig. 52.4a), the leading point of the prolapse is the upper anterior vaginal wall, Point Ba (+6). Note that there is significant elongation of the bulging anterior wall. Point Aa is maximally distal (+3) and the vaginal cuff scar is 2 cm above the hymen (C = –2). The cuff
Point Aa anterior wall
Point Ba anterior wall
Point C cervix or cuff
Genital hiatus
Perineal body
Total vaginal length
Point Ap posterior wall
Point Bp posterior wall
Point D posterior fornix
Figure 52.2. A three-by-three grid for recording the quantitative description of pelvic organ prolapse.
Complete vaginal vault eversion
Aa Ba s
s
Aa
s
Ba
s Cs s
s
sD
C
s s
Ap Bp
s
Bp
Normal support of uterine cervix
Ap
+3 Aa
+8 Ba
+8 C
–3 Aa
–3Ba
–8C
4.5 gh
1.5 pb
8 tvl
2 gh
3pb
10tvl
+3
Ap
+8
Bp
–
–3
a
Ap
–3
Bp
D
–10
b
Figure 52.3.
(a) Complete eversion; (b) normal support.
Predominant posterior support defect
Predominant anterior support defect with partial vault descent
Ba Aa s
s
Aa
s
C
s
C Bp
ss
s Ba
s
sBp
Ap +3 Aa
+6 Ba
–2 C
–3 Aa
–3 Ba
–6 C
4.5 gh
1.5 pb
6 tvl
4.5 gh
1 pb
8 tvl
_
+2
Ap
+3 a
s
Ap
–2
Bp
Ap
+5
Bp
_
b
Figure 52.4. (a) Predominant anterior prolapse; (b) predominant posterior prolapse. 775
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scar has undergone 4 cm of descent since it would be at –6 (the total vaginal length) if it were perfectly supported. In this example, the total vaginal length is not the maximum depth of the vagina with the elongated anterior vaginal wall maximally reduced, but rather the depth of the vagina at the cuff with Point C reduced to its normal full extent as specified in ‘Other landmarks and measurements’, above. In the example of the predominant posterior support defect (Fig. 52.4b), the leading point of the prolapse is the upper posterior vaginal wall, Point Bp (+5). Point Ap is 2 cm distal to the hymen (+2) and the vaginal cuff scar is 6 cm above the hymen (–6). The cuff has undergone only 2 cm of descent since it would be at –8 (the total vaginal length) if it were perfectly supported.
Ordinal staging of pelvic organ prolapse The tandem profile for quantifying prolapse just described provides a precise description of anatomy for individual patients. However, because of the many possible combinations, such profiles cannot be directly ranked; the many variations are too numerous to permit useful analysis and comparisons when populations are studied. Consequently, they are analogous to other tandem profiles such as the tumor–node–metastasis (TNM) index for various cancers. For the TNM description of individual patients’ cancers to be useful in population studies evaluating prognosis or response to therapy, they are clustered into an ordinal set of stages. Ordinal stages represent adjacent categories that can be ranked in an ascending sequence of magnitude, but the categories are assigned arbitrarily and the intervals between them cannot actually be measured. While the committee is aware of the arbitrary nature of an ordinal staging system and the possible biases that it introduces, we conclude that such a system is necessary if populations are to be described and compared, if symptoms putatively related to prolapse are to be evaluated, and if the results of various treatment options are to be assessed and compared. Stages are assigned according to the most severe portion of the prolapse when the full extent of the protrusion has been demonstrated according to the criteria in ‘Conditions of the examination’, above. In order for a stage to be assigned to an individual subject, it is essential that her quantitative description be completed first. The 2 cm buffer related to the total vaginal length in Stages 0 and IV is an effort to compensate for vaginal distensibility and the inherent imprecision of the measurement of total vaginal length. The 2 cm buffer around
the hymen in Stage II is an effort to avoid confusing a stage to a single plane and to acknowledge practical limits of precision in this assessment. Stage 0 No prolapse is demonstrated. Points Aa, Ap, Ba, and Bp are all at –3 cm and either Point C or D is between –X cm and –(X –2) cm, where X = the total vaginal length in centimeters [i.e. the quantitation value of Point C or D is ≤ –(X –2) cm]. Figure 52.3a represents Stage 0 pelvic organ prolapse. Stage I The criteria for Stage 0 are not met but the most distal portion of the prolapse is more than cm above the level of the hymen (i.e. its quantitation value is < – cm). Stage I can be subgrouped according to which portion of the lower reproductive tract is the most distal part of the prolapse using the following letter qualifiers: a = anterior vaginal wall, p = posterior vaginal wall, C = vaginal cuff, Cx = cervix, and Aa, Ap, Ba, Bp, and D for the Points of measurement already defined (e.g. I-Cx if the cervix is the most distal, I-Bp if the upper posterior wall is most distal, or I- if the junction of the distal and proximal anterior wall is the most distal part of the prolapse. Stage II The most distal portion of the prolapse is cm or less proximal to or distal to the plane of the hymen (i.e. its quantitation value is ≥ – cm but ≤ + cm). Stage II can be subgrouped according to the scheme described under Stage I (e.g. II-a, II-C, or II-Bp). Stage III The most distal portion of the prolapse is more than cm below the plane of the hymen but protrudes no further than 2 cm less than the total vaginal length in centimeters [i.e. its quantitation value is > + cm but < +(X –2) cm where X = total vaginal length]. Stage III can be subgrouped according to the scheme described under Stage I. For example, Fig. 52.4a represents State III-Ba and Fig. 52.4b represents Stage III-Bp prolapse. Stage IV Essentially complete eversion of the total length of the lower genital tract is demonstrated. The distal portion of the prolapse protrudes to at least (X –2) cm where X = the total vaginal length in centimeters [i.e. its quantitation value is ≥ +(X –2) cm]. In most instances, the leading edge of Stage IV prolapse will be the cervix or
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vaginal cuff scar. Rare exceptions to this can be noted according to the subgrouping scheme described under Stage I. Figure 52.3b represents Stage IV-C prolapse. Table 52. summarizes the staging system.
ANCILLARY TECHNIQUES FOR DESCRIBING PELVIC ORGAN PROLAPSE This series of procedures may help to further characterize pelvic organ prolapse in an individual patient. They are considered ancillary either because they are not yet standardized or validated or because they are not universally available to all patients. Authors utilizing these procedures should include the following information in their manuscripts. a. Describe the objective information they intended to generate and how it enhanced their ability to evaluate or treat prolapse. b. Describe precisely how the test was performed, any instruments that were used, and the specific testing conditions (see ‘Conditions of the examination’, above) so that other authors can reproduce the study. c. Document the reliability of the measurement obtained with the technique.
Supplementary physical examination techniques Many of these techniques are essential to the adequate preoperative evaluation of a patient with pelvic organ prolapse. While they do not directly affect either the tanTable 52.1.
ICS pelvic organ prolapse ordinal staging system
Stage 0
Points Aa, Ap, Ba, & Bp are all at –3 cm and Either Point C or D is at ≤ – (X – 2) cm
Stage I
The criteria for Stage 0 are not met and the leading edge of prolapse is < –1 cm
Stage II
Leading edge of prolapse is ≥ –1 cm but ≤ +1 cm
Stage III
Leading edge of prolapse is > +1 cm but < + (X – 2) cm
Stage IV
Leading edge of prolapse is ≥ + (X – 2) cm
X = total vaginal length in centimeters in Stages 0, III, and IV Stages I through IV can be subgrouped according to which portion of the lower reproductive tract is the leading edge of the prolapse using the following qualifiers: a = anterior vaginal wall, p = posterior vaginal wall, C = vaginal cuff, Cx = cervix, and Aa, Ba, Ap, Bp, and D for the defined points of measurement (e.g. IV-Cx, II-a, or III-Bp)
dem profile or the ordinal stage, they are important for the selection and performance of an effective surgical repair. These techniques include, but are not necessarily limited to, the following: a. performance of a digital rectal–vaginal examination while the patient is straining and the prolapse is maximally developed to differentiate between a high rectocele and an enterocele; b. digital assessment of the contents of the rectal– vaginal septum during the examination noted in a. above to differentiate between a ‘traction’ enterocele (the posterior cul-de-sac is pulled down with the prolapsing cervix or vaginal cuff but is not distended by intestines) and a ‘pulsion’ enterocele (the intestinal contents of the enterocele distend the rectal–vaginal septum and produce a protruding mass); c. Q-tip testing for the measurement of urethral axial mobility; d. measurements of perineal descent; e. measurements of the transverse diameter of the genital hiatus or of the protruding prolapse; f. measurements of vaginal volume; g. description and measurement of rectal prolapse; h. examination techniques for differentiating between various types of defect (e.g. central versus paravaginal defects of the anterior vaginal wall).
Endoscopy Cystoscopic visualization of bowel peristalsis under the bladder base or trigone may identify an anterior enterocele in some patients. The endoscopic visualization of the bladder base and rectum and observation of the voluntary constriction and dilation of the urethra, vagina, and rectum has, to date, played a minor role in the evaluation of pelvic floor anatomy and function. When such techniques are described, authors should include the type, size, and lens angle of the endoscope used, the doses of any analgesic, sedative, or anesthetic agents used, and a statement of the level of consciousness of the subject in addition to a description of the other conditions of the examination.
Photography Still photographic documentation of prolapse beyond Stage II may be utilized both to document serial changes in individual patients and to illustrate findings for manuscripts and presentations. Photographs should 777
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contain an internal frame of reference such as a centimeter ruler or tape.
Imaging procedures Different imaging techniques have been used to visualize pelvic floor anatomy, support defects, and relationships among adjacent organs. These techniques may be more accurate than physical examination in determining which organs are involved in pelvic organ prolapse. However, they share the limitations of the other techniques in this section, i.e. a lack of standardization, validation, and/or availability. For this reason, no specific technique can be recommended but guidelines for reporting various techniques will be considered.
Contrast radiography Contrast radiography may be static or dynamic and may include voiding colpo-cysto-urethrography, defecography, peritoneography, and pelvic fluoroscopy among others. All reports of contrast radiography should include the following information: a. projection (e.g. lateral, frontal, horizontal, oblique); b. type and amount of contrast media used and sequence of opacification of the bladder, vagina, rectum and colon, small bowel, and peritoneal cavity; c. any urethral or vaginal appliance used (e.g. tampon, catheter, bead-chain); d. type of exposure (e.g. single exposure, video); e. magnification – an internal reference scale should be included.
General guidelines for imaging procedures Landmarks should be defined to allow comparisons with other imaging studies and the physical examination. The lower edge of the symphysis pubis should be given high priority as a landmark. Other examples of bony landmarks include the superior edge of the pubic symphysis, the ischial spine, the obturator foramen, and the promontory of the sacrum. All reports on imaging techniques should specify the following: a. position of the patient including the position of her legs (images in manuscripts should be oriented to reflect the patient’s position when the study was performed and should not be oriented to suggest an erect position unless the patient was erect); b. specific verbal instructions given to the patient; c. bladder volume and content and bowel content, including any pre-study preparations; d. the performance and display of simultaneous monitoring such as pressure measurements that might be used to document that exposures were made at the most appropriate moment.
Ultrasonography Continuous visualization of dynamic events is possible. All reports using ultrasound should include the following information: a. transducer type and manufacturer (e.g. sector, linear, MHz); b. transducer size; c. transducer orientation; d. route of scanning (e.g. abdominal, perineal, vaginal, rectal, urethral).
Computed tomography and magnetic resonance imaging These techniques do not allow for continuous imaging under dynamic conditions. Currently available equipment usually dictates supine scanning. Details of the technique should be specified including: a. the specific equipment used, including the manufacturer; b. the plane of imaging (e.g. axial, sagittal, coronal, oblique); c. the field of view; d. the thickness of sections and the number of slices; e. the scan time; f. the use and type of contrast; g. the type of image analysis.
Surgical assessment Intraoperative evaluation of pelvic support defects is intuitively attractive but as yet of unproven value. The effects of anesthesia, diminished muscle tone, and loss of consciousness are of unknown magnitude and direction. Limitations due to the position of the patient must also be evaluated.
PELVIC FLOOR MUSCLE TESTING Pelvic floor muscles are voluntarily controlled, but selective contraction and relaxation necessitate muscle awareness. Optimal squeezing technique involves contraction of the pelvic floor muscles without contraction of the abdominal wall muscles and without a Valsalva maneuver. Squeezing synergists are the intra-
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urethral and anal sphincteric muscles. In normal voiding, defecation, and optimal abdominal-strain voiding, the pelvic floor is relaxed, whereas the abdominal wall and the diaphragm may contract. With coughs and sneezes, and often when other stresses are applied, the pelvic floor and abdominal wall are contracted simultaneously. Evaluation and measurement of pelvic floor muscle function includes: ) an assessment of the patient’s ability to contract and relax the pelvic muscles selectively (i.e. squeezing without abdominal straining and vice versa); and 2) measurement of the force (strength) of contraction. There are pitfalls in the measurement of pelvic floor muscle function because the muscles are invisible to the investigator and because patients often simultaneously and erroneously activate other muscles. Contraction of the abdominal, gluteal, and hip adductor muscles, Valsalva maneuver, straining, breath holding, and forced inspirations are typically seen. These factors affect the reliability of available testing modalities and have to be taken into consideration in the interpretation of these tests. The individual types of test cited in this report are based on both the scientific literature and current clinical practice. It is the intent of the committee neither to endorse specific tests or techniques nor to restrict evaluations to the examples given. The standards recommended are intended to facilitate comparison of results obtained by different investigators and to allow investigators to replicate studies precisely. For all types of measuring technique, the following should be specified:
any device used should be specified as should the state of undress of the patient.
a. b. c. d.
a. b. c. d. e. f. g.
patient position, including the position of the legs; specific instructions given to the patient; the status of bladder and bowel fullness; techniques of quantification or qualification (estimated, calculated, directly measured); e. the reliability of the technique.
Inspection A visual assessment of muscle integrity, including a description of scarring and symmetry, should be performed. Pelvic floor contraction causes inward movement of the perineum and straining causes the opposite movement. Perineal movements can be observed directly or assessed indirectly by movement of an externally visible device placed into the vagina or urethra. The abdominal wall and other specified regions might be watched simultaneously. The type, size and placement of
Palpation Palpation may include digital examination of the pelvic floor muscles through the vagina or rectum as well as assessment of the perineum, abdominal wall, and/or other specified regions. The number of fingers and their position should be specified. Scales for the description of the strength of voluntary and reflex (e.g. with coughing) contractions and of the degree of voluntary relaxation should be clearly described and intra- and interobserver reliability documented. Standardized palpation techniques could also be developed for the semi-quantitative estimation of the bulk or thickness of pelvic floor musculature around the circumference of the genital hiatus. These techniques could allow for the localization of any atrophic or asymmetric segments.
Electromyography Electromyography from the pelvic floor muscles can be recorded alone or in combination with other measurements. Needle electrodes permit visualization of individual motor unit action potentials, while surface or wire electrodes detect action potentials from groups of adjacent motor units underlying or surrounding the electrodes. Interpretation of signals from these latter electrodes must take into consideration that signals from erroneously contracted adjacent muscles may interfere with signals from the muscles of interest. Reports of electromyographic recordings should specify the following: type of electrode; placement of electrodes; placement of reference electrode; specifications of signal processing equipment; type and specifications of display equipment; muscle in which needle electrode is placed; description of decision algorithms used by the analytic software.
Pressure recording Measurements of urethral, vaginal, and anal pressures may be used to assess pelvic floor muscle control and strength. However, interpretations based on these pressure measurements must be made with a knowledge of their potential for artifact and their unproven or limited reproducibility. Anal sphincter contractions, rectal peristalsis, detrusor contractions, and abdominal straining 779
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can affect pressure measurements. Pressures recorded from the proximal vagina accurately mimic fluctuations in abdominal pressure. Therefore, it may be important to compare vaginal pressures to simultaneously measured vesical or rectal pressures. Reports using pressure measurements should specify the following: a. the type and size of the measuring device at the recording site (e.g. balloon, open catheter, etc.); b. the exact placement of the measuring device; c. the type of pressure transducer; d. the type of display system; e. the display of simultaneous control pressures. As noted in the section on ‘Inspection’ (above), observation of the perineum is an easy and reliable way to assess for abnormal straining during an attempt at a pelvic muscle contraction. Significant straining or a Valsalva maneuver causes downward/caudal movement of the perineum; a correctly performed pelvic muscle contraction causes inward/cephalad movement of the perineum. Observation for perineal movement should be considered as an additional validation procedure whenever pressure measurements are recorded.
DESCRIPTION OF FUNCTIONAL SYMPTOMS Functional deficits caused by pelvic organ prolapse and pelvic floor dysfunction are not well characterized or absolutely established. There is an ongoing need to develop, standardize, and validate various clinimetric scales such as condition-specific quality-of-life questionnaires for each of the four functional symptom groups (described below) thought to be related to pelvic organ prolapse. Researchers in this area should try to use standardized and validated symptom scales whenever possible. They must always ask precisely the same questions regarding functional symptoms before and after therapeutic intervention. The description of functional symptoms should be directed toward four primary areas: ) lower urinary tract; 2) bowel; 3) sexual; and 4) other local symptoms.
Urinary symptoms This report does not supplant any currently approved ICS terminology related to lower urinary tract function. However, some important prolapse related symptoms are not included in the current standards (e.g. the need to manually reduce the prolapse or assume an unusual position to initiate or complete micturition). Urinary
symptoms that should be considered for dichotomous, ordinal, or visual analog scaling include, but are not limited to, the following: a. b. c. d. e. f. g. h.
stress incontinence; frequency (diurnal and nocturnal); urgency; urge incontinence; hesitancy; weak or prolonged urinary stream; feeling of incomplete emptying; manual reduction of the prolapse to start or complete voiding; i. positional changes to start or complete voiding.
Bowel symptoms Bowel symptoms that should be considered for dichotomous, ordinal, or visual analog scaling include, but are not limited to, the following: a. b. c. d. e. f. g. h.
difficulty with defecation; incontinence of flatus; incontinence of liquid stool; incontinence of solid stool; fecal staining of underwear; urgency of defecation; discomfort with defecation; digital manipulation of vagina or perineum to complete defecation; i. feeling of incomplete evacuation.
Sexual symptoms Research is needed to attempt to differentiate the complex and multifactorial aspects of ‘satisfactory sexual function’ as it relates to pelvic organ prolapse and pelvic floor dysfunction. It may be difficult to distinguish between the ability to have vaginal intercourse and normal sexual function. The development of satisfactory tools will require multidisciplinary collaboration. Sexual function symptoms that should be considered for dichotomous, ordinal, or visual analog scaling include, but are not limited to, the following: a. b. c. d. e. f. g.
Is the patient sexually active? If she is not sexually active, why? Does sexual activity include vaginal coitus? What is the frequency of vaginal intercourse? Does the patient experience pain with coitus? Is the patient satisfied with her sexual activity? Has there been any change in orgasmic response?
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Other local symptoms We currently lack knowledge regarding the precise nature of symptoms that may be caused by the presence of a protrusion or bulge. Possible anatomically based symptoms that should be considered for dichotomous, ordinal, or visual analog scaling include, but are not limited to, the following: a. vaginal pressure or heaviness; b. vaginal or perineal pain; c. sensation or awareness of tissue protrusion from the vagina; d. low back pain; e. abdominal pressure or pain; f. observation or palpation of a mass.
ACkNOwLEDGMENTS The subcommittee would like to acknowledge the contributions of the following consultants who contributed to the development and revision of this document: W. Glenn Hurt, MD, Richmond, VA, US Bernhard Schüssler, MD, Luzern, Switzerland L. Lewis Wall, MD DPhil, New Orleans, LA, US.
REFERENCE .
Abrams P, Blaivas JG, Stanton SL, Andersen JT. The International Continence Society Committee on Standardization of Terminology. The standardization of terminology of lower urinary tract function. Scand J Urol Nephrol 988;4S:5–9 [see also Chapter 5.]
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53 Good urodynamic practices: uroflowmetry, filling cystometry, and pressure–flow studies Werner Schaefer, Paul Abrams, Limin Liao, Anders Mattiasson, Francesco Pesce, Anders Spangberg, Arthur M Sterling, Norman R Zinner, Philip van Kerrebroeck
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INTRODUCTION A good urodynamic practice comprises three main elements:
• A clear indication for and appropriate selection of, relevant test measurements and procedures;
• Precise measurement with data quality control and complete documentation;
• Accurate analysis and critical reporting of results. The aim of clinical urodynamics is to reproduce symptoms while making precise measurements in order to identify the underlying causes for the symptoms, and to quantify the related pathophysiologic processes. By doing so, it should be possible to establish objectively the presence of a dysfunction and understand its clinical implications. Thus, we may either confirm a diagnosis or give a new, specifically urodynamic, diagnosis. The quantitative measurement may be supplemented by imaging (videourodynamics). Urodynamic measurements cannot yet be completely automated, except for the most simple urodynamic procedure – uroflowmetry. This is not an inherent problem of the measurement itself, but is due to the current limitations of urodynamic equipment and the lack of a consensus on the precise method of measurement, signal processing, quantification, documentation, and interpretation. With the publication of this International Continence Society (ICS) standardization document on good urodynamic practice, it is expected that the necessary technological developments in automation will follow. Urodynamics allows direct assessment of lower urinary tract (LUT) function by the measurement of relevant physiologic parameters. The first step is to formulate the ‘urodynamic question or questions’ from a careful history, physical examination, and standard urologic investigations. The patient’s recordings of micturitions and symptoms on a frequency volume chart, and repeated free uroflowmetry with determination of postvoid residual volume, provide important, non-invasive, objective information that helps to define the specific urodynamic question(s) prior to invasive urodynamics such as filling cystometry and pressure–flow studies. Recommendations for good urodynamic practice are bullet pointed.
RECORDING MICTURITIONS AND SYMPTOMS A micturition time chart records the time of each micturition. The usefulness of such a record is significantly enhanced when the voided volumes are recorded in a frequency volume chart. The bladder diary adds to this
the relevant symptoms and events such as urgency, pain, incontinence, episodes, and pad usage. Recording for a minimum of 2 days is recommended. From the recordings, the average voided volume, voiding frequency, and, if the patient’s time in bed is recorded, day/night urine production and nocturia can be determined. This information provides objective verification of the patient’s symptoms, together with key values for plausibility control of subsequent urodynamic studies; for example, in order to prevent overfilling of the patient’s bladder.
UROFLOWMETRY Uroflowmetry is non-invasive and relatively inexpensive. Therefore, it is an indispensable, first-line screening test for most patients with suspected LUT dysfunction. Objective and quantitative information, which helps in the understanding of both storage and voiding symptoms, is provided by this simple urodynamic measurement. Adequate privacy should be provided and patients should be asked to void when they feel a ‘normal’ desire to void. Patients should be asked if their voiding was representative of their usual voiding and their view should be documented. Automated data analysis must be verified by inspection of the flow curve, artifacts must be excluded, and verification must be documented. The results from uroflowmetry should be compared with the data from the patient’s own recording on a frequency/ volume chart. Sonographic estimation of post-void residual volume completes the non-invasive assessment of voiding function.
Normal uroflow Normal voiding occurs when the bladder outlet relaxes (is passive) and the detrusor contracts (is active). An easily distensible bladder outlet with a normal detrusor contraction results in a smooth arc-shaped flow rate curve with high amplitude. Any other shapes – such as curves that are flat, asymmetric, or have multiple peaks (fluctuating and/or intermittent) – indicate abnormal voiding, but are not specific for its cause. It is assumed that it is normal for the mechanical properties of a relaxed outlet to be constant, and that the properties can be defined by the dependency of the cross-sectional area of the urethral lumen on the intraurethral pressure at the flow rate controlling zone (FRCZ). Typically, below the minimum urethral opening pressure (pmuo), the urethral lumen is closed. The lumen then opens widely with little additional pressure
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Q (ml/s)
surface of the funnel, or patient movements (see flow curves in Figs 53.3–53.8).
Accuracy of uroflowmeters 10 20
Q (ml/s)
a
b
Time (s)
10 20
Time (s)
Figure 53.1. (a) Typical normal flow; (b) constrictive flow curve (dotted line), compressive flow curve (solid line). increase. With normal detrusor contractility and low intraurethral pressure, the normal flow curve is arcshaped with a high maximum flow rate (Fig. 53.1a). A normal flow curve is a smooth curve without any rapid changes in amplitude because the shape of the flow curve is determined by the kinetics of the detrusor contraction which – arising from smooth muscle – does not show rapid variations. A decreased detrusor power and/or a constant increased urethral pressure will both result in a lower flow rate and a smooth flat flow curve. A constrictive obstruction (e.g. urethral stricture) with reduced lumen size results in a plateau-like flow curve (Fig 53.1b, dotted line). A compressive obstruction with increased urethral opening pressure (e.g. benign prostatic obstruction) shows a flattened asymmetric flow curve with a slowly declining end part (Fig. 53.1b, solid line). The same pattern may also originate from a weak detrusor in aging males and females. Fluctuations in detrusor contractility or abdominal straining, as well as variable outlet conditions (e.g. intermittent sphincter activity), will lead to complex flow rate patterns. Rapid changes in flow rate may have physiologic or physical causes that are due either to changes in outlet resistance (e.g. sphincter/pelvic floor contraction or relaxation, mechanical compression of the urethral lumen, or interference at the meatus) or to changes in driving energy (e.g. abdominal straining). These intracorporeal causes lead to true flow rate changes. Rapid changes in flow rate may also be artifacts, when the flow rate signal is extracorporeally modified through interference between the stream and the collecting funnel (the flowmeter), movement of the stream across the
Uroflowmetry measures the flow rate of the external urinary stream as volume per unit time in milliliters per second (ml/s). The ICS Technical Report1 made recommendations with respect to uroflowmetry, but did not compare different flowmeters by specific testing. There are, however, differences in the accuracy and precision of the flow rate signals that depend on the type of flowmeter, on internal signal processing, and on the proper use and calibration of the flowmeter. The desired and actual accuracy of uroflowmetry should be assessed in relation to the potential information that could be obtained from the urinary stream compared to the information actually abstracted for clinical and research purposes. Some relevant aspects of the physiologic and physical information contained in the urinary stream are outlined here. The desired clinical accuracy may differ from the technical accuracy of a flowmeter. The ICS Technical Report recommended the following standards: a range of 0–50 ml/s for Qmax, and zero to 1000 ml for voided volume, maximum time constant of 0.75 s; an accuracy of ±5% relative to full scale, although a calibration curve representing the percentage error over the entire range of measurement should be made available. However, technical specifications from the manufacturers are rare and often not in accordance with ICS recommendations; this situation should be rectified. Furthermore, as most flowmeters are mass flowmeters (e.g. a weight transducer or rotating disk), variations in the specific gravity of the fluid will have a direct influence on the measured flow rate. For example, urine of high concentration may increase apparent flow rate by 3%. With x-ray medium, the flow rate may be overestimated by as much as 10%. These effects should be corrected by calibration software. Thus, since the overall accuracy of flow rate signals will not be better than ±5%, it would not be meaningful to report a maximum flow rate of a resolution better than a full milliliter per second (ml/s). Under carefully controlled research conditions, a better resolution may be possible by flowmeter calibration and instrument selection. However, such improvements in resolution may not be required for routine clinical applications. The dynamic properties of most flowmeters will be good enough for free uroflowmetry. When pressure– flow data are analyzed, however, the limitation in signal dynamics should be taken into account because pres785
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sure will be different from flow. Flow signals have a much slower response, and are less accurate than pressure signals.
Problems in urine flow rate measurement The problems in measurement, as well as the information that can be abstracted from the flow rate signal, are rather different for free uroflowmetry compared to combined pressure–flow recordings. In free uroflowmetry, the shape of the flow curve may suggest specific types of abnormality; however, reliable, specific, and detailed information about the cause of abnormal voiding cannot be derived from a flow curve alone. Only when uroflowmetry is combined with intravesical and abdominal pressure recordings does it become possible, from the pressure–flow relationship, to analyze separately the contributions of detrusor contractility and bladder outlet function to the overall voiding pattern (see Figs 53.3–53.8). Urine flow rate measurement is affected by a number of important factors.
Detrusor contractility As the voiding function reflects the interaction between the relaxed outlet and the contracting detrusor, variation of both will affect the flow. For steady outflow conditions, all variations in flow rate are related to changes in detrusor activity alone. The detrusor contraction strength varies neurogenically and myogenically, and can cause significant variability in urine flow rate measurements (see Fig. 53.5).
Bladder outflow resistance If detrusor contractility is constant, then changes in outflow resistance will lead to changes in flow rate; for example, in patients with detrusor–sphincter dyssynergia (see Figs 53.3, 53.7, 53.8).
Bladder volume As the bladder volume increases and the detrusor muscle fibers become more stretched, there is an increase in the potential bladder power and work associated with a contraction. This is most pronounced in the range from empty up to 150–250 ml bladder filling volume. It appears that, at volumes higher than 400–500 ml, the detrusor may become overstretched and contractility may decrease again. Therefore, Qmax is physiologically dependent on the bladder volume. This dependency will vary between individuals and with the type and degree of pathology; for example, in constrictive obstruction, Qmax is almost independent of volume, and in compressive obstruc-
tion, the dependency becomes weaker with increasingly obstructed outlet conditions and lower flow rate.
Technical considerations The flow rate signal is influenced by the technique of measurement and by signal processing. The external urinary stream should reach the flowmeter unaltered and with minimal delay. However, any funnel or collecting device, as well as the flowmeter, will inevitably introduce modifications to the flow rate recording. Physically, the external urinary stream breaks into drops not far from the meatus. This fine structure of the stream has a high frequency, which can be assessed by drop spectrometry, and contains interesting information. For standard uroflowmetry, however, such high frequencies should be eliminated by signal processing. For free uroflowmetry, all intracorporeal modulations of the flow rate are physiologic artifacts and should be minimized (e.g. by asking the patient to relax and not to strain). Nevertheless, certain dynamic patterns of intracorporeal modulations can provide information about functional obstruction (e.g. typical patterns of detrusor–sphincter dyssynergia or abnormal straining). This information may be lost by excessive filtering or during analog to digital A/D conversion with a filter speed of less than 10 Hz. The precise interpretation of dynamic variations in the flow rate signal is only possible when the flow rate is viewed together with the simultaneously recorded pressure signals. Thus, only in combined pressure–flow recordings can the details of the flow signal be fully understood. For the determination of the ‘true’ maximum flow rate value, particularly during free flow, such high frequency signal variations are more likely to be misleading, and consequently they should be suppressed electronically.
Recommendations for uroflowmetry In order to facilitate the recording of urine flow rate and pattern recognition of flow curves, it is recommended that graphical scaling should be standardized as follows:
• One millimeter should equal 1 s on the x-axis and 1 ml/s and 10 ml voided volume on the y-axis. With respect to the technical accuracy of uroflowmeters, it is meaningful for routine clinical measurements to read flow rate values only to the nearest full ml/s and volumes to the nearest 10 ml. In order to make electronically read Qmax values more reliable, comparable, and clinically useful, we recom-
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mend internal electronic smoothing of the flow rate curve. It is recommended that:
• a sliding average over 2 s should be used to remove positive and negative spike artifacts. If curves are smoothed by hand, the same concept should be applied. That is, when reading Qmax graphically, the line should be smoothed by eye into a continuous curve so that in each period of 2 s, there are no rapid changes. Such a smoothed, clinically meaningful maximum free flow Qmax will be different (lower) from the peak value in the flow rate recording of electronic instruments currently available (see Figs 53.2, 53.5, 53.6, 53.8). It is recommended that:
• only flow rate values, which have been ‘smoothed’, either electronically or manually, should be reported. If a maximum flow value is determined electronically by simple signal peak detection without the recommended electronic smoothing, it should be labeled differently – Qmax.raw. Such raw data have meaning only if a detailed specification of the type of flowmeter used is given. The interpretation of any dynamic variation (signal patterns) in free flow will rely on personal experience, can be only descriptive, and in general will remain speculative. For the documentation of the results of uroflowmetry, the following recommendations are made:
residuals as VOID1 = 8/90/0 and VOID2 = 17/180/20 (see Figs 53.2, 53.5, 53.6). The adoption of these standards will aid the interpretation of uroflowmetry results. If data are not available, then a minus sign should be used; for example, if only the voided volume is known, VOID: –/340/– or, if the voided volume was missing, VOID: 10/–/90.
• If a flow/volume nomogram is used, this should be stated and referenced. Uroflowmetry data from other than free flow (e.g. measured in combination with intravesical pressure) should be reported with an additional descriptive index, p, i.e. Qmax.p, for pressure–flow recording.
INVASIVE URODYNAMICS: FILLING CYSTOMETRY, PRESSURE–FLOW STUDY OF VOIDING Introduction Invasive urodynamic procedures should not be performed without clear indications and the formulation of specific urodynamic question(s). This process will usually be aided by the a priori completion of a frequency volume chart and free uroflowmetry. There are certain key recommendations that will lead to the performance of a successful urodynamic study.
• A good urodynamic investigation should be
• Maximum (smoothed) urine flow rate should be •
•
rounded to the nearest whole number (a recording of 10.25 ml/s would be recorded as 10 ml/s); Voided volume and post-void residual volume should be rounded to the nearest 10 ml (a recording of a voided volume of 342 ml would be recorded as 340 ml); The maximum flow rate should always be documented together with voided volume and post-void residual volume using a standard format: VOID: maximum flow rate/volume voided/post-void residual volume.
For example, the automatically detected flows, Qmax.raw, are 16.6 and 21.3 ml/s with voided volumes of 86 and 182 ml, respectively. The smoothed Qmax values are 8 and 17 ml/s and should be reported with voided volumes of 90 and 180, respectively, and the estimated
•
•
performed interactively with the patient. It should be established by discussion with the patient that the patient’s symptoms have been reproduced during the test. There should be continuous and careful observation of the signals as they are collected, and the continuous assessment of the qualitative and quantitative plausibility of all signals. Artifacts should be avoided, and any artifacts that occur should be corrected immediately. It is always difficult and is often impossible to correct artifacts during a retrospective analysis. Furthermore, it is more time consuming than if the signals are continuously observed and tested at regular intervals and artifacts recognized during the urodynamic study and corrected.
At present, ambulatory urodynamic monitoring has to rely on retrospective quality control and artifact corrections. However, in principle, the same quality crite787
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ria apply for ambulatory urodynamic monitoring as for standard urodynamics.2 This makes a consensus on quality even more important, because only when such criteria are precisely defined can they be implemented in an ‘automated intelligent’ ambulatory system. Quality control relies on pattern recognition and a knowledge of normal values as well as prior identification of useful information obtained from non-invasive urodynamics and all other sources relevant for the urodynamic question. Thus, before invasive urodynamics, a frequency volume chart should be completed. Useful information obtained from non-invasive testing includes typical voided volumes and post-void residual volumes as well as the expected values for Qmax. This information should be used for the control of subsequent invasive studies. Only by good preparation can it be ensured that: 1) the proper answers to the urodynamic questions will be obtained before the study is terminated; and 2) essential modifications, additions or repetitions of measurements will have been performed in order to derive the necessary information.
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Figure 53.2. Exclusion of artifactual spikes in the flow curve, Qmax raw, and determination of a clinically relevant maximum flow rate, Qmax, by manual smoothing. The results from uroflowmetry should be reported in the standard format: Qmax/Vvoid/Vres.
The effective practice of urodynamics requires: 1) a theoretical understanding of the underlying physics of the measurement; 2) practical experience with urodynamic equipment and procedures; 3) an understanding of how to ensure quality control of urodynamic signals; and 4) the ability to analyze critically the results of the measurements. Because urodynamics deals largely with mechanical measurements such as pressure and volume and their related changes in time, and because many analytical models use mechanical concepts such as resistance to flow or contraction power, it is essential that the nature of these measurements and concepts, in particular for pressure and flow rate, are understood. Therefore, in addition to a comprehensive understanding of anatomy and physiology, some basic knowledge of biomechanics and physics is required. The quality control of urodynamic measurements must be approached on a holistic basis. Different types and levels of data quality and plausibility control should be used: 1) on a physical and technical level; 2) on a biomechanical level; and 3) on a pathophysiologic
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Figure 53.3. Full recording of filling and voiding. Starting with initial values for pves, pabd of 32 cmH2O in the typical range for a standing patient with zero pdet; testing signal quality with a vigorous cough at the beginning, and regularly repeated (here less strong) coughs. Additionally, the pressure recordings show the typical pattern of a talking patient, while the pdet trace is unaffected; a weak contraction at first desire FD; another vigorous cough before voiding; beginning of flow shows dyssynergic sphincter activity as proven by a decrease in flow with an increase in pdet.
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Figure 53.4. Good recording quality until cystometric capacity (CC) is reached; at second cough before voiding the intravesical signal is lost (no response in pves, negative spike in pdet). Dead pves – signal during voiding, which is ‘live’ again only at the second cough after voiding. Thus, pressure–flow study is lost. Careful observation of signals would have made it possible to interrupt the study immediately the signal failed and to correct this problem before voiding started. 789
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Figure 53.5. Variable flow rate due to varying detrusor contraction strength (VOID: 7/250/70).
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Figure 53.6. The first part of the traces shows typical biphasic movement artifacts. The two coughs before voiding prove good recording quality. The typical picture of an unobstructed voiding: a weak detrusor contraction with pdet of 40 cmH2O and a Qmax of 9 ml/s is supported by vigorous straining, which causes some variability in flow (VOID: 9/380/100). clinical level. A common problem in urodynamics is that clinicians often proceed immediately to a clinical interpretation, i.e. to level 3, without a critical analysis of the potential pathophysiologic information content, without considering the plausibility of the signals (level 1), without considering the biomechanical context of the measurements (level 2), and without taking into account the physical properties of the parameters, technical limitations, and accuracy of the signals. Therefore, it is recommended that:
• Invasive urodynamics should not be performed without precise indications and well-defined ‘urodynamic questions’ that are to be answered by the results of the urodynamic study.
Measurement of urine flow rate during pressure–flow studies The usefulness of the concept of a FRCZ for data analysis requires that the recorded pressure and flow rate signal
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Figure 53.7. A good recording showing the typical pattern of increasing detrusor overactivity and a dyssynergic event during voiding.
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be synchronized with respect to the FRCZ.3 Normally, no measurable time delay will exist between the intravesical pressure signal and the actual flow at the FRCZ. However, a significant delay is to be expected for the typical urodynamic flow rate recorded extracorporeally. This delay will vary with anatomy, pathology, flow rate, and the set up for measurement. Our understanding of the actual dynamics of flow rate changes is limited, and the relatively slow response of most flowmeters may not be sufficient to match the dynamics of the much faster pressure signal. The actual time difference may be from 0.5 to 2 s; the time delay between urethral closure and
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Figure 53.8. High quality recordings allow detailed interpretation. The typical pattern of rectal activity becomes clearly visible in pdet. The flow artifacts can be identified as dyssynergic events and manually corrected from Qmax.raw = 11.2 ml/s to Qmax = 9 ml/s.
the end of any flow recording may be much longer, particularly in prostatic obstruction and terminal dribbling than between the opening of the urethra and the start of a flow rate signal. Therefore, we recommend the use of more descriptive terminology for synchronizing pressure and flow values, such as pdet.Qbeg for the pressure at which flow begins instead of pdet.open, and pdet.Qend when flow ends instead of pdet.close. The time delay correction needs to be considered when analyzing pressure flow studies.3 On average, the maximum flow rate recorded during pressure–flow studies (Qmax.p) is lower than during free flow (Qmax). This, however, is not due simply to a 791
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mechanical increase of outflow resistance by the intraurethral catheter, because such a difference is also found in suprapubic pressure–flow studies. A difference has also been reported between Qmax.p during conventional and ambulatory urodynamics. This indicates more complex causes, possibly psychogenic, but also physiologic; for example, that a difference in detrusor contraction strength may be involved, and that the fast filling rate used in clinical studies may lead to reduced contractility. This could also explain the difference in results between conventional and ambulatory studies.
Measurement of intravesical and abdominal pressure • It is recommended that there is strict adherence to the ICS standardization of zero pressure and reference height. Only then can pressure recordings be compared between patients and centers. Zero pressure and reference height are concepts which are often confused in urodynamics; for example, by use of the misleading term ‘zero reference height’. As both are independent features of pressure, they must be considered separately, and both must follow recommended ICS methodology.
• Zero pressure is the surrounding atmospheric pressure. Zero pressure is the value recorded when a transducer is open to the environment when disconnected from any tubes or catheters, or when the open end of a connected, fluid-filled tube is at the same vertical level as the transducer. Only then can a ‘set zero’ or ‘balance’ be performed.
• The reference height is defined as the upper edge of the symphysis pubis. The reference height is the level at which the transducers must be placed so that all urodynamic pressures have the same hydrostatic component. It is often argued that it does not make a difference for the most relevant parameter, pdet, if the same error is introduced to pves and pabd, as they tend to cancel each other out. This is not an acceptable argument. The hydrostatic pressure is real and important, and inevitably plays a role in any intracorporeal pressure recording. Many important aspects of quality and plausibility control, such as typical resting value ranges at different patient positions, are based on the proper recording of pressures, and will not apply if
pressures are not recorded according to ICS standards. Also, it is only meaningful to subtract one pressure from the other – for example (pves – padb = pdet) – when both are recorded to the same reference level.
Pressure transducers Urodynamic techniques are developed using external pressure transducers connected to the patient with fluid-filled lines, allowing easier compliance with the standards of correct zero and reference height. Cathetermounted pressure transducers, so-called microtip transducer catheters, have become popular due to their apparent higher accuracy, better dynamic resolution, and their apparent independence from hydrostatic pressure. A catheter-mounted pressure transducer is an advantage for dynamic recordings of urethral pressures during coughing (stress profiles) as well as for ambulatory urodynamics in mobile patients. Here only the application of catheter-mounted pressure transducers for intravesical and abdominal pressure recordings will be discussed as urethral pressures are dealt with in a separate report.4 All aspects of urodynamic pressure recording outlined in the preceding section are valid and independent of transducer type. It is impossible to define the precise position of an intravesical and a rectal catheter-mounted pressure transducer as to place them at any common level, and impossible to position them at the standard level of the upper border of the symphysis pubis. It has become popular to circumvent this problem by setting the catheter-mounted pressure transducer to zero pressure when inside the body at the start of pressure recording. This, however, means that both the standard zero pressure as well the reference level are ignored, so that such recorded pressure cannot be compared between patients or centers. The fact is, the initial intravesical and abdominal resting pressures are real, are different between patients, and depend significantly on the patient’s position. Thus, there are significant potential errors: by ignoring the correct atmospheric zero pressure, an error of up to 50 cmH2O can occur, and as the reference height of catheter-mounted pressure transducers is usually undetermined, another potential error of 10 cmH2O is possible for a full bladder. In addition, when a study starts with zero abdominal pressure, then the commonly observed abdominal pressure decrease at pelvic floor relaxation during voiding will result in negative abdominal pressure values, and thus in pdet being higher than pves. The same problem of apparent independence from the existing hydrostatic pressure also applies to airfilled catheters and/or connection tubings. Due to the
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absence of a water column between the balloon-covered opening on the catheter and the external transducer, the reference height in an air-filled system will refer to the position of the sensing balloon on the catheter and not to the external transducer.
• It is recommended that external transducers connected to fluid-filled tubings and catheters be used for intravesical and abdominal pressure recording. If microtip or air-filled catheters are used, any deviation from standard zero and reference level should be minimized and taken into account at the time of data analysis.
Urodynamic catheters
The use of two separate tubes for filling and recording is less convenient. Removing the larger filling tube for voiding may appear to be an advantage because only a single small tube is left in the urethra. However, there are no data to suggest that, for example, in a compressive obstruction such as benign prostatic obstruction, a 6 Fr catheter has a detrimental influence on the pressure or flow data. There are, however, data suggesting that results from a single study may be misleading. A double lumen catheter facilitates a second fill/void study to establish reproducibility. Reintroduction of the separate filling tube for a repeated study is more invasive and complicated.
• The use of rectal balloon catheter is recommended for the measurement of abdominal pressure, pabd.
Comparison between patients and urodynamic studies performed in different centers would be facilitated by the use of standard catheters. It is recommended that:
• For the measurement of intravesical pressure and for bladder filling, the standard catheter for routine urodynamics is a transurethral double-lumen catheter. Only in small children and patients with severe constrictive obstruction (stricture) does suprapubic pressure recording have clear advantages. Intraurethral catheters should be as thin as possible, limited only by the practicality of insertion and by internal lumen sizes, which should be sufficiently large to avoid excessive damping of pressure transmission and to achieve the desired filling rate with standard pumps. A 6 Fr double lumen catheter is the smallest practical size at present. The major advantage of a double lumen catheter is that the fill/void sequence can be repeated without the need for recatheterization. Note that the use of a 6 Fr double lumen catheter can limit the infusion rate during cystometry to 20–30 ml/min, as a typical roller pump may not manage to transport a higher perfusion rate through such a small lumen. This can result in an incorrect filling volume being indicated by the machine when the filling volume is calculated from the pump setting. For example, with a filling rate set at 60 ml/min and an actually filling rate of 30 ml/min, the machine will show double the filling volume. Thus, after voiding, a high calculated residual will occur. With some equipment, higher filling rates are possible; it is essential that any system should be critically tested to: 1) measure the maximum filling rate that can be achieved by a particular catheter attached to an individual pump; and 2) correct or calibrate the indicated infused volume.
Although there are various methods for the successful recording of abdominal pressures, a flaccid, air-free balloon in the rectal ampulla gives a suitable signal for pabd to determine a meaningful pdet when pves is measured synchronously (pdet = pves – pabd). In females, vaginal recording may be more acceptable and provides comparable results. The recording of pabd allows the measurement of any abdominal (i.e. perivesical) pressure component during changes in intravesical pressure. The role of the balloon is to maintain a small fluid volume at the catheter opening and to avoid fecal blockage, which can prevent or impair pressure transmission to the transducer. Additionally, as the rectal ampulla and the vagina are not homogeneously fluid-filled spaces, the balloon prevents pressure artifacts arising from contact between the catheter opening and the wall tissue. The balloon serves this function best when it is filled to only 10–20% of its unstretched capacity. Overfilling and elastic distension of the balloon is the most common mistake in abdominal pressure recording. The resultant high balloon (not abdominal) pressure will produce a misleading pressure reading. Such an artificially elevated balloon distention pressure can be avoided by making a small hole in the balloon, although this is unnecessary if the balloon is filled properly as described above. It is also possible to record reliable abdominal pressure with a very slowly perfused (<2 ml/min) open-ended catheter. However, excessive fluid volume in the rectal ampulla may cause problems.
Equipment: minimum requirements for filling cystometry and pressure–flow studies of voiding The ICS has not yet specified definite technical standards in respect of minimum requirements for filling cystom793
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etry and pressure–flow studies beyond the ICS Technical Equipment Report1 and the appendix to the ICS document on pressure flow,3 where a data exchange software standard is recommended. Some further aspects will be discussed in more detail here.
• A higher frequency (minimum 20 kHz) is necessary for recording EMG;
• Calibration of all measurements should be possible.
The minimum recommended requirements for a urodynamic system are:
The scalings should be kept unchanged as much as possible, because urodynamic data quality control is based on pattern recognition, and the recognition of patterns depend on scaling. Therefore, it is recommended that:
• three measurement channels – two for pressure and
• During recording and for analysis, minimum scaling
Equipment recommendations
one for flow;
• a display (on printer and/or monitor) and secure • •
•
storage of three pressures (pabd, pves, pdet) and flow (Q) as tracings against time; infused volume and voided volume may be shown graphically or numerically; online display of pressures and flow, with adequate scale and resolution; scales must be clearly given on all axes; no information should be lost electronically when tracings go off-scale on display; possibilities to record standard information about sensation and additional comments (event recordings).
Meaningful plausibility assessment and quality control are possible only when the measured and derived signals are displayed continuously as curves over time, without delay (in real time), as the examination proceeds. Each displayed curve and number should be labeled according to ICS standards, with clear scaling of amplitudes and the time axis. The following sequential position of tracings is suggested: pabd at the top, then pves, pdet and Q (see Figs 53.3–53.8). It is least important when pabd goes off-scale and is cut off (see Fig. 53.6). Additional parameters such as EMG, bladder filling, and voided volumes can be displayed either as curves or digitally as numbers. The following minimum technical specifications are recommended:
• Minimum accuracy should be ±1 cmH2O for • •
•
pressure and ±5% full scale for flow and volume; Ranges of zero to 250 cmH2O, zero to 25(50) ml/s, and 1000 ml for pressure, flow, and volume, respectively; The software must ensure that no information for pressures up to 250 cmH2O and for flow rates up to 50 ml/s is lost internally, even when not displayed, and that off-scale values are clearly identified; An analog/digital (A/D) frequency of 10 Hz per channel as the lower limit for pressure and flow;
for pressure be of 50 cmH2O per cm, for flow 10 ml/s per cm, and for the time axis 1 min/cm or 5 s/mm during filling and 2 s/mm during voiding. To enable a retrospective judgment of the curves, urodynamic measurements should be documented as curves over time with comments and explanations. It is usually insufficient to document urodynamic measurements by a few numerical values alone. The same amplitude of scaling should be used for all documentation, although the time axis may be compressed. Only if there is no relevant information to be lost by reducing resolution (e.g. during filling), the time scale can be compressed. For a print-out, maximum full scale deflections of 200 cmH2O, 50 ml/s, and 1000 ml are sufficient for pressure, flow, and volume, respectively. In most cases, half the maximum full scale will be sufficient to show all relevant parts of curves. Line resolution should be better than 0.10 mm. During interventions (e.g. interruption of bladder filling or manipulation of catheters) the continuation of both measurement and recording must always be possible. Online recording of comments should be possible, to complete the documentation.
Calibration of equipment The need to calibrate pressure transducers, flowmeters, and pumps cannot be stated: simply ‘yes’ if there is a need or ‘no’ if there is not. The specification of the manufacturer should be studied. Two aspects must be considered: the intended accuracy of the system and the investigator’s experience with the system. If a new system is installed or new transducers are being used, it is recommended that regular calibration be carried out. If experience with daily calibration shows that the potential error is small (e.g. <2 cmH2O), then it will be sufficient to calibrate once a month. However, calibration should not be ignored and good urodynamic equipment
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makes it technically possible to perform a calibration. Calibration should not be confused with simple ‘zero balancing’, which is only one part of calibration. In addition to setting the zero, it must be possible to check and adjust the amplitudes of all measurement channels, i.e. to calibrate all signals. Calibration of a flowmeter can be achieved by pouring a precisely measured volume at a constant flow into the flowmeter, typically 400 ml in 20–30 s (at 15–20 ml/ s) and checking the recorded volume. Special constant-flow rate bottles are available for flow calibration. Similarly, one can test a pump by measuring the time to deliver a known volume (e.g. 100 ml) into a measuring cylinder. It is recommended that pump calibration be performed with the filling catheter connected. Such a pump calibration can only be as good as the cylinder used, which needs to have good resolution and be accurate. Some measuring beakers usually available in clinics are not accurate.
Pressure signal quality control: qualitative and quantitative plausibility It is very important to observe and to test signals carefully and to correct any problems before starting the urodynamic study. If the signals are perfect at the beginning of the study, they usually remain so without the need for major intervention. If the signals are not perfect, remedial action must be taken. If a quality problem does not disappear at once, when filling commences, it will usually deteriorate further during the study. Conscientious observation of the patient and of the signals, in particular pdet, during all parts of the study, together with continuous signal testing, are the keys to high quality urodynamics. The first aim is to avoid artifacts and the second to correct the source of all artifacts immediately they occur. The following three criteria form the minimum recommendations for ensuring quality control of pressure recordings:
• Resting values for abdominal, intravesical, and •
•
detrusor pressure are in a typical range (see below); The abdominal and intravesical pressure signals are ‘live’, with minor variations caused by breathing or talking being similar for both signals; these variations should not appear in pdet; Coughs are used (every 1 min. or, for example, 50 ml filled volume) to ensure that the abdominal and intravesical pressure signals respond equally. Coughs immediately before voiding and immediately after voiding should be included.
When standards are followed, i.e. with the transducer zeros set to atmospheric pressure, and the transducers placed at the level of the upper edge of the symphysis, a typical range for initial resting pressures values for pves and pabd is (Schäfer, unpublished communications): – supine 5–20 cmH2O; – sitting 15–40 cmH2O; – standing 30–50 cmH2O. Usually both recorded pressures are almost identical, so that the initial pdet is zero, or close to zero, i.e. zero to 6 cmH2O in 80% of cases and in rare cases up to 10 cmH2O.5 All initial pressure values should be verified and the patient’s position should be documented on the urodynamics trace. All negative pressure values, except when caused by rectal activity, should be corrected immediately. It should always be kept in mind that pabd is recorded not in order to ascertain the actual rectal pressure, but to eliminate the impact of (abdominal) pressure changes on pves. The principal aim is to determine the detrusor pressure, pdet, which is the pressure in the bladder without the influence of abdominal pressure. Therefore, pdet cannot be negative. By talking to the patient during the study, the proper dynamic response in the pressure signals can be observed and is ‘automatically’ documented (see Figs 53.3, 53.4, 53.8).
Problem solving If either detrusor or rectal contractions occur, the recorded pressures in pves and pabd will be different. Such changes can be identified and interpreted with sufficient accuracy and reliability only when the patient is observed and the relation between signal changes and patient sensation/activity are checked for plausibility and documented. Any pressure change caused by smooth muscle contractions will show a ‘smooth’ pattern (Figs 53.5, 53.7, 53.8), i.e. there should be no rapid (‘stepwise’) changes (see Fig. 53.4). If pressures increase or decrease stepwise, or with a constant slope over a long period of time, a non-physiologic cause, such as catheter movement, should be considered. If a sudden drop or increase occurs in either the pves or the pabd signal, the usual cause is the movement, blockage (see Fig. 53.4), or disconnection of a catheter. When the patient changes position, sudden changes in resting values occur and are seen equally in both pressure signals. If pves (without change in pabd) increases slowly – as 795
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is typical for a low compliance bladder – it is important to test for any other possible cause for a slow pressure increase. One cause could be a problem with the intravesical catheter measurement; for example, the hole for the pressure conducting lumen is slowly moving into the bladder neck region. This should be assessed by asking the patient to cough, if there is no other apparent artifact. Furthermore, it is recommended that bladder filling is stopped if the filling rate is above a physiologic limit of 10 ml/min. If the value of pves drops after filling is stopped, it is likely that ‘low compliance’ was, at least in part, related to fast filling. There are several common problems that must be solved before the study is started or when observed during a study: Problem: Initial resting pdet is negative, for example, –5 cmH2O. Possible explanations:
• because pabd is too high.
•
Solution: If pves is in the typical range, and both pressures are ‘live’, open the valve in the abdominal line and drain one or two drops from the rectal balloon filling volume. This will usually cause pabd to fall to a proper value. If not, gently reposition the rectal balloon and/or make a small hole in the balloon. because pves is too low. Solution: This may be due to air bubbles trapped in the catheter, the catheter not being in the bladder, or the catheter being blocked/kinked. Gently flush through the pves line (max. 10 ml). It is very important to flush slowly while observing the pressure signal because pressures above 300 cmH2O may damage the transducer. If this does not solve the problem, add some more volume to the bladder via the filling lumen. If resistance to filling is high and it does not drain easily when opened, it will be necessary to check the catheter position, and to reposition the catheter, if necessary.
Problem: Initial pdet too high, for example, 15 cmH2O. Possible explanations: The key problem here is indicated by the measurement of 15 cmH2O. The situation is different from the clear statement that ‘pdet cannot be negative’, as we do not have a definite upper limit for the normal maximum ‘resting’ value for pdet. Thus, we can only follow the present guidelines that, in most tests in an empty bladder, pdet is between zero and 5 cmH2O, and in some 90% it is between zero and 10 cmH2O. For any higher value,
• •
stringent plausibility checking must be applied. If the patient has no detrusor overactivity, a pdet of 15 cmH2O is unlikely to be valid and there may be a signal problem. First check if pabd and pves are in the expected ranges. For example, if, in a standing patient, initial pves is 30 cmH2O and pabd is 15 cmH2O, then by experience the value of pabd is too low (because pabd is too low). If in a supine patient pabd is 10 cmH2O and pves is 25 cmH2O, then the value of pves is too high (because pves is too high). Check the zero balance and proper signal response to coughing for both signals. because pabd is too low. Solution: Very slowly flush the rectal balloon with 1 or 2 ml. because pves is too high. Solution: This problem can be related to a misplaced catheter, a kink in the catheter, or contact with the bladder wall in an empty bladder, which occludes the eyehole(s) of the catheter. Proceed according to the solution of pves being too high, in the first example above. If no signal problems can be identified, the clinical study may be started, but the pdet signal deserves particular attention. If compliance is normal and the bladder normal at filling, then it is very important to record and check, for some period after the micturition, the post-voiding resting value of pdet. Only if an elevated pdet is perfectly reproducible for repeated filling and voiding studies can it be accepted. However, it is most likely that a high resting pdet will not be reproducible and will be corrected by the measures described above. In summary, if any resting value or cough response does not fit the usual values or patterns, it should be corrected before bladder filling is started. If this is not possible, the signals must be observed even more carefully and every effort made to reveal the potential source of error or artifact during the study.
Retrospective artifact correction In principle, a good pdet signal requires only that pves and pabd show the same fine structure and quality of signals before filling, during filling, and after a voiding (see Figs 53.3, 53.4, 53.7, 53.8). Both pves and pabd must have the same zero and reference level. The most common mistake is to set (balance) the initial pressure values of pves and pabd to zero with the catheters connected to the patient instead of setting zero to atmospheric pressure. This results in incorrect pves and pabd. If this is done, urodynamic studies cannot be compared between centers
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and between patients. Although it may seem convenient and easy to start with a value of pdet as zero, this practice will lead to problems later in the test. As soon as pelvic floor relaxation occurs, which is particularly common during voiding, the value of pabd, if starting at zero, becomes negative. With a negative padb, pdet will be higher than pves, a conceptually meaningless result. Furthermore, it will then be impossible to correct a negative pabd. Cough tests at regular intervals, particularly before and after voiding, document the dynamic response of the pressure channels and are fundamentally important. A typical physiologic artifact that can be easily recognized is a rectal contraction. Rectal contractions are usually of low amplitude and may or may not be felt by the patient (see Fig. 53.8). The value of pabd shows a phasic rise with no change in the pdet signal – a potentially confusing fall in pdet results from the electronic subtraction, but this is, of course, an artifact. Usually rectal contractions are relevant only because they may be misinterpreted as detrusor overactivity (see Fig. 53.8); they have no relevance to voiding. Biphasic spikes as a response to cough tests are another example of artifacts that are easy to correct. However, any other artifacts – such as a signal which is nonresponding (dead), has stepwise changes in pressure, or has negative pressures – often cannot be corrected or can be corrected only with extensive speculation about the underlying causes of the problem. Studies with such artifacts should be repeated (see the next section). Retrospective corrections require the same strategies for plausibility control as during recording, but are then are much more difficult and less successful to perform. A few common artifacts (e.g. rectal activity, biphasic spikes at cough tests, or insufficient pabd response during straining) can be accepted during the study as they can be corrected retrospectively. Usually, this is easier to do manually than through a computerized system.
Urodynamic computer software Computer applications should allow the easy use of even the most complicated analytical algorithms. However, most of the software offered by the urodynamic equipment industry is neither original nor validated. The software may, in fact, not do what the original developer(s) of the algorithm intended. Therefore, it is recommended that:
• When analytical urodynamic software is used to perform data analysis according to any published
concept, the source of the software should be specified. It should also be clearly stated if the software has been validated, i.e. proven to provide results consistent with the algorithms to which the analyses are attributed.
STRATEGY FOR REPETITION OF URODYNAMIC TESTS • It is recommended that a urodynamic test should be repeated if the initial test suggests an abnormality, leaves the cause of troublesome lower urinary tract symptoms unresolved, or if there are technical problems preventing proper analysis. It may not be necessary, however, to repeat a study which, beyond any doubt, confirms the expected pathology; for example, detrusor overactivity which correlates with the patient’s symptoms. However, if the study is inconclusive, then the consequences of not finding a clear answer to the urodynamic question(s) should be considered. If an invasive therapy is planned, the urodynamics should be repeated. Therefore, it is necessary to analyze the signals during the study and document the study immediately upon its conclusion. Only then is it possible to be sure that the urodynamic study is of a quality that answers the urodynamic question and provides an understanding about the patient’s clinical problem. Therefore, it is recommended that:
• The urodynamic findings and the interpretation of the results should be documented immediately after the study is finished, i.e. before the patient has left the urodynamic laboratory, thus allowing for a second test if required. The analysis of a good study is easy and straightforward. Indeed, an easy analysis is actually the key criterion for good urodynamics. A good study is one that is easy to read and one from which any experienced urodynamicist will abstract the same results and come to the same conclusions. For computerized analyses, high data quality is even more important than for manual graphical data analysis. The future development of urodynamic equipment and software should force investigators to conduct proper online data quality control. Analysis of ambulatory studies will remain problematic, as it is less easy to conduct online assessment of quality, and analysis is time consuming. Hence, it will be necessary to ask the patient to return, on another occasion, should the investigation require repeating, for whatever reason. 797
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CONCLUSIONS This is the first report of the ICS Standardization Committee of Good Urodynamic Practice. The authors are well aware that this is just a first step and many more will have to follow. Only the essential aspects are considered, but if these basic standards are followed, the quality of urodynamic studies will be significantly improved.
acknowledgments The Standardization Committee is grateful for the extensive editing performed by Vicky Rees, ICS Administrator. The committee is also grateful for the detailed comments received from Linda Cardozo, Paul Dudgeon, Guus Kramer, Joseph Macaluso, Gerry Timm, and Alan Wein.
2. Van Waalwijk E, Anders K, Khullar V et al. Standardisation of ambulatory urodynamic monitoring: report of the Standardisation Sub-committee of the International Continence Society. Neurourol Urodyn 2000;19:113–25. 3. Griffiths DJ, Hofner K, van Mastrigt R, Rollema HJ, Spangberg A, Gleason DM. Standardization of terminology of lower urinary tract function: pressure–flow studies of voiding, urethral resistance, and urethral obstruction. Neurourol Urodyn 1997;16:1–18. 4. Lose G, Griffiths DJ, Hosker G et al. Standardisation of urethral pressure measurement: report of the sub-committee of the International Continence Society. Neurourol Urodyn 2002;21:258–60. 5. Liao L, Kirshner-Hermanns R, Schafer W. Urodynamic quality control: quantitative plausibility control with typical value ranges. Neurourol Urodyn 1999;18(abstract 99a):365–6.
REFERENCES 1. Rowan D, James DE, Kramer AEJL, Sterling AM, Suhel PF. Urodynamic equipment: technical aspects. J Med Eng Tech 1987;11:57–64.
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Index Page numbers in italics indicate figures or tables. abdominal examination 750 abdominal (or Valsalva) leak point pressure (VLPP) 259 definition 754–5, 766 measurement 267–8 as outcome measure 455 pad tests and 208 stress urinary incontinence 306–7, 308, 309, 310 urethral pressure profile and 268 videourodynamics 305 abdominal pressure (pabd) ambulatory urodynamics 317 definition 752, 763 flow rates and 152 leak point 267, 268 measurement 229, 792, 793 quality control 227, 227 rectal contractions and 232–3, 233 urethral continence mechanism 125, 125 videourodynamics 303, 305 abdominal straining see straining abdominal surgery previous 192 suprapubic catheterization after 546 abdominal trauma, ureteric injuries 1291 abdominal wall anterior see anterior abdominal wall muscles 1154, 1155 abdominoperineal resection 575–6 ACET trial 500–1 acetylcholine 151, 158, 159 -like drugs 488–9 Acinetobacter 619 acontractile detrusor 756, 767 see also detrusor areflexia; detrusor underactivity; underactive bladder acquired immune deficiency syndrome (AIDS) 574 activities ambulatory urodynamics 316, 319 fitness see sports/fitness activities measures of overactive bladder impact 439 see also physical activity acupuncture 420 Ad-afferent fibers 147 bladder sensation 148, 159 loss of sensation via 149 micturition reflex 160 pharmacological targeting 165–6 urine storage reflexes 159 adenocarcinoma, urethral diverticulum 1253 adenosine triphosphate see ATP adenoviruses 619, 620 adherence, bacterial 617 adhesions conscious pain mapping 1175 fistula risk and 1224, 1226 laparoscopic treatment (adhesiolysis) 1173–5 laparoscopy safety and 1212 pelvic pain 1166–7, 1173–4 adolescents 46 adrenal hyperplasia, congenital 1324, 1324, 1340, 1341 adrenergic receptors 146, 163–4
advanced practice nurses (APNs) 92, 93–4, 94 education/training 93–4, 95 adverse drug reactions (ADRs) 440–3 objective tests 440–3, 441 spontaneous vs elicited reports 440–1, 441 aerobics, high impact 658, 659 afferent neurons see sensory neurons age frequency and 187, 188, 201, 202 nocturia and 187–8, 188 overactive bladder and 59, 61 pelvic organ prolapse and 1004 quality of life impairment and 66 urinary incontinence and 395–6, 698, 698, 699 Asia 54, 55, 57 Australia 42, 43 Europe 32, 32, 33, 35 United States 14, 14 urinary tract infection risk and 617–18 uroflowmetry and 218 voiding parameters and 201, 201, 202 volume voided and 201, 202 Agency for Health Care Policy and Research (AHCPR) (US) 95, 96 aging effects on continence mechanism 699–700 see also elderly AIDS 574 aids and appliances 555, 555–8 alarms, enuresis 558, 558 albuterol (salbutamol) 488 alcohol consumption 192, 410 Aldridge procedure 7, 836, 882 alfuzosin 488, 493 allantois 129, 129 Allen–Masters syndrome 1168 allergic vulvovaginitis 649, 651 allograft sling materials 846, 847–53, 885, 914 complications 850–1, 852 results 850, 851, 888 a-adrenergic agonists 515–17 a-adrenergic antagonists 488 a1-specific 493 facilitating bladder contractility 490 voiding difficulty 491–3, 589 a-adrenergic receptors (a-ARs) 144, 162, 163–4 distribution 146, 491 initiation of normal voiding 151 subtype distribution 163–4 Altemeier procedure (perineal rectosigmoidectomy) 732, 1140, 1141, 1143 ambulatory urodynamics 260, 314–24 analysis 317–18 asymptomatic volunteers 320 clinical report 318 definition 316, 751, 763 diary 318, 319, 319 equipment 314, 314–16, 315 ICS standardarization 316–20, 787–8 indications 316, 320–2 methodology 316–17
patient instructions 317, 318 patient preparation 318 pressure–flow studies 322 procedure 318–20 systems available 322, 322–3, 323 terminology 316 variables recorded 320 amenorrhea hypothalamic 659 obstetric fistula 1243 American College of Obstetricians and Gynecologists, chronic pelvic pain definition 606 American Urological Association (AUA) stress incontinence outcomes assessment 450, 804, 810, 811–20 symptom score 437 amitriptyline, painful bladder syndrome 599–600 amoxicillin 622, 623, 624 anal canal childbirth-related nerve damage 687 somatosensory evoked potentials 293–4 anal endosonography see endoanal ultrasonography anal incontinence see fecal incontinence anal neosphincters 717–18, 1127–9 anal plugs 715–16 anal reflex, neurophysiologic conduction studies 294–5 anal sphincter anatomy 1100–1, 1101 electromyography 279–81, 1125 concentric needle 283 single fiber 283, 283–4 neurophysiologic conduction studies 291, 292, 292, 294–5 obstetric injury see obstetric anal sphincter injury pregnancy-related changes 686 replacement procedures 717–18, 1127–9 surgical repair 716–17, 1125–6 factors predicting outcome 716 failure 716 primary, obstetric injury 1113–18 results 717, 1125–6, 1126 techniques 716, 1125, 1126 ultrasonography 714, 715 see also external anal sphincter; internal anal sphincter anal triangle 1100–1 anatomy 116–26 functional terms 119 laparoscopic 1154–64 lower urinary tract 116, 116–19 MRI 340–2, 341, 342, 343 pelvic floor 119–22, 120 underlying urinary continence 123–5 androgen insensitivity syndrome 1324, 1340–1 androgens receptors 697, 700 sexual differentiation 129–30 anemia, preoperative correction 828 anesthesia complications, laparoscopic surgery 1218
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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anesthesia – continued midurethral slings 892 preoperative assessment 829 SPARC sling 926 tension-free vaginal tape 918–19 anismus 1138 electromyography 280 obstructed defecation 724–5, 726 rectocele and 1037, 1039 ankylosing spondylitis 573 anococcygeal ligament 1162 anococcygeal nerves 1163 anorectal malformation 1325 anorectal manometry constipation 727–8 fecal incontinence 714, 714, 1122 rectal prolapse 1138 rectocele 1041 anterior abdominal wall 1154, 1155 laparoscopic vaginal suspension 1207 trocar placement sites 1213 vasculature 1213, 1214–15 anterior colporrhaphy 1013–16 AUA outcomes assessment 811–12, 813, 814, 818 complications 1020 history 7 operative technique 1013–16, 1014, 1015 prevention of failure 401 prosthetic augmentation 1014–15, 1015, 1016, 1019 results 1019 sacrospinous vault suspension with 1058 vs colpourethropexy 871 anterior sacral root stimulation, muscleevoked potentials 291–2, 292 anterior urethrovesical angle 331, 334 anterior vaginal wall cyst 1255, 1256 making/recording measurements 775, 775–6 masses, differential diagnosis 1255, 1256 measurement points 773, 774 anterior vaginal wall prolapse (cystocele) 1010–21 3D ultrasound 369, 369 after anti-incontinence surgery 1353 leak point pressure testing 271, 271, 274–5 after hysterectomy, prevention 399 anatomy and pathology 121, 1010, 1010–12, 1011 dynamic nature 461 evaluation 1012–13 ICS definition 751 leak point pressures and 305 making/recording measurements 775, 775–6 midline (central) defects 1010, 1010, 1012 paravaginal (lateral) defects see paravaginal defects reduction pressure–flow studies and 237–8, 239 urodynamic testing after 1013 stress incontinence with 1012, 1013 surgical repair 1013–20 abdominal repair 1018 anterior colporrhaphy see anterior colporrhaphy prevention of failure 401 rectal prolapse surgery with 1145 results 1018–20
vaginal paravaginal repair 1016–18, 1017–18 symptoms and signs 1012 terminology 773, 1003, 1010 transverse defects 1010, 1010 ultrasonography 359, 359, 361 uroflowmetry 221 videourodynamics 307, 309 antibiotics bactericidal vs bacteriostatic 622 prophylactic 625 perioperative 831 postcoital 669 urogenital fistulae 1230 resistance patterns 623 sensitivities 623, 624 trichomoniasis 650 urinary tract infections 622, 622–3 children 626 duration of therapy 623 elderly 626 pregnancy 625 anticholinergic drugs 192–3, 497–502 as cause of voiding difficulty 584 neurogenic voiding dysfunction 566–7 urinary retention 589 see also antimuscarinic agents antidepressants 488, 510–12 antidiuretic hormone (ADH) 186 -like agents 488, 520–1 antifungal agents 648, 649 anti-incontinence surgery alternative therapies 826–7 artificial urinary sphincter 962–70 biologic graft materials 846–54 colpourethropexy see colpourethropexy complications 831–3, 1346–62 immediate 1346–9 long-term 1350–6 short-term 1349–50 failed definition 809–10 leak point pressure testing 269–71, 270, 271, 272–5 preoperative risk factors 867, 868 prevention 400–1 tension-free vaginal tape for 920, 920 urethrocystoscopy 378–9 future prospects 9 history 6–8 indications 866 nulliparous women 678 obstruction complicating see under obstruction, bladder outflow outcomes 8–9, 20, 811–20 outcomes assessment 802–23 AUA guidelines 803 future considerations 808–9 ICI recommendations 805–8 questionnaires 803 Urodynamic Society recommendations 803–5 see also stress urinary incontinence (SUI), outcome measures patient selection 826 perioperative care 826–34 postoperative care 831–3 postoperative urodynamics 221, 245–6 preoperative assessment anesthetist 829 investigations 221, 246, 321–2, 828–9 preoperative considerations 826–31
previous artificial urinary sphincter 962 history taking 192 success of subsequent surgery 867, 868 prolapse surgery with see prolapse surgery, incontinence surgery with quality of life impact 1356–7 rates 20 selection of procedure 826, 866–7 sexual function after 667–8, 1353, 1354 sling procedures see sling procedures synthetic graft materials 836, 840–1 ultrasonography after 362, 362–3 voiding difficulty after see under voiding difficulty vs pelvic floor muscle training 413 antimicrobial agents see antibiotics antimuscarinic agents 488, 497–502 efficacy–tolerability ratios 443–4 overactive bladder 635–8, 638 safety 444 side effects 499 tolerability 440–3 see also anticholinergic drugs antiproliferative factor (APF) 594 apomorphine 162 appendicovesicostomy 1342–3, 1343 appliances 555, 555–8 arcus tendineus fasciae pelvis (ATFP) 121, 121, 124, 124 arcus tendineus levator ani (ATLA) 122, 122, 124, 124 Aris™ TOT 948, 949, 951 artificial bowel sphincter (ABS) 717–18, 1127–9, 1129 indications 1129 results 1129, 1130 artificial urinary sphincter (AUS) 962–70 complications 967–8, 969, 1356 device 962, 962 myelodysplasia 266 patient evaluation 962–3 patient selection 963 results 968, 969 transabdominal implantation 966, 966–7, 967 transvaginal implantation 963–6, 964, 965 ASE model, patient education 109, 109 aseptic intermittent catheterization 757 Asia, epidemiology 52–62 athletes, female elite 657, 658–9, 660 see also sports/fitness activities ATP 158, 165, 166 atropine 488, 497–8, 499 resistance 498 attitudes, public (to incontinence) 76–7 changing see continence promotion factors affecting 76, 76 AUA see American Urological Association augmentation cystoplasty fistula repair 1306 irreparable obstetric fistula 1248 overactive bladder 639–40, 1307–8 Australia epidemiology 40–50 National Continence Management Strategy (NCMS) 78–80 nurse continence advisor 93 autoaugmentation, bladder 1308–9 autologous graft materials 846–7, 883–5 periurethral injections 972–3 see also interposition grafts; pubovaginal slings (PVS), autologous
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autonomic dysreflexia 567, 572 autonomic nervous system lower urinary tract 158, 158–9, 573 neurophysiologic conduction studies 295–6 pelvis and pelvic floor 608, 1163–4 average flow rate see flow rate, average awareness, promoting continence see continence promotion azithromycin 623 back pain 192 baclofen 488 to decrease outlet resistance 494–6 detrusor overactivity 162, 513 intrathecal 495–6 bacteria biofilms, catheter systems 544, 546–7 uropathogenic 616–17, 619 urothelial adherence 617 bacterial vaginosis (BV) 647 diagnosis 646, 646 management 647 bacteriuria 614–15 asymptomatic (ASB) 614, 615, 620 pregnancy 625 significant 614 Baden–Walker system (vaginal profile) 462, 462, 1000, 1000–1 balloon expulsion test, rectal 729 barium enema 714, 726 Barrington, FJF 142 Bartholin’s glands 1100, 1100 pediatric patients 1338 bed protection products 553, 554, 558 bedwetting see nocturnal enuresis behavioral risk factors, urinary tract infections 618 behavioral therapies 468–73 continence nurse specialist 86–7 definition 757 encouraging patient participation 472 future developments 9 lifestyle changes and 471–2 overactive bladder 634–5 physical therapist 107 techniques used 468–71 benign prostatic enlargement 757 benign prostatic hyperplasia (BPH) 493, 757 benign prostatic obstruction 757 benzodiazepines 192, 494 b-adrenergic agonists 488 stress incontinence 517–18 urge incontinence 510 voiding dysfunction 493, 496 b-adrenergic antagonists 517–18 b-adrenergic receptors (b-ARs) 146, 164 distribution 491 type 3 (b3) 159, 164 b-lactamases, extended-spectrum (ESBLs) 623 bethanechol chloride 488–9, 589 pediatric patients 1332 BioArc™ sling system 940, 940–1, 941 BioArc™ TO 948, 949, 951 biofeedback constipation 730–1 definition 757 detrusor overactivity 107 electromyography 85, 104, 481, 482 equipment 104, 480, 481 evidence for effectiveness 412 fecal incontinence 715, 1122
manometry 481 pelvic floor educator 480–1, 481 pelvic floor ultrasound 481 pelvic organ prolapse 421 stress urinary incontinence 85, 104, 469, 479–81 vaginal palpation 480 see also vaginal cones/balls biofilms, catheter systems 544, 546–7 biologic prosthetic materials 846–57 allografts 847–53 autologous 846–7 complications 1354–6, 1355 cystocele repair 1015, 1019 midurethral slings 940, 940–1, 941 rectocele repair 1045–6, 1048, 1048–9 sacral colpopexy 1199 xenografts 853–4 biomechanics, lower urinary tract 236–7 BION® device 1285, 1285 biopsy, bladder see bladder biopsy bipolar electrochemical energy, laparoscopic colposuspension 1181 bladder anatomy 116, 147 augmentation see augmentation cystoplasty autoaugmentation 1308–9 biomechanics 236–7 defense mechanisms 616 distension test, interstitial cystitis 597 diverticula 385 embryological development 130–1, 134 endometriosis 191, 1168 epithelium bacterial adherence 617 defense mechanisms 616 deficiency, interstitial cystitis 594 exstrophy 1333, 1333 foreign bodies 385 hypertonic 150 innervation 158, 158–9 early studies 142, 145 malakoplakia 384 mucosal grafts, fistula repair 1303 muscle see detrusor neuronal changes, interstitial cystitis 595 overdistension injury 586 physiology 142–55 contemporary studies 146–7 early experimental studies 142–5 early urodynamic studies 145–6 structural features relevant to 147 see also micturition, clinical physiology polyps/fronds 383 somatosensory evoked potentials 293–4 squamous metaplasia 383, 384 storage function see storage, urine submucosal hemorrhages (glomerulations) 597 substitution, interstitial cystitis 601 trabeculations, endoscopy 384, 384–5 trigone see trigone bladder biopsy painful bladder syndrome 597–8 recurrent urinary tract infections 621 bladder calculi endoscopy 385, 385 obstetric fistula 1242 bladder cancer see bladder tumors bladder capacity 150 absolute 150 cystometric 18, 754, 765 drugs increasing 513–15
during filling cystometry 233, 754, 765 functional 150, 750 maximum anesthetic 754, 765 maximum cystometric (MCC) 239, 754, 765 pregnancy 683 voiding diary assessment 199 bladder compliance 149–50 calculation 753–4, 764 filling cystometry 230–1, 305, 753–4, 764 leak point pressures and 268, 271, 275, 305–6 low ambulatory urodynamics 320, 321 pathogenesis 147, 150 bladder cycle 142, 147–52 ambulatory urodynamics and 318 I (diastole; filling phase) 148–50 II (systole; emptying phase) 150–2 bladder diary see voiding diary bladder emptying 486 completeness 152 drugs facilitating 193, 488–97 impaired, urethral pressure measurements 260 incomplete, feeling of 190–1, 748 nervous control 160 physiology 150–2 see also voiding bladder erosion artificial urinary sphincter 968 midurethral slings 897–8 synthetic grafts 1356 transobturator tape 958 bladder expression 757 bladder filling 486 ambulatory urodynamics 318 artificial 751 cystometry 226, 230–1 first sensation 432, 752, 763 medium, urodynamics 227–8, 238 natural 316, 751 nervous control 159–60 physiology 148–50 rates 228 non-physiologic 752, 763 physiologic 752, 763 videourodynamics 304 see also storage, urine Bladder Health Questionnaire (BHQ) 65–6 bladder hypersensitivity 230 see also bladder sensation, increased bladder injuries anti-incontinence surgery 1347–8, 1348 colpourethropexy 871–2, 872 cystocele repair 1020 intraoperative recognition/repair 1369 laparoscopic surgery 1187, 1217 midurethral slings 895 postoperative recognition/management 1373 sacrospinous vault fixation 1060 tension-free vaginal tape 921, 921 transobturator midurethral slings 949–51 bladder leak point pressure see detrusor leak point pressure bladder neck 116, 119 childbirth-related damage 345 descent, pelvic floor ultrasound 357, 358 dysfunction, ureterocele 138, 139 embryological development 131 incision 589 intrinsic sphincter see intrinsic urethral sphincter
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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bladder neck – continued mobility 123, 124, 124 perineal ultrasound 357, 357–9 postpartum 686 Q-tip test 194 see also urethral hypermobility; urethral mobility MRI 343–4, 344 open, cystourethrography 334–5 opening, bladder emptying 150–1 position perineal ultrasound 357, 357–9 postpartum changes 686 urethrocystoscopy 379 pseudopolyps 383 reflex responses to stimulation 294 see also urethrovesical junction bladder neck plication anterior colporrhaphy with 1013–14, 1015, 1019 Neugebauer–Le Fort colpocleisis 1082 see also Kelly plication bladder neck slings see pubovaginal slings bladder neck suspension see colpourethropexy bladder outflow obstruction see obstruction, bladder outflow bladder outlet 177 classification of dysfunction 174, 177–80, 178 overactive 178, 179–80 sensory disorders 179, 180 underactive 177–9, 178 see also intrinsic urethral sphincter bladder outlet resistance drugs decreasing 491–7 drugs increasing 515–20 urine flow rate and 219, 786, 789, 791 bladder output relation (BOR) 236 bladder pain 191, 748 altered bladder sensation and 175 during filling cystometry 432, 752, 764 see also painful bladder syndrome bladder perforation after augmentation cystoplasty 1308 after bladder autoaugmentation 1309 see also bladder injuries bladder reflex triggering 757 bladder retraining see bladder training bladder sensation 148–9, 159 absent 432, 747, 752, 764 altered, and pain 175 disorders 148–9, 179, 180 drugs decreasing 165–6, 513–15 filling cystometry 230, 432, 752, 763–4 ICS definitions 432, 747, 752, 761 increased 432, 747, 752, 763–4 ambulatory urodynamics 322 filling cystometry 230 non-specific 432, 747, 752, 764 normal 747, 752, 763 reduced 747, 752, 764 voiding diary assessment 199 bladder spasm 191, 748, 761 bladder suspension defects classification 332 cystourethrography 329–32, 333, 334 bladder training 417, 418–20, 468 continence nurse specialist 86, 86–7 evidence for effectiveness 412, 418–19 factors affecting outcome 419–20 guidelines 468 overactive bladder 634–5
painful bladder syndrome/interstitial cystitis 598 physical therapist 107 prevention of urinary incontinence 397 protocols 418, 420 bladder tumors cystoscopy 379, 386, 386–7, 387 translabial ultrasound 363, 364 bladder ulcers, interstitial cystitis cystoscopic diagnosis 597 treatment 601, 601 bladder volume urine flow rate and 219, 786 see also bladder capacity bladder wall thickness increased see detrusor hypertrophy ultrasound measurement 359–60, 360 bladder washouts, catheterized patients 545, 545 bleeding see hemorrhage/bleeding blood transfusion, after colpourethropexy 871, 872 Boari flap 1294, 1295–6, 1371–2, 1372 body image 1378 body mass index (BMI) anti-incontinence surgery outcome and 867, 868 midurethral slings and 898 reduction see weight loss urinary incontinence and 19, 45, 45, 408, 471 body-worn female continence devices 558 Bolam principle 829 bone anchors 936–8 historical perspective 936 osteomyelitis complicating 938, 1349 transvaginal slings 936–8 complications 938 operative technique 936–7, 937 results 937–8 vaginal wall slings 939 bone morphogenetic protein type 4 (BMP4) 129, 133 Bonney, Victor 7 Bonney test 194 borreliosis, Lyme 574 bothersomeness overactive bladder 60, 437–8 quality of life assessment and 66–7 symptoms in nulliparous women 675 urinary incontinence epidemiologic studies 20, 53, 54 help-seeking and 56, 57 see also quality of life botulinum toxin (BTX) 166, 488 detrusor overactivity 512, 639, 1307 to facilitate bladder emptying 496–7 bovine collagen see collagen, bovine bovine pericardium, slings 854, 888 bowel frequency, normal 722 bowel injuries anti-incontinence surgery 895, 1348, 1348 laparoscopic 1215–17 underwater test 1217 see also rectal injury bowel management 87, 472 bowel preparation 828 laparoscopic surgery 1199, 1217 bowel problems after augmentation cystoplasty 1308 prolapse 780, 1139, 1140 urinary incontinence and 19 bowel retraining 730–1
brain lesions 566, 567–70 brainstem, voiding center 143 brain tumors 567, 569 branching morphogenesis, renal 132, 132 Bristol Female Lower Urinary Tract Symptoms (BFLUTS) 69, 437, 438 broad ligament 1158 Brown–Sequard syndrome 572 Brubaker, Linda 5 bulbocavernosus reflex 193 neurophysiologic conduction studies 293, 294–5 bulbospongiosus muscle 1100, 1100 bumetanide 521 buprenorphine 161 Burch, John 8 Burch colposuspension AUA outcomes assessment 814, 815 enterocele after 875, 1025, 1027 prevention 1029 failed, leak point pressures 273 intraoperative complications 871–2, 872, 1346, 1347 laparoscopic 870, 1180, 1181–4 postoperative complications 872–5, 873, 874 preoperative pressure–flow studies 246 risk factors for failure 867, 868 technique/modifications 868–9 ultrasound findings after 362, 362 urodynamic changes after 871, 872 vs other procedures 895 see also colpourethropexy cadaveric prolapse repair and sling (CAPS) procedure 853, 936 results 938 cadaveric sling materials see allograft sling materials caffeine intake 409, 471, 730 C-afferent fibers 147 pathophysiology of urgency 149 pharmacological targeting 165–6 sensory function 159 vesicospinovesical micturition reflex 160 calcium, intracellular 164 calcium antagonists 164–5, 507–8 calcium channels 163, 164–5 calcium hydroxylapatite, injectable spheres 861–2, 972, 972 Camper’s fascia 1154 Candida, urinary tract infections 619, 619 candidiasis recurrent 648 vulvovaginal 647–8, 648, 649 capsaicin 488, 513–15 mechanism of action 160, 165–6 overactive bladder 638 carbachol 163 carbon-coated zirconium oxide beads (Durasphere™) 860, 861 carbon dioxide, gas cystometry 228 carcinoma in situ, bladder 386, 387 cardiac failure 192 cardinal ligaments 120 Cardozo, Linda 6 care pathways, continence 96 caruncle, urethral 1255, 1256 categorical responses 803 catheterization 542–50 ICS definitions 757 indications 542 indwelling 757, 1309
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intermittent 757 intermittent self- see intermittent self-catheterization nurse’s role 88–9 obstetric fistulae 1244 postoperative 549–50, 588 colpourethropexy 872–3 fistula repair 1236, 1301 hysterectomy 1365 incontinence surgery 832 pubovaginal slings 910–11 sexual health and 546, 668 suprapubic 545, 545–6, 618 urethral see urethral catheterization urinary tract infections 544, 615, 618, 626–7 uroflowmetry and 219 catheters 542–50 drainage bags 546–7, 547, 548 materials 542 suprapubic 545, 545–6 urethral see urethral catheters urodynamic see urodynamic catheters valves 548, 548 cauda equina lesions electromyography 282, 284 sacral reflex responses 295 stimulation, muscle-evoked potentials 291–2, 292 syndrome 573 celiac plexus 607 cell–cell interactions, smooth muscle development 130–1 central motor pathways, neurophysiologic assessment 292–3 central nerve conduction times 292 Centrasorb™ T-Sling system 941 cephalosporins preoperative prophylactic 831 urinary tract infections 622, 624 cerebral cortex, control of micturition 143, 160 cerebral disease 566, 567–70 cerebral palsy 567 cerebral somatosensory evoked potentials (SEPs) 293, 293–4 cerebrovascular accident (CVA) 567, 568 cervical cancer, uroflowmetry 221 cervix congenital absence 1322 development 1318, 1318 cesarean section after anti-incontinence surgery 867 after uterine prolapse repair 1080 bladder injuries 1369 fecal incontinence and 686, 688 pelvic organ prolapse and 1004–5 prevention of perineal trauma 1106 prevention of urinary incontinence/ prolapse 397, 679 urinary incontinence risk and 19, 24–5, 25, 55 CGP55845 162 Chagas disease 724 chair protection products 553, 554 chaperones 476 Chassar Moir fistula repair procedure 1233 childbirth 682–93 3D ultrasound after 367, 367–8 after anti-incontinence surgery 867 artificial urinary sphincter deactivation 963
fecal incontinence related to see fecal incontinence, childbirth-related mechanisms of pelvic floor injury 682–3 MRI-based simulation 349–50, 350 pelvic floor MRI after 344–5 pelvic floor ultrasound after 358, 358 pelvic organ prolapse and 689, 1004–5 perineal trauma see perineal trauma pudendal nerve terminal motor latency after 291 rectocele formation and 1036–7 urethral diverticulum and 1252 urinary incontinence after 684–5 etiologic mechanisms 394, 394, 685–6 prevention 396–8 urodynamic changes before/after 685, 685–6 vaginal laxity after 1381–2 see also pregnancy children see pediatric patients Chlamydia trachomatis 619, 620, 621, 624 chondrocytes, autologous, periurethral injection 972–3 chronic obstructive pulmonary disease (COPD) 1005 chronic pelvic pain 606–12, 1166 after anti-incontinence surgery 1353, 1354 after colpourethropexy 874, 875 causes 1166 clinical implications 610 definitions 606 diagnostic laparoscopy 1166–7 epidemiology 606 laparoscopic treatment 1167–76 neuropathology 609–10 pelvic denervation procedures 1172–3 pharmacologic aspects 610 cimetidine, painful bladder syndrome 600 cisapride 489 clam cystoplasty 1307 clean intermittent catheterization (CIC) 757 myelomeningocele 1334 clean intermittent self-catheterization (CISC) 549, 549–50 catheter types 550 indications 549–50 neurogenic voiding dysfunction 566–7 postoperative voiding dysfunction/ obstruction 832, 986 urinary tract infections 626–7 voiding difficulty/retention 589 clenbuterol 488 detrusor overactivity 164 stress incontinence 517–18 urge incontinence 510 climacteric 696 clinical effectiveness 443–4 clinical nurse specialists 93, 94 Clinical Research Assessment Groups, ICS 741–2 clinical trials outcome measures see outcome measures quality of life assessment 65, 68–9 clitoral nerve stimulation sacral reflex responses 293, 294–5 somatosensory evoked potentials 293, 293 cloaca 128–30 division 128–30, 129 formation 128–9 molecular control of differentiation 129, 130, 130 persistent common 134, 1319, 1325 cloacal exstrophy 1333, 1334
cloacal membrane 128, 128 clonidine 491, 497 closing pressure 755, 767 clothing 556, 556 clotrimazole 648, 649 clue cells 646, 646 co-amoxiclav 622, 624 Coaptite® 862 coccygeal ganglion 1163 coccygeal plexus 1163 cognitive impairment anti-muscarinic agent-induced 440 objective measures 441, 441–2 see also dementia coital incontinence 633, 664–5 history taking 189–90, 664 pathophysiology 665 prevalence 664, 664–5 treatment 667–8 colectomy, with ileorectal anastomosis 731–2 collagen bovine, periurethral injection 861, 972, 972, 1354 deposition in bladder interstitium 147 Novasys micro-remodeling system 977, 978 pelvic floor dysfunction and 10 urinary incontinence and 677, 686 collagen vascular diseases 1005 colonic scintigraphy 727 colonic sphincter-cystoplasty 1310–11 colonic transit time normal 722–3 testing constipation 726–7, 728 rectal prolapse 1139 rectocele 1041 colonoscopy 714, 726 color Doppler ultrasound, pelvic floor 359, 359, 360 colostomy, fecal incontinence 718 colovaginoplasty 1323 colpocleisis, Neugebauer–Le Fort 1082–4, 1083 colporrhaphy see anterior colporrhaphy; posterior colporrhaphy colpourethropexy (CU) (colposuspension) 866–78 complications intraoperative 871–2, 872 postoperative 832, 872–5, 873, 874, 984 history 7–8, 866 indications 866–7 laparoscopic 866, 868, 1180–8 complications 1187, 1217 cost 1188 disadvantages 1188 methods 1180–1, 1181 non-suture methods 1187 operative technique 1181–4, 1182, 1183, 1184 success rates 869–70, 1185, 1185 ultrasound findings after 362 uterosacral plication with 1183, 1184 variations in technique 1183–4 vs open colposuspension 1186, 1186–7 vs tension-free vaginal tape 1188 minimally invasive 866, 868 results 869–70 prevention of failure 399, 868–9 prolapse repair with 1015–16 retropubic AUA outcomes assessment 811–12, 813, 814, 815
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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retropubic – continued results 9, 869–71, 870 technique 867–9, 873 see also Burch colposuspension; Marshall–Marchetti–Krantz procedure risk factors for failure 867, 868 sacrocolpopexy with 875–6 transvaginal see needle bladder neck suspension ultrasound findings after 362, 362 urodynamic changes after 245, 871, 872 vs other procedures 870–1, 871 vs tension-free vaginal tape 870, 871, 894–5, 920–1, 921 commodes 557, 557 compartment syndrome, postoperative 1348–9 complementary therapies 420, 422 complex reconstructive surgery 1290–315 compliance, bladder see bladder compliance compliance, patient behavioral therapies 472 physical therapy interventions 415 voiding diary completion 198–9 compound muscle action potential (‘M’ response) 290, 291 compound nerve action potential 290 compressor urethrae 117, 118, 118 computed tomography (CT) central nervous system 336 pelvic organ prolapse 778 upper urinary tract 327 urogenital fistulae 1229 computer software 3DSlicer 348, 350, 351 urodynamic 797 conditions, ICS definition 746, 756–7, 768 congenital adrenal hyperplasia 1324, 1324, 1340, 1341 congenital malformations see developmental abnormalities connective tissues embryological development 130–1 nulliparous women 677 pelvic floor dysfunction and 10, 686 pelvic support function 121, 123 conscious pain mapping 1175–6 consent, informed anti-incontinence surgery 829–30 capacity 829–30 knowledge 830 physiotherapy 476–7 volition 829 conservative treatment fecal incontinence 715–16, 1122 iatrogenic bladder outflow obstruction 986 painful bladder syndrome/interstitial cystitis 598, 599 pelvic organ prolapse 420–2, 422, 1029, 1041 ureteric injuries 1293–4, 1373–4 urinary incontinence 826–7 complementary therapies 420 continence nurse specialist 84, 84–9 lifestyle interventions 408–11 nulliparous women 678 outcomes 407–27 scheduled voiding regimes 417–20 summary of evidence 422 urinary vaginal fistulae 1298
see also devices, incontinence; drug treatment; pessaries; physical therapy consistency, internal 802–3 constipation 722–34 after rectocele repair 1046, 1047, 1047 causes 722 children 1332 clinical examination 726 clinical history 725–6 investigations 726–9, 727 management 87, 410, 472 pathophysiology 723–5 pelvic organ prolapse risk 395, 1005 posthysterectomy 725 postrectopexy 1141, 1142, 1143 rectocele and 1037 Rome II criteria 722 slow-transit (STC) 722, 723–4 diagnosis 725, 726–7 obstructed defecation combination syndrome 724 treatment 729, 730, 731–2 treatment 729–33 urinary incontinence and 45, 192 voiding difficulty/retention 585 continence, urinary see urinary continence continence care pathways 96 Continence Foundation (UK) 78, 555 Continence Foundation of Australia (CFA) 78–80 Continence Guard device 538 continence nurse advisor (CNA) 92–3 continence nurse practitioner (CNP) 92, 93 continence nurse specialist 82–90 assessment role 83, 83, 84 education 94–6, 95 functions 82–3 global perspective 92–4 management role 84–9 USA perspective 92–8 Continence Product Evaluation (CPE) network 550, 552–3, 557–8 continence products 550–8 assessment guidelines 551 information sources 78 see also aids and appliances; pads; pants continence promotion 77–8 International Continence Society 80 national organizations 78–80 recommendations 80 survey of national organizations 77–8, 78 Continence Worldwide 80 contraception, urinary tract infections and 618, 669 contrast media, videourodynamics 304 contrast radiography, pelvic organ prolapse 778, 1028, 1038–9, 1039, 1040 Contrelle Activguard 87, 87 coping strategies, urinary incontinence 20 corticosteroids interstitial cystitis 600 intravesical 600 urinary vaginal fistulae 1298 cosmetic vaginal surgery 1378–81 ethical considerations 1380–1 preoperative approach 1381, 1381 procedures available 1379 reasons for increased demand 1378, 1378 sexual function and 1379–80, 1380 vaginal laxity 1381–2 cost-effectiveness analysis overactive bladder 439 quality of life assessment 65
costs, economic laparoscopic colposuspension 1188 urinary incontinence 20, 35–6, 49, 82 cost–utility analysis overactive bladder 439 quality of life assessment 65 tension-free vaginal tape 922 co-trimoxazole 622 cough chronic 25, 192, 677, 1005 cystometry 227, 227, 231, 232, 233 leak point pressure 259, 268, 455 pressure–flow studies 239, 240 urethral pressure measurements 257–9 cough profile 258 pressure transmission ratio (PTR) 258–9 time separation during 259, 259 urodynamic stress incontinence 231, 232 videourodynamics 304 cough stress test (CST) epidemiologic study 18–19 as outcome measure 455 prolapse surgery 400, 1092, 1093 counseling, preoperative anti-incontinence surgery 827, 867 cosmetic vaginal surgery 1381, 1381 fistula surgery 1230 cranberry juice 622, 669 Crede maneuver 151, 304, 761 Creutzfeldt-Jakob disease (CJD) 847, 850, 885 cromakalim 165, 509 Cronbach’s coefficient alpha 803 cube pessaries 535, 538 cul-de-sac see pouch of Douglas culdoplasty, McCall see McCall culdoplasty cure overactive bladder 430 stress incontinence 450, 451, 809 cyclosporine 600 cystectomy, partial 589 cystic fibrosis 46 cystitis acute (infectious) 614, 619 eosinophilic 384 ‘honeymoon’ 668 interstitial see interstitial cystitis cystitis cystica 384 cystitis glandularis 384 cystocele see anterior vaginal wall prolapse cystodefecoperitoneography (CDP) 463 cystometry 226–34, 237 aims 226 definition 226 equipment 228, 228–9, 229 calibration 226, 794–5 minimum requirements 793–4 filling 226, 230–1 definition 752, 763 ICS good practice guidelines 787–97 ICS-recommended terminology 752–5, 763–6 normal 233 filling medium 227–8, 238 filling rates 228, 752 historical aspects 8 indications 226 measurements 229–30 method 230–1 normal 233 patient position 227, 228 pitfalls 231–3
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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preparation for 226–9 problem solving 795–6 quality control 226–7, 227, 233, 795 retrospective artifact correction 796–7 videourodynamics 305 voiding 226, 231 voiding difficulty/retention 587–8 cystoplasty augmentation see augmentation cystoplasty pediatric patients 1342, 1342–3 sphincter- 1310–11, 1311 stoma- 1310, 1311, 1311 terminology 1310 urinary reservoir reconstructions 1309–11, 1311 cystoproctography, dynamic 1028, 1038–9, 1039, 1040 cystoscopes bridges 380 flexible 381, 381 history 6 rigid 379–80, 380 sheaths 380 vs urethroscopes 380–1 cystoscopy abnormal findings 384–7 diagnostic 382 infection risk 618 normal findings 383, 383 painful bladder syndrome 597 perioperative cystocele repair 1018 midurethral slings 892, 893 pubovaginal slings 882–3, 909 SPARC sling procedure 930 tension-free vaginal tape 919 see also endoscopy, urinary tract cystotomy, inadvertent see bladder injuries cystourethrography 328–36, 330–2 continent vs incontinent elderly women 18 evaluation of bladder support 329–32, 333 limitations of static 8 obstruction 985, 986 open bladder neck/proximal urethra 334–5 residual urine measurement 333 videourodynamics 328, 329, 329 voiding (VCUG) 328, 330, 331, 332 bladder outlet obstruction 241, 242 urethral diverticulum 335, 335–6, 1256–8, 1257, 1258 urethrovaginal fistula 1266 urogenital fistulae 1228–9, 1298, 1298 cystourethroscope, flexible 381, 381 cystourethroscopy see endoscopy, urinary tract dance activities 658 Danish Prostate Symptom Score Schedule (DAN-PSS-1) 437 dantrolene 494, 496 darifenacin 488, 501–2 cognitive effects 442 overactive bladder 636, 638 da Vinci robotic surgical system 1180 DDAVP see desmopressin deep circumflex iliac artery 1213, 1215 deep transverse perineal muscle 1100 deep venous thrombosis (DVT), after colposuspension 873 defecation digital assistance 1037, 1039 disorders, rectocele and 1037–8
obstructed 724–5 diagnosis 725 functional causes 724–5 slow transit constipation combination syndrome 722, 724 structural anorectal disorders 724 treatment 729, 730–1, 732 physiology 722–3, 723 proctography see defecography defecography constipation 728–9, 729 MRI 1040–1, 1139 rectal prolapse 1139 rectocele 1038–9, 1039, 1040 DeLancey hammock theory 125, 125, 881, 946 delivery mode perineal trauma and 1106 urinary incontinence and 19, 24, 25, 54, 55 position 1106 techniques 1106 see also cesarean section; forceps delivery; vaginal delivery; ventouse/vacuum delivery Delorme procedure 732, 1140, 1141 results 1143 surgical technique 1141, 1142 dementia 192, 570 see also cognitive impairment denervation, muscle electromyography 281, 282, 284–5 neurophysiologic conduction studies 291 see also pelvic floor muscles, denervation/ nerve damage Denny-Brown, D 143–4 deodorants 558 dermal allografts, cadaveric pubovaginal slings 851–3, 885 complications 852, 852, 1355 results 851, 852–3 rectocele repair 1044, 1045–6, 1048 dermatitis, urine 1242, 1243 dermis, porcine 853, 854, 885–7 descending perineum syndrome 724, 731 enterocele formation 1026, 1026 rectocele formation 1037 desipramine 511 desmopressin 488, 520–1, 638 desquamative inflammatory vaginitis (DIV) 652 detrusor 116 acontractile 756, 767 mechanical properties 236–7 physiology see bladder, physiology wall thickness see bladder wall thickness detrusor areflexia (DA) 566, 567–8 after hysterectomy 1364 multiple sclerosis 570 spinal cord disease 571, 573–4, 575 see also detrusor underactivity; underactive bladder detrusor contractility assessment 236 drugs decreasing 497–513 drugs facilitating 488–90 impact of obstruction 236–7 postoperative voiding dysfunction and 983 urine flow rate and 218, 786, 790 detrusor contractions
after voiding (after-contraction) 231 bladder emptying 151 involuntary (IVCs) drugs decreasing 497–513 epidemiologic study 18 ICS definition 753, 764 detrusor function/activity asymptomatic volunteers 320 during filling cystometry 230, 753, 764 during voiding 755–6, 767 ICS definitions 305, 432, 753 index 320 normal during filling cystometry 233, 432, 753, 764 during voiding 755–6, 767 reflexes inducing 143 sex hormones and 700–1 spontaneous 142–3, 144, 149 stability 149 structural features relevant to 147 detrusor hyperreflexia see detrusor overactivity (DO), neurogenic detrusor hypertrophy causes 150 ultrasound 360, 360 detrusor inhibition reflex (DIR) 107 detrusor instability (DI) see detrusor overactivity detrusor leak point pressure (DLPP) 266–7 definition 755, 766 myelodysplasia 266–7 urethral pressure profiles and 267 videourodynamics 305–6 detrusor loop 116 detrusor myopathy 585–6 detrusor overactivity (DO) after urethral diverticulectomy 1265, 1265–6 ambulatory urodynamics 321, 322 asymptomatic volunteers 320 clinical presentation 633 conservative treatment 414, 416, 418 continence nurse specialist 84 continence nurse’s role 86 definition 432, 753, 764 de novo, after incontinence surgery see overactive bladder, de novo, after anti-incontinence surgery drug treatment 497–515, 635–8, 638 idiopathic 632, 753, 764 filling cystometry 230, 305 pathophysiology 632–3 incontinence 305, 632, 753, 764 neurogenic (detrusor hyperreflexia) 566– 7, 632, 753, 764 cerebral conditions 567, 568, 569, 570 with detrusor–sphincter dyssynergia 566–7 filling cystometry 230, 305 spinal cord disease 571, 574, 575 surgical treatment 1306–9 with synergistic external sphincteric function 566 see also neurogenic voiding dysfunction nulliparous women 676 pathophysiology 143 phasic 149, 230, 632, 753, 764 physical therapy 101, 107–8, 109 prevention 401 provocative maneuvers 432, 753 quality of life impairment 66 surgery 1306–9
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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detrusor overactivity (DO) – continued terminal 230, 632, 753, 764 urethral relaxation and 259 urgency and 144, 149 urodynamic diagnosis 149, 230, 231, 232, 633, 634 videourodynamics 305 see also overactive bladder detrusor pressure (pdet) ambulatory urodynamics 320 area under the curve (AUCdet) 242–3, 243, 244 definition 752, 763 filling phase 229, 305 isometric (piso) 587 isovolumetric (pdet.iso) 236 leak point see detrusor leak point pressure at maximum flow (pdetQmax) 231 bladder outlet obstruction 241, 241 maximum voiding 233 bladder outlet obstruction 242 normal values 233, 233 urinary flow relations 236–7 voiding phase 231, 306, 306 vs intravesical pressure 303 detrusor–sphincter dyssynergia (DSD) 151, 566–7 definition 756, 768 drug treatment 491, 495, 496–7 electromyography 280, 281 historical aspects 8 multiple sclerosis 570 spinal cord disease 571 videourodynamics 308, 310 detrusor underactivity 756, 767 urodynamic diagnosis 231, 232 see also detrusor areflexia; underactive bladder development, embryological see embryology developmental abnormalities 1318–28 associated with other anomalies/syndromic 1325 causing urinary incontinence 1333, 1333–7 clinical examples 133–9 complex 1322–4 imaging 1318–19, 1319 simple/isolated 1319–22 devices, incontinence 87, 534–40, 537 adverse effects 538–9 body-worn female 558 during exercise 659 effectiveness 537–8 nurse’s role 87 use before surgery 826–7 see also pessaries dextranomer macrospheres (Zuidex™) 862, 973, 973–4 diabetes insipidus 192, 520–1 diabetes mellitus 192 constipation 726 neurogenic voiding dysfunction 567, 576, 585 pelvic organ prolapse 1005 urinary incontinence 19, 25 diabetic cystopathy 576 diagnosis accuracy of clinical 186 future developments 10 historical aspects 8 DIAPPERS mnemonic 395 diary ambulatory urodynamics 318, 319, 319
voiding see voiding diary diazepam 494, 589 dicyclomine 488, 505–6 pediatric patients 1332 dietary management constipation 730 painful bladder syndrome/interstitial cystitis 598, 599 urinary incontinence 409–10 diethylenetriaminepentaacetic acid (DTPA) indium-labeled 727 technetium-labeled 621 diltiazem 507–8 dimercaptosuccinic acid (DMSA) scans 621 dimethyl sulfoxide (DMSO) ethylene vinyl alcohol suspended in (Uryx®) 861, 973, 973 intravesical 512–13, 600 dipstick tests, urinary tract infections 619–20 disability definition 102 incontinence outcome assessment 808, 821 distal urethral electrical conductance test (DUEC) 206, 316, 317 distigmine bromide 589 diuretics 192, 521 Doderlein crossbar colporrhaphy 1083 dopamine 162, 640 dopamine receptors 162 dorsal clitoral nerve stimulation see clitoral nerve stimulation dorsal root ganglia 159 doxazosin 162, 164, 488, 493 doxepin 511 doxycycline 651 drainage bags, catheter 546–7, 547, 548 dribbling postmicturition 191, 217, 748 terminal 217, 748, 761 urethral diverticulum 1253 drug history 192–3, 193 drugs affecting bladder function 635 causing voiding difficulty 584 drug treatment chronic pelvic pain 610 constipation 730, 731 fecal incontinence 715 overactive bladder 497–515, 635–8, 638 monitoring 322 painful bladder syndrome/interstitial cystitis 598–600 pediatric neurovesical dysfunction 1332 stress urinary incontinence 515–20, 977–9, 979 voiding dysfunction 486–532 bladder training with 419 circumventing the problem 520–1 CNS targets 160–2 continence nurse’s role 87 facilitating bladder emptying 193, 488–97 facilitating urine storage 193, 497–520 functional classification 487 ICI assessment 486, 488 nulliparous women 678 peripheral targets 163–6 principles 160–6, 486–8 vs bladder training 419 vs electrical stimulation 414 vs pelvic floor muscle training 412–13 Drutz, Harold 6
dry eyes, antimuscarinic-induced 441, 443 dry mouth, antimuscarinic-induced 636, 637 objective measures 441, 442–3, 443 placebo-controled trials 440 spontaneous vs elicited reports 441, 441 duloxetine 146 fecal incontinence 715 molecular structure 979 prior to surgery 826 stress urinary incontinence 518, 977–9, 979 dura mater, lyophilized, for slings 847, 885 Durasphere™ 860, 861 Durasphere EXP™ 860, 861 Dwyer, Peter 6 dye studies fistula detection 1228, 1243, 1298 ureteric injuries 1292, 1293, 1369 dynamic graciloplasty (DGP) 717, 1127, 1127 indications 1129 results 1127, 1128, 1129 dyschezia see defecation, obstructed dysmenorrhea endometriosis 1171 pelvic denervation procedures 1172, 1172–3 dyspareunia endometriosis 1171 postoperative anti-incontinence surgery 667–8, 1353, 1354 colpourethropexy 874, 875 rectocele repair 1046, 1047, 1048 sacrospinous vault fixation 1060 synthetic meshes 667–8, 841 transvaginal bone-anchor slings 938 vaginal surgery 1380 postpartum 682 urethral diverticulum 1253 dysuria 191, 748, 761 postcoital 668 urethral diverticulum 1253 eating disorders 659 economic burden measures 439, 456 urinary incontinence 20, 35–6, 49, 82 economic evaluations, quality of life assessment 65 ectoderm 128 education 9 continence nurse specialist 94–6, 95 patient see patient education public see continence promotion educational attainment overactive bladder and 59 urinary incontinence and 57 efficacy measures, overactive bladder treatments 431–9 efficacy–tolerability ratios, overactive bladder treatments 443–4 Egypt, ancient 4 Ehlers-Danlos syndrome 1005, 1056 ejaculation, female 665 elderly drug treatment 635 midurethral slings 898 Neugebauer–Le Fort colpocleisis 1082–4 tricyclic antidepressants 511, 512 urinary incontinence outcome assessment 808, 821 pathogenesis 699–700, 700 prevention 395–6
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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urinary tract infections 618, 619, 626, 704, 704 see also postmenopausal women electrical conductance test, urinary loss 206, 316, 317 electrical stimulation (ES) clitoral nerve cerebral somatosensory evoked potentials 293, 293 sacral reflexes 294–5 ICS definition 757 lower urinary tract 1276–87 BION® device 1285, 1285 history 1276 peripheral nerve stimulator 1283, 1283–4 motor cortex 292–3 pelvic floor 478–9, 479 detrusor overactivity 107–8, 108, 109 evidence for effectiveness 412, 413–14, 416–17 stress urinary incontinence 85, 104–5, 105, 479 urge urinary incontinence 479 sacral nerve roots see sacral nerve stimulation urethra, bladder and anal canal 293–4 electrocardiogram (ECG), preoperative 829 electroencephalography (EEG), quantitative 441–2 electromyography (EMG) 278–88 biofeedback 85, 104, 481, 482 concentric needle electrode (CNE) 278, 281 denervation and reinnervation 281, 282, 284–5 diagnostic usefulness 286 genuine stress incontinence 282, 285 motor-evoked potentials 292 normal findings 281–3 primary muscle disease 286 urinary retention/obstructed voiding 285–6 during voiding 239, 240 fecal incontinence 1122, 1125 kinesiologic 278, 279–81 diagnostic usefulness 281 method 279–80 normal and abnormal findings 280, 280–1 motor unit 278, 281–6 rectocele 1041 single fiber (SFEMG) 283–4 diagnostic usefulness 286 electrode 278, 283 genuine stress incontinence 285 method and normal findings 283–4 videourodynamics 306 voiding difficulty/retention 285–6, 588 electronic pelvic floor symptoms assessment questionnaire (e-PAQ) 71 electronic voiding diaries 200, 435 electrosurgical therapy bowel injuries 1216 endometriosis 1168 embryology 128–40, 697 division of cloaca 128–30 early embryogenesis 128, 128 female genital tract 1318, 1318, 1330, 1330, 1331 Müllerian differentiation 130, 131 smooth muscle differentiation 130–1 sphincters 131
trigone and upper urinary tract 131–3 see also developmental abnormalities EMG see electromyography emphysema, subcutaneous 1217–18 emptying see bladder emptying endoanal ultrasonography (EAUS) anal incontinence 714, 715 obstetric anal sphincter injury 398, 687, 687–8, 688 rectal prolapse 1138 endocervical swabs 646 endocrine disorders, urinary retention 585 endoderm 128, 130 endometriomas, ovarian 1170–1, 1171 endometriosis bladder 191, 1168 chronic pelvic pain 1166–7 conscious pain mapping 1175–6 laparoscopic diagnosis 1167, 1167, 1168 laparoscopic treatment 1167–71, 1169, 1170 peritoneal disease 1167–70 rectovaginal septum 1171, 1171 vs painful bladder syndrome 596 endopelvic fascia 120, 120–1, 121 defects, enterocele 1026, 1027, 1027, 1028 endoscopes, flexible 381, 381 endoscopy, urinary tract (urethrocystoscopy) 378–89 bladder abnormalities 384–7 iatrogenic obstruction 985 indications 378–9 instrumentation 379–81 intraoperative midurethral slings 892, 893 pubovaginal slings 882–3, 909 tension-free vaginal tape 919 normal findings 382–3 pelvic organ prolapse 777 techniques 381–2 ureteral anomalies 387–8 ureteric injuries 1293–4 urethral diverticulum diagnosis 378, 384, 384, 1254–5, 1257 urethral diverticulum therapy 1260, 1260 urethral evaluation 383–4, 388 urethrolysis 990 urethrovaginal fistula 1266 urinary incontinence evaluation 378–9 urinary tract infections 621 urogenital fistulae 378, 382, 385, 386, 1229 voiding difficulty/retention 588 see also cystoscopy Endo Stitch, sacrospinous vault suspension 1059 enemas 730, 731 Enhorning theory, stress incontinence 8, 880–1 enteric nervous system (ENS) 723 Enterobacter 619, 619, 624 Enterobacteriaceae 617, 619, 623 enterocele 1024–34 after anti-incontinence surgery 832–3, 1353 after Burch colposuspension 875, 1025, 1027 prevention 1029 after hysterectomy 399, 725, 1056 prevention 399, 1028–9 surgical repair 1057, 1058 anatomy 1024 anterior 1012, 1024, 1028
prevention after hysterectomy 1029 apical 1028 clinical assessment 1028, 1028 congenital 1027 conservative treatment 1029 definition and scope 1024 epidemiology 1027 etiology and pathophysiology 1024–7, 1136–7 iatrogenic 1027 investigations 1028, 1029, 1039, 1040 obstructed defecation 724 perineal ultrasound 361, 362 prevention 1028–9 pulsion 777, 1027 rectal prolapse with 1139, 1146 surgical treatment 1029–31, 1058 laparoscopic 1209 symptoms 1027–8 terminology 773, 774, 1003 traction 777, 1027 enterococci 624 enterovesical fistulae, cystoscopic assessment 385 enuresis definition 747, 761 nocturnal see nocturnal enuresis ephedrine 515 Ephrin B 130 epidemiology Asia 52–62 Australia 40–50 Europe 32–7 South America 24–9 USA 14–22 Epidemiology of Prolapse and Incontinence Questionnaire (EPIQ) 461 epidural anesthesia/analgesia perineal trauma and 1106 stress incontinence risk after 685 voiding difficulty after 584, 684 episiotomy 1101–3 anal sphincter damage and 398, 682, 687, 688–9, 1113 ideal rate 1103 incidence 1102, 1102 indications 1102–3 mediolateral 1101–2 midline 1101, 1102 prevention 1106–7 stress urinary incontinence and 397 structures involved 1101 see also perineal trauma epispadias, female 1335, 1336 erosion artificial urinary sphincter 968, 969 pessaries 536 synthetic meshes see under synthetic meshes Escherichia coli antibiotic resistance 623 antibiotic susceptibilities 624 microbiologic culture 620, 620 urinary tract infections 614, 616, 619, 619 Estring 625, 706 estrogen 518–20 continence mechanism and 700, 701 deficiency female athletes 659 recurrent urinary tract infections and 704, 704 urinary symptoms 696, 697–8 vaginal changes 644, 649–50 see also postmenopausal women
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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estrogen – continued lower urinary tract effects 518, 696–7 receptors 696, 697, 700 replacement therapy recurrent urinary tract infections 623– 5, 704, 705 urinary incontinence prophylaxis 702–3 urinary incontinence risk 19, 703 urinary incontinence treatment 518– 20, 701, 701–2 urogenital atrophy 705–6 see also hormone replacement therapy vaginal administration 519, 520 atrophic vaginitis 650 pessary wearers 536 postcoital urinary tract infections 669 recurrent urinary tract infections 623, 625, 704, 705 urogenital atrophy 706 vs pelvic floor muscle training 413 ethical issues, cosmetic vaginal surgery 1380–1 ethnic differences see racial differences ethylene vinyl alcohol co-polymer suspended in dimethyl sulfoxide (Uryx®) 861, 973, 973 Europe, epidemiology 32–7 European Agency for the Evaluation of Medicinal Products, Committee for Human Medicinal Products (CHMP) 450 European Association of Urology, chronic pelvic pain definition 606 evacuatory failure see defecation, obstructed event recording, ambulatory urodynamics 318–19 Everett, Houston 6 examination, physical 193–4 continence nurse specialist 84, 85 gynecologic 193–4 ICS definitions 750–1, 762 physical therapist/physiotherapist 102, 476 examination under anesthesia, urogenital fistulae 1229, 1298 exercise as cause of urinary incontinence 409, 658–9, 676, 676–7 pad tests 206, 209 pelvic floor muscles see pelvic floor muscle training preoperative 827–8 see also physical activity; sports/fitness activities explantation artificial urinary sphincter 967, 969 see also erosion exstrophy bladder 1333, 1333 cloacal 1333, 1334 external anal sphincter (EAS) 3D MRI reconstruction 348 anatomy 122, 1100–1, 1101 childbirth-related nerve damage 687 electromyography 283, 285 MRI 340, 341 obstetric damage see obstetric anal sphincter injury primary repair after obstetric injury 1114– 15, 1115, 1116–17, 1117 see also anal sphincter
external genitalia ambiguous 1324, 1324, 1340, 1341 development 129–30, 1318 hemangiomas 1339, 1340 inspection 750–1 pediatric disorders 1340–1 externally readjustable sling 975, 976 external urethral sphincter (striated urogenital sphincter; rhabdosphincter) 177 anatomy 116, 117, 117–18, 118 drugs relaxing 491, 494–7 electromyography see urethral sphincter, electromyography embryological development 131 function in neurologic disease 566, 567 mechanism of continence 119, 147, 880 MRI 344, 345 neural reflexes 160 relaxation coordination 151–2 normal voiding 151 sensory nerves 159 extraurethral incontinence 751, 762 fallopian tubes anatomy 1159, 1159–60, 1160 development 1318, 1318 family history overactive bladder 61 pelvic organ prolapse 1006 urinary incontinence 19, 54, 55, 56–7, 396 faradism, evidence for effectiveness 414 fascia autologous slings see pubovaginal slings (PVS), autologous deep, anterior abdominal wall 1154, 1155 pelvic 1158 fascia lata autologous, pubovaginal slings 883 complications 819–20, 847 harvesting 846 results 814, 883–5, 884 cadaveric (CFL) pubovaginal slings 847, 850–1, 885 complications 889 results 850, 851, 888 sacrocolpopexy 1199 fat, autologous, periurethral injections 1354–5 fecal impaction 472 fecal incontinence 712–20, 1122–33 after rectocele repair 1047, 1047 after rectopexy 1141, 1142 biofeedback 715, 1122 childbirth-related 686–9 pathogenesis 687–9, 712–13 prevention 397–8 see also obstetric anal sphincter injury etiology 712 functional rehabilitation 1122–5 history taking 192, 713 investigations 714, 714, 1122 management 714–18 pads and pants 552 pathogenesis 687–9, 712–13 patient assessment 713–14, 1122 pudendal nerve terminal motor latencies 291, 714 St. Mark’s scoring system 713, 713 surgery 716–18, 1125–9, 1130 urinary incontinence and 19 female genital mutilation (FGM) 585, 1240
ethical issues 1380 reversal 1379 Female Sexual Function Index (FSFI) 26 FemAssist® device 536 femoral nerve injury 1350 FemSoft® device 536–7, 538, 539 ferrous sulfate 828 fetal weight, pelvic organ prolapse and 1005 fiber, dietary 730 fiber density (FD) 283, 283–4 fibroblasts, autologous, periurethral injection 973 fibroids, uterine, uroflowmetry and 221 filling, bladder see bladder filling filum terminale, short 575 fimbriae, uropathogenic bacteria 617 first desire to void (FDV) 230, 233, 432, 752, 763 first sensation of bladder filling 432, 752, 763 fistulae, urogenital 1224–38, 1297–306 abdominal repair 1232, 1234, 1301–3 combined transperitoneal/ transvesical 1301–3, 1304–5 transperitoneal 1234 transvesical 1234 after anti-incontinence surgery 1349, 1350, 1350 classification 1224–7, 1297 complex 1297 vaginal repair 1301, 1302–3 conservative management 1298 endoscopic assessment 378, 382, 385, 386, 1229 etiology 1224, 1225, 1226–7, 1297 investigations 1228–9, 1297–8 obstetric see obstetric fistulae pessary-related 536 postoperative management 1235–7 preoperative care 1230 presentation 188, 1227–8 prevalence 1224 prognosis 1237 risk factors 1224, 1226 simple 1297 surgical treatment 1230–5 choice of route 1231, 1299–300 dissection principles 1231, 1232–3 instruments 1231 interposition grafting 1234–5, 1303–6, 1304–5 suture materials 1231 techniques 1231–5, 1300–6 timing 1230–1, 1298–9 vaginal repair 1231–4 dissection and repair in layers 1231–2, 1232–6 saucerization technique 1232 in specific circumstances 1232–4 testing 1235 see also specific types fitness activities see sports/fitness activities training, preoperative 827–8 ‘flat tire’ test, urinary vaginal fistulae 382 flatus incontinence, after childbirth 686 flavoxate 488, 506 vs bladder training 419 flow see urine flow flow delay 755, 767 flow rate 152, 217 accelerated (AFR), before antiincontinence surgery 246 ambulatory urodynamics 320
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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average (Qaverage) 217, 755, 766 epidemiologic study 17 healthy volunteers 220, 220 catheter effects 237 curves see uroflow curves definition 755, 766 maximum (Qmax) 217, 217, 755, 766 bladder outlet obstruction 241, 241, 242 epidemiologic study 17 healthy volunteers 220, 220 interpretation 220, 786–7 normal 233 pressure–flow studies 791–2 recording 220, 787 measurement see uroflowmetry pressure–flow studies 790–2 videourodynamics 304–5 voiding difficulty/retention 587 flow rate controlling zone (FRCZ) 784–5, 790–1 flow time 217, 217, 755, 766 healthy volunteers 220 flow/volume nomograms 219, 220 fluconazole 648, 649 fluid management after fistula repair 1235 catheterized patients 545 constipation 730 urinary incontinence 87, 409–10, 471 fluoroquinolones 622–3, 624 fluoroscopy sacral neuromodulation surgery 1278, 1278, 1279, 1279–80 videourodynamics 303–4, 328, 329, 329 flurbiprofen 509–10 follow-up losses to 808 outcomes assessment 807 forceps delivery fecal incontinence and 398, 688 pelvic organ prolapse and 1005 perineal trauma and 1106 urinary incontinence and 397 foreign bodies, bladder 385 Fowler’s syndrome, electromyography 285, 286 FOXc1 133, 135 French gauge 543–4 frequency 187, 187, 188 24-hour 750, 762 bladder training to decrease see bladder training causes of abnormal 188 classification 175 continence nurse specialist 86 daytime 750, 762 detrusor overactivity and 144 drug treatment 502, 504 epidemiologic studies 16–17, 53, 54 increased daytime 633, 747, 760 increasing, as management intervention 468–9 normal values 201, 202 overactive bladder syndrome 633 patient-centred measures 436 pregnancy 397, 683–4 frequency–volume (FV) chart 198, 198–200 definition 749, 762 see also voiding diary functional ability, measures of impact on 439 functional profile length 754, 765 functional urinary incontinence 175 fungal infections, vulvovaginal 647–8, 648
funicular meso 1158 funneling, proximal urethra, pelvic floor ultrasound 359, 359 furniture protection 558 GABA 161–2 detrusor overactivity and 640 drugs acting on 494, 495 GABAA receptors 162, 495 GABAB receptors 162, 495 gabapentin 162, 600 Gaeltec NanoLogger™ ambulatory urodynamic system 322, 322 g-aminobutyric acid see GABA ganglion impar 1163 Gartner’s duct cysts 1255, 1256 embryologic basis 130, 136 translabial ultrasound 363, 364 gas embolism 1218 Gellhorn pessary 535, 535–6 gender differences childhood enuresis 47 urinary incontinence 33, 34, 40, 40, 42, 43 general practitioners (GPs), diagnostic role 100–1 genital hiatus see urogenital hiatus of levator ani genitalia, external see external genitalia genital ligament 1158 genital mutilation, female see female genital mutilation genital tract, female see reproductive tract, female genitogram, persistent urogenital sinus 134, 136, 1336 genitoplasty, feminizing 1324, 1340 genitourinary pain syndromes 748–9, 761 genuine stress incontinence (GSI) 754, 765 see also urodynamic stress incontinence germ cell layers 128 Gibson, James 5–6 giggle incontinence 190, 675 Gillick competence 830 Gittes procedure, outcome 814, 817 glial derived neurotrophic factor (GDNF) 133 global assessment scales 71–2, 72 stress urinary incontinence 453–4 gluteus transposition, anal sphincter 717 glyceryl trinitrate 513 glycine 494 glycopyrrolate 499 glycosaminoglycans, intravesical 600 gonadectomy, androgen insensitivity syndrome 1324, 1340–1 gonadotropin-releasing hormone (GnRH) analogs 828 Good Urodynamics Practices guidelines (ICS) 784–98 filling cystometry/pressure–flow studies 226–7, 787–97 calibration of equipment 794–5 computer software 797 equipment: minimum requirements 793–4 measurement of intravesical/abdominal pressures 792 measurement of urine flow rate 790–2 pressure signal quality control 795 pressure transducers 792–3 problem solving 795–6 retrospective artifact correction 796–7 urodynamic catheters 793
recording micturitions and symptoms 784 strategy for repetition of tests 797 uroflowmetry 216, 218, 784–7 Gore-Tex mesh 889, 1084 gracilis muscle interposition, fistula repair 1235 graciloplasty dynamic see dynamic graciloplasty fecal incontinence 717 graft rejection allograft slings 850 synthetic midurethral slings 897–8 xenograft slings 853 Gram-negative bacteria 614, 619 antibiotic resistance 623 Gram stain 620, 646 grande fosse pelvienne 1024–5, 1025 Green types 1 and 2 urethral descent 8, 332, 334 G-spot amplification 1379 guarding reflex 148, 159–60 sacral nerve stimulation actions 1276, 1277 stroke patients 568 Guillain–Barré syndrome 573 gynecologic developmental abnormalities see developmental abnormalities gynecologic examination 193–4 gynecologic surgery prevention of incontinence/prolapse after 398–400 urologic complications 1290, 1368–75 see also hysterectomy; pelvic surgery gynecologic symptoms 192 habit training 86–7, 417 Haemophilus influenzae 619, 620 Halban-type pouch of Douglas obliteration 1030, 1030 laparoscopic 1209 hamartoma, urethral/vaginal wall 1256 Hamlin and Nicholson fistula repair procedure 1233 hammock theory, DeLancey 125, 125, 881, 946 handicap, definition 102 health, WHO definition 24, 438 health systems, overactive bladder impact 439 Heart and Estrogen/Progestin Replacement Study (HERS) 19, 702 help-seeking overactive bladder 60 urinary incontinence 20, 41–2, 56 factors influencing 56, 57, 58 types of practitioners consulted 56, 56, 58 hemangiomas, introital 1339, 1340 hematocolpos 585, 1320 hematologic investigations, preoperative 829 hematomas, postoperative anti-incontinence surgery 1346–7, 1347 translabial ultrasound 363, 364 hematometra 1319, 1320 hematuria 192, 1292 hemorrhage/bleeding anti-incontinence surgery 831–2, 1346–7, 1347 colpourethropexy 871, 872 laparoscopic surgery 1215, 1216 midurethral sling procedures 895 sacrospinous vault suspension 1059–60 tension-free vaginal tape 921, 922
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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heparin intravesical 600 thromboprophylaxis 830–1 hernia trocar site 1214 true, enterocele 1026–7 see also incisional hernias herpes simplex, anogenital 584 herpes zoster 574–5 hesitancy 190 definition 217, 748, 761 pregnancy 684 hiatus, genital see urogenital hiatus of levator ani Hill equation 236 Hinman syndrome 151 Hirschsprung’s disease 724 anorectal manometry 728, 728 treatment 732 history, clinical 186–93 drug 192–3, 193 neurologic 192 obstetric see obstetric history past medical 192 physical therapist/physiotherapist 102, 476 urinary symptoms 186–92 history of urogynecology 4–12 home delivery, perineal trauma and 1107 pad tests 210–11 uroflowmetry 219 hormone replacement therapy (HRT) pelvic organ prolapse and 1006 prior to surgery 831 risk–benefit balance 520 Turner’s syndrome 1325 urinary incontinence prophylaxis 396, 702–3 urinary incontinence risk 19, 25, 703 urinary incontinence therapy 518–20, 702–3 see also estrogen Hormones and Urogenital Therapy (HUT) Committee 701, 704, 706 hospital-acquired infections 619, 619 hospitals, prevalence of urinary incontinence 48–9 host defense mechanisms 616 HRT see hormone replacement therapy human immunodeficiency virus (HIV), transmission via allografts 850–1, 885 Hunner’s ulcers 6, 386 hyaluronic acid (HA) dextranomer macrospheres (Zuidex™) 862, 973, 973–4 intravesical 600 hydrogel-coated catheters 542, 543 hydrometrocolpos 1338, 1338 hydronephrosis ectopic ureter 137, 138 imaging 326, 326 hydroxychloroquine 600 21-hydroxylase deficiency 1324, 1324, 1340, 1341 hydroxyzine 599 hymen imperforate 1319–20 measurements to/from 773, 774–5 hymenoplasty/hymenorrhaphy 1379, 1380–1 hyoscyamine 488, 499 hyperalgesia, referred pain with 609–10 hypermobile stress incontinence (HSI) 866–7
see also urethral hypermobility hypersensitive female urethra 584–5 hypertension autonomic dysreflexia 572 pelvic organ prolapse and 1005 hypertonic bladder 150 hypnosis 420 hypocalcemia 726 hypogastric nerves 159, 573 early stimulation studies 142, 144 laparoscopic sacrocolpopexy and 1195 hypogastric plexus 607, 1163–4 hypothalamus, control of micturition 160 hypothyroidism 585, 726 hysterectomy abdominal sacrocolpopexy with 1070 bladder injuries 1369 constipation after 725 cystocele repair with 1018 fistulae complicating 1224, 1225, 1227 laparoscopic, complications 1217 lower urinary tract problems after 1364–5 assessment 1364 prevention 1364 symptoms 1364 treatment 1365 pelvic organ prolapse and 399, 1006 prevention of enterocele after 399, 1028–9 radical lower urinary tract problems after 576, 1364–5 uroflowmetry before/after 221 rectocele after 1042 sexual dysfunction and 666–7 urinary incontinence after 398–9, 1364 epidemiology 34, 35, 42, 45 prevention 399 uterine prolapse 1078, 1078–9 vaginal apex fixation 1054 vaginal supports/attachments after 121, 121, 1054–5, 1055, 1194 vaginal vault prolapse after see vaginal vault prolapse hysterosalpingography (HSG), developmental anomalies 1319 hysteroscopy metroplasty 1321 uterine anomalies 1319 ICI see International Consultation on Incontinence ICS see International Continence Society IgA, secretory 616 IIQ see Incontinence Impact Questionnaire ileal conduit urinary reservoir 1310 ileal segment augmentation cystoplasty 1307 ileal sphincter-cystoplasty 1310–11 ileal ureter, ureteric injuries 1294–5, 1373, 1373 ileal vaginoplasty 1323 ileorectal anastomosis, colectomy with 731–2 iliococcygeal fixation, vaginal vault 1061 iliococcygeal muscle anatomy 122, 122, 1156 MRI 340, 341, 342 imaging 326–38 future developments 10 iatrogenic obstruction 985, 986 lower urinary tract 328–36 nervous system 336 pelvic organ prolapse 463–4, 778 preoperative 829 rectocele 1038–41
upper urinary tract 326–8 urogenital fistulae 1228–9 voiding difficulty/retention 588 see also specific modalities and techniques imipramine 488, 510–11 overactive bladder 638 side-effects 511–12 stress incontinence 517 vs bladder training 419 immunosuppressive drugs, interstitial cystitis 600 impairment, definition 102 improvement overactive bladder 430 patient-centered measures 438 stress incontinence 450–1, 810 incisional hernias after colposuspension 873 after laparoscopic surgery 1214 incomplete emptying, feeling of 190–1, 748 Incontinence Impact Questionnaire (IIQ) 69, 438, 438 ICI recommendations 805 nulliparous women 675 Incontinence on the Sexual Response/RJ (IIURS-RJ) 26 Incontinence Quality of Life Questionnaire 438 Incontinence Screening Questionnaire (ISQ) 49, 49 Incontinence severity index 69 Indevus Urgency Severity Scale (IUSS) 435, 435–6 indigo carmine, fistula detection 1228 infections complicating anti-incontinence surgery 1349, 1349 surgical mesh implants 838, 840 transmission via allografts 847, 850–1, 885 vaginal 644, 645, 647–8 see also urinary tract infections; wound infections inferior epigastric artery 1213, 1214–15 laparoscopic localization 1215, 1215 management of bleeding 1215, 1216 inferior fascia of levator ani 121–2 inferior gluteal artery 1055, 1055–6 surgical injury 1056, 1060 inferior gluteal nerve 1055, 1163 inferior hypogastric plexus see pelvic plexus inferior mesenteric artery 1162 inferior mesenteric ganglia (IMF) 158 inflammation interstitial cystitis 595 vulvovaginal, voiding difficulty 584 information leaflets, patient 82, 827 information provision, preoperative 827, 830 infundibulopelvic ligament 1157, 1158 Ingelman-Sundberg, Axel 4–5, 6 inguinal hernia, androgen insensitivity and 1324 injections, urethral 860–3 see also urethral bulking agents, injectable institutional settings, urinary incontinence 48, 48–9, 82 integral (midurethra) theory (Petros & Ulmsten) 881, 890–1, 918, 926 intention to treat analysis (ITT) 431 interferential therapy 414 interlabial masses, pediatric patients 1337–9 intermittent catheterization 757 intermittent self-catheterization (ISC) 588–9 after augmentation cystoplasty 1307–8
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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clean see clean intermittent self-catheterization continence nurse’s role 88, 88 definition 757 intermittent stream 217, 748, 761 internal anal sphincter (IAS) 1101, 1101 primary repair after obstetric injury 1114–15, 1115, 1116 internal iliac artery 1162 internal pudendal artery/vein 1055, 1160, 1162 internal urinary meatus 116–17 International Association for the Study of Pain (IASP) 606 International Classification of Diseases (ICD10) 746 International Classification of Functioning, Disability and Health (ICIDH-2) 101, 102, 746 International Consultation on Incontinence (ICI) continence nursing 92 Continence Promotion, Prevention, Education and Organization (CPPEO) committee 77–8, 80 Imaging and Other Investigations committee 209, 210 outcomes assessment standards 450, 805–8 baseline data/demographics 805 clinician observations 805–6 follow-up 807 patient observations 805 quality of life measures 69, 69, 72, 807–8 specific patient groups 808, 821–2 tests 806–7 pharmacotherapy recommendations 486, 488 International Consultation on Incontinence Questionnaire (ICIQ) 64, 69–71, 72 International Consultation on Incontinence Questionnaire Short Form (ICIQ-SF) 69–71 overactive bladder 437 pad tests and 211–12 stress incontinence 451–2 International Continence Society (ICS) 1-hour pad test 206, 206, 208–9 ambulatory urodynamics standardization 316–20, 787–8 Clinical Research Assessment groups 741–2 Continence Promotion Committee (CPC) 80 Good Urodynamics Practices guidelines see Good Urodynamics Practices guidelines outcome measures 450, 460 quality of life assessment 64, 68–9 questionnaire for males (ICSmale) 437 standardization of terminology and methods see standardization of terminology and methods Standardization of Terminology Committee 757–8, 772 International Federation of Gynecology and Obstetrics (FIGO) 4 International Urogynecology Association (IUGA) history 4–6 training standards 9 International Urogynecology Journal 5
interposition grafts fistula repair 1234–5, 1246, 1303–6, 1304–5 see also Martius fat-pad grafts intersex disorders 1340–1, 1341 InterStim® system 1284 interstitial cells of Cajal 723 interstitial cystitis (IC) 594–604 capsaicin therapy 515 clinical evaluation 595–8 cystoscopic assessment 385–6, 386, 597 diagnostic criteria/definition 594 ICS recommendation 749, 761 possible etiologies 594–5 treatment 598–601 see also painful bladder syndrome Interstitial Cystitis Association 598 interureteric ridge 117 endoscopic appearance 383, 383 intervertebral disk disease 567, 572–3 intervoid interval 436, 436 intestine embryological development 128 laparoscopic anatomy 1161–2 see also bowel injuries; enterocele; rectum; sigmoidocele intra-abdominal pressure see abdominal pressure intraurethral devices (inserts) urinary incontinence 87, 536–7, 537, 538 urinary retention 589 intravaginal (resistance) devices (IVRD) 87, 87, 537 effectiveness 537–8 pelvic floor muscle training with 412 intravaginal slingplasty (IVS) 1062 3D ultrasound imaging 369–70 pelvic floor ultrasound after 363, 363 surgical technique 1062, 1062 intravenous pyelography/urography (IVP/ IVU) 326, 326–7, 327 ureteric injuries 1292 urethral diverticulum 1259, 1259 urinary tract infections 621 urogenital fistulae 1228, 1229, 1298 intravesical pressure (pves) ambulatory urodynamics 317 changes during filling phase 149 definition 752, 763 drugs increasing 488–90 early studies 143–4 flow rates and 152 measurement 228–30, 792 quality control recordings 227, 227 videourodynamics 305 vs detrusor pressure 303 intrinsic sphincter deficiency (ISD) 147 artificial urinary sphincter 962, 963, 968 classification 177–9, 178 ICS view 754, 765 pubovaginal slings 846 surgical failure rates 400 surgical options 866–7 tension-free vaginal tape 920, 920 urethral pressure measurements 257, 257 urethrocystoscopy 379, 383, 384 Valsalva leak point pressure 305 videourodynamics 307 intrinsic urethral sphincter 177, 880 continence mechanism 119, 147 drugs decreasing outlet resistance at 491–3 see also bladder outlet
introital hemangiomas 1339, 1340 Introl prosthesis 535, 536, 537–8 involuntary detrusor contractions see detrusor contractions, involuntary ion channels 164–5 iron replacement therapy 828 irritable bowel syndrome (IBS), constipationpredominant 724, 725 ischial spines, as anatomic landmarks 773 I STOP® 948, 949, 951 JO1870 513 John Paul II, Pope 6 juxtacervical fistulae 1224, 1232–3 Karram, Mickey M. 5 Kegel, Arnold 9, 469, 481 Kelly, Howard A. 6, 7 Kelly plication 7 anterior colporrhaphy 1013–14, 1015, 1019 current consensus 931, 1092 outcomes 814, 818, 1094 kidneys autotransplantation, ureteric injuries 1372 duplex 136 embryological development 131, 132, 132–3, 134, 135 pregnancy/postpartum period 683 King’s Health Questionnaire (KHQ) 69, 70, 438 minimal important difference (MID) assessment 71 pad tests and 211 Klebsiella 619, 619, 624 ‘knack,’ the 470, 478 Kralj, Bozo 5 Kretz Voluson system 365, 365 Labhardt partial colpocleisis 1083 labia minora, enlarged 1378–9 labiaplasty augmentation 1379 reduction 1378, 1379, 1379 labor management see obstetric management obstructed 1240 lactobacilli 644 effects of estrogen 704 increased levels, vaginal disease 650–1 lactulose 730 laparoscopic surgery 1152 advantages 1152 colposuspension see colpourethropexy, laparoscopic complications 1152, 1212–20 access-related 1212 anesthesia 1218 bladder injuries 1217 bowel injuries 1215–17 pneumoperitoneum-related 1217–18 trocar-associated 1212–15 ureteric injuries 1217 disadvantages/problems 1152 endometriosis 1167–71 enterocele/rectocele 1209 paravaginal repair 1180, 1188–9, 1189 rectopexy/resection rectopexy 1143, 1143–4 robotic assistance 1180, 1180, 1199 sacral colpopexy 1194–203 support procedures 1206–10 surgeon’s experience 1217
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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laparoscopic surgery – continued ureteric injuries 1217, 1290 uterine-preserving, for uterine prolapse 1086, 1207–9 vaginal agenesis 1323, 1323 laparoscopic uterine nerve ablation (LUNA) endometriosis 1170 pelvic pain 1172, 1172–3 laparoscopy, diagnostic developmental anomalies 1319 endometriosis 1167, 1167, 1168 pelvic pain 1166–7 Lapides procedure 814, 815 laser treatment bladder ulcers 601, 601 endometriosis 1168, 1168–71, 1169, 1170 pelvic adhesions 1174 lateral inguinal fossae 1157 lateral umbilical fold 1157, 1157 latex catheters 542, 543 laxatives 730, 731 Leadbetter–Politano ureteral reimplantation technique 1370, 1370 leakage, urine see urine loss leak point pressures 259, 266–76 abdominal see abdominal (or Valsalva) leak point pressure cough 259, 268, 455 detrusor see detrusor leak point pressure ICS definitions 754–5, 766 measurement technique 267–8 as outcome measures 455 stress incontinence 267–71 videourodynamics 305–6 Learmonth, J.R. 144 Le Fort colpocleisis 1082–4, 1083 leg catheter drainage bags 547, 547 leg pain, postoperative sacrospinous vault fixation 1060 transobturator tape 952–3, 958 leiomyoma, urethral/vaginal wall 1256 levator ani muscles 121–2, 122, 1155–6 3D ultrasound 366–8, 367 activity (contractions) 3D/4D ultrasound 366, 367 perineal ultrasound 360–1, 361 childbirth-related damage 3D ultrasound 367, 367–8 MRI 343, 345 MRI-based simulation 349–50, 350 connective tissue interaction 123 electromyography kinesiologic 280–1 needle electrodes 281 inferior fascia 121–2 MRI 340, 341, 342, 343–4 color thickness mapping 348, 349 racial differences 345–6 superior fascia 121–2, 124 urethral/vesical neck support 124, 124 urogenital hiatus see urogenital hiatus of levator ani see also pelvic floor muscles levator ani syndrome 724 levatorplasty, posterior colporrhaphy with 1036, 1046 levator–symphysis gap (LSG) 344 levcromakalim 509 lidocaine, intravesical 600 lifestyle factors, modifiable constipation 730 pelvic organ prolapse 421, 1005 urinary incontinence 408–11, 471–2
lifting, heavy 409, 421, 1005 Likert scales 437, 803 limb contractures, obstetric fistula 1242 linea alba 1154, 1155 local anesthesia conscious pain mapping 1175–6 midurethral slings 892 SPARC sling 926 tension-free vaginal tape 918–19 loin pain 191, 191 long-term care, overactive bladder 439 loop diuretics 521 lower motor neuron lesions 145, 566 sacral reflex responses 295 lower urinary tract (LUT) anatomy 116, 116–19 functional 123–5 biomechanics 236–7 electrical stimulation 1276–87 embryology 128–40, 697 functional terms 119 hormonal influences 696–7, 697 imaging 328–36 instrumentation, infection risk 618 nervous control 158, 158–60, 571, 573 pregnancy 683–5 reconstruction 1309–11, 1311 pediatric patients 1342, 1342–3 rehabilitation 757 lower urinary tract exercises (LUTE) 107, 109 see also pelvic floor muscle training lower urinary tract symptoms (LUTS) 186– 92, 746 after fistula repair 1237 associated with sexual intercourse 748 classification into groups 187, 187 cystometry and 226 flow-related 217 hormonal influences 697 ICS definitions 746–9, 760–2 measuring frequency, severity and impact 749–50, 762–3 overactive bladder syndrome 633 pad tests and 211–12 pathophysiology 149 poor correlation with urodynamics 321 postmenopausal 696, 697–8, 698 postmicturition 748, 761 pregnancy/postpartum 683 prolapse-related 780 quality of life impact 66–7 questionnaires 186, 186, 187, 803 recording, during urodynamics 784 severity analysis of treatment outcomes and 431 assessment 186–7, 749–50 storage 747, 760–1 urinary incontinence and 19 voiding 747–8, 761 see also symptoms lumbar intervertebral disk herniation 572–3 lumbosacral spine X-rays 336 lung disease, chronic 46 LUT see lower urinary tract LUTS see lower urinary tract symptoms Lyme disease 574 lymphatic system, pelvic 1163 Macroplastique® see silicone macroparticles magnetic resonance imaging (MRI) 10 anterior vaginal wall prolapse 1011, 1011 chemical shift artifact 347
defecography rectal prolapse 1139 rectocele 1040–1 developmental anomalies 1319, 1319 endoanal 714, 714 enterocele 1028, 1029 pelvic floor 340–53 3D reconstruction 348, 349 basic anatomy 340–2, 341, 342, 345 childbirth-related changes 344–5 childbirth simulation 349–50, 350 color thickness mapping 348, 349 data processing/evaluation tools 350, 351 imaging protocols 347–8 pitfalls 346–7 racial differences 345–6 symptomatic findings 342–4, 343, 344 pelvic organ prolapse 342, 343, 344, 463–4, 778 rectocele 1039–41, 1040 sigmoidocele 1136 slice acquisition angle 346, 346–7, 347 upper urinary tract 326, 327 urethral diverticulum 336, 336, 1259, 1259–60 urogenital fistulae 1229 voiding difficulty/retention 588 vs 3D ultrasound 365, 366 magnetic stimulation anterior sacral roots 291–2, 292 clitoris 294 motor cortex 292, 292–3 therapy 414–15, 417, 479 Mainz 2 ureterosigmoid pouch 1312 malakoplakia, bladder 384 malignant disease fistula formation 1224, 1225, 1229 fistula repair 1306 urethral diverticulum 1253, 1253 urethral/vaginal 1256 see also bladder tumors malnutrition, obstetric fistulae and 1242 Manchester procedure 1079–80, 1080, 1087 manometry anorectal see anorectal manometry biofeedback 481 Marfan syndrome 1005, 1056 Marlex mesh 836, 839 Marshall–Marchetti–Krantz (MMK) procedure 7–8, 866 complications 1346, 1347, 1350, 1351, 1353 osteitis pubis after 875, 1350 pressure–flow parameters after 245 results 814, 815 vs Burch colposuspension 868 marsupialization, transvaginal, urethral diverticulum 1260, 1261 Martius fat-pad grafts 7 fistula repair 1234–5, 1246, 1301, 1302–3 transvaginal urethrolysis 990 urethral diverticulectomy 1263, 1266 urethrovaginal fistula repair 1268, 1269, 1301 mast cells, activation in interstitial cystitis 594–5 mattress covers 558 maximum cystometric capacity (MCC) 239, 754, 765 maximum flow rate see flow rate, maximum maximum pressure 755, 767
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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maximum urethral closure pressure (MUCP) see urethral closure pressure, maximum maximum urethral pressure (MUP) see urethral pressure, maximum maximum voided volume 750, 763 Mayer–Rokitansky–Küster–Hauser syndrome 134–5, 1323, 1341, 1342 McCall culdoplasty surgical technique 1030, 1030–1 at time of hysterectomy 1028–9 vaginal vault prolapse 1061–2 McGuire technique, augmentation cystoplasty 1307 means (statistical) 430–1 meatal masses 1255 mechanical properties, synthetic meshes 839 mechanical stimulation, sacral reflexes 294–5 mechanoafferent signaling, urothelial 165 media, mass 77 medial inguinal fossae 1157 medial umbilical fold 1157, 1157 medians 430–1 median sacral artery 1162 median umbilical fold 1157 Medical, Epidemiologic and Social Aspects of Aging (MESA) study 14–15, 16–19 medical history, past 192 medical illness, pelvic organ prolapse and 1005 medicolegal issues, incontinence surgery 827, 829–30 medroxyprogesterone acetate (MPA) 520 melanoma, bladder metastases 386–7, 387 men diagnosis of incontinence type 101 ICI-recommended outcomes assessment 808, 821 physical therapy 108 prevalence of urinary incontinence 33, 34, 40, 40 severity of urinary incontinence 48, 48 Menfis Blu Runner ambulatory urodynamic system 323, 323 menopause 696–710 continence mechanism and 699–701 sexual dysfunction and 666 symptoms, prevalence 26, 27 urinary incontinence and 33–4, 34 see also perimenopausal women; postmenopausal women menstrual cycle urinary symptoms and 697 uroflowmetry and 221 menstrual flow, obstructed 1319, 1319, 1320 mental health, obstetric fistulae and 1242 mercaptoacetyl triglycine (MAG3) scans 621 Mersilene mesh/tape 836, 838, 841, 890 pectineal ligament uterine suspension 1085–6 sacrohysteropexy 1084 mesenchyme 128, 130–1 mesenteries, pelvic 1157–8 meshes, synthetic see synthetic meshes mesoderm 128 mesonephros 131 meso-ovarium 1158 mesosalpinx 1158 meta-analyses 431 metanephros 131 metastatic tumors, bladder 386–7, 387 methantheline 499 methotrexate 600 metoclopramide 489
metronidazole 650 metroplasty, hysteroscopic 1321 Meyer Weigert law 136 MIchaelis–Gutmann bodies 384 microbiologic culture urinary tract infections 620, 620 vaginitis 646, 649 microorganisms, vaginal flora 644, 644 microscopy urine 620 vaginal 646, 646, 649 micturition 486 clinical physiology 142–55 bladder cycle 142, 147–52 contemporary studies 146–7 early experimental studies 142–5 early urodynamic studies 145 structural aspects 147 development of voluntary control 147–8 habits 676 hormonal effects on control 700 pontine center see pontine micturition center preventative 676 recording, during urodynamics 784 reflexes 160 sacral nerve stimulation inhibiting 1276, 1277 sacral cord center 145, 571 time chart 749, 762, 784 urethral mobility 123, 124 middle rectal artery 1162 middle sacral artery/vein 1195, 1195 midodrine 517 midpubic line, pelvic organ prolapse 464 midurethral slings 870, 880, 890–9 after obstetric fistula repair 1248 complications 895–8 elderly patients 898 history 890 hybrid procedures 940, 940–1, 941 materials available 891 mechanism of effect 881, 881, 890–1, 918, 946 obese patients 898 obstruction complicating sling loosening/incision 988 timing of intervention 984 transvaginal sling incision 988–9, 990 operative techniques 891–3 pressure–flow parameters and 245–6 prevention of urge incontinence after 399–400 prolapse surgery with 898–9, 1016, 1019 results 894, 894–5 transpubic technique 893 transvaginal technique 892–3 see also SPARC sling; tension-free vaginal tape; transobturator midurethral slings midurethra (integral) theory (Petros & Ulmsten) 881, 890–1, 918, 926 midwifery training 1107–8 minimal important difference (MID) assessment, quality of life scores 64, 71, 453 minimum voiding pressure 755, 767 Mitrofanoff procedure, continent reconstruction 1342–3, 1343 mixed urinary incontinence 84, 100 conservative treatment 418 definition 747, 760 history taking 189
pathophysiology 143 physical therapy 108 prevalence 15, 33, 34, 53, 54, 56 tension-free vaginal tape 920, 920, 921–2 urodynamic diagnosis 232 Miya hook 1058, 1058, 1081 MMS Luna ambulatory urodynamic system 322, 322–3 mobility problems association with incontinence 19 cystometry 227 mobilization, postoperative, fistula repair 1236–7, 1247 Monarc™ 948, 949, 951 montelukast 600 morphine 160, 161 Moschcowitz procedure 1029, 1030 laparoscopic 1209 motor conduction velocity 290, 290 motor cortex stimulation, motor-evoked potentials 292, 292–3 motor-evoked potentials (MEPs) anterior sacral root stimulation 291–2, 292 motor cortex stimulation 292, 292–3 perineal/perianal stimulation 290 motor pathways, central, neurophysiologic assessment 292–3 motor unit 278, 279 motor unit potentials (MUPs) concentric needle EMG 281–3, 282 denervation and reinnervation 282, 283, 284 kinesiologic EMG 280, 280 ‘M’ response 290, 291 MRI see magnetic resonance imaging Müllerian ducts development 1318, 1318 differentiation 130, 131 Müllerian remnant cyst 1256 multichannel urodynamic recorder 302–3, 303 Multinational Interstitial Cystitis Association 598 multipara, pelvic floor MRI 340–2 multiple sclerosis (MS) 570 drug treatment 503 neurophysiologic conduction studies 292, 293 sexual dysfunction 666 voiding dysfunction 566, 567, 570 multiple system atrophy (MSA) 569 electromyography 283, 284–5 muscarinic receptors 146, 158, 163, 498 muscimol 162 muscle damage, nulliparous women 677 denervation see denervation, muscle disease, primary, electromyography 286 reinnervation, electromyography 284–5 muscle-evoked potentials see motor-evoked potentials muscle fibers classification 278 density (FD) 283, 283–4 innervation ratio 278 muscle transposition anal sphincter 717 stimulated (dynamic) 717, 1127, 1127 musculotropic relaxants 502–7 Mycobacterium tuberculosis 620 Mycoplasma hominis 620–1 mycoplasmas 619, 620, 624
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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myelodysplasia 147, 567 cystourethrography 335 detrusor leak point pressures 266–7 myelomeningocele 1333–4, 1334 drug treatment 503 electromyography 284 myoblasts, autologous, periurethral injection 973 myocutaneous flaps, vaginal reconstruction 1379 myopathy detrusor 585–6 electromyography 286 nalbuphine 161 nalidixic acid 623 naloxone 160, 161, 490 National Continence Management Strategy (NCMS) (Australia) 78–80 national continence organizations 77–80, 79 continence promotion role 78–80 results of survey 77–8, 78 National Foundation for Continence (US) 78 National Institute of Child Health and Human Development (NICHD), outcomes of treatment standards 450, 455, 456 National Institute of Diabetes, Digestive and Kidney Diseases (NIDDK), interstitial cystitis criteria 594, 597 National Institutes of Health (NIH) definition of pelvic organ prolapse 1003 Terminology Workshop for Researchers in Female Pelvic Floor Disorders 804, 809–10 needle bladder neck suspension (NBNS) (transvaginal colpourethropexy) 866, 870 complications 1346, 1347 laparoscopic 1181 postoperative voiding dysfunction 832, 984 results 9, 811–12, 813, 814, 816, 817 urethral diverticulectomy with 1260, 1261 vs retropubic colpourethropexy 871 see also Pereyra procedure; Raz procedure; Stamey procedure neobladder construction, pediatric patients 1342, 1342–3 neodymium:YAG laser, bladder ulcers 601, 601 Neomedics Acquilog ambulatory urodynamic system 323, 323 neosphincters, anal 717–18, 1127–9 neovagina formation 1323, 1323, 1342 nephrectomy, ureteric injuries 1373 nephrogenic adenoma, urethral diverticulum 1253 nephrostomy tube, ureteric injury 1293–4, 1373–4 nephroureterectomy, duplicated ectopic ureter 1336, 1337 nerve growth factor 147, 149 nerve injury anti-incontinence surgery 1349, 1350 laparoscopic surgery 1164 midurethral slings 895 obstetric fistulae 1242 sacrospinous vault suspension 1060 nerve supply female pelvis 607, 607–9, 1163–4 lower urinary tract 158, 158–60, 571, 573 nervous system, imaging 336
Neugebauer–Le Fort procedure 1082–4, 1083 neural plasticity, interstitial cystitis 595 neurogenic voiding dysfunction 566–81 ambulatory urodynamics 321 cerebral lesions 567, 568–70 classification 174, 177 clean intermittent self-catheterization 549 current issues 742 cystourethrography 334–5 drug treatment 492, 495–6, 497, 503, 506, 514 ICI-recommended outcomes assessment 808, 821–2 peripheral nervous system disease 567, 575–6 spinal cord disease 566, 567, 570–5 surgical treatment 1306–9 urodynamic diagnosis 232 videourodynamics 307–9, 310, 311 see also detrusor areflexia; detrusor overactivity (DO), neurogenic; detrusor–sphincter dyssynergia neurologic disorders 566–81, 567 urinary incontinence in childhood 1331 voiding dysfunction see neurogenic voiding dysfunction neurologic examination 193 neurologic history 192 neuromodulation, sacral see sacral nerve stimulation neuropathic bladder see neurogenic voiding dysfunction neurophysiologic conduction studies 290–9 autonomic nervous system 295–6 parameters measured 290, 290 rectocele 1041 sacral motor system 290–3 sacral reflexes 294–5 sacral sensory system 293–4 neurophysiologic tests see electromyography; neurophysiologic conduction studies neurosyphilis 573–4 NFO Worldgroup survey 20 nicotonic cholinergic receptors 158, 159, 160 nifedipine 507–8, 600 nitric oxide (NO) 147, 159 host defense role 616 initiation of voiding 151 therapies targeting 493, 513 nitric oxide synthetase inhibitors 493, 513 neuronal (nNOS) 131 nitrofurantoin 623, 624 pregnancy 625 nociception bladder 148 pelvic visceral 608–9 nociceptors mechano-insensitive (silent) 609 visceral 609 nocturia 187–8 drug-mediated control 521 ICS definitions 747, 750, 760, 762 overactive bladder syndrome 633 patient-based measurement 436–7 postmenopausal women 699–700 pregnancy 397, 683–4 prevalence 17, 54 nocturnal enuresis 190 alarms 558 childhood 1331 drug treatment 511, 520–1
urinary incontinence risk in adult life 46, 46–7 definition 747, 761 drug treatment 520–1 overactive bladder syndrome 633 prevalence 41, 42 primary 190, 1331 secondary 190 nocturnal polyuria 190, 750, 762 nocturnal urine volume 190, 750, 762 nomograms bladder outlet obstruction 236, 242 flow/volume 219, 220 non-adrenergic, non-cholinergic (NANC) neurotransmitters 147, 158, 498 non-inferiority study design 431 non-neurogenic neuropathic bladder 151 non-neurogenic voiding difficulty/retention see voiding difficulty, non-neurogenic non-relaxing urethral sphincter obstruction 756, 768 non-steroidal anti-inflammatory drugs (NSAIDs) 509–10 noradrenaline (norepinephrine) 159, 162, 640 norephedrine chloride 515 norfenefrine 515–16 normality, standardization and 740 Nottingham Health Profile 67, 68 Novasys micro-remodeling system 977, 978 nulliparous women 674–80 giggle incontinence 675 pelvic floor dysfunction etiologic factors 675–7 management 678 prevalence 674–5 prevention 678–9 significance of symptoms 675 pelvic floor MRI 340, 342 pelvic floor ultrasound 358 pelvic organ prolapse 674–5, 676 urinary tract infections 675 nurse continence advisor (NCA) 92, 93 nurse practitioners 93, 94 nurses advanced practice see advanced practice nurses continence see continence nurse specialist preoperative counseling 827 registered (RN) 94 Nurses’ Health Study 702–3 nursing assessment 83, 83, 84 nursing home residents urinary incontinence 48, 48 urinary tract infections 626 nystatin 649 OABq 437 OASI; OASIS see obstetric anal sphincter injury obesity anti-incontinence surgery and 867, 868 midurethral slings 898 pelvic organ prolapse and 1005 preoperative preparation 828 urinary incontinence and 19, 45, 408 urinary tract infections and 618, 675 weight loss 396, 408–9, 471–2 OBJECT trial 500 obstetric anal sphincter injury (OASI; OASIS) 1112–20 classification 1112, 1112 early recognition 714–15
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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fecal incontinence 686–9, 687, 688 incidence 1113, 1114 patient assessment 713 surgical repair 716–18 incidence 1113 prevention 397–8 primary repair 1113–18 definition 1112 end-to-end technique 1113, 1115 end-to-end vs overlap techniques 1115 outcome 1113, 1114 overlap technique 1113–15, 1115 principles and technique 1116–18 techniques 1113–14 secondary repair 1112 obstetric fistulae 1224, 1240–50, 1297 circumferential 1247, 1247 classification 1243–4, 1244 epidemiology 1240 etiology 1225, 1240 future 1249 immediate management 1244 investigations 1243 irreparable 1248 prevalence 1240–1 surgical repair 1244–8 absent urethra 1246, 1246–7 complications 1248 failed 1248 flap splitting technique 1245, 1245 interposition grafts 1246 postoperative care 1247–8 results 1248 route 1244–5 specific problems 1246–7 timing 1230, 1244 symptoms and signs 1241–3 obstetric history 192 urinary incontinence and 19, 24–5, 25, 28 obstetric management fecal incontinence prevention 398 perineal trauma prevention 1106–7 urinary incontinence prevention 397 obstetric trauma rectocele formation and 1036–7 see also perineal trauma obstructed defecation see defecation, obstructed obstructed labor 1240 obstruction, bladder outflow (BOO) after incontinence surgery 982–95 diagnostic evaluation 983–6 etiology 982–3 identifying risks 983 incidence 982 management 986–93, 987 presentation 983 see also voiding difficulty, after antiincontinence surgery a-adrenergic receptor subtypes and 164 before anti-incontinence surgery 246 causes 585 clean intermittent self-catheterization 549 current issues 741–2 detrusor function and 236–7 detrusor overactivity 632–3 electromyography 285–6, 588 ICS definition 756, 768 non-relaxing urethral sphincter 756, 768 prolapse reduction and 237–8, 239 symptom syndrome suggesting 749, 761–2 treatment 589 urethrolysis see urethrolysis
urodynamic definition/diagnosis 236 after incontinence surgery 984–5 pressure–flow studies 239–45, 241, 242, 243, 244 voiding cystometry 231, 232 videourodynamics 241, 244, 306, 306, 309–10, 985 see also urinary retention; voiding difficulty ObTape® 946 complications 951–2 mesh characteristics 949, 951 operative technique 948 ObTryx™ 948, 949, 951 obturator artery 1162 obturator nerve 1163 occupation overactive bladder and 59, 61 pelvic organ prolapse and 1005 urinary incontinence and 54, 55 odor control 558 omental pedicle grafts, fistula repair 1235, 1303, 1304–5, 1306 omental urethra-cystoplasty 1310–11 Onuf’s (Onufrowicz’s) nucleus 159–60, 608 degeneration, electromyography 284 pharmacological targets 160, 161 opening pressure 755, 767 opening time 755, 767 OPERA trial 500 opioid agonists 513, 730 opioid antagonists 490 opioid receptors 160–1 oral contraceptive pill 831 orchidectomy, androgen insensitivity syndrome 1324, 1340–1 oropharyngeal membrane 128, 128 Ortiz, Oscar Contreras 5 osteitis pubis 875, 1349, 1349–50 osteomyelitis, postoperative 938, 1349 Ostergard, Donald 5 outcome 740 outcome measures 740 clinician (investigator)-based 432, 454–6, 461–4 incontinence interventions 802–23 AUA guidelines 803, 810, 811–20 future considerations 808–9 ICI recommendations 805–8 NIH Terminology Workshop recommendations 809–10 Urodynamic Society recommendations 803–5, 810–21 overactive bladder 430–48 patient-centred 432, 435–9, 451–4, 460–1 pelvic organ prolapse 460–5 physiologic 432–5 primary 803 questionnaires 803 secondary 803 stress incontinence 450, 450–8 subjective vs objective 451 surrogate 456 validity and reliability 430, 460, 802–3 outcome research 740 ovarian artery/vein 1160, 1162 ovarian endometriomas 1170–1, 1171 ovarian failure, Turner’s syndrome 1325 ovarian fossa 1158 ovarian ligament 1158, 1160 ovarian plexus 1164 ovaries 1160, 1160 overactive bladder (syndrome) (OAB) 632–42
classification 174, 176, 178, 180 clinical presentation 633 de novo, after anti-incontinence surgery 833, 1352, 1352–3 colpourethropexy 873–4, 874 midurethral slings 896, 897 prevention 399–400 pubovaginal slings 886–7, 889 urethrocystoscopy 378–9 drug treatment 497–513, 635–8, 638 dry 632 estrogen therapy 702 future developments 640 history 632 outcome measures 430–48 efficacy 431–9 efficacy–tolerability ratios 443–4 placebo response 440 principles of evaluation 430 safety 444 statistical evaluation 430–1 tolerability 440–3 pathophysiology 161, 632–3 peripheral nerve stimulation 1283–4 pregnancy 397 prevalence 633–4 Asia 58–60, 59, 60, 61 Europe 34, 35 quality of life assessment 64 sacral nerve stimulation 639, 1276 spinal cord injury 145 surgical treatment 1306–9 terminology 632, 749, 761 treatment 634–40 urgency and 144, 149 urodynamic diagnosis 149, 232, 633, 634 videourodynamics 308, 310 wet 632 see also detrusor overactivity overactive bladder outlet 178, 179–80 Overactive Bladder Questionnaire 438 overactive bladder symptoms and healthrelated quality of life questionnaire (OABq) 437 overdistension injury, bladder 586 overflow incontinence 84 classification 175 ICS recommendation 756, 768 Oxford grading system, pelvic floor muscles 85, 85, 477, 477 oxybutynin 488, 503–5 cost-effectiveness analysis 439 evidence for effectiveness 500–1, 503–4 extended release (ER) 504, 636, 638 intravesical administration 504–5 overactive bladder 635–6, 638 pediatric patients 1332 placebo-controled trials 440 side effects 504, 636 tolerability measures 441, 441, 442–3, 443 transdermal (OXY-TDS) 505, 636, 638 vs bladder training 419 vs pelvic floor muscle training 412–13 pad-and-pants systems, disposable 553 pads 88, 550–5, 552 all-in-one 553, 553 bed 553, 554 disposable 552–3, 555 during exercise 659 guidelines for assessing 551 nursing management 87–8 pouch 553, 554
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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pads – continued reusable 553, 555 skin care 555 urogenital fistulae 1230 pad tests 206–14 1-hour 206, 208–9, 433 ICS standard 206, 206, 208–9 modified 209 ambulatory urodynamics 315 historical aspects 206 indications 206 long 210–11 detection limit 210 reliability and validity 210–11 overactive bladder evaluation 433, 433 paper towel test 212 Pyridium test 209–10 recommendations 751, 763, 806 reliability and validity 207 short 207–10 detection limit 207–8 reliability and validity 208–9 vs long 211 stress incontinence evaluation 455–6 symptoms/quality of life correlation 211–12 pain 191 bladder see bladder pain chronic pelvic see chronic pelvic pain conscious laparoscopic mapping 1175–6 ICS definitions 748 loin 191 pelvic see pelvic pain pelvic pathways 608 postoperative laparoscopic surgery 1152 transobturator tape 952–3, 958, 959 somatic vs visceral 609–10 syndromes, genitourinary 748–9, 761 urethral 191 visceral see visceral pain painful bladder syndrome (PBS) 594–604 clinical evaluation 594–8 ICS definition 594, 749, 761 treatment 598–601 see also interstitial cystitis pants 550 designs 554, 554 selection guidelines 552 skin care 555 paper towel test 212 paracervical ganglia 608 paracervix 1158 parachute jumping 659 paracolpium 120, 120, 121, 1054–5, 1068, 1194 see also pelvic organ support paradoxical puborectalis syndrome 1138 see also anismus parametrium 120, 120, 1054, 1158, 1194 pararectal fascia 1036 pararectal fossa (space) 1055, 1158, 1162 parasympathetic nerves bladder cycle control 148, 151 early physiologic studies 142 lower urinary tract 158, 158–9, 573 neurophysiologic studies 295 pelvis 608 parasympathomimetic agents 488–9 paraurethral glands (Skene’s glands) 119 blockage by catheters 544, 544 cyst/abscess 1255, 1256 infection 1252
pediatric patients 1337, 1337 paraurethral structures 116 paravaginal (lateral vaginal) defects 1010, 1010–11 3D ultrasound 368 causes of failed repair 401 laparoscopic repair 1180, 1188–9, 1189 MRI 1011, 1011 physical examination 1012 retropubic repair 1016 AUA outcomes assessment 814, 815 vaginal repair 1016–18, 1017–18 results 1019 vs laparoscopic repair 1189 paravaginal supports/attachments 124, 1010 3D ultrasound 367, 368 MRI 1011, 1011 paravesical fossa 1158 parity overactive bladder and 59, 61 urinary incontinence risk and Asia 54, 55 Australia 42, 44, 45, 45 Europe 34, 35 South America 24, 25, 28 Parkinson’s disease 162, 568–9 electromyography 280 voiding dysfunction 567, 568–9, 569 patient-centered outcome measures 432 overactive bladder 435–9 pelvic organ prolapse 460–1 stress urinary incontinence 451–4 patient derived outcome measures (PDO) 64 patient education constipation 730–1 physical therapy 103, 107, 108–9, 476–7 Patient Global Impression of Improvement (PGI-I) scale 72, 72, 438, 454 Patient Global Impression of Severity (PGI-S) scale 72, 72, 437, 454 patient perception of bladder condition questionnaire 71, 72, 437 peak flow rate see flow rate, maximum pectineal ligament uterine suspension 1085–6 pediatric patients 1330–44 capacity to give consent 829–30 interlabial masses 1337–9 urinary incontinence 1331–7 congenital abnormalities causing 1333–7 enuresis alarms 558 etiology 1331 functional causes 1331–2 outcomes assessment 808, 821 prevalence 47 urethral injections 862 urinary incontinence in adult life and 46, 46–7 see also nocturnal enuresis, childhood urinary symptoms, management 396, 401 urinary tract infections 617, 626 urinary tract reconstruction 1342–3 see also developmental abnormalities pelvic brim 1154–5, 1155 pelvic denervation procedures, chronic pelvic pain 1172–3 pelvic diaphragm 119–20, 121–2, 1155–6 pelvic fascia 1158 parietal 1158 visceral 1158 pelvic floor 3D reconstruction 348, 349
anatomy 119–22, 120 functional 123–5 MRI 340–2, 341 connective tissue/muscle interaction 123 mechanisms of injury 682–3 MRI see under magnetic resonance imaging repair 1379 ultrasound 356–77 viscerofascial layer 120, 120–1, 121 Pelvic Floor Distress Inventory (PFDI) 460–1 pelvic floor dysfunction (PFD) classification 177–80, 178–9 description of functional symptoms 780–1 diagnostic tools 1138–9 ICS standardization of terminology 772–81 MRI 340, 342–4, 343, 344 nulliparous women 674–80 obstructed defecation 724–5, 726, 732 pathophysiology and etiology 1138 prevention 395–401, 678–9 pelvic floor dyssynergia 724, 1138 see also anismus pelvic floor educator device 480–1, 481 pelvic floor exercises see pelvic floor muscle training Pelvic Floor Impact Questionnaire (PFIQ) 460–1 pelvic floor muscles (PFM) anatomy 121–2, 122 assessment of function 477 continence nurse specialist 85, 85 ICS recommendations 751, 778–80 Oxford grading system 85, 85, 477, 477 childbirth-related trauma 683 rectocele formation and 1036–7 connective tissue interaction 123 contraction, urethral pressure measurements 259 denervation/nerve damage childbirth-related 683, 686, 687 electromyography 285 neurophysiologic conduction studies 291 nulliparous women 677 rectocele formation and 1037 electrical stimulation see electrical stimulation, pelvic floor electromyography 280, 280–1 during voiding 239, 240 ICS recommendations 779 female athletes 658–9 inspection 779 obstetric fistulae and 1242 palpation 779 pressure recordings 779–80 see also levator ani muscles pelvic floor muscle training (PFMT) 9, 469–70, 477–8 biofeedback 104, 469, 479–81 electromyography 85, 104, 107 equipment 104, 480, 481 evidence for effectiveness 412, 421 perineal ultrasound 360 daily regimes 469–70 definition 757 detrusor overactivity 107, 108, 109 electrical stimulation with 414 evidence for effectiveness 411–13, 416, 476 female athletes 660 guidelines 106, 106 intravaginal resistance devices with 412
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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measures of efficacy 455 in men 108 overactive bladder 635 pelvic organ prolapse 421 prevention of fecal incontinence 398 prevention of urinary incontinence 397 prior to surgery 826 programs 411, 478 stress strategies (the ‘knack’) 470, 478 stress urinary incontinence 84–5, 103–4 teaching 469 urge incontinence 470, 470 vaginal cones and 86, 105–6, 480 pelvic inflammatory disease 191 pelvic (splanchnic) nerves bladder innervation 158, 159, 573 pelvis innervation 607, 608, 1164 sensory function 148, 159 stimulation studies 142 surgical injury 575–6 pelvic organ prolapse (POP) 1000–8 anatomical basis 121 classification 463, 1000, 1000–1 conservative treatment 420–2, 422, 1029 definition 1003–4 de novo, after anti-incontinence surgery 875, 1353, 1353 epidemiology 20, 395, 1003, 1004–6 estrogen deficiency and 705 hysterectomy and 399, 1006 ICS definitions 751 ICS description system 772–8 ancillary techniques 777–8 conditions for examination 772–3 imaging procedures 778 ordinal staging 776–7, 777, 1002, 1002–3 quantitative see Pelvic Organ Prolapse Quantification System surgical assessment 778 ICS standardization of terminology 772–81 leak point pressure testing 268 MRI 342, 343, 344, 463–4, 778 natural history 395 nulliparous women 674–5, 676–7 outcome measures 460–5 objective 461–4 subjective 460–1 pathogenesis 394, 394, 689 pessaries and devices 534–40, 535 physical examination 193–4, 751, 772–7 conditions for 772–3 supplementary techniques 777 prevention 395–400 reduction pressure–flow studies and 237–8, 239 to reveal stress incontinence 400, 1090, 1091 risk factors/etiology 395–7, 1003–6, 1136 nulliparous women 676–7 sexual function and 666, 780, 1028 surgery see prolapse surgery symptoms associated with 192, 748 ICS-recommended description 780–1 ultrasonography 778 3D 367, 368–9, 369 4D 366 translabial/perineal 361, 361–2, 362, 371 upper urinary tract imaging 326, 326 urodynamic diagnosis 232 uroflowmetry 221
voiding difficulty 191, 585, 586 see also anterior vaginal wall prolapse; enterocele; rectocele; sigmoidocele; uterine prolapse; vaginal vault prolapse Pelvic Organ Prolapse Quantification System (POP-Q) 773–6, 1001–3 clinical use 463, 1001 definition of anatomic landmarks 773–4, 774, 1001 making/recording measurements 774–6, 775, 1002 normal ranges 463 ordinal staging system 776–7, 777, 1002, 1002–3 as outcome measure 462, 462–3 population studies using 1003, 1003 rectocele assessment 1038 specific site defects 463 technique of use 1001–3 vs other grading systems 1000, 1000 Pelvic Organ Prolapse/Urinary Incontinence Sexual Questionnaire (PISQ) 461 pelvic organ support 120–3, 1024, 1036, 1068–9 ‘boat in a dry dock’ analogy 123, 1068 classification 1000, 1000–1 endopelvic fascia 120, 120–1, 121 level I (suspension) 121, 1054, 1055, 1068, 1068 level II (attachment) 121, 1054, 1068, 1068 level III (fusion) 121, 1054–5, 1068, 1068 muscle/connective tissue interaction 123 pelvic diaphragm 121–2, 122 pelvic pain 748, 1164–78 acute, causes 1166 chronic see chronic pelvic pain conscious pain mapping 1175–6 laparoscopic management 1164–78 pelvic denervation procedures 1172–3 syndrome 606, 749 pelvic plexus (inferior hypogastric plexus) 142, 607, 608, 1163–4 injury 575 pelvic surgery previous pelvic organ prolapse and 1006 urinary incontinence and 45, 192 radical, voiding dysfunction after 567, 575–6 urogenital fistulae complicating 1224, 1225, 1226 urologic complications 1368–75 see also gynecologic surgery pelvic-to-pudendal reflex see guarding reflex pelvic wall 1154–6, 1155, 1156 pelvis bony 1155 obstetric fistulae 1242 pelvic floor dysfunction 343 cellular tissues 1158 greater (false) 1154–5, 1155 laparoscopic anatomy 1154–64 laparoscopic visualization 1152 lesser (true) 1155, 1155 lymphatic system 1163 masses 194 nervous system 607, 607–9, 1163–4 peritoneum, fascia, fossae and ligaments 1156–9, 1157 ureteral anatomy 1368, 1368 vascular system 1160, 1162–3
penicillin, preoperative prophylactic 831 pentosan polysulfate (PPS) 598–9 percutaneous nerve evaluation (PNE) 1123, 1278–9 acute stage 1123 subchronic stage 1123 percutaneous vaginal tape (PVT) 941–2 Pereyra (and Pereyra modified) procedure 866 outcome 814, 816 sacrospinous fixation with 1093 periaqueductal gray (PAG) 159, 160 pericardium, bovine 854, 888 perimeatal masses 1255 perimenopausal women stress incontinence 26–7 urinary incontinence 32, 33, 698, 698 see also menopause; postmenopausal women perineal body 122, 1101 measurement point 774, 774, 1001 recording measurements 775, 775 perineal descent assessment 726 excessive see descending perineum syndrome perineal membrane see urogenital diaphragm perineal pain 748 syndrome 749 perineal rectosigmoidectomy see Altemeier procedure perineal stimulation motor conduction responses 290–1 reflex responses 294 perineal trauma 682, 1100 assessment 1104–5 classification 1112, 1112 definition 1101 first degree 1101, 1112 fourth degree 1112 management 1103–6 non-suture management 1103–4 prevention 1106–7 repair continuous suturing method 1104, 1105, 1105 interrupted suturing method 1104, 1105, 1105–6 procedure 1104–6 rectocele repair with 1042–3 skin closure 1104 suture material 1104 training 1107–8 second degree 1101, 1112 structures involved 1101 third degree 1112 see also episiotomy perineometer 469 perineorrhaphy, rectocele surgery 1043–4 perineum anatomy 1100, 1100–1 congenital absence 1037 embryology 128–30 inspection 750–1 manual support, during delivery 1106 massage, pregnancy and labor 1106–7 reconstruction 1379 perioperative care anti-incontinence surgery 826–34 laparoscopic sacral colpopexy 1199 see also postoperative care peripheral nerve evaluation see percutaneous nerve evaluation
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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Index
peripheral nerve stimulation 1283, 1283–4 peripheral nervous system disease 567, 575–6 peritoneal flap grafts, fistula repair 1235, 1303 peritoneal fossae 1157–8 peritoneum endometriosis 1167–70 parietal/visceral layers 1156 pelvic 1156–8 rectal 1162 periurethral glands see paraurethral glands periurethral injection therapy 860–3 see also urethral bulking agents, injectable pernicious anemia 567 peroneal neuropathy, obstetric fistula with 1242 per protocol analysis (PPA) 431 perspiration, measurement 441, 443 pessaries 534–40, 1029 adverse effects 538–9 care programs 536 choosing 534–6 effectiveness 537 incontinence 534–5, 535 rectocele 1041 space-occupying 534, 535, 535 supportive 534, 534 use before surgery 827 pessary test post-void residual volume 238 before prolapse surgery 400, 1090, 1091 Petri, Eckhard 5 Petros & Ulmsten integral theory 881, 890–1, 918, 926 PFS see pressure–flow studies pH, vaginal 644, 646 pharmacology bladder 146, 158–71 clinical concepts 486–8 pharmacotherapy see drug treatment phenazopyridine (Pyridium) fistula detection 1228 test, urinary incontinence 209–10 phenoxybenzamine (POB) 491, 492 phentolamine 491, 492 phenylephrine 164 phenylpropanolamine (PPA) 516–17, 519 photography, pelvic organ prolapse 777–8 physical activity 409 assessment of incontinence during 656, 656–7 as cause of urinary incontinence 409, 658–9, 676, 676–7 pad tests 206, 209 see also exercise; sports/fitness activities physical examination see examination, physical physical therapy (physiotherapy) 100–12, 476–84 assessment 101–2, 103, 476–7 detrusor overactivity 107–8, 109 evaluation of effectiveness 110 evidence for effectiveness 411–17, 476 factors affecting outcome 415 interventions 103–8, 476, 477–82 men 108 mixed incontinence 108 painful bladder syndrome/interstitial cystitis 598 patient education 108–9, 476–7 pelvic organ prolapse 421 process 103 referral diagnosis 100–1, 103
stress incontinence 103–6, 106, 477–82 physiologic outcome measures, overactive bladder 432–5 physiotherapy see physical therapy pili, uropathogenic bacteria 617 pinacidil 165, 509 pirenzepine 498 placebo response, overactive bladder 439 plastic catheters 542, 543, 550 plastics, technology 837–8 pneumoperitoneum, complications 1217–18 poliomyelitis 575 pollakisuria 633, 747, 760 see also frequency polydipsia 188 polymer technology 837–8 polyomaviruses 619, 620 polypropylene mesh 836, 838, 839, 840 cystocele repair 1019 SPARC sling system 927 tension-free vaginal tape 918 transobturator midurethral slings 949, 951 polypropylene sling, distal urethral 941–2 polyps bladder 383 urethral 1339, 1340 polysynaptic inhibitors 513 polytetrafluoroethylene (PTFE) see Teflon polyuria ICS definition 750, 762 nocturnal 190, 750, 762 pontine micturition center (PMC) 160, 571 discovery 143 pharmacological targets 160, 162 sex hormone influences 700 POP see pelvic organ prolapse POP-Q see Pelvic Organ Prolapse Quantification System porcine dermis 853, 854, 885–7 porcine small intestinal submucosa (SIS) 854, 887–8 position, patient childbirth 1106 cystometry 227, 228 intraoperative, complications due to 1348–9 leak point pressure testing 268 pelvic floor ultrasound 356, 357–8 pressure-flow studies 238 SPARC sling procedure 926 videourodynamics 302, 304 see also posture positive pressure urethrography (PPUG), urethral diverticulum 335–6, 1258, 1260, 1260 postanal repair (PAR) 717 postcolposuspension syndrome 874, 875, 1353 posterior colporrhaphy 732, 1036 levatorplasty with 1036, 1046 operative technique 1044–5 results and complications 1046 vs transanal rectocele repair 1047–8 posterior intravaginal slingplasty see intravaginal slingplasty posterior urethrovesical angle (PUV) (retrovesical angle) 8 cystourethrography 329–32, 331, 334 epidemiologic study 18 obliteration during micturition 123 pelvic floor ultrasound 357, 358 posterior vaginal wall
ICS-defined points for measurement 774, 774 making/recording measurements 775, 776 posterior vaginal wall prolapse ICS definition 751 making/recording measurements 775, 776 terminology 774 see also enterocele; rectocele postmenopausal women estrogen therapy see estrogen, replacement therapy pelvic organ prolapse risk 1006 recurrent urinary tract infections 704, 704, 705 statistics 696, 696 urinary incontinence 698, 698, 699 urinary symptoms 696, 697–8, 698 urogenital atrophy 705–6 see also elderly; hormone replacement therapy; menopause postmicturition dribble 191, 217, 748 postmicturition symptoms 748 postoperative care abdominal sacrocolpopexy 1071–2 fistula repair 1235–7, 1247–8, 1301 incontinence surgery 831–3 midurethral slings 893 pubovaginal slings 883, 910–11 SPARC sling 931–2, 932 ureteric injuries 1295–7 urethral diverticulectomy 1264 urinary catheterization 588 postpartum period anal sphincter morphology 686 early voiding difficulty 585 lower urinary tract changes 683 pudendal nerve terminal motor latencies 291, 686 urinary retention 684 urodynamic values 685, 685–6 uroflowmetry 221 post-polio syndrome 575 posture preventing urinary incontinence 410 uroflowmetry and 219 see also position, patient post-void residual (volume) (PVR) 756, 767 after urethral reconstruction surgery 1264, 1271 cystourethrography 333 epidemiologic study 17–18 prolapse reduction and 238 uroflowmetry 220, 787 potassium-channel openers 165, 509 potassium channels 165 ATP-sensitive (KATP) 163, 165 large conductance calcium-activated (BKCa) 165 potassium sensitivity testing (PST) 597 pouch of Douglas (rectouterine pouch) 1157, 1157, 1162 anatomy 1024 depth, enterocele formation and 1024–5, 1025, 1027 endometriosis 1171 obliteration 1029–31 prophylactic 1028–9 surgical techniques 1030, 1030–1 Poussan urethral advancement technique 6–7 PRAFAB-score 102
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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prazosin 193, 491, 492–3 pregnancy 682–93 after obstetric fistula repair 1243 after urinary tract reconstruction 1343, 1343 after uterine prolapse repair 1080, 1082, 1085 anal sphincter morphology 686 artificial urinary sphincter deactivation 963 cervical atresia 1322 fecal incontinence after see fecal incontinence, childbirth-related irritative symptoms 397 lower urinary tract changes 683 mechanisms of pelvic floor injury 682–3 non-communicating rudimentary uterine horn 1322 pelvic organ prolapse and 1004–5 pessaries 534 prevention of pelvic floor dysfunction after 679 Turner’s syndrome 1325 urinary incontinence during/after 42–4, 684–5 etiologic mechanisms 394, 394, 685–6 risk factors 19, 24–5, 25, 28, 396–7 urinary tract infections 615, 625 urodynamic values 685, 685–6 uroflowmetry 221 see also childbirth; postpartum period premicturition pressure 755, 767 prenatal diagnosis, congenital anomalies 134–5, 137, 138 preoperative assessment 828–9 anesthetist 829 investigations 221, 246, 321–2, 828–9 preoperative considerations anti-incontinence surgery 826–31 midurethral slings 891–2 pubovaginal slings 882 preoperative management, urogenital fistulae 1230 preoperative preparation incontinence surgery 826–8 alternative therapies 826–7 psychological 827 informed consent 829–30 thromboprophylaxis 830–1 pre-ovarian fossa 1158 presacral nerve (superior hypogastric plexus) 607, 608, 1163–4 presacral neurectomy 1173 presacral space 1195, 1195 laparoscopic approach 1197, 1198 pressure at maximum flow rate 755, 767 pressure–flow studies (PFS) 152, 226, 236–49 after anti-continence surgery 245–6 ambulatory urodynamics 322 biomechanical aspects 236–7 defining bladder outflow obstruction 239– 45, 241, 242, 243, 244 equipment, minimum requirements 793–4 factors affecting 237–8 ICS definitions 755–6, 766–8, 767 ICS good practice guidelines 787–97 interpretation 239, 240 normal volunteers 243 predictive value 246 pressure measurements 755 quality control 239, 795 recording 237
retrospective artifact correction 796–7 troubleshooting 238, 795–6 urethrolysis and 246–7 videourodynamics 306, 306 pressure sores 555 pressure transducers abdominal pressure measurements ambulatory urodynamics 314, 314–15, 318 cystometry 229, 229 ICS recommendations 792–3 videourodynamics 304 calibration 226, 317, 794–5 fixation 229, 317, 318 intravesical pressure measurements (urethral) ambulatory urodynamics 314, 314–15, 318 cystometry 228–9, 229 ICS recommendations 792–3 videourodynamics 304 reference levels (heights) 227, 317, 792–3 urethral pressure measurements 252–5 balloon catheters 254, 255 catheter-tip transducer catheters 254, 254–5 perfused catheters with side holes 252, 254 zeroing to atmospheric pressure 226, 317, 792 see also urodynamic catheters pressure transmission ratio (PTR) 258–9, 754, 765 preterm labor 625 proctalgia fugax 724 proctography, defecation see defecography proctologic examination 1138 progesterone continence mechanism effects 700–1 lower urinary tract effects 696–7 receptors 696–7 voiding difficulty and 493 progestogens 520, 700–1, 703 prokinetic agents 730 prolapse, pelvic organ see pelvic organ prolapse prolapse surgery 1194 anterior vaginal wall prolapse 1013–20 bone anchors 936 enterocele 1029–31, 1058 incontinence surgery with 1015, 1092–6 indications 1092 as prophylactic measure 400 results 1019, 1094–5, 1096 selection of continence procedure 1092 vaginal vault prolapse 1199–200 laparoscopic 1194–203, 1206–10 midurethral slings with 898–9 prevention of failure 401 rectocele 1042–9 sexual function after 667–8, 1020 SPARC sling procedure with 931 synthetic mesh 836, 840–1 urinary incontinence after 1090–8 definitions 1090 diagnosis 400, 1091–2 management 1092–6, 1093 pathophysiology 1090–1 prevention 400 summary of study results 1094–5 uterine prolapse 1078–87 see also specific procedures
Prolene mesh 836, 838, 890 promotion, continence see continence promotion prompted voiding 417 pronephros 131 propantheline bromide 488, 498–9, 503 pediatric patients 1332 propiverine 488, 506–7, 637–8 propranolol 517 proprioception, bladder 148 prostaglandins (PGs) inhibitors 509–10 intravesical administration 489–90, 589 prostatectomy, incontinence after 101, 108 prostatic enlargement, benign 757 prostatic hyperplasia, benign (BPH) 493, 757 prostatic obstruction benign 757 bladder instability 149 prostatodynia 749 prosthetic materials categories 836–7, 837 see also biologic prosthetic materials; synthetic prosthetic materials Proteus (mirabilis) 619, 624 provocative maneuvers ambulatory urodynamics 319 cystometry 231, 232 cystourethrography 328–9 detrusor overactivity 432, 753 videourodynamics 304 see also cough; Valsalva maneuver pseudoephedrine 515 pseudohermaphroditism female 1340, 1341 male 1340–1 Pseudomonas aeruginosa 619, 619, 623, 624 psoas hitch 1294, 1370–1, 1371 psychogenic retention of urine 285, 286, 585 psychological factors, cosmetic vaginal surgery 1378, 1382 Psychosocial Adjustment to Illness Scale 67 puboanal muscle 122, 122 pubocervical fascia 121 pubococcygeal line 1038, 1039–40, 1040 pubococcygeus muscle 122, 1156, 1156 electromyography 280, 280 puboperineal muscle 122, 122 puborectalis muscle 122, 122, 1156, 1162 childbirth-related disruption 344–5 MRI 341, 342, 344 neurophysiologic conduction studies 293 pubourethral ligaments 123, 124, 125, 918 pubovaginal muscle 122, 122 pubovaginal slings (PVS) 880, 881–90, 908–15 allografts 846, 847–53, 885, 914 complications 850–1, 852 results 850, 851, 888 autologous 846–7, 883–5 complications 847, 849–50, 885, 886–7 current and future role 914 harvesting 846, 882 operative technique 881–2, 908–10 results 847, 848, 883–5, 884 biologic materials 846–54 bone anchors 936–8 complications 913, 1346, 1347 history 881–2 myelodysplasia 266–7 obstruction complicating timing of intervention 984 transvaginal sling incision 988–9, 989
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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pubovaginal slings (PVS) – continued operative technique 881–2, 908–10, 909–12 postoperative management 883, 910–11 pressure–flow studies 245, 246 results 882–90, 911–13, 913 synthetic materials 888–9, 914 with urethrovaginal fistula repair 1267 xenografts 846, 853, 853–4, 885–8, 914 pubovesical ligaments 124–5, 1157, 1159, 1161 pubovesical muscles 116, 124, 124–5 pubovisceral muscle 122, 341 pudendal nerve anatomy 607, 608, 1163 childbirth-related damage 683 anal incontinence and 687, 712–13 rectocele formation and 1037 urinary incontinence and 686 electrical stimulation (BION® device) 1285, 1285 reflex responses to stimulation 294 sensory function 148, 159, 180 somatic function 159, 573 somatosensory evoked potentials 293 terminal motor latencies (PNMTL) 290–1 after childbirth 686, 687, 712–13 constipation 729 fecal incontinence 291, 714 pudendal neuropathy 291 pudendal neurovascular complex 1055, 1055 surgical injury 1056, 1060 puerperium see postpartum period PVT (percutaneous vaginal tape) 941–2 pyelography intravenous see intravenous pyelography/urography retrograde, urogenital fistulae 1228 pyelonephritis 625 Pyridium see phenazopyridine Qmax see flow rate, maximum QT (QTc) interval drug-induced prolongation 508 measurement 440, 441, 442 Q-tip test 194 qualitative data 430 quality adjusted life years (QALYs) 64, 65, 439 quality assessment, ambulatory urodynamics 317–18 quality assurance, role of standards 738 quality control ambulatory urodynamics 317 cystometry 226–7, 227, 233, 795 invasive urodynamics 787–90 pressure–flow studies 239, 795 pressure signals 795 quality of life (QoL) 10, 64–74 after anti-incontinence surgery 1356–7 assessment 64, 67–73 applications 65–6, 66, 67–8 clinical measures and 66–7 ICI recommendations 69, 69, 72, 807–8 methods 65 overactive bladder 438, 438–9 pelvic organ prolapse 460–1 stress incontinence 453 definition 64, 438 dimensions 65 pad tests and 211–12 predictors of impairment 66 questionnaires 64, 65, 67–72
computerization 71 disease-specific 68–71, 69 generic 67–8 minimal important difference (MID) assessment 64, 71, 453 simple global scoring systems 71–2, 72, 453–4 urinary incontinence impact 17, 25–6, 45 vs bothersomeness 437 Quality of life in persons with urinary incontinence (I-QoL) 69 quantitative data 430 quantitative electroencephalography (qEEG) 441–2 questionnaires outcomes assessment 803–4 quality of life see quality of life (QoL), questionnaires racial differences attitudes to incontinence 674 connective tissue 677 pelvic floor MRI 345–6 pelvic organ prolapse 1005–6, 1037 urethral diverticulum 1252 urinary incontinence 14, 27 radiation fistulae 1224, 1225 prognosis 1237 surgical repair 1306 timing of surgery 1230 radiation injury, ureters 1291 radiofrequency therapy, stress urinary incontinence 976–7, 977, 978 radiologic imaging see imaging radiopaque markers, colonic transit testing 727, 728 raphe nuclei 161 Raz procedure (vaginal wall sling) 938–40 complications 817, 940 operative technique 938–9, 939 results 814, 940 receiver operator characteristics (ROC), bladder outlet obstruction 241, 241, 244 reconstructive surgery biologic prosthetic materials 846–57 complex 1290–315 fecal incontinence 1125–9 pediatric patients 1342, 1342–3 synthetic prosthetic materials 836–43 recovery, laparoscopic surgery 1152 rectal balloon catheters abdominal pressure measurements 229, 229, 793 see also pressure transducers rectal balloon expulsion test 729 rectal contractions, during cystometry 232–3, 233 rectal examination 194, 726, 751 rectal injury isolated obstetric 1112, 1113, 1116 surgical 1060 rectal intussusception 1137 rectal ligament 1158 rectal mucosal intussusception 724, 725 rectal mucosal prolapse 1137 rectal prolapse 1136–48, 1137 classification 1137–8 complete (procidentia) 1137, 1137 diagnostic tools 1138–9 genital prolapse with 1136 diagnostic evaluation 1139, 1140 pathophysiology and etiology 1136–8
surgical techniques 1145–6 history and examination 725, 726 pathophysiology and etiology 724, 1025, 1027, 1137–8 surgical techniques 732, 1139–45 abdominal 1140, 1141–4 perianal 732, 1140, 1141 rectal resection pelvic nerve injury 575–6 rectopexy with see rectopexy, resection rectoanal inhibitory reflex (RAIR) 723, 728, 728 rectocele 1036–51 3D ultrasound 369, 369, 370 after anti-incontinence surgery 832–3, 1353 anatomical basis 121, 1036 etiology 1036–7 investigations 1038–41 management 1041–2 obstructed defecation 724 physical examination 1038 surgical repair 1042–9 defect-specific 1042–4, 1043, 1044 results and complications 1046, 1046 indications 1041 laparoscopic 1209 mesh or graft augmentation 1045, 1045–6 results and complications 1048, 1048–9 rectopexy with 1145 results and complications 1046–9 selection of procedure 1042 transanal (transrectal) approach 732, 1045 results and complications 1047, 1047–8 transvaginal approach see posterior colporrhaphy symptoms 1037, 1037–8 terminology 774, 1003 ultrasonography 361, 362 rectopexy 732, 1141–4 anterior sling 1142 choice of procedure 1144–5 genital prolapse surgery with 1145–6, 1146 Ivalon sponge 1141–2 laparoscopic methods 1143, 1143–4 posterior mesh 1142, 1143 resection 732, 1142–3, 1144 laparoscopic 1143, 1143–4 suture 1141, 1142, 1143 rectosigmoidectomy, perineal see Altemeier procedure rectosigmoid junction 1162 rectouterine fold 1157 rectouterine pouch see pouch of Douglas rectovaginal fascia (septum) 121, 1024, 1036 defects, rectocele 1038, 1042, 1043 surgical repair 1042–3, 1043, 1044 endometriosis 1171, 1171 enterocele formation and 1026 laparoscopic anatomy 1157 rectovaginal fistula, obstetric 1241, 1247, 1248 rectovaginal space see pouch of Douglas rectum contrast medium, cystourethrography 328, 332 development 129, 129–30 laparoscopic anatomy 1161–2 rectus fascia slings 883
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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complications 819–20, 847 harvesting 846, 882, 908, 908 results 814, 883–5, 884 see also pubovaginal slings, autologous rectus sheath 1154, 1155 reference height, urodynamics 227, 317, 792 referred visceral pain, mechanisms 609–10 reflex incontinence 753 registered nurse (RN) 94 rehabilitation functional, fecal incontinence 1122–5 lower urinary tract 757 see also physical therapy reinnervation, muscle, electromyography 284–5 rejection, graft see graft rejection reliability 430, 460, 802–3 alternate form 802 interobserver and intraobserver 802 pad tests 207, 208, 210–11 test–retest 802 urethral pressure measurements 255, 256 voiding diary 199 Remeex system 975, 976 renal failure 192 renal function, diabetic cystopathy 576 reproductive tract, female 1159, 1159–60 development 1318, 1318, 1330, 1330, 1331 developmental abnormalities 1318–28 obstetric injury 1241–2 research outcome 740 outcome measures see outcome measures residual urine 152 clean intermittent self-catheterization 549–50 measurement 333 normal 233 see also post-void residual resiniferatoxin (RTX) 166, 488, 513–15, 638 responder analyses 431 responsiveness, test 460 restriction in participation (handicap), definition 102 retention of urine see urinary retention retrograde pyelography, urogenital fistulae 1228 retropubic colpourethropexy see colpourethropexy, retropubic retropubic space see space of Retzius retropubic suspension, uterovaginal prolapse (Nesbit) 1086 retrorectal space 1157 retrovesical angle see posterior urethrovesical (PUV) angle Retzius, space of see space of Retzius rhabdomyosarcoma, vaginal 1338–9, 1339 rhabdosphincter see external urethral sphincter Rho-kinase 163 ring pessaries 534, 535, 535–6 Roberts catheter 543, 543 Robertson, E.G. 143–4 Robertson, Jack Rodney 4, 5, 6 robotic-assisted laparoscopic surgery 1180, 1180 sacral colpopexy 1199 round ligament 1157 laparoscopic uterine suspension with 1208–9 mesentery 1158 sling operation for stress incontinence 7
Royal Dutch Foundation for Physiotherapy (KNGF) 106 rural–urban differences see urban–rural differences Sabre™ sling system 941 sacral colpohysteropexy, laparoscopic 1207, 1207–8 sacral colpopexy see sacrocolpopexy sacral dysgenesis, videourodynamics 311 sacral micturition center 145, 571 sacral nerve roots 608 sacral nerve stimulation (SNS) constipation 732–3 fecal incontinence 718, 1122–5 acute test stimulation 1123 implant placement 1123–4, 1124, 1125 results and complications 1124–5, 1125 subchronic test stimulation 1123 history 1276 lower urinary tract 1276–87 anatomic landmarks 1278, 1278 clinical results 1281–3, 1283 complications 1284–5, 1285 future directions 1285–6 indications 1282 mechanisms of action 1276, 1276, 1277 patient selection 1276–8 surgical techniques 1278–81, 1279–81 muscle-evoked potentials 291–2, 292 overactive bladder 639, 1276 painful bladder syndrome/interstitial cystitis 601 voiding difficulty/retention 589, 1276, 1282–3, 1283 sacral parasympathetic nucleus (SPN) 158, 160, 608 sacral plexus 607, 1163 sacral promontory anatomy 1195, 1195 laparoscopic appearance 1197, 1197 prosthesis fixation methods 1199 sacral reflexes 193, 294–5 sacral sympathetic trunks 1163 sacrocolpopexy (abdominal) 1068–74 anatomic considerations 1194–5 colpourethropexy with 875–6 enterocele repair with 1031 laparoscopic (LSC) 1073, 1194–203, 1206 complications 1201, 1217 concomitant anti-incontinence surgery 1199–200 contraindications 1196 patient assessment/selection 1195–6 perioperative care 1199 prosthesis types 1198–9 results 1200, 1200–1 robotic assistance 1199 surgical technique 1196–9, 1197, 1198 vs vaginal sacrospinous colpopexy 1061 patient selection and evaluation 1069, 1069–70 results and complications 1072–3, 1073 surgical principles 1201–2 surgical technique 1070–2, 1071, 1072 vs sacrospinous colpopexy 1061, 1072–3, 1194 sacrohysteropexy/sacrocervicopexy 1084, 1084–5 laparoscopic (LSH) 1200, 1201, 1207–8 sacrospinous ligament 1055, 1055
sacrospinous uterosacral fixation (sacrospinous hysteropexy) 1080–2, 1081, 1082 sacrospinous vault suspension (sacrospinous colpopexy) 1057–61 complications 1059–60 contraindications 1057 failures 1060–1 indications 1057 laparoscopic extraperitoneal 1207 Pereyra suspension and 1093 results 1059 surgical techniques 1057–9 vascular structures at risk 1056 vs abdominal sacrocolpopexy 1061, 1072–3, 1194 safety overactive bladder treatments 444 stress incontinence treatments 456 salbutamol 488 saline, cystometry filling medium 227–8 saliva production, measurement 442–3, 443 sarcoma botyroides 1338–9, 1340 saucerization technique fistula repair 1232 urethral diverticulum 1260 Scarpa’s fascia 1154 scheduled voiding regimes 417–20 schizophrenia 192 sciatic nerve 1055, 1163 surgical injury 1060 scopolamine 499 scrotal pain 748 syndrome 749 selective serotonin reuptake inhibitors (SSRIs) 161 sensation bladder see bladder sensation pelvic visceral 608–9 sensitization, visceral nociceptors 609 sensory action potential 290 sensory disorders 179, 180 sensory neurons (primary afferents) 148, 159, 573, 608 capsaicin-sensitive (CSPAs) 514–15 childbirth-related damage 687 drugs targeting 165–6, 513–15 serotonergic pathways 161, 640 serotonin (5-HT) receptors 161 sex steroid hormones continence mechanism and 700–1 lower urinary tract effects 696–7, 697 see also androgens; estrogen; progesterone sexual abuse, previous 1166 sexual differentiation, external 129–30 sexual dysfunction 665–8 after anti-incontinence surgery 667–8, 1353, 1354 after prolapse surgery 1020, 1046, 1047 after rectocele repair 732 after vaginal surgery 1380 prevalence 25–6, 26, 27, 665 treatment 667–8 urinary incontinence and 665–7, 666 see also dyspareunia sexual function 664–72 assessment 460, 461 catheterization and 546, 668 cosmetic vaginal surgery and 1379–80, 1380 epidemiologic studies 25–6 pelvic organ prolapse and 666, 780, 1028 sexual intercourse
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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sexual intercourse – continued symptoms associated with 748 urinary incontinence during see coital incontinence urinary tract infections and 618, 668–9 sexually transmitted diseases (STDs) 645 shapes test, colonic transit 727, 728 Sharp technique, sacrospinous vault suspension 1059 Sherrington, C.S. 142–3 Short Form 36 (SF36) health status questionnaire 67, 68, 72 Shy–Drager syndrome 567, 569 Sickness Impact Profile (SIP) 67–8 Sidaway v Board of Governors of Bethlem Royal Hospital [1985] 830 sigmoidocele 1039, 1136, 1136–7 after hysterectomy 725 classification 1136 sigmoidoscopy 714, 726 sigmoid segment augmentation cystoplasty 1307 signs, lower urinary tract dysfunction clinical assessment (ICS) 749–51, 762–3 definition 746 see also examination, physical silicone catheters 542, 543 silicone macroparticles (Macroplastique®) 862–3 3D ultrasound 370, 371 perineal ultrasound 363, 364 siliconized catheters 542, 543 simplified urinary outcome score (SUIOS) 911, 913 Sims, Marion 6 single photon emission computed tomography (SPECT) 336 Skene’s glands see paraurethral glands skin care urinary incontinence 555 urogenital fistulae 1230 sling procedures 880–906 3D ultrasound imaging 369–70, 370 AUA outcomes assessment 811–12, 813, 814, 819–20 biologic materials 846–54 bone anchor 936–8 externally readjustable 975, 976 failed, leak point pressures 269–71, 270, 271, 273 history 7–8 minimally invasive 9 myelodysplasia 266–7 perineal ultrasound after 363, 363 postoperative voiding problems 832 prolapse repair with 1015–16 synthetic materials 836, 840 vaginal wall 938–40, 939 variants 936–43 vs colpourethropexy 871 see also midurethral slings; pubovaginal slings; specific procedures slow stream 191, 217, 748, 761 small intestinal submucosa (SIS), porcine 854, 887–8 smoking cessation advice 87, 678, 679, 828 pelvic organ prolapse and 1005 urinary incontinence and 25, 45–6, 409, 677, 677 smooth muscle bladder see detrusor embryological development 130–1
social consequences, obstetric fistulae 1242 Society for Urodynamics and Female Urology see Urodynamic Society Society of Urologic Nurses and Associates (SUNA) 94, 96–7 socioeconomic impact 35–6 measures 456 socioeconomic status overactive bladder and 59, 61 urinary incontinence and 40, 54–6, 57, 57 sodium bicarbonate cytolytic vaginosis 651 intravesical 600 solifenacin 488, 501–2 overactive bladder 636, 637, 638 side effects 636, 637 vs tolterodine 636, 637 solitary rectal ulcer syndrome 724, 725 somatic nerves, pelvic 158, 159, 573, 608 somatosensory evoked potentials (SEPs), cerebral 293, 293–4 somatosensory perception, bladder 148, 159 sonic hedgehog (Shh) 129, 130, 130 South America, epidemiology 24–9 space of Retzius 124, 1156–7, 1161 hematomas, postoperative 1346–7, 1347 MRI 344 SPARC sling 926–33 3D ultrasound imaging 369–70 BioArc version 940, 940–1, 941 concomitant procedures 931 device design 927 mechanism of action 926 pelvic floor ultrasound after 363, 363 postoperative care 931–2, 932 postoperative extrusion 932 pressure–flow studies after 246 surgical technique 926–31, 928, 929, 930, 931 Spence technique, urethral diverticulum 1260, 1261 sphincter-cystoplasty 1310–11, 1311 sphincter electromyography 279, 279–86, 284 videourodynamics 306 sphincters see anal sphincter; urethral sphincter spina bifida see myelomeningocele spinal cord disease neurophysiologic conduction studies 292, 293 voiding dysfunction 566, 567, 570–5 spinal cord injury (SCI) 571 autonomic dysreflexia 572 bladder instability 149 cystourethrography 334–5 drug therapy 489, 492, 495, 497, 514 electromyography 284 physiologic studies 144, 145, 146 somatosensory evoked potentials 293, 293 videourodynamics 308, 310 voiding dysfunction 566, 567, 571, 572 spinal shock 571 spinal surgery, previous 192 spiroperidol 162 splitting, urine stream 217, 748, 761 sponge, intravaginal 87 sports/fitness activities 656–62 as cause of urinary incontinence 658–9, 676, 676–7 stress incontinence during assessment 656–7, 657 consequences 658
prevalence 657 prevention 659 treatment 660 spraying, urine stream 217, 748, 761 squamous cell carcinoma bladder, cystoscopic evaluation 386 urethral diverticulum 1253 squamous metaplasia, bladder 383, 384 St. Mark’s fecal incontinence scoring system 713, 713 St. Mark’s stimulator 291, 294 Stamey procedure outcome 814, 816 postoperative voiding problems 832 standardization of terminology and methods (ICS) ambulatory urodynamic monitoring 316–18 lower urinary tract dysfunction 760–70 current issues 741–2 future needs 742, 742–3 purpose 738–44 Standardisation Subcommittee report (2002) 746–58 units of measurement/symbols 768, 768, 769 pelvic organ prolapse/pelvic floor dysfunction 772–81 see also Good Urodynamics Practices guidelines standards 738–40 application and acceptance 738–9 creation and institution 739 methods, measurements and terms 739–40 normality and 740 updating and revising 739 staphylococci 619, 619, 624 Staphylococcus aureus 619, 624 Staphylococcus saprophyticus 619, 624 statistical analysis, treatment outcomes 430–1 stenting, ureteric 1293–4, 1373, 1374 steps model, patient education 109, 109 stigma, of incontinence 76–80 basis 76–7 definition 76 survey of national organizations 77–8 tackling 77–80 see also continence promotion Stoller afferent nerve stimulator (SANS) 1283, 1283–4 stoma-cystoplasty 1310, 1311, 1311 stomas, fecal incontinence 718, 1129 stop test 236 storage, urine 148–50, 486 congenital abnormalities affecting 1333, 1333–4 drugs facilitating 193, 497–520 symptoms related to 747, 760–1 see also bladder filling Storz, Karl 5 straining defecation pelvic floor changes 723, 723 rectocele formation and 1037 urinary incontinence and 410 to void 190, 217 iatrogenic obstruction 984 ICS definition 748, 761 urinary incontinence and 676 uroflowmetry 219 see also Valsalva maneuver strangury 191, 748, 761
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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Stratasis TF™ sling system 941, 941 streptococci 624 Streptococcus pneumoniae 619, 620 Stress Incontinence Surgical Treatment Efficacy Randomized (SISTER) trial 245 stress tests, provocative see provocative maneuvers stress urinary incontinence (SUI) 83–4, 100 after fistula repair 1237, 1246–7, 1248 after hysterectomy 1364 after prolapse surgery 400, 1090–6 after sacrospinous vault fixation 1060 ambulatory urodynamics 321 anterior vaginal wall prolapse with 1012, 1013 classification 307 conservative treatment see under conservative treatment cure 450, 451, 809 cystourethrography 332–3 definition 656, 747, 760 drug treatment 515–20, 977–9, 979 electromyography 280, 282, 285 estrogen therapy 518–20, 701, 701–2 etiology/pathogenesis 880–1, 890–1, 918 hammock theory 125, 125, 881, 946 hypothesis 394, 394 integral theory see midurethra theory failure of treatment 809–10 function/activity-based classification 175, 176 historical aspects 7–8 history taking 186, 189 improvement 450–1, 810 injection therapy 860–3 leak point pressures 267–71 surgical failures 269–71, 270, 271, 272–5 worst cases 268–9, 269, 270 masked 1090 diagnosis 1090, 1091 management 1092, 1093 surgical procedures 1094–5 medical correlates 19 natural history 394–5 new technologies in treatment 972–80 evolutionary 972–5 novel approaches 976–9 nursing assessment 84–5, 85 nursing management 84, 84–9 outcome measures 450, 450–8 AUA guidelines 804 economic 456 investigator observations 454–6 NIH Terminology Workshop for Researchers in Female Pelvic Floor Disorders recommendations 804, 809–10 patient observations 451–4 standards 450, 450 pelvic floor MRI 342–3, 344, 344, 345 pelvic floor ultrasound 358–9, 359, 360 pessaries and devices 534–40, 535 physical examination 194, 750–1, 762 physical therapy 103–6, 477–82 potential 1090–1 diagnosis 1090, 1091 prevention 400, 1092–3 surgical procedures 1094 vaginal vault prolapse 1200 pregnancy/childbirth-related 684–5 etiologic mechanisms 685–6
pressure–flow studies 243 prevalence Asia 53, 54, 56 Australia 42 during sports/fitness activities 657 Europe 33, 34 postmenopausal women 698, 699 South America 26–7, 27 United States 15, 15 prevention 395–400 quality of life impact 17, 66 recurrence after interventions for obstruction 987, 987, 991 urethrocystoscopy 379 sports/fitness activities see under sports/ fitness activities surgical treatment see anti-incontinence surgery type I 177, 307 videourodynamics 306, 308 type II 177 type IIa 307 videourodynamics 306–7, 308, 309 type IIb 307 videourodynamics 307, 309 type III 177–9, 307 artificial urinary sphincter 962 cystourethrography 335 leak point pressure testing 271, 271, 272 videourodynamics 307, 310 see also intrinsic sphincter deficiency ureterocele 138, 139 urethral pressure measurements 257, 257–9, 258, 258, 259 urgency/urge incontinence with see mixed urinary incontinence urodynamic diagnosis see urodynamic stress incontinence uroflowmetry 221 vaginal vault prolapse and 1057, 1069, 1199–200 videourodynamics 306–7, 307, 308–10, 310–11 stroke (cerebrovascular accident) 567, 568 strong desire to void (SDV) 230, 432, 752, 763 subsymphysial fistulae 1224 vaginal repair 1233 sugar substitutes 471 superficial circumflex iliac artery 1213 superficial epigastric artery 1213, 1215 superior fascia of levator ani 121–2, 124 superior gluteal nerve 1163 superior hypogastric plexus 607, 608, 1163–4 superior rectal artery 1162 superior vesical artery 1162 suprapubic arc sling see SPARC sling suprapubic catheterization 545, 545–6 infection rates 618 supravesical fossa 1157 surgical assessment, pelvic organ prolapse 778 surgical treatment constipation 731–3 fecal incontinence 716–18 overactive bladder 639–40 painful bladder syndrome/interstitial cystitis 601 postoperative obstruction 986–93, 987 prolapse see prolapse surgery stress urinary incontinence see antiincontinence surgery
voiding difficulty/retention 589 see also specific procedures Surgipro mesh 838 SURx transvaginal system 976–7, 977 suture materials fistula repair 1231 perineal repair 1104 repair of obstetric anal sphincter injury 1116 sweating, measurement 441, 443 Sweden population studies 32–4, 33, 34 socioeconomic costs 35–6 symbols, ICS recommendations 768, 769 sympathetic chain ganglia 159, 607, 608 sympathetic nerves early physiologic studies 142, 144 lower urinary tract 158, 159, 573 pelvis 608 urine storage reflex 159 sympathetic skin responses 295–6, 296 sympathomimetic drugs 193, 515–17 symphysis orifice distance 332, 334 symphysis pubis bladder neck distance, perineal ultrasound 357, 358 pelvic organ descent, perineal ultrasound 361, 361 reference height (urodynamics) 227, 317, 792 symptoms 746 diaries 452, 452–3 gynecologic 192 history taking 186–92 lower urinary tract see lower urinary tract symptoms pelvic organ prolapse 748 prolapse-related, ICS guidelines 780–1 scales/assessment 435–7, 451–2 ICI recommendations 805, 806 Symptom Severity Index (SSI) 69, 211 symptom syndromes, suggesting lower urinary tract dysfunction 748–9, 761–2 synthetic meshes 3D ultrasound 370, 371 absorbable 837, 837 bonded 839, 839, 840 classification 839–40, 840, 841 combined genital and rectal prolapse surgery 1145 current surgical practice 840–1 dyspareunia caused by 667–8, 841 erosion/extrusion 836, 840–1 abdominal sacrocolpopexy 1073 anti-incontinence surgery 1355, 1356 cystocele repair 1019 laparoscopic sacral colpopexy 1201 midurethral slings 897–8 rectocele repair 1049 SPARC procedure 932 transobturator approach 951–2, 958, 959 filament types 838 incontinence surgery laparoscopic colposuspension 1180–1, 1187 pubovaginal slings 889 SPARC sling 927 tension-free vaginal tape 836, 838, 840, 840, 891, 918 transobturator midurethral slings 949, 951 infections 838, 840
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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synthetic meshes – continued mechanical properties 839 non-absorbable 837–40 pore size 838, 838–9 prolapse surgery 836, 840–1 cystocele repair 1015, 1015, 1016, 1019, 1058 laparoscopic sacral colpopexy 1197–8, 1198 other laparoscopic techniques 1207–8 rectocele repair 1044, 1045–6, 1048, 1048–9 rectopexy 1142, 1143 sacrocolpopexy 1070–1, 1072 sacrohysteropexy 1084, 1084 technology 838–40 weave 839 weight 839 synthetic prosthetic materials 836–43 3D ultrasound 369–70, 370, 371 categories 836–7, 837 complications 1354–6, 1355 history of use 836 perineal ultrasound 363, 363 periurethral bulking agents 862–3 polymer technology 837–8 pubovaginal slings 888–9, 914 systematic reviews 431 tabes dorsalis 567, 573–4 Tamm–Horsfall protein 616 tampons anal 715–16 vaginal 87, 537, 537, 538 tamsulosin 488, 493 tear production, measurement 443 Teflon (PTFE) mesh 836, 838, 839 sacrohysteropexy 1084 particles, injectable 861 complications 1354, 1355 tegaserod 730 telemetry, ambulatory urodynamics 314 teleoscopy, laparoscopic colposuspension 1181 temperature, perineal, urine leakage detection 206, 315–16 tension-free vaginal tape (TVT) 9, 918–23 3D ultrasound imaging 369–70, 370 bleeding complications 921, 922, 1346–7, 1347 complications 895–8, 921, 921–2, 1356 development 918–19 elderly patients 898 obese patients 898 obstruction complicating tape loosening or cutting 988 timing of intervention 984 transvaginal tape incision 988–9, 990 operative technique 919 pelvic floor ultrasound after 363, 363 postoperative leak point pressures 270, 271, 272 postoperative pressure–flow studies 245–6 postoperative uroflowmetry 221 preoperative pressure–flow studies 246 prepubic 974, 974–5 prevention of urge incontinence after 399–400 prolapse surgery with 898–9, 1019, 1200 rationale 918 results 894–5, 919–21, 920, 921 sexual function after 668
synthetic materials 836, 838, 840, 840, 891, 918 vs colposuspension 870, 871, 894–5, 920–1, 921 vs laparoscopic colposuspension 1188 vs transobturator tape 949, 952 tension-free vaginal tape-obturator (TVT-O) 947 mesh characteristics 949, 951 operative technique 948 terazosin 488, 492, 493 terbutaline 488, 493, 496, 510 terminal dribble 217, 748, 761 terminology, standardization of see standardization of terminology and methods terodiline 440, 508 testicular feminization (androgen insensitivity) 1324, 1340–1 tethered cord syndrome 575 tetracycline 622, 624 therapeutic index 443–4, 444 thiphenamil hydrochloride 513 3DSlicer software 348, 350, 351 three-dimensional (3D) reconstruction, pelvic floor 348, 349 three swab test, fistula detection 1228, 1243, 1298, 1299 thromboembolism prophylaxis 830–1, 1236–7 risk assessment 830 thymoxamine 491 Tiemann catheter 543, 543 timed voiding 86–7, 417, 420 time to maximum flow 217, 755, 766 healthy volunteers 220 tissue engineering, vaginal reconstruction 1379 toilet aids 556, 556 ‘mapping’ 79 type 55, 61 toileting aided 556, 556 scheduled 417–20 toilet training 107 early childhood 147–8 tolerability definition 440 overactive bladder treatments 439–43 tolterodine 488, 500–1 bladder training with 419 cost-effectiveness analysis 439 evidence for effectiveness 500–1 extended release (ER) 635–6 overactive bladder 635–6, 638 placebo-controled trials 440 side effects 500, 636, 637 tolerability measures 442–3, 443 vs bladder training 419 vs solifenacin 636, 637 tomoxetine 511 TOT see transobturator midurethral slings total pelvic floor repair (TPFR) 717 traditional medical practitioners 56, 58 training 9 continence nurse specialists 94–6, 95 laparoscopic surgery 1152 perineal repair 1107–8 tramadol 161 tranexamic acid 832 transducers 3D ultrasound 365
pressure see pressure transducers transitional cell carcinoma (TCC), bladder 386, 386, 387 transobturator midurethral slings (transobturator tape; TOT) 946–54, 956–60 complications 949–53, 951, 958, 959, 1346, 1356 inside-out technique 893, 948 mechanism of action 946, 956, 956 operative technique 893, 948, 956–8, 957, 958 outside-in technique 948 pressure–flow studies after 245–6 prolapse surgery with 1019 results 895, 949, 950, 958, 958 surgical anatomy 946–8, 947 transureteroureterostomy 1371, 1372 transverse myelitis 574 transverse vaginal septum 1320 transverse vesical fold 1157 transversus abdominis muscle training 659, 659 trauma perineal see perineal trauma ureteric injuries 1291, 1292 treatment functional classification 487 ICS definitions 746, 757 outcome measures see outcome measures trichomoniasis 648, 648–9, 650 tricyclic antidepressants 488, 510–12 trigone anatomy 116–17, 117 during bladder emptying 150–1 embryological development 131–3, 134 endoscopic appearance 383 trimethoprim 622, 623, 624 pregnancy 625 trocars, laparoscopic placement sites 1213 primary 1212–14, 1214 secondary 1214–15 tropical spastic paraparesis 574 trospium chloride 488, 506–7 overactive bladder 636–7, 638 TRPV1 receptors 609 T-Sling 941 tubo-ovarian recess 1158 turbine valve, intraurethral 589 Turner’s syndrome 1325 TVT see tension-free vaginal tape UDI see Urogenital Distress Inventory ultrasonography 10 3D 10, 364–70, 365, 371 display modes 365, 365–6 practical applications 366–70 4D 365 developmental anomalies 1319 endoanal see endoanal ultrasonography enterocele 1028 intraurethral 10 introital 356 pelvic floor 356–77 pelvic organ prolapse see under pelvic organ prolapse rectocele 1041 translabial/transperineal 356, 356–63, 370–1 biofeedback 481 vs urethrocystoscopy 379 transvaginal 356
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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urethral diverticulum 362, 362, 1258, 1258 urogenital fistulae 1229 voiding difficulty/retention 588 umbilical artery 1162 umbilical peritoneal folds 1157 umbilicus 1154, 1155 uncategorized incontinence 751, 762 underactive bladder 174 classification 178–9, 180 clean intermittent self-catheterization 549 see also detrusor areflexia; detrusor underactivity underactive bladder outlet 177–9, 178 underwater test, bowel injury 1217 United Kingdom (UK), continence nurse specialists 82–90, 92–3 United States continence nurse specialist 92–8 epidemiology 14–22 units of measurements 768, 768 upper motor neuron lesions 145, 566 upper urinary tract (UUT) damage, obstetric fistulae 1242 embryological development 131–3, 132 imaging 326–8 investigations, urinary tract infections 621 urachus 129 UraTape® 948 complications 951–2 mesh characteristics 949, 951 urban–rural differences overactive bladder 59, 61 urinary incontinence 55, 57 Ureaplasma urolyticum 619, 621 ureter(s) cystoscopic evaluation 387–8 descending 1160 dilation, pregnancy 683 ectopic 136–7, 138 cystoscopic evaluation 387 duplicated 136, 1334–6, 1336, 1337 embryological basis 134 imaging 326, 327 urinary incontinence 1336–7 vaginal 136 embryological development 131, 133, 134, 135 intraligamentary 1160 laparoscopic anatomy 1160–1, 1161 lumbar 1160 orifices 116–17 cystoscopy 383, 383 pelvic anatomy 1368, 1368 polyps/fronds 383 reimplantation techniques 1370, 1370–1, 1371 retroligamentary 1160 retrovesical 1160 stenting 1293–4, 1373, 1374 stricture formation 1291 uterine artery relations 1160–1, 1161, 1293 ureterectomy, duplicated ectopic ureter 1336, 1337 ureteric buds abnormal development 136, 137 branching morphogenesis 132, 132 formation 131, 132, 133 Mackie & Stephens hypothesis 132, 134, 136 ureteric fistulae 1291, 1292 conservative management 1293 see also ureterovaginal fistulae
ureteric injuries 1290–7 colpourethropexy 872 diagnosis 1292 gynecologic surgery 1368–74 iatrogenic 1290–1 prevention 1292–3 risk factors 1290 types 1291 intraoperative recognition and repair 1292, 1293, 1368–73 lower ureter procedures 1369–71 midureter procedures 1371–2 role of urologic consultant 1369 upper ureter procedures 1372–3 laparoscopic surgery 1217, 1290 non-iatrogenic 1291 obstetric 1241 postoperative management 1293–7, 1373–4 conservative methods 1293–4, 1373–4 diagnosis 1291–2, 1373–4 open surgical repair 1294–5, 1294–6 postoperative care/follow-up 1295–7, 1374 timing of surgery 1293 ureterocele 138–9 cystoscopic evaluation 387–8 ectopic 1256 prolapsed 1255, 1256, 1338, 1338 ureteroneocystostomy, ureteric injuries 1294 ureteroscopy, ureteric injuries 1291, 1293 ureterosigmoidoscopy 1310, 1312 ureteroureterostomy 1294, 1294, 1369, 1369–70 ureterovaginal fistulae conservative treatment 1298 diagnosis 1298, 1299 endoscopic ‘flat tire’ test 382 iatrogenic 1292 imaging 327 Uretex® TO 948, 949, 951 urethra 3D ultrasound 366 absent, fistula surgery 1233, 1246, 1246–7 anatomy 116, 117–19 biomechanics 237 caruncle 1255, 1256 compression, in prolapse 1090 connective tissue 118–19 duplication, endoscopic evaluation 383, 383, 388, 388 electrical conductance, urinary loss 206, 316, 317 embryological development 129, 129–31, 131 endoscopic evaluation 382, 382–4, 388 fibrosed drainpipe 188 glands see paraurethral glands hypersensitive female 584–5 innervation 158, 158–9 kinking, in prolapse 1090 knee angle 946 laparoscopic anatomy 1161 malignant neoplasms 1256 masses, differential diagnosis 1255, 1256 MRI anatomy 344, 345 mucosa 118 mucosal prolapse 1255, 1256 pain 191 polyps 1339, 1340 position 123–5, 124 pregnancy-related changes 683, 685 proximal
funneling, pelvic floor ultrasound 359, 359 open, cystourethrography 334–5 pseudopolyps 383 reflex responses to stimulation 294 sensory nerves 159 smooth muscle 118, 119 somatosensory evoked potentials 293–4 stress relaxation 257, 258 submucosal vasculature 118, 124 supporting tissues 123–5, 124 surgical injuries 1348 unstable 754, 765 urethra-cystoplasty 1310–11 urethral bulking agents, injectable 860–3 3D ultrasound 370, 371 complications 1354–5, 1355 history of use 7 materials available 861 materials in development 861–3 new materials 972–4 optimal attributes 860–1 perineal ultrasound 363, 364 recurrent stress incontinence 991 urethral catheterization 542–5 complications 544–5 indwelling 1309 intermittent self- see intermittent self-catheterization urinary tract infections 544, 618 urethral catheters 88, 542–5 care 545 clean intermittent self-catheterization 550 design 543, 543 drainage bags 546–7, 547, 548 effects on flow rates 237 infection-inhibiting 544 leakage, bypassing and blockage 544–5 materials 542, 543 nursing management 88–9 pressure measurements see under pressure transducers selection 543–4 size and length 543–4, 544 urinary loss measurement 316 urodynamics 228, 229, 793 valves 548, 548 urethral closure mechanism incompetent 754, 765 normal 754, 765 urethral closure pressure (UCP) filling cystometry 231 low see intrinsic sphincter deficiency maximum (MUCP) 255, 255–6, 754, 765 colpourethropexy success and 867, 868 drugs increasing 515, 516, 517 intrinsic sphincter deficiency 257, 257 MRI-detected puborectalis disruption and 345 normative and comparative data 256 reliability 256 measurement 252, 253 as outcome measure 455 pregnancy/postpartum 685 profile 754, 765 urethral crest 382, 382–3 urethral dilation 589 postoperative obstruction 986 urethral diverticulectomy 1260–6 postoperative care 1264 preoperative preparation 1260 results and complications 1264–6, 1265
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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urethral diverticulectomy – continued surgical technique 1261, 1261–4, 1262, 1263, 1264 urethral diverticulum (UD) 1252–66, 1271 associated complications 1252–3 carcinoma 1253, 1253 classification 1254, 1257 diagnosis 596, 1254–60 differential diagnosis 1254, 1255, 1256 etiology and pathophysiology 119, 1252 history 1252 incidence/patient profile 1252 presentation 1253, 1253–4, 1254 radiologic imaging 335, 335–6, 336, 1255–60 recurrent 1265, 1266 stones 1252 treatment 1258–66 endoscopic 1258 history 1258 observation 1258 results and complications 1264–6, 1265 vaginal flap technique 1258–64 ultrasonography 362, 362, 1258, 1258 urethral pressure measurements 260 urethroscopic diagnosis 378, 384, 384, 1254–5, 1257 urethral erosions artificial urinary sphincter 968 midurethral slings 897–8 synthetic grafts 1356 urethral fistulae see urethrovaginal fistulae urethral function abnormal 768 bladder emptying 150–1 continence and 266–7 during filling cystometry 231, 754–5, 765–6 during voiding 756, 768 endoscopic evaluation 379, 382 normal 756, 768 quantitative measures 455 sex hormones and 701 urethral hypermobility 754, 765 colpourethropexy 867–8, 868 midurethral slings and 891 radiofrequency thermal therapy 976–7 surgical options 866–7 urethral inclination 334 urethral injection therapy 860–3 see also urethral bulking agents, injectable urethral mobility 123–5, 124 leak point pressure test 269, 270, 271, 273–4 Q-tip test 194 see also urethral hypermobility urethral occlusive devices 536–7, 537, 538 urethral pain 748 syndrome 749, 761 urethral pressure cross-sectional area (CA) relationship 256–7, 257 definition 252 fluctuations 754, 765 functional profile length 754 ICS definition 754, 765 maximum (MUP) 255, 256, 754, 765 drugs increasing 515 transmission ratio (PTR) 258–9, 754, 765 urethral pressure measurements 252–63 ambulatory urodynamics 260, 317 circumstances/types 252
clinical measurements and parameters 255–60 continuous recording 252, 252 during coughing/pelvic floor contraction 257–9 dynamic, in resting urethra 257, 258 ICS recommendations 754–5, 765 new catheter-free methods 260 reliability 255, 256 research tool 260 static, in resting urethra 255–7, 257 techniques 252–5 urethral pressure profile (UPP) 252, 253 abdominal leak point pressure and 268 cough 258 detrusor leak point pressure and 267 functional length 754, 765 ICS definition 754, 765, 765 stress 252, 253, 257–9 urethral pressure profilometry (UPP) 252, 253 epidemiologic study 18 ICS definitions of terms 255, 754, 765, 765 reliability 255 urethral prolapse after anti-incontinence surgery 1353 mucosal 1255, 1256 pediatric patients 1338, 1339 urethral reflectometry 260 urethral relaxation incontinence 259, 754, 765 urethral resistance 237 bladder outlet obstruction 241 drugs decreasing 491–7 measurement 266, 267 as outcome measure 455 urethral retroresistance pressure (URP) 260 urethral sphincter congenital abnormalities 1334–6 congenital abnormalities bypassing 1336–7 continence mechanism 880 electromyography kinesiologic 279–81 needle (‘motor unit’) 281, 282 stress urinary incontinence 285 urinary retention/obstructed voiding 285–6 videourodynamics 306 hypertrophy 586 mechanism of continence 119, 147 neurophysiologic conduction studies 292, 292, 293 obstruction, non-relaxing 756, 768 see also external urethral sphincter; intrinsic urethral sphincter urethral strictures/stenosis after urethral diverticulectomy 1265, 1266 treatment 589 urethral pressure measurements 260 urethrocystography see cystourethrography urethro-cystoplasty 1311 urethrocystoscopy see endoscopy, urinary tract urethrography, positive pressure (PPUG), urethral diverticulum 335–6, 1258, 1260, 1260 urethrolysis 989–93, 1352 after SPARC sling 932 failed 993 predictors of success 985, 986–7 pressure–flow studies and 246–7 results 986–7, 987 retropubic 992, 992–3
timing aspects 984 transvaginal 989–92, 991 urethropelvic angle (UP) 332, 334 urethropelvic ligaments, MRI 343, 344 urethropexy see colpourethropexy urethroscopes 380–1, 381 history 5 urethroscopy dynamic 381–2 urethral diverticulum 378, 384, 384, 1254–5, 1257 see also endoscopy, urinary tract urethrovaginal fistulae (UVF) 1266–71 after urethral diverticulectomy 1265, 1266 complications of surgery 1270–1 diagnosis 1266 presentation 1228, 1266 results of surgery 1270 secondary to urethral diverticulum 1252 surgical repair 1266–70, 1267–9, 1270, 1301 urethrovaginal sphincter 117, 118, 118 urethrovesical angle anterior 331, 334 posterior see posterior urethrovesical angle urethrovesical junction (UVJ) 1161 endoscopic evaluation 379, 382, 383 poor support, surgical options 866–7 see also bladder neck urge 633 suppression strategies 470 Urge Impact Scale 438 Urge Incontinence Impact Questionnaire (Urge – IIQ) 69, 438 urgency classification 175 continence nurse specialist 86 definition 747, 760 de novo, after anti-incontinence surgery 982 detrusor overactivity and 144, 149 filling cystometry 230, 752, 764 history taking 189, 190 motor 752, 764 overactive bladder syndrome 633 pathophysiology 143, 144, 148–9 patient-centred measurement 435–6 prevention 396 sensory 752, 764 drug treatment 513–15 see also bladder sensation, increased symptom syndromes 749 urodynamic definition 432 urgency–frequency syndrome 632, 749 sacral nerve stimulation 1282, 1283 see also overactive bladder Urgency Perception Scale (UPS) 435–6, 436 urge syndrome 632, 749 see also overactive bladder Urge – UDI 69 urge urinary incontinence (UUI) 84, 100, 632 behavioral training 470, 470 classification 175, 176 conservative treatment 415, 418 continence nurse’s role 86 definition 747, 760 de novo, after anti-incontinence surgery 982 midurethral slings 896, 897 prevention 399–400 pubovaginal slings 886–7, 889, 913 tension-free vaginal tape 921, 922
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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transvaginal bone-anchor slings 938 drug treatment 504, 507, 510 history taking 189 medical correlates 19 motor and sensory 741 overactive bladder syndrome 633 pathophysiology 143, 149 physical therapy 479 postmenopausal women 698, 699, 702 pregnancy 397 prevalence Asia 53, 54, 59 Europe 33, 34 United States 15, 15 prevention 396 sacral nerve stimulation 1282, 1283 stress incontinence with see mixed urinary incontinence Urilos monitor 8, 206 ambulatory urodynamics 315, 315 urinals, female 557, 557–8 urinalysis, preoperative 829 urinary continence DeLancey hammock theory 125, 125, 881, 946 effects of aging 699–700 extrinsic 119, 147 intrinsic 119, 147 mechanism 147, 880–1, 881, 1161 menopause and 699–701 midurethra theory see midurethra theory sex hormones and 700–1 urethral supports 123–5, 125 urinary diversion 1309–11 continent 1309, 1310–11, 1311, 1312 pediatric patients 1342, 1342 free-draining 1309 interstitial cystitis 601 irreparable obstetric fistula 1248 options available 1309–10 overactive bladder 640 pregnancy after 1343 sexual function after 668 terminology 1309, 1310–11 voiding difficulty/retention 589 urinary incontinence (UI) after fistula repair 1237, 1248 after prolapse surgery 400, 1090–6 after urethral diverticulectomy 1265, 1265–6 aids and appliances 555, 555–8 behavioral therapies see behavioral therapies catheterization see catheterization, urinary causes 24–5, 25, 42–4, 189 conservative treatment 407–20, 422, 826–7 continuous 188, 747, 761, 1227 coping strategies 20 definition 14, 24, 32, 632, 747, 760 current issues 741 devices see devices, incontinence duration, quality of life impairment and 66 economic burden 20, 35–6, 49, 82 ectopic ureter 136–7 endoscopic evaluation 378–9 extraurethral 751, 762 fistula related 1227–8 functional 175 help-seeking see help-seeking, urinary incontinence history of management 6–8 history taking 188–90
incidence 14–15, 16 medical correlates 19, 25 natural history 394–5 nocturnal see nocturnal enuresis overactive bladder 436, 437 pediatric patients see under pediatric patients physical examination 193–4, 750–1, 762 physical therapy see physical therapy prevalence 24, 82 Asia 53, 54, 56 Australia 40, 49, 49–50 Europe 32, 32–5, 33, 34 institutional settings 48, 48–9, 82 men vs women 33, 34, 40, 40 nulliparous women 674–5 postmenopausal women 698, 698, 699 by severity 16, 40, 41, 47, 47–8, 48 by type 15, 15, 24, 33, 34, 41, 53, 54 United States 14, 14 prevention 395–401, 678–9, 702–3 quality of life impact 17, 25–6, 45 radiologic imaging 330–1, 332–3, 336 remission 14–15 risk factors 395–7 Asia 54–6, 55 Australia 44, 44–6, 45 Europe 34–5, 35 nulliparous women 675–7 South America 24–5, 25 United States 19 severe intermittent 188 severity assessment 189 epidemiologic studies 16, 16, 47, 47–8 help-seeking and 56 pad test-based staging 206, 207, 433, 433 pad test correlations 211 quality of life impairment and 66 situational 747, 761 stigma see stigma, of incontinence surgery see anti-incontinence surgery treatment experience 41–2 uncategorized 751, 762 ureterocele 138 urethral diverticulum 1252 videourodynamics 306–7, 307 see also specific types Urinary Incontinence Quality of Life Instrument 438 Urinary Incontinence Severity Score, pad tests and 211 urinary retention 584–91 acute 756, 768 causes 584–6, 585 cerebrovascular accident 568 chronic 756, 768 drug treatment 489–90, 496–7, 589 electromyography 285–6, 588 investigations 587–8 non-neurogenic see voiding difficulty, non-neurogenic peripheral nerve injury 575–6 postoperative 832 anti-incontinence surgery 983, 1350–2, 1351 hysterectomy 1364–5 see also voiding difficulty, after antiincontinence surgery postpartum 684 pregnancy 684 presenting symptoms 586–7
prolapse reduction and 238 prophylactic treatment 588 psychogenic 285, 286, 585 sacral nerve stimulation 589, 1276, 1277, 1282–3, 1283 signs 587 spinal cord injury 571 treatment 588–9 see also obstruction, bladder outflow; voiding difficulty urinary symptoms see lower urinary tract symptoms urinary tract anatomy 1160–1, 1161 embryology 128–33 see also lower urinary tract; upper urinary tract urinary tract infections (UTI) 614–30 after ambulatory urodynamics 319–20 after augmentation cystoplasty 1308 AIDS 574 catheter-associated 544, 615, 618, 626–7 causative organisms 619 clinical symptoms 619 complicated 615, 615, 625–7 congenital anomalies 137, 139 definitions 614–15 history taking 192 hospital- vs community-acquired 619, 619 host defenses 616 interstitial cystitis and 595 intraurethral devices and 538–9 investigations 619–21, 620, 621 nulliparous women 675 nursing advice 87 pathogenesis 615–17 postcoital 618, 668–9 postoperative colpourethropexy 873, 873 tension-free vaginal tape 921, 921 prevalence 614 prophylaxis 621, 625 recurrent 615 after anti-incontinence surgery 1351, 1352, 1354 estrogen deficiency and 704, 704, 705 investigations 621 risk factors 615 treatment/prophylaxis 623–5 urethral diverticulum 1252 urinary incontinence risk 24, 25, 42, 44, 45, 45 relapse 615 risk factors 617, 617–18 treatment 621–5 urinary tract injuries anti-incontinence surgery 1347–8, 1348 gynecologic surgery 1368–75 see also bladder injuries; ureteric injuries urine 24-hour production 750, 762 extravasation, ureteric injuries 1292 residual see residual urine storage see storage, urine urine dermatitis, fistula-associated 1242, 1243 urine flow continuous 218, 218, 755, 766 curves see uroflow curves detrusor pressure relations 236–7 ICS definitions 755, 766 intermittent 218, 218, 755, 766, 766 measurement see uroflowmetry rate see flow rate
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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Index
urine flow – continued symptoms related to 217, 747–8 time see flow time see also urine stream urine loss (leakage) color Doppler ultrasound 359, 360 pad tests 206–12, 433, 433 paper towel test 212 pelvic floor ultrasound 359 quantification methods 206 ambulatory urodynamics 315–16, 317 voiding diary 199 see also leak point pressures urine stream hesitancy see hesitancy intermittent 217, 748, 761 slow 191, 217, 748, 761 splitting or spraying 217, 748, 761 see also urine flow urine volume nocturnal 190, 750, 762 post-void residual see post-void residual voided see voided volume urocolpos 1335, 1336 urodynamic catheters ambulatory urodynamics 314, 314–15, 318 cystometry 229, 229 effects on flow rates 237 ICS recommendations 793 urethral pressure measurements 252–5 videourodynamics 304 urodynamic observations ICS definition 746, 763 ICS recommendations 751–6, 763–8 urodynamics (UDS) 142 ambulatory see ambulatory urodynamics bladder cycle components measured 148–52 computer software 797 conventional 751, 763 cystometry see cystometry development 145 early studies 145–6 epidemiologic study 17–19 flow measurements see uroflowmetry iatrogenic obstruction 984–5 ICS good practice guidelines see Good Urodynamics Practices guidelines inconclusive 320–1 indications 226 leak point pressures see leak point pressures limitations of standard 314 outcomes assessment ICI recommendations 806–7 overactive bladder 432, 432–3 stress incontinence 454–5 painful bladder syndrome 596–7 poor correlation with symptoms 321 pregnancy/postpartum 685, 685–6 pressure-flow studies see pressure–flow studies prolapse surgery candidates 1091 repetition 797 units of measurements and symbols 768, 768, 769 urethral diverticulum 1255–6, 1257 urethral pressure measurements see urethral pressure measurements video- see videourodynamics voiding difficulty/retention 587–8 vs endoscopy 378 vs pad tests 207, 208–9, 211
Urodynamic Society (UDS), outcomes assessment standards 450, 804–5, 810–21 urodynamic stress incontinence (USI) classification 176, 177–9 diagnosis/definition 231, 232, 754, 765 pad tests 208 treatment outcome evaluation 454–5 urethrocystoscopy 383, 384 see also stress urinary incontinence uroflow curves 152, 218, 218 definitions 755, 766, 766 normal patterns 218, 784–5 smoothing recommendations 219–20, 786–7 uroflowmeters 216–17 accuracy 216–17, 785–6 calibration 794 electronic dip-stick 216 gravimetric 216 rotating disk 216 technical problems 219, 786 videourodynamics 303, 304 uroflowmetry 216–23, 237 in clinical practice 221 data from healthy volunteers 220 epidemiologic study 17 history 8, 216 ICS good practice guidelines 216, 218, 784–7 ICS terminology 755, 766, 766 parameters 217, 217–18 pressure–flow studies 790–2 problems 218–19, 786 recommendations 219–20, 786–7, 788–91 videourodynamics 304–5 voiding difficulty/retention 220, 221, 587 see also pressure–flow studies urogenital atrophy, postmenopausal 705–6 urogenital diaphragm (perineal membrane) 123, 1100, 1100 MRI 344 Urogenital Distress Inventory (UDI) 69, 437, 805 urogenital hiatus of levator ani (genital hiatus) 122 3D imaging 366, 367, 368 making/recording measurements 775, 775 measurement point 774, 774, 1001 pathophysiology of prolapse 1056 surgical repair, rectocele 1043 urogenital sinus 130, 131, 1318 persistent 133–4, 136, 1335, 1336 urogenital triangle 1100 urography, intravenous see intravenous pyelography/urography urogynecologist, definition 10 urogynecology, history 4–12 uropharmacology 9 urorectal septum 129, 129, 130 urothelium bacterial adherence 617 embryological development 130–1 host defenses 616 mechanoafferent signaling 165 Uryx® solution 861, 973, 973 uterine anomalies 1320–2 American Fertility Society classification 1320, 1321 diagnosis 1319, 1319 uterine artery 1160, 1162 relations to ureter 1160–1, 1161, 1293
uterine horn, non-communicating rudimentary 1322, 1322 uterine nerve ablation, laparoscopic (LUNA) endometriosis 1170 pelvic pain 1172, 1172–3 uterine prolapse 1078–88 after anti-incontinence surgery 1353 anatomical basis 121 and enterocele, surgical repair 1031 history 1078 hysterectomy 1078, 1078–9 with laparoscopic sacrocolpopexy 1196 vaginal apex fixation see vaginal apex, fixation perineal ultrasound 361, 361 treatment options 1078, 1078 uterus-preserving procedures 1078, 1078–87 abdominal 1084–6 combined vaginal/abdominal 1086 indications 1078–9 laparoscopic 1086, 1207–9 vaginal 1079–84 uterosacral ligaments 120, 1158–9 uterosacral ligament-vault suspension, laparoscopic 1206, 1206–7 uterosacral suspension/plication enterocele 1030, 1030, 1031 uterine prolapse 1080 laparoscopic 1183, 1184, 1208, 1208 uterovaginal anastomosis 1322 uterus anatomy 1159, 1159, 1160 bicornuate 1321 development 130, 1318, 1318 didelphic 1322 septate 1321 support by pelvic floor 123 unicornuate 1321–2 UTI see urinary tract infections vacuum delivery see ventouse/vacuum delivery vagina abdominal pressure measurements 793 anatomy 1159, 1159, 1160 congenital absence 1323, 1341, 1342 congenital anomalies 134–5, 137, 1320 cosmetic surgery 1378–81 ecosystem 644 embryological development 130, 131, 1318, 1318 laxity 1381, 1381–2 malignant neoplasms 1256 masses, pediatric patients 1337–9 normal flora 644, 644 effects of estrogen 704 pelvic supports/attachments 121, 121, 1054–5, 1055, 1068, 1068 connective tissue/muscle interaction 123, 1068 posthysterectomy 121, 1194 see also pelvic organ support rhabdomyosarcoma 1338–9, 1339 tissue engineering 1379 vaginal apex anatomic supports 121, 1054–5, 1055 fixation abdominal approach 1068–75, 1194 laparoscopic techniques 1194–203, 1206–7 rectopexy with 1145, 1146 vaginal approach 1054–66
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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vaginal vs abdominal routes 1061, 1072–3, 1194 measurement point 773–4, 774 prolapse ICS definition 751 see also vaginal vault prolapse vaginal artery/vein 1160, 1162 vaginal atresia 130, 134–5, 137 vaginal axis enterocele formation and 1025–6 rectocele formation and 1036–7 vaginal cones/balls 480, 480 continence nurse specialist 86, 86 evidence for effectiveness 412, 413, 416 physical therapist 105, 105–6 vaginal delivery 682 after anti-incontinence surgery 867 mechanisms of pelvic floor injury 682–3 pelvic floor muscle EMG changes 285 pelvic organ prolapse and 1004–5 pudendal nerve terminal motor latency after 291 urinary incontinence risk 19, 24, 25, 54, 55, 396–7 see also childbirth vaginal dilators 1323, 1323 vaginal discharge 644 vaginal erosion artificial urinary sphincter 968 midurethral slings 897 pessaries 536, 538 synthetic grafts 1356 synthetic mesh slings 840–1 transobturator midurethral slings 951–2 vaginal examination 194, 751 vaginal fistulae, urinary 1297–306 see also ureterovaginal fistulae; urethrovaginal fistulae; vesicovaginal fistulae vaginal length, total measurement 774, 774, 1001 recording measurements 775, 775 vaginal pain 748 syndrome 749 vaginal profile (Baden–Walker) 462, 462, 1000, 1000–1 vaginal prolapse history taking 192 leak point pressure testing 271, 271, 274–5 see also anterior vaginal wall prolapse; enterocele; posterior vaginal wall prolapse; rectocele; sigmoidocele vaginal septum longitudinal 1320 transverse 1320 vaginal speculum, notched 1058, 1058 vaginal vault fistulae 1224 abdominal repair 1234 vaginal repair 1232–6, 1233–4 vaginal vault prolapse 399 after anti-incontinence surgery 1353 anatomy 1194–5 cystourethrography 328–9, 333 and enterocele, surgical repair 1031, 1058 etiology and pathophysiology 1056, 1068–9 making/recording measurements 775, 775 prevalence 1194 prevention 399 and rectocele, surgical repair 1045–6 stress incontinence with 1057, 1069, 1199–200
surgical repair abdominal approach 1068–74, 1194 laparoscopic sacral colpopexy 1194–203 other laparoscopic techniques 1206, 1206–7 recurrent stress incontinence after 400 vaginal approach 1054–66 vaginal vs abdominal routes 1061, 1072–3, 1194 symptoms, presentation and evaluation 1056–7, 1069, 1069–70 vaginal voiding 1332, 1332 vaginal wall anterior see anterior vaginal wall cyst 1255, 1256 flap, urethrovaginal fistula repair 1269, 1270 posterior see posterior vaginal wall slings see Raz procedure vaginitis 644–53 atrophic 649–50, 651 causes 645, 647–52 chronic 652 desquamative inflammatory (DIV) 652 epidemiology 644 history and examination 645, 645–6 investigations 646, 646–7 vaginoplasty androgen insensitivity syndrome 1324 esthetic 1379 obstetric fistula repair with 1247 vaginal agenesis 1323, 1323, 1342 vaginosis bacterial see bacterial vaginosis cytolytic 651 lactobacillus 651 validity 430, 460, 803 concurrent 803 concurrent criterion 803 construct 803 content 803 external 430 internal 430 pad tests 207, 208, 210–11 predictive criterion 803 voiding diaries 199, 434–5 Valsalva leak point pressure see abdominal leak point pressure Valsalva maneuver 190 3D/4D ultrasound 365, 367, 367 bladder emptying 151 pelvic floor MRI 348 transperineal/translabial ultrasound 357, 358, 358, 359, 359, 360 urethrocystoscopy 383 videourodynamics 304 see also straining van Geelen, Hans 6 vanilloid agents 513–15 vanilloid receptors 165–6 vascular injuries, laparoscopic surgery 1212, 1213–15 management 1215, 1216 prevention 1212–15, 1215 vasculature anterior abdominal wall 1213, 1214–15 pelvic 1160, 1162–3 urethral submucosal 118, 124 vasopressin analogs 488, 520–1 VATER syndrome 134 VBN micturition model 243 Vecchietti procedure, laparoscopic 1323, 1323
ventouse/vacuum delivery fecal incontinence and 398, 688 perineal trauma and 1106 urinary incontinence and 397 verapamil 507–8 vesical ligament 1158 vesical neck see bladder neck vesical/urethral sensory threshold 752, 764 Vesica™ procedure 936 vesicoanal reflexes 294 vesicobulbovesical micturition reflex 160 vesicocervical fistulae presentation 1227–8 vaginal repair procedures 1232–3 vesicospinovesical micturition reflex 160 vesicospinovesical storage reflex 159 vesicoureteral reflux children 626 cystoscopic evaluation 387 infection risk 618 videourodynamics 307, 309, 310, 311 vesicourethral reflexes 294 vesicouterine fistula, presentation 1227–8 vesicouterine ligaments 1159 vesicouterine pouch 1157, 1157 vesicovaginal fistulae 1297 abdominal repair 1301–6 complex 1301, 1302–3, 1306 conservative treatment 1298 diagnosis 382, 1297–8 endoscopic assessment 385, 386, 1229 etiology 1240 history of treatment 6 imaging 1228–9 interposition grafting 1303–6, 1304–5 obstetric 1240, 1241, 1241 surgical repair 1245, 1245 see also obstetric fistulae vaginal repair 1231–3, 1300, 1300–1 dissection and repair in layers 1231–3, 1232–6, 1300–1 postoperative care 1301 vestibular bulb 1100, 1100 videourodynamics (v-UDS) 302–12, 329 development 8 equipment 302, 302–4, 303, 304 fluoroscopy 303–4, 328, 329, 329 future developments 311–12 indications 306–10 obstruction 241, 244, 306, 306, 309–10, 985 pitfalls 310–11 technique 304 tests performed 304–6 voiding difficulty/retention 588, 588 vs pad tests 207, 208–9, 211 vs ultrasound 356–7, 357 vs urethrocystoscopy 379 viral infections, lower urinary tract 619 virilization, female genitalia 1324, 1324 visceral injuries anti-incontinence surgery 1348, 1348 see also bowel injuries; rectal injury visceral nociceptors 609 visceral pain pelvic, neurobiology 607, 607–9 referred, mechanisms 609–10 vs somatic pain 609–10 visual accommodation, antimuscarinic effects 441, 442 visual analog scale (VAS) 803 bothersomeness 437 dry mouth 442–3, 443 frequency 436
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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voided volume 755, 766 ambulatory urodynamics 320 maximum 750, 763 uroflowmetry 217, 217 healthy volunteers 220 recording 220, 787 voiding diary values 201, 202 voiding ambulatory urodynamics 318 center, brainstem see pontine micturition center dysfunctional 756, 768 infrequent 587 interval between 436, 436 neural control 160, 571 obstructed see obstruction, bladder outflow phase, bladder cycle 148, 150–2 physiology see micturition, clinical physiology pressure–flow studies see pressure–flow studies prompted 417 reflexes 160 scheduled 417–20 see also bladder training symptoms related to 747–8, 761 timed 86–7, 417, 420 vaginal 1332, 1332 videourodynamics 304 see also bladder emptying voiding cystometry 226, 231 voiding cystourethrography (VCUG) see cystourethrography, voiding voiding diary (bladder diary) 198–203 duration 199–200 electronic 200, 435 ICI recommendations 806 ICS definition 750, 762 instructions 198–9 intelligent character recognition 200, 200 normative values 201, 201, 202 overactive bladder evaluation 433–5, 434, 436 painful bladder syndrome 596 paper 101, 198, 198, 200 physiotherapy assessment 476 stress incontinence evaluation 452, 452–3 therapeutic use 471 validity and reliability 199, 434–5 voiding difficulty/retention 587 voiding difficulty after anti-incontinence surgery 245–6, 832, 982–95
allograft slings 852, 889 autologous slings 847, 849–50, 885, 886–7 colpourethropexy 872–3, 873, 874, 875 combined with prolapse surgery 899 diagnostic evaluation 983–6 etiology 982–3 identifying risks 983 incidence 982 management 986–93 midurethral slings 895–7, 896 persistent 1350–2, 1351 presentation 983 SPARC sling 931–2 tension-free vaginal tape 921, 921, 952 transient 1350, 1351 transobturator tape 952, 952, 958, 959, 959 after hysterectomy 1364–5 after prolapse surgery 1020 after sacrospinous vault fixation 1060 children 1331–2 drug treatment 488–97, 589 non-neurogenic 584–91 causes 584–6, 585 investigations 587–8 presenting symptoms 586–7 signs 587 postpartum 585 pregnancy 684 prophylactic treatment 588 psychogenic 585 sacral nerve stimulation 589, 1276, 1277 symptoms 190–1 treatment 588–9 uroflowmetry 220, 221, 587 see also urinary retention voiding dysfunction classification 174–81 expanded to include pelvic floor activity 177–80, 178–9 by function/activity 174–6, 175, 176 by symptoms 174 complex, videourodynamics 310, 311 drug treatment 486–532 infection risk 618 neurogenic see neurogenic voiding dysfunction voiding time 217, 755, 766 healthy volunteers 220, 220 vulval pain 748 syndrome 749 vulvar lipoplasty 1379
vulvodynia 749 vulvovaginal candidiasis 647–8, 648, 649 vulvovaginitis allergic 649, 651 voiding difficulty 584 ‘warning time’ effects of darifenacin 501–2 measurement 433–4 water, cystometry filling medium 227–8 water births 1107 Watson, B.P. 7 Watts factor 236 websites, national continence organizations 78 weight loss 408–9, 471–2 nulliparous women 678 preoperative 828 prevention of incontinence 396 whiff test 646 whistle-tipped catheter 543, 543 willingness-to-pay assessment 65, 68, 439 wolffian ducts 131, 132, 133, 134 müllerian duct interactions 130, 131 Women’s Health Australia 40, 42, 44–6 Women’s Health Initiative 20, 395, 461, 520, 703 work heavy lifting 409, 421, 1005 measures of overactive bladder impact 439 pelvic organ prolapse and 1005 World Health Organization (WHO) definition of health 24, 438 definition of quality of life 438 episiotomy recommendation 1103 Wound, Ostomy and Continence Nurses Society (WOCN) 94, 96 wound infections anti-incontinence surgery 1349, 1349 colpourethropexy 873, 873 laparoscopic surgery 1214 prophylaxis 831 tension-free vaginal tape 921 transvaginal bone-anchor slings 938 xenografts, for slings 846, 853, 853–4, 885–8, 914 X-rays, lumbosacral spine 336 yolk sac 128, 128 zero pressure 226, 317, 792 Zuidex™ system 862, 973, 973–4
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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Volume 2
Textbook of Female Urology and Urogynecology Second edition Editors-in-Chief Linda Cardozo md frcog Professor of Urogynecology, King’s College Hospital, London, UK
David Staskin md Head, Section of Female Urology, New York Presbyterian Hospital, Cornell Associate Professor of Urology, Weill-Cornell Medical College, New York, NY, USA
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© 2001, 2006 Informa Healthcare, an imprint of Informa UK Ltd First edition published in the United Kingdom in 2001 by Isis Medical Media Ltd. Second edition published by Informa Healthcare, an imprint of Informa UK Ltd, 2 Park Square, Milton Park, Abingdon, Oxon OX14 4RN Tel: +44 (0)20 7017 6000 Fax: +44 (0)20 7017 6699 Email:
[email protected] Website: www.tandf.co.uk/medicine All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior permission of the publisher or in accordance with the provisions of the Copyright, Designs and Patents Act 1988 or under the terms of any licence permitting limited copying issued by the Copyright Licensing Agency, 90 Tottenham Court Road, London W1P 0LP. Although every effort has been made to ensure that all owners of copyright material have been acknowledged in this publication, we would be glad to acknowledge in subsequent reprints or editions any omissions brought to our attention. Although every effort has been made to ensure that drug doses and other information are presented accurately in this publication, the ultimate responsibility rests with the prescribing physician. Neither the publishers nor the authors can be held responsible for errors or for any consequences arising from the use of information contained herein. For detailed prescribing information or instructions on the use of any product or procedure discussed herein, please consult the prescribing information or instructional material issued by the manufacturer. A CIP record for this book is available from the British Library. Library of Congress Cataloging-in-Publication Data Data available on application ISBN10: 1-84184-358-X ISBN13: 978-1-84184-358-2 Distributed in North and South America by Taylor & Francis 6000 Broken Sound Parkway, NW, (Suite 300) Boca Raton, FL 33487, USA Within Continental USA Tel: 800 272 7737; Fax: 800 374 3401 Outside Continental USA Tel: 561 994 0555; Fax: 561 361 6018 Email:
[email protected] Distributed in the rest of the world by Thomson Publishing Services Cheriton House North Way Andover, Hampshire SP10 5BE, UK Tel: +44 (0)1264 332424 Email:
[email protected] Composition by Phoenix Photosetting UK Printed and bound in Singapore by Kyodo Printing Co (S’pore) Pte Ltd Chapter title image courtesy of Geoffrey W Cundiff md facog Cover image courtesy of Science Photo Library (photographer: Cristina Pedrazzini)
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Contents List of Contributors Foreword Preface
x xix xx
VOLUME 1
Volume 1, Section 1 – 1 History of urogynecology and female urology Background Jane A Schulz, Jack R Robertson, Harold P Drutz Section Editor: 2a Epidemiology: USA cornelius J Kelleher Brandon S Rubens, William D Tissot, Ananias C Diokno 2b Epidemiology: South America Paulo Palma, Miriam Dambros 2c Epidemiology: Europe Ian Milsom 2d Epidemiology: Australia Richard J Millard 2e Epidemiology: Asia Peter H C Lim, Marie Carmela Lapitan 3 Quality of life and urinary incontinence Cornelius J Kelleher, Stephen Radley 4 Tackling the stigma of incontinence – promoting continence worldwide David Fonda, Diane K Newman 5a The roles of the continence nurse specialist Ellie Stewart 5b The roles of the continence nurse specialist – global perspective Diane K Newman 6 The role of the pelvic physical therapist Bary Berghmans
Volume 1, Section 2 – 7 Basic Science: Structure and Function of 8 Lower Urinary and Ano- Rectal Tracts in women 9 Section Editor: Jacek L Mostwin 10 11
Anatomy John O L DeLancey Embryology of the female urogenital system with clinical applications Jenny Lassmann, Stephen A Zderic Clinical physiology of micturition Jacek L Mostwin Pharmacology of the bladder Karl-Erik Andersson Classification of voiding dysfunction in the female patient David Staskin, Alan J Wein
Volume 1, Section 3 – 12 Diagnostic Evaluation, Incontinence and Prolapse 13 Section Editor: Sender Herschorn 14 15 16
History and examination Vikram Khullar, Lesley K Carr Voiding diary Matthew Parsons Pad tests Marie-Andrée Harvey Uroflowmetry Jean-Jacques J M Wyndaele Cystometry Hashim Hashim, Paul Abrams
3 13 23 31 39 51 63 75 81 91 99 115 127 141 157 173 185 197 205 215 225
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17 18 19 20 21 22 23 24 25 26 27
Pressure–flow plot in the evaluation of female incontinence and postoperative obstruction Philippe Zimmern, Jason P Gilleran Urethral pressure measurements Gunnar Lose Leak point pressures Edward J McGuire Electromyography David B Vodušek, Clare J Fowler Clinical neurophysiologic conduction studies David B Vodušek, Clare J Fowler Videourodynamics Sender Herschorn, Jerome Green, Dudley Robinson Ambulatory urodynamics Stefano Salvatore, Vikram Khullar, Linda Cardozo Radiologic imaging Andrea Tubaro, Antonio Carbone, Alberto Trucchi Magnetic resonance imaging (MRI) and the female pelvic floor Lennox Hoyte Pelvic floor ultrasound Hans P Dietz Endoscopy Geoffrey W Cundiff, Gary E Lemack
Volume 1, Section 4 – 28 Natural history and prevention of incontinence and prolapse Non-Surgical treatment Robert M Freeman of Incontinence, Prolapse 29 Outcomes of conservative treatment and related conditions Don Wilson Section Editor: Eric S Rovner 30a Outcome measures in women with lower urinary tract symptoms: overactive bladder Catherine E DuBeau, Eboo Versi 30b Outcome measures in women with lower urinary tract symptoms: stress incontinence Richard C Bump, Ilker Yalcin 30c Outcome measures in women with lower urinary tract symptoms: pelvic organ prolapse Peggy A Norton 31 Behavioral therapies and management of urinary incontinence in women Kathryn L Burgio 32 Physiotherapy for urinary incontinence Jeanette Haslam 33 Drug treatment of voiding dysfunction in women Alan J Wein, M Louis Moy 34 Pessaries and devices for non-surgical treatment of pelvic organ prolapse and stress incontinence Ingrid E Nygaard 35 Catheters; pads and pants; appliances Kate Anders, Su Foxley
235 251 265 277 289 301 313 325 339 355 377 393 407
429
449
459
467 475 485
533 541
vi
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Contents
Volume 1, Section 5 – Associated Disorders Section Editor: Philip Toozs-Hobson
Volume 1, Section 6 – Appendices
36 37 38 39 40 41 42 43 44 45 46 47 48 49
Neurologic disorders Ricardo R Gonzalez, Renuka Tyagi, Alexis E Te Non-neurogenic voiding difficulty and retention Amitabha Majumdar, Philip Toozs-Hobson Painful bladder syndrome Deborah R Erickson The neuropathology of chronic pelvic pain Ursula Wesselmann Lower urinary tract infections – simple and complex James Gray, Dudley Robinson The overactive bladder syndrome Philip Toozs-Hobson, Matthew Parsons Vaginitis Brian G Wise, Gopalan Vijaya Sports and fitness activities Kari Bø Problems associated with sexual activity Andrew Hextall, Nicholas Christofi Nulliparous women Katharine H Robb, Philip Toozs-Hobson Pregnancy and childbirth and the effect on the pelvic floor Charlotte Chaliha Menopause Andrew Hextall, Dudley Robinson Anal incontinence Michael Walker, Simon Radley Constipation Jason Goh, Iqbal Khan
50 The purpose of standardization of terminology and methods in patients with lower urinary tract dysfunction Anders Mattiasson 51a The standardization of terminology of lower urinary tract function: Report from the Standardization Subcommittee of the International Continence Society (ICS) Paul Abrams, Linda Cardozo, Magnus Fall, Derek Griffiths, Peter Rosier, Ulf Ulmsten, Philip van Kerrebroeck, Arne Victor, Alan J Wein 51b The standardization of terminology of lower urinary tract function recommended by the ICS 2002 Samih Al-Hayek, Paul Abrams 52 The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction Richard C Bump, Anders Mattiasson, Kari Bø, Linda P Brubaker, John O L DeLancey, Peter Klarskov, Bob L Shull, Anthony R B Smith 53 Good urodynamic practices: uroflowmetry, filling cystometry, and pressure-flow studies Werner Schaefer, Paul Abrams, Limin Liao, Anders Mattiasson, Francesco Pesce, Anders Spangberg, Arthur M Sterling, Norman R Zinner, Philip van Kerrebroeck Index
565 583 593 605 613 631 643 655 663 673 681 695 711 721
737
745
759
771
783
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VOLUME 2 Volume 2, Section 7 – 54 The assessment of outcomes used for incontinence interventions Surgery for Urinary in women Incontinence Emily E Cole, Harriette M Scarpero, Roger R Dmochowski Section Editor: 55 Peri- and postoperative care Roger R Dmochowski Maria Vella, John Bidmead 56 Synthetic materials for pelvic reconstructive surgery Mark Slack 57 Biologic materials for reconstructive surgery Harriette M Scarpero, Emily E Cole, Roger R Dmochowski 58 Urethral injections for incontinence Rodney A Appell 59 Abdominal and transvaginal colpourethropexies for stress urinary incontinence Michelle Y Morrill, Karl M Luber 60 An overview of pubovaginal slings: evolution of technology Emily E Cole, Harriette M Scarpero, Roger R Dmochowski 61 Pubovaginal fascial sling for the treatment of all types of stress urinary incontinence: surgical technique and long-term outcome Jerry G Blaivas, David Chaikin 62 Tension-free vaginal tape procedure for treatment of female urinary stress incontinence Carl Gustaf Nilsson 63 SPARC – midurethral sling suspension system David Staskin, Renuka Tyagi 64 Other sling variants Kristie A Blanchard, J Christian Winters 65a Transobturator midurethral sling technique for stress urinary incontinence Jonathan S Starkman, Harriette M Scarpero, Roger R Dmochowski 65b Transobturator approach Calin Ciofu, Francois Haab 66 The artifical urinary sphincter for treatment of stress urinary incontinence in women Emily E Cole, Harriette M Scarpero, Roger R Dmochowski 67 New technologies for stress urinary incontinence Jay-James R Miller, Peter K Sand 68 Diagnosis and treatment of obstruction following incontinence surgery – urethrolysis and other techniques Chad Huckabay, Victor W Nitti Volume 2, Section 8 – 69 Surgery for Urogenital Prolapse 70 Section Editor: Bernhard Schuessler 71 72 73 74
Classification and epidemiology of pelvic organ prolapse Steven Swift Anterior vaginal wall prolapse Mark D Walters Enterocele Kaven Baessler, Bernhard Schuessler Rectocele – anatomic and functional repair William A Silva, Mickey M Karram Vaginal approach to fixation of the vaginal apex May Alarab, Harold P Drutz Abdominal approach to fixation of the vaginal apex Wesley Hilger, Jeffrey Cornella
801 825 835 845 859
865 879
907
917 925 935
945 955
961 971
981 999 1009 1023 1035 1053 1067
viii
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Volume 2, Section 9 – Laparoscopy Section Editor: Anthony R B Smith
Volume 2, Section 10 – Complex problems Section Editor: Rodney A Appell
75 76 77 78 79 80
Preservation of the prolapsed uterus Vasiliki Varela, Adam Magos Urinary incontinence following prolapse surgery Brigitte Fatton, Bernard Jacquetin, Rufus Cartwright Episiotomy and perineal repair Ranee Thakar, Christine Kettle Primary repair of obstetric anal sphincter injury Abdul H Sultan Surgery for fecal incontinence Klaus E Matzel, Manuel Besendörfer Combined genital and rectal prolapse Vanessa Banz, Jürg Metzger, Bernhard Schuessler
81 82 83 84 85 86 87
The role of laparoscopic surgery Anthony R B Smith Pelvic anatomy through the laparoscope Edmund Edi-Osagie Laparoscopic treatment of pelvic pain Christopher Sutton, Richard Dover Laparoscopic colposuspension and paravaginal repair Rohna Kearney, Alfred Cutner Laparoscopic sacrocolpopexy Marcus P Carey Other laparoscopic support procedures Peta Higgs Prevention, recognition, and treatment of complications in laparoscopic pelvic floor surgery Christopher Maher
88 89 90 91 92 93 94 95 96 97 98
Urogenital fistulae – surgical Paul Hilton Urogenital fistulae – obstetric Andrew Browning Urethral diverticulum and fistula Kenneth C Hsiao, Kathleen C Kobashi Electrical stimulation of the lower urinary tract Firouz Daneshgari Complex reconstructive surgery Christopher R Chapple, Richard T Turner-Warwick Gynecologic developmental abnormalities Melissa C Davies, Sarah M Creighton Pediatric urogynecology Andrew J Kirsch, Howard M Snyder Complications of surgery for stress incontinence Walter Artibani, Maria Angela Cerruto, Giacomo Novara The effect of hysterectomy (simple and radical) on the lower urinary tract Heinz Koelbl Recognition and management of urologic complications of gynecologic surgery Kevin R Loughlin Cosmetic vaginal surgery James Balmforth, Linda Cardozo
Index
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1077 1089 1099 1111 1121 1135 1151 1153 1165 1179 1193 1205
1211 1223 1239 1251 1275 1289 1317 1329 1345
1363
1367 1377 I-1
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Contributors Paul Abrams md frcs Professor of Urology, Bristol Urological Institute, Southmead Hospital, Bristol, UK May Alarab mb chb mrcog mrcpi Department of Obstetrics and Gynecology, University of Toronto, Toronto, ON, Canada Samih Al-Hayek md lmssa lrcp(lond) lrcs(eng) mrcs Bristol Urological Institute, Southmead Hospital, Bristol, UK Kate Anders rgn bsc Nurse Specialist in Urogynaecology, Surrey, UK Karl-Erik Andersson md phd Department of Clinical and Experimental Pharmacology, Lund University Hospital, Lund, Sweden Rodney A Appell md frcs Professor of Urology and Chief, Division of Voiding Dysfunction and Female Urology, Baylor College of Medicine, F. Brantley Scott Chair in Urology St. Luke’s Episcopal Hospital, Houston, TX, USA Walter Artibani md Professor of Urology, Chief of Urology Department, University of Padova Via Giustiniani, Padova, Italy Kaven Baessler md Department of Obstetrics and Gynecology, Cantonal Hospital, Lucerne, Switzerland James Balmforth mrcog Department of Urogynaecology, Kings College Hospital, Denmark Hill, London, UK Vanessa Banz md Department of Surgery, Cantonal Hospital, Lucerne, Switzerland Bary Berghmans phd msc rpt Health Scientist, Epidemiologist, AZM University Hospital Maastricht, The Netherlands Manuel Besendörfer md Chirurgische Klinik mit Poliklinik der Universität Erlangen, Germany John Bidmead mb bs mrcog Research Fellow, Department of Urogynaecology, King’s College Hospital, London, UK Kristie A Blanchard md Department of Urology, Ochsner Clinic Foundation, New Orleans, LA, USA Jerry G Blaivas md Clinical Professor of Urology, Cornell Medical Center, UroCenter of New York, New York, NY, USA Kari Bø phd Professor, Norwegian University of Sport and Physical Education, Oslo, Norway Andrew Browning mb bs mrcog Gynecologist, Addis Ababa Fistula Hospital, Ethiopia, Addis Ababa, Ethiopia Linda P Brubaker md facog facs Professor and Director, Section of Urogynecology and Reconstructive Plastic Surgery, Loyola University Medical Center, Maywood, IL, USA Richard C Bump md Eli Lilly and Company Corporate Center, Indianapolis, ID, USA
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Contributors
Kathryn L Burgio phd Department of Veterans Affairs Medical Center, Birmingham/Atlanta Geriatric Research, Education and Clinical Center, Birmingham, AL, USA Antonio Carbone Associate Professor of Urology, Department of Urology, I.C.O.T. Hospital, Rome, Italy Linda Cardozo md frcog Professor of Urogynaecology, Department of Urogynaecology, King’s College Hospital, London, UK Marcus P Carey mb bs franzcog Director of Urogynaecology, Royal Women’s Hospital, Melbourne, Australia Lesley K Carr md frcs Division of Urology, Sunnybrook and Women’s College Health Science Centre, Toronto, ON, Canada Rufus Cartwright ma mb bs Department of Urogynaecology, King’s College Hospital, London, UK Maria Angela Cerruto md Assistant Professor, Department of Urology, University of Verona, Verona, Italy David Chaikin md Clinical Assistant Professor, Department of Urology, Cornell Medical Center, New York, NY; Associate Attending Urologist, Morristown Memorial Hospital, Morristown, NJ, USA Charlotte Chaliha ma mb bchir mrcog Sub-specialist trainee in Urogynaecology, St Mary’s Hospital, London, UK Christopher R Chapple bsc md frcs Urology Department, Royal Hallamshire Hospital, Sheffield, UK Nicholas Christofi mb bs Fellow in Urogynaecology, St Albans City Hospital, West Hertfordshire Hospitals NHS Trust, St Albans, UK Calin Ciofu md Urology Department, Tenon Hospital, Paris, France Emily E Cole md Fellow, Department of Urology, Vanderbilt University Medical Center, Nashville, TN, USA Jeffrey Cornella md Chair, Pelvic Reconstructive Surgery, Associate Professor, Mayo Medical School Mayo Clinic Scottsdale, Department of Gynecology, Scottsdale, AZ, USA Sarah M Creighton md frcog Consultant Gynaecologist, Elizabeth Garrett Anderson Hospital, University College Hospitals, London, UK Geoffrey W Cundiff md Professor, Department of Gynecology and Obstetrics, Johns Hopkins School of Medicine, Baltimore, MD, USA Alfred Cutner md mrcog Consultant Gynaecologist, University College London Hospitals NHS Foundation Trust, London, UK Miriam Dambros md phd Urogynaecology Research, Division of Urology, State University of Campinas, UNICAMP, São Paulo, Brazil Firouz Daneshgari md Glickman Urological Institute, The Cleveland Clinic Foundation, Cleveland, OH, USA
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Textbook of Female Urology and Urogynecology
Melissa C Davies mrcs Clinical Research Fellow, Academic Department of Obstetrics & Gynaecology, University College London, London, UK John O L DeLancey md Normal F Miller Professor of Gynecology, Director, Pelvic Floor Research Group Director, Fellowship in Female Pelvic Medicine and Reconstructive Surgery, Ann Arbor, MI, USA Hans P Dietz Associate Professor in Obstetrics and Gynaecology, Western Clinical School, University of Sydney, Penrith, NSW, Australia Ananias C Diokno md facs Department of Urology, William Beaumont Hospital, Royal Oak, MI, USA Roger R Dmochowski md facs Professor, Department of Urology, Vanderbilt University Medical Center, Nashville, TN, USA Richard Dover mb bs Consultant Obstetrician and Gynaecologist, Royal North Shore Hospital, Sydney, Australia Harold P Drutz md Professor and Head Division of Urogynecology, Department of Obstetrics and Gynecology, University of Toronto, Toronto, ON, Canada Catherine E DuBeau Section of Geriatrics, University of Chicago, Chicago, IL, USA Edmond Edi-Osagie md mrcog Consultant Gynaecologist, St. Mary’s Hospital, Manchester, UK Deborah R Erickson md Professor of Surgery, Division of Urology, University of Kentucky College of Medicine, Lexington, KY, USA Magnus Fall md phd Professor of Urology, Senior Consultant, Department of Urology, Sahgrenska University Hospital, Göteborgs, Sweden Brigitte Fatton Gynaecologic Surgeon, Maternité de l’Hotel-Dieu, Centre Hospitalier Universitaire, France David Fonda mb bs bmed sci fracp fafrm Associate Professor of Medicine, Monash University, Consultant Geriatrician, Cabrini Medical Centre, Malvern, VIC, Australia Clare J Fowler mb bs msc frcp Department of Uro-Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London, UK Su Foxley rgn dip ns Nurse Consultant Incontinence, King’s College Hospital, London, UK Robert M Freeman md frcog Consultant, Urogynaecology Unit, Directorate of Obstetrics and Gynaecology, Derriford Hospital, Plymouth, UK Jason P Gilleran md Assistant Professor, Division of Urology, 4980 University Hospital Clinics, Columbus, OH, USA Jason Goh md GI Unit, University Hospital Birmingham, UK Ricardo R Gonzalez md Instructor in Urology, Weill Cornell Medical College, New York, NY, USA xii
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Contributors
James Gray mrcpath Department of Microbiology, Birmingham Women’s Hospital, Birmingham, UK, Department of Urogynaecology, King’s College Hospital, London, UK Jerome Green md frcsc Fellow in Urodynamics, Sunnybrook and Women’s College Health Sciences Centre, Toronto, ON, Canada Derek Griffiths md Geriatric Continence Unit, Montefiore Hospital, Pittsburgh, PA, USA Francois Haab md Urology Department, Tenon Hospital, Paris, France Marie-Andrée Harvey md sc(epi) frcsc faclog Assistant Professor of Obstetrics, Gynaecology and Urology, Queen’s University, Kingston, ON, Canada Hashim Hashim mb bs mrcs Urology Research Registrar, Bristol Urological Institute, Southmead Hospital, Bristol, UK Jeanette Haslam MPhil Grad Dip Phys mcsp Senior Visiting Fellow, University of East London, Honorary Visiting Lecturer, University of Bradford, Bradford, UK Sender Herschorn bsc mdcm frcsc Division of Urology, Sunnybrook and Women’s College Health Sciences Centre, Toronto, ON, Canada Andrew Hextall md mrcog Consultant Urogynaecologist, West Hertfordshire Hospitals NHS Trust, St Albans, UK Peta Higgs mb bs franzcog Urogynaecology Department, Royal Women’s Hospital, Melbourne, Australia Wesley Hilger md Fellow, Female Pelvic Medicine and Reconstructive Surgery, Mayo Clinic Scottsdale Department of Gynecology, Scottsdale, AZ, USA Paul Hilton md frcog Consultant Gynaecologist, Royal Victoria Infirmary, Newcastle upon Tyne, Senior Lecturer in Urogynaecology, University of Newcastle upon Tyne, UK Lennox Hoyte md mseecs facog Assistant Professor of Obstetrics/Gynecology and Radiology, Harvard Medical School, Director of Clinical Research in the Division of Urogynecology, Dept of Obstetrics/Gynecology, Senior Clinical Research Scientist, Surgical Planning Laboratory, Dept of Radiology, Brigham and Womens Hospital, Boston, MA, USA Kenneth C Hsiao md Fellow, Female Urology, The Continence Center at Virginia Mason Medical Center, Seattle, WA, USA Chad Huckabay md Fellow, Department of Urology, New York University School of Medicine, New York, NY, USA Bernard Jacquetin md Head, Department of OBGYN, Maternité de l’Hotel-Dieu, Centre Hospitalier Universitaire, France Mickey M Karram md Division of Urogynecology and Pelvic Reconstructive Surgery, Department of Obstetrics and Gynecology, Good Samaritan Hospital, Cincinnati, OH, USA
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Textbook of Female Urology and Urogynecology
Rohna Kearney mrcog mrcpi Subspecialty Trainee Urogynaecology, University College London Hospitals NHS Foundation Trust, London, UK Cornelius J Kelleher md mrcog Consultant Physician, Department of Obstetrics and Gynaecology, Guy’s and St Thomas’s Hospital Trust, London, UK Christine Kettle srn scm dip mid phd Professor of Women’s Health, Academic Unit of Obstetrics & Gynaecology, University Hospital of North Staffordshire & Staffordshire University, UK Iqbal Khan phd GI Unit, University Hospital Birmingham, UK Vikram Khullar bsc mrcog Department of Reproductive Science and Medicine, Division of Paediatrics, Obstetrics and Gynaecology, Mint Wing, St Mary’s Campus, Imperial College London, South Kensington Campus, London, UK Andrew J Kirsch md faap facs Clinical Professor of Urology, Emory University School of Medicine, Director Pediatric Urology Fellowship, Georgia Urology, Private Practice Peter Klarskov md phd Department of Neurology, Glostrup Hospital, Glostrup, Denmark Kathleen C Kobashi md Co-Director, The Continence Center at Virginia Mason Medical Center, Seattle, WA, USA Heinz Koelbl md Department of Obstetrics and Gynecology, Johannes-Gutenberg University, Mainz, Germany Jenny Lassmann md Fellow in Pediatric Urology, The Children’s Hospital Philadelphia, Philadelphia, PA, USA Marie Carmela Lapitan md Asia Pacific Continence Advisory Board, Gleneagles Hospital Singapore, Philippine General Hospital, Manila, Philippines Gary E Lemack md Associate Professor and Residency Program Director Holder of the Rose, Mary Haggar Professorship in Urology, University of Texas Southwestern Medical Center, Dallas, TX, USA Limin Liao md Professor of Urology, Chairman of Department of Urology, China Rehabilitation Research Center, Beijing, China Peter H C Lim am mb bs mmed durol fams(urol) miurol (hon) Senior Consultant Urological Surgeon, Andrology, Urology and Continence Centre, Gleneagles Hospital, Singapore Gunnar Lose md dmsc Chief Gynecologist, Department of Gynecology, Glostrup Hospital, Glostrup, Denmark Kevin R Loughlin md Division of Urology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA Karl M Luber md Department of Obstetrics and Gynecology, Division of Female Pelvic Medicine and Reconstructive Surgery, Southern California Permanenete Medical Group, San Diego, CA, USA Adam Magos bsc md frcog Consultant Gynaecologist, Minimally Invasive Therapy Unit and Endoscopy Training Centre, University Department of Obstetrics and Gynaecology, Royal Free Hospital, London, UK xiv
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Contributors
Christopher Maher franzcog Royal Women’s and Mater Urogynaecology, Brisbane, Queensland, Australia Amitabha Majumdar mb bs Research Fellow, Department of Urogynaecology, Birmingham Women’s Hospital, Birmingham, UK Anders Mattiasson md Department of Urology, University Hospital, Lund, Sweden Klaus E Matzel md Chirurgische Klinik mit Poliklinik der Universität Erlangen, Erlangen, Germany Edward J McGuire md Professor of Urology, The University of Michigan, Ann Arbor, MI, USA Jürg Metzger md Head of Department Visceral Surgery, Cantonal Hospital of Lucerne, Switzerland Richard J Millard mb bs frcs fracs Associate Professor and Head, Department of Urology, Prince of Wales Hospital, Randwick, Sydney, NSW, Australia Jay-James R Miller md Evanston Continence Center, Feinberg School of Medicine, Northwestern University Evanston, IL, USA Ian Milsom md phd Professor of Obstetrics and Gynecology, Department of Obstetrics and Gynecology, Sahlgrenska Academy at Göteborg University and Consultant Gynecologist at Sahlgrenska University Hospital, Göteborg, Sweden Michelle Y Morrill md Senior Fellow, Female Pelvic Medicine and Reconstructive Surgery, University of California, San Diego, USA Assistant Professor, Division of Urology, University of Pennsylvania Health System, PA, USA Jacek L Mostwin md dphil Professor of Urology, James Buchanan Brady Urological Institute, Johns Hopkins Medical Institutions, Baltimore, MD, USA M Louis Moy md Attending Surgeon, Division of Urology, Hospital of the University of Pennsylvania, PA, USA Diane K Newman rnc msn crnp faan Co-Director, Penn Center for Continence and Pelvic Health, Division of Urology, University of Pennsylvania Medical Center, Philadelphia, PA, USA Carl Gustaf Nilsson md phd Department of Obstetrics and Gynecology, Helsinki University Central Hospital, Finland Victor W Nitti md Associate Professor and Vice Chairman, Department of Urology, New York University School of Medicine, New York, NY, USA Peggy A Norton md Professor of Obstetrics and Gynecology, Chief of Urogynecology and Reconstructive Pelvic Surgery, University of Utah School of Medicine, UT, USA Giacomo Novara md University of Padova, Padova, Italy Ingrid E Nygaard md Professor, University of Iowa, Department of Obstetrics and Gynecology, Iowa City, IA, USA xv
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Textbook of Female Urology and Urogynecology
Paulo Palma md phd Head, Division of Urogynaecology, Department of Urology, State University of Campinas, UNICAMP, São Paulo, Brazil Matthew Parsons mrcog Urogynaecology Fellow, King’s College Hospital, London, UK Francesco Pesce md Specialist in Urology and Neurology, University of Verona, Italy Simon Radley md frcs Consultant Surgeon, University Hospital Birmingham, Edgbaston, Birmingham, UK Stephen Radley mb bs frcs ed mrcog Senior Registrar in Obstetrics and Gynaecology and Research Fellow in Urogynaecology, Royal Hallamshire Hospital, Urology Research, Sheffield, UK Katharine H Robb mrcog Research Fellow in Urogynaecology, Birmingham Women’s Hospital, Birmingham, UK Jack R Robertson md Urogynecologist and Professor Emeritus, University of Nevada Medical School, Reno, NV, USA Dudley Robinson mrcog Department of Microbiology, Birmingham Women’s Hospital, Birmingham UK, Department of Urogynaecology, King’s College Hospital, London. UK Peter Rosier md Department of Urology, UMC Utrecht, Heidelberglaan, Utrecht, The Netherlands Eric S Rovner md Assistant Professor of Urology, Division of Urology, Department of Surgery, Hospital of the University of Pennsylvania, PA, USA Brandon S Rubens md House Officer in Urology, William Beaumont Hospital, Royal Oak, MI, USA Stefano Salvatore md Divisione di Ginecologia Chirurgica, Ospedale Bassini, Università di Milano, Milan, Italy Peter K Sand md Evanston Continence Center, Feinberg School of Medicine, Northwestern University Evanston, IL, USA Harriette M Scarpero md Assistant Professor, Department of Urology, Vanderbilt University Medical Center, Nashville, TN, USA Werner Schaefer di Associate Professor of Medicine, Director, Continence Research Unit, University of Pittsburgh, Montfiore Hospital, Pittsburgh, PA, USA Bernhard Schuessler md Department of Obstetrics and Gynecology, Cantonal Hospital, Lucerne, Switzerland Jane A Schulz md Urogynecologist and Associate Professor, Department of Obstetrics and Gynecology, University of Alberta, Edmonton, Canada Bob L Shull md Vice-Chairman, Scott & White Women’s Health Center, Temple, TX, USA William A Silva md Division of Urogynecology and Pelvic Reconstructive Surgery, Department of Obstetrics and Gynecology, Good Samaritan Hospital, Cincinnati, OH, USA
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Contributors
Mark Slack mmed mrcog Simms Black Professor of Gynaecology , Head of Urogynaecology, Addenbrooke’s Hospital, Cambridge, UK; Lead Clinician, Department of Urogynaecology, Addenbrooke’s Hospital University of Cambridge NHS Foundation Trust, Cambridge, UK Anthony R B Smith mb chb frcog md Consultant Gynaecologist, St Mary’s Hospital for Women & Children, Manchester, UK Howard M Snyder md Division of Pediatric Urology, Children’s Hospital of Philadelphia, PA, USA, Clinical Professor of Urology, Emory University School of Medicine, Director Pediatric Urology Fellowship Georgia Urology, Private Practice Anders Spangberg md phd Urologist, Consultant, Department of Urology, University Hospital, Linkoping, Sweden Jonathan S Starkman md Department of Urologic Surgery, Vanderbilt University Medical Center, Nashville, TN, USA David Staskin md Head, Section of Female Urology, New York Presbyterian Hospital, Cornell Associate Professor of Urology, Weill-Cornell Medical College, New York, NY, USA Ellie Stewart rgn dip ns Clinical Nurse Specialist Urogynaecology, Guys and St Thomas NHS Trust, London, UK Abdul H Sultan mb chb md frcog Mayday University Hospital, Croydon, Surrey, UK Christopher Sutton md Professor of Gynaecological Surgery, University of Surrey, Honorary and Emeritus Consultant, Royal Surrey County Hospital, Guildford, Emeritus Consultant, Chelsea and Westminster Hospital, London, UK Steven Swift md Department of Obstetrics and Gynecology, Medical University of South Carolina, Charleston, SC, USA Alexis E Te md Associate Professor of Urology, Weill Cornell Medical College, New York, NY, USA Ranee Thakar md mrcog Academic Unit of Obstetrics and Gynaecology, University Hospital of North Staffordshire and Staffordshire University, UK William D Tissot md House Officer in Urology. William Beaumont Hospital, Royal Oak, MI, USA Philip Toozs-Hobson mb bs mrcog Consultant Urogynaecologist, Birmingham Women’s Hospital, Birmingham, UK Alberto Trucchi md febu Assistant Professor of Urology, Department of Urology, Sant’Andrea Hospital, Rome, Italy Andrea Tubaro md febu Associate Professor of Urology, Department of Urology, Sant’Andrea Hospital, Rome, Italy Richard T Turner-Warwick md Emeritus Surgeon, The Middlesex Hospital, London, UK Renuka Tyagi md Associate Professor of Urology, Weill Cornell Medical College, New York, NY, USA Ulf Ulmsten† Philip van Kerrebroeck md phd fellow ebu Professor of Urology, University Hospital Maastricht, The Netherlands xvii
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Textbook of Female Urology and Urogynecology
Vasiliki Varela md Visiting Clinical Fellow, Minimally Invasive Therapy Unit & Endoscopy Training Centre, University Department of Obstetrics and Gynaecology, Royal Free Hospital, London, UK Maria Vella mrcog Clinical Research Fellow, Department of Urogynaecology, King’s College Hospital, Denmark Hill, London Eboo Versi md phd Department of Obstetrics and Gynecology, United Medical and Dental School, New Brunswick, NJ, USA Arne Victor md Medical Product Agency, Uppsala, Sweden Gopalan Vijaya mrcog Specialist Registrar, Department of Obstetrics and Gynaecology, Medway Maritime Hospital, Kent, UK David B Vodusˇek md Medical Director, Division of Neurology, University Medical Center, Ljubljana, Slovenia Michael Walker bsc mb chb mrcs Specialist Registrar in General Surgery, Department of Surgery, University of Birmingham, Birmingham, UK Mark D Walters md Head, Section of General Gynecology, Urogynecology and Pelvic Reconstructive Surgery, The Cleveland Clinic Foundation, Department of Obstetrics and Gynecology, Cleveland, OH, USA Alan J Wein md Professor and Chief of Urology, Hospital of the University of Pennsylvania, Urology Division, Philadelphia, PA, USA Ursula Wesselmann md phd Departments of Neurology, Neurological Surgery and Biomedical Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD, USA Don Wilson md frcs franzcog cu Professor of Obstetrics and Gynaecology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand J Christian Winters md facs Department of Urology, Ochsner Clinic Foundation, New Orleans, LA, USA Brian G Wise mb bs md mrcog Consultant Urogynaecologist, William Harvey Hospital, Ashford, Kent, UK Jean-Jacques J M Wyndaele md Department of Urology and Center for Urological Rehabilitation, University Hospital Antwerp, Belgium Ilker Yalcin phd Eli Lilly and Company Corporate Center, Indianapolis, ID, USA Stephen A Zderic md Professor of Surgery, University of Pennsylvania, School of Medicine, Attending Surgeon, Division of Urology, The Childrens Hospital of Philadelphia, Philadelphia, PA, USA Philippe Zimmern md Department of Urology, University of Texas Southwestern Medical Center, Dallas, TX, USA Norman R Zinner md ms facs Medical Director, Western Clinical Research Inc, Torrance, CA, USA
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Foreword Female urology / urogynecology is a blooming subspecialty. We owe our gratitude to the prior outstanding masters from multiple disciplines who have contributed to a solid foundation of practical knowledge from the past. Fortunately, a unique multi-disciplinary culture has flourished over the last decade, and even in the early evolution of this collaborative effort we have embraced a new approach that incorporates the entire ‘pelvic floor’. This core approach will continue to be a catalyst from which current and future generations can generate new information and novel techniques based on creativity, innovation, and evidence based analysis of the results. This new and updated edition of the Textbook of Female Urology and Urogynecology continues a tradition from the first volume which is already considered a classic in the field. The text provides the reader with a comprehensive high-quality and inclusive review of the subject of female urology and urogynecology. This book is a vital and important reflection of the standardised and validated approach put forth for the management of female pelvic floor disorders, following the pathways indicated by the International Continence Society (ICS), the Society of Urodynamics and Female Urology (SUFU), the International Urogynecological Association (IUGA) and the International Consultation on Incontinence (ICI). This book should be listed as a must in the personal library of those interested and involved in female urology and urogynecology. Reading, incorporating and referring to the various chapters of the book will be a pleasure and enrichment both for beginners as well as for experts. Walter Artibani md Chief of Urology Department University of Padova
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Preface Our decision to produce a second edition of this textbook, a formidable undertaking, is due to the many rapid advances which have occurred in urogynecology/ female urology. The first edition was well received by readers and we had an overwhelmingly favorable response from the contributors to update and where necessary re-write their chapters. In addition, a number of new authors have taken on the task of creating new chapters relating to topics which had not previously been covered and enhancing many areas covered in the previous edition. We are truly grateful to all those whose hard work has resulted in this finished product, of which we can all be very proud. Our vision was, once again, to assemble an international group of experts as authors, but on this occasion we have been able to recruit the invaluable help of section editors who have guided the authors and prevented too much “overlap” from occurring in the various chapters of the book. Because our authors represent both gynecologists and urologists, as well as some non-medical clinicians, with a true international perspective, we have been able to avoid the polarization of ideas which occurs in many textbooks as a natural product of geography and the training and interests of the contributors. So a muchísimas gracias - grazie infinite - danke sehr – merci beaucoup to our section editors, the authors from the first edition and the new authors who have brought fresh ideas and new areas of interest to this textbook. As previously our mission was to produce a comprehensive textbook which would chronicle past contributions, document the present state of the art, and serve as a foundation, preparing the reader for future developments in the field. The text is arranged in sections enabling the reader to access areas of interest with an extensive bibliography intended to facilitate further study of this fascinating and rapidly changing subject. The section on surgery has been formatted to serve as both evidence based text and an atlas which should provide information pertaining to the decision making process as well as the technical aspects of the surgical procedures. We do however recognize that as this text goes to press, it is impossible to cover all aspects of female urology and urogynecology comprehensively and that the rapid pace of advances makes it difficult to be completely up to date. We will to try to amend any deficiencies in our 3rd edition! As editors we are truly grateful to all those authors who have contributed. Researching and writing demands a considerable amount of time and effort and is often a thankless task. We are really grateful to the individuals who sacrificed much of their “quality time and family life” outside of their required hours of clinical and scientific work, to make this project a reality. Once again we would like to thank the publishers for producing a well illustrated book of high quality which should enhance the minds, practices and book shelves of those who own it. Finally, we recognize the contribution from our patients who place their trust in all of us, and without whom this work would be futile. We hope that the textbook contributes to their quality of care and to the ability of those who care for them today and in the future. Linda Cardozo David Staskin
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Section 7 surgery for urinary incontinence Section Editor Roger R Dmochowski
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54 The assessment of outcomes used for incontinence interventions in women Emily E Cole, Harriette M Scarpero, Roger R Dmochowski
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Textbook of Female Urology and Urogynecology
INTRODUCTION Urinary incontinence is a common condition that affects up to 13–15 million individuals in the United States alone. Urinary incontinence (UI) is described as the involuntary loss of urine. The term incontinence denotes a symptom, a sign, and a condition. The symptom is the patient or caregiver’s direct report of involuntary loss of urine, the sign is the objective demonstration of urinary loss on physical examination, and the condition relates to the pathophysiologic reason for urine loss which may be determined via clinical and/or urodynamic testing. Increased public awareness regarding voiding dysfunction and incontinence has produced heightened interest in the effects of incontinence on the quality of an individual’s life. Furthermore, a marked increase in options for the treatment of incontinence has led to the need for accurate assessment as to the impact of any intervention upon the quality of life of the individual. To assess the results of specific therapies for incontinence adequately, outcomes need to be measured and quantified in a standard and consistent manner that permits objective conclusions to be made. Historically, outcomes assessment for incontinence has been founded on physician-reported results, often established on the basis of patient interview, physician opinion, non-validated surveys, and a variable combination of physical examination, voiding diaries, symptom scores, and urodynamic evaluation. Non-standardized results reporting has prevented critical analysis not only of the overall influence of incontinence on the individual, but also of the success of treatment interventions. Currently we have objective measures such as urodynamics, pad tests, and physical examination with stress test. Additionally there are the semi-objective measurements of diaries, logs and other tools for assessing voiding frequency, urinary loss, and diurnal variations. Finally, there are the completely subjective (yet validated and psychometrically correct) patient symptom appraisals and quality of life metrics. Various groupings of these modalities have achieved ‘standardization’ level for reporting, but universal acceptance has not yet been achieved. This chapter reviews the assessment of outcomes and the utilization of these outcomes in the establishment of diagnostic and treatment guidelines for the management of urinary incontinence.
GENERAL CONSIDERATIONS Whereas the physician and surgeon are concerned with the individual patient, outcomes reporting research is concerned with symptoms, signs, and conditions of entire patient populations and with how specific treat-
ment strategies work with respect to safety, efficacy, and the economic impact on all involved parties. While physicians generate non-quantifiable assessments of UI by patient history, physical examination, laboratory tests, urodynamics and cystoscopy, outcomes reporting must focus on quantifiable variables assessed via validated instruments. Minimal requirements for results reporting include not only certain specified elements with which to assess outcomes, but also longevity of data follow-up and the manner with which data are collected. The elements in question should attempt to capture a blend of subjective and objective outcomes factors so as to present the most comprehensive assessment of the final result for the group of patients under analysis. Outcome instruments must be reliable, valid, and quantifiable.
Reliability Reliability refers to how reproducible the instrument is over time. Questionnaires that measure the same characteristics should produce similar responses from a subject. Additionally, the same questionnaire should produce similar results for a subject over short intervals of time. Reliability is a quantifiable assessment of these sources of error in measuring devices.1 There are five measures of reliability: 1) alternate form; 2) test–retest; 3) interobserver; 4) intraobserver; and 5) internal consistency.
• Alternate form reliability refers to using two or more
•
•
•
alternate wordings of questionnaire items in an attempt to obtain the same information about a specific domain of an instrument. The degree of agreement between the two responses represents alternate form reliability.2 Test–retest reliability measures the reproducibility of a response over time. This is evaluated by repeat administration of the questionnaire to subjects over a period of time. Sufficient time should have elapsed for the subjects to forget their responses to the items, but no change in their symptoms should be evident. Correlation coefficients generally used to measure this property include the interclass correlation coefficient, Pearson correlation coefficient, and Spearman rank correlation.3 Interobserver and intraobserver reliability addresses the degree of consistency among two or more observations of the same variable by one or more observers, respectively.2 Internal consistency measures the similarity of responses among items that are designed to address
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Assessment of outcomes used for incontinence interventions in women
the same variable. Because items in a questionnaire query related aspects of the same condition, a relationship should exist between responses to these items. The degree of agreement is measured by Cronbach’s coefficient alpha. This statistical tool ranges from 0 to 1, with lower numbers representing lesser degrees of internal consistency.3
Validity Validity refers to how accurately an instrument measures what it intends to measure. There are five methods of assessing validity: 1) content validity; 2) construct validity; 3) concurrent criterion validity; 4) predictive criterion validity; and 5) face validity.
• Content validity refers to the relationship of the
• • • •
measuring device to the condition being measured. Questions should cover all of the important aspects of the condition. Content validity is often established by using focus groups of potential subjects and by asking experts to evaluate the questionnaire. Construct validity is a theoretic measure of how meaningful the instrument is. Concurrent criterion validity measures how well an item correlates with a gold standard method of measurement of the same variable. Predictive criterion validity is a measure of how well a domain of investigation is shown to predict future observations.
Questionnaires For history taking and patient report of status, the basic element of outcomes assessment has been the questionnaire. In the setting of lower urinary tract symptoms (LUTS), a questionnaire might serve several purposes. It can aid the practitioner in gathering relevant information about the patient’s problem, helping to determine the nature of the problem, and the frequency and extent of the symptoms. Questionnaires are useful in assessing the impact the condition has upon the patient’s activities and well-being. Ideally, a questionnaire might be able to elucidate the cause of a patient’s condition, limiting the need for more costly and/or invasive studies. Following treatment, questionnaires can track the outcomes of treatment strategies, providing more standardized outcome data than informal data retrieval.4 Specific items used in LUTS questionnaires may vary widely, depending on the purpose and target subjects of the outcomes measurement.5 To accomplish these tasks, symptom
questionnaires must be relevant to clinical practice. Paul Abrams identified four characteristics of a good symptom questionnaire: 1) the questionnaire should be facile; 2) each item of the questionnaire should have a known causal relationship to the condition being measured; 3) the score should help determine appropriate therapeutic options; and 4) use of the questionnaire should directly improve patient management and the effect should be demonstrable.6 Questionnaires consist of a series of questions called items. Each item consists of a stem (question or statement) and a response. Responses may be: 1) a categorical response; 2) a Likert response; or 3) a visual analog or 1-item metric:
• A categorical response consists of choices that are ‘mutually exclusive and collectively exhaustive’;
• A Likert response is composed of several levels of •
agreement or disagreement; A visual analog response utilizes a visual scale usually defined on either end with a word or phrase representing the extreme range of variability.
Outcomes reporting can be divided into primary and secondary outcome measures. Primary outcome measures refer to those variables that directly assess continence including: 1) number of incontinent episodes over a specifically defined time period; 2) the volume of urinary loss; 3) the ease with which the incontinence can be provoked; and 4) the type of incontinence. These variables can be assessed via patient questionnaires, diaries, pad tests, physical examination, and urodynamics. Secondary outcome measures represent factors affecting patient satisfaction and the effect of treatment, including any resulting complication(s) and/or morbidity.2 In contemporary times, there are many who would assert that – when undertaking an intervention to correct a problem that mostly comprises an effect on a patient’s quality of life – patient satisfaction should be considered a primary outcome, if not the most important outcome of all. In addition to utilizing valid and reliable instruments for measuring signs, symptoms, and specific responses to treatment(s), it is imperative that researchers specify the outcome measures that will be used to define cure, failure, and improvement for each individual study protocol. Outcome after treatment for urinary incontinence should be defined not only in terms of symptoms, signs, and testing, but also in terms of associated symptoms and unwanted side effects resulting from an intervention, after return to baseline activities and medications. Specific definitions of outcomes – such as the 803
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National Institutes of Health Terminology Workshop for Researchers in Female Pelvic Floor Disorders’ recommendations for outcomes after treatment for stress urinary incontinence – should be developed to assist in the standardization of outcomes terminology. These recommendations are detailed in Appendix I.7
AUA GUIDELINES The American Urologic Association synthesized an extensive literature review in an attempt to assess the success of interventions for urinary incontinence.8 The goal of their resultant guidelines was to examine specifically the existing medical literature regarding the surgical treatment of stress urinary incontinence (SUI) in women. The index patient was defined as the otherwise healthy woman, without significant pelvic organ prolapse, who had decided to undergo surgical correction for SUI as either primary or secondary therapy. The panel evaluated the medical literature pertaining to the treatment of SUI from 1950 to 1993: over 5000 articles were identified, of which 457 were selected for data retrieval. Articles were excluded if there was insufficient follow-up (<12 months postoperatively), if more than 50% of the initial cohort of patients was lost to follow-up, or if specific outcome data (number cured or failed) were unstated. The explicit data analysis method was utilized to evaluate abstracted results. Owing to the large number of individual procedure types reviewed and the lack of significant difference in outcome data between these types, the panel grouped the surgical approaches into four broad categories: retropubic suspensions, slings, transvaginal suspensions, and anterior repairs. The procedural types were evaluated for surgical success (cure of incontinence: dry, improved, failed) as well as outcomes such as postoperative urgency/urge incontinence, urinary retention, urinary outflow obstruction and pelvic prolapse, and complications. Given variations in reporting of surgical complications, six general categories were defined by the panel: general medical complications, intra- and perioperative complications, subjective complications, complications requiring surgery, and transfusions. The data collected by the panel are shown in Appendix II. Based on the compendium of compiled data, the panel made several recommendations for patient evaluation, citing certain crucial aspects of the preoperative workup: 1) history (including impact of incontinence on the patient’s quality of life); 2) physical examination with demonstration of incontinence; 3) urinalysis; 4) diagnostic studies to assess relative contributions of detrusor dysfunction, hypermobility and intrinsic sphincteric
deficiency (ISD) to overall presentation; 5) estimation of the severity and frequency of incontinence; and 6) assessment of the patient’s expectations for therapeutic outcome. The panel considered that determination of the patient’s quality of life comprised a significant component of pre- and postoperative evaluation. In addition, as above, they addressed the consideration of the patient’s understanding of, and expectations for, treatment results. In order to facilitate appropriate decision making by both patient and physician, extensive counseling and communication are necessary during the informed consent process. A specific recommendation concerning choice of procedure was not made by the panel. Difficulties in formulating a true representation of outcomes were encountered due to aberrations in data reporting. The guidelines were criticized for their lack of specific recommendations. However, their assimilation of existing data highlighted the inconsistencies in results reporting and clearly indicated the need for future development of specific outcomes reporting strategies.
RECOMMENDATIONS OF THE URODYNAMIC SOCIETY The demographics of female voiding dysfunction continue to evolve on the basis of emerging population-based data as extracted from questionnaire-based instruments. Depending on age, it is estimated that as many as 50% of women may experience urinary incontinence at some point in life.9 As previously mentioned, incontinence represents a symptom complex, a sign, and a condition. Regarding symptoms, associated aspects of voiding dysfunction include irritative (urgency, frequency) and obstructive (hesitancy, intermittency, incomplete bladder emptying) symptoms, and the complicated component of nocturnal voiding dysfunction. Further confounding the delineation of incontinence is the relatively minor degree of morbidity associated with the symptom complex, except in those women with concomitant recurrent urinary tract infection and related sequelae, or in those patients who have bladder storage abnormalities that compromise renal function. In 1997, Blaivas et al.10 introduced minimal standards by which the efficacy of therapy for urinary incontinence may be assessed (Appendix III). These standards were developed by a committee of the Urodynamic Society and were adopted as official recommendations of the American Urologic Association and the Urodynamic Society. They recommended that all clinical trials should
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include a pre- and post-treatment evaluation that conforms to recommended standards. They mandated that post-treatment evaluation be conducted no less often than 1, 6, and 12 months after treatment and at yearly intervals thereafter, continuing as long as possible. They specified the importance of defining a clear definition of the criteria for success and failure of an intervention and included specific recommendations for pharmacologic studies and studies which examine repetitive therapies (e.g. injection therapy).
RECOMMENDATIONS OF THE INTERNATIONAL CONSULTATION ON INCONTINENCE The International Consultation on Incontinence (ICI) of 2002 aimed to expand upon the recommendations of the AUA and the Urodynamic Society to improve clinical research design and outcomes reporting. They emphasized that, due to the complexity of incontinence, no single measure can fully express the outcome of an intervention, whether pharmacologic or surgical. They stressed the importance of the correlation of information in the understanding as to why one treatment is better than another, and as to why one treatment works for one patient and not for another. They recommended the collection of detailed data on improvement and deterioration in anatomy, symptoms, lower urinary tract function, complications of the intervention, and the effect on quality of life to help in the understanding of the disease process and how the chosen intervention(s) may benefit. For clarity, they structured their recommendations as follows:11 1. Baseline data 2. Observations: a. Patient’s observation/subjective measures b. Clinician’s observation/objective measures 3. Tests a. Quantification of symptoms – voiding diary/pad tests b. Urodynamics 4. Follow-up 5. Quality of life measures
Baseline data/demographics The ICI recommended that data collection for research purposes should begin with a complete demographic assessment of each subject including age, race, sex, duration of symptoms, prior treatments, medical co-morbidities, medications, etc. Obstetric and gynecologic history is important in women.7
Observations – patient One or more validated symptom instruments should be administered to accurately define baseline symptoms and other areas in which the proposed treatment may produce an effect. There is a variety of validated questionnaires available for the assessment of the incontinent patient. It is important to include instruments that address both specific symptoms and the respondent’s overall opinion of the condition. The Urogenital Distress Inventory (UDI) and Incontinence Impact Questionnaire (IIQ) provide a multicomponent quantification of the effects of the symptoms associated with incontinence and bother on the individual’s daily activities.12 Shortened versions of these questionnaires can be easily administered over minimal time intervals and can be used for cross-comparison of results of intervention. Validated questionnaires that assess symptomatic urge and stress incontinence, pad usage and incontinence volume, as well as validated visual analog scales that assess bothersomeness of symptomatic incontinence, are also currently available.13 In summary, the ICI recommendations for the reporting of patient observations include the following:
• One or more validated symptom instruments
•
should be chosen at the outset of a clinical trial to accurately define baseline symptoms and other areas in which the treatment may produce an effect; The same instruments should be administered after intervention throughout follow-up.11
Observations – clinician According to the ICI, an important and often overlooked element of patient evaluation is the investigation of the possible presence of anatomic changes in the lower urinary tract and its supporting structures. It is paramount to report these observations both before and after any treatment intervention. There are few papers addressing outcomes of stress incontinence surgery that report both functional and anatomic results. These objective measures are particularly important in the explanation of treatment failures. For example, functional results may provide some idea as to the effectiveness of a certain procedure, however, there is no information to explain what happened in cases of failure. Did the treatment fail due to technical factors (e.g. recurrent hypermobility) or due to an inherent limitation of the procedure (e.g. ISD)? In summary, the ICI recommendations for the reporting of clinicians’ observations include the following: 805
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• Clinicians’ observations of anatomy should • •
be recorded using standardized, reproducible measurements; Pelvic muscle and voluntary sphincter function should be reported using a quantifiable scale; These measures should be repeated after intervention and correlated with primary clinical outcome measures.11
Tests Quantification of symptoms Measures that have been utilized to measure the severity of symptomatic incontinence include standardized diaries and pad-weighing tests. The voiding diary is a self-monitored record of selected lower urinary tract function that is kept for a specific time period. Voiding diaries commonly assess fluid intake, micturition frequency, volume voided, number and degree of incontinence episodes, and pad use.14 The International Continence Society (ICS) utilizes the largest voided volume recorded in the patient’s diary as the definition of functional bladder capacity.15 Diaries are routinely kept for discrete 24-hour periods and are repeated for 48- to 72-hour periods.16 Their accuracy is defined by the patient’s ability to follow specific directions. The circumstances under which a diary is kept should mimic everyday life and should be similar before and after intervention to allow for meaningful comparisons. Pad tests provide a semi-objective method for assessing the degree (volume) of urine loss over a specified time period. Several time periods and testing modalities have been described for pad testing, including 1-, 6-, and 24-hour intervals.15,17,18 Pad weighing quantifies the amount of urine lost over the measured time period. Pad testing can be supplemented with the ingestion of phenazopyridine hydrochloride, which provides a visual corollary to the actual change in weight of the pad. Pad testing is subject to significant variability between and within individuals. This modality is best correlated with the patient’s own assessment of urinary loss. Various types of pad test have previously been validated and subjected to testing reliability; however, poor test–retest validation and variability in performance of testing limit widespread usage.8 In summary, the ICI recommendations concerning the use of tests include the following:
• Clinical trials of incontinence and LUTS should include bladder diaries as an essential baseline and outcome measure;
• The diary should include measured voided volume (for at least 1 day if a multi-day diary is utilized);
• 24-hour diaries are adequate for most studies; • Clinical trials of incontinence and LUTS should include a pad test as an essential baseline and outcome measure.11
Urodynamics The ICI also details the recommendations for the usage of urodynamics in clinical research. They caution that due to the lack of universal availability of urodynamic testing and to the lack of 100% sensitivity and/or specificity, subjects should not be stratified into study groups based on urodynamic diagnosis but should be enrolled based on carefully defined symptoms. They call for continued data collection to work towards the determination of the predictive value of urodynamic testing prior to intervention and for the development of new and better tools to improve the sensitivity and specificity of testing. The ICI recommends the use of urodynamic testing to accurately characterize baseline lower urinary tract function and dysfunction. Preintervention studies can assist in the understanding of the pathophysiology of the disease process. They also recommend that, when possible, post-treatment studies be performed to further clarify the actual effects of the intervention(s). The problem of interobserver variability is addressed, emphasizing the importance of utilizing standardized techniques at baseline and follow-up. In addition, it is recommended that, when possible, a central blinded reader for urodynamic tracings be assigned in order to reduce investigator bias, particularly in multicenter trials. In summary, the ICI recommendations for the use of urodynamic testing in clinical research include the following:
• At this time, clinical studies should enroll subjects •
• • •
by carefully defined symptoms, not urodynamic findings; To determine the predictive value of urodynamic tests, urodynamics must be performed at baseline but subjects should be enrolled without prejudice of urodynamic test results; In the ideal clinical study, urodynamic tests are performed at baseline and at exit to correlate symptom changes with physiologic changes; When these ideal conditions cannot be met, urodynamic tests should be performed on a subset of the larger group; In all trials, standardized urodynamic protocols (based on ICI recommendations) are defined at the
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outset. In multicenter trials, urodynamic tests should be interpreted by a central reader to minimize bias.11
Follow-up The ICI report concurs with the minimal standards for follow-up recommended by Blaivas et al.10 in the report approved by the Urodynamic Society. As previously described, in addition to standard pre- and postintervention evaluation, they recommend evaluation of surgical, prosthetic, and implant therapies no less often than 1–3 months and 12 months after treatment, and thereafter at yearly intervals for as long as possible. They recommend the specific definition of the following:
• the method by which data are to be collected; • the identification of the individual(s) collecting data (e.g. research nurse, clinician);
• the interval between the time of evaluation and the last treatment;
• the identification of the exact type of data collected at each time point in follow-up;
• the specific criteria by which treatment success or failure is to be determined. In addition, they recommend the mandatory inclusion of the following data at each follow-up interval: 1) the total number of patients treated; 2) the number of subjects actually evaluated in the study; and 3) the total number of subjects lost to follow-up and the reasons why they were lost.
Quality of life measures The major impact of incontinence is on the sufferer’s quality of life and the related physical activity, social, emotional, and psychological limitations. Global assessment of the impact of incontinence implies the necessity for health-related quality of life (HRQOL) measures that reflect the broader impact of this symptom complex. HRQOL is a multidimensional construct that refers to an individual’s perceptions of the effect of a health condition and its treatment on quality of life. Primary domains of HRQOL include physical, psychological, and social functioning; overall life satisfaction and well-being; and perceptions of health status. Secondary domains include somatic sensations (symptoms), sleep disturbances, intimacy and sexual functioning, and personal productivity. Considering the complexity of voiding dysfunction and the variety of treatment modalities available, it is important to
know not only how well interventions eliminate incontinence, but also how a treatment affects the patient globally. HRQOL measures can be classified into three broad types: 1) generic – allowing assessment and comparison of quality of life across populations but not reflecting the specifics of the disease or symptom in question; 2) condition specific – providing more critical analysis of the condition under investigation but lacking the capability for cross-population or group comparison; and 3) dimension specific – designed to assess a single component of HRQOL, such as emotional distress. The trend in assessing HRQOL outcomes has been toward the use of a multidimensional generic and/or condition-specific instrument, supplemented with a dimension-specific instrument as needed.19 The selection of a HRQOL instrument should be based on the purpose of the study. Descriptive epidemiologic studies should consider the use of both generic and condition-specific instruments. Intervention studies should focus more on conditionspecific instruments, with the use of dimension-specific instruments when more detail about a focused subdomain of HRQOL is desired. In the description of study design, a clear description of selected HRQOL measures and of data collection should be presented. Selected instruments should be reliable and sensitive and, if available, information about reliability data should be provided. Despite the importance of HRQOL measures in defining outcomes, HRQOL should never be used as the sole endpoint of clinical research. The ICI recommends that the focus must always be on the combination of HRQOL with how successfully the target condition or symptom is treated. If a treatment is effective but does not improve HRQOL, possibly due to some adverse event, the treatment can be better. The combination of HRQOL and specific objective postintervention endpoints can add understanding to the reasons behind the success or failure of certain treatment modalities. In summary, the ICI recommendations concerning the use of HRQOL measures in clinical research include the following:
• Research in incontinence and LUTS should include •
both generic and condition-specific HRQOL instruments; Changes in HRQOL after therapy should be correlated with changes in individual symptoms and with physiologic and anatomic outcome measures to ascertain how that particular therapy is working.11 807
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Considerations for specific patient groups The ICI report also included specific recommendations for certain patient groups (Appendix IV). They concurred with the recommendations of the ICS report on ‘Outcome Measures for Research in Treatment in Adult Males with Symptoms of Lower Urinary Tract Dysfunction’ in addressing the factors unique to adult men, the presence of the prostate, and the possible presence of benign prostatic obstruction.20 Concerning females, they referenced recommendations from Blaivas et al. and the Urodynamic Society, the ICS, and the Proceedings of the NIH Terminology Workshop for Researchers in Female Pelvic Floor Disorders to define unique factors influencing research on incontinence and LUTS in women including: 1) hormonal effects on the lower urinary tract; 2) obstetric history and the influence of vaginal childbirth on the development of pelvic floor disorders; 3) assessment of pelvic organ prolapse and other measures on physical examination; 4) definitions of outcomes after treatment of lower urinary tract symptoms; and 5) sexual functioning.7,10,21,22 The ICI also addressed study design and outcomes in frail older and disabled people, agreeing with recommendations reported in the ICS subcommittee on ‘Outcome Measures for Research of Lower Urinary Tract Dysfunction in Frail Older People’.23 Concerning children, the ICI referenced the official report from the United States National Institutes of Health (NIH) from 1998, calling for increased and improved pediatric medical research.24 This report detailed specific responsibilities of each involved party and emphasized the importance of full understanding of the levels of risk and the corresponding nature of assent required for participation. For investigations involving patients with neuropathic lower urinary tract dysfunction, specific recommendations emphasizing the classification of the neurogenic patient and utilization of objective measures (e.g. urodynamic studies) in assessing baseline and post-treatment outcomes were made.25
FUTURE CONSIDERATIONS At present, the ideal manner with which to report the outcomes of surgical interventions remains unsettled. Although this particular issue is significant for any intervention, for interventions designed to lessen the impact of particular symptoms that are significant for quality of life disruption (e.g. incontinence), this quandary becomes more marked. Without established and gener-
ally accepted criteria, the quality of literature outcomes reporting for urinary incontinence will never develop to the level seen for other symptom or disease states (e.g. oncologic outcomes reporting). Currently, efforts are underway to make sense of the multiple factors involved in the evaluation and treatment of incontinence and to provide a workable taxonomy. However, these criteria – such as the above-mentioned ICI recommendations – are inclusive and somewhat cumbersome. Yet these reporting criteria are as important (and in some cases, more so) as isolated efficacy parameters. There is a paucity of literature addressing the quandary of what to do with those patients who fail to follow-up. Ward et al. reported a prospective trial comparing tension-free vaginal tape and colposuspension for the primary treatment of stress incontinence.26 They reported outcomes based on several different assumptions and had very different results. By analyzing only data available at 2 years follow-up and ignoring withdrawals, objective cure rates were 81% for TVT and 80% for colposuspension, with no significant difference between the two. If all patients who failed to follow-up were considered successes, the objective cure rates were 85% and 87% for TVT and colposuspension, respectively, again with no statistically significant difference between the two methods. However, if all those who failed to follow-up were considered to be failures, the objective cure rates fell to 63% and 51%, respectively, the difference statistically favoring TVT. Minassian et al. echoed these findings in their comparison of patients with good follow-up versus those with poor follow-up following the TVT procedure.27 Based on telephone interview of those patients who did not follow-up as scheduled, they found significantly higher subjective and objective cure rates among the patient group with good follow-up. Clearly, how we address the proportion of patients lost to follow-up is important in the assessment of treatment outcomes. In 1999, Chaikin et al.28 evaluated 84 women before and after pubovaginal sling. They evaluated the patients pre- and postoperatively with a voiding diary, pad test, symptom questionnaire (administered by a blinded third party), and operating physician evaluation (history and physical examination). At 1 year postoperatively, they compared patient assessment (cured, improved, failure) to the outcome of the pad test, voiding diary, and physician assessment. Agreement was excellent among the four instruments for outcome assessment with respect to cure/improved versus failure, but only good for cured versus improved versus failure. The conclusions from this study confirmed that these four instruments were reliable outcomes measures; however, none was perfect. In response to this and to other studies emphasizing
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inconsistencies between subjective and objective results, Groutz et al. introduced an incontinence score incorporating several non-invasive outcomes measures to potentially evaluate therapeutic intervention.29 They evaluated 94 women who underwent pubovaginal sling by the same surgeon, including pre- and postoperative patient questionnaire, 24-hour voiding diary, and 24-hour pad test. Postoperative outcomes were classified twice: once by considering all of the evaluation methods separately, and once by assigning a simple outcomes score based on a combination of responses/results from all methods. The new score was divided into five categories: 1) cure; 2) good response; 3) fair response; 4) poor response; and 5) failure. Comparison of the two evaluation methods indicated that the outcomes score gave a more accurate measure of postsurgical status. According to the older criteria, 64–69% of patients were classified as cured. Utilizing the newer strict outcomes definition, only 44.7% of patients could be classified as cured, with 26.6% of patients classified as a good response. These findings echoed the consideration that gross classification of results into cured, improved, and failed may not accurately reflect the real clinical status. These results were supported by similar findings in more isolated patient populations such as those with simple stress urinary incontinence and those with mixed urinary incontinence.30,31 The use of this outcomes score, combining subjective and objective measurement tools, is a step in the positive direction in the movement towards a standardization of results reporting. There are issues that remain to be addressed by all of the described contemporary recommendations. Although all of the factors detailed in the above discussion have great importance, perhaps what should be asked for is a set study defining primary and secondary outcome variables while honestly reporting the side effects of those complications for the population undergoing the intervention. The concept of a carefully defined therapeutic index, providing a balance between the polar components of outcomes should be a starting point. The blended efficacy analyzes a summation of two, three, or four factors that can then be balanced with the tolerability issues for an ultimate appraisal of the therapy. In addition, the relatively uncharted territory of improvement needs to be better understood and more effectively assessed. It remains clear that the well-informed patient is critical in the overall estimation of procedural outcome. Patients are receptive and happy with improvement and not cure after our interventions, just so long as they are aware that cure is not a universal phenomenon. It is clear that in the field of urinary incontinence, a standard method of outcome evaluation and reporting
is necessary in order to appreciate accurate assessments of treatment efficacy. As is evident in the above discussion, multiple components are paramount in the establishment of a ‘result’. In addition to a clear definition of cure, various degrees of improvement, and failure, and a combination of subjective and objective measures need to be utilized to address all aspects of outcome – connecting anatomic and physiologic results with patient assessment of quality of life and satisfaction...we recommend…
AppENDIx I OUTCOMES AFTER TREATMENT FOR STRESS URINARY INCONTINENCE: RECOMMENDATIONS OF THE NIH TERMINOLOGY WORkSHOp FOR RESEARCHERS IN FEMALE pELVIC FLOOR DISORDERS CURE OF STRESS URINARY INCONTINENCE IS DEFINED AS: 1. Resolution of stress urinary incontinence symptoms; 2. Resolution of the sign (negative full bladder cough stress test, performed under the same conditions as pretreatment). In studies using urodynamics after intervention, absence of genuine stress incontinence should be documented; 3. No new symptoms or side effects. New symptoms or side effects should be specifically described and could include: a. new urinary symptoms such as urinary urgency, frequency, urge incontinence, with or without urodynamic changes of detrusor overactivity; b. change in sexual function; c. development or worsening of pelvic organ prolapse; d. adverse effect on bowel function; e. onset of urinary tract infections; f. surgical complications, such as foreign body reaction to grafts, or development of fistulae or diverticula; g. osteitis or osteomyelitis; h. neuropathy; i. other
FAILURE OF TREATMENT OF STRESS URINARY INCONTINENCE IS DEFINED AS ANY ONE OF: 1. Persistent stress symptoms with the number of incontinent episodes unchanged, or worse, by voiding diary; 809
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2. Positive full bladder cough stress test (performed under the same conditions as pretreatment) or genuine stress incontinence confirmed by urodynamic studies; and 3. Presence or absence of new symptoms or side effects as listed above.
IMpROVEMENT OF STRESS INCONTINENCE INCLUDES:
a. b. c. d. e.
2.
1. Persistent stress symptoms but with the number of incontinent episodes decreased by voiding diary; 2. Positive full bladder cough stress test (performed under the same conditions as pretreatment) or genuine stress incontinence confirmed by urodynamic studies; and 3. Presence or absence of new symptoms or side effects as listed above.
AppENDIx II OUTCOMES REpORTED BY THE AUA GUIDELINES COMMITTEE See Tables 54.1–54.7.
AppENDIx III STANDARDS OF EFFICACY FOR EVALUATION OF TREATMENT OUTCOMES IN URINARY INCONTINENCE: RECOMMENDATIONS OF THE URODYNAMIC SOCIETY
3.
GENERAL CONSIDERATIONS At each post-treatment interval, the following data should be recorded:
4.
• The total number of patients treated during that
5.
time interval.
• The total number of patients actually evaluated during that time interval.
• The total number of patients lost to follow-up during that time interval.
• The reasons why patients were lost to follow-up. pRETREATMENT EVALUATION SHOULD CONSIST OF: 1. Structured micturition history or questionnaire including at least:
number of micturitions/day number of micturitions/night number of incontinent episodes/day number of incontinent episodes/night type of incontinence (stress, urge, unconscious, continuous) f. description of voiding (emptying) symptoms Structured physical examination with full bladder including at least: a. Neurourologic examination i. Perianal sensation ii. Anal sphincter tone and control iii. Bulbocavernosus reflex iv. Brief screening neurologic examination b. (Women) vaginal examination i. Demonstration of urinary leakage 1. spontaneous/continuous 2. synchronous with stress 3. after stress ii. Presence and degree of 1. cystocele 2. urethrocele 3. uterine prolapse 4. enterocele 5. rectocele c. (Men) prostate examination i. Size and consistency of prostate ii. Demonstration of urinary leakage 1. continuous 2. synchronous with stress 3. after stress Micturition diary – self-reported by patient a. Time of micturition b. Time and type of incontinence c. Voided volume Pad test – a quantitative or semi-quantitative pad test should be done to estimate the amount of urinary loss Urodynamics – videourodynamics is the most comprehensive method of evaluation. The minimum evaluation should consist of: a. Cystometry (liquid) with simultaneous measurement of vesical and abdominal pressure for determination of detrusor pressure b. Synchronous detrusor pressure/uroflow study c. Simple uroflow d. Assessment of the relative contribution of urethral hypermobility and intrinsic sphincteric deficiency, such as the Q-tip test and leak point pressure e. Estimation of post-void residual urine, e.g. by ultrasound or catheterization
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23/1870 17/2196
48 months and longer
24/1941 18/2204
24–47 months
48 months and longer
1/6 8/241
For patients with no urgency but with DI preoperatively
For patients with no urgency and no DI preoperatively
Days in the hospital (panel survery)
Permanent
Longer than 4 weeks
5/340
6/319
For patients with urgency and no DI preoperatively
Retention
6/78
For patients with urgency and DI preoperatively
Postoperative urgency
16/961
12–23 months
Cure/dry/improved
15/943
24–47 months
5
11
4
36
66
90
88
86
84
84
84
(3–7)
(8–16)
(0–33)
(22–52)
(50–79)
(87–92)
(85–91)
(80–90)
(79–88)
(80–88)
(77–89)
6/479
6/150
1/3
6/33
4/292
8/424
13/700
4/292
8/424
13/700
(4–8)
(3–10)
5
5
(0–54)
(35–73)
(73–89)
(71–83)
(74–87)
(53–79)
(50–77)
(71–86)
6/1101
3/113
6/310
5/1088
3/113
6/310
G/P
From 0 to 5 days
73
95
78
61
85
68
Median
Anterior repair
Less than 5%
CI (2.5–97.5)%
7
54
82
78
82
67
65
79
Median
G/P
CI (2.5–97.5)%
G/P
Median
Transvaginal suspension
Retropubic suspension
Comparative outcomes for procedure categories
12–23 months
Cure/dry
Outcomes
Table 54.1.
(70–76)
(89–98)
(65–88)
(47–72)
(69–95)
(55–80)
CI (2.5–97.5)%
7/578
7/140
4/36
5/110
4/45
7/473
7/344
5/135
7/473
7/34
5/135
G/P
8
7
20
34
46
87
85
91
83
82
82
Median
Sling procedure
(6–11)
(3–11)
(5–45)
(13–61)
(24–68)
(80–92)
(77–91)
(84–96)
(75–88)
(73–89)
(73–89)
cont.
CI (2.5–97.5)%
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CI (2.5–97.5)%
G/P
Median
Anterior repair
7/1549
Not significant
(1–3)
2
15/1575
24/1412
54/3330
40/2814
25/1835
5/532
7/646
10/805
10/1083
2
11
12
7
5
2
4
2
3
(1–4)
(8–15)
(9–15)
(5–9)
(4–8)
(1–5)
(1–9)
(1–3)
(1–6)
2/1074
3/341
13/2322
5/970
1/313
1/294
3/650
5/1005
3/857
0
2
16
2
0
1
8
2
3
DI, detrusor instability; G, number of groups/treatment arms extracted; P, number of patients in these groups; CI, confidence interval. Reprinted with permission of the American Urological Association.
15/2718
(5–15)
9
Complications requiring surgery
(14–15)
14
13/1001
64/6044
(3–5)
(1–4)
3 4
Subjective complications
Not significant
Significant
(1–3)
(1–4)
2
(2–3)
2
(3–8)
2
5
40/3598
16/2284
Not significant
Perioperative complications
13/1992
Significant
Intraoperative complications
21/3136
Significant
General medical complications
(0–1)
(1–6)
(10–23)
(1–5)
(0–1)
(0–2)
(2–17)
(1–3
(1–9)
11/1119
4/301
26/1916
20/1723
19/1077
6/326
2/258
14/1127
6/279
3
6
12
7
8
3
6
4
4
9/1131
Median
Transfusion
G/P
Death rate for all procedures presumed to be no different than for other types of elective vaginal/abdominal surgery: approximately 5 out of 10,000
CI (2.5–97.5)%
Sling procedure
Death
Typically 6 weeks for all treatment modalities
Median
G/P
CI (2.5–97.5)%
G/P
Median
Transvaginal suspension
Retropubic suspension
Comparative outcomes for procedure categories (cont.)
Resumption of normal activities
Outcomes
Table 54.1.
(2–5)
(2–13)
(8–17)
(5–10)
(5–12)
(1–6)
(3–10)
(2–5)
(2–7)
CI (2.5–97.5)%
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21/3136 6/1000
Cardiovascular
Pulmonary
6/730 5/1003
Ureteral complication
Urethral complication
5/349 9/766
Pain
Sexual dysfunction
4/744
Stone formation
2
(1–4)
(1–2)
(3–12)
6 1
(3–10)
6
(6–24)
(5–8)
(12–14)
(3–7)
1/7
14/1568
10/609
16/1151
4/119
61/4096
33/1598
21/1392
2/128
1/255
25/1835
5/516
10/805
16
2
8
10
16
7
10
4
3
1
5
4
2
(2–50)
(1–3)
(6–11)
(7–14)
(6–32)
(6–8)
(7–13)
(3–5)
(1–8)
(0–2)
(4–8)
(1–11)
(1–3)
CI (2.5–97.5)%
2/1074
3/341
7/1806
11/1743
3/889
1/313
3/650
5/1005
1/519
G/P
1
2
(0–1)
(1–6)
(6–17)
(5–16) 10
(1–6) 9
(0–1)
(2–17)
(1–3)
(0–1)
CI (2.5–97.5)%
3
0
8
2
0
Median
Anterior repair
G, number of groups/treatment arms extracted; P, number of patients in these groups; CI, confidence interval; UTI, urinary tract infection. Reprinted with permission of the American Urological Association.
15/2718
Fistula
Complications requiring surgery
3/175
Dysuria
13
7
57/5633
Subjective complications
Wound complication
46/4141
5 13
19/1608
UTI
(0–3)
(1–4)
2 1
(2–4)
(1–3)
3
(2–3)
2
(1–22)
3
6
Bleeding
Perioperative complications
16/2284
Bladder complication
Intraoperative complications
1/19
Abdominal complication
Median
G/P
CI (2.5–97.5)%
G/P
Median
Transvaginal suspension
Retropubic suspension
Comparative outcomes for procedure categories
General medical complications
Outcomes
Table 54.2.
2/417
10/829
1/69
1/54
2/178
30/2499
14/984
4/500
6/326
19/1077
2/258
14/1127
1/88
G/P
3
3
2
4
8
9
12
3
3
8
6
4
1
Median
Sling procedure
(1–7)
(1–5)
(0–7)
(1–11)
(1–25)
(6–12)
(7–19)
(1–6)
(1–6)
(5–12)
(3–10)
(2–5)
(0–5)
CI (2.5–97.5)%
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9/756 6/529
24–47 months
48 months and longer
3/1006
48 months and longer
60
94
71
2/17
24–47 months
61
96
(18–94)
(67–100)
2/91
3/208
2/35
Synthetic
71
82
86
98
69
62
74
61
81
73
69
76
75
(59–81)
(70–91)
(68–96)
(92–100)
(39–91)
(38–83)
(62–84)
(31–86)
(73–88)
(33–96)
(40–90)
(40–97)
(62–86)
(83–96)
(69–93)
(70–95)
(76–88)
(75–89)
(55–85)
CI (2.5–97.5)%
3/202
1/84
Other
1/82
Vaginal wall
1/20
3/281
Other
2/96
3/87
2/66
Stamey
1/41
2/98
Lapides
G/P
85
82
95
75
93
65
52
67
44
86
Median
MMK, Marshall–Marchetti–Krantz procedure; G, number of groups/treatment arms extracted; P, number of patients is these groups; CI, confidence interval. Reprinted with permission of the American Urological Association.
48 months and longer
1/6
12–23 months
(68–92)
2/98
48 months and longer
82
1/52
Homologous
1/10 (72–90)
1/67
Fascia lata
2/82
1/62
2/40
24–47 months
82
(41–77)
(83–99)
(54–84)
Other
12–23 months
Abdominal fascia
2/51
Sling procedure
4/270
24–47 months
Kelly plication
12–23 months
Anterior repair
48 months and longer
1/108
(21–49)
2/49 1/41
24–47 months
Gittes
12–23 months 34
5/205 2/196
Raz
(70–86)
48 months and longer
79 2/168
1/99
90
83
85
83
83
72
Median
Pereyra – modified
24–47 months
12–23 months
Pereyra
3/258
(83–92)
48 months and longer
Transvaginal suspension
5/298
Other
6/1156
10/718
3/107
MMK
G/P
4/192 88
(75–90)
(79–88)
(78–91)
CI (2.5–97.5)%
24–47 months 1/213
83
84
85
Median
12–23 months
Paravaginal
8/644
12–23 months
Burch
G/P
Comparative outcomes forindividual procedures – cure/dry detail
Retropubic suspension
Table 54.3.
(71–93)
(73–89)
(89–98)
(54–90)
(88–96)
(47–80)
(33–70)
(48–83)
(30–59)
(60–98)
CI (2.5–97.5)%
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MMK
Lapides
Paravaginal
G/P
8/1557
2/231
G/P
3
8
Median
(1–4)
(4–14)
CI (2.5–97.5)%
1/63
G/P
2
Median
(0–7)
CI (2.5–97.5)%
1/146
2/359
G/P
2
2
Median
(1–5)
(0–9)
CI (2.5–97.5)% 3/327
G/P
4/454
1/156
Urethral complication
17/1667
1/117
Stone formation 3
2 (1–7)
(0–5) 1/270
9/1867
2/217
0
1
10
2
18
8
7
4
1
0
2
1
(0–2)
(1–2)
(0–49)
(0–8)
(6–39)
(6–11)
(5–10)
(2–7)
(0–4)
(0–2)
(1–3)
(0–3)
2/75
4
(1–12
2/359
1/146
1/213
2
11
1
(0–5)
(7–17)
(0–2)
2/357
3/383
1/100
1/100
13/928
8/555
5/506
1/37
2/152
1/175
2
1
6
6
7
10
3
3
1
3
3
6
5
Median
(1–4)
(0–3)
(3–12)
(3–12)
(4–11)
(5–17)
(1–6)
(0–12)
(0–4)
(1–6)
(1–6)
(1–22)
(1–13)
CI (2.5–97.5)%
MMK, Marshall–Marchetti–Krantz procedure; G, number of groups/treatment arms extracted; P, number of patients in those groups; CI, confidence interval; UTI, urinary tract infection. Reprinted with permission of the American Urological Association (AUA). Analysis of individual procedures complications (Tables 54.4–54.7). Subgroupings of complications for the various individual procedures under each of the four major procedure groupings are displayed in Tables 54.4–54.7. Under the retropubic suspension grouping (Table 54.4), the individual procedures are: Burch, MMK, Lapides, Paravaginal and Other. For transvaginal suspensions (Table 54.5), the individual procedures are Pereyra, Modified Pereyra, Stamey, Raz, Gittes and Other. For the anterior repair grouping (Table 54.6), the Kelly plication and Other are the only procedures listed (because of condiserable variabilty in types of procedures in the Other category). Finally Table 54.7 summarizes sling procedures: Abdominal fascia, Fascia lata, Vaginal wall, Homologous materials, Synthetic materials and Other. The Other category in each of these tables contains combined procedures as well as a variety of additional procedure modifications. A technical supplement to this report, Evidence Working Papers (available from the AUA) contains a full listing of procedures in the Other category. Rates of complications are generally between the types of retropubic suspensions (Table 54.4), with some exceptions. For example, the Burch procedure appears to have a higher UTI rate (median 24%) than other retropubic procedures. In the panel’s opinion, such differences are due to reporting variances between studies and to small overall sample sizes. For transvaginal suspension procedures (Table 54.5), complication rates are also generally similar. Inconsistencies are due to small numbers of patient groups and/or patients. This is true of the transfusion rate of Pereyra (17%) and of the dysuria rate forStamey (41%). Complication rates for anterior repairs (Table 54.6) are generally low and reflect differences in reporting and older literature references rather than real differences from the other procedure groupings. Table 54.7 displays complication rates for sling procedures. Differences in data reported are due to small sample size and older literature.
3/468
Fistula
Complications requiring surgery
(2–10)
7/639
Sexual dysfunction 5
2/75 1/60
3/189
23/2604
19/2036
8/400
4/847
1/239
8/1613
Pain (2–14)
(4–9)
(17–33)
(3–12)
(0–2)
(1–5)
(2–10)
3/535
Dysuria
Subjective complications 6
6
17/1341
Wound complication
24
6/702
UTI
7
0
2
5
(1–8)
3
Bleeding
Perioperative complications
6/519
Ureteral complication
1/77
Bladder complication
Intraoperative complications
Pulmonary
(1–4)
2
1/19
(1–7)
CI (2.5–97.5)%
4/517
3
Median
Cardiovascular
8/916
2/214
Other
Abdominal complication
General medical complications
Transfusion
Burch
Death rate for all procedures presumed to be no different than for other types of elective vaginal/abdominal surgery: approximately 5 out of 10,000
Death
Retropubic suspension
Comparative outcomes for retropubic suspension procedures: complications details
Outcomes
Table 54.4.
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Stamey
5/614
Wound complication
Stone formation
Fistula
Complications requiring surgery
Sexual dysfunction 3/420
1
(0–2)
3/393
1/114
1/114
Pain
9/611
6/216
3/177
1/82
1/225
7/539
1/30 (19–37)
(3–11)
6
27
(7–17)
(2–9)
(0–10)
11
5
3
(2–8)
1/225
1/30
1/93
G/P
Dysuria 1/99
3/306
UTI
Subjective complications
3/310
1/46
4
(0–2)
1
1/186 6/565
(0–4)
(10–25)
CI (2.5–97.5)%
1
17
Median
2/285
1/95
Bleeding
Perioperative complications
Urethral complication
Ureteral complication
Bladder complication
Intraoperative complications
Pulmonary
Cardiovascular
Abdominal complication
General medical complications
Transfusion
G/P
1
(0–3)
(10–23)
(0–6)
2 16
(0–15)
(5–12)
(6–26)
(1–7)
4
8
14
3
(0–6)
(0–2)
1 1
(2–9)
(0–2)
(1–20)
(3–13)
CI (2.5–97.5)%
4
1
7
7
Median
1/7
3/147
2/62
11/584
1/44
25/1481
14/684
7/386
5/189
2/85
6/465
4/457
G/P
16
(2–50)
(3–19)
(1–23)
8 9
(9–15)
(27–56) 12
41
(8–16)
(4–11)
7 12
(2–6)
(6–19)
(0–18)
(1–4)
(0–3)
cont.
CI (2.5–97.5)%
4
12
5
2
1
Median
Death rate for all procedures presumed to be different than for other types of elective vaginal/abdominal surgery: approximately 5 out of 10,000
Pereyra – modified
Pereyra
Death
Transvaginal suspensions
Comparative outcomes for transvaginal suspension procedures: complications details
Outcomes
Table 54.5.
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Other
5/384
Wound complication
(0–1)
(1–12)
4 0
(2–12)
(3–14)
7
5
(4–36)
(3–33)
(1–16)
(0–4)
CI (2.5–97.5)%
15
13
6
1
Median
2/72
5/286
2/106
3/177
2/54
1/20
G/P
3
(0–12)
(3–11)
(1–19) 6
(1–8)
6
(2–19)
(17–57)
CI (2.5–97.5)%
4
8
35
Median
4/402
3/114
1/107
2/45
12/720
6/225
4/325
3/346
1/25
2/132
G/P
1
4
3
9
9
4
3
1
1
6
Median
G, number of groups/treatment arms extracted; P, number of patients is those groups; CI, confidence interval; UTI, urinary treact infection. Reprinted with permission of the American Urological Association.
Stone formation
Fistula
1/206
2/247
Sexual dysfunction
Complications requiring surgery
2/247
Pain
Dysuria
Subjective complications
1/17 2/61
UTI
2/142
2/306
Bleeding
Perioperative complications
Urethral complications
Ureteral complications
Bladder complications
Intraoperative complications
Pulmonary
Cardiovascular
Abdominal complication
General medical complications
G/P
(0–2)
(1–10)
(1–7)
(2–22)
(6–13)
(7–23)
(1–7)
(0–3)
(0–9)
(1–20)
CI (2.5–97.5)%
Death rate for all procedures presumed to be different than for other types of elective vaginal/abdominal surgery: approximately 5 out of 10,000
Gittes
Raz
Death
Transvaginal suspensions
Comparative outcomes for transvaginal suspension procedures: complications details
Outcomes
Table 54.5.
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Table 54.6
Comparative outcomes for anterior repair procedures: complications details Anterior repairs
Outcomes
Kelly plication
Death
Death rate for all procedures presumed to be no different than for other types of elective vaginal/abdominal surgery: approximately 5 out of 10,000 G/P
Transfusion
Median
Other
CI (2.5–97.5)%
G/P
Median
CI (2.5–97.5)%
3/857
3
(1–9)
Abdominal complication
1/519
0
(0–1)
Cardiovascular
4/965
1
(0–3)
1/40
3
(0–11)
Pulmonary
2/610
7
(1–23)
1/40
5
(1–15)
1/313
0
(0–1)
Bleeding
2/849
2
(0–7)
1/40
3
(0–11)
UTI
9/1689
8
(3–15)
2/54
22
(4–55)
Wound complication
5/1706
13
(7–20)
2/100
3
(1–9)
2/319
1
(0–4)
1/22
5
(0–19)
2/1074
0
(0–1)
General medical complications
Intraoperative complications Bladder complication Ureteral complication Uretheral complication Perioperative complications
Subjective complications Dysuria Pain Sexual dysfunction Complications requiring surgery Fistula
Stone formation G, number of groups/treatment arms extracted; P, number of patients in those groups; CI, confidence interval; UTI, urinary tract infection. Reprinted with permission of the American Urological Association.
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Stone formation
Fistula
Complications requiring surgery
Sexual dysfunction
Pain
Dysuria
Subjective complications 1/80
2/77 3/157
UTI
3/171
2/77
2/114
Wound complication
Bleeding
Perioperative complications
Uretheral complication
Ureteral complication
Bladder complication
Intraoperative complications
Pulmonary
Cardiovascular
Abdominal complication
General medical complications
Transfusion
G/P
1
(0–6)
(1–67) (2–17)
7
(1–7)
(2–64)
(1–9)
CI (2.5–97.5)%
18
3
21
3
Median
2/93
4/421
2/258
1/170
2/147
2/258
4/405
1/88
1/10
G/P
6
(1–16)
(4–14)
(5–14)
9 8
(0–3)
1
(5–23)
(3–10)
5 12
(1–5)
(0–5)
(0–22)
CI (2.5–97.5)%
2
1
2
Median
1/54
1/82
1/54
1/82
1/54
1/54
G/P
4
3
4
3
2
0
Median
(1–11)
(1–8)
(1–11)
(1–8)
(0–8)
(0–5)
cont.
CI (2.5–97.5)%
Death rate for all procedures presumed to be no different than for other types of elective vaginal/abdominal surgery: approximately 5 out of 10,000
Vaginal wall
Death
Fascia lata
Abdominal fascia
Sling procedures
Comparative outcomes for sling procedures: complications details
Outcomes
Table 54.7.
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G/P
1/20
4/339
4/399
2/80
Wound complication
(1–5) (1–7)
3
(0–7)
(9–23)
(6–15)
(5–19)
(1–20)
(1–21)
(4–14)
(1–5)
(1–13)
CI (2.5–97.5)%
3
2
15
10
11
7
6
2
2
5
Median
1/160
8/791
1/21
1/205
2/135
5/422
2/145
G/P
0
9
6
1
2
5
7
Median
G, number of groups/treatment arms extracted; P, number of patients in those groups; CI, confidence interval; UTI, urinary tract infection. Reprinted with permission of the American Urological Association.
2/417
1/69
1/98
13/1038
Stone formation
(9–61)
7/576
31
1/10
Fistula
Complications requiring surgery
Sexual dysfunction
Pain
Dysuria
Subjective complications
40
1/10
7/564
(15–70)
(1–38)
(1–38)
CI (2.5–97.5)%
UTI
11
11
Median
2/125
1/10
1/10
G/P
Bleeding
Perioperative complications
Urethral complication
Ureteral complication
Bladder complication
Intraoperative complications
Pulmonary
Cardiovascular
Abdominal complication
General medical complications
Transfusion
(0–2)
(4–16)
(1–20)
(0–3)
(0–6)
(2–10)
(1–21)
CI (2.5–97.5)%
Death rate for all procedures presumed to be no different than for other types of elective vaginal/abdominal surgery: approximately 5 out of 10,000
Vaginal wall
Death
Fascia lata
Abdominal fascia
Sling procedures
Comparative outcomes for sling procedures: complications details (contd.)
Outcomes
Table 54.7.
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pOST-TREATMENT EVALUATION SHOULD CONSIST OF: 1. Structured micturition history or questionnaire at each follow-up. 2. Structured physical examination with full bladder at least once during follow-up. 3. Micturition diary at each follow-up. 4. Pad test at each follow-up. 5. Uroflow at least once during follow-up. 6. Estimation of post-void residual urine at least once during follow-up. 7. Other urodynamic techniques are optional.
AppENDIx IV RECOMMENDATIONS OF THE INTERNATIONAL CONSULTATION ON INCONTINENCE: CONSIDERATIONS FOR SpECIFIC pATIENT GROUpS MEN WITH LUTS, INCLUDING INCONTINENCE • If treatment could change prostate volume, • •
measurements of volume should be performed before and after treatment. Consider stratifying patients by prostate volume. Whenever feasible, detrusor pressure/uroflow studies should be performed before and after treatment to document the presence and degree of change in bladder outlet obstruction.
WOMEN WITH LUTS AND INCONTINENCE • Data on hormonal status should be collected on •
•
•
•
women in all studies of incontinence and LUTS. At a minimum, data on vaginal parity should be collected on women in all studies. Additional obstetric history should be obtained as appropriate for individual studies. Studies of surgical treatment of incontinence (and other study types as appropriate) should include assessment for pelvic organ prolapse using the ICS staging system, the Pelvic Organ Prolapse Quantification (POP-Q) system. Outcomes (cure, failure, improvement) relating to symptoms and signs must be clearly defined at the onset of all studies. Complications and side effects may be included in outcomes but should be reported separately. Assessment of sexual function should be included in all studies.
FRAIL OLDER AND DISABLED pEOpLE • This is a heterogeneous population requiring
• •
a detailed study design and careful description of baseline clinical data if results are to be interpretable. There is a need for validation of all instruments and procedures used in incontinence research for the population of frail elderly patients. ‘Clinically significant’ outcome measures and relationships of outcome to socioeconomic costs are critically important to establish the utility of treating urinary incontinence in this population.
INCONTINENCE IN CHILDREN • We support the National Institutes of Health (NIH)
• •
statement calling for increased clinical research in children. All investigators that work with children should be aware of the details of the document and particularly the issues surrounding informed consent. Long-term follow-up is of critical importance in the pediatric population in order to ascertain the effect of a treatment on normal growth and development. Research is needed to develop standardized outcome measures including validated, age-specific symptom and disease-specific quality of life outcome measures.
NEUROpATHIC LOWER URINARY TRACT DYSFUNCTION • Detailed urodynamic studies are required for
•
•
•
classification of neurogenic lower urinary tract disorders in research studies because the nature of the lower urinary tract dysfunction cannot be accurately predicted from clinical data. Videourodynamic studies are preferred but not mandatory. Change in detrusor leak point pressure should be reported as an outcome as appropriate, and can be considered a primary outcome in addition to a symptom response. An area of high priority for research is the development of a classification system to define neurogenic disturbances. Relevant features would include the underlying diagnosis, the symptoms, and the nature of the urodynamic abnormality. It may sometimes by appropriate to group patients with urodynamically similar neurogenic bladder disorders of different etiologies in a clinical trial. 821
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However, great caution must be used if patients with progressive disease (e.g. multiple sclerosis) are grouped with patients having a stable deficit (e.g. traumatic spinal cord injury). LUTS, lower urinary tract symptoms.
REFERENCES 1. McDowell J, Newell C. Measuring Health: A Guide To Rating Scales And Questionnaires. New York: Oxford University Press, 1996; 10–36. 2. Blaivas JG. Outcome measures for urinary incontinence. Urology 1998;51(Suppl 2A):11–19. 3. Graham CW, Dmochowski RR. Questionnaires for women with urinary symptoms. Neurourol Urodyn 2002;21:473–81.
14. Larsson G, Victor A. Micturition patterns in a healthy female population studied with a frequency/volume chart. Scand J Urol Nephrol 1988;114:53–7. 15. Abrams P, Blaivas JG, Stanton SL et al. The standardization of terminology of lower urinary tract function. Scand J Urol Nephrol 1988;114(Suppl):5–19. 16. Hahn I, Fall M. Objective quantification of stress urinary incontinence: a short, reproducible, provocative pad weighing test. Neurourol Urodyn 1991;10:475–81. 17. Lose G, Gammelgard J, Jorgensen TJ. The one hour pad weighing test: reproducibility and the correlation between the test result, start volume in the bladder and the diuresis. Neurourol Urodyn 1986;5:17–21. 18. Fantl JA, Harkins SW, Wyman JF et al. Urinary incontinence in adults: acute and chronic management. Clinical Practice Guideline. Rockville, MD: United States Department of Health and Human Services, 1996; 1–65.
4. Sirls LT, Keoleian CM, Korman HJ, Kirkemo AK. The effect of study methodology on reported success rates of the modified Pereyra bladder neck suspension. J Urol 1995;85(Suppl 1):1732–5.
19. Shumaker SA, Wyman JF, Uebersax JS et al. Health related quality of life measures for women with urinary incontinence: the Incontinence Impact Questionnaire and the Urogenital Distress Inventory. Qual Life Res 1994;3:291–306.
5. Donavan J, Naughton M, Gotoh M et al. Symptoms and quality of life assessment. In: Khoury S, Wein A (eds) Incontinence: 1st International Consultation on Incontinence. Plymouth, UK: Health Publication, 1999; 296–331.
20. Nordling J, Abrams P, Ameda JT et al. Outcome measures for research in treatment of adult males with symptoms of lower urinary tract dysfunction. Neurourol Urodyn 1998;17:263–71.
6. Abrams P. A critique of scoring systems. Prog Clin Biol Res 1994;386:109–23.
21. Blaivas JG, Appell RA, Fantl JA. Definition and classification of urinary incontinence: recommendations of the Urodynamic Society. Neurourol Urodyn 1997;16:145–7.
7. Weber AM, Abrams P, Brubaker L et al. The standardization of terminology for researchers in female pelvic floor disorders. Int Urogynecol J Pelvic Floor Dysfunct 2001;12(3):178–86. 8. Leach GE, Dmochowski RR, Appell RA et al. Female stress urinary incontinence clinical guidelines panel. Summary report on the surgical management of female stress urinary incontinence. J Urol 1997;158:875–9. 9. Holroyd-Leduc JM, Straus SE. Management of urinary incontinence in women: clinical applications. JAMA 2004;291:996–9. 10. Blaivas JG, Appell RA, Fantl A et al. Standards of efficacy for evaluation of treatment outcomes in urinary incontinence: recommendations of the Urodynamic Society. Neurourol Urodyn 1997;16:145–7. 11. Payne C, Van Kerrebroeck P, Blaivas J et al. Research methodology in urinary incontinence. In: Wein A (ed) Incontinence: 2nd International Consultation on Incontinence. Plymouth, UK: Health Publication, 2002; 1045–77. 12. Wyman JF, Harkins SC, Choi SC et al. Psychosocial impact of urinary incontinence in women. Obstet Gynecol 1987;70:378–81. 13. Romanzi L, Blaivas JG. Office evaluation of incontinence. In: O’Donnell PD (ed) Urinary Incontinence. St Louis: Mosby, 1997; 475–9.
22. Lose G, Fantl JA, Victor A et al. Outcome measures in adult women with symptoms of lower urinary tract dysfunction. Neurourol Urodyn 1998;17:255–62. 23. Fonda D, Resnick NM, Colling J et al. Outcome measures for research of lower urinary tract dysfunction in frail older people. Neurourol Urodyn 1998;17:273–81. 24. National Institutes of Health (NIH) policy and guidelines on the inclusion of children as participants in research involving human subjects, Release Data: March 6, 1998, National Institutes of Health. Online. Available: http://grants.nih.gov/grants/guide/notice-files/ not98-024.html. 25. Wein AJ. Pathophysiology and categorization of voiding dysfunction. In: Walsh PC, Retik AB, Vaughan ED Jr, Wein AJ (eds) Campbell’s Urology, 7th ed. Philadelphia: WB Saunders, 1998; 917–26. 26. Ward KL, Hilton P. A prospective multicenter randomized trial of tension-free vaginal tape and colposuspension for primary urodynamic stress incontinence: two year followup. Am J Obstet Gynecol 2004;190:324–31. 27. Minassian VA, Al-Badr A, Pascali DU et al. Tension-free vaginal tape: do patients who fail to follow-up have the same results as those who do? Neurourol Urodyn 2005;24:35–8.
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28. Chaikin DC, Blaivas JG, Rosenthal JE et al. Results of pubovaginal sling for stress incontinence: a prospective comparison of 4 instruments for outcome analysis. J Urol 1999;162:1670–7. 29. Groutz A, Blaivas JG, Rosenthal JE. A simplified urinary incontinence score for the evaluation of treatment outcomes. Neurourol Urodyn 2000;19:127–35.
30. Groutz A, Blaivas JG, Hyman MJ et al. Pubovaginal sling surgery for simple stress urinary incontinence: analysis by an outcome score. J Urol 2001;165:1597–1600. 31. Chou EC, Flisser AJ, Panagopoulos G et al. Effective treatment for mixed urinary incontinence with a pubovaginal sling. J Urol 2003;170(2 Pt 1):494–7.
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55 Peri- and postoperative care Maria Vella, John Bidmead
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INTRODUCTION A great deal of a surgeon’s attention is naturally focused on the technical performance of an operation. Although surgical technique is a major factor influencing outcome, other factors such as appropriate patient selection, preoperative investigation and preparation, and postoperative care also have a major influence on the results of surgery. Most urogynecologic surgery is elective. Urinary incontinence and urogenital prolapse, although undeniably distressing, are rarely life threatening. Urogynecologic surgery can therefore be planned in advance and time is available for preparation, which can be used to improve the outcome of surgery. The elective nature of most urogynecologic surgery means that operative morbidity must be kept to a minimum. Adequate preparation and intervention to reduce surgical and anesthetic complications is mandatory, as is the provision of preoperative counseling.
PReOPeRaTIve CONsIDeRaTIONs Procedure selection and discussion of alternative therapies One of the most important factors governing the success of any gynecologic surgery is patient selection. This applies as much to the selection of procedure by the woman herself as it does to the selection of an operation for a patient by the surgeon. In gynecology, the type of surgery performed may have a profound influence on the emotional, psychological, and sexual well-being of a woman. It is, therefore, vital that, before proceeding to an irreversible surgical procedure, a woman should feel that she has had the opportunity to take part in the decision process. Information on the possible effects of surgery on physical, hormonal, reproductive, and sexual function should be provided. The possible effects of any pathology on these functions also need to be explored, to allow the pros and cons of surgery to be weighed. The full range of therapeutic measures available, both conservative and surgical, should be discussed to allow an informed choice. It is also important to give a realistic view of any possible complications, their likelihood and possible sequelae. A woman is much more likely to accept slight voiding difficulties after a continence procedure, for example, if this has been explained in advance. Explaining unanticipated difficulties ‘after the event’ can be fraught and is much more likely to lead to medicolegal action, often with unsatisfactory outcomes for both parties.
Patient selection It has often been said that the key to successful surgery lies not only with the technical skills of the surgeon but also with the ability to select cases appropriately. This means that the skill and experience of the surgeon should be used during consultation to help guide a woman in making the right choices about treatment.
Use of alternative therapies Time is also available to permit a number of alternative therapies to be tried before surgical intervention is undertaken. Recently, alternative conservative treatments for incontinence have become available that offer increased choice for those women unsuitable or unwilling to undergo surgery. Pelvic floor physiotherapy, with or without electrical stimulation, remains the mainstay of conservative management of genuine stress incontinence (GSI). Many studies have shown excellent results, although it is clear that closely monitored therapy by a physiotherapist interested and experienced in this area is necessary. Vague instructions to perform pelvic floor exercises (PFE) are ineffective and may even be counterproductive: fewer than 70% of women are able to perform these exercises correctly without tuition.1 The use of PFE was first described by Kegel in 1948.2 In a series of studies Kegel was able to demonstrate an impressive success rate of 84% in women with stress incontinence. More recent studies have confirmed good long-term results.3,4 Although there are no published data to suggest that prior effective pelvic floor physiotherapy improves the eventual outcome of surgery, this is the impression of many urogynecologists. As the success rate of physiotherapy is good and its influence on surgical outcome may be beneficial, it is recommended that surgical intervention is not resorted to until a woman has had an adequate course of physiotherapy. A new drug has recently been developed, specifically for the treatment of stress incontinence. Duloxetine is a potent and balanced serotonin and noradrenaline inhibitor (SNRI) that enhances urethral sphincter activity via a centrally mediated pathway.5 The evidence reported to date suggests that duloxetine offers an effective alternative to surgery and may be complementary to the use of PFEs in the initial management of women with stress incontinence.6,7 It is given in a 40 mg dose twice daily. A number of mechanical devices have also become available recently. These may be useful in a number of situations: for example, they may be helpful in the
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short term, allowing women to regain continence while undergoing physiotherapy or while awaiting surgery.8 Some women, particularly those with mild GSI only on exercise, may choose to use them as an alternative to surgery (e.g. during aerobics classes or tennis). Lastly, there remains a group of women for whom surgery has failed and where further surgery is inadvisable: women in this group are able to use devices to regain control or manage their incontinence. Devices vary, as do the women who use them, and so it is often worth trying more than one. Prosthetic devices for the control of prolapse are also available. Those most commonly used today are a silicon ring pessary which can control vaginal prolapse very effectively if pelvic floor tone is good. Uterovaginal prolapse may be more effectively controlled with a shelf pessary. Although these pessaries may not be suitable for younger women, they can be useful for older women wishing to avoid surgery. Use of such devices/medical therapy while awaiting surgery can improve a woman’s quality of life in the short term; they may also be advantageously employed while a woman is undergoing a course of physiotherapy and while coming to a final decision regarding surgery.
Psychological preparation for surgery Whereas it may be considered desirable to bring any intervention to a satisfactory conclusion as rapidly as possible, the very nature of this surgery allows time for both surgeon and patient to consider all the available options and select the most appropriate. Time is also available to consider factors that may improve the likelihood of a satisfactory outcome and to take measures to reduce the possibility of adverse outcomes. Finally, the effect of surgery on lifestyle can be considered and planning for any period of convalescence initiated. It is well documented that only 10% of verbal information given during a consultation is remembered by the patient afterwards. This can be substantially increased by the use of written information given to patients during a consultation.9 Patient information leaflets can be particularly useful if they have been written locally to reflect practice in a particular unit. Written information leaflets can also be re-read at leisure by women, allowing them time to consider treatment options and think of any questions that may be addressed at subsequent consultations. Although the primary objective of patient information leaflets is not to save the surgeon’s time, it would be impractical to discuss all aspects of all the treatment options at a single consultation.
Although not a primary objective, the use of such written information and documentation of this may be particularly useful medicolegally. Many medicolegal disputes arise because patients complain of sequelae about which they feel they were not warned. It is often the case that such problems were discussed but that this was not among the 10% of the consultation remembered by the patient. The documentation of written information being given may be useful in such circumstances.
Use of a nurse counselor Involvement of nursing staff may be particularly beneficial. Increasingly, a number of units are offering a preoperative counseling service. This is often provided by suitably experienced and trained nursing staff and allows discussion of any anxieties in a more relaxed and leisurely fashion than is possible on a traditional preoperative ward round. It is particularly helpful if a woman has the opportunity to discuss a procedure with an experienced member of the nursing team preoperatively so that she can discuss aspects of surgery that she may have felt unable to discuss with the surgical staff. Nursing staff are also appropriately placed to give information about pre- and postoperative care, catheter regimes, drains, dressings, and ward routine. Ideally, the nurse should be one of the team providing care on the ward. As previously stated, because most urogynecologic surgery is elective, any investigations can be carried out in advance of any proposed intervention and plans can be modified as a result. There should be no need for a procedure to be performed under conditions of undue stress and there should be no hesitation in deferring an operation until an appropriate time available on a theater list, for example. If a procedure is felt to be inappropriate, further investigations necessary or the patient’s condition not optimal, then surgery should be deferred. Finally, the surgeon has the ultimate sanction and, if it is felt that an intervention is inappropriate or not in a patient’s best interest, then (after appropriate explanation) it may be wise to refer back to the general practitioner or suggest a further opinion, or investigations. Although this may seem to be an extreme measure, it is preferable to continuing on a course of action that may have untoward results for both patient and doctor!
Physical preparation for surgery Fitness Before undergoing any surgical procedure it is essential that a woman is as fit, physically, as possible. The elec827
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tive nature of most urogynecologic procedures allows surgery to be deferred if any intercurrent illness has reduced a woman’s fitness. In addition to exercising the pelvic floor muscles, a program of exercise may be beneficial in reducing morbidity and speeding up postoperative recovery. Preoperative exercise will also enhance weight loss if this is a concern. The physiotherapist is in an ideal position to advise a woman on preoperative exercise.
(500 mg three times daily) alone or in combination with tranexamic acid (1 g four times daily).10 Gonadotropin-releasing hormone (GnRH) analogs may be useful, with or without ‘add-back’ hormone replacement therapy (HRT), in extreme cases to suppress menstruation prior to surgery.11 GnRH analogs have also been shown to be useful in reducing the volume of uterine fibroids prior to hysterectomy or myomectomy, and in reducing blood loss at myomectomy or hysterectomy.12
Smoking In addition to its well known effects on general health, smoking increases the risk of postoperative problems, such as thromboembolism (see ‘Thromboembolism and thromboprophylaxis’, below). Pulmonary atelectasis and subsequent pneumonia is a particular risk following general anesthesia and this is substantially increased by smoking. In addition, chronic cough is a factor in development or recurrence of urogenital prolapse. For these reasons it is worth impressing on women the importance of stopping smoking preoperatively.
Weight It comes as a surprise to many women that obesity is a major cause of surgical difficulty. In addition to the technical difficulties faced by the surgeon, obesity also increases virtually all perioperative risks. For the anesthetist, intravenous access, induction of anesthesia and intubation are all more difficult. Postoperatively, obesity increases the risk of thromboembolism, wound infection, hematoma, and respiratory infection. Although there is little published evidence, it appears that obesity, by raising intra-abdominal pressure, increases the recurrence of urogenital prolapse. For these reasons the obese woman should be encouraged to lose weight prior to surgery. Rather than giving a general instruction to ‘lose some weight’, it is more effective to set a reasonable target to be achieved. Referral to a dietitian is often helpful and appetite suppressants may be useful in the short term.
Anemia Anemia may well be a problem in women presenting for urogynecologic surgery with concomitant menorrhagia. As well as reducing the safe margin for intraoperative blood loss, anemia increases the risk of postoperative wound infection and delays full recovery. Mild-to-moderate anemia may respond to simple oral iron replacement in the form of ferrous sulfate (200 mg daily). Other measures to reduce menstrual loss and allow replenishment of iron stores include the use of mefenamic acid
Bowel preparation It is worth paying attention to preoperative bowel preparation. In women with normal bowel habit undergoing routine surgery, complicated preoperative regimens are unnecessary. However, it is worth ensuring an empty rectum prior to surgery as this may avoid postoperative discomfort and constipation. A single mild aperient such as sodium lauryl sulfoacetate enema given the evening before surgery should suffice. Women undergoing pelvic reconstructive surgery, such as colposuspension or vaginal repair, may benefit from more thorough bowel preparation (to prevent a loaded rectum interfering with surgery) and a regimen of postoperative laxatives (to reduce postoperative straining that may compromise the repair). A sachet of sodium picosulfate taken the afternoon before surgery will ensure an empty rectum; postoperatively, a stool softener such as lactulose will prevent discomfort and straining due to constipation. Prior to undertaking operations which require complete access to the sacral promontory and where mobilization of the rectum may be required, more thorough bowel preparation is necessary. A full rectum may make the performance of sacrocolpopexy difficult or impossible. A low-residue, low-fiber diet for 48 hours prior to surgery, together with a half-sachet of sodium picosulfate daily, will help to ensure an empty rectum. A disposable phosphate enema can be given preoperatively to women with a history of constipation.
Preoperative investigations The majority of preoperative investigations should be performed on an outpatient basis with the results available for review prior to admission to allow time for any remedial action to be taken. An exhaustive list of preoperative investigations is beyond the scope of this chapter and should be tailored to an individual woman’s general health and any existing medical problems. Basic preoperative investigations may include hematologic and biochemical investigations, urinalysis, electrocardiography (ECG), and imaging.
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Hematologic investigations Every woman should have a full blood screen performed to include a hemoglobin, hematocrit, white cell count and differential, and hemoglobinopathy screen where appropriate. For all procedures where there is a significant risk of transfusion, typing should be performed and serum retained for cross-matching at short notice.
Biochemical investigations For the majority of women, no particular biochemical investigations are necessary. However, in women with pre-existing disease such as hypertension or diabetes, biochemical screening may be necessary. Renal function tests should be performed if there is any suspicion of renal failure or ureteric obstruction.
Urinalysis Simple ward urinalysis is useful to exclude glycosuria and infection. Urine should be tested for beta human chorionic gonadotrophin if there is any possibility of pregnancy.
ECG ECG traces are not required for most fit women undergoing surgery, but may be required if there is a history of hypertension or cardiac disease. Most anesthetic departments now have guidelines for preoperative ECG testing.
ried out prior to admission. The most appropriate type of anesthetic (general, regional or local) should also be selected. The advice of the relevant specialist should also be sought in the case of significant existing medical conditions. The specialist team will be able to give advice on preoperative preparation and therapy in the immediate postoperative phase.
Informed consent Before embarking upon any surgical procedure it is imperative that adequate informed consent has been obtained and documented. Increasingly, medicolegal claims involving the issue of consent are being pursued and, as an aspect of good practice as well as risk management, it is important to understand the ethical and legal issues surrounding the concept of informed consent. When considering the issue of informed consent, the British courts use what is known as the Bolam principle. This was developed in the case Bolam v Friern Hospital Management Committee, [1957] 1 Wlr 582. This states that ‘a Doctor is not negligent when he acts in accordance with a practice accepted as proper by a responsible body of medical men skilled in that particular art’. Consent is difficult to define succinctly but requires three elements: volition, capacity, and knowledge.
Volition Imaging The roles of plain and contrast radiology, computed tomography, ultrasonography, and magnetic resonance imaging are discussed in the relevant sections of this book. Routine preoperative chest radiography is now rarely required except in women with cardiac or pulmonary disease. Most anesthetic departments now have guidelines for preoperative chest radiography. An intravenous urogram should be performed if an anatomic abnormality suggests that the course of the ureters may be aberrant, if malignancy is suspected or in major prolapse where ureteric obstruction is a possibility.
anesthetic pre-assessment Preoperative assessment by the anesthetist is essential to ensure the safe and smooth running of the list. It is good practice for the patient to be seen the evening before surgery with the notes and results of investigations available. Where major medical problems exist, or if there have been previous anesthetic problems such as difficult intubation, anesthetic consultation may be car-
Volition is based on the principles of self-determination and a respect for individual integrity. This requires that a woman is able to make a decision regarding consent without undue pressure from a third party, either a relative or a member of the medical staff. Legally, a spouse or relative cannot give or withhold consent on a woman’s behalf, although it is considered good practice to involve the spouse, particularly where the treatment proposed will affect fertility.
Capacity Capacity to consent requires that a woman has sufficient intellect to appreciate information discussed prior to giving consent, and the mental capacity to appreciate the risks and the consequences of the operation proposed. This is a particularly difficult area when dealing with women whose mental capacity is limited as a result of either intellectual handicap or psychiatric illness. In these situations it is important to seek additional professional opinion and to seek legal clarification where time allows. The situation when dealing with minors (in the UK under 16 years of age) is another delicate area. In gen829
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eral, both the parents and child would be involved in giving informed consent. However, in the UK the circumstances of minors giving consent without parental approval or knowledge has recently been clarified in the case of Gillick v West Norfolk and Wisbech Health Authority, [1985] 3 All ER 402, in which the House of Lords ruled that parental rights give way to a child’s right to make her own decision upon sufficient maturity to understand the nature and consequences of that decision. This has led to the concept of ‘Gillick’ competency, where a medical practitioner must make a clinical judgment as to whether a minor has sufficient maturity to give informed consent. Although this has clarified the situation in the UK, it is important that practitioners are aware of the law regarding minors in their own country or state.
Knowledge The third aspect of consent is that of knowledge. This implies that a woman should have sufficient information concerning the diagnosis and prognosis to make a reasoned decision regarding treatment. A woman must also be given sufficient information about alternative treatments and also any reasonably foreseeable adverse effects of the proposed treatment. This is another difficult area, as women’s ability to understand the technicalities of a medical condition and its treatment may vary. Similarly, it would be unreasonable to describe in depth every conceivable complication arising from surgery. This area was clarified in the case of Sidaway v Board of Governors of Bethlem Royal Hospital, [1985] 1 All ER 643, in which the courts applied the Bolam principle to information about potential risks. In general, the information given should conform to that given by a responsible body of medical opinion. Those risks that are commonly associated with a procedure should certainly be discussed; more uncommon complications need not be. It is left to the medical practitioner to decide on an individual patient’s ability or wish to discuss these issues. The need to discuss complications also varies with their potential severity and implications for future health. This means that it is essential to discuss the possibility of a complication that may be relatively remote but which would have a major impact on a woman’s life. A good example of this is to perform hysterectomy to control hemorrhage at myomectomy; although this is well reported it is, in fact, a relatively uncommon occurrence. However, as myomectomy is primarily performed to preserve fertility and the loss of the uterus has such major implications for a woman wishing to bear future children, the remote possibility of this should always be discussed and recorded beforehand.
Oophorectomy performed without specific consent has been the subject of a number of recent court actions – both civil cases for negligence and criminal cases for assault. It is essential that the possibility of oophorectomy, either as a technical necessity or for an unforeseen indication, is discussed and documented. The risks of surgical complications such as bladder trauma requiring catheterization and wound infection should also be discussed, as appropriate. The issue of informed consent has become clearer in recent years, with some guidance from the cases cited above. The final decision regarding a woman’s capacity to give consent and her ability to understand the information given is left to the professional judgment of the surgeon. Most practitioners will use a standard consent form and record any particular information on this. However, the concept of informed consent embraces more than just a signature and so it is important that good records are kept of any discussion and information given prior to informed consent.
Thromboembolism and thromboprophylaxis Thromboembolism accounts for around 20% of perioperative hysterectomy deaths.13 As prophylaxis has been shown to be effective in reducing the risk of thromboembolism, women undergoing gynecologic surgery should be assessed for clinical risk factors and overall risk of thromboembolism, and should receive prophylaxis according to the degree of risk: this is highest for surgery associated with malignancy, less in abdominal hysterectomy, and lowest for vaginal hysterectomy.14 Other risk factors associated with the disease or surgical procedure include infection, polycythemia, and heart failure. Risk factors associated with the patient are age over 37 years, obesity, previous deep vein thrombosis (DVT), blood group other than O, and the presence of congenital or acquired thrombophilias. Assessment of these risk factors allows categorization into low-, medium- or high-risk categories. The Royal College of Obstetricians and Gynaecologists (RCOG) has issued guidelines on the use of thromboprophylaxis in gynecologic surgery.15 Patients deemed at low risk require attention to hydration and early mobilization only. Those at moderate risk should receive specific prophylaxis with either low molecular weight heparin (doses varying depending on the heparin used, for example enoxaparin and tinzaparin) or intermittent pneumatic compression. Patients deemed to be high risk should be given heparin as above and in addition be fitted with graduated compression stockings.
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The use of heparin is associated with a small increase in the risk of wound hematoma but no significant fall in postoperative hemoglobin or increase in the need for blood transfusion. In many units these guidelines are exceeded and heparin, intermittent compression, and compression stockings are used for all but minor day case procedures. In patients who are high risk, a hematologist is actively involved in the management.
Combined oral contraceptive pill The combined oral contraceptive (COC) pill has been implicated as a risk factor for postoperative thromboembolism. A study by Vessey et al.16 showed a modest increased risk in users of the COC. Recent RCOG guidelines suggest that the COC should be discontinued at least 4 weeks before major surgery when immobilization is anticipated. Hormonal methods do not need to be discontinued before minor surgery without immobilization. When indicated, the COC should be discontinued at least 4 weeks before surgery and alternative contraception discussed.
Hormone replacement therapy Recent studies have suggested an increased risk of venous thrombosis in women taking hormone replacement therapy (HRT). There is at present no evidence associating HRT, at physiologic levels, with an increase in postoperative DVT.17 Therefore there seems little to be gained by stopping HRT prior to surgery and exposing the patient to a recurrence of perimenopausal symptoms. However, routine assessment of risk and appropriate prophylaxis should be undertaken, as many patients in this age group will have other, more significant, risk factors for thrombosis.18 Atrophic changes in the vaginal skin can cause difficulty during vaginal reconstructive surgery and compromise postoperative wound healing. Preoperative treatment with topical estrogen for 6 weeks is worthwhile and carries little risk.
antibiotic prophylaxis in both abdominal and vaginal hysterectomy.5,6 This reduction was also seen in a study of antibiotic prophylaxis in both general and gynecologic surgery.7 Adverse reactions to prophylactic antibiotic regimens are reported rarely, with an incidence of less than 1%. The cost of antibiotic cover is outweighed by the considerable economic savings, most notably the reduction in inpatient stay. The clinical and economic evidence clearly demonstrates the effectiveness of routine perioperative antibiotic prophylaxis. The choice of antibiotic appears to be between a broad-spectrum penicillin or cephalosporins, either alone or in combination with an aminoglycoside or metronidazole. There appears to be little difference between the penicillins and cephalosporins. The studies showing the greatest reduction in postoperative infection are those when an aminoglycoside was used as part of the combination. As the pattern of microbial resistance varies, the most appropriate combination of agents should be selected after consultation with the local microbial service, and should be reviewed at regular intervals. The development of microbial resistance is a particular concern. Given the clear advantages of routine chemoprophylaxis, it is sensible to continue this; however, to reduce bacterial resistance, short courses should be used with routine ‘first line’ agents. Newer agents should be reserved for treatment of established antibiotic-resistant infections. As the aim of chemoprophylaxis is the prevention rather than the treatment of established infection, regimens used should aim to achieve a high tissue concentration of the chosen antibiotics at the time of surgery when inoculation of the wound occurs. However, as this would mean the administration of intravenous antibiotics some hours prior to surgery, a more practical compromise is to give the first dose at the time of induction of anesthesia, with a further two doses in the first 24 hours postoperatively.
POsTOPeRaTIve PROBLeMs
Prophylactic antibiotics
Immediate postoperative care
Prophylactic antibiotics have been clearly shown to reduce the risk of postoperative wound infection. The use of perioperative antibiotic prophylaxis has been shown, in a systematic review, to reduce markedly the risks of febrile morbidity after elective and emergency cesarean section.19 A similar reduction in infectious morbidity has been shown with the use of broad spectrum
Normal clinical monitoring of postoperative patients with pulse and blood pressure recording is adequate for most gynecologic patients. In high risk cases, the hourly urine output is a sensitive measure of peripheral circulation. When massive blood loss occurs, which is rare in a urogynecologic setting, a consumptive coagulopathy 831
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may develop as all coagulation factors are exhausted. It is therefore important to monitor the coagulation status of the patient repeatedly during resuscitation and if an abnormality develops, expert advice from a hematologist should be sought. One way of controlling blood loss is the use of tranexamic acid by intravenous infusion. Tranexamic acid impairs fibrin dissolution and is sometimes used in an acute blood loss setting to try to prevent the development of consumption coagulopathy. Occasionally, embolization of actively bleeding blood vessels using intervention radiology techniques may be an effective alternative to surgery. It requires a skilled team of interventional radiologists who are able to provide an emergency service. This generally avoids very difficult surgery in very sick patients. It is often the more reliable and the faster method of controlling the bleeding. Decision regarding re-exploration may be difficult and the advice and help of the most experienced person should be sought. As a rule of thumb, the sooner after the surgery the bleeding presents, the more likely that re-exploration will identify a single obvious bleeding vessel.
anticipation of postoperative voiding problems Voiding difficulties may occur acutely following any pelvic surgery; after continence procedures in particular, voiding difficulties may persist in the medium or long term. The importance of relieving acute urinary retention cannot be overstated. Acute overdistension of the bladder leads to damage of the detrusor syncytium with ischemic damage to the postsynaptic parasympathetic fibers. This may result in insidious deterioration of detrusor function and, later, the onset of voiding dysfunction.20 A number of factors that increase the risk of acute postoperative retention have been identified, including increased age, long operation time, high doses of opiate analgesia and patient-controlled analgesia, together with large amounts of intravenous fluids.21 In view of the possible long term sequelae of acute overdistension of the detrusor, it is important that steps are taken to prevent this. Postoperative indwelling urethral catheterization should be used following surgery, although some authors prefer intermittent catheterization.22 In women judged clinically or urodynamically to be at high risk of retention, suprapubic catheterization may be preferable; this may be performed easily at the time of surgery and avoids the need for repeated urethral catheterization. Following removal of a catheter, close monitoring of fluid balance should be continued to prevent recurrent retention.
As previously stated, voiding difficulties are particularly common following continence procedures initially and may persist for a variable time following surgery. After colposuspension they are particularly common in women with preoperative flow rates of less than 15 ml/s or maximum voiding detrusor pressure below 15 cmH2O. Between 12 and 25% of women are reported to suffer delayed voiding postoperatively and 11–20% have increased residual volumes and reduced flow rates when measured at 3 months postoperatively.23 In a study by Smith and Cardozo24 of 100 women undergoing colposuspension, 21% experienced significant voiding difficulties for up to 6 months following their surgery, although this persisted beyond 6 months in only 2%. Hilton and Stanton25 performed postoperative urodynamic studies on women 3 months after colposuspension and found highly significant reduced flow rates and increased voiding pressure. Voiding problems are also common following needle suspension procedures, although published figures vary. Ashken et al.26 noted no significant changes in flow rate, voiding pressures or urine residual volume in a study of 60 women after successful Stamey procedure; Hilton and Mayne27 studied 100 women undergoing Stamey procedure and found increased functional urethral length and improved pressure transmission but no significant changes in resting urethral profile or voiding pressure; Mundy28 found a higher incidence of voiding difficulties and irritative symptoms compared to colposuspension. Sling procedures are particularly prone to causing voiding difficulty as their mechanism of action is to increase outflow resistance.25,29 Whichever continence procedure is to be performed, it is important that women are counseled adequately. The need for suprapubic catheterization, which may occasionally be prolonged, should be carefully explained preoperatively. The occasional need for clean intermittent self-catheterization (CISC) should be discussed. When voiding difficulty is predicted by urodynamic studies, it may be worth teaching CISC prior to surgery. Even though perhaps only a minority of these women will need to self-catheterize, from the psychological standpoint short-term voiding problems are much better dealt with when they have been anticipated.
enterocele and rectocele formation The formation of enteroceles and rectoceles is thought to occur as a result of elevation of the anterior vaginal wall creating a posterior defect and causing intra-abdominal pressure to be transmitted directly to the posterior
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vaginal wall. The incidence of postoperative posterior compartment defects is estimated to be 7–17%.30 It is important that this is discussed with women preoperatively, together with the potential need for interval posterior vaginal repair.
6. Duff P, Park RC. Antibiotic prophylaxis in vaginal hysterectomy: a review. Obstet Gynecol 1980;55(Suppl):193–202.
De novo detrusor instability
8. Choe JM, Staskin DR. Clinical usefulness of urinary insert devices. Int Urogynecol J 1997;8:307–13.
It has been shown that detrusor instability (DI) arises de novo in 12–18.5% of women postoperatively,31 and occurs more commonly following previous continence surgery. It seems likely that a number of cases reflect preexisting DI not detected at cystometry preoperatively. In addition, it has been suggested that damage to the autonomic nerve supply occurs during lateral displacement of the bladder during surgery.32 The presence of postoperative DI should be excluded with urodynamic investigations. Where DI is present, a trial of anticholinergic therapy should be carried out. This will ensure that symptoms of frequency and urgency can be controlled and that the woman is able to tolerate the side effects of anticholinergic therapy if it is required postoperatively. Such women should be warned that symptoms of frequency and urgency may persist after surgery for stress incontinence and this should be recorded in the case notes.
9. Collings LH, Pike LC, Binder A et al. Value of written information in a general practice setting. Br J Gen Pract 1991;41:466–7.
CONCLUsIONs Adequate preparation for surgery has an important role in ensuring an optimal outcome and reducing morbidity. The elective nature of most urogynecologic surgery allows time to ensure that all women are well prepared, both psychologically and physically, before undergoing the chosen operation.
ReFeReNCes 1. Laycock J. The Investigation and Management of Urinary Incontinence in Women. London: RCOG Press, 1995. 2. Kegel AH. Progressive resistance exercise in the functional restoration of the perineal muscles. Am J Obstet Gynecol 1948;56:238–48. 3. Tapp AJS, Hills B, Cardozo L. Who benefits from physiotherapy? Neurourol Urodyn 1988;7:259–65. 4. Bo K, Talseth T. Five year follow-up of pelvic floor exercise for the treatment of stress urinary incontinence. Neurourol Urodyn 1994;13:374–6. 5. Hemsall DL, Molly C, Heard RA et al. Single dose prophylaxis for vaginal and abdominal hysterectomy. Am J Obstet Gynecol 1987;157:498–501.
7. Regiori A, Ravera M, Coccozza E et al. Randomised study of antibiotic prophylaxis for general and gynaecological surgery from a single centre in rural Africa. Br J Surg 1996;83:356–9.
10. Bonnar J, Sheppard BL. Treatment of menorrhagia: a randomized controlled trial of etamysylate, mefenamic acid and tranexamic acid. Br Med J 1996;313:579–82. 11. Thomas EJ, Okuda M, Thomas NM. The combination of a depot GnRH analogue and cyclical HRT for dysfunctional uterine bleeding. Br J Obstet Gynaecol 1991;98:1155–9. 12. Sternquist M. Treatment of uterine fibroids with GnRH analogues prior to hysterectomy. Acta Obstet Gynecol Scand Suppl 1997;194:94–7. 13. Department of Health Report of the National Enquiry into Perioperative Deaths. London: HMSO, 1993. 14. Bergquist D. Postoperative Thromboembolism. London: Springer-Verlag 1983; 106–7. 15. Royal College of Obstetricians and Gynaecologists. Report of RCOG Working party on prophylaxis against thromboembolism in gynaecology and obstetrics. London: RCOG, 1995. 16. Vessey MP, Mant D, Smith A, Yeates D. Oral contraceptives and venous thromboembolism. Br Med J 1986;292:526–31. 17. Carter CJ. Thrombosis in relation to oral contraceptives and hormone replacement therapy. In: Greer IA, Turpie AAG, Forbes CD (eds) Haemostasis and Thrombosis in Obstetrics and Gynaecology. London: Chapman and Hall, 1992; 371–88. 18. Lowe G, Greer I, Cooke T et al. Risk and prophylaxis for venous thromboembolism in hospital patients. Br Med J 1992;305:567–74. 19. Smaill F. Prophylactic antibiotics in caesarean section (all trials). In: Keirse MJNC, Renfrew MJ, Neilson JP, Crowther C (eds) The Cochrane Pregnancy and Childbirth Database, Issue 2. Oxford: Oxford University Press, 1994. 20. Osborne JL. Urodynamics and the Gynaecologist. Alec Bourne Lecture. London: RCOG Press, 1981. 21. Tammela T, Konturri M, Lukkarien O. Postoperative urinary retention 1. Incidence and predisposing factors. Scand J Urol Nephrol 1986;20:197–201. 22. Smith NGK, Murrant JD. Postoperative urinary retention in women: management by intermittent catheterization. Age Ageing 1990;19:337–40. 23. Stanton SL, Cardozo LD, Williams JE et al. Clinical and
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urodynamic features of failed incontinence surgery in the female. Obstet Gynecol 1978;51:515–20. 24. Smith RN, Cardozo L. Early voiding difficulties after colposuspension. Br J Urol 1997;160:911–4. 25. Hilton P, Stanton SL. A clinical and urodynamic assessment of the Burch colposuspension for genuine stress incontinence. Br J Obstet Gynaecol 1983;90:934–9. 26. Ashken MH, Abrams PH, Lawrence WT. Stamey endoscopic bladder neck suspension for stress incontinence. Br J Urol 1984;56:629–34. 27. Hilton P, Mayne C. The Stamey endoscopic bladder neck suspension: a clinical and urodynamic investigation including actuarial follow up over four years. Br J Obstet Gynaecol 1991;98:1141–9.
28. Mundy AR. A trial comparing the Stamey bladder neck suspension with colposuspension. Br J Urol 1983;55:687–90. 29. Beck RP, McCormack RN. Treatment of urinary stress incontinence with anterior colporrhaphy. Obstet Gynecol 1982;59:269–74. 30. Burch JC. Coopers ligament urethrovesical suspension for urinary stress incontinence. Am J Obstet Gynecol 1968;100:764–72. 31. Alcalay M, Monga A, Stanton SL. Burch colposuspension: a 10–20 year follow-up. Br J Obstet Gynaecol 1995;102:740–5. 32. Cardozo LD, Stanton SL, Williams JE. Detrusor instability following surgery for GSI. Br J Urol 1979;58:138–42.
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56 Synthetic materials for pelvic reconstructive surgery Mark Slack
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INTRODUCTION Pelvic organ prolapse and urinary incontinence are common conditions affecting thousands of women worldwide. One study indicated that 11.1% of women aged 20 years will undergo an operation for prolapse or incontinence by the age of 60. Of this group, a staggering 30% will require reoperation for the condition.1 There are indications that the rates of pelvic organ prolapse (POP) surgery are increasing.2 As a result of these figures, together with a perception among the scientific community that the traditional vaginal surgical approach to POP may have limited success, there has been a move to correction with abdominal procedures.3 Crucial to the success of abdominal procedures has been the utilization of synthetic materials to help with the provision of durable support. The ideal properties of a synthetic mesh to be placed in the body are that it should be inert, resistant to infection, pliable and biocompatible, and that it should maintain mechanical integrity. Additionally, it must be easily fabricated and sterilizable. The perfect synthetic material for placement in the body has yet to be discovered. However, significant strides have been made, leading to the increasing availability of materials that match up to the properties described above. There are, however, concerns that the use of synthetic materials in gynecologic surgery could be associated with significant morbidity, especially if surgeons are not familiar with the principles behind their use and the properties of the individual materials.
HISTORY The use of synthetic mesh in surgery is not new. Some of the earliest descriptions involve the use of a tantalum mesh for the closure of chest wall defects.4 Although initial results were encouraging, there was fragmentation and disintegration of the mesh, resulting in extrusion of fragments, draining sinuses, and painful wounds.5 Teflon (polytetrafluoroethylene, PTFE) was thought to be a promising mesh because it appeared to be covered completely by granulation tissue. It also appeared to withstand infection. However, it proved too weak and developed fraying. To increase its strength it was more tightly woven, and although this did increase tensile strength, it required removal when infected. It was concluded that because of the proximity of the fibers, drainage was prevented and granulation tissue could not grow through the interstices.6 In a series of animal experiments, Usher and Gannon compared loose and tightly woven Teflon with Marlex (polypropylene) mesh.7 Little tissue ingrowth was noted with the Teflon
mesh as opposed to good fibrous infiltration into and through the Marlex mesh. Adhesions to bowel and omentum were noted. Contemporaneously, the vascular surgery community identified that the ingrowth of tissue is determined by the porosity of the graft material.8 Surgical mesh made of polypropylene became available from 1962. It was noted to be sterilizable without loss of its properties.9 Soon after, the makers of Marlex (Ethicon Ltd, Edinburgh) produced a new mesh made of polypropylene (Prolene) and one made of polyester (Mersilene). Surgeons experienced good results in the surgery for stress urinary incontinence (SUI) using the Aldridge sling.10 Because of the morbidity associated with graft harvesting, surgeons soon started experimenting with sling operations that utilized a synthetic sling. The first to be described was probably by Bracht in 1951 where a nylon cord was used.11 In the United Kingdom, Chassar Moir – on reporting a new operation using Mersilene mesh – encouraged the use of the material in operations for the treatment of SUI.12 This publication made no mention of the possible complications associated with the use of synthetic materials. The procedures were not without complications, with reported erosion rates of between 2 and 16% and the need to revise or remove the sling in between 2 and 35% of cases.13 General dissatisfaction with the procedure led to the abandonment of the operation by most surgeons in the UK. Following the success with the use of synthetic materials in the ‘tension-free’ surgical management of inguinal hernias, interest in the use of these materials in SUI surgery and POP surgery was renewed.14 The publication of articles on the tension-free vaginal tape (TVT) procedure, and the widespread marketing that accompanied the launch, led to the rapid introduction of this operation.15,16 Subsequent 7-year data on safety are now available for the TVT.17 Unfortunately, success with this product has led to the development of a range of procedures using a variety of tapes for the treatment of SUI and POP. Most of these new procedures lack any real or substantive data for their safety or success.
SYNTHETIC MESH FOR USE IN HUMAN SURGERY There are numerous differences in the various mesh materials. These occur as a result of the different ways of creating the mesh and by the substance from which they are created Artificial materials used for surgical prostheses are divided into whether they are biologic or synthetic (Fig. 56.1). Synthetic meshes are further classified into
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Prothesis
Biological
Allografts
Xenografts
Synthetic
Autologous
Absorbable
Nonabsorbable
Figure 56.1. Categorization of surgical prostheses for incontinence and prolapse. Cardoza Fig 56.1
whether they are absorbable or non-absorbable (Fig. 56.2).
Absorbable mesh Limited data are available on the use of absorbable mesh in urologic or gynecologic surgery. On first principles it is probably an unsatisfactory prosthesis as it has been demonstrated that adequate fibrous tissue incorporation does not occur before hydrolysis of implanted polyglactin mesh.18 In this animal model, which compared abdominal wall defect repair with an absorbable mesh versus a non-absorbable mesh, it was demonstrated that after 12 weeks 25% of the animals in the absorbable group had demonstrable gross hernias compared to none in the animals with synthetic repairs. A similar finding was demonstrated by another group.19 Two clinical studies have produced conflicting results from randomized trials comparing standard surgery for prolapse with surgery utilizing surgical prostheses: the first study showed an advantage when using mesh,20 the second study did not.21
Synthetic
Absorbable
Polyglactin
Polyglycolic acid
Non-absorbable
Multi
Mono
Mixed
Vypro
Vypro II
Figure 56.2. Categorization of synthetic surgical prostheses Cardoza Fig 56.2 for the treatment of incontinence and prolapse.
Corrective surgery for abdominal wall defects has been used as a surrogate for other indications for materials evaluation. Obviously surgery for abdominal wall hernias is very different from prolapse and incontinence work. Although synthetic grafts woven from rapidly hydrolyzed materials such as vicryl may be inadequate, there may be a place for the use of meshes created from materials with a longer life such as polydioxanone (PDS). An absorbable mesh which remains in place long enough for a significant three-dimensional fibrous ingrowth to occur remains an aspirational goal. With current knowledge the use of absorbable mesh cannot be recommended for reconstructive or incontinence surgery.
Non-absorbable mesh This represents a complex area dependent on an intricate knowledge of the science behind the technology. This chapter will attempt to give an overview of the science behind the synthetic, non-absorbable mesh materials.
POLYMER TECHNOLOGY Most of the synthetic meshes are plastics categorized by their chemical nature, the polymerization process that forms them, and their processibility. The manufacture involves procuring the raw materials, synthesizing the basic polymer, compounding the polymer into a useful material for fabrication, and then molding or shaping it into its final form. Originally, most plastics were made from resins derived from vegetable matter such as cellulose, which is derived from cotton. The initial unit produced is the monomer. The production of nylon was originally based on coal, air and water, although most such products are now derived from petrochemicals. The chemical nature of a plastic is defined by the monomer. This divides them into categories such as acrylics, styrenes, vinyl chloride, polyesters, polyurethanes, polyamides, polyethers, acetals, phenolics, cellulosics, and amino resins. The first stage in manufacture is polymerization. This is either a condensation reaction (nylon, polyurethane and polyester) or an addition reaction (polyethene, polypropene and polystyrene). Addition polymers have larger molecular weights than the condensation ones. Chemical additives are often used to produce some desired characteristic. In industry antioxidants are used to protect a polymer from chemical degradation by ozone or oxygen. Plasticizers can make it more flexible and pigments can alter the color. Changes to the sur837
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face tension can be created by additives. Each company holds the key to its particular formula and will resist any attempts to declare the exact nature of the finished product. It is these additives that impart a degree of individuality to each product. As such, not even mesh derived from the same monomer units is the same. The final stage employs techniques to shape and finish the polymer. In medicine one of the commonest techniques is that of extrusion. An extruder is a device that pumps plastic through a desired die or shape. Using this technique, long strands of polymer can be produced. These strands can then be woven into mesh. Alternatively, some meshes are made by a bonding process where short strands of polymer are almost stuck together. Because plastics are relatively inert, the final products do not normally present health hazards. This should not make us complacent as some monomers used in the manufacture of plastics have been shown to have carcinogenic properties.22
MESH TECHNOLOGY Differences in the type and composition of the individual fibers (e.g. weight, mono- or polyfilament, additives) will impart further differences. In addition, the individual characteristics of the mesh such as pore size, porosity, and weave will further determine how it behaves in the body. Differences will occur in relation to foreign body reaction, ability to withstand infection, shrinkage, and erosion. There are also mechanical differences between the various types. Mechanical differences are more likely to be an issue in hernia and other forms of abdominal wall surgery.
size of the interstices between mono- and multifilament mesh. Interstices smaller than 10 microns allow infection by bacteria, which on average are less than 1 micron whereas most macrophages and neutrophilic granulocytes are larger than 10 microns. Examples of multifilament mesh are polyester mesh (Mersilene), PTFE (Teflon) and polypropylene mesh (Surgipro). If infections occur in multifilament implants, removal is usually necessary.24,25 Infection of a monofilament macroporous mesh does not require its removal.
Pore size The pore size is measured by taking the two longest perpendicular axes of the pore (Fig. 56.3). They can be classified as macroporous (>75 microns) or microporous (<10 microns). The size of the pore imparts similar properties experienced with mono- and multifilament fibers. As such, it can be seen that microporous mesh types exhibit a greater propensity to infection.24,25 Pore size is also implicated in the ingrowth of fibrous tissue. The pore size determines the success of the graft as a scaffold. It has been determined that the optimal pore size is greater than 90 microns but smaller than 5 mm. Pores that are too large incorporate too slowly.26 The quantity reaches a maximum at 6 weeks without any increase over the next year.27 This large size is necessary for the rapid ingrowth of vascularized connective tissue. The smaller size does not leave sufficient space for capillary penetration.28 There is also evidence that flexibility and stiffness are related to pore size. The larger the pore, the greater the
Type of filament It appears that meshes constructed with a monofilament fiber induce a different foreign body reaction when compared with multifilamentous mesh types.23 This 1996 study compared the foreign body reaction of the monofilament polypropylene mesh (Prolene) and the multifilament Surgipro mesh. Both materials were widely used in hernia work at the time. Mesh was implanted in 12 sites in six pigs. At each of 3, 5 and 12 weeks two animals were sacrificed and the tissue specimens were harvested for histologic examination. The study found that there was a significantly greater foreign body reaction with the multifilamentous mesh than the monofilament insert. The greater the amount of foreign material, the greater the possibility of harboring or perpetuating infection. This is probably due to the difference in the
Figure 56.3.
TVT polypropylene type I tape.
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flexibility.29 The importance of this in the clinical setting has yet to be established. Pore size is not the only determinant of tissue ingrowth. Teflon mesh has a pore size 157 microns × 67 microns but has less tissue ingrowth than Marlex, which has a pore size of only 68 × 32 microns. It is believed that this can be attributed to the very low critical surface tension of the fibers, which are only 18.5 dynes/cm, making it difficult for fibroblasts to attach to, and spread on, the fibers.30
Weight The density and weight of the mesh are important factors because of their relationship to healing. The extent of chronic inflammation in the tissues adjacent to the mesh is directly related to the amount of foreign material left in the patient.31 Theoretically, a mesh with a similar pore size to successful mesh materials but with a lower weight might induce an even lower inflammatory response. New materials with a lower weight have demonstrated less of an inflammatory response over time.32
Weave Most articles advocate an open weave as the one that will produce the optimum porosity. Pore size is different from porosity. Porosity, or openness of a fabric, can be defined as the difference between the total fabric area and the area covered by the fabric. Using a sophisticated measuring system combining digitized scanning electron microscope images with custom-built software, this measurement can be calculated accurately. Obviously, the less fabric, the better. This is an alternative method of assessing the nature of the mesh if pore size proves difficult to measure.33
Bonded mesh Bonded mesh is created by fusion welding of the polypropylene fibers (Fig. 56.4). This gives it a very different appearance from mesh made with an open weave. In the experimental setting, it appears to behave in a fashion very similar to type III fibers and therefore should be used with caution until further evidence of clinical safety is established.
Mechanical properties A range of physical tests can be used to differentiate the mechanical properties of mesh fabrics.
Figure 56.4.
Bonded mesh – Porges Mentor.
• Tensile breaking strength of woven mesh is assessed by grab, modified grab, and strip tests.
• Bursting strength is used for materials that do not • •
have yarns or where the yarns are not aligned in any given direction (e.g. knits of bonded mesh). Flexural rigidity is measured by the cantilever test, the principle of which is based on the level of bend of the specimen under its own weight. Wrinkle resistance measures the degree of recovery in a mesh that has undergone controlled creasing.
All of these tests should take place in temperature-controlled environments to ensure that there is uniformity in the test.29 Numerous authors have looked at the differences in mechanical properties between the various materials. It is easy to show differences in strength and elasticity in the laboratory but what impact this has on behavior in the body is poorly understood.34,35 Most of the current materials have the calculated strength to withstand the pressures associated with rises in intraabdominal pressure. Meshes do not need to withstand much more than 16 N/cm of force. Meshes on the market can usually withstand pressures from 30 to 50 N/cm.36 More studies looking at the mechanical properties of explanted materials are required.
Classification of mesh types Using the above physical characteristics, Amid proposed a classification of mesh types which could help the consumer with choice (Table 56.1).24 Based on the experimental work done on mesh, it would appear that type I mesh materials have much lower rates of infection and, if infected, can be treated without removal.37 The large pore meshes admit macrophages and allow rapid angiogenesis.38 Type II and type 839
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Table 56.1
Amid classification of mesh types
Type
Properties
Pore size
Product
I
Macroporous
>75 microns
Atrium Marlex Prolene Monarc TVT
II
Microporous
<10 microns
Goretex Obtape PTFE
III
Macroporous with multifilamentous filaments
>75 microns
PTFE Mersilene Surgipro
IV*
Submicronic
Not applicable
Silastic
* Type IV mesh is not suitable for gynecologic use as it is a relatively solid sheet and will totally resist incorporation. PTFE, polytetrafluoroethylene; TVT, tension-free vaginal tape.
III mesh materials, however, can harbor bacteria and by so doing can promote growth of the bacteria.39,40 These features, added to the better incorporation rates, make type I mesh materials the preferred fabric (Fig. 56.5).41
New classification The Amid classification fails to cover all the categories of mesh types. Considering recent modifications, a more encompassing classification is outlined in Table 56.2. If manufacturers adopted this new classification, researchers would be able to compare the various materials more easily and comparisons would become clinically relevant.
CURRENT CLINICAL PRACTICE Mesh is used in operations for the treatment of SUI and in the management of POP. This article will not cover a
a
Figure 56.5.
b
review of the clinical results but will instead try to concentrate on the overall picture and the principles that should be adopted when dealing with mesh. Generally the articles on the various operations are small series with limited follow-up. These are covered in the relevant chapters. The success of the TVT procedure42 and the demonstration that the risk of erosion is very small has led to the development of many similar operations. The evidence surrounding the advantages and disadvantages of the types of mesh material is limited, with follow-up of less than a year in most early reports. Some of the operations may differ by the instrumentation, technique, and/or type of sling material. Some of the materials are similar to the loosely knitted 4-0 polypropylene utilized in TVT, but others fall into the type II and III Amid classification.43 The enthusiasm for these new procedures does not, it appears, reflect any anxiety about the absence of safety data on the different mesh types. It is worth remembering that synthetic sling erosion can create urethral damage requiring reconstructive surgery. This can be associated with postoperative incontinence in 44–83% of women.44 An infection rate requiring removal in 7.4% of patients who had undergone surgery with multifilament tapes was recently described.45 Another series described an erosion rate of 33% in patients treated 3–24 months previously with suburethral polyester slings.46 The increased erosion rate was attributed to those cases where the vaginal mucosa was closed with a locked suture. The use of mesh in prolapse surgery has become increasingly more common. Reports demonstrating that the abdominal repair with mesh has a better outcome than vaginal surgery with a sacrospinous fixation47 have resulted in numerous publications supporting the use of mesh in vaginal surgery. Most of the reported case series described a purely abdominal approach and avoided vaginal surgery. Another surgical trial by Maher and colleagues reached a similar conclusion.48 Very small rates of erosion were identified in these series. Most of the
c
Scanning electron micrographs of (a) type I mesh; (b) type III mesh, and (c) bonded mesh.
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Table 56.2
Suggested new classification of mesh types
Type
Properties
Pore size
I
Macroporous
>75 microns
Ia
Lightweight (<5 mg/cm2)
<5 mg/cm2
Ib
Heavyweight (>5 mg/cm2)
>5 mg/cm2
II
Microporous
<10 microns
III
Macroporous/multifilamentous
>75 microns
IV
Composite mesh (combination of absorbable and non-absorbable)
>75 microns
V
Bonded mesh
<10 microns
VI
Submicronic
Not applicable
studies have concentrated on the surgical technique and outcomes without performing any analysis on the influence of the mesh types. Visco and colleagues suggested that mesh placed vaginally had a much higher erosion rate (40%) than when placed abdominally (3.2%).49 The mesh used in this series was Mersilene, which is a type III mesh; vaginal placement of a type I mesh may not create the same problems. It is also not clear which suture types were used to fix the mesh. Defining suture type is essential since erosion is more likely to occur at a suture line than through epithelium that has not previously been incised. The role of intra-operative antibiotic irrigation should also be defined for any mesh type. A recent paper has described a doubling of dyspareunia rates with the use of mesh for transvaginal repair and a 13% erosion rate.50 Although not a randomized study, the authors previously demonstrated that an identical surgical technique without mesh had a much lower dyspareunia rate.51 The newer operations for prolapse are transvaginal procedures and use a wide variety of mesh materials.52 The risk and benefit of utilizing a newer material or technique, and the indication for the procedure in the index patient and in subpopulations, should be considered. Each new procedure should declare the properties of the grafts and supply data on erosion and infection rates. Each operation should also supply data on bowel, bladder, and sexual function.
CONCLUSION The use of mesh in surgery for SUI and POP represents one of the most active areas of clinical and basic research in the science of pelvic reconstruction. Evidence exists to support the use of type I mesh materials in the surgery for SUI. Reporting criteria for any
procedure using a new approach and/or material should include the type of mesh employed, technique used, and any special procedural or patient group circumstances. New techniques should also be supported by clinical trial data for the operation that has sufficient follow-up to ensure safety. The use of these materials should only be carried out in controlled trials or under strict audit. A national registry in each country represents an ideal circumstance. Evidence exists to support the use of synthetic mesh in abdominal surgery for POP. Less evidence exists for the use of the material transvaginally. Furthermore, there is no consensus on the type of suture used to fix the mesh, the vaginal closure technique or the use of antibiotic irrigation to prevent infection. In summary, it appears that there are multiple reasons that may increase the risk of erosion. These include the route of surgery, the concomitant surgeries performed, the epithelial closure technique, the mesh type, the suture material used to fix the mesh, and the use of prophylactic antibiotics. The prolapse operations employ a much greater volume of mesh than that used in incontinence surgery and this too may be an issue. One may suggest that stricter governance be employed in the introduction of these techniques. The size of surgical series, the number of cases, and the duration of follow-up are open to standardization. Conversion of all vaginal operations to those employing the use of mesh may be associated with an increase in mesh erosion and clinical morbidities that have been outlined in this chapter, and the risk and benefit of incorporation of mesh into the procedure should be carefully assessed.
REFERENCES 1. Olsen AL, Smith VJ, Bergstrom JO et al. Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 1997;89:501–6. 2. Boyles S, Weber A, Meyn L. Procedures for pelvic organ prolapse in the United States, 1979–1997. Am J Obstet Gynecol 2003;188:108–15. 3. Maher CF, Qatawneh AM, Dwyer PL et al. Abdominal sacral colpopexy or vaginal sacrospinous colpopexy for vaginal vault prolapse: a prospective randomized trial. Am J Obstet Gynecol 2004;190:20–6. 4. Morrow AG. The use of tantalum gauze in the closure of a full thickness defect in the chest wall. Surgery 1951;28:1016–21. 5. Effler DB. Prevention of chest wall defects: use of tantalum and steel mesh. J Thorac Surg 1953;26:419–23. 6. Harrison JH. Teflon weave for replacing tissue defects. Surg Gynecol Obstet 1957;104:584–90.
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7. Usher FC, Gannon JP. Marlex mesh, a new plastic mesh for replacing tissue defects. I. Experimental studies. AMA Arch Surg 1959;78:131–7.
tions to monofilament and braided polypropylene mesh used as preperitoneal implants in pigs. Eur J Surg 1996;162:823–5.
8. Wesolowski SA, Fries CC, Karlson KE et al. Porosity: primary determinant of ultimate fate of synthetic vascular grafts. Surgery 1961;50:91–6.
24. Amid PK. Classification of biomaterials and their related complications in abdominal wall hernia surgery. Hernia 1997;1:15–21.
9. Usher FC. Hernia repair with knitted polypropylene mesh. Surg Gynecol Obstet 1963;117:239–40.
25. Amid PK, Shulman AG, Lichenstein IL. Selecting synthetic mesh for the repair of groin hernia. Postgrad Gen Surg 1992;4:150–5.
10. Aldridge AH. Transportation of fascia for relief of urinary incontinence. Am J Obstet Gynecol 1942;44:398–411. 11. Ghoniem GM, Shaaban A. Sub-urethral slings for treatment of stress urinary incontinence. Int Urogynecol J 1994;5:228–39. 12. Chassar Moir J. The gauze hammock operation: a modified Aldridge sling procedure. J Obstet Gynaecol Br Commonw 1968;75:1–9. 13. Jensen JK, Rufford HJ. Sling procedures – artificial. In: Cardozo L, Staskin D (eds) Textbook of Female Urology and Urogynaecology, 1st ed. London: Martin Dunitz, 2001; 544–61. 14. Lichenstein IL, Shulman AG, Amid PK et al. The tensionfree hernioplasty. Am J Surg 1989;157:188–93. 15. Ulmsten U, Johnson P, Rezapour M. An ambulatory surgical procedure under local anaesthesia for treatment of female urinary incontinence. Int Urogynecol J 1996;9:81–6. 16. Ulmsten U, Falconer C, Johnson P et al. A multicentre study of tension-free vaginal tape (TVT) or surgical treatment of stress urinary incontinence. Int Urogynecol J 1998;9:210–3. 17. Nilsson CG. Latest advances in TVT tension-free support for urinary incontinence Surg Technol Int 2004;12:171–6.
26. Bobyn JD, Wilson GJ, McGregor DC et al. Effect of pore size on peel strength of attachment of fibrous tissue to poroussurfaced implants. J Biomed Mater Res 1975;181:728–34. 27. Rath AM, Zhang J, Amouroux J, Chevrel JP. [Abdominal wall prostheses. Biomechanic and histological study.] Chirurgie 1996;121:253–65. 28. Chavpil H, Holusa R, Kliment K et al. Some chemical and biological characteristics of a new collagen-polymer compound material. J Biomed Mater Res 1969;3:315–22. 29. Chu CC, Welch L. Characterization of morphologic and mechanical properties of surgical mesh fabrics. J Biomed Mater Res 1985;19:903–16. 30. Usher FC, Gannon JP. Marlex mesh, a new plastic mesh for replacing tissue defects. I. Experimental studies. Arch Surg 1959;78:175–7. 31. Bleichrodt RP, Simmermacher RKG, van der Lei B et al. Expanded polytetrafluoroethylene patch versus polypropylene mesh for the repair of contaminated defects of the abdominal wall. Surg Gynecol Obstet 1993;176:18–24. 32. Schumpelick V, Klosterhalfen B, Muller M et al. Minimized polypropylene mesh for preperitoneal net plasty (PNP) of incisional hernias. Chirurg 1999;70:422–30. 33. Pourdeyhimi B. Porosity of surgical mesh fabrics: new technology. J Biomed Res 1989;23:145–52.
18. Lamb JP, Vitale T, Kaminski DL. Comparative evaluation of synthetic meshes used for abdominal wall replacement. Surgery 1983;93:643–8.
34. Dietz HP. Mechanical properties of implant materials used in incontinence surgery. Int Urogynecol J Pelvic Floor Dysfunct 2003;14(4):239–43; discussion 243.
19. Tyrell J, Silberman H, Chandrasoma P et al. Absorbable versus permanent mesh in abdominal operations. Surg Gynecol Obstet 1989;169:227–32.
35. Sandhu DR, Staskin D, Slack M. Physical characteristics of suburethral sling material. Int Urogynecol J 2005. (In press).
20. Sand PK, Koduri S, Lobel RW et al. Prospective randomised trial of polyglactin 910 mesh to prevent recurrence of cystoceles and rectoceles. Am J Obstet Gynecol 2001;184:1357–64.
36. Rosch R. Junge K. Quester R et al. Vypro II mesh in hernia repair: impact of polyglactin on long-term incorporation in rats. Surgical Research 2003;35(5):445–50.
21. Weber AM, Walters MD, Piedmonte MR et al. Anterior colporrhaphy: a randomised trial of three surgical techniques. Am J Obstet Gynecol 2001;185:1299–1306. 22. Fuller RA, Rosen J. Materials for medicine. Sci Am 1986;255:118–125. In: Szycher M (ed) High Performance Biomaterials: A Comprehensive Guide to Medical and Pharmaceutical Applications. Lancaster, PA: Technomic Publishing; 1991. 23. Beets GL, Peter NY, Go H et al. Foreign body reac-
37. Law N, Ellis H. A comparison of polypropylene mesh and expanded PTFE patch for the repair of contaminated abdominal wall defects. Surgery 1991;109:652–6. 38. Arnaud JP, Eloy R, Adloff M et al. Critical evaluation of prosthetic materials in repair of abdominal wall hernias. Am J Surg 1977;133:338–45. 39. Martin RE, Surech S, Classen JN. Polypropylene mesh in 450 hernia repairs: evaluation of wound infection. Contemp Surg 1982;20:46–8. 40. Usher FC, Fries JC, Ochsner JL et al. Marlex mesh: a
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new plastic mesh for replacing tissue defects. Arch Surg 1959;78:138–45. 41. Slack MJ, Sandhu S, Staskin DR et al. In vivo comparison of suburethral sling materials. Int Urogynec J Pelvic Floor Dysfunct 2005 Jul 2; [Epub ahead of print]. 42. Nilsson CG, Falconer C, Rezapour M. Seven-year follow-up of the tension-free vaginal tape procedure for treatment of urinary incontinence. Obstet Gynecol 2004;104(6):1259–62. 43. deTayrac R, Deffieux X, Droupy S et al. A prospective randomized trial comparing tension-free vaginal tape and transobturator suburethral tape for surgical treatment of stress urinary incontinence. Am J Obstet Gynecol 2004;190:602–8. 44. Blaivas JG, Sandhu J. Urethral reconstruction after erosion of slings in women. Curr Opin Urol 2004;14:335–8. 45. Bafghi A, Benizri E, Trastour C et al. Multifilament polypropylene mesh for urinary incontinence: 10 cases of infection requiring removal of the sling. Br J Obstet Gynaecol 2005;112:376–8. 46. Nemunaitis-Keller J, Alford W, Hopkins M. Experience with polyester fabric grafts when used in suburethral sling operations. J Pelvic Surg 2002;8:78–82.
47. Benson JT, Lucente V, McClellan E. Vaginal versus abdominal colpopexy for the treatment of pelvic support defects: a prospective randomized study with long-term outcome evaluation. Am J Obstet Gynecol 2004;175:1418–21. 48. Maher CF, Qatawneh AM, Dwyer PL et al. Abdominal sacral colpopexy or vaginal sacrospinous colpopexy for vaginal vault prolapse: a prospective randomized trial. Am J Obstet Gynecol 2004;190:20–6. 49. Visco AG, Weidener AC, Barber MD et al. Vaginal mesh erosion after abdominal sacral colpopexy. Am J Obstet Gynecol 2001;184:297–302. 50. Milani R, Salvatore S, Soligo M et al. Functional and anatomical outcome of anterior and posterior vaginal prolapse repair with prolene mesh. Br J Obstet Gynaecol 2005;112:107–11. 51. Milani R, Soligo M, Salvatore S et al. Fascial defect repair for symptomatic rectocele: anatomical and functional outcome. Proceedings of the 33rd Meeting of the International Continence Society: Florence, 5–9 October 2003. 189–90. 52. Hung MJ, Liu FS, Shen PS et al. Factors that affect recurrence after anterior colporrhaphy procedure reinforced with four-corner anchored polypropylene mesh. Int Urogynecol J 2004;15:399–406.
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57 Biologic materials for reconstructive surgery Harriette M Scarpero, Emily E Cole, Roger R Dmochowski
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INTRODUCTION The autologous pubovaginal sling has been used for decades to treat anatomic, functional, and recurrent stress urinary incontinence with excellent and long lasting results. In 1997, the American Urological Association (AUA) Female Stress Incontinence Clinical Guidelines Panel concluded that retropubic suspensions and slings were the most efficacious and durable procedures for stress urinary incontinence (SUI).1 In their review of the English language peer-reviewed literature, sling success rates were found to be greater than 80% at 48 months follow-up or longer. These results refer to continence achieved with a traditional autologous fascial sling. Whether the same outcome can be expected from another sling material is not clear. The classic pubovaginal sling requires the harvest of autologous fascia for sling material. Modifications such as alternative sling materials, bone anchor suspension, and midurethral slings have been developed to reduce operating time, surgical morbidity and postoperative complication. The term ‘sling procedure’ can now mean a variety of procedures that can differ in sling material, sling size, anchoring technique, and placement of sling. Numerous alternative biologic materials are commercially available and obviate the need to harvest autologous fascia. Critical analysis of alternative biologic materials and comparison to standard autologous sling outcomes is hampered by the lack of long-term results and direct prospective randomized comparisons. Use of these tissues poses new questions and concerns regarding biocompatibility, reaction or integration with host tissue, and disease transmission. Allografts and xenografts are meant to function as scaffolding for the ingrowth of native tissue that ultimately will replace the graft, but recent data question the permanence of some materials. Although there is evidence that such transformation occurs in some orthopedic and ophthalmic applications, its ability to do this in the vaginal environment is not confirmed. Very little is known about biologic responses to allografts and xenografts in comparison to autologous tissue after vaginal implantation. The vaginal microenvironment differs from that of the abdominal wall, orbital cavity, or knee joint in several important ways. First, the histology is different. The vagina is composed of many layers of cells: stratified squamous epithelium and smooth muscle bundles intermixed with collagen bundles. The vagina is highly vascular, richly innervated and is not sterile but maintains a natural flora. The vaginal flora may be altered by hormonal changes, medications or illness. How the graft behaves in the human vagina may alter surgical success, durability, and complication rate. Despite a lack
of knowledge about the long-term behavior of alternative biologic materials in vaginal procedures, patient desires for alternatives to self-harvest continue to drive the use of them. This chapter examines currently available biologic sling materials to elucidate their unique characteristics and their role in the correction of SUI.
AUTOlOgOUs MATeRIAls Autologous fascia is an attractive sling material because it is cost-effective, available, and biocompatible by definition. Rectus fascia and fascia lata are the autologous sling materials of choice. The harvest of rectus fascia can be accomplished by extending the suprapubic incision that will be made for passage of the ligature carriers and expanding the dissection over the rectus fascia. If the surgeon is willing to struggle with the reduced exposure provided by a smaller incision, the harvest-site incision does not have to be much larger than the typical suprapubic incision for sling sutures alone. Even in the case of prior abdominal surgery or prior rectus fascial sling surgery, it is commonly possible to harvest more fascia for the sling. Fascia lata is another option that may be chosen first line or when poor or insufficient fascia is encountered abdominally. Unlike the harvest of rectus fascia, the harvest of fascia lata requires patient repositioning, prepping of the patient’s thigh, and additional instrumentation to strip the muscle. Regardless of the material used, the pubovaginal sling attempts to restore sufficient outlet resistance to prevent stress urinary incontinence without compromising normal voiding or producing voiding dysfunction. Historically, the pubovaginal sling was reserved for SUI due to intrinsic sphincteric deficiency (ISD) or prior surgical failure; however, the evolution of our theories of the pathophysiology of SUI has extended the use of pubovaginal slings to all types of SUI. We no longer think of SUI as being purely anatomic or purely functional. Instead, it is felt that all women with SUI and hypermobility also have some degree of ISD since not all women with hypermobility leak. The pubovaginal sling, therefore, may be applied universally in SUI. The choice of what anti-incontinence procedure to perform and by what technique is still based on a variety of factors: patient choice, patient characteristics, and the surgeon’s experience and comfort level with a particular technique. Analysis of success of autologous slings is complicated by the varied definitions of cure and different outcome measures used in studies. It is well identified that results based on retrospective chart review tend to be more favorable than results collected by questionnaire or
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objective measurements.1 Numerous studies document the excellent results with autologous materials, even in the long-term. In studies with at least 12 months’ followup, cure rates vary from 50 to 100% with an average cure rate of 84%2–42 (Table 57.1). Use of autologous materials provides the security of known efficacy, consistent durability, and lack of immunogenicity. An important part of critical evaluation of any surgical procedure also includes patient satisfaction and improvement in quality of life. Three recent studies have examined patient satisfaction with autologous slings.14,31,41 Latini et al.41 retrospectively surveyed 100 women who had undergone an autologous fascia lata sling. At a mean follow-up of 4.4 years, 85% of women stated that they were dry or improved, and 83% felt that it had a positive effect on their life. Similar rates of improvement in quality of life and satisfaction from rectus fascial slings are reported by Richter et al.31 and Morgan et al.14 Complications (Table 57.2) unique to autologous tissues are related to the harvest site such as harvest-site infection, seroma or hematoma formation, herniation, or pain at the site. Transient obstructive symptoms that resolve within a few weeks are quite common. Urinary retention requiring urethrolysis occurs in 1–2% of cases, and rates may be slightly higher in fascia lata slings as compared to rectus fascial slings. No cases of rejection have been reported with autologous materials, and the few reported cases of erosion were likely due to excessive sling tension or overly aggressive periurethral dissection.43 Autologous sling materials remain the ‘gold standard’ against which other sling materials are measured. Success of other available sling materials is judged against our results from autologous slings. While clinical results are solid with autologous materials, some investigators have put available materials to test in an in vivo rabbit model.44 In an investigation of time-dependent changes in tensile strength, stiffness, shrinkage, and distortion among cadaveric fascia, porcine dermis, porcine small intestine submucosa (SIS), polypropylene mesh, and autologous fascia, only mesh and autologous fascia showed no difference in tensile strength from baseline. Conversely, a significant loss of tensile strength and stiffness occurs in porcine and cadaveric materials within 12 weeks.
AllOgRAfTs The term allograft refers to non-autologous material taken from an organism of the same species or cadaveric tissues. The appeal of cadaveric tissue has been to avoid the time and morbidity of fascial harvest, yet
maintain a perceived greater biocompatibility and lower risk of erosion compared to synthetics. In the case of sling allografts, the material includes lyophilized dura mater, pericardium, several preparations of fascia lata, and acellular dermis. These tissues have been used for more than 20 years in ophthalmic and orthopedic procedures, but have been used widely in sling surgery only since the mid 1990s. Allografts are commonly used in orthopedic reconstructive surgery for joint arthroplasties, spinal surgery, pediatric, and sports medicine orthopedic procedures. Bone allografts may be used to replace bone and joints lost to metallic implants or the excision of tumors. Orthopedic surgeons cite tissue availability, reduced surgical times, and lack of donor site morbidity as reasons in support of their use. In 2001, approximately 875,000 musculoskeletal allografts were distributed by tissue processors.45 Remarkably, few cases of disease transmission have been cited with the use of musculoskeletal grafts. The first use of allografts in sling surgery was reported by Jarvis and Fowlie in 1985.46 Subsequently, Handa et al. followed with a description of the successful implantation of cadaveric fascia lata (CFL) for genuine stress incontinence which sparked widespread interest in the use of allografts.47 Success rates with cadaveric allografts from studies with at least 12 months’ follow-up vary from 40 to 100% with an average cure rate of 79%.24,32,33,48–63 Prospective evaluation of subjective outcome, specifically patient satisfaction with CFL allograft sling in 102 patients with a mean time out from surgery of 35 months, found significant improvement in symptoms by validated questionnaire:54 80% of patients were better or much better, and 90.2% were somewhat or completely satisfied with their progress. The use of cadaveric tissue sparks several concerns, however: biocompatibility, rejection, disease transmission, and durability. Lyophilized human dura mater has been used in a variety of urologic procedures in the past, including Peyronie’s plaque excision, urethroplasty, and bladder augmentation, and as an interposition material in vesicovaginal fistula repairs. It has been used as a sling material in a few small series, but is a less common allograft for this use. Cure rates with lyophilized dura slings vary from 89 to 92% with follow-up of 6–48 months. No complications from the use of this material have been reported.64,65 Of considerable concern to any surgeon using this material is a case report of the transmission of Creutzfeldt–Jakob’s disease (CJD) in a male patient who received a cadaveric dura graft 12 years earlier for a non-urologic indication.66 To date there have been no cases of the transmission of infection from the use of lyophilized dura mater in urologic surgery. 847
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Table 57.1.
Results of autologous fascial slings*
Author
Material
Sling length (cm)
Mean F/U (months)
Kaufman2
R
15
15
<48
93.3
Schultz-Lampel et al.
R
11
–
24
63.6
Loughlin4
R
22
5
15
72.7
Mason & Roach
R
63
4
12
Zaragoza6
R
60
6–8
25
100
Siegel et al.7
R
20
–
185
80
Carr et al.8
R
96
11–13
22
97.9
3
5
9
No. of patients
Cure (%)
93.7
Barbalias et al.
R
32
12
>30
65.6
Chaikin et al.10
R
251
15
37
72.9
R
43
–
17.4
95.3
Hassouna & Ghoniem
R
82
7
41
Kane et al.13
R
13
5
26
Morgan et al.14
R
247
6–8
51
82.2
Kochakarn et al.15
R
100
–
12.1
94
R
67
15
34
67.2
R
24
20
24
95.8
Borup & Nielsen
R
31
12
60
96.8
Gormley et al.19
R
41
–
>74
95.1
11
Maheshkumar et al.
12
16
Groutz et al. 17
Kuo
18
20
89.1 100
De Rossi
R
27
8
20
100
Lucas et al.21
R
156
–
>30
76
Chou et al.
R
98
12
36
95
Pfitzenmaier et al.23
R
50
–
60
63.9
22
24
Almeida et al.
R
30
–
33
70
Rodrigues et al.25
R
126
–
70.3
74.4
26
Kreder & Austin
R/FL
27
–
22
96.3
Golomb et al.27
R/FL
18
15
30.7
88.9
Haab et al.
R/FL
37
12–15
48.2
73
Wright et al.29
R/FL
33
13–15
16
93.9
Petrou & Frank
R/FL
14
10
17
50
Richter et al.31
R/FL
57
24
42
84
R/FL
71
12
44
90.1
Chien et al.
R/FL
23
10
30.5
94.1
Low34
FL
36
>24
>24
94.4
28
30
Flynn & Yap
32
33
35
Addison et al.
FL
97
–
12
86.6
Beck et al.36
FL
170
>17
>24
98.2
Karram & Bhatia
FL
10
5×7
>12
90
Govier et al.38
FL
30
>24
14
69.7
Berman & Kreder
FL
14
>17
14.9
71.4
Phelps et al.40
FL
27
>20
20
77.8
Latini et al.
FL
63
18–22
53
85
Ellerkmann et al.42
FL
39
>24
>24
92.3
37
39
41
* Limited to studies with minimum of 12 months’ follow-up. Adapted from ref. 97. Cure (%), percentage of patients cured; FL, fascia lata; F/U, follow-up period; R, rectus.
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Table 57.2.
Complications of autologous slings*
Author
De novo storage symptoms (%)
Voiding dysfunction
Other complications
Kaufman2
–
Obstruction 33% Excision 7%
–
Schultz-Lampel et al.3
0
–
–
Loughlin
6
Transient retention 23%
–
Mason & Roach5
–
Obstruction 3% Excision 2%
DVT 2%
Zaragoza6
12
–
–
Siegel et al.
–
Lysis 30%
–
Carr et al.8
–
Obstruction 3% Excision 1%
–
0
–
–
Chaikin et al.
8
–
Bladder perforation 1%
Maheshkumar et al.11
–
CIC 42% Incision 5%
–
0
Pain 25%
8
Dilation 8%
Wound infection 15%
Morgan et al.
7
Lysis 2%
–
Kochakarn et al.15
5
Mean CIC time = 8.9 wks 39%
Wound infection 1%
–
–
Lysis 4%
Subcutaneous hematoma 8%
Obstruction 16% Lysis 3%
Sling erosion 8%
–
–
–
7
–
Bladder perforation 14%
43
CIC 8%
–
Chou et al.
4
Lysis 1%
–
Pfitzenmaier et al.23
–
–
–
4
7
Barbalias et al.9 10
Hassouna & Ghoniem12 13
Kane et al.
14
16
Groutz et al.
21
10
17
Kuo
8 18
Borup & Nielsen Gormley et al.19 20
De Rossi
21
Lucas et al.
22
24
Almeida et al.
13
–
–
–
25
–
Obstruction 11%
–
26
Kreder & Austin
12
Long-term CIC 7%
Thigh hematoma 4%
Golomb et al.27
5
Refractory urge 6%
Haab et al.28
27
Refractory urge 24% CIC 3%
–
Wright et al.29
10
Rodrigues et al.
Lysis 3%
–
0
Long-term CIC 7%
–
Richter et al.
–
High PVR 16% CIC 7%
–
Flynn & Yap32
5
Lysis 1%
–
Chien et al.
–
–
–
Low34
–
–
UVF 8%
Petrou & Frank30 31
33
cont.
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Table 57.2.
Complications of autologous slings* (cont.)
Author
De novo storage symptoms (%)
Voiding dysfunction
Other complications
Addison et al.35
–
Obstruction 6%
Bladder perforation 8% Wound infection 2% PE 1%
Beck et al.36
–
Lysis 3%
Wound infection 5% FL hematoma 1% Seroma 4% PE 1% DVT %
Karram & Bhatia37
–
38
Govier et al.
14 39
Berman & Kreder 40
Phelps et al.
– –
Latini et al.41 42
Ellerkmann et al.
–
–
Lysis 3%
Leg pain 3%
–
Leg hematoma 14%
Retention/lysis 3% CIC 2%
–
–
–
–
–
–
* Limited to studies with minimum of 12 months’ follow-up. Adapted from ref. 97. CIC, clean intermittent catheterization; De novo storage symptoms (%), percentage of patients with de novo storage symptoms (i.e. urgency, frequency, urge incontinence); DVT, deep vein thrombosis; FL, fascia lata; Incision, sling incision; Lysis, urethrolysis; PE, pulmonary embolism; PVR, post-void residual; UVF, urethrovaginal fistula.
Cadaveric fascia lata (CFL) debuted as a sling material in the mid 1990s. Not all cadaveric fascia lata is the same. A major source of variability in CFL originates from its technique of processing, either solvent dehydration and gamma irradiation (Tutoplast®) or freeze-drying (tissue banks and FasLata®). Freeze-dried CFL has been implicated as a cause for suture pull-through and immediate failure.67 Recent studies offer conflicting results regarding whether the method of processing and sterilization structurally weakens tissue. While one study found no statistical difference in tissue thickness or maximum load to failure between freeze-dried CFL, solvent-dehydrated CFL, and acellular cadaveric dermis, another suggested that freeze-dried CFL was less stiff and had a significantly lower maximum load to failure.68,69 The issue of tissue processing and how it affects tissue strength and longevity is still under investigation, and no consensus exists. Although many series find results similar to autologous slings in the short-term, newer published allograft sling outcomes suggest an early failure rate (Table 57.3). Fitzgerald et al. reported failure rates as high as 20% within 3 months of surgery with allograft slings.70 When they reoperated on eight women for persistent or recurrent SUI after allograft sling, the original graft was absent in 14% and degenerated in 6%, suggesting autolysis. Other authors subsequently published failure rates of 28–38% and their observation of similar findings at re-exploration.59,71,72 Recently, a series of intermediate-
term CFL sling failures has been published, prompting significant concern.73 Freeze-dried CFL was implicated more often than other types of processing. No standardization of processing, sterilization, and packaging of allografts exists. Mechanisms of failure and the factors responsible for early allograft loss are not known, but may include the processing technique leading to destabilization of structural integrity of the material, contamination/infection by vaginal flora, host versus graft reaction, accelerated immunity or autolysis. Tissue rejection remains a concern with the nonautologous tissues but has not specifically been reported to date. Since inflammation is difficult to distinguish from rejection without the use of specific tissue staining, it is not yet clear whether true rejection after allograft implant occurs. The concern of disease transmission from an allograft sling remains a real threat. DNA has been detected in freeze-dried CFL, solvent-dehydrated CFL, and acellular dermis, but to date there has been no reported cases of disease transmission. All cadaveric tissues undergo serologic screening for human immunodeficiency virus (HIV) and hepatitis B, but false-negative results are possible. The risk of HIV transmission from a frozen allograft has been estimated to be 1 in 8 million, while the risk of developing CJD is approximately 1 in 3.5 million.44,74 It is not known whether the genetic material found in these allografts is transmissible or poses any long-term health risk. In 1985, HIV was transmitted
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Table 57.3.
Results of allograft slings*
Author
Sling length (cm)
Mean F/U (months)
26
12
15
76.9
FD
91
15
19.4
62.6
CFL
FD
104
24
12
66.3
CFL
FD
8
>20
24
CFL
FD
31
10
13.5
93.5
CFL
FD
63
12
29
87.3
CFL
–
83
10
27.4
90.1
Bodell & Leach
CFL
SD
186
7
16.4
75.8
Richter et al.54
CFL
FD
102
25
35
75
CFL
–
36
>20
20
83.3
CFL
–
34
7
12.5
83.3
Almeida et al.
CFL
FD
30
6–8
36
40
56
Gurdal et al.
CFL
SD
42
4
16
88
Park et al.57
CFL
FD
60
20
>36
85
CFL
FD
27
–
12
59
CFL
SD
32
>24
>24
90.5
Soergel et al.
CFL
FD
12
10
6
Crivellaro et al.60
CAD
Repliform®
253
4
18
78
Wang et al.61
CAD
Repliform®
111
–
36
95
CAD
–
18
3×7
28
89.5
CAD
DuraDerm®
24
14.8
32
Elliott & Boone48 49
Amundsen et al.
50
Brown & Govier
Vereecken & Lechat Walsh et al.52 Flynn & Yap
32
33
Chien et al.
53
40
Phelps et al.
55
Hartanto et al.
24
58
Fitzgerald et al.
42
Ellerkmann et al. 59†
62
Chung et al.
63
Owens & Winters
51
Material
Processing
CFL
SD
CFL
No. of patients
12
Cure (%)
100
33.3
† This study reported 6-month follow-up of the autologous slings, but only short-term follow-up for the allografts. It is noteworthy for its high allograft failure rate within the first 3 months. Adapted from ref. 97. CAD, cadaveric dermis; CFL, cadaveric fascia lata; Cure (%), percentage of patients cured; FD, freeze-dried; F/U, follow-up period; SD, solvent-dehydrated.
from a bone allograft from a tissue donor seronegative for HIV.75,76 More sophisticated donor screening has since been developed and has decreased the risk of seronegative transmission. Bacterial infections are a rare complication of allografts; however, after the reported death of a 23-yearold male recipient of an allograft contaminated with Clostridim, the Centers for Disease Control investigated and identified 26 other cases of allograft-associated infections.77 A case of invasive disease with Streptococcus pyogenes after reconstructive knee surgery using contaminated allograft tissue was reported in 2003.78 Tissue processing and sterilization differs among tissue banks, and clearly there is a need for improved tissue evaluation and processing standards. A questionnairebased study regarding allograft acquisition in 340 hospitals in the United States revealed that in approximately 85% of the institutions, those responsible for providing
surgeons with the allografts had little or no knowledge of the practices of tissue banking and allograft transplantation biology.79 The surgeon was involved in the selection of the source of allografts in only 15% of hospitals. Given the recognition of the risk of disease transmission, it has become wise, if not imperative, for the surgeons who use allografts to be actively involved in determining the source and processing of the grafts they place in patients. Cadaveric acellular dermal allografts are an additional biologic alternative to CFL. In this tissue, epidermal and dermal cellular elements are removed, leaving basement membrane behind to act as a framework into which the patient’s own cells can grow. Acellular dermis has been shown in animal studies to integrate into tissue consistently without any foreign body reaction. Additionally, it persists up to 6 months after implantation and shows evidence of extensive cellular infiltration 851
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and neovascularization. A potential risk of hair follicle and sebaceous gland ingrowth does exist, as does the risk of disease transmission from this material. Several acellular dermal allografts are commercially available as slings: Alloderm™, Repliform®, and Dermal Allograft®. Mechanical load-to-failure testing demonstrates dermal allografts to be strong and to perform in a similar fashion to autologous tissues. To date, there are very few clinical data on the use of cadaveric dermis for sling surgery60–63 (see Table 57.3). In a prospective series of 253 patients treated with a human dermal allograft sling and bone anchors, Crivellaro et al. demonstrated a 57% dry rate in type II SUI and a 55% dry rate in type III SUI at 18 months.60 Overall cured and improved rate was 78%. Wang et al. observed a 95% cured and improved rate in 111 patients treated with a dermal allograft sling at 36 months.61 In a study examining outcomes of cadaveric dermis for combined cystocele and sling surgery, 16 of 18 patients were cured at 28 months, and one patient experienced graft infection and failure.62 Conversely, Owens and Winters found disappointing results with dermal allograft slings.63 At 14.8 months follow-up, only 32% of patients were dry; 24% of the failures occurred within 6–14 months postoperatively. Of the eight failures, one opted to undergo Table 57.4.
Complications of allograft slings*
Author Elliott & Boone48 49
Amundsen et al. 50
Brown & Gover
Vereecken & Lechat51 Walsh et al.
52
Flynn & Yap
an autologous sling. At the time of her surgery, the graft was almost completely absent without evidence of infection or excessive inflammation. Their finding suggests that the material fails, not because of rejection or infection, but because host infiltration either does not occur or does not occur at a fast enough rate to make the graft permanent. Complication rates are similar to those seen with other sling materials (Table 57.4). Two recent reports of vaginal erosion after dermal allograft slings are the first with these materials.80 The cause of the graft erosion in these cases is not clear. Pathologic examination of the graft material was not specific for rejection or inflammation. Although short-term outcomes have been equivalent to those in autologous slings, newer data call into question the durability of allografts. Outcomes data remain limited, particularly in allografts other than CFL, so it is difficult to draw conclusions, but cadaveric dermal allografts reflect short- and medium-term outcomes similar to cadaveric fascia. The mechanisms of failure with allografts need further elucidation. Host factors may play as big as or a bigger role than tissue processing in failure rates. As Owens and Winters point out in the discussion of their series of intermediate-term dermal
32
33
De novo storage symptoms (%)
Voiding dysfunction
Other complications
13
–
–
44
Lysis 1%
–
Long-term retention 2%
–
Lysis 13%
–
CIC at 1 year 3%
–
Retention 2%
–
– 13 – 28
Chien et al.
–
–
–
Bodell & Leach53
–
–
Osteitis 1%
–
Impaired emptying 58%
–
Phelps et al.
–
Lysis 3% CIC 2%
–
Hartanto et al.55
–
–
–
Almeida et al.24
–
–
–
–
CIC for mean of 20 days 12%
–
Park et al.
5
Elevated PVR at 30 days 5% CIC for 1 month 2%
Bladder perforation 2% Blood transfusion 7%
Crivellaro et al.60
5.5
Prolonged catheterization 2%
Vaginal infection 1.7%
54
Richter et al.
40
56
Gurdal et al. 57
* Limited to studies with minimum of 12 months’ follow-up. Adapted from ref. 97. CIC, clean intermittent catheterization; De novo storage symptoms (%), percentage of patients with de novo storage symptoms (i.e. urgency, frequency, urge incontinence); PVR, post-void residual.
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allograft sling failures,63 the scarification of the sling into proper position is not the major factor for long-term success with these materials. The apparent rapid degradation of the sling and failure of host remodeling must be explained. As part of informed consent, patients undergoing allograft sling procedures should be told of data suggesting intermediate failures that do not appear to occur with autologous tissues, the lack of long-term data, and the possibility of disease transmission. The benefits of allograft may only be relevant in a select group of patients unwilling or unable to undergo a fascial harvest, yet not all outcomes are poor. Results of the cadaveric prolapse repair and sling (CAPS), which uses cadaveric fascia lata for the simultaneous repair of a cystocele and placement of a pubovaginal sling by means of a transvaginal approach, continue to show promise.81 At a maximum of 28 months’ follow-up (mean 12.4 months), only 9.8% had recurrent or de novo apical vaginal prolapse. Only 24 of the 132 patients (18.2%) had stress incontinence of any degree.
XeNOgRAfTs The term xenograft refers to the sling material originating from an organism of a different species (non-human). The first animal tissue for urologic use was a porcine corium treated with proteolytic enzymes to remove non-collagenous material. Additional cross-linking of the collagen with glutaraldehyde was needed to reduce antigenicity and then the product was freeze-dried and sterilized with gamma irradiation. Commercially available porcine corium today (DermMatrix™, Pelvicol™, InteXen™) is cross-linked by diisocyanate which is nontoxic and causes no graft mineralization as can occur after cross-linking with glutaraldehyde. Published series of xenograft outcomes are scarce46,82–86 (Table 57.5). In one study, Nicholson and Brown cured 79% of 24 patients with a porcine dermis sling at a mean follow-up of over 48 Table 57.5.
months.83 Thirteen percent of these patients developed urinary retention more than 1 year postoperatively. No cases of sling extrusion or erosion were reported. Porcine dermis has been used at the midurethra with a cure rate of 89% at 12 months.87 Complications included de novo storage symptoms in 6% and urethral obstruction in 7%. Porcine dermis is the only xenograft with long-term follow-up and randomized comparison to other sling alternatives.84 In a randomized comparison of Pelvicol™ pubovaginal slings and tension-free vaginal tape (TVT) synthetic midurethral slings in 142 women, results and complication rates were similar at a median follow-up of 12 months. The patient-determined cure rate was 85% in the TVT group and 89% in the Pelvicol™ group. Rates of postoperative voiding dysfunction and de novo urge incontinence were 3.4% and 9% in the TVT group, and 1.4% and 6% in the Pelvicol™ group, respectively. While rejection has not been reported with porcine dermis, reports of its unpredictable tissue response exist. Cole and colleagues encountered encapsulation of a porcine dermis sling noted at reoperation for retention, 4 months postoperatively.88 Although the material is meant to act as a scaffold for the ingrowth of native tissue, the encapsulated porcine sling was completely acellular without any host tissue proliferation. Gandhi and colleagues observed a trend toward porcine graft preservation in eight women with persistent urinary retention at up to 42 weeks postoperatively.89 The histology of the slings removed demonstrated minimal tissue remodeling, and collagen deposition was present only on the periphery of the sling. Inflammation and foreign body reaction were seen in half of the specimens. In women undergoing reoperation for recurrent SUI, the porcine slings were difficult to identify and histologically the graft material was absent. These findings suggest that porcine dermis is in fact immunogenic. Further studies of the long-term tissue characteristics of implanted porcine dermis are needed.
Results of xenograft slings*
Author
Material 46
No. of patients
Sling length (cm)
Mean F/U (months)
Cure (%)
21
82
18–48
88.7
49
79.2
12
89
Jarvis & Fowlie
PD
50
–
Iosif 82
PD
53
30
PD
24
–
PD
74
Rutner et al.
SIS
115
–
36
94
Pelosi et al.86
BP
22
9
20
95
83
Nicholson & Brown
84
Arunkalaivanan & Barrington 85
10–12
* Limited to studies with minimum of 12 months’ follow-up. Adapted from ref. 97. BP, bovine pericardium; Cure (%), percentage of patients cured; F/U, follow-up period; PD, porcine dermis; SIS, porcine small intestine submucosa.
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Porcine SIS is another animal tissue that has recently been marketed for pubovaginal sling use (STRATASIS®). It is harvested from small intestine and the extracellular collagen matrix remains intact. In theory, through the preservation of collagen, growth factors, glycosaminoglycans, proteoglycans, and glycoproteins, host cells may proliferate through the SIS layers, remodeling and replacing these with host connective tissue. SIS has been used in urologic surgery for urethroplasty, Peyronie’s plaque excision, and ureteral interposition. The tensile strength of SIS has been challenged by a report of the mean suture pull-through load of freeze-dried SIS being less than that of freeze-dried CFL.90 Immunogenicity is also a potential concern. Biopsies of SIS slings at reoperation for recurrent SUI found no evidence of inflammation or foreign body reaction at 9, 12, and 17 months, but other investigators have found evidence to the contrary.91 Two small series of the use of 8-ply SIS tension-free slings describe the development of erythema and inflammation at the suprapubic incisions after implantation.92,93 Another xenograft – bovine pericardium – is available in several preparations. The UroPatch™, a purified and detoxified bovine pericardium cross-linked with glutaraldehyde, has shown a 95% cure rate at a mean follow-up of 20 months in a small series of bone anchored slings.86 A second preparation of the bovine pericardium is a non-cross-linked, propylene oxidetreated, acellular collagen matrix marketed as Veritas™ Collagen Matrix. This tissue is reportedly thinner than freeze-dried or solvent-dehydrated CFL, but possesses greater tensile strength.94 DNA has been identified within the bovine pericardium, but the amount is less than that found in either freeze-dried or solvent-dehydrated CFL, or cadaveric dermis. As with the other tissues, it is not known whether this DNA is transmissible. Two recent Brazilian studies reported rejections of bovine pericardium in 11 of a combined 15 patients. In all cases, vaginal extrusion and wound dehiscence necessitated sling removal.95,96 While all of the available xenografts claim biocompatibility, excellent tensile strength, lack of immunogenicity, and lack of viruses or prions, clinical outcomes suggest that these claims must be strongly scrutinized when considering a xenograft as a sling material. To date, only porcine dermis and 4-ply SIS have shown non-immunogenicity. Porcine dermis is also the only xenograft to have sufficient reports of long-term efficacy.
CONClUsIONs Pubovaginal slings remain a reliable surgical procedure for the correction of all forms of SUI, but not all sling
materials produce equivalent results. The classic autologous fascial sling can be relied upon to provide a cure rate of 84% or better. Complications related to fascial harvest are possible but acceptable. Outcomes and complications associated with the use of cadaveric and animal tissues are less predictable. Sling surgery with most alternative biologic materials produces short-term success rates comparable to autologous fascia. Rates of postoperative voiding dysfunction and urinary retention also appear similar. Allografts and xenografts undoubtedly shorten operative times and obviate the morbidity of fascial harvest, but these shortcuts may be costly in the long term. Current literature points to higher risks of early failure and immunogenicity leading to rejection and poor tissue healing. DNA of unclear transmissibility has been isolated in several sling products including CFL, cadaveric dermis, and bovine pericardium. With so many available sling options, it is imperative that the surgeon be familiar with the nature, behavior, and outcomes of the sling materials as well as the complications of the procedure itself. Patients must be counseled preoperatively and informed consent must include information regarding the sling material to be used. Further studies into the long-term behavior of allografts and xenografts in the vaginal environment are needed to clarify the efficacy and safety of these materials for the correction of SUI.
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29. Wright EJ, Iselin CE, Carr LK et al. Pubovaginal sling using cadaveric allograft fascia for the treatment of intrinsic sphincter deficiency. J Urol 1998;160:759–62. 30. Petrou SP, Frank I. Complications and initial continence rates after a repeat pubovaginal sling procedure for recurrent stress urinary incontinence. J Urol 2001;165:1979–81. 31. Richter HE, Varner E, Sanders E et al. Effects of pubovaginal sling procedure on patients with urethral hypermobility and intrinsic sphincter deficiency: Would they do it again? Am J Obstet Gynecol 2001;184:14–9. 32. Flynn BJ, Yap WT. Pubovaginal sling using allograft fascia lata versus autograft fascia for all types of stress urinary incontinence: 2-year minimum follow-up. J Urol 2002;167:608–12. 33. Chien GW, Tawadroas M, Kaptein JS et al. Surgical treatment for stress urinary incontinence with urethral hypermobility. What is the best approach? World J Urol 2002;20:234–9. 34. Low JA. Management of severe anatomic deficiencies of urethral sphincter function by a combined procedure with a fascia lata sling. Am J Obstet Gynecol 1969;105:149–55. 35. Addison WA, Haygood V, Parker RT. Recurrent stress urinary incontinence. Obstet Gynecol Annu 1985;14:254–65. 36. Beck RP, McCormick S, Nordstrom L. The fascia lata sling procedure for treating recurrent genuine stress incontinence of urine. Obstet Gynecol 1988;72:699–703. 37. Karram MM, Bhatia NN. Patch procedure: modified
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transvaginal fascia lata sling for recurrent or severe stress urinary incontinence. Obstet Gynecol 1990;75:461–3. 38. Govier FE, Gibbons RP, Correa RJ et al. Pubovaginal slings using fascia lata for the treatment of intrinsic sphincter deficiency. J Urol 1997;157:117–21. 39. Berman CJ, Kreder KJ. Comparative cost analysis of collagen injection and fascia lata sling cystourethropexy for the treatment of type III incontinence in women. J Urol 1997;157:122–4. 40. Phelps J, Lin L, Liu C. Laparoscopic suburethral sling procedure. J Am Assoc Gynecol Laparosc 2003;10:496–500. 41. Latini JM, Lux MM, Kreder KJ. Efficacy and morbidity of autologous fascia lata sling cystourethropexy. J Urol 2004;171:1180–4. 42. Ellerkmann RM, McBride AW, Bent AE et al. Comparison of long-term outcomes of autologous fascia lata slings to Suspend Tutoplast™ fascia lata allograft slings for stress incontinence. J Pelvic Med Surg 2004;10(Suppl 1):S28 [oral poster 38]. 43. Webster TM, Gerridzen RG. Urethral erosion following autologous rectus fascial sling. Can J Urol 2003;10:2068–9. 44. Dora CD, Dimarco DS, Zobitz ME et al. Time dependent variations in biomechanical properties of cadaveric fascia, porcine dermis, porcine small intestine submucosa, polypropylene mesh and autologous fascia in the rabbit model: implications for sling surgery. J Urol 2004;171:1970–3. 45. Kainer MA, Linden JV, Whaley DN et al. Clostridium infections associated with musculoskeletal-tissue allografts. N Engl J Med 2004;350:2564–71. 46. Jarvis GJ, Fowlie A. Clinical and urodynamic assessment of the porcine dermis bladder sling in the treatment of genuine stress incontinence. Br J Obstet Gynaecol 1985;92:1189–91. 47. Handa VL, Jensen JK, Germain MM et al. Banked human fascia lata for the suburethral sling procedure: a preliminary report. Obstet Gynecol 1996;88:1045–9. 48. Elliott DS, Boone TB. Is fascia lata allograft material trustworthy for pubovaginal sling repair? Urology 2000;56:772–6. 49. Amundsen CL, Visco AG, Ruiz H et al. Outcome in 104 pubovaginal slings using freeze-dried allograft fascia lata from a single tissue bank. Urology 2000;56(Suppl 6A):2–8.
53. Bodell DM, Leach GE. Update on the results of the cadaveric transvaginal sling (CATS). J Urol 2002;167(Suppl):78 [abstract 308]. 54. Richter HE, Burgio KL, Holley RL et al. Cadaveric fascia lata sling for stress urinary incontinence: a prospective qualityof-life analysis. Am J Obstet Gynecol 2003;189:1590–6. 55. Hartanto VH, DiPiazza D, Ankem MK et al. Comparison of recovery from postoperative pain utilizing two sling techniques. Can J Urol 2003;10:1759–63. 56. Gurdal M, Tekin A, Huri E et al. Pubovaginal sling using cadaveric allograft fascia for all types of stress urinary incontinence. XIXth European Association of Urology Congress, March 25, 2004; Abstract 317. 57. Park S, Kim S, Choo M et al. Long term follow-up result of pubovaginal sling with cadaveric fascia lata in the management of female stress urinary incontinence. XIXth European Association of Urology Congress, March 25, 2004; Abstract 319. 58. Fitzgerald MP, Edwards SR, Fenner D. Medium-term follow-up on use of freeze-dried, irradiated donor fascia for sacrocolpopexy and sling procedures. Int Urogynecol J Pelvic Floor Dysfunct 2004;15:238–42. 59. Soergel TM, Shott S, Heit M. Poor surgical outcomes after fascia lata allograft slings. Int Urogynecol J 2001;12:247–53. 60. Crivellaro S, Smith JJ, Kocjancic E et al. Transvaginal sling using acellular human dermal allograft: safety and efficacy in 253 patients. J Urol 2004;172:1374–8. 61. Wang D, Bresette JF, Smith JJ. Initial experience with acellular human dermal allograft (Repliform®) pubovaginal sling for stress urinary incontinence. J Pelvic Med Surg 2004;10:23–6. 62. Chung SY, Franks M, Smith CP, Lee JY, Lu SH, Chancellor M. Technique of combined pubovaginal sling and cystocele repair using a single piece of cadaveric dermal graft. Urology 2002;59(4):538–41. 63. Owens DC, Winters JC. Pubovaginal sling using Duraderm graft: intermediate follow-up and patient satisfaction. Neurourol Urodyn 2004;23:115–8. 64. Rottenberg RD, Weil A, Brioschi PA et al. Urodynamic and clinical assessment of the Lyodura sling operation for urinary stress incontinence. Br J Obstet Gynaecol 1985;92:829–34.
50. Brown SL, Govier FE. Cadaveric versus autologous fascia lata for the pubovaginal sling: Surgical outcome and patient satisfaction. J Urol 2000;164:1633–7.
65. Enzelsberger H, Helmer H, Schatten C. Comparison of Burch and Lyodura sling procedures for repair of unsuccessful incontinence surgery. Obstet Gynecol 1996;88:251–6.
51. Vereecken RL, Lechat A. Cadaver fascia lata sling in the treatment of intrinsic sphincter weakness. Urol Int 2001;67:232–4.
66. Liscic RM, Brinar V, Miklic P et al. Creutzfeldt–Jakob disease in a patient with a lyophilized dura mater graft. Acta Med Croatica 1999;53:93–6.
52. Walsh IK, Nambirajan T, Donellan SM et al. Cadaveric fascia lata pubovaginal slings: early results on safety, efficacy, and patient satisfaction. BJU Int 2002;90:415–9.
67. Chaikin DC, Blaivas JG. Weakened cadaveric fascial sling: an unexpected cause of failure. J Urol 1998;160:2151. 68. Sutaria PM, Staskin D. A comparison of fascial ‘pull
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through’ strength using four different suture fixation techniques. J Urol 1999;161(Suppl 4):79–80.
incontinence: a questionnaire-based study. Int Urogynecol J 2003;14:7–23.
69. Lemer ML, Chaikin DC, Blaivas JG. Tissue strength analysis of autologous and cadaveric allografts for the pubovaginal sling. Neurourol Urodyn 1999;18:497–503. 70. Fitzgerald MP, Mollenhauer J, Brubaker L. Failure of allograft suburethral slings. BJU Int 1999;84:785–8.
85. Rutner AB, Levine SR, Schmaelzle JF. Porcine small intestinal submucosa implanted as a pubovaginal sling in 115 female patients with stress urinary incontinence: A 3 year series evaluated for durability of the results. Society for Urology and Engineering, 17th Annual Meeting, 2002.
71. Carbone JM, Kavaler E, Hu J et al. Pubovaginal sling using cadaveric fascia and bone anchors: disappointing early results. J Urol 2001;165:1605–11.
86. Pelosi MA II, Pelosi MA III, Pelekanos M. The YAMA UroPatch sling for treatment of female stress urinary incontinence: a pilot study. J Lap Adv Surg Tech 2002;12:27–33.
72. Huang YH, Lin ATL, Chen KK et al. High failure rate using allograft fascia lata in pubovaginal sling surgery for female stress urinary incontinence. Urology 2001;58:943–6.
87. Barrington JW, Edwards AS, Arunkalaivanan AS et al. The use of porcine dermal implant in a minimally invasive pubovaginal sling procedure for genuine stress incontinence. BJU Int 2002;90:224–7.
73. O’Reilly KJ, Govier FE. Intermediate term failure of pubovaginal slings using cadaveric fascia lata: a case series. J Urol 2002;167:1356–8. 74. Buck BE, Malinin TI. Human bone and tissue allografts: preparation and safety. Clin Orthop 1994;303:8–17. 75. Simonds RJ, Holmberg SD, Hurwitz RL et al. Transmission of human immunodeficiency virus type 1 from a seronegative organ and tissue donor. N Engl J Med 1992;326:726–32. 76. Tomford WW. Transmission of disease through transplantation of musculoskeletal allografts. J Bone Joint Surg 1995;77:1742–54. 77. Update: allograft-associated bacterial infections – United States 2002. MMWR Morb Mortal Wkly Rep 2002;15:207–10. 78. Centers for Disease Control and Prevention (CDC). Invasive Streptococcus pyogenes after allograft implantation – Colorado, 2003. MMWR Morb Mortal Wkly Rep 2003;52:1174–6. 79. Lavernia CJ, Malinin TI, Temple T et al. Bone and tissue allograft use by orthopedic surgeons. J Arthroplasty 2004;19:430–5. 80. Bradley CS, Morgan MA, Arya LA et al. Vaginal erosion after pubovaginal sling procedures using dermal allografts. J Urol 2003;169:286–7. 81. Kobashi KC, Leach GE, Chon J et al. Continued multicenter follow-up of cadaveric prolapse repair with sling. J Urol 2002;168:2063–9. 82. Iosif CS. Porcine corium sling in the treatment of urinary stress incontinence. Arch Gynecol 1987;240:131–6. 83. Nicholson SC, Brown ADG. The long-term success of abdominovaginal sling operations for genuine stress incontinence and a cystocele: a questionnaire-based study. J Obstet Gynaecol 2001;21:162–5. 84. Arunkalaivanan AS, Barrington JW. Randomized trial of porcine dermal sling (Pelvicol™ implant) vs. tension-free vaginal tape (TVT) in the surgical treatment of stress
88. Cole E, Gomelsky A, Dmochowski RR. Encapsulation of a porcine dermis pubovaginal sling. J Urol 2003;170:1950. 89. Gandhi S, Kubba LA, Abramov Y et al. Histopathologic changes of porcine dermal implants used for transvaginal suburethral slings. J Pelvic Med Surg 2004;10(Suppl 1): S12 [paper 29]. 90. Kubricht WS, Williams BJ, Eastham JA et al. Tensile strength of cadaveric fascia lata compared to small intestinal submucosa using suture pull through analysis. J Urol 2001;165:486–90. 91. Wiedemann A, Otto M. Small intestinal submucosa for pubourethral sling suspension for the treatment of stress incontinence: first histopathological results in humans. J Urol 2004;172:215–8. 92. Ho KLV, Wittie MN, Bird ET. 8-Ply small intestinal submucosa tension-free sling: spectrum of postoperative inflammation. J Urol 2004;171:268–71. 93. Dalota SJ. Small intestinal submucosa tension-free sling. Postoperative inflammatory reactions and additional data. J Urol 2004;172:1349–50. 94. Oray NB, Lambert A, Wonsetler R et al. Physical and biochemical characterization of a novel non-crosslinked, propylene-oxide treated acellular collagen matrix: comparison with solvent-extracted and freeze-dried cadaveric fascia lata. Society for Urology and Engineering, 17th Annual Meeting, 2002. 95. Martucci RC, Ambrogini A, Calada AA et al. Pubovaginal sling with bovine pericardium for treatment of stress urinary incontinence. Braz J Urol 2000;26:208–14. 96. Candido EB, Triginelli SA, Siva FAL. The use of bovine pericardium in the pubovaginal sling for the treatment of stress urinary incontinence. Rev Bras Ginecol Obstet 2003;25:525–8. 97. Gomelsky A, Scarpero HM, Dmochowski RR. Sling surgery for stress urinary incontinence in the female: what surgery, which material? AUA Update Series 2003;XXII(Lesson 34):266–76.
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58 Urethral injections for incontinence Rodney A Appell
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INTRODUCTION Emphasis on minimally invasive options for the surgical treatment of incontinence (both stress and urge types) has resulted in the development of agents and techniques that improve these conditions substantially towards social continence, but, at this time, suboptimal cure/dry rates. The application of injectable therapy as an office procedure implies the potential for costefficient treatment for selected patients with urinary incontinence. Continuous advancements in materials technology have provided the possibility that multiple new urethral bulking agents will soon be available. Experience continues to accrue in clinical trials for urethral bulking with these agents while parallel utilization for the indication of pediatric vesicourethral reflux has also provided evidence of biologic activity related to these compounds. The agents that are closest to complete analysis are synthetic and represent a variety of material types and characteristics. As these materials evolve, understanding of preferential injection technique is also being gained. Delivery method and site may prove to alter the biologic activity of these compounds substantially. Both stress urinary incontinence (SUI) and urge incontinence (UI) continue as an increasingly significant health concern for millions of women. According to recent estimates, approximately 180,000 surgical procedures are now performed for genuine stress urinary incontinence (GSUI) alone. The lack of one single, reproducible, permanent and yet minimal risk procedure has led to the development of several minimally invasive options that provide the hope of reasonable efficacy associated with minimal morbidity. Reimbursement trends have also placed an emphasis on interventions that require minimal hospitalization or, more optimally, can be performed entirely in the ambulatory office location without requirements for general or regional anesthesia and attendant recuperative facilities. Injection therapy has been used sparingly for the management of SUI for nearly two decades, but has been limited by durability and antigenicity issues associated with bovine collagen. Recent Food and Drug Administration (FDA) approval of carbon particulate technology (DurasphereTM) has provided another option for bulking, but one that had been somewhat limited by difficulty with the injection (due to carrier extrusion resulting in injection needle obstruction). Due to these concerns, many physicians would only use DurasphereTM in the controlled setting of the operative suite, thus detracting from the financial benefit associated with inoffice bulking therapy. This was addressed by the manufacturer and an improved formulation (Durasphere
EXPTM) was introduced following FDA approval in October 2003, making its injection as easy as collagen. Therefore, the use of bulking therapy had been less than optimal to that date. However, the advent of several new bulking agents, each with unique tissue interaction characteristics and holding the promise of greater durability, with fewer actual injection sessions and no antigenicity, promises to dramatically alter the role of bulking therapy in the overall management schema for SUI. Selection of patients appears crucial to the outcome of the intraurethral injection of bulking agents. The ideal candidate for this procedure is one who has good anatomic support, a compliant stable bladder, and a malfunctioning urethra evidenced by a low leak point pressure.1 Other subsets of patients who may benefit from the procedure are patients with high leak point pressure and minimal hypermobility, and elderly women with bladder base mobility who are less active and are a poor surgical risk for other interventions.
INJECTABLES FOR SUI The successful use of periurethral bulking agents is dependent on several factors including the composition of the material, facility of agent use (ease of preparation and implantation), and a receptive host environment (optimized hormonal environment, integrity of urethral anatomic components, and intact periurethral fascia). Three categories of material have been investigated for periurethral bulking: human (autologous or allograft), xenograft, and synthetic. The optimal attributes for bulking materials are:
• biocompatibility; • minimal or no immunogenicity (hypoallergenic); • integrity of the material formulation – there should •
be little or no separation of agent subcomponents (carrier and particulate solid); rheologic (deformation within tissue) characteristics of the agent should also be positively affected by adequate material viscosity, surface tension, and tissue response (wound healing).
These attributes for any specific agent should also be reproducible. Tissue response characteristics should further demonstrate minimal fibrotic ingrowth, little extracapsular inflammatory response (if encapsulation occurs), and agent volume after injection should be retained with minimal resorption. The ideal scenario for any soft tissue-bulking agent would be a single injection with permanent tissue residence of the agent (and partial or total incorporation into the host tissues).
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However, the current reality for the available agents is that they do not ideally fulfill the above criteria, either due to isolated or combined agent and host factors (e.g. lack of resorption, agent admixture separation, etc.). The goal of endoscopic injection therapy for SUI is to provide a minimally invasive, effective, and safe alternative to open surgery. Although the technique has been available for decades, the ideal injectable has yet to be developed. In addition to safety issues by being biocompatible, non-antigenic, non-infectious, and noncarcinogenic, any material must demonstrate ‘anatomic integrity’. This implies that the material conserves its volume over time. Despite the safety of using bovine collagen as a material for injection treatment for SUI, it lacks this ‘anatomic integrity’. This reduces the ability of collagen to be cost effective. A significant volume is required at each injection session and multiple injection sessions are the rule, not the exception, thus reducing not only the cost effectiveness of this material but also translating into patient inconvenience and, ultimately, to patient dissatisfaction with collagen and (perhaps) injectable therapy in general. Information on the use of collagen in SUI has been well documented.2
DurasphereTM pyrolytic carbon-coated zirconium oxide beads This product was approved by the FDA in 1999. The beads are suspended in a water-soluble β-glucan vehicle. The randomized, multicenter, double-blind study3 accepted by the FDA compared collagen to DurasphereTM and showed similar outcomes, the original DurasphereTM offering a slight benefit. DurasphereTM is more viscous than collagen and, as mentioned above, its injection was more technically demanding until the introduction of Durasphere-EXPTM. Recently, renewed concern has been expressed about material migration after injection,4 despite lack of clear evidence demonstrating migration. Microcrystalline components of the bulking agent should be composed of uniform spheroidal particles with sizes above 80 microns (approximate size required to avoid migration, determined in studies involving polytetrafluoroethylene [Teflon]). Migration is clearly influenced by the ability of host macrophages to phagocytize particles, and smaller particle sizes have been shown to migrate to distant locations with Teflon injection. However, direct embolization of material is caused by high pressure injection resulting in material displacement into vascular or lymphatic spaces. Injection technique should therefore rely on larger particle sizes administered with low pressure injection instrumentation. This should not become a problem with Durasphere-EXPTM, as its smallest particle
is 95 microns with a range up to 200 microns, significantly smaller than the original DurasphereTM (200–550 microns), but still in the size greater than the 80 micron minimum needed for safety.
Ethylene vinyl alcohol co-polymer suspended in dimethyl sulfoxide (DMSO) or Uryx® solution Approved by the FDA in December 2004, this bulking agent is so new that few data are currently available as it still awaits commercial launch for this indication, although it is considered safe as it has already been in use for neurovascular embolization of arteriovenous malformations and small aneurysms. Upon injection and exposure to solution (blood or extracellular space) at physiologic temperatures, the DMSO diffuses from the co-polymer and causes the ethylene vinyl alcohol to precipitate into a complex spongiform mass. This phase change requires diligent separation of agent and body temperature fluids until implantation occurs. Early experience with this agent suggested that optimal results were obtained with injection in a slightly more distal location within the urethra (approximately 1.5 cm distal to the bladder neck), with a slower rate of injection (at least 30 s/ml/injection site), and without the need to observe visual coaptation at the completion of injection, as the volume injected is limited to 2.5 ml on each side of the urethra. Using these endpoint criteria, results with this agent have been intriguingly good. Again, the interesting difference with this material is that injection consists of this set volume and not an endpoint of coaptation of the urethra/bladder neck at the time of injection. A large scale North American trial incorporated 237 women with GSUI, and used a prospective, randomized (2:1 Uryx® to bovine collagen) schema.5 All treated patients were followed for 1 year after their last injection. Interestingly, at 12 months, 74% of the Uryx® patients were dry as compared to 40% of the collagen patients. Rates of postimplantation urgency and dysuria were essentially the same between the two arms. This result suggests that, unlike collagen, Uryx® maintains a durability of response not noted with biologic agents and may provide the first synthetic material to do this without substantive complication issues.
Specific agents in development Calcium hydoxylapatite Synthetic calcium hydoxylapatite is identical to the same material found in human teeth and bones. The agent is composed of hydroxylapatite spheres (which are extremely uniform in shape, smooth, and 75–125 microns in size) in an aqueous gel composed of sodium 861
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carboxylmethylcellulose (trade name, Coaptite®). Plain film radiography or ultrasonography may be used to localize this material and can be useful adjuncts to assessing implantation. In fact, the first FDA approved indication for this material has been obtained, specifically for soft tissue marking (as an adjunct to radiographic focusing for radiotherapeutics). Agent injection is carried out with a small bore (21-gauge needle), with standard cystoscopic instruments. A large-scale North American pivotal trial has been completed, accruing more than 250 women. In a preliminary report, when 21 women who had received Coaptite® and 18 who had received collagen and had been followed for 1 year since last injection,6 the average number of injections was 2.0 for Coaptite® and 2.3 for collagen. The total volume injected was 3.7 ml for Coaptite® and 7.4 ml for collagen. Eighty-six percent of Coaptite® patients improved by at least one Stamey grade, 67% improved by two grades, and 38% were completely continent (compared to women who received collagen with 66%, 55%, and 44%, respectively). Overall pad weight reduction in the 1-hour stress pad test was at least 75% in 77% of Coaptite® patients but in only 55% of collagen patients, and a 90% reduction or greater was found in 46% (Coaptite®) and 33% (collagen), respectively. No prolonged retention, urgency, or periurethral erosion or abscess was seen in either group. This agent has similar injection characteristics to collagen, and thus far appears to require less injected volume for somewhat more durable effect than collagen.
ZuidexTM Zuidex™ – another biologic agent – consists of dextranomer microspheres in a cross-linked hyaluronic acid (HA) vehicle. HA is a water-insoluble, complex glycosaminoglycan composed of disaccharide units, which form molecules of 23 million molecular weight, and is dissolved in normal saline for urethral bulking purposes. This composite gel has significant elasticity and high viscosity. These biologic characteristics have led to the use of hylan gels for soft tissue bulking purposes. It is completely biodegradable and non-immunogenic. Hyaluronic acid functions as the transport compound and is resorbed within 2 weeks after injection. The dextranomer microspheres actually function as the bulking agent, are 80–200 microns in size and do not show fragility with insertion, remaining in the injection site for about 4 years. Injection is performed using standard cystoscopic equipment, with minimal injection pressure. A clinical trial has just begun in the US to evaluate this agent for SUI.
Of interest is that the technique requires no endoscopy. A small device (called the ‘Implacer’) is inserted into the urethra and the four needles direct the injected material in 0.7 ml aliquots at the midurethra. Substantive data existed for the efficacy and safety of this agent, allowing FDA approval in the US for the indication of vesicoureteral reflux and for pediatric incontinence. It is therefore unlikely that there will be any safety issues in the evaluation of adult incontinence treatment. The incontinence injections are at the bladder neck for the collagen used in this trial whereas the Zuidex™ is placed at the midurethra; it remains to be seen if this affects efficacy. Results of dextranomer injection for pediatric incontinence show no associated adverse events, and substantial improvement at 12 months postinjection;7 however, these children were injected at the bladder neck. Sixteen patients (with a variety of underlying etiologies for their incontinence) underwent a mean of 2.3 injections with a mean volume of 2.8 ml with subsequent annual follow up. Seventy-five percent were improved at 6 months and 50% at 12 months as determined by 1-hour pad tests and diary data. Further follow-up at 2 years indicated relative stability of incontinence parameters as compared with the 1-year data. No local injection site complications or immunologic sequelae resulted. Similar durability and safety findings have been identified with this material when used for the reflux indication.
Synthetic agents Synthetic agents would seem to pose a potential benefit as bulking agents due to their stability (non-biodegradability). Silicone is a hydrogel suspension composed of polyvinylpyrrolidone (povidone) as the carrier (which also acts as a lubricant for the injection system) while the bulking agent is solid polydimethylsiloxane elastomer (vulcanized silicone). The elastomer is a particulate of varying shapes and conformal configurations. Particle size is markedly variable with 25% of particles less than 50 microns in size, and some greater than 400 microns in largest dimension. Silicone delivery also requires high-pressure administration, but, with newer equipment, this material is more easily delivered. Although well established in Europe, concerns regarding silicone stimulation of the immunologic response have limited evaluation of this agent in the US. However, a clinical trial evaluating this agent (Macroplastique®) for this indication is now in progress in North America. A recent Scandinavian report followed 22 women long term (2 years postinjection) who had received this agent.8 Subjective and objective criteria showed stability and persistent benefit for those patients. Overall pad test
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data showed dramatic reduction (147 g mean pretreatment reduced to 9 g post-treatment). No long-term local or systemic complications were noted. A requirement for FDA trials with these agents is active comparison with bovine collagen. No current head-to-head data exist between these evolving agents for the indication of GSUI. However, a recently completed trial did compare Macroplastique® to dextranomer/hyaluronic acid for the treatment of ureteral reflux in children.9
CONCLUSIONS It is clear that injectable treatment for SUI can be effective and safe; however, it is also clear that durability of the positive results remains a primary concern when implementing this minimally invasive technique. With time and further research, improvements in the use of injectables for SUI are inevitable.
REFERENCES 1. Winters JC, Appell R. Periurethral injection of collagen in the treatment of intrinsic sphincteric deficiency in the female patient. Urol Clin North Am 1995;22:673–8. 2. Kershen RT, Dmochowski RR, Appell RA. Beyond collagen: injectable therapies for the treatment of female stress uri-
nary incontinence in the new millennium. Urol Clin North Am 2002;29:559–74. 3. Lightner D, Calvosa C, Andersen R et al. A new injectable bulking agent for treatment of stress urinary incontinence: results of a multicenter, randomized, controlled, doubleblind study of Durasphere. Urology 2001;58:12–5. 4. Ritts RE. Particle migration after transurethral injection of carbon coated beads. J Urol 2002;167:1804–5. 5. Dmochowski RR, Herschorn S, Corcos J et al. Multicenter randomized controlled study to evaluate Uryx urethral bulking agent in treating female stress urinary incontinence. J Urol 2002;167:LB-10 (A). 6. Dmochowski R, Appell RA, Klimberg I et al. Initial clinical results from coaptite injection for stress urinary incontinence, comparative clinical study. In: Program of the International Continence Society, Heidelberg, Germany, August 2002. 7. Caione P, Capozza N. Endoscopic treatment of urinary incontinence in pediatric patients: 2-year experience with dextranomer/hyaluronic acid. J Urol 2002;168:1868–71. 8. Peeker R, Edlund C, Wennberg AL et al. The treatment of sphincter incontinence with periurethral silicone implant (Macroplastique). Scand J Urol Nephrol 2002;36:194–8. 9. Aboutaleb H, Bolduc S, Upadhyay J et al. Subureteral polydimethyl-siloxane injection versus extravesical reimplantation for primary low grade vesicoureteral reflux in children: a comparative study. J Urol 2002;169:313–6.
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59 Abdominal and transvaginal colpourethropexies for stress urinary incontinence Michelle Y Morrill, Karl M Luber
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Introduction There have been over 100 procedures described for the surgical correction of stress urinary incontinence (SUI), but credit for the first retropubic colposuspension belongs to Marshall, Marchetti and Krantz. In 1949, in an early example of cooperation between pelvic surgeons, this team of two gynecologists and one urologist described their first series of the correction of stress urinary incontinence by simple vesicourethral suspension in a series of 50 patients including 12 men at risk for incontinence following prostatectomy.1 Others subsequently recognized the value of this approach for women with SUI and, with modifications, it became a gold standard procedure for SUI that has withstood many years of critical review.2–5 In 1991, Vancaillie and Schuessler introduced a laparoscopic approach to the retropubic space that facilitated a minimally invasive approach to colpourethropexy.6 The efficacy of this approach has not supported it as a replacement for the open colpourethropexy (CU). Although the role of CU is changing as new, less invasive procedures are introduced, it remains an important technique in the armamentarium of the female pelvic reconstructive surgeon. Transvaginal needle procedures, originally developed through the pioneering work of Armand Pereyra in the late 1950s, represented a remarkable insight into less invasive surgery.7 Although transvaginal needle bladder neck suspensions (NBNS) were commonly used for over three decades, recent critical meta-analysis has shown that long-term outcomes compare unfavorably to other available procedures and their use has been largely abandoned.5,8,9
Indications Before surgery for female SUI is undertaken, it is important that non-surgical care be offered and encouraged.10 Contemporary non-surgical care has demonstrated good results and exposes women to fewer potential risks.11 However, even with optimal non-surgical care, there are many women who will elect for surgical intervention. In 1998 nearly 135,000 women in the United States had inpatient surgery for SUI.12 Four percent of US women responding to a national postal survey said that they had undergone surgery for SUI.13 With the vast array of surgical options currently available, recommending the optimal surgical procedure for an individual patient has grown more complex but should remain based upon existing methods of evaluation along with ongoing assessment of available outcome data. Careful evaluation should be undertaken prior to offering a patient surgery for SUI and should include
a detailed history of their condition and background medical history to identify other potential contributors such as chronic coughing, limited mobility, etc. A voiding diary is useful to assess storage ability, but must be interpreted in light of the patient’s symptoms; for example, a patient may present with small voided volumes and it could easily be assumed that this reflected an overactive bladder. However, further questioning may reveal she has learned to void more frequently to avoid stress loss. The physical examination should include a directed neurologic evaluation, grading of pelvic floor muscle strength, and assessment of vaginal and urethral support, preferably using the pelvic organ prolapse quantification (POPQ) grading system14 for prolapse and the Q-tip test for hypermobility.15 A post-void residual urine volume and stress testing, preferably undertaken in the context of urodynamic testing, are appropriate prior to making any recommendation to surgery. Many surgeons also prefer baseline voiding information to allow for better assessment and care of potential postoperative voiding difficulties. Once stress incontinence is established and a patient expresses the desire to explore surgical options, consideration must be given to what represents appropriate surgery for that individual. For many years, surgeons have considered women with SUI in three groups based upon two components: support of the urethrovesical junction (UVJ) and the intrinsic function of the urethral closure mechanism. The first group includes women with poor UVJ support, known as urethral hypermobility, who otherwise have good urethral function. The term hypermobile stress incontinence (HSI) is often applied to this group. The second group is composed of women with good urethral support, but poor urethral function. Historically this group has been referred to as Type III incontinence, but is now commonly known as intrinsic sphincter deficiency (ISD).16 The third group is made up of those women who have both hypermobility (HSI) of the UVJ and poor urethral function (ISD). Recommendations for treatment follow this categorization. HSI is treated primarily by stabilizing the UVJ with a CU, a suburethral sling or, of historical interest, a NBNS. ISD without hypermobility (HM) can be treated with a suburethral sling, often with mobilization of the urethra, or with bulking agents designed to improve urethral coaptation. As women in this group already have good urethral support, a procedure such as CU or NBNS – which functions by improving support – is not likely to provide relief of their symptoms. Therefore, there is no role for CU or NBNS in caring for women with ISD without HM.17 This leaves debate about the optimal manage-
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ment for that group of women with both hypermobility and poor urethral function (ISD). Low maximum urethral closure pressure (MUCP; 20 cmH2O or lower) has been studied as a risk factor for failure of colpourethropexies. McGuire et al. were the first to report that women with HSI who had persistent SUI following colpourethropexy were more likely to have a low preoperative MUCP than women with a successful outcome.18 They concluded that a low MUCP reflected poor urethral function and that simply stabilizing such a urethra would not correct the SUI. Subsequent investigators confirmed these findings. Sand and colleagues noted that 54% of patients with low urethral pressures continued to have stress incontinence after a Burch procedure compared to only 18% of women with maximum urethral closure pressures of greater than 20 cmH2O.19 This led to the broad use of MUCP to identify women with ISD along with HSI and the recommendation to use a sling procedure, rather than a stabilization procedure, to correct their SUI. More recently, both Richardson et al.20 and Sand et al.21 have reported clinical series in which women with low MUCP achieved success rates of 78% and 90%, closely approximating those of women with normal MUCP. This issue is made more difficult by the lack of agreement on definition and diagnosis of ISD. Thus, in the absence of a randomized controlled trial, the importance of urethral function to the success of CU is unclear although most thought leaders recommend against CU in patients with evidence of ISD. Current work undertaken by the National Institutes of Health (NIH) sponsored Urinary Incontinence Treatment Network (UITN) is currently investigating this, and the data being generated promises to improve our understanding of this issue. In the early 1990s, several thought leaders in the surgical care of female SUI began sharing data from clinical series in which suburethral sling procedures were used to treat women with HSI regardless of urethral function.22 They emphasized that careful sling placement and the absence of tensioning against the urethra reduced the risk of postoperative obstruction to levels comparable to CU. Prior to this, many practitioners felt that the mechanical effect of the graft should be visually confirmed as an indentation on the proximal urethra noted on urethroscopy. As a result, postoperative obstruction rates were troublesomely high. The concept that successful cure of SUI could occur with less obstruction by using a tension-free suburethral sling technique led to a movement away from retropubic urethropexy and needle bladder neck suspension. As this philosophy was adopted, preoperative assessment of urethral func-
tion became less critical as the role of CU was reduced and the use of slings was expanded. Many variables have been examined as risk factors for failure of colpourethropexies, including obesity and previous anti-incontinence surgery. Table 59.1 examines studies of commonly considered risk factors for failure of Burch procedures. Contrary to common recommendations, patients with previous incontinence surgery have outcomes similar to women who have not undergone previous anti-incontinence procedures. Obesity has been identified as a risk factor for SUI23 and many have taught that it is likewise a risk factor for failure of anti-incontinence surgery. This was not supported in a 5-year follow-up study of incontinence surgery and patient body mass index (BMI) where 87% of the obese patients (BMI >30) were continent.24 Although obesity may create insurmountable technical difficulties for the surgeon, evidence does not support a reduction in the efficacy of CU in treating women with elevated body mass indices. In clinical practice, it is common to encounter questions surrounding the route of delivery following surgery for SUI. Unfortunately, there are no studies in the literature designed to answer questions about women who deliver children after surgery for incontinence. Survey studies conducted through the American Urogynecologic Society have revealed that 67% of respondents would recommend performing a cesarean section for a patient after an anti-incontinence procedure rather than allowing subsequent vaginal delivery. Physicians reported outcomes of their patients who delivered after surgery. Forty women delivered vaginally and 22 (55%) were known to be continent. Forty-seven had cesarean sections, after which 35 (74%) were continent.25 It is not known how many of those women labored before delivering abdominally. The decision to operate on a woman who plans future childbearing mandates a thorough discussion with the patient of the risks and benefits as they relate to subsequent delivery. Finally, patients anticipating CU or any other form of surgery to correct SUI should be counseled extensively about the risks and benefits. Counseling should include an accurate sense of the long-term correction of SUI along with information about the immediate and long-term risks, especially overactive bladder (OAB) symptoms and voiding dysfunction as outlined in Tables 59.7 and 59.8.
Technique The goal of CU is to create, or more accurately, recreate a backboard against which the hypermobile urethra 867
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Table 59.1. Success rates for specific preoperative factors Preoperative factor
Objective success (%)
Subjective success (%)
n
Follow-up
Reference
Low UCP
46
N/A
41
3 months
Sand et al.19
Low UCP HM data not presented
50
N/A
6
1 year
Bergman et al.58
Low UCP with HM
78
–
29
–
Richardson et al.20
Low UCP, ‘poor bladder neck mobility was not a risk factor for failure’
67
90
21
4–36 months (mean 15)
Maher et al.59
Low UCP and HM
90
95
19
3 months
Sand et al.21
Low UCP and HM
84.6
93
28
33–116 months (mean 72.6)
Culligan et al.60
No hypermobility (Q-tip change of <30 degrees)
45
N/A
9
3–12 months
Bergman et al.17
Negative Q-tip test
50
N/A
12
1 year
Bergman et al.58
Previous incontinence surgery
82.9
N/A
35
5–10 years
Feyereisl et al.51
Previous incontinence surgery
81
80% rated surgery highly successful
53
4–72 months (mean 9)
Maher et al.47
BMI >30
87
N/A
15
5 years
Zivkovic et al.24
BMI, body mass index; HM, hypermobility; n, number of subjects in colpourethropexy arm of trial; N/A, not applicable; UCP, urethral closure pressure.
can be compressed during stress. This is done by stabilizing the endopelvic connective tissue that provides the underlying support of the proximal urethra. This underlying support is provided by the anterior vaginal wall and consists of fibromuscular tissue with lateral attachment to the arcus tendineus fascia pelvis.26 Historically, there has been an emphasis on restoring the urethra to an intra-abdominal location in which the zone of pressure within the abdomen will be equally exerted upon the urethra and the bladder, thus closing the urethra and resisting passage of urine during stress.27 However, this is not consistent with anatomic observations in cadaver dissections or during surgical procedures, and has given way to the more contemporary explanation above. Although CUs are commonly undertaken as part of more comprehensive reconstructive surgery, they can be performed as isolated procedures using a laparoscope, a 5–6 cm mini-laparotomy, or a full-sized transverse or midline incision. The cosmetic advantages of laparoscopic surgery and mini-laparotomy are immediately obvious to the patient. The surgical outcomes of open versus laparoscopic CU are discussed later in this chapter. The original colposuspension was designed to elevate the urethrovesical junction to the pubic symphysis. The initial modification of this was published in 196128 when Burch, after becoming frustrated with the inconsistency of support and suture pullout from the midline periosteum, chose to attach them to Cooper’s ligament. A
meta-analysis of two subsequent trials comparing these two procedures has demonstrated a significant improvement in outcome, with a relative risk of failure for Burch compared to the Marshall–Marchetti–Krantz (MMK) procedure at 1–5 years of 0.38 and a decrease in postoperative retention with the Burch procedure.29 Failures following CU can be attributed to several causes. Mechanical failure caused by suture pullout with subsequent loss of urethral support, as well as compromise of urethral function caused by periurethral dissection that can create ISD, can both contribute to failure. Additionally, a subset of women experience successful correction of their SUI only to find that they have developed de novo detrusor overactivity or worsening of pre-existing overactive bladder (OAB) symptoms. It has been observed that development or worsening of urge symptoms is commonly associated with voiding difficulties. This has led many to speculate that new postoperative urge symptoms are the result of a postobstructive phenomenon analogous to urge in the male associated with benign prostatic hyperplasia. By analyzing these failures, we can develop guidelines by which we strive to avoid them. In his landmark article of 1976,3 Tanagho outlined technical variations of the Burch procedure that recommended avoiding dissection of the midline neurovascular supply to the urethra to protect against compromising urethral function and creating ISD. Tanagho also sug-
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gested that overcorrection of the urethral support not only failed to improve success rates, but was also associated with voiding dysfunction and, often, irritative voiding symptoms. This resulted in the now broadly accepted recommendation that sutures be placed lateral to the urethra and tied in such a way as to support the urethra without excessive elevation and without compression of the urethra against the posterior of the symphysis pubis. The parallel concepts of protecting the midline structures and correcting support while avoiding overcorrection are key to providing the best outcomes for patients. Mechanical failure of CU is most probably caused by suture pullout from the endopelvic connective tissue of the anterior vaginal wall rather than the sturdier Cooper’s ligament. This emphasizes the importance of optimizing the weakest link of the procedure by ensuring that sutures placed into the anterior vaginal wall achieve optimal purchase. This can be accomplished by confident full thickness bites of the endopelvic connective tissue placed with sufficient precision that the operator does not hesitate for fear of injuring adjacent structures, particularly the urinary tract. A triangle of safety can be visualized intraoperatively by creating a line approximately 2 cm from and parallel to the urethra, a second line along the distal aspect of the bladder, and a third along the pelvic sidewall (Fig. 59.1). Within this zone of safety, the surgeon can be confident that deep, elongated bites will provide optimal support without fear of collateral damage to the urinary tract. Longer, full thickness suture placements are also less likely to tear through the venous plexus of the anterior vaginal wall than more tentative bites, making them a hemostatically safer alternative as well.
Results Outcomes of retropubic colpourethropexy The long-term goals of reconstructive surgery differ fundamentally from those of extirpative surgery. A procedure designed to create a functional improvement for a patient must stand a different test of cure than an operation intended to remove a mass or a dysfunctional organ. With reconstructive surgery, the adverse effects are weighed against the duration and degree of improvement in the primary symptom. This makes the definition of success a moving target that is difficult to define. When assessing stress incontinence surgery, the successful management of SUI is balanced against intraoperative and long-term functional risks. The potential functional risks of anti-incontinence surgery include
voiding difficulties and obstruction, de novo or worsened OAB symptoms, chronic pain, osteitis pubis, and dyspareunia. Results of colposuspension have been reported using both objective and subjective measures. Objective success rates range from 68 to 95.6% (Table 59.2). The results of colposuspension in the first 5 years after surgery are consistently better than 80%. The 1997 American Urological Association guidelines panel meta-analysis found that success at 48 months averaged 84% with a confidence interval of 79–88%.5 The Cochrane Review of open retropubic colposuspension focused on randomized controlled trials and found a slow decline in cure to 70% as patients were followed over 5 years.29 Reports attempting to study women with follow-up of greater than 10 years often lack objective data and suffer from the inevitable drop in follow-up rates. The retrospective studies in Table 59.2 reporting success rates of 90% and 94% at 15 years plus postoperatively are unlikely to be indicative of expected results. Further studies are needed to clarify the longer-term results of colposuspension. Subjective measures are predictably difficult to metaanalyze because there is great variability in the metrics used to assess outcomes subjectively. However, subjective outcomes are very important. It is essential to understand the effects of surgery on a patient who leaks during an office stress test but states that she does not consider her leakage to be significant or bothersome. The International Continence Society has recognized this by including in the definition of incontinence that it is ‘a social or hygienic problem for the patient’.30 Among studies that provide both subjective and objective outcome data, continence rates can differ by more than 20% (see Table 59.1). Only three of the studies listed in Table 59.2 reported subjective cure rates. Alcalay et al.31 and Ward and Hilton32 found subjective cure rates of 73.5% and 62%, respectively. Jarvis’ meta-analysis33 reported a much higher 89.6% subjective cure rate in over 1700 patients. Subjective cure rates in patients evaluated for preoperative risk factors for failure ranged from 80 to 93% (see Table 59.1). Accepting their limitations, subjective measures of success following surgery for SUI remain an important outcome variable that does not always agree with objective data. Laparoscopic or minimally invasive approaches to colposuspension were developed to speed patient recovery, both in the hospital and after discharge. Descriptions of both extraperitoneal (approaching the space of Retzius without entering the peritoneal cavity) and transperitoneal (incising the peritoneum cephalad to the bladder from a pneumoperitoneum) techniques have been reported. A review published in the Cochrane Database34 869
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Table 59.2. Success rates of retropubic urethropexy Follow-up Study
n
Study design
Cure (objectively dry) (%)
1–5 years
Jarvis33
1726
Meta-analysis
84.3
≥1 year
Colombo et al.61
40
Prospective randomized
80
2–7 years (mean 3.1)
Leach et al.5
2196
Meta-analysis
84
≥4 years
Su et al.62
46
Prospective randomized
95.6
≥1 year
2403
Meta-analysis
85–90
1 year
169
Prospective randomized
80 in 86 who were followed up 68 if LOCF
2 years
87
Retrospective cohort
81.6
5–10 years
Lapitan et al.29 Ward & Hilton
32
Feyereisl et al.51 36
Bergman & Elia
5–10 years
>10 years
33
Prospective randomized
82
5 years
29
Lapitan et al.
2403
Meta-analysis
Approx. 70
5 years
Alcalay et al.31
109
Retrospective review
90
10–20 years (mean 13.8)
Langer et al.63
127
Retrospective review
94
10–15 years (mean 12.4)
LOCF, last observation carried forward; n, number of subjects in colpourethropexy arm of trial.
reported an increased objective failure rate for laparoscopic Burch procedures compared to the open technique (relative risk 2.30). The authors note that one of the three studies had problems with randomization and consistency of suture usage. With that one study removed from the analysis there was no significant difference between laparoscopy and laparotomy up to 18 months after surgery. However, most experts feel that 18 months is not an adequate test of time for an anti-incontinence procedure.5 Long-term published and unpublished data from Burton were utilized in the Cochrane Database. Burton’s data indicate that laparoscopic CU failed to maintain continence as well as open Burch procedures at both 3 and 5 years. In the Cochrane Review, laparoscopy resulted in a shorter hospital stay and shorter time to return to normal activities. The complication rates of voiding dysfunction and de novo urgency were not significantly different. Clinicians are faced with many surgical choices to treat SUI. Table 59.3 lists studies in which colposuspension has been compared to other procedures. Anterior colporrhaphy (Kelly plication) was one of the first surgeries described to treat SUI in women.35 Several wellexecuted randomized controlled trials and carefully performed meta-analyses have shown that anterior colporrhaphy does poorly compared to colposuspension and its use as an anti-incontinence procedure should be
considered for historic interest only.5,36,37 Needle bladder neck suspensions were heralded as a minimally invasive procedure for stress incontinence and underwent innumerable minor modifications over more than 30 years of use. However, like anterior repairs, both clinical trials and meta-analyses revealed the poor longevity of needle bladder neck suspensions and they no longer play a major role in the surgical management of female SUI.5,33 Midurethral slings, developed in the mid 1990s by Ulmsten and colleagues,38 have offered a minimally invasive alternative to colpourethropexy. Data from clinical trials have been encouraging and a randomized trial between Burch and one type of midurethral sling – the tension-free transvaginal tape (TVT) – has shown that these two procedures have similar success rates after 2 years.32 In a randomized trial between laparoscopic Burch and the TVT procedure, Paraiso et al. determined that there was no statistically significant difference in cure rates between the two procedures, although the study did not have the necessary power to show such a difference.39 The results tended toward improved outcome for TVT with a 1-year postoperative SUI rate of 3.2% compared to 18.8% in the laparoscopic patients. The TVT procedure was noted to take a significantly shorter length of operative time (mean = 79 versus 132 minutes, p=0.003).
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Table 59.3. Comparison studies between colpourethropexy and other procedures Study
Alternate procedure
Success CU (%) vs. other (%)
n CU vs. n other
Follow-up
Bergman et al.58
Vs. anterior colporrhaphy
89 vs. 63
38 vs. 35
1 year
82 vs. 37
33 vs. 30
5 years
Black & Downs
85 vs. 50–70
Meta-analysis
1 year
Leach et al.5
84 vs. 61
Meta-analysis
≥4 years
89 vs. 31
18 vs. 15
1 year
74 vs. 42
35 vs. 33
14.2 years vs. 13.9 years
89 vs. 65
38 vs. 34
1 year
82 vs. 43
33 vs. 30
5 years
85 vs. 50–70
Meta-analysis
1 year
84 vs. 67
Meta-analysis
≥4 years
Difference not significant
Meta-analysis
1 year
84 vs. 83
Meta-analysis
≥4 years
80 vs. 81 68 vs. 78
108 vs. 137 followed-up 175 vs. 169 LOCF
2 years
Bergman et al.36 64
37
Kammerer-Doak et al. 54
Colombo et al.
Bergman et al.58
Vs. NBNS
36
Bergman et al.
64
Black & Downs 5
Leach et al.
64
Black & Downs
Vs. sling
Leach et al.5 Ward & Hilton
32
Vs. TVT
CU, colpourethropexy; LOCF, last observation carried forward; n, number of subjects in arm of trial; NBNS, needle bladder neck suspensions; TVT, tension-free vaginal tape.
A great deal of emphasis has been placed on urodynamic changes following colpourethropexy in the past. As seen in Table 59.4, there is a significant increase in urethral resistance after Burch colposuspension associated with an alteration in the physiology of micturition and the prevention of leakage in these patients. Changes to flow rates are not consistently significant but a trend can be seen toward slower rates. These are changes which patients may notice and they should be reassured that such changes are common and not worrisome. Maximum capacity and post-void residual volumes do not change significantly in these women. Interestingly, urethral closure pressures do not show significant changes. Of the six studies in Table 59.4, none demonstrated a significant difference in pre- and postoperative urethral closure pressure (UCP). This may be because urethral pressure profiles represent a portion of the urethral sphincter mechanism that is not affected by colposuspension. It is interesting to note that UCP is also unchanged in women who are made continent after periurethral collagen injection.40
Intraoperative complications Operating in the retropubic space or space of Retzius is a delicate procedure that requires specialized training. It is important to be prepared to recognize and manage
possible complications that can occur during surgery as listed in Table 59.5. It is equally important to recognize the morbidity associated with functional long-term complications following CU, specifically voiding dysfunction and irritative symptoms.
Hemorrhage and transfusion The space of Retzius has a robust collection of blood vessels crossing the area dissected for colposuspension. The approach to this area is therefore cautious and it is important to maintain meticulous hemostasis throughout the retropubic space. The proximity of the obturator canal and its neurovascular bundle is another threat that surgeons must be aware of and avoid.41 The risk of hemorrhage and the possibility of transfusion should be discussed with all patients as part of a complete consent process.
Lower urinary tract trauma During CU, bladder trauma is possible with dissection, retraction, or suture placement. As the bladder is amenable to repair, it is imperative that this damage is recognized at the time of surgery. Urethropexy sutures passed into the bladder should be removed to avoid stone formation. Their small diameter does not require 871
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Table 59.4. Urodynamic changes Preop → postop change
Follow-up
n
0.035 → 0.055
3–12 months
48
0.07 → 0.62
3.1 years (range 2–7 years)
40
0.166 → 0.332
≥1 year
46
Qmax
23.2 → 22 (NS)
3–12 months
48
Colombo et al.
Qmax
21.6 → 13.0
3.1 years (range 2–7 years)
40
Maher et al.59
Qmax
38 → 29
15 months (range 4–36 months)
21
Qmax
27.6 → 24.3 (NS)
12.4 years (range 10–15 years)
109
Qavg
14.5 → 8.8
3.1 years (range 2–7 years)
40
Maher et al.
Flow rate
27 → 20
9 months (range 4–72 months)
53
Su et al.62
MUCP
83.1 → 82.5 (NS)
≥1 year
46
Reference
Urodynamic measurement 65
2 max
Bhatia et al.
Urethral resistance (pves/Q
Colombo et al.61
Urethral resistance (pdet/Qmax2)
62
)
2 max
Su et al.
Urethral resistance (pves/Q 45
Bhatia et al.
61
63
Langer et al.
61
Colombo et al. 47
)
MUCP
40 → 46 (NS)
9 months (range 4–72 months)
53
63
MUCP
46.9 → 43.1 (NS)
12.4 years (range 10–15 years)
109
63
Maher et al.47 Langer et al.
MUCP
53.2 → 46.8 (NS)
12.4 years (range 10–15 years)
109
47
Maher et al.
PVR
5 → 7 (NS)
9 months (range 4–72 months)
53
Maher et al.59
PVR
2 → 5 (NS)
15 months (range 4–36 months)
21
PVR
19.4 → 24.6 (NS)
12.4 years (range 10–15 years)
109
MCC
342 → 335 (NS)
≥1 year
46
Maher et al.
MCC
482 → 500 (NS)
15 months (range 4–36 months)
21
Langer et al.63
MCC
486.2 → 459.5 (NS)
12.4 years (range 10–15 years)
109
Langer et al.
63
Langer et al. 62
Su et al.
47
MCC, maximal cystometric capacity; MUCP, maximal urethral closure pressure; n, number of subjects in colpourethropexy arm; NS, change not significant; pdet, detrusor pressure at Qmax; pves, ‘vesical pressure at voiding’; PVR, post-void residual.
Table 59.5. Intraoperative complications Complication Hemorrhage (>1000 ml) Transfusion
Reference
Incidence (%)
n
Maher et al.
0
53
Kenton et al.66
2
151
5 (CI 3–8%)
1131
Maher et al.
0
53
Kenton et al.66
0.7
151
67
1.2
82
Maher et al.
2
53
Ward & Hilton68
2
146
Kenton et al.66
1.3
151
Cosson et al.67
1.2
82
66
0.7
151
47
5
Leach et al.
47
Cosson et al. Cystotomy
47
Suture in bladder Kenton et al.
CI, confidence interval; n, number of subjects in colpourethropexy arm.
repair and another suture may be placed, taking care to remain away from the bladder. Ureteral injury following CU has been reported to be as high as 4/60.42 Ureteral kinking may occur as the anterior vaginal wall is pulled forward. This is an uncommon complication and if care is taken to remain within the triangle of safety described earlier in this chapter, the ureters should not be at risk. Cystoscopy is recommended after colposuspension43 and should note efflux from both ureters as well as the absence of suture in the urothelium.
Postoperative complications Brief urinary retention is common after colposuspension and all patients should be prepared for this (Table 59.6). Retention can be managed with a suprapubic or transurethral catheter or with intermittent self-catheterization. Ideally, these options can be discussed with the patient prior to surgery, allowing the patient to be prepared for whichever technique she finds most comfortable. Most patients will void on their own within 2 weeks,
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Urethra
Area safe for suture placement
Symphysis pubis Anterior vaginal wall
Cooper’s ligament Pelvic sidewall obturator internus
Obturator fossa Bladder
Figure 59.1. Safe placement of sutures in colpourethropexy.
although it is estimated that between zero and 21% will experience long-term voiding difficulty as discussed below (Table 59.7). Prophylactic measures can be taken to decrease some postoperative complications. Confirmation of sterile urine and appropriate perioperative antibiotics for all patients will decrease urinary tract and wound infections.44,45 Urinary tract infection after catheterization is common and should be anticipated in postcolposuspension patients. A low threshold for testing and treating possible urinary tract infections after pelvic surgery is acceptable. Prophylactic antibiotics in a patient with a suprapubic catheter have been shown to reduce the risk of urinary tract infection and should be administered.46 Wound complications include infections, seromas, and hernia formation. Infection rates range from 3.5 to 7% after Burch. Attention to the incision site and active management of any signs of infection with antibiotics will minimize this.
Incisional hernias occur in 3–4% of patients.32,47 Wide bites should be taken in the fascia while closing the wound to reduce the risk of hernia formation. The risk of deep venous thrombosis (DVT) is present in any pelvic surgery. A DVT rate of 2% has been reported in patients following a Burch procedure and the American College of Obstetricians and Gynecologists quotes a risk of 7–29% in general gynecologic surgery in their guidelines.48 Sequential compression stockings are recommend for all appropriate patients to reduce the risk of this complication.
Overactive bladder De novo urgency has been reported following pelvic surgery, particularly after anti-incontinence procedures. The cause is unclear and may involve alteration in the afferent nerves, a shift in the parasympathetic versus sympathetic motor nerves, or a reprogramming of the
Table 59.6. Immediate postoperative complications Complication
Reference
Incidence (%)
n
Notes
Urinary tract infection
Bergman 58
11
38
>1000 col/ml by SPC
8
53
32
146
2.4
82
5
21
47
Maher et al.
Ward & Hilton
68
Cosson et al.67 Wound infection
59
Maher et al.
Ward & Hilton
68
7
146
66
3.5
151
67
Cosson et al.
3.7
82
Colombo et al.54
25
35
Ward & Hilton68
12
146
Kenton et al. Retention (1 week–1 month)
Within 6 weeks after surgery. Note very high catheter use
Did not resume voiding before discharge from hospital after a mean of 6.7 days
n, number of subjects in colpourethropexy arm; SPC, suprapubic catheter.
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Table 59.7. Long-term complications of colposuspension Complication Retention >1 month
Reference
Incidence (%)
n
Notes
0
38
SPC
5 (CI 3–7%)
Meta-analysis
6
53
One patient had ‘voiding difficulties’ before and after surgery
Colombo et al.54
0
35
SPC
68
21
146
0.7
151
Wiskind et al.
Decreased from before surgery
131
Colombo et al.54
8
24
Langer et al.63
3.9
127
12
50
Postcolposuspension syndrome
2.3
87
Postcolposuspension syndrome
4
53
‘Persistent wound pain’
58
Bergman et al. 5
Leach et al.
47
Maher et al.
Ward & Hilton 66
Kenton et al. Dyspareunia
Chronic pain
52
Galloway et al.50 51
Feyereisl et al. 47
Maher et al.
Both with concomitant posterior colporrhaphy
n, number of subjects in colpourethropexy arm; SPC, suprapubic catheter.
neural control loops secondary to the increase in outflow resistance created by the anti-incontinence procedure. It is possible that a portion of the reported de novo postoperative urgency is persistence of OAB present prior to surgery but less symptomatic because of patients’ limited bladder capacity due to SUI; when finally able to hold a larger volume, the patient may pass a threshold volume triggering the sensation of urgency. Table 59.8
lists studies of OAB symptoms following surgery. In a patient with no OAB symptoms, the risk of developing de novo urgency is 5–30%. Paradoxically, resolution of OAB symptoms is reported in 20–73% of women undergoing CU. Because no consistent predictors of outcome of OAB symptoms have been defined, it is appropriate to discuss the possibility of changes in or the development of OAB symptoms with patients considering surgery.
Table 59.8. Postoperative changes in overactive bladder symptoms Postoperative change De novo OAB symptoms
Reference
Incidence (%)
n
5
40
Alcalay et al.
15.4
104
Su et al.62
6.5
46
11 (CI 8–16%)
241
6
53
5
21
61
Colombo et al. 31
5
Leach et al.
47
Maher et al.
59
Maher et al.
69
Resolution of OAB symptoms
Klutke & Ramos
30
23
Langer et al.63
17
102
Kenton et al.66
8
99
31
Alcalay et al.
Notes
By CMG
20
5
47
Maher et al.
60
5
In previous surgery patients
Maher et al.59
60
5
In low urethral closure pressure patients
63
52
25
66
73
52
Langer et al.
Kenton et al.
By CMG
CMG; cystometrogram; n, number of subjects; OAB, overactive bladder.
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Urinary retention There are reports of urinary retention after 1 month ranging from 0.7 to 21% (see Table 59.7). Each of these studies limited the definition of this complication to those women who required catheterization. The wide discrepancy is therefore not explained by a difference in diagnosis. It is possible that this inconsistency is a result of the subjective variation in the tension on the vaginal sutures as they are tied to Cooper’s ligament or to differences in the populations studied. Physicians are cautioned to avoid overcorrection when tying sutures. Less frequently reported are the more subtle, but none the less problematic changes in voiding such as double voiding, positional voiding, and prolonged voiding associated with these procedures. There is debate about the timing of surgical management of postoperative voiding dysfunction. Although it is commonly taught that there is no harm in a watch and wait approach, recent basic science using animal models of obstruction has demonstrated structural changes that occur within the first 4 weeks.49 Care should be taken to assess obstructive symptoms and early intervention should be considered.
Dyspareunia and chronic pain Any surgery carries with it the risk of chronic pain. CU can change the axis of the vagina in relation to other organs and supporting structures, causing discomfort. Adhesions and nerve damage can result in pelvic pain. Postcolposuspension syndrome has been described as a pain in the groin that may be relieved by release of the ipsilateral sutures.50,51 Dyspareunia, although more commonly attributed to surgery to the posterior vagina, has been reported in 3.9–8% of CU trials. It is notable that in one study there was a decrease in painful coitus after colposuspension.52
Pelvic organ prolapse In 1968, Burch described a high rate of enterocele development after colposuspension, and ‘special attention was therefore directed to the cul-de-sac as the most vulnerable part of the repair’.53 Since then, surgeons have attributed prolapse in various compartments to the colposuspension itself. Colombo et al. demonstrated that the Burch procedure is not an adequate treatment for cystocele and should not be considered a surgery for anterior prolapse.54 Wiskind et al. published a 26.7% rate of reoperation for prolapse after Burch procedure.52 However, Olsen et al. estimated that 11.1%
of women under 80 will have a prolapse requiring surgery, followed by a reoperation rate nearing 30%.55 It is believed that the high reoperation rate is due in part to a physiologic predisposition to pelvic floor disorders that necessitated the initial surgery. It is logical that a woman who developed incontinence from a loss of support for the urethra would be at risk of failure of support in other uterovaginal compartments. A recent large study randomizing women to Burch or TVT found a significantly greater number of women had another surgery for prolapse within 2 years after colposuspension (4.8% versus zero).32 However, the high urinary retention rate of 21% seen in the Burch arm of that study suggests that the retropubic sutures were tied very tightly and thus could alter the anatomy of the pelvic organs and permit abdominal pressures to create or worsen defects in pelvic floor support. Whether or not colposuspension is a risk factor for prolapse is not yet clear and physicians are well advised to follow Burch’s advice to thoroughly evaluate and treat pelvic floor defects at the time of surgery.
Osteitis pubis Osteitis pubis – an inflammatory condition related to periosteal trauma which causes pain at the symphysis, possibly radiating to the perineum, thighs, and abdomen – has been reported in 2–3% of women undergoing a MMK CU.56 Pain is aggravated by the use of adjacent musculature such as with ambulation and coughing. There is no literature regarding non-infectious osteitis pubis related to Burch colposuspension. There is one case report of a woman with pseudomonas infection causing osteitis pubis following a Burch procedure.57 The MMK procedure should be recognized as a significant step forward in the management of SUI but in light of the evidence above, the Burch and its modifications are preferred for colposuspension.
Summary With the current availability of less invasive surgery, the role of CU in the care of women with SUI has evolved. Although it is routinely offered as a first line therapy for women with surgically managed SUI, women increasingly elect less invasive procedures. In this way, the role of CU has become most important during abdominal reconstruction for pelvic organ prolapse. The gold standard sacrocolpopexy is often combined with a CU in women with advanced stage pelvic organ prolapse and urodynamic SUI. Recent evidence from the NIH Pelvic Floor Disorders Network indicates that 875
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inclusion of a CU may be appropriate for all women undergoing sacrocolpopexy regardless of preoperative testing results. When patients are properly selected and the procedure is performed according to contemporary recommendations, patient and surgeon can anticipate durable results with minimal complications whether the CU is performed as a stand-alone procedure for SUI or as a component of more comprehensive surgery for pelvic organ prolapse.
REFERENCES 1. Marshall VF, Marchetti AA, Krantz KE. The correction of stress incontinence by simple vesicourethral suspension. Surg Gynecol Obstet 1949;88:509–18. 2. Burch JC. Urethrovaginal fixation to Cooper’s ligament for correction of stress incontinence, cystocele, and prolapse. Am J Obstet Gynecol 1961;81:281–90. 3. Tanagho EA. Colpocystourethropexy: the way we do it. J Urol 1976;116:751–3. 4. Green TH Jr. Urinary stress incontinence: differential diagnosis, pathophysiology, and management. Am J Obstet Gynecol 1975;122:368–400. 5. Leach GE, Dmochowski RR, Appell RA et al. Female Stress Urinary Incontinence Clinical Guidelines Panel summary report on surgical management of female stress urinary incontinence. The American Urological Association. J Urol 1997;158:875–80. 6. Vancaillie TG, Schuessler W. Laparoscopic bladder neck suspension. J Laparoendosc Surg 1991;1:169–73. 7. Pereyra AJ. A simplified surgical procedure for the correction of stress incontinence in women. West J Surg Obstet Gynecol 1959;67:223–6. 8. Kim HL, Gerber GS, Patel RV et al. Practice patterns in the treatment of female urinary incontinence: a postal and internet survey. Urology 2001;57:45–8. 9. Jha S, Arunkalaivanan AS, Davis J. Surgical management of stress urinary incontinence: a questionnaire based survey. Eur Urol 2005;47:648–52. 10. Fantl JA, Newman DK, Colling J et al. Urinary incontinence in adults: acute and chronic management. Clinical Practice Guideline, No. 2, 1996 Update. Rockville, MD: US Department of Health and Human Services. Public Health Service, Agency for Health Care Policy and Research. AHCPR Publication No. 96-0682. March 1996. 11. Viktrup L, Koke S, Burgio KL et al. Stress urinary incontinence in active elderly women. South Med J 2005;98:79–89. 12. Waetjen LE, Subak LL, Shen H et al. Stress urinary incontinence surgery in the United States. Obstet Gynecol 2003;101:671–6. 13. Diokno AC, Burgio K, Fultz H et al. Prevalence and
outcomes of continence surgery in community dwelling women. J Urol 2003;170:507–11. 14. Bump RC, Mattiasson A, Bo K et al. The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 1996;175:10–7. 15. Karram MM, Bhatia NN. The Q-tip test: standardization of the technique and its interpretation in women with urinary incontinence. Obstet Gynecol 1988;71:807–11. 16. Blaivas JG. Classification of stress urinary incontinence. Neurourol Urodyn 1983;2:103–4. 17. Bergman A, Koonings PP, Ballard CA. Negative Q-tip test as a risk factor for failed incontinence surgery in women. J Reprod Med 1989;34:193–7. 18. McGuire EJ, Lytton B, Pepe V et al. Stress urinary incontinence. Obstet Gynecol 1976;47:255–64. 19. Sand PK, Bowen LW, Panganiban R et al. The low pressure urethra as a factor in failed retropubic urethropexy. Obstet Gynecol 1987;69:399–402. 20. Richardson DA, Ramahi A, Chalas E. Surgical management of stress incontinence in patients with low urethral pressure. Gynecol Obstet Invest 1991;31:106–9. 21. Sand PK, Winkler H, Blackhurst DW et al. A prospective randomized study comparing modified Burch retropubic urethropexy and suburethral sling for treatment of genuine stress incontinence with low-pressure urethra. Am J Obstet Gynecol 2000;182:30–4. 22. Appell RA. Argument for sling surgery to replace bladder suspension for stress urinary incontinence. Urology 2000;56:360–3. 23. Bump RC, Sugerman HJ, Fantl JA et al. Obesity and lower urinary tract function in women: effect of surgically induced weight loss. Am J Obstet Gynecol 1992;167:392–7; discussion 397–9. 24. Zivkovic F, Tamussino K, Pieber D et al. Body mass index and outcome of incontinence surgery. Obstet Gynecol 1999;93:753–6. 25. Dainer M, Hall CD, Choe J et al. Pregnancy following incontinence surgery. Int Urogynecol J Pelvic Floor Dysfunct 1998;9:385–90. 26. DeLancey JO. Structural support of the urethra as it relates to stress urinary incontinence: the hammock hypothesis. Am J Obstet Gynecol 1994;170:1713–20; discussion 1720–3. 27. Germain MM, Ostergard DR. Retropubic Surgical Approach for Correction of Genuine Stress Incontinence in Urogynecology and Urodynamic: Theory and Practice. Baltimore: Williams and Wilkins, 1996. 28. Burch JC. Urethrovaginal fixation to Cooper’s ligament for correction of stress incontinence, cystocele, and prolapse. Am J Obstet Gynecol 1961;81:281–90. 29. Lapitan MC, Cody DJ, Grant AM. Open retropubic colposuspension for urinary incontinence in women. Cochrane Database Syst Rev 2003;CD002912.
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30. Weber AM, Abrams P, Brubaker L et al. The standardization of terminology for researchers in female pelvic floor disorders. Int Urogynecol J Pelvic Floor Dysfunct 2001;12:178–86. 31. Alcalay M, Monga A, Stanton SL. Burch colposuspension: a 10–20 year follow up. Br J Obstet Gynaecol 1995;102:740–5. 32. Ward KL, Hilton P. A prospective multicenter randomized trial of tension-free vaginal tape and colposuspension for primary urodynamic stress incontinence: two-year followup. Am J Obstet Gynecol 2004;190:324–31. 33. Jarvis GJ. Surgery for genuine stress incontinence. Br J Obstet Gynaecol 1994;101:371–4. 34. Moehrer B, Carey M, Wilson D. Laparoscopic colposuspension: a systematic review. BJOG 2003;110:230–5. 35. Kelly HA, Dumm WM. Urinary incontinence in women, without manifest injury to the bladder. Surg Gynecol Obstet 1914;18:444–450. 36. Bergman A, Elia G. Three surgical procedures for genuine stress incontinence: five–year follow-up of a prospective randomized study. Am J Obstet Gynecol 1995;173:66–71. 37. Kammerer-Doak DN, Dorin MH, Rogers RG et al. A randomized trial of Burch retropubic urethropexy and anterior colporrhaphy for stress urinary incontinence. Obstet Gynecol 1999;93:75–8. 38. Ulmsten U, Henriksson L, Johnson P et al. An ambulatory surgical procedure under local anesthesia for treatment of female urinary incontinence. Int Urogynecol J Pelvic Floor Dysfunct 1996;7:81–5; discussion 85–6. 39. Paraiso MF, Walters MD, Karram MM et al. Laparoscopic Burch colposuspension versus tension-free vaginal tape: a randomized trial. Obstet Gynecol 2004;104:1249–58. 40. Monga AK, Stanton SL. Urodynamics: prediction, outcome and analysis of mechanism for cure of stress incontinence by periurethral collagen. Br J Obstet Gynaecol 1997;104:158–62. 41. Shull BL. Anterior paravaginal defects. In: Rock JA, Thompson JD (eds) Te Linde’s Operative Gynecology, 8th ed. New York: Lippincott, Williams & Wilkins, 1997: 997–9. 42. Harris RL, Cundiff GW, Theofrastous JP. The value of intraoperative cystoscopy in urogynecologic and reconstructive pelvic surgery. Am J Obstet Gynecol 1997;177:1367–71. 43. Dwyer PL, Carey MP, Rosamilia A. Suture injury to the urinary tract in urethral suspension procedures for stress incontinence. Int Urogynecol J Pelvic Floor Dysfunct 1999;10:15–21. 44. Hamasuna R, Betsunoh H, Sueyoshi T et al. Bacteria of preoperative urinary tract infections contaminate the surgical fields and develop surgical site infections in urological operations. Int J Urol 2004;11:941–7. 45. Bhatia NN, Karram MM, Bergman A. Role of antibiotic
prophylaxis in retropubic surgery for stress urinary incontinence. Obstet Gynecol 1989;74(4):637–9. 46. Rogers RG, Kammerer-Doak D, Olsen A et al. A randomized, double-blind, placebo-controlled comparison of the effect of nitrofurantoin monohydrate macrocrystals on the development of urinary tract infections after surgery for pelvic organ prolapse and/or stress urinary incontinence with suprapubic catheterization. Am J Obstet Gynecol 2004;191:182–7. 47. Maher C, Dwyer P, Carey M et al. The Burch colposuspension for recurrent urinary stress incontinence following retropubic continence surgery. Br J Obstet Gynaecol 1999;106:719–24. 48. ACOG Practice Bulletin Number 21, October 2000. 49. Austin JC, Chacko SK, DiSanto M et al. A male murine model of partial bladder outlet obstruction reveals changes in detrusor morphology, contractility and myosin isoform expression. J Urol 2004;172:1524–8. 50. Galloway NT, Davies N, Stephenson TP. The complications of colposuspension. Br J Urol 1987;60:122–4. 51. Feyereisl J, Dreher E, Haenggi W et al. Long-term results after Burch colposuspension. Am J Obstet Gynecol 1994;171:647–52. 52. Wiskind AK, Creighton SM, Stanton SL. The incidence of genital prolapse after the Burch colposuspension. Am J Obstet Gynecol 1992;167:399–404; discussion 404–5. 53. Burch JC. Cooper’s ligament urethrovesical suspension for stress incontinence. Nine years’ experience – results, complications, technique. Am J Obstet Gynecol 1968;100:764–74. 54. Colombo M, Vitobello D, Proietti F et al. Randomised comparison of Burch colposuspension versus anterior colporrhaphy in women with stress urinary incontinence and anterior vaginal wall prolapse. BJOG 2000;107:544–51. 55. Olsen AL, Smith VJ, Bergstrom JO et al. Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 1997;89:501–6. 56. Lentz SS. Osteitis pubis: a review. Obstet Gynecol Surv 1995;50:310–5. 57. Michiels E, Knockaert DC, Vanneste SB. Infectious osteitis pubis. Neth J Med 1990;36:297–300. 58. Bergman A, Ballard CA, Koonings PP. Comparison of three different surgical procedures for genuine stress incontinence: prospective randomized study. Am J Obstet Gynecol 1989;160:1102–6. 59. Maher CF, Dwyer PL, Carey MP et al. Colposuspension or sling for low urethral pressure stress incontinence? Int Urogynecol J Pelvic Floor Dysfunct 1999;10:384–9. 60. Culligan PJ, Goldberg RP, Sand PK. A randomized controlled trial comparing a modified Burch procedure and a suburethral sling: long-term follow-up. Int Urogynecol J Pelvic Floor Dysfunct 2003;14:229–33; discussion 233.
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61. Colombo M, Scalambrino S, Maggioni A et al. Burch colposuspension versus modified Marshall–Marchetti– Krantz urethropexy for primary genuine stress urinary incontinence: a prospective, randomized clinical trial. Am J Obstet Gynecol 1994;171:1573–9. 62. Su TH, Wang KG, Hsu CY et al. Prospective comparison of laparoscopic and traditional colposuspensions in the treatment of genuine stress incontinence. Acta Obstet Gynecol Scand 1997;76:576–82. 63. Langer R, Lipshitz Y, Halperin R et al. Long-term (10–15 years) follow-up after Burch colposuspension for urinary stress incontinence. Int Urogynecol J Pelvic Floor Dysfunct 2001;12:323–6; discussion 326–7. 64. Black NA, Downs SH. The effectiveness of surgery for stress incontinence in women: a systematic review. Br J Urol 1996;78:497–510. 65. Bhatia NN, Bergman A, Karram M. Changes in urethral
resistance after surgery for stress urinary incontinence. Urology 1989;34:200–4. 66. Kenton K, Oldham L, Brubaker L. Open Burch urethropexy has a low rate of perioperative complications. Am J Obstet Gynecol 2002;187:107–10. 67. Cosson M, Boukerrou M, Narducci F et al. Long-term results of the Burch procedure combined with abdominal sacrocolpopexy for treatment of vault prolapse. Int Urogynecol J Pelvic Floor Dysfunct 2003;14:104–7. 68. Ward K, Hilton P. Prospective multicentre randomised trial of tension-free vaginal tape and colposuspension as primary treatment for stress incontinence. BMJ 2002;325:67–70. 69. Klutke JJ, Ramos S. Urodynamic outcome after surgery for severe prolapse and potential stress incontinence. Am J Obstet Gynecol 2000;182:1378–81.
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60 An overview of pubovaginal slings: evolution of technology Emily E Cole, Harriette M Scarpero, Roger R Dmochowski
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INTRODUCTION Urinary incontinence has been discussed in the writings of physicians since ancient Egyptian times.1 During the past century, many corrective procedures have been described showing varying degrees of success. Since the first description of the sling procedure nearly 100 years ago, the popularity of slings has waxed and waned. Initially, the sling was associated with high complication rates and was therefore reserved for the treatment of recurrent or refractory stress urinary incontinence (SUI). In the past 30 years, great strides have been made in the understanding of the pathophysiology of incontinence, leading to a resurgence in the popularity of pubovaginal slings. In 1997, the American Urological Association (AUA) Female Stress Incontinence Clinical Guidelines Panel concluded that suburethral slings, along with retropubic bladder suspensions, were the most efficacious procedures for long-term success in the treatment of SUI.2 With a greater than 80% probability of improvement of symptomatic SUI at 48 months or longer, the pubovaginal sling has become the gold standard for surgical correction of SUI. Technologic advances resulting in novel methods of suspension, such as the minimally invasive midurethral sling, have contributed to decreased surgical time and shorter postoperative convalescence. At the same time, the glut of technology and the continuous introduction of new suspension techniques have made interpretation of results more difficult. This, combined with controversy surrounding the lack of standardization in outcomes reporting, leads to many questions. Has enthusiasm for new technology been supported by long-term efficacy? Have de novo complications outweighed the utility and efficacy of novel techniques and materials? This chapter will address the current sling techniques and materials available with a systematic evaluation of the contemporary literature. The goal is to discuss the techniques, safety, tolerability, and efficacy of the standard bladder neck sling and the midurethral sling, and potentially identify which procedure is appropriate in certain situations.
PATHOPHYSIOLOGY OF STRESS INCONTINENCE The popularity of pubovaginal and midurethral slings has mirrored advances in the understanding of the pathophysiology of SUI. In order to understand how a sling prevents SUI, it is first important to appreciate normal pelvic floor adaptation to increases in intraabdominal pressure. Traditionally, the urethral continence mechanism was considered to be composed of two components: the internal sphincter, which repre-
sents a continuation of the detrusor smooth muscle, and the striated external sphincter.3 From a clinical standpoint, the bladder neck/proximal urethra functions as a sphincteric mechanism in both sexes; however, there is no identifiable anatomic sphincter as such. Rather, a complex interaction of several factors – including smooth and striated muscle, intracellular matrix, and intrinsic mucosal factors – interplay to account for the components of a functional sphincter.4–6 The principles underlying the function of this complex are: 1) watertight apposition of the urethral lumen; 2) compression of the wall around the lumen; 3) structural support to keep the proximal urethra from moving during increases in pressure; 4) a means of compensating for abdominal pressure changes; and 5) neural control.7 While the complex interactions resulting in these functional principles are not completely understood, several factors are known to assist in the maintenance of continence in the neurologically intact female. At rest, a seal composed of richly vascularized submucosal connective tissue compresses mucosal urethral folds to create a watertight closure.8 This ‘mucosal seal’ is augmented by heightened wall tension created by luminal secretions from the periurethral glands. In addition, slow-twitch muscle fibers in the paraurethral layer of the external urethral sphincter maintain passive continence by tonic contraction of the urethra.9,10 This collective mechanism undergoes several changes in the face of increased intra-abdominal pressure. Reflex contraction of the levator ani musculature and urogenital diaphragm elevates suburethral support tissue, compressing the proximal urethra. These muscle complexes form a broad hammock upon which the pelvic viscera lie. The fascial covering of the levator ani consists of two leaves: the endopelvic fascia (abdominal side) and the pubocervical fascia (vaginal side). The two leaves envelop the proximal urethra and bladder neck medially and fuse laterally to insert along the tendinous arc of the obturator internus.11 Augmenting the effects of the support network, striated muscle in the urethrovaginal sphincteric mechanism and compressor urethrae aid in compressing the urethra during intra-abdominal pressure transmission. The net result of the interplay of these changes is increased outlet resistance and continence. Specific aspects of the continence mechanism have led to several theories about the pathophysiology of continence/incontinence. Until the early 1980s the understanding of stress incontinence was mainly based on the Enhorning theory.12 Enhorning suggested that pressure transmission from the bladder to the urethra occurs because the urethra lies with the bladder within the abdomen. Based on this theory, increases in intra-
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abdominal pressure were thought to be transmitted directly to the bladder neck and urethra, compressing them and preventing leakage. Stress incontinence was thought to occur due to the descent of the bladder neck, the proximal urethra thereby not residing within the abdomen, and not able to be compressed when subjected to increases in intra-abdominal pressure. Thus, most surgical procedures aimed not only to support but also to elevate the bladder neck and urethra so that they would respond once again to changes in abdominal pressure.13 The 1990s witnessed a change in approach stimulated by DeLancey’s hammock theory.14 According to DeLancey, continence was due to tension arising within a subcervical hammock composed of muscle (anterior pubourethral bundle of the levator ani) held by two ligaments (pubourethral and conjunctive) connected to the endopelvic fascia. In the normal continent female, this musculofascial support provides a hammock upon which the urethra is compressed during increases in intra-abdominal pressure. This support mechanism constitutes a hammock under the urethra in its upper and middle portions. The hammock is composed of a segment of the anterior vaginal wall that is attached to the muscles of the pelvic floor and to the arcus tendineus. When either active or passive supports are altered, the urethra and bladder neck are no longer well supported, resulting in a defect in transmission of intra-abdominal pressure to the urethra. Based on the hammock theory, to restore continence the bladder neck and proximal urethra do not have to be elevated, but should be provided with adequate underlying support. This view advocates the placement of slings beneath the bladder neck. More recently, much attention has been given to a new class of slings placed at the midurethra rather than the bladder neck. The midurethra has previously been found to be the site of maximal intraurethral pressure.15 With this in mind, Petros and Ulmsten proposed in their ‘integral theory’ that the midurethra, rather than the bladder neck, may be the key mechanism involved in urinary continence.16 Their theory is based on the idea that the opening and closure of the urethra and bladder neck are mainly controlled by three anatomical structures: 1) the tension within the pubourethral ligaments; 2) the activity of the pubococcygeus and levator ani muscles; and 3) the condition of the suburethral vaginal hammock. All of these structures are interconnected by connective tissues. Tension in the pubourethral ligaments ensures that the muscular component of support and the hammock provided by the vaginal wall interact correctly. If tension is adequate, three opposing forces result in kinking of the urethra and bladder neck
and subsequent continence. The three forces (vectors) that influence the opening and closure of the inner urethra and bladder neck include: 1) forward force resulting from contraction of the pubococcygeus muscle; 2) backward force caused by contraction of the levator ani musculature; and 3) inferior force controlled by the longitudinal muscle of the anus. The midurethral sling was described according to this theory in order to correct the lack of tension in the pubourethral ligaments, to restore the attachment of the urethra to the pubic bone, and to restore the connections of the urogenital structures (Fig. 60.1).
PUBOVAGINAL SLINGS History At the beginning of the 20th century, the first slings were performed entirely from an abdominal approach and utilized autologous tissues. Initial attempts to increase outlet resistance using detached or tunneled muscle flaps met with severe complications, such as urethral
a
b
Figure 60.1. Pressure transmission changes associated with the implantation of bladder neck (a) and midurethral support (b). (Courtesy of Professor D. Staskin, Harvard Medical School, Boston, USA.) 881
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sloughing, fistula formation, and bladder outlet obstruction. In 1942, Aldridge and colleagues performed the first abdominovaginal sling, proving that careful anatomic dissection revealed an ‘almost bloodless plane’ on either side of the urethra, permitting minimally traumatic entry into the space of Retzius.17 Despite reports of long-term success, the complication rate continued to be high, and the popularity of the procedure waned over the following several decades. As long-term efficacy of needle suspensions began to be questioned in the 1970s, there was a resurgence of interest in the pubovaginal sling. Improving on Aldridge’s technique, McGuire and Lytton isolated a strip of rectus fascia and left it attached laterally on one side.18 The free end of the strip was passed through the body of the rectus muscle, positioned under the urethra and reattached to the rectus fascia on the other side. Blaivas and Jacobs further modified the technique by completely detaching the fascial strip on both ends, and perforating the endopelvic fascia from below.19
Operative technique (bladder neck slings) Preoperative considerations Informed consent should involve a discussion of the risks, benefits, and options for sling surgery. Risks include, but are not limited to, bleeding, infection, injury to the bladder or urethra, dyspareunia, formation of anterior or apical prolapse, vesico-vaginal fistula formation, urinary retention, and de novo or worsening storage symptoms. An hour prior to surgery, parenteral antibiotics are given (ampicillin and gentamicin or a fluoroquinolone). Antiembolic stockings and sequential compression devices are applied prior to induction of anesthesia. Following induction of general or regional anesthesia, the patient is carefully placed in a slightly exaggerated dorsal lithotomy position with appropriate pressure points adequately padded. Betadine or Hibiclens preparation solution is used to scrub the surgical field from umbilicus to mid-thigh, including the vagina. The patient is draped in standard surgical fashion, and a urethral catheter is placed for continuous drainage.
Harvest of rectus fascia (not performed if using alternative biologic materials) An approximately 7 cm Pfannenstiel incision is made and carried down through the subcutaneous tissues, exposing the rectus fascia. A strip of rectus fascia approximately 2 × 7 cm is marked and excised using cut electrocautery. The sling is soaked in antibiotic solution while the fascial defect is closed with No. 1 delayed absorbable sutures. The skin is left open to assist in the passage of
the sling sutures later in the procedure. Meanwhile, the sling is prepared for placement by securing No. 1 polypropylene sutures at either end. If autologous rectus fascia is not to be utilized, the graft of choice may be placed in antibiotic solution at any time.
Vaginal dissection The urethral catheter balloon is palpated to confirm the location of the bladder neck. An inverted U is the incision of choice for maximal exposure of the bladder neck. The apex of the U should be based at the midurethra and the ends should extend laterally to the level of the bladder neck. A vertical midline incision from the midurethral to the bladder neck or beyond may be used if concomitant procedures are planned. With either incision, the vaginal mucosa is carefully dissected from the underlying surface of the pubourethral or pubocervical fascia using scissors. Lateral dissection should continue to the inferior edge of the pubic symphysis. Using an index finger as a guide, the endopelvic fascia is perforated sharply bilaterally. When performing this maneuver, it is recommended that the point of the scissors be oriented towards the ipsilateral shoulder and should remain just under the pubic symphysis. Once this is complete, an index finger can be used to carefully develop the space of Retzius. The openings in the endopelvic fascia should be large enough to accommodate an arm of the fascial sling, allowing the sutured ends of the sling material to reside in the retropubic space.
Suture passage Ligature carriers are passed into the retropubic space just superior to the pubic symphysis, approximately 2 cm lateral to the midline on each side. Each needle should be guided down along the pubic bone through the opening in the endopelvic fascia using a finger in the retropubic space as a guide. The needle is guided through the fascial opening and out of the lateral aspect of the vaginal incision on each side.
Cystoscopy Cystourethroscopy should now be performed to ensure the integrity of the bladder, ureters, and urethra. Ureteral integrity can be confirmed with the visualization of efflux from bilateral ureteral orifices. If difficult to assess, indigo carmine can be administered to improve visualization. A 70-degree lens is utilized to check the dome and superolateral aspects of the bladder where penetration with needles is most likely to occur. It is important to visualize the entire path of the needle from the dome to the bladder neck and proximal urethra to rule out injury to these structures. If the bladder has been pen-
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etrated, the offending needle should be removed and can be re-passed once the bladder has been completely drained. Cystoscopy should be repeated following each pass to confirm bladder and urethral integrity.
The pre-placed sling sutures are fed through the eyes of the passed needles. The needles are then withdrawn, pulling the sling sutures up and out of the abdominal incision. The sling is positioned in the midline at the level of the bladder neck and is fixed to the periurethral fascia bilaterally with 4-0 vicryl sutures. The vaginal incision is closed with 2-0 absorbable sutures. Sling tension is set in the abdominal incision. Typically, the suture ends are tied together loosely, commonly with two fingers easily able to be inserted under the knot. After two knots have been thrown, a hemostat is used to secure the knot. The urethral catheter is removed and the cystoscope is inserted. If there is no ‘road bump’ when the cystoscope is passed, this indicates that sling tension is not too great and additional knots can be added to the sutures. If there is a ‘road bump’, the existing knots should be untied and the sling should be loosened. The abdominal wound is irrigated and closed in several layers with absorbable sutures. The vagina is packed with premarin-coated gauze. Saline-soaked gauze may be utilized in premenopausal women.
cedures for SUI by conducting a comprehensive review of published results. The panel concluded that suburethral slings, along with retropubic bladder suspensions, are the most efficacious procedures for the treatment of SUI.2 There was a greater than 80% probability of improvement or cure at 48 months following a suburethral sling. It should be noted that at the time of the panel’s report, slings were not yet standard treatment for primary SUI, but were reserved for complicated cases in which prior surgery had failed. It can be extrapolated from this information that if slings were utilized as initial treatment in cases of primary SUI, the success rates would have been even higher. Although mediumto long-term data have only recently been available for the use of slings in the treatment of intrinsic sphincter deficiency (ISD), it was the opinion of the panel that slings would also be an effective treatment for patients with primary ISD. Since the release of this report, pubovaginal slings have been considered the gold standard for treatment of SUI. With the increased popularity, however, came a desire for improvement of the procedure. Novel sling materials and methods of suspension have decreased operative times and reduced postoperative convalescence. With a rapid influx of new products has come a plethora of short-term results and claims that each procedure is better than the last. There is currently no clear evidence as to which sling material is the best.
Postoperative course
Autologous materials
Patients are usually admitted for overnight observation. The vaginal packing is removed on the following morning and the urethral catheter may or may not be removed. A voiding trial should be performed and if the patient cannot void to completion, the catheter may be replaced or the patient may be discharged with plans for intermittent self-catheterization. If the bladder was penetrated at any time during the procedure, the patient should be discharged with the urethral catheter in place, with plans for an outpatient voiding trial in 2–3 days. Early ambulation is encouraged, but strenuous exercise and heavy lifting should be avoided. Patients should refrain from sexual intercourse until their vaginal incision is completely healed (approximately 6 weeks). Patients can usually be released to full activity at 6 weeks.
The first autologous tissues used to increase bladder outlet resistance included gracilis muscle,20 pyrimidalis flaps,21 and levator ani.22 Although Aldridge popularized the use of rectus fascia in the 1940s,17 this material only achieved widespread use nearly 40 years later when its efficacy was confirmed.18,19 Price23 introduced the use of fascia lata as a sling material, a practice that has been widely used in the past. Both of these materials are durable, available in most patients, and are not predisposed to rejection. The drawback to the use of this material is that the harvest does require an additional incision and extended convalescence. While the extra incision and dissection associated with the sling harvest does add operating time, in most cases both parts of the procedure can be completed within 1 hour. In our experience, the postoperative convalescence is typically brief and the patient is at full level of activity in less than 6 weeks. The results of autologous slings with rectus fascia are summarized in Table 60.1. Data supporting the use of autologous materials in sling surgery are abundant. While the subjective and objective cure rates range from 5053 to 100%,27,35,42 the
Setting sling tension
Pubovaginal sling results Overview The AUA Female Stress Incontinence Clinical Guidelines Panel investigated the efficacy of different surgical pro-
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Table 60.1.
Results of rectus fascia and fascia lata slings
Author
Material
No. of patients
Sling length (cm)
Mean F/U (months)
Cure (%)
Kaufman24
R
15
15
<48
93.3
Schultz-Lampel et al.
R
11
–
24
63.6
Loughlin26
R
22
5
15
72.7
Mason & Roach
R
63
4
12
93.7
Zaragoza28
R
60
6–8
25
100
Siegel et al.29
R
20a
–
185
80
Carr et al.
R
96
11–13
22
97.9
Barbalias et al.31
R
32
12
>30
65.6
Chaikin et al.
R
251
15
37
72.9
Maheshkumar et al.33
R
43b
–
17.4
95.3
Hassouna & Ghoneim34
R
82
7
41
89.1c
Kane et al.35
R
13
5d
26
100
R
247
6–8
51
82.2
Kochakarn et al.
R
100
–
12.1
94
Groutz et al.38
R
67
15
34
67.2
Kuo39
R
24
20
24
95.8
Borup& Nielson
R
31
12
60
96.8
Gormley et al.41
R
41
–
>74
95.1
De Rossi
R
27
8
20
100
Lucas et al.43
R
156
e
>30
76
Chou et al.44
R
98
12
36
95c
R
50
–
60f
63.9
25
27
30
32
36
Morgan et al.
37
40
42
Pfitzenmaier et al.45 46
Guatelli et al.
g
h
R
35
>20
26
74.2
Almeida et al.
R
30
–
33
70
Rodrigues et al.48
R
126
–
70.3
74.4
Kreder & Austin49
R/FL
27
–
22
96.3
Golomb et al.
R/FL
18
15
30.7
88.9
Haab et al.51
R/FL
37
12–15
48.2
73
Wright et al.52
R/FL
33
13–15
16
93.9
Petrou & Frank
R/FL
14
10
17
50
Richter et al.54
R/FL
57i
24
42
84
R/FL
71
12
44
90.1
R/FL
23
10
30.5
94.1c
FL
36
>24
>24
94.4
Addison et al.
FL
97
–
12
86.6
Beck et al.59
FL
170
>17
>24
98.2
Karram & Bhatia
FL
10
5×7
>12
90
Govier et al.61
FL
30
>24
14
69.7
Berman & Kreder62
FL
14
>17
14.9
71.4
47
50
53
Flynn & Yap
55
Chien et al.56 57
Low
58
60
63
h
Phelps et al.
FL
27
>20
20
77.8
Latini et al.64
FL
63
18–22
53
85c
Ellerkmann et al.65
FL
39
>24
>24
92.3
a
, includes one non-rectus sling; b, 18 patients had sling attached to Cooper’s ligament; c, includes cured and improved patients; d, suprapubic bone anchors; e, includes full-length and short ‘sling on a string’; f, median follow-up; g, includes seven porcine dermis slings; h, attachment point is Cooper’s ligament; i, includes Aldridge-style rectus slings. Cure (%), percentage of patients cured; FL, fascia lata, F/U, follow-up period; R, rectus,
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mean cure rate is nearly 87%, with follow-up exceeding 10 years in some studies. De novo storage symptoms are reported in 0–27% of studies. After many early studies reported long-term voiding dysfunction (refractory urge incontinence, urinary retention requiring clean intermittent catheterization, and sling revision) in up to 33% of patients, more recent reports have quoted these findings in less than 10% of patients. Other reported complications are detailed in Table 60.2. Both rectus fascia and fascia lata have predictable wound healing characteristics; however, it is our experience that rectus fascia may be stronger than fascia lata due to fiber organization and specimen thickness. In summary, rectus fascia slings are durable and safe and should be considered the ‘gold standard’ of materials available for sling surgery.
Allograft slings Cadaveric allograft materials have been widely used in ophthalmic and orthopedic procedures for more than 20 years. The main advantage of allograft materials is the elimination of the need for an additional incision and dissection, causing increased operative time and extended postoperative convalescence. The theoretical advantage includes the use of human tissue with proposed increased biocompatibility and decreased chances of rejection and/or erosion. With any implantation of foreign materials comes concern about potential disease transmission. Although all cadaveric tissues are serologically screened for human immunodeficiency virus (HIV) and hepatitis, and are treated and rendered acellular prior to surgical implantation, false-negative results are possible. The estimated risk for transmission of HIV from a frozen allograft is 1 in 8 million,67 and the risk of transmission of Creutzfeldt–Jakob disease is 1 in 3.5 million. There are multiple cadaveric allografts available for implantation. Those utilized in sling surgery have included lyophilized dura mater, cadaveric fascia lata, and acellular dermal grafts. With follow-up ranging from 6 to 150 months, cure rates of lyophilized dura slings have ranged from 86 to 94%.68–70 While there have been no complications specific to this material reported in the urologic literature, there has been a case of presumed transmission of Creutzfeldt–Jakob disease following implantation of a dural graft, raising concern about the long-term safety of this material.71 The use of cadaveric fascia lata (CFL) as a sling material was initially reported in 1996.72 There are two main processing techniques for CFL materials, both designed to remove cellular materials and preserve integrity: 1) solvent dehydration and gamma irradiation; and 2)
freeze drying. Regardless of processing technique, CFL requires 15–30 minutes in saline for rehydration. Results and complications for CFL slings are reported in Tables 60.3 and 60.4, respectively. Dermal allografts are strong and more pliable than CFL grafts, exhibiting properties similar to autologous tissues in mechanical tests. Acellular dermis has been found to integrate into tissue consistently; however, there is the potential for sebaceous gland and hair follicle ingrowth. Studies regarding the strength of the available allograft tissues have revealed conflicting results. Sutaria and Staskin found no statistically significant difference in tissue thickness or maximum load to failure between freeze-dried CFL, solvent-dehydrated CFL, and acellular cadaveric dermis.85 Lemer et al. found that solvent-dehydrated CFL and acellular dermis had a similar load to failure as autologous fascia, whereas freeze-dried CFL was significantly inferior.86 The literature has suggested that there is a real risk of early allograft failure (within 3 months of implantation), particularly with the used of freeze-dried CFL.87–89 Several mechanisms of graft loss have been proposed (autolysis, graft-versus-host reaction, etc.); as of yet, however, there has been no consensus on this subject. Concerning risk for disease transmission, DNA has been detected in freeze-dried CFL, solvent-dehydrated CFL, and acellular dermis.90,91 These findings have unknown consequences, and raise concern about the potential health risks resulting from the implantation of foreign genetic material. In summary, the use of allograft materials decreases operative times and potentially reduces postoperative convalescence by eliminating the need for additional dissection. Short- to medium-term cure rates approach those of autologous slings; however, long-term data for a single material is lacking. In addition, the presence of DNA in these materials raises questions about their longterm safety. Additional rigorous long-term surveillance with well-defined outcomes reporting is needed before adequate conclusions can be made about the global use of these materials.
Xenograft slings Like cadaveric allografts, treated animal tissues have been utilized in surgical reconstructive procedures for many years. More recently, the use of porcine dermis has been popularized in the urologic community. The tissues are initially treated with proteolytic enzymes to remove non-collagenous material, and then are freeze-dried and sterilized with gamma irradiation. These materials are available as either a cross-linked or a non-cross-linked graft. Cross-linking involves treatment with a non-toxic 885
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Table 60.2.
Complications of autologous slings
Author
De novo storage symptoms (%)
Voiding dysfunction
Other complications
Kaufman24
–
Obstruction (33%) Dilation/VIU (27%) Excision (7%)
–
Schultz-Lampel et al.25
0
–
–
Loughlin26
6
Short-term retention/dilation (23%)
–
Mason & Roach
–
CIC at 3 months (19%), at 6 months (6%) Long-term CIC (3%) Revision (2%)
DVT (2%)
Zaragoza28
12
–
–
–
Incision (30%)
–
–
Refractory urinary incontinence (6%) CIC at 3 months (7%) Permanent CIC (3%) Early revision (1%)
–
0
–
–
Chaikin et al.
8
CIC >1 month (2%)
Bladder perforation (1%)
Maheshkumar et al.33
–
CIC (42%) Incision (5%)
–
Hassouna & Ghoneim34
21
Strain to void (1%)
Pain from procedure (25%)
8
Dilation/VIU (8%)
Wound (15%)
Morgan et al.
7
Urethrolysis (2%)
Pelvic hematoma (1%) Incisional hernia (1%) DVT (<1%) PE (<1%)
Kochakarn et al.37
5
Mean time of CIC = 8.9 weeks (39%)
Wound (1%)
Groutz et al.38
10
Weak stream at 3 weeks (22%)
–
Kuo
8
Urethrolysis (4%)
Subcutaneous hematoma (8%) Persistent dysuria (4%)
Borup & Nielson40
13
CIC at 6 months (39%) CIC at 1 year (16%) Revision at 1 year (3%)
Sling erosion (8%)
Gormley et al.41
–
–
–
De Rossi
7
Weak stream (7%)
Bladder perforation (14%)
Giannitsas et al.66
43
CIC (8%) De novo voiding problems (33%)
–
4
Revision (1%)
–
–
–
–
6
Obstruction (6%) Incision (3%)
–
–
–
–
27
29
Siegel et al. 30
Carr et al.
Barbalias et al.31 32
35
Kane et al.
36
39
42
Chou et al.44 45
Pfitzenmaier et al. 46
Guatelli et al.
Almeida et al.47 48
Rodrigues et al.
49
Obstruction (11%)
Kreder & Austin
12
Long-term CIC (7%)
Thigh hematoma (4%) Death from MI (4%)
Golomb et al.50
5
Refractory urge (6%)
– cont.
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Table 60.2.
Complications of autologous slings (cont.)
Author
De novo storage symptoms (%)
Voiding dysfunction
Other complications
Haab et al.51
27
Refractory urge (24%) CIC (3%)
–
10
Urethrolysis (3%)
–
Petrou & Frank
0
Long-term CIC (7%)
–
Richter et al.54
–
High PVR (16%) Posture (4%) CIC (7%)
–
Flynn & Yap55
5
Retention >45 days (3%) Urethrolysis (1%)
–
Chien et al.56
–
–
–
–
–
UVF (8%)
Addison et al.
–
Long-term retention (6%)
Bladder perforation (8%) Wound (2%) PE (1%)
Beck et al.59
–
Mean period of voiding dysfunction = 2 months Incision (3%)
Wound (5%) FL hematoma (1%) Seroma (4%) PE (1%) DVT (1%)
Karram & Bhatia60
–
Mean time to spontaneous void = 20 days; Maximum = 39 days
–
Govier et al.61
14
Mean CIC = 3.3 weeks; CIC at 4 months (3%) Incision (3%)
Leg pain (3%)
Berman & Kreder62
–
–
Leg hematoma (14%)
Phelps et al.63
–
Retention/incision (3%) CIC (2%)*
–
–
–
–
–
–
–
Wright et al.52 53
57
Low
58
Latini et al.64 65
Ellerkmann et al.
* Percentages include totals for 27 fascia lata slings and 36 cadaveric fascia lata slings. CIC, clean intermittent catheterization; De novo storage symptoms (%), percentage of patients with de novo storage symptoms (i.e. urgency, frequency, urge incontinence); Dilation, urethral dilation; DVT, deep vein thrombosis; FL, fascia lata; Incision, sling incision; MI, myocardial infarction; PE, pulmonary embolism; PVR, post-void residual; Revision, sling revision; UVF, urethrovaginal fistula; VIU, visual internal urethrotomy; Wound, wound infection or complication.
substance such as diisocyanate to render them more resistant to degradation by the host. Although crosslinking was initially thought to reduce antigenicity of the graft, cases of encapsulation have raised questions about the remodeling characteristics of tissues treated in this manner.92 Success rates of porcine dermal slings have been good, but – as with allograft materials – longterm consistent data have been lacking. In one study, Nicholson and Brown reported a cure rate of 79% in 24 patients undergoing porcine dermal sling with a follow-up of more than 48 months. Thirteen percent of their patients developed urinary retention more than a year postoperatively.93 Cure rates in another study with
mean follow-up of 12 months approached 89%, with 7% of patients requiring sling release for obstructive voiding.94 There have been no reports of sling extrusion or erosion. Porcine small intestinal submucosa (SIS) has recently been marketed for pubovaginal sling surgery. SIS is harvested from small intestine and the extracellular matrix is maintained intact. The collagen, growth factors, glycosaminoglycans, proteoglycans, and glycoproteins promote host cell proliferation through SIS layers. The SIS ultimately provides a scaffold for tissue remodeling and ingrowth of host connective tissue structures. SIS is currently available for use in pelvic surgery in 1- and 887
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Table 60.3.
Results of cadaveric fascia lata slings
Author
Processing
No. of patients
Sling length (cm)
Mean F/U (months)
Cure (%)
Elliott & Boone
SD
26
12
15
76.9
Amundsen et al.74
FD
91
15
19.4
62.6
FD
104
24
12
66.3a
FD
8
>20
24
100
FD
31
10
13.5
93.5
FD
63
12
29
87.3
Chien et al.
–
83
10
27.4
90.1b
Bodell & Leach79
SD
186
7c
16.4
75.8d
Richter et al.80
FD
102
25
35
75b
–
36
>20
20
83.3
73
75,76
Govier
Vereecken & Lechat77 Walsh et al.
78
Flynn & Yap55 56
63
Phelps et al.
81
Hartanto et al.
c
–
34
7
12.5
83.3
Almeida et al.
FD
30
6–8
36
40
82
SD
42
4
16
88
Park et al.
FD
60
20
>36
85
Fitzgerald et al.84
FD
27
12
59
SD
32
>24
90.5
47
Gurdal et al. 83
65
Ellerkmann et al.
>24
a
, updated cure rate with eight additional failures between 4 and 13 months postoperatively88; b, includes cured and improved patients; c, transvaginal bone anchors; d, patients reporting >50% improvement and no subjective SUI. Cure (%), percentage of patients cured; FD, freeze-dried; F/U, follow-up period; SD, solvent-dehydrated.
4-ply sheets for prolapse repairs, and 4- and 8-ply slings. Results for the use of this material in the urologic literature are lacking. Rutner et al. reported results of a SIS sling suspended with bone anchors in 115 adults.95 At 36 months follow-up, 94% were continent, while only one patient required urethrolysis from excessive sling tension. Palma and colleagues cured 93% of their 28 patients with a mean follow-up of 8 months.96 The tensile strength of SIS remains questionable. Kubricht et al. found the mean suture pull through load of freeze-dried SIS to be less than freeze-dried CFL.97 In addition, questions remain about the immunogenicity of SIS. There have been multiple reports of significant inflammatory responses following implantation of SIS slings.98–100 Bovine pericardium is currently available in a crosslinked and non-cross linked variety. The material is reportedly thinner than CFL, but may possess greater tensile strength.101 As with SIS, long-term experience with this material does not yet exist. Pelosi et al. reported a 95% cure rate in 22 patients having undergone use of the YAMA urology patch sling with crosslinked bovine pericardium at a mean follow-up of 20 months.102 As with other allograft and xenograft materials, immunogenicity is a concern with bovine pericardium. Studies have confirmed the presence of DNA in
these materials; however, the amount extracted may be much smaller than either CFL or cadaveric dermis.103 Additionally, the biocompatibility of bovine pericardium has come into question with recent reports of frequent rejections following implantation.104,105 In summary, despite claims that xenograft materials are biocompatible, have excellent tensile strength, are non-immunogenic, and are devoid of viruses and prions, there is insufficient evidence as yet to support these claims. Long-term follow-up is only available for porcine dermis slings, with success and complication rates approaching those of autologous slings. All of the described materials appear to have tensile strength similar to cadaveric allografts; however, claims of biocompatibility and non-immunogenicity should be met with intense scrutiny. Ultimately, ingrowth of native human tissue into a xenograft-derived scaffolding of acellular matrix may offer the ideal material for use in sling operations. Efforts to create these materials are ongoing.
Synthetic slings In situations when no suitable native tissues were available, experimentation was performed with synthetic materials. In the 1950s, nylon and perlon were used for sling construction.106 Due to the narrow nature of the
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Table 60.4.
Complications of cadaveric fascia lata slings
Author Elliott & Boone73 74
Amundsen et al. 75,76
Govier
Vereecken & Lechat
77
De novo storage symptoms (%)
Voiding dysfunction
Other complications
13
–
–
44
Urethrolysis (1%)
–
–
Long-term retention (2%)
–
13
Incision (13%)
–
Walsh et al.78
–
Posture to void (77%) CIC at 4 months (35%) CIC at 1 year (3%)
–
Flynn & Yap55
28
Retention at 56 days (2%)
–
Chien et al.56
–
–
–
–
Osteitis (1%)
–
Difficulty emptying bladder (58%)
–
–
Retention/incision (3%) CIC (2%)*
–
–
–
–
Almeida et al.
–
–
–
82
–
CIC for mean of 20 days (12%)
–
5
High PVR at 30 days (5%) Suprapubic suture removal (3%) CIC for 1 month (2%)
Bladder perforation (2%) Blood transfusion (7%)
–
–
–
–
–
–
Bodell & Leach79 80
Richter et al.
63
Phelps et al.
Hartanto et al.81 47
Gurdal et al. 83
Park et al.
Fitzgerald et al.84 65
Ellerkmann et al.
* Percentages include totals for 27 fascia lata slings and 36 cadaveric fascia lata slings. CIC, clean intermittent catheterization; De novo storage symptoms (%), percentage of patients with de novo storage symptoms (i.e. urgency, frequency, urge incontinence); Incision, sling incision; PVR, post-void residual.
strips of material, ‘strangulation’ of the bladder neck commonly resulted in high rates of urethral obstruction. Additionally, high rates of suprapubic abscess and urethrovaginal fistula formation led to several authors condemning synthetics as inappropriate sling materials. Despite the implementation of wider strips and a decrease in complication rates,107 the interest in synthetic materials waned. While all synthetic sling materials are strong and non-toxic, they differ in many ways. Almost all are permanent, though experimentation has been performed only with absorbable types. Sling types can also differ in composition (monofilament versus multifilament), pore size, and flexibility. Multifilament meshes contain interstices that are much smaller than standard pores. These small interstices may be large enough to allow bacteria (1 µm) to migrate into the mesh, but may be too small to allow entry of mediators of the body’s immune response such as macrophages and lymphocytes (50 µm).108 In theory, these very small pores may also inhibit the influx of host fibroblasts and deter the
ingrowth of new connective tissue, thereby preventing proper sling integration and remodeling. More recently, there has been a resurgence of the use of synthetic sling materials. Permanent synthetic materials are easily accessible, relatively inexpensive to produce, strong, and non-carcinogenic. All are associated with success rates similar to those of autologous materials. Dense, multifilament meshes such as GoreTex and Silastic may not integrate into host tissue well and therefore may be associated with prohibitively high complication rates. Despite larger pore size, high rates of erosion and sinus formation have been seen with other multifilament meshes such as Mersilene. Impregnation with antibiotic protectants has not reduced the complication rates of these materials. Loose monofilament meshes have resulted in greatly reduced complication rates and are clearly the better choice for utilization in sling surgery. Due to the large pore size, monofilament construction, and flexibility, Prolene is currently the synthetic material of choice for use in pelvic reconstructive surgery. 889
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Conclusions Since the introduction of the pubovaginal sling nearly 100 years ago, there have been countless variations and ‘improvements’ made to the techniques and materials involved. Only with the introduction of DeLancey’s hammock theory did we truly begin to understand why and how the pubovaginal sling has a positive effect in the treatment of SUI. The pubovaginal or bladder neck sling is the support mechanism that was described by DeLancey. The object of the procedure is to provide the necessary backing (i.e. sling) to the bladder neck and proximal urethral to build the framework for adequate closure of the urethra during times of increased abdominal stress. Even in cases with a fixed, open urethra as is seen in the patient with severe ISD, the pubovaginal sling can provide enough of a support backing to ensure continence. The resurgence of the pubovaginal sling, along with the reduction of the morbidity associated with the procedure, has truly revolutionized surgical treatment of stress urinary incontinence. However, as mentioned previously, the introduction of new technology should always be met with increased scrutiny as to the accuracy of the results reported. As determined by the AUA panel, autologous rectus fascia pubovaginal slings are viewed as the gold standard in the treatment of SUI. How do the other materials measure up? Are the reductions in operative time and postoperative morbidity worth the possibility for reduced material strength, immunogenicity, and even disease transmission? These questions will remain unanswered until reliable, standardized data are accessible for every new material available.
MIDURETHRAL SLINGS History With the above discussion of technologic advances in treatments for SUI, it is natural that what follows is a discussion about midurethral slings. Since its introduction onto the clinical market in 1994–95 by Petros and Ulmsten,109 the minimally invasive tension-free midurethral sling has achieved widespread acceptance as a first-line treatment for SUI. Initially, this operation was called the ‘combined intravaginal sling and tuck operation’ and involved minimal dissection at the level of the midurethra and no perforation of the endopelvic fascia. Specialized tunnelers were passed through the urogenital diaphragm from below up through the abdo-
men, staying just posterior to the pubic symphysis. A 45 cm segment of Mersilene tape was positioned loosely around the midurethra, and the ends were guided up into the abdominal incisions through the tunnelers. The free tape ends were cut and removed entirely 4–8 weeks following the surgery. The authors’ initial study reported a cure rate of 82% at 12 months, and 76% at 36 months.110 An interesting concept of this procedure was the use of synthetic material in order to reduce the morbidity related to autologous tissue use. Initially, Mersilene was the material of choice, with larger pore sizes and more flexibility than Gore-Tex. However, as more reports of erosion of Mersilene circulated in the literature, and with its ultimate recall in 1999, experimentation was carried out with other materials.111–113 Ultimately, loosely woven monofilament Prolene mesh was shown to be the best material available for sling construction, and was adopted as the material of choice for midurethral slings.114
Why does it work? The midurethral sling procedure was initially developed to restore the fulcrum-like interaction between the pubourethral ligament and the anterior vaginal wall. The procedure stemmed from the ‘integral theory’ previously described by Petros and Ulmsten.109 Its development was based on the idea that the opening and closure of the proximal urethra and bladder neck are mainly controlled by a direct interaction between the pubourethral ligaments and the suburethral vaginal wall and its muscular support, the levator ani and the pubococcygeus muscles. If the tension in the pubourethral ligaments and the interplay between all involved factors are adequate, then during times of increased intra-abdominal stress the forward contraction of the pubococcygeus muscles and the backward contraction of the levator ani muscles result in kinking of the urethra. Stress incontinence is thought to result when these interactions are interrupted in any way. The midurethral sling was designed to correct the lack of tension in the pubourethral ligaments and to re-establish the connection between the urethra and the pubic bone, thereby re-creating the urethral kinking phenomenon in times of stress, but not affecting the urethra during times of rest. This concept has been supported by studies such as that of Sarlos et al.115 that have investigated the effects of a midurethral sling with perineal ultrasound. The positions of the implanted tape, the bladder neck, and the urethra were sonographically documented at rest and
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with abdominal straining. These images were compared with preoperative examinations. The authors reported dynamic kinking of the urethra in 36 of 40 cases, and movement of the tape against the pubic symphysis, causing compression of the tissue between the tape and the symphysis, in all cases. There was no change in bladder neck position or mobility between pre- and postoperative studies. The authors proposed that even if stress incontinence did not result from defective pubourethral ligaments, the midurethral sling was nonetheless effective by causing urethral kinking and compression during times of intra-abdominal stress. These findings have been echoed by other imaging studies.116 Interestingly, studies such as that just described have reported no change in bladder neck and proximal urethral position during straining in those patients who have undergone midurethral sling operation. According to DeLancey’s hammock hypothesis, proximal urethral hypermobility would be directly involved in the pathogenesis of genuine stress incontinence, and therefore restoration of vaginal support to the bladder neck and urethra would most effectively cure incontinence. Several studies, however, have demonstrated that the midurethral tape, while curing incontinence, actually has very little clinical effect on the positioning or support of the bladder neck or proximal urethra. Klutke et al.117 and Lukacz et al.118 described the results of Q-tip tests both before and after the placement of a midurethral sling. Both centers found some change in the mean straining Q-tip angle; however, in both studies, the majority of patients, despite being cured of their stress incontinence, did have significant postoperative urethral hypermobility. Lo et al.119 assessed the position and mobility of the bladder neck in 90 women before and after placement of a midurethral tape using ultrasound with the pubic bone as a reference point. Although cure of incontinence occurred in 93%, there were no significant differences in measurements of urethral position and mobility with straining. Halaska et al.120 reported similar findings determined by dynamic magnetic resonance images. More recently, Atherton et al.121 compared the effect of midurethral sling and Burch colposuspension on bladder neck mobility using perineal ultrasound, both preoperatively and 4 weeks after surgery. They found that both procedures resulted in more acute resting bladder neck angles and decreased Valsalva angles; however, the Burch procedure produced more dramatic changes than the midurethral sling. These studies raise important questions with their unanimous conclusion that the cure of stress incontinence does not necessarily require correction of urethral hypermobility.
The potential for the reduction in postoperative voiding difficulties has been an important consideration in the development of the midurethral sling. Many authors propose that normal voiding depends on mobility of the proximal urethral for its initiation. It is well accepted that surgical procedures can adversely affect voiding, especially in cases in which they interfere with the proximal urethra. The midurethral sling was designed with this in mind. With minimal vaginal dissection, minimal change in the architecture of the vagina, and minimal effect on the mobility of the proximal urethra, the hypothesis was that incontinence can be corrected with little effect on normal voiding patterns.
Materials available Since the introduction of the concept of the midurethral sling and its establishment as an acceptable surgical treatment for incontinence, there has been an influx of new procedural methods and surgical tools. Originally, the technique was introduced as the tension-free vaginal tape (TVT), a procedure that involved minimal vaginal dissection, followed by passage of trocars and tape from the vaginal incision, along the pubic bone, and out through two small abdominal stab incisions. Multiple variations of the TVT, including different operative techniques and different tape materials, have been marketed. A transpubic method was introduced in which the trocars are guided much the way as Stamey needles, i.e. from abdominal stab incisions just above the pubic symphysis, along the pubic bone, and into a small vaginal incision. Additionally, a transobturator technique has been introduced involving passage of trocars through the obturator foramen bilaterally. Thus far, there have been no head-to-head trials comparing the different techniques for midurethral tape placement. We would assert that the choice should be made based on surgeon comfort, and that new techniques should be met with skepticism until adequate success and complications data are available.
Operative techniques Preoperative considerations As with traditional slings, each patient being considered for midurethral tape placement should be evaluated with a comprehensive history, physical examination, and urodynamic assessment. It is important to characterize the incontinence and to document the presence of urgency, frequency, and/or urge incontinence to assist in preoperative counseling. 891
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Informed consent should involve a discussion of the risks, benefits, and options for sling surgery. Risks include, but are not limited to, bleeding, infection, injury to the bladder or urethra, dyspareunia, formation of anterior or apical prolapse, vesico-vaginal fistula formation, urinary retention, and de novo or worsening storage symptoms. An hour prior to surgery, parenteral antibiotics are given (ampicillin and gentamicin or a fluoroquinolone). Antiembolic stockings and sequential compression devices are applied prior to induction of anesthesia. Following induction of general or regional anesthesia, the patient is carefully placed in a slightly exaggerated dorsal lithotomy position with appropriate pressure points adequately padded. Betadine or Hibiclens preparation solution is used to scrub the surgical field from umbilicus to mid-thigh, including the vagina. The patient is draped in standard surgical fashion, and a urethral catheter is placed for continuous drainage.
Anesthetic considerations At the time of the introduction of the TVT, the preference was to perform the procedure under local anesthesia with sedation. Authors suggested that the procedure was less morbid when performed under local anesthesia and they stressed the importance of being able to perform an adequate stress test during the procedure to set adequate, but not excessive, tension on the sling.122,123 Klutke and Klutke argued that, when properly placed, the local anesthetic does not paralyze the musculature of the pelvic floor, ensuring that biofeedback will be accurate in determining the degree of resistance necessary at the bladder outlet. They also suggested that local anesthetic injected into areas of the pelvis through which the sling would pass will also create tissue ‘hydrodissection’ that allows easier passage of the trocar. They recommended a long-acting local anesthetic with or without epinephrine.122 Some surgeons, however, are uncomfortable performing the procedure under a local anesthetic. More recently, there have been reports that bladder outlet obstruction and urinary retention rates are not influenced by the mode of anesthesia, provided that the tape is positioned loosely.124 Spinal, general, and local anesthesia have yielded comparable results, but there has yet to be a prospective, randomized study comparing results with specific anesthetic techniques.
Transvaginal midurethral sling The transvaginal technique has changed little since its first introduction. A midline vaginal incision is made
beginning 1.0 cm from the external urethral meatus that encompasses the midurethra and extends 1.5 cm in length. The anterior vaginal epithelium is dissected from the midline incision for a distance of approximately 5 mm on either side. The purpose of this initial sharp dissection is to align the trocar tip in the proper plane and to minimize the risk of vaginal tape exposure later on. After satisfactory initial dissection, the bladder is emptied and a catheter guide is inserted into the urethral catheter. The catheter can then be used as a rigid probe to mobilize the urethra and the bladder neck away from the path of the trocar. Two suprapubic stab incisions are made approximately one fingerbreadth cephalad and lateral to the pubic tubercles on either side. The introducer is attached to one trocar, and the tip of the trocar is guided into the lateral aspect of the anterior vaginal wall incision and aimed towards the lateral vaginal sulcus on that side. Once the tip reaches this position, it is directed towards the ipsilateral shoulder in a ventral–lateral direction. The trocar is slowly advanced until a ‘give’ is felt, indicating that the trocar has breached the endopelvic fascia. Once in the retropubic space, lateral passage stops and the introducer is dropped, rotating the trocar upwards along the inferior pubic ramus and up to the abdominal fascia. The trocar is then guided through the abdominal stab incision. The introducer is removed from the trocar, the urethral catheter is removed, and cystoscopy is performed with the 70-degree lens to ensure bladder integrity. Bladder penetration typically occurs in the upper lateral aspect of the bladder, so it is important to inspect the dome and superior bladder neck. Should bladder penetration occur, the bladder is drained, the cystoscope removed, and the trocar is backed out completely. A second pass may then be attempted. If no penetration occurs, the introducer is removed from the end of the trocar and the trocar with the attached tape is pushed upward vaginally and pulled out through the skin incision. The same sequence is repeated with the other trocar on the opposite side. Once both trocars have been passed, tension of the tape can be adjusted. Initial tension adjustment is performed using a spacer instrument such as Mayo scissors, a No. 8 Hagar dilator, or a right angle clamp. The plastic sheath around the tape is removed following detachment of the trocars from either end of the tape. The spacing instrument is placed under the tape, and the plastic sheaths are removed by pulling up on each end with hemostats. The free ends of the excess tape are then cut at the level of the skin. The suprapubic stab incisions are closed with 4-0 vicryl and Steri-strips. The vaginal incision is closed
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with 2-0 vicryl. A vaginal pack can be left at the surgeon’s preference.
Transpubic midurethral tape The transpubic procedure is very much a combination of the transvaginal midurethral sling and the traditional sling techniques. The initial steps are identical. Two suprapubic stab incisions and a 1.5 cm midline vaginal incision are made. Minimal dissection is performed to elevate the vaginal epithelium from the underlying tissue. The trocars, however, are passed in much the same way as Stamey needles are passed during a traditional bladder neck sling. The trocar is introduced into the abdominal incision and the rectus fascia is penetrated. The trocar is guided downwards and slightly medially in very close approximation to the pubic bone. The trocar is then guided through the endopelvic fascia and out of the vaginal incision. This maneuver is repeated on the contralateral side. The urethral catheter is then removed and cystoscopy is performed with the 70-degree lens to ensure bladder and urethral integrity. Once this has been confirmed, the tape ends are connected to the trocar bilaterally, and the trocars are withdrawn through the abdominal incisions, bringing the tape ends out with them. The tape is positioned beneath the midurethra and the trocars are cut off. Tension is adjusted as the plastic sheath is removed in the same manner as that described for the transvaginal approach.
Transobturator midurethral sling Delorme initially described the transobturator tape technique in 2001.125 The patient is positioned in an exaggerated dorsal lithotomy position, with the thighs bent back onto the abdomen at an angle of 120 degrees. A vertical midline vaginal incision is made and dissection is performed in the same fashion as that described above. The lateral margin of the ischiopubic ramus is identified between an index finger placed in the lateral vaginal fornix and the thumb placed in front of the obturator foramen. A puncture incision is made 15 mm lateral to the ischiopubic ramus on a horizontal line level with the preputium clitoridis. The tunneler is held in the same hand as the side on which the operator is working. The tunneler is held vertically with the handle downwards. It is introduced through the skin incision and is guided across the obturator membrane. As the membrane is crossed, some resistance should be felt. The tunneler is then turned to the horizontal position, with the handle pointing medially. The tip of the tunneler is led medially towards the urethra, aiming
above the urethral meatus and underneath the symphysis pubis. The safest method is to lead the tunneler around the ischiopubic ramus while remaining in contact with it. A finger is placed in the vaginal incision to ensure that the tunneler is not piercing the vagina and to hold the urethra superiorly, protecting it from the trocar. The finger should make contact with the tunneler laterally underneath the symphysis pubis. The tunneler can then be delivered through the vaginal incision under fingertip guidance. The same procedure is repeated on the opposite side. Although some authors state that cystoscopy to ensure safe trocar passage is not a necessary step in this procedure,125,126 bladder perforation has been reported127 and anecdotal experience confirms this to be a risk of this procedure. We recommend cystourethroscopy following trocar placement to ensure safe passage. Following confirmation of safe passage, the tape may be secured to the trocar tips and pulled through the lateral stab incisions. Tension can be adjusted as described above for transvaginal and transpubic techniques. Since this initial description, new Helical tunnelers have been introduced and tailored based on patient anatomy, facilitating the safe passage of the trocars and tape. More recently, authors have presented an ‘insideout’ technique in which the trocars are guided from the vaginal incision out to the thigh folds in the opposite trajectory of that described above.128 Anatomic studies have detailed that when passed in this manner, the tape avoids the pelvic compartment completely. The proponents of this technique argue that it is more protective against injury to the bladder, urethra, or dorsal nerve of the clitoris.129
Postoperative care Patients are usually discharged home following a brief recovery room stay. The vaginal packing and the urethral catheter are removed prior to discharge. A voiding trial should be performed and if the patient cannot void to completion, the catheter may be replaced or the patient may be discharged with plans for intermittent self-catheterization. If the bladder was penetrated at any time during the procedure, the patient should be discharged with the urethral catheter in place, with plans for an outpatient voiding trial in 2–3 days. Early ambulation is encouraged, but strenuous exercise and heavy lifting should be avoided. Patients should refrain from sexual intercourse until their vaginal incision is completely healed (approximately 6 weeks). Patients can usually be released to full activity at 6 weeks. 893
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Results The midurethral sling has become a mainstay of antiincontinence therapy. TVT has been the most well known product in this market, having been performed in over 200,000 women in Europe. In the original study group from Scandinavia, 91% were cured and 7% were significantly improved at a minimum of 12 months.130 Nilsson et al. recently published results of 90 women having undergone midurethral sling placement after 7 years of follow-up.131 They reported subjective and objective cure rates of 81.3% at a mean follow-up of 91 months. De novo urge symptoms were seen in 6.3% of patients, recurrent urinary tract infections were seen in 7.5%, and asymptomatic pelvic organ prolapse was seen Table 60.5.
in 7.8%. No other long-term adverse effects of the procedure were detected. Medium- and long-term results from several large European and American centers have been published and results of studies with 12 or more months of follow-up are summarized in Table 60.5. Several studies have reported results comparing the tension-free midurethral tape with other anti-incontinence procedures. Ward and Hilton reported results of a prospective randomized study comparing TVT (175 patients) with open colposuspension (169 patients).154 They utilized questionnaires, clinical examination, and 1-hour pad tests to assess outcomes with a follow-up of 24 months. When patients who failed to follow-up were considered failures, the cure rates for TVT and colposuspension were 63% and 51%, respectively. Overall per-
Results for midurethral slings
Author
No. of patients
Mean F/U (months)
Cure (%)
51
36
90
Moran et al.
40
12.3
80
Jacquetin134
156
12–36
89
120
15.2
87
62
16.8
87
73
27
86
67
12
81
85
56
85
404
21
92
34
48
91*
Rezapour et al.
49
48
86*
Rezapour & Ulmsten141
80
48
89*
Buscant et al.142
30
36
84
68
24
90
Glavind & Larsen
15
12
93
Kinn145
75
24
80
112
25
89
132
Olsson & Kroon 133
135
Soulie et al.
124
Haab et al.
Wang & Chen
136
Azam et al.137 138
Nilsson et al.
108
Meschia et al.
139
Rezapour & Ulmsten 140
143
Liapis et al.
144
146
Jeffry et al.
De Val et al.
147
187
27
90
148
Lo et al.
45
20
91
Chung & Chung149
91
12
100*
Adamiak et al.150
103
13
95
158
26
86
45
12
87
Arunkalaivanan & Barrington
68
12
85
Tsivian et al.153
55
55
79
80
91
81
151
Brophy et al.
152
Sander et al.
94
131
Nilsson et al.
* Includes cured and improved patients. Cure (%), percentage of patients cured; F/U, follow-up period.
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ceived health status was better in the TVT group, and enterocele and/or vault prolapse was seen more commonly in the colposuspension group. The discrepancy in these reported results with others in the literature may be due to strict criteria for cure and/or methods of statistical evaluation. The authors felt that, based on their data, they could conclude that TVT ‘appears’ to be as effective as colposuspension for the treatment of stress urinary incontinence. Their results raise interesting questions concerning outcomes analysis in antiincontinence surgery, particularly how to address those patients who fail to follow-up. Paraiso et al.155 reported a randomized comparison of 36 patients undergoing laparoscopic Burch colposuspension with 36 patients undergoing TVT. They reported a higher rate of urodynamic stress incontinence at 1 year in the colposuspension group (18.8% versus 3.2%). They reported a significant improvement in the number of incontinent episodes per week and in Urogenital Distress Inventory and Incontinence Impact Questionnaire scores in both groups at 1 and 2 years after surgery. However, postoperative subjective symptoms of incontinence were reported significantly more often in the laparoscopic Burch colposuspension group than in the TVT group (p<0.04). Another study reported results of a prospective randomized trial comparing porcine dermis pubovaginal sling with TVT with a median follow-up of 36 months.156 They utilized a questionnaire to measure outcomes. Statistical analysis failed to detect significant differences in cure rates or complications between the two groups. As of yet, there has been no large scale prospective randomized study utilizing objective criteria to compare results of pubovaginal slings with midurethral tape procedures. Large trials with extended follow-up detailing results and/or complications of the transobturator technique have yet to be published. DeTayrac et al.157 reported a 1year cure rate of 84% with the transobturator approach. Delorme et al.158 recently presented results in 32 patients with a minimum of 1-year follow-up (mean 17 months) following transobturator tape placement with an outsidein technique. They reported that 90.6% of patients were cured and 9.4% of patients were improved. One patient had complete postoperative retention, which resolved following 4 weeks of intermittent catheterization. Five patients had voiding difficulties suggesting outflow obstruction, and two patients developed de novo urge incontinence. De Leval reported initial results following the inside-out technique.159 He reported a 91% cure and 4% improvement rate in 107 patients with a mean follow-up of 10 months. He reported a 4% incidence of postoperative de novo urge incontinence.
Complications As with any surgical intervention, strict adherence to standard surgical procedure will minimize the occurrence of complications. The midurethral sling has been demonstrated to be a safe and effective method for the treatment of stress incontinence; however, it is important to be aware of potential complications. A review of currently available complications data is detailed in Table 60.6.
Intraoperative The majority of intraoperative complications are due to aberrant passage of the trocars. Rates of bladder perforation in smaller series have been reported as high as 61%.151 However, the incidence of bladder injury seems to be inversely related to experience, as the rate of bladder perforation in studies of over 1000 patients is 3– 4%.160,161 In the majority of cases of inadvertent bladder injury, proper repositioning of the trocar and urethral catheter drainage for 1–2 days is sufficient treatment. In cases of more severe injuries, endoscopic bladder repair has been described.162 Ileoinguinal and obturator nerve injury or entrapment may approach 0.1% in large series.108,133,161,163 Bowel injury from passage of trocars has also been described.160,164–166 Vascular complications, including retropubic hematoma and blood loss over 200 cc, may be seen in over 3% of patients.138 The incidence of major vessel injury approaches 0.1%,161 and injuries to the external iliac artery have been reported.167,168 Most commonly, hemorrhagic complications can be managed conservatively;169 however, as many as 0.5% of patients in large series have required surgery to address the site of hemorrhage.108,170
Voiding complications It is generally accepted that anti-incontinence procedures have an obstructive effect on the urethra that may affect voiding.171–173 Traditional anti-incontinence procedures carry a risk of permanent voiding dysfunction requiring surgical reversal in 1–20% of cases.174 Although the midurethral sling is placed without tension at the level of the midurethra, there appear to be significant effects on the voiding phase of micturition. It is well accepted that most obstructive symptoms are transient, requiring only temporary indwelling or intermittent catheterization.175 However, longer-term urinary retention rates for TVT of between 1.4 and 9% have been reported.133,160,161,176–178 Most reported data on postoperative urinary retention has been in the form of case reports and case series. In general, there is a paucity of subjective and/or objective outcomes data that address voiding function 895
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Table 60.6.
Complications for midurethral slings
Author
De novo storage symptoms (%)
Voiding dysfunction
Other complications
Moran et al.133
3
Retention (5%)
Obturator nerve injury (3%) Periostitis (3%)
Jacquetin134
4
–
–
Soulie et al.
–
–
Bladder perforation (10%) Pelvic hematoma (2%)
Haab et al.124
6
Voiding dysfunction (8%) Incision (2%)
–
Azam et al.137
7
Voiding dysfunction (4%)
Bladder perforation (19%)
Nilsson et al.138
8
–
Bladder perforation (1%) Pelvic hematoma (3%) >200 ml blood loss (3%)
Meschia et al.108
–
Voiding dysfunction (4%) Incision (0.5%)
Bladder perforation (6%) Pelvic hematoma (1.5%) Vaginal erosion (0.5%) Surgery for bleeding (0.5%) Obturator nerve injury (0.25%)
–
–
Bladder perforation (3%)
–
–
Urethrovaginal fistula (3%)
Kinn
–
Incision (1%)
Bladder perforation (4%) Vaginal erosion (3%)
Jeffry et al.146
26
Voiding dysfunction (12%) Retention (9%)
Bladder perforation (12%) Hemorrhage (2%)
De Val et al.147
31
Retention (6%) Incision (2%)
Bladder perforation (10%) Hemorrhage (3%) Pain (1%)
–
–
Bladder perforation (4%)
135
Rezapour et al.140 144
Glavind & Larsen 145
Lo et al.148 150
Adamiak et al.
6
–
Bladder perforation (9%)
151
–
–
Bladder perforation (61%)
152
Sander et al.
2
CIC (4%) Urethrolysis (2%)
–
Arunkalaivanan & Barrington94
9
Retention 6 weeks (2%) CIC (4%) Dilation (2%) Incision (3%)
Hemorrhage (3%)
Voiding dysfunction (3%)
Bladder perforation (5%) Urethra injury (2%) Erosion (5%)
–
–
Brophy et al.
Tsivian et al.153
Nilsson et al.131
6
CIC, clean intermittent catheterization; De novo storage symptoms (%), percentage of patients with de novo storage symptoms (i.e. urgency, frequency, urge incontinence); Dilation, urethral dilation; Incision, sling incision.
after midurethral tape placement. This is compounded by the fact that data from existing series are difficult to compare due to a lack of consensus definitions for obstruction and/or voiding dysfunction. Sander et al.152 reported a 78% rate of ‘voiding difficulty’ in 45 patients undergoing TVT procedures. Voiding difficulty was
defined as hesitancy, dysuria, and the use of abdominal straining to void, or a sensation of incomplete emptying. Wang et al.179 utilized objective (post-void residual >100 ml) and subjective (frequency of more than six voids per day and more than two voids per night, and an abnormal stream of urine per patient report) criteria
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to evaluate 57 patients who had undergone TVT placement. Using this definition, 15 patients (26%) were classified as having voiding dysfunction. Klutke et al.176 reported a 2.8% rate of urinary retention or symptoms consistent with obstruction lasting more than 1 week from the date of the procedure in their experience with 600 TVT procedures. Prospective objective voiding data are also limited. Wang180 described his experience with 79 patients who underwent TVT. Patients were classified as ‘dysfunctional voiders’ or ‘normal voiders’ based on symptoms and a urinary free flow ≤12 ml/s and a detrusor pressure at maximum flow of >20 cmH2O. Both groups were found to have a statistically significant decrease in maximum urinary free flow 1 year postoperatively. Factors highly correlated with postoperative abnormal voiding included abnormal preoperative uroflow, preoperative vaginal vault prolapse or enterocele, concurrent vault suspension procedure, and postoperative urinary tract infection. Lukacz et al. prospectively evaluated 65 patients undergoing TVT placement.181 Voiding was assessed with patient questionnaires, non-invasive urinary flow rate, and pressure–flow studies both preoperatively and at 1 year postoperatively. Subjective voiding did not change; however, maximum free flow rates decreased from 29 ml/s to 16 ml/s (43% change). Post-void residual measurements revealed no clinically significant increases, changing from a median of 15 to 30 ml postoperatively. Thirty-eight patients (37%) required postoperative catheterization for urinary retention (median duration 4 days). No risk factors could be identified that predicted a requirement for postoperative catheterization. Eight patients (8%) required sling release and were not included in the voiding analysis. In cases of persistent urinary retention, several treatments have been advocated including stretching of the tape,152 interposition of mesh,182 simple transection,178 and complete urethrolysis.183
De novo urge incontinence/overactive bladder De novo urge incontinence and de novo overactive bladder symptoms are known risks of anti-incontinence procedures. De novo detrusor overactivity (DO) has been reported to occur in 0-30% of patients after antiincontinence surgery.184 The incidence of DO following pubovaginal sling procedures has been reported to be between 3 and 24%.2 Initial thoughts were that due to the lack of tension at the level of the midurethra, the TVT would result in lower rates of de novo storage symptoms. However, studies have demonstrated that placement of a midurethral tape does have potential to cause new onset stor-
age symptoms in between 0 and 31% of patients (Table 60.6). Conversely, Segal et al.185 demonstrated resolution of urge incontinence in 63.1% of patients and resolution of overactive bladder symptoms in 57.7% following TVT placement. Further prospective analyses are required prior to formulating consensus recommendations concerning the onset or fate of storage symptoms following midurethral tape placement.
Graft rejection Reported complications related to the use of synthetic permanent material for tension-free midurethral slings have been relatively rare. In their 2000 review of complications data, Yonneau et al.186 emphasized the low incidence of vaginal, urethral or bladder erosion with the midurethral tape procedure when performed with Prolene mesh versus other materials. Nilsson and Kuuva,187 in a study of 161 patients followed for 16 months, found no cases of tape erosion. Ulmsten et al.,188 in a 3-year followup study involving 50 patients, also reported no cases of tape erosion. Karram et al.189 reviewed their series of 350 TVT procedures and reported poor healing or erosion in three patients. Kuuva and Nilsson,161 in a nationwide questionnaire-based analysis of complications associated with TVT procedures in 1455 patients, found an incidence of 7/1000 of defective vaginal healing. Possible reasons for vaginal erosion include inadequate vaginal incision suturing, wound infection, impaired wound healing, or foreign body (tape) rejection. Patients with vaginal erosion may present in a variety of ways. They may complain of vaginal discharge, discomfort reported by their spouse during intercourse, vaginal or pelvic pain, or vaginal bleeding. Most groups recommend removal of the exposed areas of tape to treat vaginal erosions.190–192 Kobashi and Govier,193 however, presented four cases of vaginal erosion of polypropylene mesh successfully managed with conservative measures alone. Urethral or bladder erosion can certainly be caused by technical error during the procedure. Urethral erosion is speculated to be due to excessive tension of the sling on the urethra, or due to technical error during the dissection under the urethra, resulting in compromised thickness of suburethral tissues. A few cases of intravesical erosion have been reported.162,190,194,195 It is possible that intraoperative bladder perforation had been missed, but theoretically, pressure necrosis with eventual penetration of the tape through the bladder mucosa is a concern. Anecdotal experience with intravesical erosions presenting several years after successful TVT placement raises questions about the significance of the latter theory. Patients with urethral or bladder tape 897
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erosions can present with storage and/or voiding symptoms, hematuria, dysuria, pelvic pain, and/or recurrent urinary tract infections. It is well accepted that in cases of urethral or bladder erosion, it is necessary to remove the offending portions of tape.
Specific patient groups Obese patients Stress urinary incontinence has been positively associated with obesity in numerous studies.196–198 Although weight loss may improve stress incontinence in these patients, definitive treatment may be best obtained through surgical intervention.199 There have been mixed reports with regard to the success rates of anti-incontinence surgery in obese patients. Some studies have indicated a significantly diminished success rate among patients with a body mass index (BMI) greater than 30 kg/m2, whereas other data suggest that obesity is not a risk factor for 200–205 failure of corrective surgery. Anecdotally, increased technical difficulty, increased perioperative morbidity, and increased postoperative convalescence are often encountered in obese patients. An effective method for cure of stress incontinence that is technically sound and minimally invasive is an ideal concept in this patient population. Lovatsis et al.206 examined the success rate of TVT in 43 patients with a BMI ≥35 kg/m2, compared to nonobese controls. They reported a success rate of 89% in the obese group versus 91% in the non-obese group, a difference that was not statistically significant. They reported no difference in complication rates between the two groups. These findings were echoed by Mukherjee and Constantine in a non-comparative study.207 Some authors propose that good success rates and decreased peri- and postoperative morbidity may make the midurethral sling the ideal surgical modality for correction of stress incontinence in this patient population. Elderly patients Large prevalence studies have shown that urinary incontinence in women increases with age. It is estimated that over 35% of community-dwelling elderly women have urinary incontinence.208 Incontinence has been shown to affect the psychological, occupational, domestic, and sexual lives of 15–30% of women of all ages.209 Due to comorbidities in the elderly population, injectable therapy has often been the treatment of choice in an attempt to avoid operative morbidity; however, long-term efficacy and durability of this material has in many cases been inadequate.210 Reports of vaginal and retropubic suspen-
sion procedures for stress incontinence in the elderly have suggested a variable rate of success.211–213 Much like in the obese patient population, there are anecdotal concerns with performing invasive surgery on elderly patients. Many patients have multiple medical co-morbidities, making them risky surgical candidates. Additionally, postoperative convalescence is expected to be more complicated and longer in this population. A less invasive procedure with reduced postoperative morbidity such as the midurethral sling would be ideal for this patient population. Walsh et al.214 reported their evaluation of quality of life outcomes in community-dwelling elderly women compared with younger patients, all of whom underwent TVT for incontinence treatment. They found significantly improved quality of life scores (80% and 91%, respectively) following surgery in both groups; however, the rate of improvement was slightly less in the elderly cohort. Although this study confirms that the midurethral tape procedure is successful in elderly patients, further reports detailing results and complication data are necessary before adequate conclusions should be drawn concerning the use of the midurethral sling as first-line therapy in this population. Patients with prolapse Stress urinary incontinence in women is frequently associated with other pelvic floor defects. A vaginal approach to repair is often preferred because anterior, apical, and posterior defects can be addressed by the same approach and without a large abdominal incision. At the present time, pubovaginal sling surgery is advocated as the best choice for treatment of occult incontinence. Recently, interest has piqued about the use of the less invasive midurethral sling during concomitant prolapse repair. Conceptually, there has been concern about the tendency of the midurethral tape to migrate towards the bladder neck if all repairs are done through a common incision. This phenomenon could cause an increased propensity for postoperative urinary retention and/or storage symptoms. Several studies have investigated the use of the midurethral sling in women with occult stress incontinence undergoing prolapse repair. Reported objective cure rates have been between 85 and 94%, with one exception.215–221 Pang et al. reported 1-year urodynamic and quality of life outcomes in 45 patients who underwent concomitant TVT insertion during pelvic floor reconstruction surgery.222 They reported a worse objective cure rate in patients having undergone concomitant cystocele repair when compared with patients at their institution who had undergone TVT alone (38% versus
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67%). The discrepancy in results could potentially be due to the stringent outcomes criteria utilized to define cure, a concept that deserves close attention. Rafii et al.223 reported different findings when they compared cure rates in patients who underwent TVT alone with those who underwent TVT and prolapse repair. No statistical difference was found between the two groups (93.0% versus 93.1%). Multiple surgical strategies for placement of a midurethral sling during prolapse repair have been described. Pang et al.222 and Jomaa216 inserted the TVT needles prior to performing repair of the anterior compartment through an extended anterior vaginal incision. Meschia et al.217 inserted the vaginal tape prior to anterior repair, but did so through a separate sagittal vaginal incision. In contrast, Lo et al.215 inserted the tape after coaptation of the paravesical fascia for anterior repair. In all of the above cases, the tension of the TVT tape was adjusted after the necessary prolapse procedures had been completed. The most common reported perioperative complication in patients undergoing TVT and concurrent prolapse surgery has been transient urinary retention (11–43%).215–220,222 The mean period of catheterization in these patients was between 3.7 and 5.1 days. Several cases of unresolved urinary retention have been reported. Rafii et al.223 reported four cases of sling adjustment and three cases of sectioning of the midurethral tape in a series of 186 patients who underwent TVT with or without prolapse repair. Partoll218 and Meltomaa et al.224 reported that the time to resolution of retentive voiding was significantly higher in patients who underwent concurrent anterior and/or posterior repair when compared to those who underwent midurethral tape placement alone.
CONCLUSIONS As can be inferred from the above discussion, a plethora of literature exists that details experiences with various surgical techniques designed to treat stress incontinence. The pubovaginal sling has remained the gold standard; however, with the introduction of minimally invasive techniques – specifically the midurethral tape – questions have been raised as to what is the most appropriate treatment in specific cases. Although no single intervention is optimal for all circumstances, the variety of technologies and procedures currently available provide the surgeon with viable options for most patients. No doubt, continued development will further improve morbidity associated with sling interventions with the hope that greater efficacy can also be achieved.
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spective quality of life analysis. Am J Obstet Gynecol 2003;189:1590–6. 81. Hartano VH, DiPiazza D, Ankem MK et al. Comparison of recovery from postoperative pain utilizing two sling techniques. Can J Urol 2003;10:1759–63. 82. Gurdal M, Tekin A, Huri E et al. Pubovaginal sling using cadaveric allograft fascia for all types of stress urinary incontinence. XIXth European Association of Urology Congress, March 25, 2004; Abstract 317. 83. Park S, Kim S, Choo M et al. Long term follow-up result of pubovaginal sling with cadaveric fascia lata in the management of female stress urinary incontinence. XIXth European Association of Urology Congress, March 25, 2004; Abstract 319. 84. Fitzgerald MP, Edwards SR, Fenner D. Medium-term follow-up on use of freeze-dried, irradiated donor fascia for sacrocolpopexy and sling procedures. Int Urogynecol J Pelvic Floor Dysfunct 2004;15:238–42. 85. Sutaria PM, Staskin DR. A comparison of fascial ‘pullthrough’ strength using four different suture fixation techniques. J Urol 1999;161:79–80. 86. Lemer ML, Chaikin DC, Blaivas JG. Tissue strength analysis of autologous and cadaveric allografts for the pubovaginal sling. Neurourol Urodyn 1999;18:497–503. 87. Chaikin DC, Blaivas JG. Weakened cadaveric fascial sling: an unexpected cause of failure. J Urol 1998;160:2151. 88. Fitzgerald MP, Mollenhauer J, Bitterman P et al. Functional failure of fascia lata allografts. Am J Obstet Gynecol 1999;181:1339–46. 89. Fitzgerald MP, Mollenhauer J, Brubaker L. Failure of allograft suburethral slings. BJU Int 1999;84:785–8. 90. Choe JM, Bell T. Genetic material is present in cadaveric dermis and cadaveric fascia lata. J Urol 2001;166:122–4. 91. Hathaway JK, Choe JM. Intact genetic material is present in commercially processed cadaver allografts used for pubovaginal slings. J Urol 2002;168:1040–43. 92. Cole EE, Gomelsky A, Dmochowski R. Encapsulation of a porcine dermis pubovaginal sling. J Urol 2003;170:1950. 93. Nicholson SC, Brown ADG. The long-term success of abdominovaginal sling operations for genuine stress incontinence and cystocele: a questionnaire-based study. J Obstet Gynecol 2001;21:162–5. 94. Arunkalaivanan AS, Barrington JW. Randomized trial of porcine dermal sling (Pelvicol implant) vs. tension-free vaginal tape (TVT) in the surgical treatment of stress incontinence: a questionnaire-based study. Int Urogynecol J 2003;14:17–23. 95. Rutner AB, Levine SR, Schmaelzle JF. Porcine small intestinal submucosa implanted as a pubovaginal sling in 115 female patients with stress urinary incontinence: a 3-year series evaluated for durability of the results. Society for Urology and Engineering, 17th Annual Meeting, 2002.
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for the diagnosis and management of female urinary incontinence. Scand J Urol Nephrol 1993;153:1–93. 111. Melnick I, Lee RE. Delayed transection of urethra by Mersilene tape. Urology 1976;8:580–1. 112. Smith DN, Rackley RR, Fralick R et al. Biocompatibility analysis of Meadox material for sling formation. J Urol 1997;157(Suppl):459A.
126. Dargent D, Bretones P, George P et al. Insertion of a suburethral sling through the obturator membrane for treatment of female urinary incontinence. Gynecol Obstet Fertil 2002;30:576–82. 127. Minaglia S, Ozel B, Klutke C et al. Bladder injury during transobturator sling. Urology 2004;64:376–7.
113. Kobashi KC, Dmochowski RR, Mee SL. Erosion of woven polyester pubovaginal sling. J Urol 1999;162:2070–2.
128. De Leval J. Novel surgical technique for the treatment of female stress urinary incontinence: transobturator vaginal tape inside-out. Eur Urol 2003;44:724–30.
114. Ulmsten U. An introduction to tension-free vaginal tape (TVT) – a new surgical procedure for treatment of female urinary incontinence. Int Urogynecol J 2001;12(Suppl 2):S3–S4.
129. Bonnet P, Waltregny D, Reul O et al. Transobturator vaginal tape inside out for the surgical treatment of female stress urinary incontinence: anatomical considerations. J Urol 2005;173:1223–8.
115. Sarlos D, Kuronen M, Schaer GN. How does tension-free vaginal tape correct stress incontinence? Investigation by perineal ultrasound. Int Urogynecol J 2003;14:395–8.
130. Ulmsten U, Falconer C, Johnson P et al. A multicenter study of tension-free vaginal tape (TVT) for surgical treatment of stress urinary incontinence. Int Urogynecol J 1998;9:210–3.
116. Masata J, Martan A, Kasikova E et al. Ultrasound study of effect of TVT operation on the mobility of the whole urethra. Neurourol Urodyn 2002;21:286–8. 117. Klutke JJ, Carlin BI, Klutke CG. The tension-free vaginal tape procedure: correction of stress incontinence with minimal alteration in proximal urethral mobility. Urology 2000;55:512–4. 118. Lukacz ES, Luber KM, Nager CW. The effects of the tension-free vaginal tape on proximal urethral position: a prospective longitudinal evaluation. Int Urogynecol J Pelvic Floor Dysfunct 2003;14(3):179–84; discussion 184. 119. Lo TS, Wang AC, Horng SG et al. Ultrasonographic and urodynamic evaluation after tension-free vaginal tape procedure (TVT). Acta Obstet Gynecol Scand 2001;80:65–70. 120. Halaska M, Otcenasek M, Havel R et al. Suspension of the lower third of the urethra in out-patient practice – minimally invasive treatment of stress urinary incontinence of urine: technique and initial experience. Ces Gynek 2000;1:4–9.
131. Nilsson CG, Falconer C, Rezapour M. Seven-year follow-up of the tension-free vaginal tape procedure for treatment of urinary incontinence. Obstet Gynecol 2004;104:1259–62. 132. Olsson I, Kroon U. A three-year post-operative evaluation of tension-free vaginal tape. Gynecol Obstet Invest 1999;48:267–9. 133. Moran PA, Ward KL, Johnson D et al. Tension-free vaginal tape for primary genuine stress incontinence: a twocentre follow-up study. BJU Int 2000;86:39–42. 134. Jacquetin B. [Use of ‘TVT’ in surgery for female urinary incontinence.] J Gynecol Obstet Biol Reprod (Paris) 2000;29:242–7. 135. Soulie M, Delbert-Juhes F, Cuvillier X et al. [Repair of female urinary incontinence with prolene ‘TVT’: preliminary results of a multicenter and prospective survey.] Prog Urol 2000;10:622–8. 136. Wang AC, Chen MC. Randomized comparison of local versus epidural anesthesia for tension-free vaginal tape operation. J Urol 2001;165:1177–80.
121. Atherton MJ, Stanton SL. A comparison of the bladder neck movement and elevation after TVT and colposuspension. Br J Obstet Gynaecol 2000;107:1366–70.
137. Azam U, Frazer MI, Kozman EL et al. The tension-free vaginal tape procedure in women with previous failed stress incontinence surgery. J Urol 2001;166:554–6.
122. Klutke JJ, Klutke CG. Tension-free vaginal tape procedure. AUA Update Series 2003;XXII:Lesson 10.
138. Nilsson GG, Kuuva N, Falconer C et al. Long-term results of the tension-free vaginal tape (TVT) procedure for surgical treatment of female stress urinary incontinence. Int Urogynecol J 2001;12(Suppl 2):S5–S8.
123. Ulmsten U. The basic understanding and clinical results of tension-free vaginal tape for stress urinary incontinence. Urologe A 2001;40:269–73. 124. Haab F, Sananes S, Amarenco G et al. Results of the tension-free vaginal tape procedure for the treatment of type II stress urinary incontinence at a minimum followup of 1 year. J Urol 2001;165:159–62. 125. Delorme E. La bandelette transobturatrice: un procede mini-invasif pour traiter l’incontinence urinaire de la femme. Prog Urol 2001;11:1306–13.
139. Rezapour M, Ulmsten U. Tension-free vaginal tape (TVT) in women with recurrent stress urinary incontinence – a long-term follow-up. Int Urogynecol J 2001;12(Suppl 2):S9–S11. 140. Rezapour M, Falconer C, Ulmsten U. Tension-free vaginal tape (TVT) in stress incontinent women with intrinsic sphincter deficiency (ISD) – a long-term follow-up. Int Urogynecol J 2001;12(Suppl 2):S12–S14.
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141. Rezapour M, Ulmsten U. Tension-free vaginal tape (TVT) in women with mixed urinary incontinence – a long-term follow-up. Int Urogynecol J 2001;12(Suppl 2):S15–S18. 142. Buscant F, Roumeguere T, Anaf V et al. [A new approach in techniques to treat urinary incontinence: TVT (tension free vaginal tape).] Rev Med Brux 2001;22:166–9.
156. Abdel-Fattah M, Barrington JW, Arunkalaivanan AS. Pelvicol pubovaginal sling versus tension-free vaginal tape for treatment of urodynamic stress incontinence. Eur Urol 2004;46:629–35.
143. Liapis A, Bakas P, Creatsas G. Management of stress urinary incontinence in women with the use of tension free vaginal tape. Eur Urol 2001;40:548–51.
157. DeTayrac R, Deffieux X, Droupy S et al. A prospective randomized trial comparing tension-free vaginal tape and transobturator suburethral tape for surgical treatment of stress urinary incontinence. Am J Obstet Gynecol 2004;190:602–8.
144. Glavind K, Larsen EH. Results and complications of tension-free vaginal tape (TVT) for surgical treatment of female stress urinary incontinence. Int Urogynecol J 2001;12:370–2.
158. Delorme E, Droupy S, deTayrac R et al. Transobturator tape (Uratape): a new minimally-invasive procedure to treat female urinary incontinence. Eur Urol 2004;45:203–7.
145. Kinn AC. Tension-free vaginal tape evaluated using patient self-reports and urodynamic testing: a two year follow-up. Scand J Urol Nephrol 2001;35:484–90.
159. De Leval J. Reply to V. Delmas: Letter to the editor. Eur Urol 2004;46:134–6.
146. Jeffry L, Deval B, Birsan A et al. Objective and subjective cure rates after tension-free vaginal tape for treatment of urinary incontinence. Urology 2001;58:702–6. 147. De Val B, Jeffry L, Al Najjar F et al. Determinants of patient dissatisfaction after a tension-free vaginal tape procedure for urinary incontinence. J Urol 2002;167:2093–7. 148. Lo TS, Huang HJ, Chang C.L et al. Use of intravenous anesthesia for tension-free vaginal tape in elderly women with genuine stress incontinence. Urology 2002;59:349–53. 149. Chung MK, Chung RP. Comparison of laparoscopic Burch and tension-free vaginal tape in treating stress urinary incontinence in obese women. JSLS 2002;6:17–21. 150. Adamiak A, Milart P, Skorupski P et al. The efficacy and safety of the tension-free vaginal tape procedure do not depend on the method of analgesia. Eur Urol 2002;42:29–33. 151. Brophy MM, Klutke JJ, Klutke GG. Urethral function testing prior to tension-free vaginal tape: does valsalva leak point pressure make a difference? J Urol 2002;167(Suppl):104. 152. Sander P, Moller LM, Rudnicki PM et al. Does the tension-free vaginal tape procedure affect the voiding phase? Pressure–flow studies before and one year after surgery. BJU Int 2002;89:694–8. 153. Tsivian A, Mogutin B, Kessler O et al. Tension-free vaginal tape procedure for the treatment of female stress urinary incontinence: long-term results. J Urol 2004;172:998–1000. 154. Ward KL, Hilton P. A prospective multicenter randomized trial of tension-free vaginal tape and colposuspension for primary urodynamic stress incontinence: two-year followup. Am J Obstet Gynecol 2004;190:324–31. 155. Paraiso MF, Walters MD, Karram MM et al. Laparoscopic BURCH colposuspension versus tension-free vaginal tape: a randomized trial. Obstet Gynecol 2004;104:1249–58.
160. Tamussino KF, Hanzal E, Kolle D et al. Tension-free vaginal tape operation: results of the Austrian registry. Obstet Gynecol 2001;98:732–6. 161. Kuuva N, Nilsson CG. A nationwide analysis of complications associated with the tension-free vaginal tape (TVT) procedure. Acta Obstet Gynecol Scand 2002;81:72–7. 162. Jorion JL. Endoscopic treatment of bladder perforation after tension-free vaginal tape procedure. J Urol 2002;168:197. 163. Geis K, Dietl J. Ileoinguinal nerve entrapment after tension-free vaginal tape (TVT). Int Urogynecol J 2002;13:136–8. 164. Brink DM. Bowel injury following insertion of tensionfree vaginal tape. S Afr Med J 2000;90:450–2. 165. Peyrat L, Boutin JM, Bruyere F et al. Intestinal perforation as a complication of tension-free vaginal tape procedure for urinary incontinence. Eur Urol 2001;39:603–5. 166. Meschia M, Busacca M, Pifarotti P et al. Bowel perforation during insertion of tension-free vaginal tape (TVT). Int Urogynecol J Pelvic Floor Dysfunct 2002;13:263–5. 167. Zilbert AW, Farrell SA. External iliac artery laceration during tension-free vaginal tape procedure. Int Urogynecol J 2002;12:141–3. 168. Primicerio M, De Matteis G, Montanino OM et al. Use of the TVT (tension-free vaginal tape) in the treatment of female urinary stress incontinence: preliminary results. Minerva Ginecol 1999;51:355–8. 169. Walters MD, Tulikangas PK, LaSala C et al. Vascular injury during tension-free vaginal tape procedure for stress urinary incontinence. Obstet Gynecol 2001;98:957–9. 170. Vierhout ME. Severe hemorrhage complicating tensionfree vaginal tape (TVT): a case report. Int Urogynecol J 2001;12:139–40. 171. Wall LL, Hewitt JK. Voiding function after Burch colposuspension for stress incontinence. J Reprod Med 1996;41:161–5. 172. Klutke JJ, Klutke CG, Bergman J. Bladder neck suspen-
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sion for stress urinary incontinence: how does it work? Neurourol Urodyn 1999;18:623–7. 173. Bhatia NN, Ostergard DR. Urodynamic effects of retropubic urethropexy in genuine stress incontinence. Am J Obstet Gynecol 1981;140:936–41. 174. Goldman HB, Rackley RR, Appell RA. The efficacy of urethrolysis without resuspension for iatrogenic urethral obstruction. J Urol 1999;161:196–8. 175. Cross CA, Cespedes RD, English SF et al. Transvaginal urethrolysis for urethral obstruction after anti-incontinence surgery. J Urol 1998;159:1199–201. 176. Klutke C, Siegel S, Carlin B et al. Urinary retention after tension-free vaginal tape procedure: incidence and treatment. Urology 2001;58:697–701. 177. Niemczyk P, Klutke JJ, Carlin BJ et al. United States experience with tension-free vaginal tape procedure for urinary stress incontinence: assessment of safety and tolerability. Tech Urol 2001;7:261–5. 178. Rardin CR, Rosenblatt PL, Kohli N et al. Release of tension-free vaginal tape for the treatment of refractory postoperative voiding dysfunction. Obstet Gynecol 2002;100:898–902. 179. Wang KH, Neimark M, Davilla GW. Voiding dysfunction following TVT procedure. Int Urogynecol J 2002;13:353–8. 180. Wang AC. The correlation between preoperative voiding mechanism and surgical outcome of the tension-free vaginal tape procedure, with reference to quality of life. BJU Int 2003;91:502–6.
188. Ulmsten U, Johnson P, Rezapour M. A three-year followup of tension free vaginal tape for surgical treatment of female stress urinary incontinence. Br J Obstet Gynaecol 1999;106:345–50. 189. Karram MM, Segal JL, Vassallo BJ et al. Complications and untoward effects of the tension-free vaginal tape procedure. Obstet Gynecol 2003;101:929–32. 190. Volkmer BG, Nesslauer T, Rinnab L et al. Surgical intervention for complications of the tension-free vaginal tape procedure. J Urol 2003;169:570–2. 191. Boublil LJ, Blaivas JG. Complications of urethral sling procedures. Curr Opin Obstet Gynecol 2002;14:515–8. 192. Clemens JQ, DeLancey JO, Faerber GJ et al. Urinary tract erosions after synthetic pubovaginal slings: diagnosis and management strategy. Urology 2000;56:589–92. 193. Kobashi KC, Govier FE. Management of vaginal erosion of polypropylene mesh slings. J Urol 2003;169:2242–3. 194. Sweat SD, Itano NB, Clemens JQ et al. Polypropylene mesh tape for stress urinary incontinence: complications of urethral erosion and outlet obstruction. J Urol 2002;168:144–6. 195. Wyczolkowski M, Klima W, Piasecki Z. Reoperation after complicated tension-free vaginal tape procedure. J Urol 2001;166:1004–6. 196. Mommsen S, Foldspang A. Body mass index and adult female urinary incontinence. World J Urogynecol 1994;12:319–22. 197. Dwyer PL, Lee ET, Hay DM. Obesity and urinary incontinence in women. Br J Obstet Gynaecol 1988;95:91–6.
181. Lukacz ES, Luber KM, Nager CW. The effects of the tension-free vaginal tape on voiding function: a prospective evaluation. Int Urogynecol J 2004;15:32–8.
198. Yarnell JW, Voyle GJ, Sweetnam PM et al. Factors associated with urinary incontinence in women. J Epidemiol Community Health 1982;36:58–63.
182. Kolle D, Stenzl A, Koelbl H et al. Treatment of postoperative urinary retention by elongation of tension-free vaginal tape. Am J Obstet Gynecol 2001;185:250–1.
199. Cummings JM, Rodning CB. Urinary stress incontinence among obese women: review of pathophysiology therapy. Int Urogynecol J 2000;11:41–4.
183. Romanzi LJ, Blaivas JG. Protracted urinary retention necessitating urethrolysis following tension–free vaginal tape surgery. J Urol 2000;164:2022–3.
200. Stanton SL, Cardozo L, Williams JE et al. Clinical and urodynamic features of failed incontinence surgery in the female. Obstet Gynecol 1978;51:515–20.
184. Kershen RT, Appell RA. De novo urge syndrome and detrusor instability after anti-incontinence surgery: current concepts, evaluation and treatment. Curr Urol Rep 2002;3:345–53.
201. Zivkovic F, Tamussino K, Pieber D. Body mass index and outcome of incontinence surgery. Obstet Gynecol 1999;3:753–6.
185. Segal JL, Vassallo B, Kleeman S et al. Prevalence of persistent and de novo overactive bladder symptoms after the tension-free vaginal tape. Obstet Gynecol 2004;104:1263–9. 186. Yonneau L, Chartier-Kastler E, Bohin D et al. Materials used for treatment of stress urinary incontinence with suburethral sling. Prog Urol 2000;10:1238–44. 187. Nilsson CG, Kuuva N. The tension-free vaginal tape procedure is successful in the majority of women with indications for surgical treatment of urinary stress incontinence. Br J Obstet Gynaecol 2001;108:414–9.
202. Brieger G, Korda A. The effect of obesity on the outcome of successful surgery for genuine stress incontinence. Aus N Z J Obstet Gynaecol 1992;32:71–2. 203. Gillon G, Engelstein D, Servadio C. Risk factors and their effect on the results of Burch colposuspension for urinary stress incontinence. Isr J Med Sci 1992;28:354–6. 204. Hutchings A, Griffiths J, Black NA. Surgery for stress incontinence: factors associated with a successful outcome. Br J Urol 1998;82:634–41. 205. Cummings JM, Boullier JA, Parra RO. Surgical correction of incontinence in the morbidly obese woman. J Urol 1998;160:754–5.
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206. Lovatsis D, Gupta C, Dean E et al. Tension-free vaginal tape procedure is an ideal treatment for obese patients. Am J Obstet Gynecol 2003;189:1601–4.
prolapse repair under local anesthesia in patients with symptoms of both urinary incontinence and prolapse. Gynecol Obstet Invest 2001;51:184–6.
207. Mukherjee K, Constantine G. Urinary stress incontinence in obese women: tension-free vaginal tape is the answer. BJU Int 2001;12(Suppl):881–3.
217. Meschia M, Pifarotti P, Spennacchio M et al. A randomized comparison of tension-free vaginal tape and endopelvic fascia plication in women with genital prolapse and occult stress urinary incontinence. Am J Obstet Gynecol 2004;190:609–13.
208. Diokno AC, Brock BM, Brown MB et al. Prevalence of urinary incontinence and other urological symptoms in the noninstitutionalized elderly. J Urol 1986;136:1022–5. 209. Thomas TM, Plymat KR, Blannin J et al. Prevalence of urinary incontinence. Br Med J 1980;281:1243–5. 210. Groutz A, Blaivas JG, Kesler SS et al. Outcome results of transurethral collagen injection for female stress incontinence: assessment by urinary incontinence score. J Urol 2000;164:2006–9. 211. Gillon G, Stanton SL. Long-term follow-up of surgery for urinary incontinence in elderly women. Br J Urol 1984;56:478–80. 212. Schmidbauer CP, Chiang H, Raz S. Surgical treatment for female geriatric incontinence. Clin Geriatr Med 1986;2:759–63. 213. Couillard DR, Deckard-Janatpour K, Stone AR. The vaginal wall sling: a compressive suspension procedure for recurrent incontinence in elderly patients. Urology 1994;43:203–8. 214. Walsh K, Generao SE, White MJ. The influence of age on quality of life outcome in women following a tension-free vaginal tape procedure. J Urol 2004;171:1185–8. 215. Lo TS, Chang TC, Chao AS et al. Tension-free vaginal tape (TVT) procedure on genuine stress incontinent women with coexisting genital prolapse. Acta Obstet Gynecol Scand 2003;82:1049–53. 216. Jomaa M. Combined tension-free vaginal tape and
218. Partoll LM. Efficacy of tension-free vaginal tape with other pelvic reconstructive surgery. Am J Obstet Gynecol 2002;186:1292–5. 219. Huang KH, Kung FT, Liang HM et al. Concomitant surgery with tension-free vaginal tape. Acta Obstet Gynecol Scand 2003;82:948–53. 220. Gordon D, Gold RS, Pauzner D et al. Combined genitourinary prolapse repair and prophylactic tension-free vaginal tape in women with severe prolapse and occult stress urinary incontinence: preliminary results. Urology 2001;58:547–50. 221. Darai E, Jeffry L, Deval B et al. Results of tension-free vaginal tape in patients with or without vaginal hysterectomy. Eur J Obstet Gynecol Reprod Biol 2002;103:163–7. 222. Pang MW, Chan LW, Yip SK. One-year urodynamic outcome and quality of life in patients with concomitant tension-free vaginal tape during pelvic floor reconstruction surgery for genitourinary prolapse and urodynamic stress incontinence. Int Urogynecol J Pelvic Floor Dysfunct 2003;14:256–60. 223. Rafii A, Paoletti X, Haab F et al. Tension-free vaginal tape and associated procedures: a case-control study. Eur Urol 2004;45:356–61. 224. Meltomaa S, Backman T, Haarla M. Concomitant vaginal surgery did not affect outcome of the tension-free vaginal tape operation during a prospective 3-year follow-up study. J Urol 2004;172:222–6.
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61 Pubovaginal fascial sling for the treatment of all types of stress urinary incontinence: surgical technique and long-term outcome Jerry G Blaivas, David Chaikin
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IntroductIon Although a plethora of surgical techniques has been devised for the treatment of stress urinary incontinence, over the last decade two have emerged as the gold standards – the Burch colposuspension and the pubovaginal sling. Historically, pubovaginal sling had been reserved for women with complicated, severe and/or recurrent sphincteric incontinence; however, recently it has been advocated for almost all types of sphincteric incontinence – simple and complicated. Fueled by a stampede of commercial innovations in sling materials, allograft and synthetic sling operations have become the most common operations performed for sphincteric incontinence in women.1 Over the last few years, many surgeons have paid increasing attention to synthetic and allograft materials to replace autologous tissue for slings in order to decrease operative time and perhaps to decrease operative morbidity. As more synthetics are used for sling surgery, hopefully there will be sufficient studies using validated outcome instruments to show that they compare favorably to autologous slings with respect to efficacy and morbidity. The objective of this chapter is to provide the reader with an update on surgical technique and long-term outcome of the full-length autologous rectus fascial sling for sphincteric incontinence in women and to describe their role in the armamentarium of the pelvic surgeon.
Figure 61.1. Abdominal incision. For most patients a short (6–8 cm) transverse incision is made just above the pubis below the pubic hairline (the horizontal portion of the incision). In obese patients, a larger incision may be necessary (the incision as shown).
operatIve technIque The procedure is performed in the dorsal lithotomy position. For most patients a short (6–8 cm) transverse incision is made just above the pubis below the pubic hairline (Fig. 61.1). In obese patients a larger incision is usually necessary. The incision is carried down to the surface of the rectus fascia which is dissected free of subcutaneous tissue. Two parallel horizontal incisions, 2 cm apart, are made in the midline of the rectus fascia, approximately 2 cm above the pubis (Fig. 61.2). Using Mayo scissors, the incisions are extended superolaterally towards the iliac crest following the direction of the fascial fibers. The wound edges are retracted laterally on either side to permit a sling of approximately 16 cm to be obtained. The undersurface of the fascia is freed from muscle and scar and each end of the fascia is secured with a 2-0 delayed absorbable monofilament suture using a running horizontal mattress placed at right angles to the direction of the fascial fibers (Fig. 61.3). The fascial strip is excised (Fig. 61.4) and placed in a basin of saline. The wound is temporarily packed with saline-soaked sponges and attention turned to the vagina.
Figure 61.2. A 2 cm wide graft is outlined, keeping the incision parallel to the direction of the fascial fibers. A weighted vaginal retractor is placed in the vagina and a Foley catheter inserted into the urethra. The labia are retracted with sutures. The vesical neck is identified by placing gentle traction on the Foley catheter and palpating the balloon, and a gently curved horizontal incision is made in the anterior vaginal wall with the apex of the curve over the vesical neck, approximately 2 cm proximal to the palpable distal edge of the balloon (Fig. 61.5). It is important that this incision is made superficial to the pubocervical fascia. This is accomplished by the technique outlined in Figures 61.6–61.12.
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Figure 61.3. A plane is created between the fascia and rectus muscle with Mayo scissors and an index finger places traction on the fascia as the incision is extended superolaterally to the point where the rectus fascia divides to pass around the external oblique muscle. If further length is needed, the incision is extended superiorly. At this point, it is important to avoid the underlying peritoneum. A No. 2-0 non-absorbable running horizontal mattress suture is placed across the lateral-most portion of the graft and the ends are left long.
Figure 61.4. Each end of the fascial graft is transected approximately 0.5 cm lateral to the mattress suture. Five ml of indigo carmine are given intravenously and cystoscopy performed to ensure that there has been no damage to the urethra, vesical neck, bladder or ureters. The sling is put on tension by pulling up on the sutures and the position of the sling is noted by observing where
Figure 61.5. A 4 cm transverse or slightly curved incision is made in the anterior vaginal wall about 2 cm proximal to the proximal edge of the Foley catheter balloon. This is the approximate site of the vesical neck. The depth of this incision extends just superficial to the pubocervical fascia. the urethra coapts. Historically, the sling has been intentionally placed at the bladder neck and we continue to place it there, but if cystoscopy shows that the sling is distal to the bladder neck, we do not attempt to reposition it. This is not the proper forum to discuss whether it is better to place the sling at the midurethra or vesical neck. Suffice it to say that the results presented herein are based on placing the sling at the vesical neck, not the midurethra. However, if cystoscopy shows that the sling is inadvertently placed proximal to the vesical neck, it is removed and a new tunnel created more distally. We generally place a trocar 14 Fr suprapubic tube percutaneously into the bladder and its position is visually inspected to ensure that it is well away from the trigone. While this is not necessary in all patients, we find that it facilitates the postoperative voiding trial. The sutures attached to the sling are pulled through the separate stab wounds in the inferior leaf of the rectus fascia on either side (not pictured here) and the rectus fascia is closed with a continuous 2-0 delayed absorbable monofilament suture. The long sutures attached to the ends of the fascial graft are tied to one another in the midline, securing the sling in place without tension (see Fig. 61.12). In order to ensure that excessive tension is not placed on the sling, we utilize several techniques. 909
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Push up with index finger on vaginal wall
Traction of clamp
Figure 61.6. An Allis clamp is placed on the cranial edge of the vaginal incision in the midline. The clamp is grasped by the left hand of the surgeon and caudad traction is applied while, at the same time, the left index finger pushes upward. A plane is created superficial to the pubocervical fascia by dissecting with Metzenbaum scissors at an angle of 60–90 degrees to the undersurface of the vaginal incision. The proper plane is identified by noting the characteristic shiny white appearance of the undersurface of the anterior vaginal wall. A small posterior vaginal flap is made for a distance of about 2 cm, just wide enough to accept the sling.
• With the cystoscope in the bladder, the sutures on
• •
•
each end of the fascial strip are grasped and gently pulled upward while downward pressure is applied to the cystoscope. This depresses the vesical neck and puts the sling on stretch. The sutures are then released, removing the excess tension from the sling. Next, the cystoscope is removed and a welllubricated Q-tip is placed in the urethra. With the table exactly parallel to the floor, the urethral angle is measured. If the angle is negative, downward pressure is placed on the Q-tip at the bladder neck until the angle is 0° or greater. The sutures attached to the sling are then tied over the rectus fascia with no added tension. It is usually possible to place two fingers comfortably between the sutures and the rectus fascia.
Figure 61.7. The lateral edges of the wound are grasped with Allis clamps and retracted laterally (not pictured here). The dissection continues just beneath the vaginal epithelium with Metzenbaum scissors pointed in the direction of the patient’s ipsilateral shoulder until the periosteum of the pubis is palpable. During this part of the dissection, it is important to stay as far lateral as possible to ensure that the urethra, bladder and ureters are not injured. This is accomplished by dissecting with the concavity of the scissors pointing laterally and exerting constant lateral pressure with the tips of the scissors against the undersurface of the vaginal epithelium. Once the periosteum is reached, the endopelvic fascia is perforated and the retropubic space entered.
The completed procedure is depicted in Figure 61.13. A vaginal pack is usually not left, unless there has been excessive bleeding. If one is used, it is soaked in sterile lubricating jelly to facilitate its painless removal postoperatively.
postoperatIve management If a vaginal pack was used it is removed the day after surgery. Voiding trials are begun as soon as the patient is comfortable, usually on the first or second postoperative day. If the patient is unable to void by the time she is to be discharged, she is taught intermittent self-catheterization.
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Figure 61.8. Alternatively, the endopelvic fascia is perforated with the index finger and the retropubic space entered. The bladder neck and proximal urethra are bluntly dissected free of their vaginal and pelvic wall attachments. Over 90% of patients void well enough by 1 week so that intermittent catheterization is not necessary and over 99% are catheter-free by 1 month. Permanent intermittent catheterization or urethral obstruction requiring surgery is necessary in less than 1% of patients.
results Our own results have been published in four reports over the last 15 years and are summarized below.2–5 Since 1988, all women who undergo pubovaginal sling have been evaluated by structured history and physical examination, voiding diary, pad test, videourodynamics and cystoscopy. Postoperatively, the diaries, pad tests, uroflow and post-void residual urine are repeated at each follow-up visit. Other outcome instruments – including questionnaires, symptom scores and patient satisfaction indices – have been added over the years. The most accurate tool, in our estimation, is the simplified urinary outcome score (SUIOS).5 The SUIOS is comprised of three components: a 24-hour voiding diary, 24-hour pad test and a patient outcome questionnaire, each with a range of scores from 0 to 2 (Table 61.1). Cure is defined as 0 points, consisting of the patient’s statement that she is cured, a dry pad test and no incontinence episodes on a voiding diary. Scores of 2–5 are considered improve-
Figure 61.9. A Kocher clamp is placed on the inferior edge of the rectus fascia in the midline and the fascia pulled upward (not pictured). The left index finger is reinserted into the vaginal wound, retracting the vesical neck and bladder medially. The tip of the finger palpates the right index finger, which is inserted just beneath the inferior leaf of the rectus fascia and guided along the undersurface of the pubis until it meets the left index finger from the vaginal wound.
ment and 6 is failure (Table 61.2). For the purposes of outcome analysis, we divided patients into two groups: simple and complex incontinence. Complex incontinence was defined as sphincteric incontinence with one or more of the following conditions: urge incontinence, ‘pipe stem urethra’ (a fixed scarred urethra), urethral or vesicovaginal fistula, urethral diverticulum, grade 3 911
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Tie loosely with no tension
Index finger between clamp, urethra & bladder at all times
Figure 61.10. A long curved clamp (DeBakey) is inserted into the incision and directed to the undersurface of the pubis. The tip of the clamp is pressed against the periosteum and directed toward the left index finger, which retracts the vesical neck and bladder medially. At all times, the left index finger is kept between the tip of the clamp and the bladder and urethra, protecting these structures from injury. In this fashion, the clamp is guided into the vaginal wound.
Figure 61.12. Two small stab wounds are made in the rectus fascia, just above the pubis (not pictured). The ends of the sutures attached to the sling are pulled through the stab wounds on either side and the rectus fascia closed with a 2-0 continuous delayed absorbable monofilament suture. The sutures attached to the ends of the fascial graft are tied to one another in the midline, securing the sling in place without tension, and the wound is closed.
Figure 61.11. When the tip of the clamp is visible in the vaginal wound, the long suture attached to the fascial graft is grasped and pulled into the abdominal wound. The procedure is repeated on the other side. The fascial sling is now positioned from the abdominal wall on one side around the undersurface of the vesical neck and back to the abdominal wall on the other side.
Figure 61.13. procedure.
Anatomic drawing of the completed
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table 61.1.
table 61.3.
Urinary incontinence instruments Score
Instrument
0
1
2
24-hour incontinence episodes
0
1–2
≥3
24-hour pad test (weight gain in grams)
≤8
9–20
Patient questionnaire, subjective assessment
Cure
Improve
table 61.2.
Urinary incontinence outcome score after pubovaginal sling in patients with simple and complex sphincteric incontinence
Outcome
Total score
≥21
Cure
0
45%
Good response
1–2
27%
Fail
Fair response
3–4
14%
Poor response
5
7%
Failure
6
7%
Urinary incontinence outcome score
Outcome
Total score
Cure
0
Good response
1–2
Fair response
3–4
Outcome
Total score
Poor response
5
Cure
0
67%
Failure
6
Good response
1–2
21%
Fair response
3–4
9%
Poor response
5
3%
Failure
6
0%
or 4 cystocele, or neurogenic bladder. In the absence of any of these, the incontinence was considered to be simple. Overall, with a mean follow-up of 4 years, the cure/ improve versus fail rate for 325 simple and complicated patients was 93% and 7%, respectively (Table 61.3); for 67 patients with uncomplicated incontinence it was 100% cure/improve (Table 61.4).3 It should be noted, however, that, from an objective perspective, patients with scores of 5 and 6 might well be considered as failures, but are included as improved because, despite persistent incontinence, the patients themselves stated that they were improved. Further, we have had two short-term failures that were not included in these reports because they occurred after the end of the study period, and two patients who were initial successes failed because of recurrent stress incontinence 9 years postoperatively. In a separate analysis of 98 women, no difference was found in the cure/improve versus fail rate in those with stress (97%) versus mixed (93%) incontinence (p=0.33) using a SUIOS = 4 as the cut-off between cure/improve and fail.6 In that study patients were also analyzed in two groups: cured versus not cured.4 For the patients with mixed incontinence, there was no difference between cured and not cured with respect to age, surgery, menopausal status, bladder capacity, leak point pressure, pad weight or type of overactive bladder. However, patients who failed had more daily preoperative urgency (5.6 versus 4.1) and urge incon-
table 61.4.
Urinary incontinence outcome score after pubovaginal sling in patients with simple sphincteric incontinence
tinence episodes (5.1 versus 3) than those who were cured, and they voided much more frequently (12 versus 8). This suggests that the more severe the overactive bladder, the less likely the patient is to respond favorably to surgery. In our combined series, most failures occurred either within the first 6 months or after 9 years, and the most common cause of failure was persistent urge incontinence, not stress incontinence. De novo urge incontinence occurred in about 3% of our series. Over the years, significant complications have been uncommon. There was one death in over 500 patients (<0.2%) due to a cardiac arrhythmia in an 80-year-old woman. Other complications included wound infections (1%), incisional hernia (1%) and unexpected long-term urethral obstruction requiring surgery or intermittent catheterization (1%). It was not possible to identify any preoperative prognostic factors associated with urinary retention, in no small part due to the fact that it was so uncommon that it would take an enormous number of patients to power a study sufficiently to detect differences. Empirically, however, there are two causes: grades 3 and 4 pelvic organ prolapse and placing the sling under too much tension. Adjusting tension comes in large part from experience; there has been no long-term urethral obstruction requiring surgery or long-term catheterization in our last 300 pubovaginal slings. 913
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dIscussIon In a meta-analysis of the peer review English literature, the AUA Female Stress Urinary Incontinence Clinical Guidelines Panel concluded that, with a short (1 year) and medium term (4 years) success rate of over 80%, pubovaginal sling and retropubic suspension are the most efficacious procedures for stress incontinence.7 Although there was insufficient data to study subpopulations, it was felt that slings are likely to be more effective for intrinsic sphincter deficiency than retropubic procedures. In that same study, the authors decried the paucity of scientifically valid outcome studies and recommended that better outcome instruments be developed and used in prospective trials. Since that report, a number of outcome instruments have been developed, including the SUIOS, and we are hopeful that future studies will be better. Many peer review studies have corroborated the guideline panel’s conclusions (albeit with the same scientific pitfalls), reporting persistent urge incontinence rates of 11–57% and de novo urge incontinence rates of zero to 30%.2–6,8–24 Urethral obstruction requiring surgery or long-term intermittent catheterization was reported in 1–7%. A new AUA guidelines panel is currently reviewing the literature and their report is expected within the next few years. Traditionally, patients were classified on an anatomic (types 0–3) or functional basis (urethral hypermobility or intrinsic sphincter deficiency), and the type of surgery was based in part on such classification.25 We no longer use either of these classification systems, but characterize incontinence by two parameters: leak point pressure and degree of urethral mobility (Q-tip angle). No matter what the type, we and others advocate autologous fascial pubovaginal sling.3,16,25
current and Future role oF autologous tIssue For slIngs In our judgment, autologous fascial pubovaginal sling remains the gold standard against which other surgeries for sphincteric incontinence should be compared. We have demonstrated that it can be performed in a reproducible fashion with minimal morbidity. Using a validated objective, semi-objective and subjective outcome instrument, cure/improve rates of over 90% have been documented. Urinary retention following the procedure should be minimal, as the sling is not tied with excessive tension. Persistent and de novo urge incontinence remain a vexing problem about which the patient should be counseled preoperatively.
While we believe that some form of synthetic or allograft sling will be shown to have equal or better efficacy and less morbidity in the future, none has yet achieved that status. When and if allograft and synthetic slings are shown to be as safe and efficacious as autologous tissue, there will be little need for the latter except in certain specific circumstances. Before describing those circumstances in more detail, it is important to state emphatically that that time has not yet come; none of these new materials has met the test of time – the future is not now! There is mounting evidence (largely unpublished except in abstract form) that, by 3 years postoperatively, both allograft and xenograft slings have an unacceptably high failure rate, approaching 40%, and there is some evidence that synthetics placed by a transobturator technique may not be as efficacious for intrinsic sphincter deficiency as an autologous fascial bladder neck sling.26–28 Whether the retropubic techniques for passing synthetics will fare as well is unknown. The time saved may come with a price in the long term. At the present time, we believe that, because of the likelihood that allograft and xenograft slings have an unacceptably high failure rate, autologous fascia should be used whenever synthetic slings are relatively contraindicated: 1) after urethral erosion of a prior synthetic sling; 2) at the time of urethral reconstruction; 3) in patients at high risk for wound infection (e.g. chronic steroid use); 4) in patients with intrinsic sphincter deficiency who have failed prior sling surgery; and 5) in patients for whom planned intermittent catheterization is necessary.
reFerences 1. Appell RA. Primary slings for everyone with genuine stress incontinence? The argument for. Int Urogynecol J 1998;9:249–51. 2. Blaivas JG, Jacobs BZ. Pubovaginal fascial sling for the treatment of complicated stress incontinence. J Urol 1991;145:1214–8. 3. Chaikin DC, Rosenthal J, Blaivas JG. Pubovaginal fascial sling for all types of stress urinary incontinence: long-term analysis. J Urol 1998;160:1312–6. 4. Chou EC, Flisser AJ, Panagopopous G, Blaivas J. Effective treatment of mixed urinary incontinence with a pubovaginal sling. J Urol 2003;170:494–7. 5. Groutz A, Blaivas JG, Hyman MJ, Chaikin DC. Pubovaginal sling surgery for simple stress urinary incontinence: analysis by an outcome score. J Urol 2001;165:1597–600. 6. Barrington JW, Fulford S, Bales G, Stephenson TP. The
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modified rectus fascial sling for the treatment of genuine stress incontinence. J Obstet Gynaecol 1998;18:61–2. 7. Leach GE, Dmochowski RR, Appell RA et al. Female Stress Urinary Incontinence Clinical Guidelines Panel summary report on surgical management of female stress urinary incontinence. J Urol 1997;158:875–80. 8. Cross CA, Cespedes RD, McGuire EJ. Our experience with pubovaginal slings in patients with stress urinary incontinence. J Urol 1998;159:1195–8. 9. Fulford SCV, Flynn R, Barrington J, Appanna T, Stephenson TP. An assessment of the surgical outcome and urodynamic effects of the pubovaginal sling for stress incontinence and the associated urge syndrome. J Urol 1999;162:135–7. 10. Hassouna ME, Ghoniem GM. Long-term outcome and quality of life after modified pubovaginal sling for intrinsic sphincter deficiency. Urology 1999;53:287–91. 11. Kochakarn W, Leenanupunth C, Ratana-Olarn K, Roongreungsilp U, Siripornpinyo N. Pubovaginal sling for the treatment of female stress urinary incontinence: experience of 100 cases at Ramathibodi Hospital. J Med Assoc Thai 2001;84:1412–5. 12. McGuire EJ, Lytton B. Pubovaginal sling procedure for stress incontinence. J Urol 1978;119:82–4. 13. McGuire EJ, Bennet CJ, Konnak JA, Sonda LP, Savastano JA. Experience with pubovaginal slings for urinary incontinence at the University of Michigan. J Urol 1987;138:525–6. 14. McGuire EJ, Lytton B, Pepe V et al. Value of urodynamic testing in stress urinary incontinence. J Urol 1980;124:256–8. 15. Morgan TO, Westney OL, McGuire EJ. Pubovaginal sling: 4-year outcome analysis and quality of life assessment. J Urol 2000;163:1845–8. 16. Zaragoza MR. Expanded indications for the pubovaginal sling: treatment of type 2 or 3 stress incontinence. J Urol 1996;156:1620–2. 17. Siegel SB, Allison S, Foster HE. Long term results of pubovaginal sling for stress urinary incontinence. American Urological Association Annual Meeting, New Orleans, LA, 1997. Abstract 1798.
18. Borup K, Nielsen JB. Results in 32 women operated for genuine stress incontinence with the pubovaginal sling procedure ad modum Ed McGuire. Scand J Urol Nephrol 2002;36(2):128–33. 19. Gormley EA, Latini J, Hanlon L. Long-term effect of pubovaginal sling on quality of life. American Urological Association Annual Meeting, Orlando, FL, 2002. Abstract 418. 20. Rodrigues P, Hering F, Meler A, Campagnari JC, D’Imperio M. Pubo-fascial versus vaginal sling operation for the treatment of stress urinary incontinence: a prospective study. Neurourol Urodyn 2004;23(7):627–31. 21. Beck RP, McCormick S, Nordstrom L. The fascia lata sling procedure for treating recurrent genuine stress incontinence of urine. Obstet Gynecol 1988;72(5):699–703. 22. Karram MM, Bhatia NN. Patch procedure: modified transvaginal fascia lata sling for recurrent or severe stress urinary incontinence. Obstet Gynecol 1990;75(3 Part 1):461–3. 23. Govier FE, Gibbons RP, Correa RJ, Weissman RM, Pritchett TR, Hefty TR. Pubovaginal slings using fascia lata for the treatment of intrinsic sphincter deficiency. J Urol 1997;157(1):117–21. 24. Latini JM, Lux MM, Kreder KJ. Efficacy and morbidity of autologous fascia lata sling cystourethropexy. J Urol 2004;171(3):1180–4. 25. Blaivas JG, Olsson CA. Stress incontinence: classification and surgical approach. J Urol 1988;139:727–31. 26. Colvert JR III, Kropp BP, Cheng EY et al. The use of small intestinal submucosa as an off-the-shelf urethral sling material for pediatric urinary incontinence. J Urol 2002;168(4 Part 2):1875–6. 27. Palma PCR, Dambros M, Riccetto CLZ, Herrmann V, Netto NR Jr. Pubovaginal sling using the porcine small intestinal submucosa for stress urinary incontinence. Braz J Urol 2001;27(5):483–8. 28. Rutner AB, Levine SR, Schmaelzle JF. Porcine small intestinal submucosa implanted as a pubovaginal sling in 115 female patients with stress urinary incontinence: a 3 year series evaluated for durability of the results. Society for Urology and Engineering, 17th Annual Meeting, Orlando, FL, 2002.
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62 Tension-free vaginal tape procedure for treatment of female urinary stress incontinence Carl Gustaf Nilsson
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IntroductIon The tension-free vaginal tape (TVT) procedure for treatment of female urinary stress incontinence is a sling operation. For over a century sling operations have been developed and performed with a satisfactory degree of success in terms of achieved dryness. The classic sling operations as described by Goebbel,1 Frangenheim,2 Stoeckel,3 and Aldridge4 are all major invasive surgical procedures, with the inevitable risk of complications, postoperative morbidity and voiding difficulties. Slings of many different materials – allografts, xenografts, and synthetics – have been used. Classic slings are placed at the bladder neck in order to correct hypermobility and to enhance transmission of intra-abdominal pressure provoked by straining. This mechanism of action is consistent with the most popular theories of the past century describing the causes of urinary incontinence.5 Growing awareness of the magnitude of the urinary incontinence problem in the aging population of the developed world has regenerated increasing interest in finding more effective, less invasive, and more affordable methods of curing incontinence. As hypermobility of the bladder neck correlates poorly with symptoms of incontinence and severity of leakage,6 a shift of interest from correcting anatomic changes to an attempt to restore function of the urethral closure mechanism has occurred. Many findings through the years have identified the midurethra as the focus of interest when dealing with female stress incontinence, with anatomic, physiologic, and histologic investigations consistently supporting the concept of the midurethra as being important in maintaining urinary continence in the female. Pubourethral ligaments, inserting at the midurethra, were identified by Zaccharin in the 1960s,7 and further demonstrated by DeLancey in the 1990s.8 Histologic evaluation of the female urethra by Huisman revealed prominent vascularization specifically at the midurethra.9 The early urodynamic investigations by Asmussen and Ulmsten10 further strengthened the impression of the more distal parts of the urethra playing a major role in the closure mechanism. The maximal closure pressure is located at the midurethra and in fertile women pulsatility can be demonstrated at the same location, indicating strong vascular support.10 Ingelman-Sundberg found that the ventral parts of the pubococcygeal muscles inserted into the anterior vaginal wall at the site of the midurethra and utilized this finding in his sling plasty.11 Furthermore, Westby and colleagues showed elegantly in radiographic experiments how, in continent women, the urethra closes at its middle section on holding urination and that the maxi-
mal closure pressure is situated at the same level of the urethra.12 By combining these findings, a new theory for describing the causes of female urinary incontinence was presented by Petros and Ulmsten – the ‘midurethra theory’ (in early literature the ‘integral theory’).13 According to this theory, damage to the pubourethral ligaments supporting the urethra, impaired support of the anterior vaginal wall to the midurethra, and weakened function of the part of the pubococcygeal muscles that inserts adjacent to the urethra are responsible for causing stress urinary incontinence. Connective tissue is an important element of the involved structures since the quality of this tissue has an influence on continence.14
tHE tVt procEdurE development of the procedure The TVT procedure was developed based on the elements of the midurethra theory. The goal was to create a minimally invasive operation that would reinforce the pubourethral ligaments, strengthen the support of the urethra by the anterior vaginal wall, and achieve conditions that would favor ingrowth of fresh connective tissue into the region. The procedure was performed under local infiltration anesthesia from the very beginning in order to facilitate early same day discharge from hospital. Several different sling materials were evaluated. The one finally chosen is a synthetic polypropylene monofilamentous mesh, with a pore size between 75 and 150 microns, which is optimal for ingrowth of fibrous tissue and allows leukocytes and macrophages to enter into the mesh, thus avoiding colonization of bacteria. The special weave of this type I mesh has favorable properties in terms of elasticity and strength.15 An effort was made to standardize the operation in order to facilitate training of doctors to perform the procedure in a manner that includes certain in-built safety features and makes good clinical results possible. The use of local anesthesia – prilocaine (2.5 mg/ml) with epinephrine (2 mcg/ml), diluted with saline to 0.25% – causes vasoconstriction in the operating region, thus decreasing the risk of intraoperative bleeding and hematoma formation. The recommended anesthetic volume of 75–100 ml results in hydrodissection of tissues at the operation site and facilitates passage of the specially designed instrument, with the attached polypropylene tape, through the correct layers of tissue, thus avoiding complications such as bladder injury.
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If the local anesthesia is placed only in the region where the tape should be positioned, deviation by the instruments from this safe sector during performance of the operation causes the patient to react and, thereby, guides the surgeon to correct his performance. Local anesthesia interferes least with the function of the pelvic floor and allows intraoperative testing of optimal tension-free placement of the tape by a cough test in order to avoid postoperative voiding difficulties.
operation technique The TVT device consists of an 11 mm wide × 40 cm long tape of polypropylene, both ends of which are attached to stainless steel, specially curved, 5 mm diameter insertion needles. The tape is covered by plastic sheets to protect it from contamination and to facilitate its passage through the tissues. A reusable handle fits to the needles and is used to insert the needles. A rigid catheter guide is placed into an 18 Fr Foley catheter and helps to deflect the bladder away from the path of needle insertion. The patient is placed in a lithotomy position, avoiding more than 70 degrees of flexion of the thighs. After premedication with, for example, 0.5 mg midazolam, the local anesthetics are placed. The operation requires three small incisions: two 1-cm wide suprapubic skin incisions at the upper rim of the pubic bone, each 2–2.5 cm lateral to the midline, and a vaginal midline incision not more than 1.5 cm wide starting 0.5 cm from the external meatus of the urethra. Five cc of anesthetics are placed under the skin at the site of the planned skin incisions. Another 20 cc are placed on each side retropubically, closely following the posterior surface of the pubic bone down to the urogenital diaphragm. Vaginal infiltration of the anesthetics includes 10 cc on each side paraurethrally up to the urogenital diaphragm and another 5 cc under the vaginal mucosa at the site of the midurethra. The skin incisions facilitate passing of the needles through the skin. After the vaginal incision is made, careful minimal blunt dissection, using Metzenbaum scissors, should be undertaken paraurethrally between the vaginal mucosa and the pubocervical fascia to a depth of not more than 2 cm. The TVT needle is placed in its starting position within the dissected paraurethral tunnel with the needle tip between the index finger of the surgeon’s hand in the vagina and the lower rim of the pubic ramus. With slow controlled pressure, the needle is brought through the urogenital diaphragm, the space of Retzius, and the rectus muscle fascia using the skin incision as a point of direction. It is important to keep the needle in close contact with the dorsal surface
of the pubic bone at all times in order to avoid bladder perforation or entrance into the abdominal cavity. The same procedure is repeated on the other side. After passing each needle to the extent that the needle tip is visible at the skin incision, cystoscopy, using a 70-degree optic, is performed to confirm bladder integrity. If bladder perforation is noted, the needle is withdrawn and passed once more, ensuring that it stays close to the pubic bone and within the safe sector. Once bladder integrity is confirmed, both needles and the tape are brought through and the final adjustment of the tape can take place. The recommendation is to fill the bladder with 300 cc of saline and perform a cough test. The patient is asked to cough vigorously while the tape is adjusted to a point when leakage is only a drop of saline at the urethral meatus. This procedure will ensure tension-free placement of the tape and minimize risks of postoperative voiding problems. After the final adjustment of the tape has been made, the plastic sheets are taken off. At this point it is important to make sure that no further tightening of the tape occurs by placing Metzenbaum scissors between the urethra and the tape when removing the plastic sheets. No fixation of the tape is required.
clinical performance The results of the first clinical trial of the TVT operation were encouraging, with an objective cure rate of 80%.16 Surgeons at six different centers were given personal hands-on training in the TVT technique, after which a multicenter, two-country, prospective clinical trial was initiated. The aim of this study was to investigate the performance of the procedure in a normal clinical setting. A total of 131 carefully selected primary cases of genuine stress incontinence were enrolled. The 1-year followup results revealed an objective cure rate of 91%, with a further 7% of patients being significantly improved. Only 2% were regarded as failures. The complication rate was low, and included one case of bladder injury and one wound infection. Three patients had short-term (≤3 days) voiding problems and only one patient experienced retention symptoms for 12 days.17 These promising results prompted further studies in unselected groups of women with indications for surgical treatment of their urinary incontinence. In a prospective clinical trial of 161 consecutive TVT operations, which included 28% with prior failed incontinence surgery, 37% with mixed incontinence and 11% with intrinsic sphincter deficiency (ISD), the overall objective cure rate at 16 months of follow-up was 87%, 7% were significantly improved and only 5% were classified as failures.18 No 919
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serious complications occurred. The bladder perforation rate was 3.7%, and 4.3% of the women experienced short-term voiding difficulties. De novo urge symptoms were noted in 3% of the women, while as many as 80% of those women who preoperatively complained of urge symptoms were relieved of these symptoms at their 16month follow-up visit. The next step was to study the effectiveness of the TVT procedure in special groups of patients. Table 62.1 shows the objective cure rates found in patients with prior failed incontinence surgery, patients with mixed incontinence, and patients with ISD. From the results it can be concluded that the performance of the TVT procedure is as good in recurrent and mixed incontinence cases as it is in primary cases of urinary incontinence. The cure rates found in patients with ISD appear to be somewhat lower than in other forms of incontinence, a finding also encountered with other types of incontinence operation.
Long-term results Table 62.2 shows the objective cure rates in the long-term follow-up trials published to date. Some of the problems of evaluating long-term results of incontinence surgery include the growing number of patients lost to followup, and the fact that, in many of these often elderly patients, new illnesses appear that might affect bladder function and thus complicate estimation of long-term effectiveness and safety of an anti-incontinence surgical intervention.
table 62.1.
Objective cure rate and time of follow-up in recurrent, mixed and intrinsic sphincter deficiency (ISD) cases of incontinence n
Follow-up
Cure rate (%)
51
24 months
89.6
Lo et al.
41
12 months
82.9
Rezapour & Ulmsten21
34
3–5 years
82.0
33
20 months
70/90*
Nilsson & Kuuva18
59
16 months
81.4
Rezapour & Ulmsten23
80
3–5 years
85.0
18
16 months
77.8
49
3-5 years
74.0
Recurrent Kuuva & Nilsson19 20
22
Liapis et al. Mixed
ISD Nilsson & Kuuva18 24
Rezapour & Ulmsten
* 70% with fixed urethra, 90% with mobile urethra.
table 62.2.
Objective cure rate during long-term follow-up n
Follow-up
Cure rate (%)
Olsson & Kroon
51
3 years
90
26
Ulmsten et al.
50
3 years
86
Nilsson et al.27
90
5 years
84.7
28
90
7 years
81.3
25
Nilsson et al.
The rate of loss to follow-up in the long-term reports, the results of which are presented in Table 62.2, ranges between zero and 11%. This low rate demonstrates a reliable picture of the actual performance of the TVT operation over time. The cure rates at 7 years after surgery are in line with those reported in the initial early trials, suggesting minimal decline in effectiveness over the years. Attempts to predict the risk of failure or declining effectiveness of the TVT procedure have been described in many reports; however, it has not been possible to identify any single significant factor. A tendency towards higher failure rates appears to be associated with older age at the time of operation and the presence of a low pressure urethra. An important finding of long-term follow-up is the absence of signs of rejection or adverse tissue reaction to the polypropylene tape material. No erosion of the tape into the urethra or the bladder was seen.
randomized clinical trials A randomized clinical trial is the preferred method of comparing new treatment methods with established ones. Colposuspension has, for decades, been regarded as the ‘gold standard’ of incontinence operations. Colposuspension is performed either as an open laparotomy procedure or as a laparoscopic operation. Four randomized clinical trials comparing the TVT operation with colposuspension have been published. The largest one by Ward and Hilton compared TVT with open colposuspension in a 14-center study in the UK and Ireland.29 Valpas et al. compared TVT with laparoscopic colposuspension using mesh in a six-center trial,30 while Persson et al. (single center study)32 and Paraiso et al. (two-center study)31 used four Gore-Tex and four polyester sutures, respectively, in their laparoscopic colposuspension operations. Table 62.3 shows the results of these trials. There was no difference in cure rate between the TVT procedure and open colposuspension, but there was a significantly more rapid recovery after surgery in the TVT group and significantly more patients in the colposuspension group needed later surgery for uro-
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table 62.3.
Cure rates in randomized clinical trials comparing tension-free vaginal tape (TVT) with colposuspension (Colpo)
Ward & Hilton29 Valpas et al.
30
Paraiso et al.31 32
Persson et al.
n (TVT/Colpo)
Follow-up
Cure rate (%) (TVT/Colpo)
175/169
24 months
63/51
70/51
12 months
86/57
36/36
18 months
97/81
37/31
12 months
94/100
genital prolapse. The cure rate in the TVT group in the trials of Valpas et al. and Paraiso et al. was significantly higher than in the colposuspension group. No difference in cure rates between the groups in the Persson et al. study could be detected.
complications Quality of life has become an important concept when discussing the outcome of incontinence surgery. Quality of life for the incontinent woman is governed not only by the absence of urinary leakage, but also by the absence of voiding difficulties, urinary tract infections and other adverse symptoms caused by complications associated with the surgical procedure. Minimal invasiveness and standardization of a surgical intervention is a means of bringing down the rate of complications. Systematic prospective registering of complications is the only way to get an accurate picture of the risk and the rate of specific complications. Fortunately, two such registers have been established and published. The one from Finland is unique, as it comprises every single TVT procedure performed in the country as it was introduced to the table 63.4.
clinics within a systematic hands-on training program.33 The Finnish material also includes the learning curve of all the surgeons involved. The other registry is from Austria and includes nearly 3000 cases, but does not involve all the clinics of the country.34 A few other more comprehensive studies focusing on complication rates have been published. The rates of the most common complications associated with incontinence surgery in these studies and the two registries are shown in Table 62.4. It is interesting to note that the rate of bladder injury is fairly consistent in these reports, being around 4% on average. The definition of voiding difficulties varies between the reports but mostly refers to the need for short-term intermittent catheterization within the first two postoperative days. In the report by Abouassaly et al. (which has the highest rate of voiding difficulties), only one patient needed an indwelling catheter for more than 48 hours.37 The risk of postoperative urinary tract infection (UTI) also varies somewhat, with the highest rate being reported in the Austrian material. This may be the result of adhering to a policy of using an indwelling catheter postoperatively (63% of the cases). The recommendation is to perform the TVT operation under local anesthesia, a situation that does not necessitate the use of a postoperative catheter in the bladder. In a report by Bodelsson et al. it was found that the risk of bladder perforation was three times higher if the TVT operation was performed under spinal anesthesia compared to local anesthesia.38 The TVT operation has been found to be effective in the treatment of women with stress incontinence complicated by the simultaneous existence of urge symptoms or/and urge incontinence. The cure rates reported in these cases of mixed incontinence are more than 80%.18,23
Rate of complications (%) associated with the TVT procedure Kuuva & Nilsson33
Tamussino et al.34
Karram et al.35
Levin et al.36
Abouassaly et al.37
Nilsson & Kuuva18
n: 1455
n: 2795
n: 350
n: 313
n: 241
n: 161
Bladder injury
3.8
2.7
4.9
5.1
5.8
3.7
Bleeding
1.9
2.3
0.9
nr
2.5
1.8
Voiding difficulties
7.6
nr
4.9
2.5
19.7
4.3
Hematoma
2.4
nr
1.7
nr
1.9
1.2
Wound infection
0.8
nr
nr
nr
0.4
1.8
Urinary tract infection
4.1
17
10
nr
nr
6.2
Defect healing
0.7
nr
0.9
1.3
0.4
nr
De novo urge
0.2
nr
12
8.3
15
3.1
nr, not reported.
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Pre-existing urge symptoms resolve in 50–80% of cases.18,39 Occurrence of de novo urge symptoms varies between 0.2 and 15% (Table 62.4). Seven years of follow-up suggest that there is no risk of the number of cases with de novo urge problems increasing over time, the rate of these symptoms being 6% at 7 years postoperatively.28 Although the TVT operation is a partly blind procedure, the risk of excessive (>200 ml) intraoperative bleeding and retropubic hematoma formation is rare. Excessive bleeding occurs on average in 2% of cases (Table 62.4) and is mostly managed by manual compression and tamponade. In a systematic evaluation of the occurrence of postoperative retropubic hematoma formation, Flock et al. reported a rate of 4.1% among 249 consecutive cases, with only four cases exceeding 300 ml and requiring surgical intervention.40 The potential for more serious vascular complications exists with a partly blind procedure; however, the incidence of such has been very low. The rate of serious vascular complications in the Finnish registry report was 0.07%, with the Austrian registry reporting bowel perforation in 0.04%.
Summary Available data obtained from published clinical reports show that the TVT operation is effective in curing stress incontinence. In prospective trials where strict criteria for cure and significant improvement have been used, approximately 95% of women having a TVT operation are found to be cured or significantly improved of their stress incontinence. Furthermore, the TVT procedure appears to perform well in all categories of patients for whom incontinence surgery is traditionally recommended, i.e. in primary cases of stress incontinence, cases of prior failed incontinence surgery, and in cases with mixed incontinence and in those with ISD. The risk of intraoperative and short-term postoperative complications is low if proper training is provided and the operation is performed in a standardized way. No long-term adverse effects of the procedure have been reported. In a cost-utility analysis by Manca et al., the TVT operation was found to be cost saving compared with open colposuspension.41
rEFErEncES 1. Goebbel R. Zur operativen Beseitigung der angeborenen Incontinentia vesicae. Ztschr f Gynäk u Urol 1910;2:187–91.
2. Frangenheim P. Zur operativen behandlung der inkontinenz der männlichen hahnröre. Verhandl d Deutsch Gesellsch f Chir 1914;43:149–54. 3. Stoeckel W. Uber die verwendung der musculi pyramidales bei der operativen behandlung der incontinentia urinae. Zentralbl f Gynäk 1917;41:11–9. 4. Aldridge HA. Transplantation of fascia for relief of urinary stress incontinence. Am J Obstet Gynecol 1942;44:398–411. 5. Enhörning G. Simultaneous recording of intravesical and intraurethral pressure. Acta Chir Scand 1961;276(Suppl):1–68. 6. Peschers UM, Fanger G, Schaer GN et al. Bladder neck mobility in continent nulliparous women. BJOG 2001;108:320–4. 7. Zaccharin RF. The anatomic supports of the female urethra. Obstet Gynecol 1968;21:754–9. 8. DeLancey JOL. Structural support of the urethra as it relates to stress urinary incontinence: the hammock hypothesis. Am J Obstet Gynecol 1994;170:1713–23. 9. Huisman AB. Aspects on the anatomy of the female urethra with special relation to urinary continence. Contrib Gynecol Obstet 1983;10:1–31. 10. Asmussen M, Ulmsten U. On the physiology of continence and pathophysiology of stress incontinence in the female. Contrib Gynecol Obstet 1983;10:32–50. 11. Ingelman-Sundberg A. Urinary incontinence in women, excluding fistulas. Acta Obstet Gynecol Scand 1953;31:266–95. 12. Westby M, Asmussen M, Ulmsten U. Location of maximal intraurethral pressure related to urogenital diaphragm in the female subject as studied by simultaneous urethrocystometry and voiding urethrocystography. Am J Obstet Gynecol 1982;144:408–12. 13. Petros P, Ulmsten U. An integral theory of female urinary incontinence. Experimental and clinical considerations. Acta Obstet Gynecol Scand 1990;153(Suppl):7–31. 14. Ulmsten U, Ekman G, Giertz G et al. Different biochemical composition of connective tissue in continent and stress incontinent women. Acta Obstet Gynecol Scand 1987;66:455–7. 15. Dietz HP, Vancaille P, Svehla M et al. Mechanical properties of implant materials used in incontinence surgery. Proceedings of the International Continence Society 31st Annual Meeting, Seoul, Korea, September 18–21, 2001. 16. Ulmsten U, Henriksson L, Johnson P et al. An ambulatory surgical procedure under local anesthesia for treatment of female urinary incontinence. Int Urogynecol J 1996;7:81–6. 17. Ulmsten U, Falconer C, Johnson P et al. A multicenter study of tension-free vaginal tape (TVT) for surgical treatment of stress urinary incontinence. Int Urogynecol J 1998;9:210–3.
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18. Nilsson CG, Kuuva N. The tension-free vaginal tape procedure is successful in the majority of women with indications for surgical treatment of urinary stress incontinence. BJOG 2001;108:414–9. 19. Kuuva N, Nilsson CG. Tension-free vaginal tape procedure: an effective minimally invasive operation for treatment of recurrent stress urinary incontinence. Gynecol Obstet Invest 2003;56:93–8. 20. Lo TS, Hornig SG, Chang CL et al. Tension-free vaginal tape procedure after previous failure in incontinence surgery. Urology 2002;60:57–61. 21. Rezapour M, Ulmsten U. Tension-free vaginal tape (TVT) procedure in women with recurrent stress urinary incontinence – a long-term follow up. Int Urogynecol J 2001;12(Suppl 2):9–11. 22. Liapis A, Bakas P, Lazaris D et al. Tension-free vaginal tape in the management of recurrent stress incontinence. Arch Gynecol Obstet 2004;269:205–7. 23. Rezapour M, Ulmsten U. Tension-free vaginal tape (TVT) in women with mixed urinary incontinence – a long term follow up. Int Urogynekol J 2001;12(Suppl 2):15–8. 24. Rezapour M, Ulmsten U. Tension-free vaginal tape (TVT) in stress incontinent women with intrinsic sphincter deficiency (ISD) – a long term follow up. Int Urogynecol J 2001;12(Suppl 2):12–4. 25. Olsson I, Kroon UB. A three-year postoperative evaluation of tension-free vaginal tape. Gynecol Obstet Invest 1999;48:267–9. 26. Ulmsten U, Johnson P, Rezapour M. A three-year follow up of tension free vaginal tape for surgical treatment of female stress urinary incontinence. BJOG 1999;106:345–50. 27. Nilsson CG, Kuuva N, Falconer C et al. Long-term results of the tension-free vaginal tape (TVT) procedure for surgical treatment of female stress urinary incontinence. Int Urogynecol J 2001;12(Suppl 2):5–8. 28. Nilsson CG, Falconer C, Rezapour M. Seven-year follow up of the tension-free vaginal tape procedure for treatment of urinary incontinence. Obstet Gynecol 2004;104:1259–62. 29. Ward KL, Hilton P. A prospective multicenter randomized trial of tension-free vaginal tape and colposuspension for primary stress incontinence. Two-year follow-up. Am J Obstet Gynecol 2004;190:324–31.
30. Valpas A, Kivelä A, Penttinen J et al. Tension-free vaginal tape and laparoscopic mesh colposuspension for stress urinary incontinence. Obstet Gynecol 2004;104:42–8. 31. Paraiso M, Walters M, Karram M et al. Laparoscopic Burch colposuspension versus tension-free vaginal tape: a randomized trial. Obstet Gynecol 2004;104:1249–58. 32. Persson J, Teleman P, Eten-Bergqvist C et al. Cost-analyses based on a prospective, randomized study comparing laparoscopic colposuspension with tension-free vaginal tape procedure. Acta Obstet Gynecol Scand 2002;81:1066–73. 33. Kuuva N, Nilsson CG. A nationwide analysis of complications associated with the tension-free vaginal tape (TVT) procedure. Acta Obstet Gynecol Scand 2002;81:72–7. 34. Tamussino K, Hanzal E, Kölle D et al. Tension-free vaginal tape operation: results of the Austrian registry. Obstet Gynecol 2001;98:732–6. 35. Karram M, Segal JL, Vassallo BJ et al. Complications and untoward effects of the tension-free vaginal tape procedure. Obstet Gynecol 2003;101:929–32. 36. Levin I, Groutz A, Gold R et al. Surgical complications and medium-term outcome results of tension-free vaginal tape: a prospective study of 313 consecutive patients. Neurourol Urodyn 2004;23:7–9. 37. Abouassaly R, Steinberg JR, Lemieux M et al. Complications of tension-free vaginal tape surgery: a multi-institutional review. BJU Int 2004;94:110–3. 38. Bodelsson G, Henriksson L, Osser S et al. Short term complications of the tension-free vaginal tape operation for stress urinary incontinence in women. BJOG 2002;109:566–9. 39. Segal JL, Vassallo B, Kleeman S et al. Prevalence of persistent de novo overactive bladder symptoms after the tension-free vaginal tape. Obstet Gynecol 2004;104:1263–9. 40. Flock F, Reich A, Muche R et al. Hemorrhagic complications associated with tension-free vaginal tape procedure. Obstet Gynecol 2004;104:989–94. 41. Manca A, Sculpher MJ, Ward K et al. A cost–utility analysis of tension-free vaginal tape versus colposuspension for primary urodynamic stress incontinence. BJOG 2003;110:255–62.
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63 SPARC – midurethral sling suspension system David Staskin, Renuka Tyagi
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INTRODUCTION Minimally invasive slings placed at the level of the mid- to distal urethra have simplified the treatment of genuine stress urinary incontinence (GSI)1 with minimal morbidity. Variations in surgical technique, materials, and shape of the slings used have resulted from the drive to decrease surgical morbidity associated with autologous fascia harvesting without affecting long-term surgical outcomes.2–9 The effective and long-term treatment of stress incontinence due to urethral hypermobility and intrinsic sphincter deficiency has been documented following placement of Burch urethropexy and classic pubovaginal slings.10–13 In addition, similar cure rates between midurethral slings and the Burch colposuspension have been documented in prospective randomized studies.14,15 The SPARC sling system is a minimally invasive sling procedure using a loosely knitted, self-fixating, 1 cm wide, 4-0 polypropylene mesh, which is placed at the level of the midurethra by passing the suspension needle via a suprapubic to vaginal approach.16–18
MECHANISM OF ACTION Continence is dependent upon multiple factors: resting urethral tone, active sphincter contraction, external compression, pressure transmission, and integrity of anatomic configuration. The success of midurethral sling techniques has prompted a re-evaluation of the pathophysiology of GSI and the paradigm for its surgical correction. The mechanism of action for midurethral slings is presumed to be mimicking of the support provided by the pubourethral ligaments and suburethral fascial support. 19 The importance of urethral stabilization from rotational motion has generally been accepted and has been introduced as the ‘integral theory’ from data collected during radiologic evaluation of micturition.20 This correlated with structures documented on anatomic dissection and dubbed an anatomic hammock.21 The importance of urethral configuration suggests that midurethral support prevents the separation of the posterior urethral wall from anterior urethral wall during rotational motion around the inferior portion of the pubic ramus, which appears integral to continence.22 Suburethral support and stability in conjunction with urethral coaptation appear to be the critical factors in the restoration of continence, and elevation of the bladder neck may no longer be a prerequisite.
DEVICE DESIGN The SPARC sling system is illustrated in Figure 63.1.
SURGICAL TECHNIQUE Anesthesia Anesthesia may be selected as per patient and surgeon preference and include general, spinal or epidural, or local anesthesia with/without intravenous sedation. If a local anesthetic is selected, it should be noted that the primary source of discomfort for the patient is contact with the periosteum of the pubic bone during needle passage. Local injections should include two approaches: 1) the abdominal surface with the local anesthetic of the abdominal skin, rectus fascia and muscle; and 2) a paravaginal approach to anesthetize the inferior border of the pubic ramus.
Positioning A standard or modified lithotomy position may be selected based on surgical preference and concomitant procedures, with a supine, pelvis-inclined (Trendelenburg) position recommended. Adequate distal vaginal exposure for a 1.5 cm midurethral incision is required; however, vaginal retraction sutures or complex retractor is usually not required for sling placement alone. A weighted speculum and placement of a Foley catheter (14–18 Fr) per urethra to drain the bladder completely is preferred.
Incisions Two parallel 15-blade stab incisions are made over the pubic symphysis 1.5 cm from the midline (3 cm apart). The surgeon should avoid incisions lateral to this area to avoid impingement of the ilioinguinal nerve exiting from the external ring (Fig. 63.2). Next, the bladder neck should be identified; the submeatal fold may be elevated using an Allis clamp, and a midline incision performed through the vaginal mucosa over the midurethra. This incision, centered over the midurethra, may vary between 1.5 and 3 cm as per surgeon preference (Fig. 63.3). If the procedure is performed without local anesthetic, a saline injection at the level of the midurethra, extending laterally, may be elected to aid in development of the plane of dissection between the vaginal epithelium and the periurethral fascia. Submucosal dissection is performed bilaterally with Metzenbaum scissors, creating a tunnel to the inferior border of the pubic ramus at the level of the midurethra. The tunnel may be small enough (1.5 cm) for only the needle and dilator–connector to traverse the distance, or wide enough (3 cm) for the fingertip to
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a
b
c
d
Figure 63.1. SPARC sling system: (a) Suspension needles: disposable ergonomic, 0.118 in. diameter, 8.2 in. long, and noncutting. (b) Dilator–connectors: create the sling tract and enable the suspension needles to be of small diameter and minimizing trauma, do not require sling attachment and tract formation until the needle position is confirmed, and permit untwisting of the mesh after attachment. (c) Plastic sheath: permits smooth placement of self-fixating mesh. Absorbable tensioning suture: placed within the mesh sling and knotted at various intervals; this absorbable suture prevents ‘pre-tensioning’ of the mesh sling during the removal of the plastic sheath and permits intra- and postoperative sling adjustment. (d) Mesh sling: biocompatible 4-0 loosely knitted polypropylene. be inserted. The ‘small tunnel’ approach involves placement of the fingertip in the paravaginal fornix outside of the incision in order to palpate needle perforation through the endopelvic fascia (recommended). The ‘large tunnel’ approach allows the surgeon to palpate the perforation point of the periurethral fascia from within the incision and to guide the needle under direct fingertip control.
Needle passage Effective needle passage is divided into two phases with entrance into and traversing of the retropubic space first, followed by perforation of the endopelvic and peri-
urethral fasciae. Needle passage may be described in five substeps: 1. Needle passage to the superior surface of pubic symphysis: Holding the needle itself with the fingertips of both hands, the needle is passed through the stab incisions above the pubic symphysis directly down to the bone. During this maneuver the needle handle is pointed toward the surgeon (Fig. 63.4). 2. Rotation around the superior surface of the pubic symphysis: The needle tip is guided along the superior surface of the bone and then directed downward to perforate the rectus fascia and muscle. Grasping the needle itself near the end with the 927
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Figure 63.4. Needle passage along the superior surface of pubic symphysis. Figure 63.2. Suprapubic skin incisions. Stab incisions through the skin 3 cm apart, flanking the abdominal midline.
Figure 63.5. Rotation of needles around the superior pubic symphysis onto the posterior (retropubic) surface.
Figure 63.3. length.
Midline vaginal incision, 1.5–2.0 cm in
fingertips rather than the handle permits more control of the straight portion of the curved needle. After fascial perforation, the needle handle should rotate to 90 degrees (up to the ceiling) as the needle is advanced to keep the tip of the needle on the posterior surface of the pubic bone (Fig. 63.5).
3. Traversing the retropubic space: The needle is guided inferiorly, with the handle rotated 10 degrees medially – ‘walked downward along the bone’ – again with the fingertips, until the endopelvic fascia is encountered (Fig. 63.6). 4. Placement of the needle tip at the perforation point: Grasping the handle of the needle, the needle tip is palpated with the alternate index finger beneath the vaginal wall and is guided to the desired point of perforation. Remember: ‘Find the needle point beneath the vaginal wall with the finger’ and guide it to the perforation point, rather than ‘Find the finger
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B
C
A
Angle handle cranially
45o
Figure 63.6. Needle traverses the retropubic space on the posterior surface of the pubic symphysis. placed at the perforation point’ with the needle. The perforation point is as lateral as possible against the inferior border of the pubic ramus, at the level of the midurethra (Fig. 63.7). 5. Perforation of the endopelvic/periurethral fascia and directing the needle through the vaginal incision: Perforation of the fascia can be performed by pushing the needle through the endopelvic and periurethral fasciae without placing a finger within the vaginal incision (recommended) or by placing a finger in the incision (preferred for less experienced surgeons). A finger placed outside of the incision against the bone within the fornix is most effective. Once the needle perforates the fasciae and can be felt only beneath the epithelial layer, it can be guided through the dissected tunnel with or without a finger placed within the vaginal incision. Be sure the needle has perforated the fasciae before directing it medially. If necessary, allow needle-point perforation of the vaginal epithelium, withdraw the needle and then guide it out of the incision. Failure to perforate the fasciae completely before medial direction of the needle out of the incision decreases the distance between the perforation point and the urethra (Fig. 63.8). The following guidelines are suggested to avoid intraoperative ‘misadventures’ during needle passage.
Figure 63.7. Placement of the needle tip at the point of endopelvic fascia perforation.
Figure 63.8. Perforation of the endopelvic/periurethral fascia and maneuvering the needle tip through the vaginal incision.
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• To avoid urethral trauma, pass the needle directly
•
against the surface of the inferior portion of the pubic ramus at the level of the midurethra onto the tip of the index finger, while deviating the urethral catheter medially with the superior surface of the finger. Major vessel injury and bowel injury should be avoided by adhering to the surface of the pubic bone. The inferior epigastric artery and vein and the endopelvic veins are subject to inadvertent trauma with any needle passage. The iliac and obturator veins are not in the direct surgical field and are not in the direction of needle passage or the force vector of perforation with suprapubic needle passage, as distinct from periurethral or endopelvic fascia perforation from the vaginal approach. Small and large bowel should not be adherent to the pubic bone except in the case of prior abdominal surgery that entered the retropubic space, or the presence of a lower abdominal incisional or inguinal hernia.
Cystoscopy After passage of both needles, cystoscopy is performed with a minimum of 350 cc in the bladder to ensure that the needles are not in a bladder fold or ‘mucosal pinch’. Needle perforation, if present, is often noted at 10 or 2 o’clock near the bladder neck, and additional care should be taken to view the urethra on scope insertion and/or removal. The bladder is left distended upon scope removal.
Sling attachment and transfer 1. The plastic sheath containing the sling material may be irrigated with sterile saline or water prior to attachment to aid in smooth removal of the plastic. 2. The sling is positioned for attachment to the needles by placing the markings in the center facing the surgeon. 3. The connectors are attached to the needle tips using gentle pressure until a ‘snap’ is felt and a ‘click’ is heard. The center of the sling is clearly marked with arrow radiating from the center (Fig. 63.9). 4. The surgeon confirms that the sling is correctly positioned flat and with the markings on the outside of the mesh. The connectors can be twisted on the needle tips to adjust the sling position. 5. The needles are directed to the retropubic space by placing the index finger at the tip of the connector and pushing the connector/needle
Figure 63.9. Sling with connector positioned for attachment to the needle tip. Note the marked arrow radiating from the center of the sling. back into the retropubic space. This ‘pushing’ maneuver minimizes disruption of the periurethral and endopelvic fasciae. The surgeon should avoid pulling the handle of the needle until the white connector has been ‘pushed’ back into the retropubic space through the periurethral fascia. 6. The needle and needle handle are utilized to complete retrograde removal of the suspension needle. Gentle traction on the needle at the level of the skin permits complete needle removal with minimal dilation at the skin level. The sling is pulled through the skin incision for several centimeters on each side. 7. Before adjusting sling tension, the plastic sheath should be re-examined at the vaginal incision for leakage from the bladder. If there is any suspicion of leakage, a repeat cystoscopy should be performed. If the sling is identified within the bladder, it should be cut closely below the white dilator– connector, withdrawn within the plastic sheath, and repositioned with an alternative ‘free suspension needle’ by suturing the plastic to the needle tip. The Foley catheter is now replaced for drainage of the bladder.
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Sling tensioning and fixation To adjust the sling tension, the sling is pulled up through the suprapubic incisions against a spacer placed in the vaginal loop; individual surgeon preference may be a scissor (large) or dilator (No. 8 Hagar preferred). Optimal sling tension is demonstrated when slight movement of the instrument within the mesh loop initially occurs. The sling and plastic sheath are cut at the level of the ‘blue dots’ below the dilator–connectors (Fig. 63.10). Hemostats are placed on each of the cut plastic sheaths using care to avoid the mesh. The suburethral spacer is stabilized with one hand as the plastic sheath on each side is removed with the other. The mesh is then cut below the skin level, with gentle traction on the ends to allow retraction of the mesh beneath the skin level (Fig. 63.11).
Closure Steri-strips are applied to the suprapubic incisions and the vaginal incision is closed using a running 2-0 absorbable suture.
completed prior to placement of the SPARC sling. In particular, if a cystocele repaired is planned, the cystocele repair should be performed with repair of the bladder base but not the bladder neck area. A Kelly repair is not recommended as it may elevate bladder neck support, and may disrupt the pressure transmission to the midurethra by altering bladder neck motion with reference to the sling. In addition, utilizing a separate incision, if possible, for placement of the SPARC sling avoids extension of a hematoma or drainage from the cystocele repair and prevents resultant disruption of the incision over the sling.
POSTOPERATIVE CARE The patient is sent to the recovery room with a Foley catheter in place. It is important, especially after epidural or spinal anesthesia, that the patient be fully ambulatory and free of any residual anesthetic prior to the voiding trial (Table 63.1) to avoid iatrogenic–anesthetic retention.
Managing postoperative retention
If additional pelvic organ prolapse repair procedures are planned, apical and anterior vaginal repairs may be
The SPARC procedure results in placement of the sling below the midurethra with no tension and minimal disruption of normal proximal urethral mobility. This change in sling placement has resulted in a substantial
Figure 63.10. Removal of the needles and connectors. The sling and plastic sheath are cut at the level of the ‘blue dots’.
Figure 63.11. Excess mesh is cut at the abdominal incision. Note gentle traction is placed on the mesh end to allow retraction of the mesh below the skin incision.
CONCOMITANT PROCEDURES
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Table 63.1.
Voiding trial
1. Fill the bladder via the Foley catheter to 300 cc or until full. 2. Remove the catheter and commence the voiding trial. 3. Measure the void: a void of >200 cc (two-thirds of capacity) or a residual measured by ultrasound of <100 cc (one-third of capacity) is considered adequate for discharge. 4. If the residual is >100 cc, the patient is rechecked following an additional void. The patient may elect to be discharged with a leg bag and repeat the voiding trial in the office the following day.
decrease in urinary retention, and is similar to other minimally invasive pubovaginal slings.18 Loosening of the SPARC sling may be initiated intraoperatively if the sling is tensioned too tightly during removal of the plastic sheath, or postoperatively if the patient presents with urinary retention or symptomatic impaired voiding. The tensioning suture within the sling mesh provides a restraint to sling stretching during loosening of the sling tension. The sling can be loosened by placement of a right angle beneath the sling, and then pulling the sling down with a right angle clamp or with a No. 1 Prolene suture that has been placed around the sling. The timing of postoperative sling adjustment should be within 2–3 weeks following implantation, as local tissue ingrowth and biodegradation of the tensioning suture begin to affect the ability to ‘move’ the sling. Pulling on the sling will result in a ‘pop’ and slight patient discomfort at the suprapubic site, indicating that the sling has moved at the rectus fascia layer. Late postoperative retention that does not improve with conservative management or early adjustment of sling tensioning may be addressed with urethrolysis. A midline urethrolysis may be performed if there is no significant tissue ingrowth into the sling. If significant ingrowth exists, a lateral approach is recommended to avoid urethral injury. Following identification of the sling, a nerve hook or right angle clamp may be used to mobilize the sling and hold it on tension. The sling may then be transected with scissors and sling tension adjusted.
Managing postoperative sling extrusion The disadvantages of synthetic mesh graft include the risk of infection, rejection, extrusion, and erosion. Erosion should refer to the entrance (or placement) of the sling within the urinary tract (the bladder or urethra), whereas extrusion refers to the migration or exposure of the sling material into the vagina. Extrusion of
sling mesh into the vagina can be managed immediately in the postoperative period by thorough antibiotic irrigation and wound closure. Delayed closure may involve mobilization of the vaginal edges. Observation and conservative management until the vaginal wall completely heals over the sling mesh may be elected for late extrusion. If the vaginal wall heals ‘through the mesh’, the exposed portion of the mesh should be excised. The vaginal wall can be closed primarily or may be left to heal secondarily. Complication rates with artificial materials may be underreported since erosion can occur relatively late, at 1–4 years postoperatively. In fact, the American Urological Association Female Stress Urinary Incontinence Clinical Guidelines Panel recommends 5-year follow-up as a true test of time for such continence procedures. Initial success with a novel graft material must therefore be judged cautiously until long-term results are available. Given the fact that the midurethral polypropylene slings are made of loosely knitted mesh, and are placed under no tension, the incidence of significant problems appears to be lower than previously anticipated, in the region of 1–6%.17,23,24
REFERENCES 1. Leach GE, Dmochowski RR, Appell RA. Female stress urinary incontinence clinical guidelines (AUA). J Urol 1997;158:875–80. 2. Beck RP, McCormick S, Nordstrom L. The fascia lata sling procedure. Obstet Gynecol 1988;72:699–703. 3. Hilton P. A clinical and urodynamic study comparing the Stamey bladder neck suspension and suburethral sling procedures in the treatment of genuine stress incontinence. Br J Obstet Gynecol 1989;96:213–20. 4. Niknejad K, Plzak LS 3rd, Staskin DR, Loughlin KR. Autologous and synthetic urethral slings for female incontinence. Urol Clin North Am 2002;29(3):597–611. 5. Staskin DR, Plzak L. Synthetic slings: pros and cons. Curr Urol Rep 2002;3(5):414–7. 6. Ghoniem GM, Shaaban A. Sub-urethral slings for treatment of stress urinary incontinence. Int Urogynecol J 1994;5:228–39. 7. Morgan JE, Heritz DM, Stewart FE, Connolly JC, Farrow GA: The polypropylene pubovaginal sling. J Urol 1995;154:1013–5. 8. Jarvis GJ. Surgery for genuine stress incontinence. Br J Obstet Gynaecol 1994;101:371–4. 9. Kersey J. The gauze hammock sling operation in the treatment of stress incontinence. Br J Obstet Gynaecol 1983;90:945–9. 10. Bergman A, Elia G. Three surgical procedures for
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genuine stress incontinence: five-year follow-up of a prospective randomized study. Am J Obstet Gynecol 1995;173(1):66–71.
17. Deval B, Levardon M, Samain E et al. A French multicenter clinical trial of SPARC for stress urinary incontinence. Eur Urol 2003;44:254–9.
11. El-Toukhy T, Mahadevan S, Angharad E et al. Burch colposuspension: a 10 to 12 years follow up. J Obstet Gynaecol 2000;20(2):178–9.
18. Staskin DR, Tyagi R. The SPARC sling system. Atlas Urol Clin 2004;12:185–95.
12. Maher CF, Dwyer PL, Carey MP, Moran PA. Colposuspension or sling for low urethral pressure stress incontinence? Int Urogynecol J Pelvic Floor Dysfunct 1999;10(6):384–9. 13. Bidmead J, Cardozo L, McLellan A, Khullar V, Kelleher C. A comparison of the objective and subjective outcomes of colposuspension for stress incontinence in women. BJOG 2001;108(4):408–13. 14. Ward KL, Hilton P. UK and Ireland TVT Trial Group. A prospective multicenter randomized trial of tension-free vaginal tape and colposuspension for primary urodynamic stress incontinence: two-year follow-up. Am J Obstet Gynecol 2004;190(2):324–31.
19. Papa Petros PE, Ulmsten U. An anatomical classification – a new paradigm for management of urinary dysfunction in the female. Int Urogynecol J Pelvic Floor Dysfunct 1999;10(1):29–35. 20. Petros P, Ulmsten U. An integral theory on female urinary incontinence. Acta Obstet Gynecol Scand 1990;153(Suppl):7–31. 21. DeLancey JOL. Structural support of the urethra as it relates to stress incontinence: the hammock hypothesis. Am J Obstet Gynecol 1994;170:1713–20. 22. Plzak L, Staskin D. Genuine stress incontinence: theories of etiology and surgical correction. Urol Clin North Am 2002,29:527–35.
15. Ward K, Hilton P. Prospective multicentre randomized trial of tension-free vaginal tape and colposuspension as primary treatment for stress incontinence. BMJ 2002;325:67–70.
23. Tseng LH, Wang AC, Lin YH, Li SJ, Ko YJ. Randomized comparison of the suprapubic arc sling procedure vs tension-free vaginal taping for stress incontinent women. Int Urogynecol J Pelvic Floor Dysfunct 2005;16(3):230–5.
16. SPARC Sling System. Patent 6,612,977, Appl. No. 917443. Minnetonka (MN): American Medical Systems Inc, September 2, 2003.
24. Kobashi KC, Govier FE. Perioperative complications: the first 140 polypropylene pubovaginal slings. J Urol 2003;170(5):1918–21.
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IntroductIon As the evidence becomes clearer that pubovaginal sling procedures are most efficacious in the surgical management of stress urinary incontinence, innovation and technology have merged to create pubovaginal sling procedures that strive to obtain the clinical efficacy of autologous fascia slings while minimizing morbidity. Many novel concepts were designed to eliminate the need for an abdominal incision, improve sling fixation, and promote the preservation of normal postoperative voiding. Transvaginal placement of bone anchors eliminated the need for an abdominal incision, and provided stabilization of the suburethral sling. The use of the vaginal wall in a variety of sling techniques eliminated the need for an additional fascial harvest. New generation self-fixating slings provide the advantages of minimally invasive tension-free midurethral sling placement combined with biologic materials which decrease the potential for erosion. These procedures can be utilized in place of the conventional autologous fascia sling in special circumstances, and have been documented to achieve acceptable levels of efficacy while decreasing morbidity. In this chapter we will profile these procedures, and how they may be utilized by pelvic surgeons.
Bone-Anchor SlIngS Bone anchors in incontinence surgery: historical perspective Benderev1 introduced a novel procedure with the use of a bone anchor and a variation of suture placement that essentially facilitated transvaginal bladder neck stabilization.2 The VesicaTM procedure introduced many urologists to the principles of bone anchor insertion. Although initial results with this procedure were encouraging,3 subsequent data revealed a lack of long-term efficacy.4 Bone anchor technology was also utilized in pubovaginal sling surgery. Appell introduced the in-situ vaginal wall sling performed with suprapubic bone anchor implantation and preservation of the endopelvic fascia.5 Favorable results were achieved with minimal complications in patients without significant intrinsic sphincteric deficiency. Hom et al. used a synthetic graft and suprapubic bone anchors to perform a pubovaginal sling,6 and Nativ et al.7 utilized an entirely transvaginal approach to perform cystourethropexy. Bone anchors were inserted by a transvaginal route, and the sutures from the bone anchor were utilized to complete fixation of the sling to the undersurface of the pubic bone.
The operative time was only 28 minutes, and at 1 year follow-up 82% of the patients were dry. Important findings in these patients were the minimal need for narcotics and early ambulation. Subsequently, many surgeons have utilized transvaginal bone anchor placement with biologic allografts to perform a pubovaginal sling.8,9 These procedures are presently the most widely utilized operations for stress incontinence employing bone anchor technology. The transvaginal anchor sling procedures were coupled with repair of anterior compartment defects to provide a stable point of fixation, augmenting the prolapse repair. Leach and colleagues reported on a cadaveric prolapse repair and sling (CaPS) procedure utilizing a large patch of cadaveric fascia.10 Distally the patch was fashioned as a sling anchored to the pubic bone, and the proximal extension of the patch extended to the vaginal apex to reinforce the anterior repair. Shah et al. described a repair of complete vaginal prolapse utilizing transvaginally placed bone anchors combined with mesh fixation to the sacrospinous ligament.11 Both series have reported excellent reduction of prolapse and correction of stress urinary incontinence.
transvaginal bone anchor slings Technique After positioning in the dorsal lithotomy position, the operation commences with an anterior vaginal wall incision. An inverted ‘U’ incision is created unless an anterior repair is performed. In this instance, a midline incision is chosen. The dissection proceeds laterally to the level of the endopelvic fascia, which is perforated. The retropubic space is entered, and the tissue is swept off the pubic bone to facilitate placement of the transvaginal bone anchor insertion tool. However, it is not necessary to perforate the endopelvic fascia, but to develop just enough space behind the pubic bone to insert the anchor insertion tool. The anchor insertion tool is introduced through the vaginal incision and positioned behind the pubic bone. The device should be placed perpendicular to the bone, and the tool should be felt firmly against the bone. This is done by gently ‘scraping’ the tool behind the bone to test for position. (Fig. 64.1) The anchor is placed into the bone positioned on the undersurface of the pubic bone approximately 2–3 cm from the urethra on each side. The suspension sutures are removed through the insertion tool, and the strength of fixation to the undersurface of the pubic bone can be verified by pulling on these sutures (Fig. 64.2). The wound is liberally irrigated with antibiotic solution.
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Figure 64.1. Placement of anchors into pubic bone via transvaginal approach.
Biologic graft material is most commonly utilized as sling material, but autologous or synthetic material may be used. A 2 × 5–7 cm segment is chosen. A tacking suture is then placed to position the sling in its proximal location, which is determined by palpation of the Foley balloon. The proximal suture is placed just beyond the bladder neck in the midline to ensure that the sling supports the bladder neck and proximal urethra. The suspension sutures from the anchors are then threaded through the edges of the sling by placing the sutures though a hollow core needle passed through the sling. Tension is adjusted by placing a large right-angle clamp between the urethra and the sling. One side of the sling is secured to its attachment. The second side of the sling is then tied loosely with the clamp still in place between the sling and the urethra, thus preventing the sling from being tied too tightly. Using the previously placed proximal suture, the sling is then fastened at the level of the bladder neck with 3-0 absorbable suture. An additional suture is then placed distally in the midline to extend the sling across the proximal urethra. Additional sutures are placed as needed to spread out the sling and prevent it from rolling over (Fig. 64.3). Liberal antibiotic irrigation of the wound follows. Cystoscopy is performed to verify lower urinary tract integrity. Vaginal closure is then completed with 2-0 absorbable suture.
Results When interpreting the results of the transvaginal anchorbased slings, it should be noted that the follow-up is limited by a small number of studies and short follow-up duration. Elias and associates reported a 92.5% rate of Urethra
Sling Vagina
Figure 64.2. Anchors utilized to secure permanent sutures to pubic bone. These two sutures will be used to secure the sling.
Figure 64.3. Final suburethral sling position utilizing transvaginal bone anchors. 937
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‘complete cure’ in 40 patients followed for an average of 6.5 months.12 In 15 patients undergoing an isolated transvaginally anchor-based sling, Payne noted that 14 were discharged on the same day.13 Overall, he utilized this procedure in 54 patients with minor complications; two early sling failures were encountered in patients with low leak point pressures (<50 cmH2O). More recently, however, success rates have been reported to be less than 80%, with Franco et al. reporting a success rate of 71% in 65 patients after 30 months.14 After 18 months, 78% of 234 patients experienced success with 53% totally dry.15 Carbone et al. reported a disappointing success rate of only 62% in 154 patients observed for an average of 10.9 months.16 When the patients underwent repeat surgery following failed transvaginal anchor sling, all anchors were properly positioned. The cadaveric grafts appeared to be fragmented, attenuated or absent in all cases. Utilizing the CaPS procedure10 in the correction of urinary stress incontinence and cystocele, 82% of the patients had no stress incontinence and only 12.9% had recurrence of cystocele at a mean follow-up of 12.4 months.17
Complications Most authors report low complication rates from transvaginal bone anchor sling procedures. Bladder perforation was the most common intraoperative complication, ranging from 2.1 to 4.5%.15,16 Almost all series report a low incidence of prolonged urinary retention. Dyspareunia is seen in 8.5–13% of patients following transvaginal sling, with 4–6% complaining of significant pelvic or suprapubic pain. Although most report the incidence of de novo bladder instability to be less than 10%, Franco et al. reported that 16 out of 30 patients (53%) developed de novo postoperative urge incontinence.14 Infection is perhaps the most feared complication involving bone anchor procedures. Osteomyelitis is an infectious condition which is progressive until adequate treatment is rendered. Pain and wound drainage are common complaints.18 In its early stages, it is often very difficult to distinguish osteomyelitis from osteitis pubis, a non-infectious inflammatory condition involving the pubic bone. Osteomyelitis results in progressive bone loss until adequately treated, usually requiring surgical debridement with removal of the bone anchors and 4–6 weeks of culture-specific antibiotics. Graham and Dmochowski published nine cases of osteomyelitis; only three patients were continent and pain-free following treatment.18 Although severe, osteomyelitis after transvaginal bone anchor placement is rare, with a reported incidence of less than 1% in bone anchor procedures.19,20 Appell reported osteomyelitis in two
women after suprapubic placement of bone anchors, both of whom were taking steroids.21 Leach reported only five cases of osteomyelitis in 7000 bone anchor procedures.22 Surgical removal of bone anchors has also been necessary in patients who developed severe pain and vaginal granulomas.23,24 Additionally, there are reports of anchors becoming dislodged from the pubic bone. Tsivian et al. identified 12 anchors becoming detached in eight patients:25 two required cystoscopic removal from the bladder, and three were spontaneously expelled through the vagina; the other seven anchors were detected in the retropubic space on x-ray.
VAgInAl WAll SlIngS The vaginal wall sling was originally described by Raz et al.26 to provide compression and coaptation to the urethra, utilizing midline vaginal mucosa and underlying periurethral support structures to form the sling. The anterior vaginal wall is ideally located and allows the sling to be easily tailored to the length and width necessary to provide an even distribution of pressure over a long urethral segment. It also requires no extravaginal harvesting incision which minimizes morbidity and postoperative pain. The major limiting factor of this procedure is the fact that long-term durability relies on the integrity of the periurethral tissue which may be weak or attenuated and potentially stretch over time. Additionally, sutures may become dislodged or pull through points of fixation. Relative contraindications to this procedure include sexually active women with short vaginal lengths and women with atrophic vaginitis who have thin attenuated vaginal walls.
Technique An inverted ‘U’ incision is made with the apex about 1 cm proximal to the urethral meatus and the base several centimeters proximal to the bladder neck. Lateral dissection and perforation of the endopelvic fascia is performed bilaterally. A transverse incision is then made at the level of the bladder neck to create a rectangular island of vaginal wall that will function as the sling. The vaginal wall proximal to the sling is undermined to form a flap, which will be advanced to cover the sling (Fig. 64.4). Non-absorbable sutures are placed at the four corners of the rectangle, including all layers of the underlying fascial supportive tissues (Fig. 64.5) The sutures are transferred through a small suprapubic incision using a double-pronged ligature carrier and then tied to the rectus fascia. Cystoscopy is performed to confirm bladder integrity and ureteral patency. The proximal vagi-
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Figure 64.5. Placement of helical permanent sutures into four corners of isolated vaginal segment.
Figure 64.4. Isolation of anterior vaginal wall segment to be used for sling. nal wall flap is then advanced over the sling to provide an epithelial covering and restore the integrity of the vagina (Fig. 64.6). Appell27 modified this technique using bone anchors placed in each pubic tubercle to secure the sling and leaving the endopelvic fascia intact. The sutures from the bone anchor are then transferred via needle under finger guidance into the vaginal lumen. A horizontal mattress suture is performed by placement of the suture onto a free Mayo-type needle and beginning the pass of the suture from behind the sling to incorporate the pubocervical fascia, after which the suture is passed back out of the sling proximally. The suture is then transferred to the abdominal wound and the procedure repeated on the opposite side. After cystoscopy confirms urinary tract integrity, the sling sutures are tied without excessive tension using a suture spacer over the pubic tubercle. This procedure was devised to utilize the advantages of the vaginal wall as a sling, and a minimally invasive route of fixation.
Figure 64.6. Advancement of vaginal wall flap to cover vaginal wall sling. 939
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Results Raz et al. noted that urinary continence was achieved in 29 of 32 patients undergoing the vaginal wall sling procedure.26 Juma et al. published the results of this procedure in 54 patients with an average follow-up of 24 months.28 Results were excellent in 90.7% and good in 3.7% for an overall success rate of 94.4%. Kaplan et al.29 retrospectively compared outcomes in patients undergoing autologous rectus fascia pubovaginal slings and those undergoing vaginal wall slings: 89% of patients following fascial slings and 94% of patients following vaginal wall slings were satisfied with the surgical outcome. In addition, the vaginal wall sling patients had significantly less morbidity. These findings led the authors to conclude that vaginal wall slings should be the preferred method of surgical treatment of intrinsic sphincter deficiency (ISD), although the follow-up in the patients undergoing fascial slings was longer. The efficacy of the vaginal wall sling in the treatment of stress urinary incontinence was documented at 18 months in 18 elderly patients. All patients were completely dry and 17/18 were voiding freely.30 In another study, using the in-situ sling technique, 20 patients were followed for at least 24 months, and a success rate of 95% was reported. Two patients developed de novo detrusor instability, which resolved after 2 months.31 Several authors have noted that the anterior vaginal wall procedures are more successful in cases of genuine stress urinary incontinence than for those patients with ISD;32 in fact, in one of these reports the success rate of vaginal wall sling was only 42% when the leak point pressure was less than 50 cmH2O.33
Complications
ability to maintain continence at the level of the midurethra. Despite encouraging results, there are several situations in which placing mesh below the urethra may be problematic. Thus, in these patients, alternate choices of sling placement should be considered. In this population, a ‘hybrid’ biologic or biodegradable midurethral sling may be advantageous. These sling procedures combine the minimally invasive nature of the tension-free midurethral synthetic slings with the lower risk of erosion from biologic tissue.
BioArc™ The BioArc™ (Fig. 64.7) is a version of the SPARC™ procedure that allows the surgeon to interpose any type of sling graft into a SPARC™ delivery system. Essentially, the long continuous mesh strips are equipped with two clamps that allow the surgeon to suture the biologic tissue of choice into the system. This leaves two self-fixating mesh arms to secure the sling, with a central biologic material acting as the suburethral graft. Positioned without tension below the urethra, there is little worry about retention. Additionally, the suburethral portion of the sling is not a mesh, but a biologic or autologous graft which may be less likely to erode. Future applications of this sling may be placement by a transobturator tape (TOT) approach, and to facilitate prolapse reconstruction by incorporating a larger graft in the sling, augmenting anterior compartment repairs.
Technique This is essentially the same as described for the SPARC™ procedure. Prior to placement, the material chosen to comprise the suburethral component of the sling must
A major advantage of this procedure is that there appear to be few associated complications. Complications reported include suture abscesses, dyspareunia, persistent suprapubic pain, and de novo instability in 9–15% of patients.28,32,34 The most bothersome and persistent complication has been detrusor instability. There has also been a report of an epithelial inclusion cyst formation requiring surgical incision;35 this occurrence is probably underreported.
‘hyBrId’ mIdurethrAl SlIngS There has been an explosion in the number of midurethral tension-free tape procedures for the surgical management of stress urinary incontinence. The hallmark of these procedures is the minimal morbidity and excellent results obtained via these methods. These procedures utilize a polypropylene mesh material to restore the
Figure 64.7. BioArc™ sling system. (Courtesy of American Medical Systems, Minneapolis, MN.)
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be incorporated. A length of approximately 7–8 cm is preferable, and the edges of this material should be trimmed to the same width as the mesh in order to facilitate the tunneling process. The surgeon may choose to have the central portion of the sling material slightly wider (approximately 2 cm) by tapering the edges or have a 1 cm graft throughout. The material is incorporated into the mesh by placing it into the clamps that are pre-attached to the mesh. A permanent suture is utilized to attach the graft to the mesh. Following this, the clamps are removed, and the tape sleeves are advanced over the suture. The sling is inserted and tensioned in a manner similar to the SPARC™ procedure (Fig. 64.8). Figure 64.9. Stratasis TF™ sling system. (Courtesy of Cook Urological, Spencer, IN.)
other hybrid midurethral slings The basic premise of these sling variants is to place a non-synthetic material below the urethra via a minimally invasive approach. This can be accomplished by using a degradable material that will dissolve over time, or by fashioning a biologic sling material in such a way as to facilitate self-fixation. Examples of these sling variants are the T-Sling with Centrasorb™ which contains a central portion of absorbable suture and the Sabre™ which is a completely biodegradable sling system. The Stratasis TF™ (Fig. 64.9) sling can be applied by an antegrade
Urethra
Mesh
Biological Material
Vagina
Figure 64.8. Final placement of BioArc™ sling system. Note: Biologic material in suburethral position.
or retrograde retropubic approach. This sling is a completely biologic natural biomaterial (small intestinal submucosa) that reportedly remodels with host tissue. Fashioned in a manner to promote self-fixation, this sling is placed in a fashion similar to SPARC™ or TVT™ techniques.
Results Clinical data with these sling variants are scarce. Much of the data are on feasibility and ease of use. Anger et al.36 noted that BioArc™ was an effective alternative in the surgical correction of stress urinary incontinence in women with more severe SUI requiring a more coaptive sling to provide continence. Eisenberg and Badlani37 demonstrated the versatility of the BioArc™ system in women with SUI and pelvic organ prolapse. Although the clinical follow-up is too short to offer meaningful conclusions regarding efficacy, the use of these sling systems appears safe and offers the surgeon more flexibility to tailor the procedure to meet the needs of the patient. Ho et al.38 reported a series of inflammatory reactions utilizing small intestinal submucosa.
PolyProPylene SlIng/‘PVt’ The most widely used tension-free midurethral slings utilize insertion kits that ‘tunnel’ the sling into the retropubic or transobturator position. These procedures have made many surgeons more at ease with the use of synthetic material as a sling graft. Based on this, Rodriguez et al.39 reported on their experience using a modified polypropylene sling for the treatment of stress urinary incontinence. Based on the principles of traditional pubovaginal sling placement, the authors described a procedure that achieves placement of a 941
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thinly woven polypropylene mesh under the distal urethra without tension. This is accomplished via two small lateral incisions in the anterior vagina, perforation of the endopelvic fascia, and tunneling under the anterior vagina. The mesh is positioned without tension utilizing two Allis-type clamps to ensure that the graft is properly positioned when the sutures are tied. This procedure has also been described by Rackley and colleagues40 who coined the term ‘PVT’, or percutaneous vaginal tape. They concluded that the PVT procedure is reproducible, and achieves excellent results. Both groups note the significant cost advantage when this approach to midurethral polypropylene sling is performed.
Results Rodriguez and Raz41 reported that following polypropylene sling only 2.3% of 301 patients required treatment for persistent stress urinary incontinence. In 92 patients with at least 12 months follow-up, the objective cure rate was 92% and the subjective cure rate was 89%. These authors also concluded that Valsalva leak point pressure (LPP) was of minimal benefit in predicting outcome after polypropylene sling, as patients did well following this procedure regardless of LPP.42 Complication rates following these procedures appear minimal.
concluSIonS The success and exponential rise in the use of the tension-free midurethral sling procedures (TVT™, SPARC™, TOT) have dramatically altered the approach to the surgical management of stress urinary incontinence in women. Bone anchor slings, vaginal wall slings, and bladder neck slings incorporating biologic graft materials are being utilized much less frequently, and these procedures have almost assumed a role of historical interest. However, there are occasions when the use of mesh may be precarious, or the type of stress urinary incontinence requires tighter compression of the bladder neck. It is in these situations, coupled with other factors (age, prolapse, vaginal wall integrity, and detrusor overactivity), that the pelvic surgeon may consider any of the procedures described in this chapter. Utilizing the techniques described above, excellent early and intermediate results are reported with few complications. This leads one to question whether the less frequent utilization of these sling variants has occurred because they are not as efficacious, or because the newer generation of slings achieves similar results more quickly and with less morbidity.
reFerenceS 1. Benderev T. Anchor fixation and other modifications of endoscopic bladder neck suspension. Urology 1992;40:409–18. 2. Marshall V, Marchetti A, Krantz K. The correction of stress urinary incontinence by simple vesicourethral suspension. Surg Gynecol Obstet 1949;88:509–18. 3. Appell R, Rackley R, Dmochowski R. Vesica percutaneous bladder neck stabilization. J Endourol 1996;10:221–5. 4. Schultheiss D, Hofner K, Oelke M, Grunewald V, Jonas U. Does bone anchor fixation improve the outcome of percutaneous bladder neck suspension in female stress urinary incontinence? Br J Urol 1998;82:192–5. 5. Appell R. The use of bone anchoring in the surgical management of female stress urinary incontinence. World J Urol 1997;15:300–5. 6. Hom D, Desautel M, Lumerman J, Feraren R, Badlani G. Pubovaginal sling using polypropylene mesh and Vesica bone anchors. Urology 1988;51:708–13. 7. Nativ O, Levine S, Madjar S, Issaq E, Moskovitz B, Beyar M. Incisionless per vaginal bone anchor cystourethropexy for the treatment of female stress incontinence: experience with the first 50 patients. J Urol 1997;158:1742–4. 8. Payne C. A transvaginal sling procedure with bone anchor fixation. Urol Clin North Am 1999;26:423–30. 9. Kovac S, Cruikshank S. Pubic bone suburethral stabilization sling for recurrent urinary incontinence. Obstet Gynecol 1997;89:624–7. 10. Kobashi KC, Mee SL, Leach GE. A new technique for cystocele repair and transvaginal sling: the cadaveric prolapse repair and sling (CAPS). Urology 2000;56(6 Suppl 1):9–14. 11. Shah DK, Paul EM, Rastinehad AR, Eisenberg ER, Badlani GH. Short-term outcome analysis of total pelvic reconstruction with mesh: the vaginal approach. J Urol 2004;171:261–3. 12. Elias I, Schahar M, Alex C et al. Per vaginal pubovaginal sling procedure using a bone anchor device and synthetic sling for the treatment of stress urinary incontinence. J Urol 1999;161:912A. 13. Payne C. A transvaginal sling procedure with bone anchor fixation. Urol Clin North Am 1999;26:423–30. 14. Franco N, Shobeiri S, Echols K. Medium-term follow-up of transvaginal suburethral slings: variance in outcome success using two different evaluation methods. Urology 2002;60:607–11. 15. Crivellaro S, Smith J, Kocjancic E, Bresette J. Transvaginal sling using acellular human dermal allograft: safety and efficacy in 253 patients. J Urol 2004;172:1374–8. 16. Carbone J, Kavaler E, Hu J, Raz S. Pubovaginal sling using cadaveric fascia and bone anchors: disappointing early results. J Urol 2001;165:1605–11.
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17. Kobashi K, Leach G, Chon J, Govier G. Continued multicenter followup of the cadaveric prolapse repair with sling. J Urol 2002;168:2063–8. 18. Graham C, Dmochowski R. Pubic osteomyelitis following bladder neck surgery using bone anchors: a report of 9 cases. J Urol 2002;168:2055–8. 19. Fredrick R, Carey J, Leach G. Osseous complications after transvaginal bone anchor fixation in female pelvic reconstructive surgery: report from single largest prospective series and literature review. Urology 2004;64:669–74. 20. Rackley R, Abdelmalak J, Madjar S et al. Bone anchor infections in female pelvic reconstructive procedures: a literature review of series and case reports. J Urol 2001;165:1975–8.
31. Vasavada S, Rackley R, Appell R. In situ vaginal wall sling formation with preservation of the endopelvic fascia for the treatment of stress urinary incontinence. Int Urogynecol J 1988;9:379–84. 32. Litwiller S, Nelson R, Fone P et al. Vaginal wall sling: long-term outcome analysis of factors contributing to patient satisfaction and surgical success. J Urol 1997;157:1279–82. 33. Goldman HB, Rackley RR, Appell RA. The in situ anterior vaginal wall sling: predictors of success. J Urol 2001;166:2259–62. 34. Raz S, Stothers L, Young G et al. Vaginal wall sling for anatomic incontinence and intrinsic sphincter dysfunction: efficacy and outcome analysis. J Urol 1996;156:166–70.
21. Appell R. The use of bone anchoring in the surgical management of female stress urinary incontinence. World J Urol 1997;15:300–5.
35. Baldwin DD, Hadley HR. Epithelial inclusion cyst formation after free vaginal wall sling procedure for stress urinary incontinence. J Urol 1997;157:952.
22. Leach G. Local anesthesia for urologic procedures. Urology 1996;48:284–8.
36. Anger J, Amundsen C, Webster G. The use of a polypropylene mesh sling with suburethral insert of biologic material: a minimally invasive approach to treating intrinsic sphincteric deficiency with minimal urethral mobility. J Urol 2004;171(Suppl 4):1240A.
23. Fialkow M, Lentz G, Miller E et al. Complications from transvaginal pubovaginal slings using bone anchor fixation. Urology 2004;64:1127–32. 24. Schultheiss D, Hofner K, Oelke M et al. Does bone anchor fixation improve the outcome of percutaneous bladder neck suspension in female stress urinary incontinence? Br J Urol 1998;82:192–5. 25. Tsivian A, Shtricker A, Levin S et al. Bone anchor 4corner cystourethropexy: long-term results. J Urol 2003;169:2244–5. 26. Raz S, Siegel A, Short J et al. Vaginal wall sling. J Urol 1989;141:43–6. 27. Appell R. In situ vaginal wall sling. Urology 2000;56:499– 503. 28. Juma S, Little N, Raz S. Vaginal wall sling: four years later. Urology 1992;39:424–8.
37. Eisenberg E, Badlani G. BioArc™: a versatile and minimally invasive sling system for stress urinary incontinence and pelvic prolapse. J Urol 2004;171(Suppl 4):V936. 38. Ho K, Witte M, Bird E. 8-ply small intestinal submucosa tension-free sling: spectrum of postoperative inflammation. J Urol 2004;171:268–71. 39. Rodriguez L, Berman J, Raz S. Polypropylene sling for treatment of stress urinary incontinence as an alternative to tension-free vaginal tape. Tech Urol 2001;7:87–9. 40. Rackley R, Abdelmalak J, Tchetgen M, Madjar S, Jones S, Noble M. Tension-free vaginal tape and percutaneous vaginal tape sling procedures. Tech Urol 2001;7:90–100.
29. Kaplan S, Santarosa P, Te A. Comparison of fascial and vaginal wall slings in the management of intrinsic sphincteric deficiency. Urology 1996;47:885–9.
41. Rodriguez L, Raz S. Prospective analysis of patients treated with a distal urethral polypropylene sling for symptoms of stress urinary incontinence: surgical outcome and satisfaction determined by patient driven questionnaires. J Urol 2003;170:857–63.
30. Couillard D, Deckard-Janatpour K, Stone A. The vaginal wall sling: a compressive suspension procedure for recurrent incontinence in elderly patients. Urology 1989;43:203–8.
42. Rodriguez L, de Almeida F, Dorey F, Raz S. Does Valsalva leak point pressure predict outcome after the distal polypropylene sling? Role of urodynamics in the sling era. J Urol 2004;172:210–4.
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65a Transobturator midurethral sling technique for stress urinary incontinence Jonathan S Starkman, Harriette M Scarpero, Roger R Dmochowski
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IntroductIon Over the past decade there have been a number of new minimally invasive surgical procedures for the treatment of stress urinary incontinence. The introduction of the tension-free vaginal tape (TVT) procedure by Ulmsten in 1996 revolutionized the field and has gained widespread acceptance due to its systematic and prospective evaluation.1,2 In a recent review of the surgical techniques used to correct stress urinary incontinence in European hospitals, 83.9% of all procedures were midurethral synthetic slings.3 Of the synthetic slings, the transobturator approach was used in 26.9% of the procedures. As the number and variety of transobturator slings continue to expand, the overall number of procedures is anticipated to increase. A successful minimally invasive surgical procedure should at the very least provide acceptable long-term efficacy, as well as a low incidence of short- and longterm complications. Retropubic midurethral sling procedures (i.e. TVT, SPARC, etc.) have shown efficacy in a variety of clinical situations including: 1) primary stress incontinence; 2) recurrent stress incontinence; 3) mixed urinary incontinence; and 4) intrinsic sphincter deficiency.4–6 In 2001, Delorme7 described the placement of a synthetic polypropylene mesh via a novel transobturator route. The procedure was simple to perform, eliminated complications typically seen with retropubic needle passage, and did not require routine cystoscopy. Currently there is a wide variety of transobturator slings available, all of which are variations on a common theme. In this chapter we review the pathophysiology, relevant anatomy, variations of technique and sling materials, potential complications, and results in the literature of the transobturator midurethral slings.
PathoPhysIology of MIdurethral slIngs for suI A common anatomic abnormality found in women with stress urinary incontinence is urethral hypermobility. Procedures including retropubic and transvaginal suspension have attempted to correct the stress urinary incontinence associated with urethral hypermobility by fixing the proximal urethra and bladder neck in a high retropubic position. In 1994, DeLancey8 suggested that increased urethral closure pressure is achieved by the urethra being compressed against a hammock-like supportive layer consisting of the anterior vaginal wall, endopelvic fascia, and the arcus tendineus fascia pelvis (ATFP). Along similar lines, Petros and Ulmsten9 proposed that laxity in vaginal and ligamentous support
were responsible for the symptoms of stress urinary incontinence and served as a basis for the ultimate success of the TVT procedure. These anatomic observations and the high success rates associated with tension-free midurethral sling procedures have made it apparent that providing suburethral support, rather than correcting hypermobility, is the critical factor in the resolution of stress incontinence.1,10,11 Much of our understanding of the mechanism of action for transobturator platform slings is extrapolated from studies investigating the mechanical forces involved in successful TVT procedures. Studies utilizing perineal ultrasonography show that, in patients cured of stress incontinence with TVT, a functional kinking of the urethra during stress occurs when the tape is placed at the midurethra.12 In a 3-year follow-up study by the same group, 92% of patients with the tape identified at the midurethra had sonographic evidence of functional urethral kinking, which they refer to as the ‘urethral knee angle’. Placement of the tape at the proximal urethra in their series only resulted in three of five patients being continent (60%), most likely due to the lack of a fulcrum effect by the tape.13 A study by Minaglia et al.14 utilizing ObTape showed no difference in resting urethral angles after placement of the tape. Although there was a statistical difference in the urethral angle with straining, urethral hypermobility was maintained in most women, and the authors concluded that correction of urethral hypermobility is not necessary to achieve continence. In fact, continence was seen in 90.4% of their patients with documented hypermobility and in only 50% of patients without urethral mobility. Despite the fact that a subanalysis of their patients was not performed to ascertain which factors predicted failure, the study concluded that a persistent positive Q-tip test was predictive of a successful outcome. Concomitant prolapse surgery or previous anti-incontinence surgery did not predict outcomes in their series. It appears that minimally invasive midurethral slings, including the transobturator approach, restore the supportive hammock as described by DeLancey. This creates a backboard of support with increases in abdominal pressure that enhances urethral compression to restore continence.
surgIcal anatoMy of the transobturator aPProach (Fig. 65a.1) Successful results achieved with transobturator midurethral slings depend on a detailed understanding of the surgical anatomy of the obturator foramen, adductor
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stage 2 dissection (obturator region) Adductor longus m. Obturator n. Urethra
Femoral a. Femoral v.
Adductor brevis m. Obturator externus m. Gracilis m.
Ischiopubic Ramus
Adductor magnus m.
After Bonnet
Figure 65a.1 Illustration of the anatomic postion of a transobturator midurethral sling within the pelvis and its relationship to other pelvic structures (Adapted from Bonnet et al15). musculature, and relevant neurovascular structures, as well as the pertinent pelvic and perineal anatomic relationships. This is of critical importance to optimize efficacy and minimize potential complications. An outstanding illustrative review was performed by Bonnet et al.15 defining the relevant anatomy in cadaveric dissections using the ‘inside-out’ transobturator technique as described by Jean de Leval. The tension-free vaginal tape-obturator (TVT-O) technique was performed in 13 cadavers and anatomic dissections were performed to determine the path of the tape and its relationship to nearby neurovascular structures and organs. Cadaveric dissection was started at Scarpa’s femoral triangle and extended medially through the adductor and obturator externus muscle toward the inferior pubic ramus. The perineal space was entered by removing the obturator internus membrane and muscle and sectioning the inferior ramus and pubic bone. This was followed by dissection of the superficial anterior perineum and pelvis. Important points observed during the dissections are summarized further.
stage 1 dissection (region of scarpa’s femoral triangle) 1. The tape never penetrated the adductor longus muscle (since this is the medial boundary of the femoral triangle, there was sufficient distance from major neurovascular structures); 2. The tape constantly traversed the adductor magnus and gracilis, and adductor brevis in 70% of the cases; 3. No adductor tendinous structure was perforated by the tape
1. At the level of the obturator region the tape penetrated the obturator externus muscle, the obturator membrane, and the obturator internus muscle; 2. The shortest distance between the tape and obturator nerve was 22 mm (range 22–30 mm), with a mean distance of 26.2 mm ± 2 mm at the level of the obturator membrane; 3. The rotational trajectory of the helical passer, as well as positioning the patient with thighs in hyperflexion, contributes to divergence of the obturator nerve from the track of the tape; 4. The anterior branch of the obturator artery is protected from injury by the bony architecture of the inferior pubic ramus.
stage 3 dissection (sectioning of inferior pubic ramus) 1. Tape location corresponds to the most anterior compartment of the ischiorectal fossa; 2. This corresponded to a triangular avascular region bounded by the levator ani (medial and cranial), perineal membrane (caudal), and the obturator internus muscle (lateral); 3. Tape topography was always outside the pelvic space. The tape did not traverse the levator ani muscles.
stage 4 dissection (pelvis) 1. Complete pelvic dissection never revealed the presence of the synthetic mesh, confirming that the levator musculature was never compromised; 2. The anterior perineal pathway showed consistent tape placement above the perineal membrane; 3. The dorsal nerve of the clitoris is consistently caudal to the perineal membrane. These key observations confirmed the highly reproducible anatomic relationships associated with passage of the synthetic mesh via an ‘inside-out’ approach. Cadaveric dissections performed by Delmas et al.16 utilizing the ‘outside-in’ approach on 10 female cadavers have also provided pertinent information and anatomic detail relevant to this minimally invasive technique. Femoral dissection verified that the tape follows a path consistently 4 cm opposite and caudal to the obturator canal, confirming that injury to 947
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major neurovascular structures is minimal. The tape is in a plane between the perineal membrane and levator ani musculature above the pudendal pedicle (the pudendal pedicle is protected by the bony architecture of the inferior pubic ramus). In pelvic dissections, the tape courses posterior to Santorini’s plexus. Thus, these authors conclude that passage of the tunneler too far anteriorly risks injury to the bladder, while passage in an exaggerated posterior direction risks vaginal perforation. In a separate study by Whiteside and Walters17 involving six female cadaveric dissections of the obturator region, the following anatomic observations were made:
• • • •
• The synthetic mesh passed on average 2.4 cm
the tunneler is turned medially, advanced on the tip of the index finger, and brought out the vaginal incision. At this point, inspect the vaginal fornix and urethra to ensure that perforation of these structures has not occurred. The tape is then loaded onto the tunneler and brought out the inner thigh stab incision and the procedure repeated on the contralateral side. It is important to ensure that the tape exerts no tension by allowing a clamp to pass easily between the tape and the urethra. The excess tape is cut flush with the skin at the inner thigh and the incisions are closed with absorbable suture.
inferomedial to the obturator canal;
• The anterior and posterior divisions of the obturator •
nerve are 3.4 and 2.8 cm from the pathway of the transobturator tunneler, respectively; The tunneling device passed on average 1.1 cm away from the most medial branch of the obturator vessels.
Given that the tunneling device and tape are within 1–3 cm of neurovascular structures, the authors emphasize that risk of injury is not negligible.
description of the operative technique An in-depth description of the surgical technique is beyond the scope of this review. The critical points are reviewed in the following section and the reader is referred for a more extensive discussion.7,10,18
Transobturator outside-in ObTape, UraTape, Aris TOT, Monarc, BioArc TO, Uretex TO, ObTryx, I STOP® • The patient is placed in the lithotomy position in 120-degree hyperflexion. • A vertical midline incision is made at the level of the midurethra and the dissection is carried laterally toward the ischiopubic ramus with Metzenbaum scissors. • A puncture incision is made 15 mm lateral to the ischiopubic ramus at the level of the clitoris. • Using the ‘Hook’ or ‘Helical’ tunneler, the obturator membrane is perforated, at which point a specific resistance is noted by the surgeon. • With the index finger in the incision palpating the ischiopubic ramus and obturator internus muscle,
Transobturator inside-out TVT-O There are three specific surgical instruments unique to TVT-O: 1. a stainless steel helical passer; 2. polyethylene plastic tubes; 3. a stainless steel introducer.
• The initial vaginal portion of the procedure is essentially identical to the ‘outside-in’ technique.
• 5 mm stab incisions are made 2 cm superior to a
• •
• • •
•
horizontal line level with the urethra and 2 cm lateral to the thigh folds. This is the exit point of the helical passer. Once the upper part of the ischiopubic ramus is reached, the obturator membrane is perforated sharply with scissors. The introducer is passed at 45 degrees relative to the urethral sagittal plane until it reaches and perforates the obturator membrane with the open side facing the surgeon. The distal end of the tubing is mounted on the spiral segment of the helical passer and slipped along the open gutter of the introducer. Once aligned parallel to the sagittal axis, the passer is rotated so the pointed tip of the tubing exits the inner thigh stab incision. The tubing is pulled from the supporting passer until the first few centimeters of the tape become externalized. The procedure is repeated on the contralateral side. The plastic sheaths are removed simultaneously from both ends of the tape and the tape is centered at the midurethra without tension.
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results with transobturator approach Since the original description of the transobturator midurethral sling in 2001 by Delorme,7 excellent continence results have been noted with relatively short-term follow-up (Table 65a.1). Continence outcomes range from 80.5 to 96% using various objective and subjective tools such as the cough stress test, uroflowmetry, and questionnaire/quality of life instruments. These studies include a variety of patients with mixed incontinence, those who have failed previous anti-incontinence procedures, and patients who had concomitant prolapse repairs. In the studies by Delorme et al.19 and Mellier et al.20 15.6% and 28% of patients had intrinsic sphincter deficiency, respectively. High success rates were consistently reported despite a relatively diverse patient population. These studies, however, failed to perform a subanalysis of their patient outcomes based upon preoperative clinical and urodynamic parameters. Therefore, we do not know which variables are predictive of success and failure with the transobturator sling. Does intrinsic sphincter deficiency (ISD), coinciding prolapse repair or mixed incontinence have a negative impact on the durability and efficacy of this technique? These questions should be answered with further prospective studies and longer follow-up, as in the TVT literature. Two non-randomized studies compared the transobturator tape (TOT) to the TVT procedure and found no statistical difference in terms of continence outcomes, postoperative obstructive symptoms, and complications.11,20 There were more bladder injuries (10% versus 0%) and hemorrhage (10% versus 2%) with TVT than with TOT, but this did not reach statistical significance. It is anticipated that the long-term results of the transobturator procedure will parallel the excellent long-term results experienced in the TVT and SPARC literature.1,21 Synthetic sling procedures may be differentiated by technique, anatomic position of the sling, and the conformation of the mesh/tape. The major difference between the different transobturator slings, aside from subtle modifications to the tunneling device and ancillary equipment, is the composition of the synthetic sling material. The properties of the mesh have a profound influence upon the local inflammatory response, ingrowth of collagen and fibrous tissue, and integration of the tape into the surrounding host tissues (Table 65a.2). These properties may have important consequences with regard to infection, erosion, and rejection. In a study by Slack et al.,22 in vivo studies comparing three different polypropylene meshes confirmed similar
inflammatory responses, while the amount of fibrous collagen, capillary ingrowth and tissue integration was superior for the larger pore, open knit polypropylene meshes. These in vivo observations have been supported by similar data in the general surgical literature.23 Although data from in vivo studies support the utilization of open knit, large diameter monofilament mesh for implantation, further clinical correlation is needed to guide surgical preferences.
• The ObTape and UraTape polypropylene meshes
• •
comprise small pore, non-knitted, thermally bonded mesh with a 15 mm silicone suburethral component. The Mentor Corporation has recently developed a second generation transobturator tape called the Aris™ TOT which has a larger 200 micron pore size to allow improved tissue ingrowth with less encapsulation. ObTryx, TVT-Obturator, Monarc, I STOP, and Uretex-TO are large pore (macropore), open knit polypropylene meshes. BioArc is unique in that it allows the surgeon to suture a biological graft material to the polypropylene tape which is placed in a suburethral position.
coMPlIcatIons of the transobturator aPProach Although the transobturator approach is minimally invasive, a number of peri- and postoperative complications have been described in the literature (Table 65a.3).
bladder perforation Bladder perforation is the most common complication observed with midurethral sling procedures via the retropubic approach, with an incidence of 2–11% in the reported literature.11,24,25 With the initial description of the transobturator technique it was felt that the risk of cystotomy during tunneler passage was negligible.7 However, with greater experience, a number of surgical series have shown that the risk of bladder injury should be considered with the technique. Minaglia et al.14 reported three cases of intraoperative bladder injury while performing the transobturator technique. All injuries were recognized intraoperatively, as cystoscopy is performed routinely at their institution. The procedure was completed with placement of the sling followed by catheter drainage for 7 days postoperatively. There were no further sequelae or complications from their management. 949
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12 months
30
80
94
de Tayrac & 3 Madelenat
Cindolo et al.26
Mellier et al.20
604 (140 1–3 months with 1-year in 572; 1 f/u) year in 140
18 months
12.8 months (2–20)
85.5% satisfied at 1 year
45/47 (96%)
95%; 4%; 1%
92% objective cure; 97% subjective; 96% overall satisfaction
90%; 3.3%; 6.7%
80.5%; 7.5%; 12%
90.6%; 9.4%; 0
56 (39–79)
Questionnaire/ quality of life instrument
Subjective questioning
Questionnaire
57
55 (40–69)
Telephone-based 58.1 questionnaire (± 9.3)
54.7
56 (29–87)
64 (50–81)
Patient age (years)
Cough stress test/ questionnaire
Cough stress test/ questionnaire
Cough stress test; Uroflow
Cured/improved/ Assessment of failed outcome
3
27.3%
18 (56%)
Mixed UI
47.3%
47
94 (100%) defined on 3 grade scale
52.7%
0
12 (13%) preoperative urgency
62 with 22 +Q-tip test (28%) (78%)
27
53%
14 (44%)
Pure SUI
Not reported
Not reported
Not applicable
28 (30%)
26 (28%) (MUCP <30 cm)
3
16 (20%)
4
14.2%
5 (15.6%)
Not reported
Not applicable
17 (18%)
Not applicable
2 (4 previous prolapse symptoms)
25.7%
5 (15.6%)
8%
0
None
None
None
26 (14.2%)
0
Previous Concomitant Previous hysterectomy prolapse antirepair incontinence surgery
Not applicable
4
10 (5.4%) (MUCP <20 cm)
5 (15.6%)
ISD
f/u, follow-up; ISD, intrinsic sphincter deficiency; MUCP, maximum urethral closure pressure; SUI, stress urinary incontinence; UI, urinary incontinence.
Krauth et al.36
Queimadelos 47 40 et al.
7 months (1–21)
183
Costa et al.27
4 months (1–8)
150 (32 17 months with 1-year (13–29) f/u)
Delorme et al.19
Follow-up
n
Outcomes
Study
table 65a.1.
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table 65a.2.
Mesh characteristics
Company
Brand name
Mesh material
Pore size
Mentor
ObTape
Prolene, 15 mm silicone
50 micron
UraTape
Prolene, 15 mm silicone
50 micron
Aris
Polypropylene
200 micron
Monarc
Knitted polypropylene
Large, open knit
AMS
BioArc
Polypropylene with biologic suburethral component
Large, open knit
GyneCare
TVT-Obturator
Polypropylene
Large, open knit
Bard
Uretex-TO
Polypropylene
Large pore
Boston Scientific
ObTryx
Polypropylene with detangled suburethral segment
Large pore, >100 microns
CL Medical, France
I STOP
Monofilament Prolene
>75 microns, low weight/area weave
table 65a.3.
Adverse events
Study
n 19
Delorme et al. de Leval18
32 107
Domingo et al.30 27
Costa et al.
65 183
de Tayrac & Madelenat3
Adverse events None reported 1 superficial vein thrombosis with abscess; ?(27/107) 15.9% transient thigh pain 9 vaginal mesh erosions 3 vaginal erosions; 2 urethral erosions; 1 bladder perforation; 1 vaginal perforation; 2 urethral perforations
30
6 uncomplicated UTI; 1 obturator hematoma
80
1 vaginal erosion with inguinal abscess
Mellier et al.
94
2% intraoperative hemorrhage (300 cc); 1 urethral perforation
Queimadelos et al.40
47
None reported
26
Cindolo et al.
20
36
Krauth et al.
604 (140 with 1-year follow-up)
0.3% vaginal erosion; 2.5% UTI; 0.5% bladder perforation; 0.33% vaginal perforation; 2.3% perineal pain
UTI, urinary tract infection.
Cindolo et al.26 and Costa et al.27 also reported a single bladder laceration in their series which was recognized and managed intraoperatively. Furthermore, anatomic studies have shown that with tunneler passage via the ‘outside-in’ transobturator approach, the needle passes through the retropubic space and true pelvis, which can result in cystotomy.17,28 Based on the published literature, there have been no published cases of bladder injury when performing the TOT via an ‘inside-out’ approach using the TVT-O. In our opinion, cystoscopy should continue to be performed in select cases.
Vaginal tape erosion Since the introduction of synthetic mesh as a sling material for the correction of stress urinary incontinence,
mesh erosion has been observed with varying frequency. A 1997 meta-analysis of synthetic slings quoted a vaginal erosion rate of 0.7% and a rate of urethral erosion greater than 2.7%.29 This complication is thought to be due to the intrinsic characteristics of the mesh utilized in the reconstruction. Although the mechanism of erosion is unclear, subclinical infection and mechanical friction between the sling and host tissues may predispose to this phenomenon.30,31 Recently, Domingo et al.30 reported a relatively high incidence of vaginal erosion (13.8%) in their series utilizing UraTape and ObTape. They hypothesized that the characteristics of the polypropylene mesh (fusion welded, thermally bonded, non-woven, non-knitted) reduced the pore size to 50 microns. These characteristics of the tape led to encapsulation and poor tissue ingrowth, which contributed to the higher vaginal ero951
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sion rate. They concluded that a synthetic mesh with larger pore size facilitates vascular and tissue ingrowth, optimizing mesh integration with the host tissues.23,30 Successful management of this complication includes complete removal of the tape via a transvaginal approach and, if indicated, a combined transobturator approach. Despite tape removal, continence status was good at 78% in their series.30 An alternative to complete tape removal was suggested by Kobashi and Govier32 who managed vaginal tape erosion conservatively after SPARC and observed excellent results due to the exceptional tissue ingrowth and granulation tissue associated with this polypropylene mesh. Since most obturator tapes utilize a macropore, open-knit polypropylene mesh, it seems reasonable to conclude that they may behave in a similar fashion.
Postoperative voiding dysfunction Midurethral slings can be complicated by postoperative bladder outlet obstruction, manifesting as urinary retention, high post-void residual urine, de novo urgency, and worsening of preoperative urgency. De novo urgency has been reported to occur in zero to 20.6% of patients following TVT.33 The incidence following TOT procedures has been between 2.1 and 6.7% in the reported literature (Table 65.6). Two non-randomized studies comparing TVT and TOT showed no statistical differences with regard to efficacy and postoperative voiding dysfunction, including bladder outlet obstruction and urinary retention.11,34 The rate of obstructive voiding after the transobturator midurethral sling can be seen in 1.5–15.6% of patients (Table 65.6). This is usually a transient problem with exceedingly few patients requiring clean intermittent table 65.6.
catheterization or a tape release procedure. Long-term retention after TVT is a rare complication (0.6–3.8%) and can be expected to be equally infrequent in the TOT population based on a similar pathophysiologic mechanism of action, namely recreating DeLancey’s supportive hammock. Patients with refractory voiding dysfunction after TOT can be managed successfully with release of the tape, which in most cases will improve the patient’s symptoms without compromising continence status.11 In patients presenting with early voiding symptoms suggestive of obstruction, downward displacement on the tape to reduce tension under local anesthesia has been shown to provide symptomatic relief.35 The risk of postoperative voiding dysfunction after transobturator sling placement is low and, if recognized in a timely fashion, active intervention can provide symptomatic relief.
other coMPlIcatIons One interesting complication with this approach is the finding of postoperative leg pain. In de Leval’s series,18 15.9% of patients had temporary groin pain which abated by the second postoperative day. In the series by Krauth et al.,36 14 patients (2.3%) had postoperative perineal/groin pain. The pain was transient in all but one case, responding to non-steroidal anti-inflammatory medications. The etiology of the pain is unclear and may be related to subclinical hematoma or transient neuropathic pain. Although the pain reported by these investigators was transient in nature, case reports have shown that isolated leg pain may be the first manifestation of an occult erosion.37 Therefore, persistent leg pain that does not
Voiding dysfunction
Study
n 19
Delorme et al.
32
Urinary retention
De novo urgency
5 (15.6%) with obstructive voiding (Qmax <15/PVR >20%); 1 with urinary retention CIC × 4 weeks
2 (6.25%)
de Leval18
107
3 required tape release
Not reported
Costa et al.27
183
7 (3.3%); 3 required tape release; 2 on CIC (PVR >100 cc) at 1 year
4 (2.1%)
30
PVR >100 cc (4 POD 1 [13.3%]; 3 POD 2; 1 after day 2)
2 (6.7%)
80
None
2 (2.5%)
94
7% PVR >100 cc on POD 1; no patients on long-term CIC
4 (4.2%)
47
None
None
9 (1.5%) transient retention; no CIC; 1 required tape release
5.2% at 3 months; 1.5% at 1 year
de Tayrac & Madelenat 26
Cindolo et al.
20
Mellier et al.
40
Queimadelos et al. Krauth et al.36
3
604 (140)
CIC, clean intermittent catheterization; POD, postoperative day; PVR, post-void residual.
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respond to conservative measures should prompt an appropriate investigation to identify mechanical causes for the pain. Other less common complications have been described anecdotally and include thigh abscess requiring drainage and infected obturator hematoma requiring bilateral transobturator exploration.18,38,39
conclusIon The transobturator suburethral sling has excellent shortterm continence results. Pathophysiologically, efficacy appears to relate to a platform of suburethral support at the midurethra as described by DeLancey’s hammock hypothesis. The technique is easy to learn and master, has short operative time, and acceptable complication rate. Moreover, major vascular and bowel complications have not been reported as the retropubic space is not violated. Initial retrospective comparisons with TVT have shown no statistically significant differences in outcomes. Prospective, randomized studies with longer follow-up are needed to confirm the initial good results.
references 1. Nilsson CG, Falconer C, Rezapour M. Seven-year follow-up of the tension-free vaginal tape procedure for treatment of urinary incontinence. Obstet Gynecol 2004;104:1259–61. 2. Ulmsten U, Henriksson L, Johnson P et al. An ambulatory surgical procedure under local anesthesia for treatment of female urinary incontinence. Int Urogynecol J Pelvic Floor Dysfunct 1996;7:81–6. 3. de Tayrac R, Madelenat P. [Evolution of surgical routes in female stress urinary incontinence]. Gynecol Obstet Fertil 2004;32:1031–8. 4. Kuuva N, Nilsson CG. Tension-free vaginal tape procedure: an effective minimally invasive operation for the treatment of recurrent stress urinary incontinence? Gynecol Obstet Invest 2003;56:93–8. 5. Rezapour M, Falconer C, Ulmsten U. Tension-free vaginal tape (TVT) in stress incontinent women with intrinsic sphincter deficiency (ISD) – a long-term follow-up. Int Urogynecol J Pelvic Floor Dysfunct 2001;12(Suppl 2):S12. 6. Ulmsten U, Falconer C, Johnson P et al. A multicenter study of tension-free vaginal tape (TVT) for surgical treatment of stress urinary incontinence. Int Urogynecol J Pelvic Floor Dysfunct 1998;9:210–3.
9. Petros PE, Ulmsten UI. An integral theory and its method for the diagnosis and management of female urinary incontinence. Scand J Urol Nephrol Suppl 1993;153:1–93. 10. Delorme E, Droupy S, de Tayrac, R et al. [Transobturator tape (UraTape). A new minimally invasive method in the treatment of urinary incontinence in women.] Prog Urol 2003;13:656–9. 11. de Tayrac R, Deffieux X, Droupy S et al. A prospective randomized trial comparing tension-free vaginal tape and transobturator suburethral tape for surgical treatment of stress urinary incontinence. Am J Obstet Gynecol 2004;190:602–8. 12. Lo TS, Wang AC, Horng SG et al. Ultrasonographic and urodynamic evaluation after tension free vaginal tape procedure (TVT). Acta Obstet Gynecol Scand 2001;80:65–70. 13. Lo TS, Horng SG, Liang CC, Lee SJ, Soong YK. Ultrasound assessment of midurethra tape at three-year follow up after tension free vaginal tape procedure. Urology 2003;63:671–5. 14. Minaglia S, Ozel B, Klutke C et al. Bladder injury during transobturator sling. Urology 2004;64:376–7. 15. Bonnet P, Waltregny D, Reul O et al. Transobturator vaginal tape inside out for the surgical treatment of female stress urinary incontinence: anatomical considerations. J Urol 2005;173:1223–8. 16. Delmas V, Hermieu J, Dompeyre P et al. The UraTape transobturator sling in the treatment of female stress urinary incontinence: mechanism of action. Eur Urol Supplement 2003;2:196. 17. Whiteside JL, Walters MD. Anatomy of the obturator region: relations to a trans-obturator sling. Int Urogynecol J Pelvic Floor Dysfunct 2004;15:223–6. 18. de Leval J. Novel surgical technique for the treatment of female stress urinary incontinence: transobturator vaginal tape inside-out. Eur Urol 2003;44:724–30. 19. Delorme E, Droupy S, de Tayrac R et al. Transobturator tape (UraTape): a new minimally invasive procedure to treat female urinary incontinence. Eur Urol 2004;45:203–7. 20. Mellier G, Benayed B, Bretones S et al. Suburethral tape via the obturator route: is the TOT a simplification of the TVT? Int Urogynecol J Pelvic Floor Dysfunct 2004;15:227–32.
7. Delorme E. [Transobturator urethral suspension: miniinvasive procedure in the treatment of stress urinary incontinence in women.] Prog Urol 2001;11:1306–13.
21. Tseng LH, Wang AC, Lin YH et al. Randomized comparison of the suprapubic arc sling procedure vs. tension-free vaginal taping for stress incontinent women. Int Urogynecol J Pelvic Floor Dysfunct 2005;16(3):230–5.
8. DeLancey JO. Structural support of the urethra as it relates to stress urinary incontinence: the hammock hypothesis. Am J Obstet Gynecol 1994;170:1713–20.
22. Slack M, Sandhu JS, Staskin DR et al. In vivo comparison of suburethral sling materials. Int Urogynecol J Pelvic Floor Dysfunct 2005 Jul 2; [Epub ahead of print].
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23. Amid PK, Lichtenstein IL. [Current assessment of Lichtenstein tension-free hernia repair.] Chirurg 1997;68:965–9.
32. Kobashi KC, Govier FE. Management of vaginal erosion of polypropylene mesh slings. J Urol 2003;169:2242–3.
24. Olsson I, Kroon U. A three-year postoperative evaluation of tension-free vaginal tape. Gynecol Obstet Invest 1999;48:267–9.
33. Peschers UM, Tunn R, Buczkowski M et al. Tension-free vaginal tape for the treatment of stress urinary incontinence. Clin Obstet Gynecol 2000;43:670–5.
25. Kobashi KC, Govier FE. Perioperative complications: the first 140 polypropylene pubovaginal slings. J Urol 2003;170:1918–21.
34. Mansoor A, Védrine N, Darcq C. Surgery of female urinary incontinence using trans-obturator tape (TOT): a prospective randomised comparative study with TVT. Neurourol Urodyn 2003;22:526.
26. Cindolo L, Salzano L, Rota G et al. Tension-free transobturator approach for female stress urinary incontinence. Minerva Urol Nefrol 2004;56:89–98. 27. Costa P, Grise P, Droupy S et al. Surgical treatment of female stress urinary incontinence with a trans-obturator-tape (T.O.T.) Uratape: short term results of a prospective multicentric study. Eur Urol 2004;46:102–6; discussion 106–7. 28. Hermieu JF, Messas A, Delmas V et al. [Bladder injury after TVT transobturator.] Prog Urol 2003;13:115–7. 29. Leach GE, Dmochowski RR, Appell RA et al. Female Stress Urinary Incontinence Clinical Guidelines Panel summary report on surgical management of female stress urinary incontinence. American Urological Association. J Urol 1997;158:875–80. 30. Domingo S, Alama P, Ruiz N et al. Diagnosis, management and prognosis of vaginal erosion after transobturator suburethral tape procedure using a nonwoven thermally bonded polypropylene mesh. J Urol 2005;173:1627–30. 31. Kobashi KC, Dmochowski R, Mee SL et al. Erosion of woven polyester pubovaginal sling. J Urol 1999;162:2070–2.
35. Ozel B, Minaglia S, Hurtado E et al. Treatment of voiding dysfunction after transobturator tape procedure. Urology 2004;64:1030. 36. Krauth JS, Rasoamiaramanana H, Barletta H et al. Suburethral tape treatment of female urinary incontinence – morbidity assessment of the trans-obturator route and a new tape (I-STOP): a multi-centre experiment involving 604 cases. Eur Urol 2005;47:102–6; discussion 106–7. 37. Mahajan ST, Kenton K, Bova DA et al. Transobturator tape erosion associated with leg pain. Int Urogynecol J Pelvic Floor Dysfunct 2005 Jun 18; [Epub ahead of print]. 38. Game X, Mouzin M, Vaessen C et al. Obturator infected hematoma and urethral erosion following transobturator tape implantation. J Urol 2004;171:1629. 39. Goldman HB. Large thigh abscess after placement of synthetic transobturator sling. Int Urogynecol J Pelvic Floor Dysfunct 2005 Jun 29; [Epub ahead of print]. 40. Queimadelos MA, Cimadevilla GA, Lema GJ, Rodrigues NH, Perez FD, Lamas CP. Monarc transobturator suburethral sling: eighteen months’ experience. ICS/IUGA, France, 2004; Abstract 559.
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65b Transobturator approach Calin Ciofu, Francois Haab
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INTRODUCTION Since 2001, when Delorme first published the transobturator insertion of a suburethral sling for the treatment of stress urinary incontinence,1 few articles have been published on the technique, despite the principle of the technique being considered both interesting and promising. The technique was developed in order to avoid the risk of urethral, bladder, and bowel injury. The paucity of articles in the literature permits only expert opinion-based and no evidence-based considerations. The former were limited to retrospective case controls, classifying the technique as having a grade B of recommendation. Nevertheless, based on DeLancey’s anatomic studies, the technique – comprising insertion and passage of the suburethral tape from one foramen obturator to the other (transobturator tape, or TOT) – appears to restore the physiologic support more effectively and, therefore, continence (Fig. 65b.1).
THE ANATOMIC RATIONALE FOR TRANSOBTURATOR TAPE The mechanism of continence is still controversial. Many authors correlate incontinence with urethral hypermobility. DeLancey’s hammock theory suggests that urinary continence is due to muscular, ligamentous and fascial support of the urethra. In order to correct incontinence, the surgical procedure has to restore urethral support. Tension-free vaginal tape (TVT) and TVT-like procedures restore this support, replacing the muscular structures with a polypropylene U-shaped tape.2
The two main concerns of the TVT technique (obstruction and bleeding) can be avoided by the anatomic specificity of TOT. In the TOT technique, the polypropylene tape inserted through the lower part of the foramen obturator is closer to the physiologic shape of the hammock. Between the left and the right part of the tape there is a very large open angle. Anatomic studies showed that the direction of the tape keeps the same transverse orientation as the muscular fibers of the hammock.3 This implies, at least from a theoretical point of view, that it is difficult to obstruct the urethra. On the other hand, anatomic studies showed that the tape passes through spaces where vascular and neurologic structures are very scarce (although not completely absent). Perineal dissection showed that the tape passes between the perineal membrane and the muscular levator ani; pelvic dissection showed that the tape is situated far behind the pubovesical and pubourethral venous plexus (Santorini). Perforation of the obturator membrane is performed in its lowest part, far below the vascular structures and nerves. In its lateral progress from the foramen obturator to the mediofemoral region, the tape crosses the adductor muscles and, here again, there are no important vessels or nerves.4 This makes hemorrhage and nerve injury less probable, although not entirely impossible.
THE OPERATIVE TECHNIQUE The procedure can be performed under either spinal or general anesthesia; however, local anesthesia is not excluded. The patient is placed in the lithotomy position, with the thighs in hyperflexion on the abdomen and the buttocks at the edge of the table. A 16 Fr Foley catheter is inserted in the bladder and retained throughout the entire operation in order to facilitate the identification and protection of the urethra. Several specifically designed devices are needed for the procedure (Fig. 65b.2):
• An ‘introducer’, a several centimeters long stainless steel gutter.
• Two ‘passers’, sometimes improperly named
Figure 65b.1. Tape position once inserted through the foramen obturator.
•
‘needles’, also made of stainless steel. Each is composed of a handle and a curved needle. The curve describes a 90-degree angle with the handle. One passer has a curve designed to fit the right side; the other, the left. The tape, which is of polypropylene, has both ends fixed in a polyethylene tube. This plastic tube has
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Figure 65b.2. Devices necessary for the transobturator tape procedure. Right: the introducer; central and left: the passer. The curved part of the needle is protected by a plastic sheath that has been removed from the central device.
above the line of the urethral meatus, 2 cm outside the thigh folds. The passer within the polyethylene tube is then guided through the hollow part of the introducer until its distal end reaches the foramen obturator (Fig. 65b.3). The introducer is removed and the passer pulled further with a rotational movement in order to reach and exit through the previously made skin incision (Fig. 65b.4). The top of the plastic tube is then grasped with a clamp and the introducer removed. The same technique is applied to the opposite side. The two tubes are then extracted on both sides. Traction is exerted simultaneously on both sides in order to adjust the position of the tape. The top of the Mayo scissors should be kept between the tape and the urethra until the final position is found in order to avoid excessive tension. Once the correct tension is applied to the tape, its plastic sheath is removed. The tape ends are then cut at the subcutaneous layer. The femoral skin and vaginal mucosal incisions are closed with resorbable sutures. The indwelling bladder catheter is retained for 24 hours. The absence of post-voiding residue should be
a lateral opening through which the curve of the passer is guided up to its end. The mid-third of the urethra is identified and the vaginal mucosa incised for 1–2 cm, along the median line, between two Allis clamps. The incision must penetrate the thickness of the vaginal wall. The dissection is continued, with fine dissection scissors, starting from the incision and directed laterally and horizontally towards the upper part of the ischiopubic ramus. The dissection can be helped by earlier hydrodissection, performed before incising the vagina. The dissection should be done with care in order not to perforate the vaginal wall or vestibular mucosa. Once bone contact is perceived, the dissection is stopped. The introducer is inserted, with the hollow part of the gutter facing the operator and keeping contact with the upper margin of the ischiopubic ramus. The obturator membrane is then perforated and the introducer’s progression stopped. The future cutaneous exit point is then located by a 0.5 cm vertical incision of the skin several millimeters
Figure 65b.3. The passer takes a circular direction, perforating the obturator membrane. 957
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RESULTS In the few retrospective series published to date, cure and improvement rates with TOT at 1 year appear to be similar to those of TVT. Cure rate is 90–95% and improvement rate 3–9%; however, the follow-up period is still very short (Table 65b.1). Complications are few. Perioperative hemorrhage is exceptional and not important. One case report notes an infected hematoma with urethral erosion.8 The urethral risk is less important than in the TVT technique. It is perhaps more important in the outsidein technique, but protection of the urethra by the operator’s finger can easily avoid any lesion, thus obviating the need for cystoscopy as is necessary with the TVT technique. In addition, the bladder is situated more cranial to the direction of the passer and is therefore difficult to injure. Nevertheless, bladder erosion of the tape has been highlighted9 by several operators. Erosion is less a postoperative consequence than a problem of graftversus-host reaction,10,11 indicating that erosion may also occur with the TOT operation. Prolonged retention (2.8%) and pain have been recognized as complications of the TOT procedure. Pain usually lasts for 1–3 days and can be treated with nonopioid analgesics (Table 65b.2). Figure 65b.4. the thigh.
The passer exits through the skin incision at
DISCUSSION
checked after catheter ablation. If voiding is incomplete, intermittent self-catheterization for several days can be suggested. An indwelling catheter is sometimes necessary but should never be retained for more than 1 week. The duration of the operation is approximately 15 minutes (14–16 minutes) and hospitalization does not usually exceed 48 hours. Several variations of the technique are mentioned. It was initially suggested that the tape be passed through, not from the vagina to the femoral region (inside-out technique), but inversely (outside-in technique). The main variation of the technique concerns the shape and curves of the passer.
Table 65b.1.
The results of treatment with the transobturator tape procedure as reflected by the literature
Authors
No. of patients
Method of evaluation
Delorme et al.5
150
Mellier et al.6 7
Cindolo et al.
Transobturator insertion of suburethral tape is a new technique and current follow-up does not exceed 1 year. It is probable that in the following years more complications will be identified. The results at 1-year follow-up appear to be as good as those with the TVT technique although these results are conclusions of retrospective non-randomized series. Prospective randomized series are necessary to confirm these initial results. If DeLancey’s hammock theory is correct, the transobturator tape appears to restore suburethral support most closely to the physiologic aspect. This led Delorme et al.13 to suggest that there should be no reason for patients to develop de novo bladder hyperactivity. We only partially agree with this opinion because the
Follow-up (months)
Cure (%)
Improvement (%)
Failure (%)
Clinical assessment by independent 17 investigator: cough test
90.6
9.4
0
94
Telephone questionnaire
3
95.0
4.0
1
80
Questionnaire
4
94.0
3.0
3
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Table 65b.2.
Peri- and postoperative complications of the transobturator tape procedure as reflected by the literature
Authors
De Leval12
Delorme et al.5
Mellier et al.6
Cindolo et al.7
No. of patients
107
150
94
80
Perioperative complications
None
None
Hemorrhage <200 ml (2 patients)
Bladder neck laceration (1 patient)
Pain (%)
15.9
0
?
Erosion
0
0
0
Superficial venous thrombosis (%)
0.8
–
De novo bladder hyperactivity (%)
–
1.33
4.1
Postoperative retention (%)
2.8
0
1.0
Voiding dysfunction (%)
–
3.33 (Qmax <15 ml/s)
natural hammock is a muscular structure, physiologically able to contract, whereas the artificial tape is not able actively to obstruct the urethra during stress. On the other hand, the TOT procedure respects the orientation of muscle fibers better than the TVT operation, and the dissection is less extensive, making tape migration less likely to occur. From the anatomic point of view one could be tempted to add that voiding difficulty should be less frequent than with TVT series. This appears to be confirmed by two studies comparing TVT and TOT retrospectively, not simultaneously, and non-randomized.6,14 Postoperative retention appears to be less frequent with TOT. These data need confirmation with prospective randomized series.
CONCLUSIONS There are several proven advantages concerning the feasibility of the TOT technique compared to the TVT procedure:
• the short duration of the operation; • the low risk of urethral and bladder lesion, making • •
–
cystoscopy redundant; the absence of risk of bowel lesion; the low risk of hemorrhage.
Initial results appear to suggest a cure rate similar to that of the TVT procedure but these data need confirmation and longer follow-up.
REFERENCES 1. Delorme E. [Transobturator urethral suspension: mini-
? Vaginal + inguinal abscess (1 patient) –
25 (‘some difficulty to void’)
2.5 – –
invasive procedure in the treatment of stress urinary incontinence in women.] Prog Urol 2001;11:1306–13. 2. Haab F, Traxer O, Ciofu C. Tension-free vaginal tape: why an unusual concept is so successful. Curr Opin Urol 2001;11:293–7. 3. Delmas V, Hermieu J, Dompeyre P et al. The Uratape transobturator sling in the treatment of female stress urinary incontinence: mechanism of action. Eur Urol (Suppl) 2003;2:776. 4. Delmas V, Hermieu JF, Dompeyre P et al. The transobturator slingtape Uratape: anatomical dangers. Eur Urol (Suppl) 2003;2:777. 5. Delorme E, Droupy S, de Tayrac R, Delmas V. Transobturator tape (Uratape): a new minimally-invasive procedure to treat female urinary incontinence. Eur Urol 2004;45(2):203–7. 6. Mellier G, Benayed B, Bretones S, Pasquier JC. Suburethral tape via the obturator route: is the TOT a simplification of the TVT? Int Urogynecol J Pelvic Floor Dysfunct 2004;15:227–32. 7. Cindolo L, Salzano L, Rota G, Bellini S, D’Afiero A. Tensionfree transobturator approach for female stress urinary incontinence. Minerva Urol Nefrol 2004;56(1):89–98. 8. Game X, Mouzin M, Vaessen C, Malavaud B, Sarramon JP, Rischmann P. Obturator infected hematoma and urethral erosion following transobturator tape implantation. J Urol 2004;171:1629. 9. Hermieu JF, Messas A, Delmas V, Ravery V, Dumonceau O, Boccon-Gibod L. Plaie vésicale après bandelette transobturatrice. Prog Urol 2003;13:115–7. 10. Boublil V, Ciofu C, Traxer O, Sebe P, Haab F. Complications of urethral sling procedures. Curr Opin Obstet Gynecol 2002;14:515–20. 11. Dietz HP, Vancaillie P, Svehla M, Walsh W, Steensma AB, Vancaillie TG. Mechanical properties of urogynecologic implant materials. Int Urogynecol J Pelvic Floor Dysfunct 2003;14:239–43.
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12. de Leval J. Novel surgical technique for the treatment of female stress urinary incontinence: transobturator vaginal tape inside-out. Eur Urol 2003;44(6):724–30. 13. Delorme E, Droupy S, de Tayrac R, Delmas V. [Transobturator tape (Uratape). A new minimally invasive method in
the treatment of urinary incontinence in women.] Prog Urol 2003;13:656–9. 14. Ansquer Y, Marcollet A, Yazbeck C et al. The suburethral sling for female stress urinary incontinence: a retropubic or obturator approach? J Am Assoc Gynecol Laparosc 2004;11:353–8.
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66 The artificial urinary sphincter for treatment of stress urinary incontinence in women Emily E Cole, Harriette M Scarpero, Roger R Dmochowski
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INTRODUCTION The artificial urinary sphincter (AUS) is an effective alternative to pubovaginal and/or midurethral slings and periurethral injection therapy in the management of urinary incontinence, particularly in those patients in whom the above-mentioned procedures have failed. Historically, the AUS has been reserved for treatment of incontinence due to primary urethral sphincter deficiency – type III stress urinary incontinence, or intrinsic sphincter deficiency (ISD).1–3 The primary pathophysiology of ISD is characterized by an inability of the urethra to function as a sphincter, either at rest or in response to minimal stress activity. ISD may be the result of urethral scarring related to prior anti-incontinence procedures, neurologic disorders (myelomeningocele, peripheral neuropathy), radical pelvic operations, pelvic radiation therapy, and, in some cases, the effects of aging and estrogen deficiency on the urethra and anterior vaginal wall. Current thinking denotes the pubovaginal sling to be the gold standard for the treatment of ISD; however, it is clear that not all patients will have adequate results despite several attempts.4 A patient in this situation with documented urethral weakness and good anterior vaginal wall support may benefit from treatment with an AUS. The AUS allows for higher intraurethral pressures by increasing pressure evenly around the urethra, thereby preventing incontinence due to the transmission of intra-abdominal forces. The placement of an AUS may be accomplished via either a transabdominal or a transvaginal approach. The device is composed of three parts: the inflatable cuff, the pressure-regulating balloon, and the pump. The cuff is placed circumferentially around the bladder neck, the pressure-regulating balloon is positioned in the prevesical space, and the pump is placed in the labium majus. When the pump is compressed, fluid within the system is transferred from the cuff into the regulating balloon. This decompression opens the bladder neck, allowing the patient to void. After 1–2 minutes, the pressureregulating balloon promotes cuff refilling by transfer of fluid through a resistor in the pump, re-establishing urethral compression, coaptation, and continence. The American Medical System AMS 800 is the only AUS currently available for implantation (Fig. 66.1).
EVALUATION Patients undergoing a workup for stress urinary incontinence (SUI) who may be considered as candidates for implantation of an AUS require a detailed evaluation including a focused urologic history and physical examination. The patient with genuine SUI due to primary
Figure 66.1. Single Cuff AMS 800™ Urinary Control System. (Courtesy of American Medical Systems, Inc., Minnetonka, MN.) urethral sphincter deficiency will typically report a significant loss of urine with abdominal straining. However, particular attention should be paid to the characterization of incontinence as purely stress, associated with urgency, spontaneous, or mixed, to rule out coexistence of detrusor overactivity. In addition, the degree of incontinence and resultant bother should be quantified to counsel the patient accurately about options. A detailed past surgical history should be obtained. A history of prior anti-incontinence surgery may affect the vascularity and thickness of the periurethral tissue and anterior wall of the vagina, thereby making dissection in the bladder neck and periurethral areas difficult. The history should also assess the patient for any neurologic or orthopedic disorders that may affect the patient’s abilities to manipulate the labial pump mechanism. A complete physical examination should be performed, paying special attention to the vaginal and lower abdominal components. Examination may confirm previous surgical procedures in many cases. Findings such as a weakened pelvic floor, anterior and/or posterior compartment defect(s) or atrophic vaginitis are identified and considered when future surgical options are discussed. Urethral hypermobility should be assessed by direct examination or the Q-tip test. A hypermobile bladder neck or urethra may respond more appropriately to a standard suspension or sling procedure. The size of the vaginal vault and basic anatomic structures should be assessed. Objective demonstration of stress
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urinary incontinence in the supine or upright position is recommended. Besides a urine sample for analysis and culture, the patient should undergo at least a simple urodynamic evaluation to assess bladder function. Urine storage at low intravesical pressures is critical before proceeding with increasing urethral resistance with the AUS. A cystometrogram (CMG) determines filling pressures and whether there is adequate bladder capacity. Highpressure urinary storage is a contraindication to AUS placement. The CMG is also helpful in the detection of detrusor overactivity, which may be treated with anticholinergic medications. Measurement of abdominal leak point pressure (LPP) is necessary to assess sphincteric competency and to confirm a diagnosis of ISD. Some authors recommend the utilization of urethral pressure profilometry to confirm low urethral closure pressures (<25 cmH2O).5 Uroflowmetry and measurement of postvoid residual urine reflect bladder emptying. Incomplete emptying may indicate the necessity for intermittent catheterization postoperatively. Radiographic evaluation should include a voiding cystourethrogram (VCUG) with resting and straining views. A well-supported urethra with an open bladder neck at rest is consistent with ISD. The VCUG will also confirm the absence of fistulae and vesicoureteral reflux.
PATIENT SELECTION The AUS is indicated for those patients who suffer from intrinsic sphincter deficiency who demonstrate lowpressure urinary storage. As in all cases, conservative measures should be considered prior to operative intervention. Non-invasive measures such as timed voiding, fluid restriction, pelvic floor exercises, vaginal estrogen therapy, and anticholinergic medications to address any urge component may be considered. If these measures are not sufficient, or if the degree of incontinence is as such, operative intervention may be considered. Patients who demonstrate elevated intravesical storage pressures are subject to upper tract deterioration when outlet resistance is increased. These patients should demonstrate a urodynamically confirmed response to anticholinergic therapy prior to AUS implantation. Simultaneous or staged augmentation cystoplasty should be considered in those patients who demonstrate persistently high pressures despite maximal pharmacologic therapy. Patients with incomplete emptying and high preoperative post-void residuals may be considered for AUS implantation. These patients may require intermittent self-catheterization following the procedure, and should
be adequately counseled preoperatively. Those who are unwilling or unable to perform intermittent catheterization but can operate the labial pump may be considered for AUS implantation. When compared to the pubovaginal sling, the AUS is less likely to cause permanent urinary retention. Following decompression of the cuff, the bladder may be emptied by Credé maneuvers. These patients should be carefully selected, demonstrating preoperatively a clear ability to empty via abdominal strain. Women of childbearing age are eligible for sphincter implantation. Many investigators believe that if the patient becomes pregnant, the device should be deactivated in the third trimester to diminish excessive pressure on the cuff and bladder neck. If the situation will not allow for deactivation throughout the third trimester, it should be deactivated during labor and delivery to permit bladder emptying. There is no contraindication to cesarean section as the components are within the retropubic space.6
TRANSVAgINAL ImPLANTATION The advantage inherent in the transvaginal approach for AUS cuff placement, compared with a purely abdominal approach, is the accessibility of the poorly defined urethrovaginal plane. The dissection of this plane is even more difficult following one or more anti-incontinence procedures, and direct visualization during the procedure can be helpful. A controlled surgical entrance and optimal closure of the anterior vaginal wall eliminates the need for dissection of this difficult plane from within the retropubic space, eliminating the risk for an inadvertent and potentially unrecognized injury to the vaginal wall.7,8 The patient is admitted to the hospital on the day of the operation. Preoperative broad-spectrum antibiotics are administered parenterally at least 1 hour prior to surgery. Following the administration of regional or general anesthesia, the patient is placed in the dorsal lithotomy position. The lower abdomen and vagina are shaved and prepared with a 10-minute scrub with povidone-iodine (Betadine) or Hibiclens solution. A posterior-weighted vaginal retractor is placed for exposure of the anterior vaginal wall. Lateral labial retraction sutures or a LoneStar retraction system can be utilized for retraction of the labia. A 14 Fr Foley catheter is inserted in sterile fashion and the bladder is drained. A midline incision is made in the anterior vaginal wall. The incision should extend from a point midway between the bladder neck and urethral meatus to the proximal bladder neck (Fig. 66.2). With sharp dissection, a plane under the vaginal wall is created on each 963
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Figure 66.2. With the patient in the dorsal lithotomy position, a midline vaginal incision is performed. side of the incision. Sufficiently thick vaginal flaps are created in anticipation of closure of the vagina over the AUS cuff. If the patient has not had a prior procedure involving dissection around the bladder neck, blunt finger dissection may be used to separate the endopelvic fascia from its lateral attachments to the pubic rim. The fascia should be swept from lateral to medial, creating a window into the retropubic space (Fig. 66.3). In cases of prior operations, the retropubic space should be entered sharply, using Metzenbaum scissors positioned against the pubic symphysis pointed in the direction of the ipsilateral shoulder. Once the retropubic space is entered bilaterally, the urethra and bladder neck can be separated posteriorly and laterally from the vagina
and pelvic sidewall utilizing a combination of sharp and blunt dissection. Attention should then be directed to the anterior aspect of the proximal urethra and bladder neck to free the attachments from the pubic symphysis. If possible, blunt finger dissection through the vaginal incision should be used to perform this part of the procedure. In the patient who has had a previous retropubic operation, dense scarring may be encountered in this area, making this dissection particularly difficult. To facilitate exposure of the dorsal urethra, a separate suprameatal incision (1–2 cm) may be used (Fig. 66.4a).9 Through this incision, sharp dissection can be performed in the midline below the pubic symphysis (Fig. 66.4b). After the bladder neck and urethra are separated from the pubic symphysis, lateral blunt dissection can be performed to complete the dissection to the retropubic space previously opened through the initial vaginal incision. Overly aggressive dissection during this stage of the procedure may lead to unintentional bladder or urethral tear. If
a
b
Figure 66.3. Using a combination of sharp and blunt dissection, the vaginal mucosa is dissected off the underlying tissues and the retropubic space is entered bilaterally.
Figure 66.4. (a) If dense scarring is encountered anterior to the urethra, a separate incision can be made above the urethral meatus. (b) The suprameatal dissection is performed in the midline, just below the pubic symphysis.
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this occurs, conventional wisdom may dictate that the procedure be abandoned. However, Salisz and Diokno reported on successful repair of this type of injury with subsequent successful implantation of the device.10 After the proximal urethra and bladder neck have been freed circumferentially, a right-angle clamp is passed around the urethra from left to right. The cuff measuring tape is grasped and passed around the bladder neck and the circumference of the bladder neck is measured. If the circumference is equivocal, it is best to err in favor of a slightly larger cuff size. Using a rightangle clamp, the appropriate sized cuff is placed around the bladder neck (Fig. 66.5). If the AUS pump is to be placed into the right labum majus, the cuff should be drawn from right to left, and vice-versa. The cuff is then locked in place and rotated 180 degrees so that the locking button of the cuff lies anteriorly, away from the anterior vaginal wall (Fig. 66.6). On the side on which the pressure-regulating balloon and pump mechanism are to be implanted, a transverse suprapubic incision (approximately 4 cm) is made. A straight clamp is passed under fingertip guidance from the suprapubic incision lateral to the midline down to the ipsilateral side of the vaginal incision. The cuff tubing is grasped and the clamp is withdrawn, pulling the tubing up into the suprapubic incision. Shods (rubber sleeves) should be utilized during this phase of the procedure to ensure that the end of the tubing is not open
Figure 66.6. The cuff is rotated 180 degrees clockwise so that the locking button lies anterior to the urethra, away from the anterior vaginal wall. to the field. The anterior rectus sheath is then incised vertically and the retropubic space is developed adjacent to the bladder. The pressure-regulating balloon is inserted into this space. The reservoir may be selected to be in the 50–70 cm H2O pressure range, and may contain 22–25 cm H2O. The choice of apropos pressure and volume is dependent on surgeon preference and patient specific factors (such as degree of urethral atrophy and history of pelvic radiation etc.)
Figure 66.5. The cuff of the artificial urinary sphincter is passed around the bladder neck and locked into place. 965
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From the suprapubic incision, a subcutaneous tunnel into the labium majus is created with blunt and sharp dissection. The pump is passed into the labium majus to rest at the level of the urethral meatus with the deactivation button facing anteriorly. A Babcock clamp is used to secure the pump in this position. The tubing is trimmed to the appropriate lengths and the ends are irrigated to remove any air or debris. Preparation of the cuff and the reservoir is performed according to the instructions specified by the manufacturer. A straight connector is then placed between the pump and the balloon reservoir. A right-angle connector attaches the pump to the cuff. Quick connectors provided in the implantation kits are used to secure these attachments. The suprapubic and vaginal incisions are irrigated copiously with antibiotic solution. The wounds are then closed in several layers with absorbable sutures to ensure coverage of implanted materials with healthy tissue. If the integrity of the anterior vaginal wall is in question, the interposition of a vascularized flap (e.g. Martius flap) should be considered. Following closure, vaginal packing is placed. Prior to awakening the patient, deactivation of the AUS cuff should be ensured. The vaginal packing and Foley catheter can be removed on the first postoperative day. The cuff should be left in the deactivated position for a period of 6 weeks.
As the dissection approaches the bladder neck, it should proceed laterally and may be facilitated by a finger or sponge stick in the vagina (Fig. 66.7). The bladder neck is located by palpation of the Foley catheter balloon and the endopelvic fascia is entered approximately 2 cm on either side of the bladder neck. The dissection of the vesicovaginal plane is continued through the periurethral fascia until the vagina is completely visible. The bladder neck is then dissected from the vagina below the periurethral fascia in both directions at the level of the catheter balloon. Extreme caution must be taken during these steps to avoid perforation of the vaginal wall. In extremely difficult cases, an intentional anterior cystotomy may aid in identification of the bladder neck and facilitate separation within the vesicovaginal plane. To verify the integrity of the bladder, it can be filled with sterile water dyed with methylene blue. Any inadvertent cystotomies may be repaired (preferably in multiple layers) with absorbable sutures. Any accidental perforations of the vaginal wall should be repaired directly. In cases of extensive injury, it may be advisable to convert to a pubovaginal sling. If AUS is determined to be the only option,
Fingers in the vagina
TRANSAbDOmINAL ImPLANTATION Some centers favor the transabdominal approach for its easy access to the retropubic space and lack of an anterior vaginal wall incision.11 As in the transvaginal approach, the patient should be admitted to hospital on the day of the procedure and should receive parenteral broad-spectrum antibiotics 1 hour prior to the start of the operation. Following induction of anesthesia, the patient should be placed in the dorsal lithotomy position allowing access to both the abdomen and vagina. The abdominal wall and vagina should be shaved and a 10minute skin preparatory scrub should be performed. A 14 Fr Foley catheter is placed and the bladder drained. A lower midline or Pfannenstiel incision should be made to allow appropriate access to the retropubic space. The incision is carried down through the fascial layers, and the retropubic space is developed using a combination of sharp and blunt dissection. This dissection can be complicated in those patients who have had prior pelvic procedures. In cases where the space does not develop easily, the dissection should follow the posterior face of the pubic bone, trying not to injure the anterior bladder wall. Repair of any cystotomy should be performed with absorbable sutures.
Defect created in endopelvic fascia
Recti muscles transected
a
b
Figure 66.7. Aiding the dissection with an intravaginal finger: (a) frontal view; (b) lateral view.
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it is preferable to implant the cuff and close the vaginal wall following the interposition of a Martius flap. When the bladder neck has been freed circumferentially, the cuff sizer is used, again taking care to choose the larger size in cases of intermediate measurement. The appropriate sized cuff is drawn around the bladder neck with a right-angle clamp and positioned so that the locking button lies on the opposite side from the labium majus in which the pump is to be placed (Fig. 66.8). The appropriate pressure-regulating reservoir is chosen as previously described. The balloon is placed on the same side as the labium majus where the pump will be placed. The system is primed and filled as previously described. A subcutaneous tunnel is created from the suprapubic incision down into the labium majus using sharp and blunt dissection. The pump is placed in the labium majus to rest at the level of the urethral meatus with the deactivation button facing anteriorly. A Babcock clamp is utilized to hold the pump in place. An absorbable suture can be placed within the tunnel to prevent migration. The tubing is then connected as described previously. The cuff is deflated and the device is deactivated. Following inspection for adequate hemostasis, the wound is copiously irrigated with antibiotic solution. The abdominal incision is then closed without drainage. Figure 66.9 illustrates the device in place.
2 cm a
b
d
c
e
Figure 66.8. (a, b) Insertion of right-angle clamp; (c, d) right-angle clamp in place; (e) clamp, catheter and finger in position.
Figure 66.9.
Artificial urinary sphincter in place.
The Foley catheter can be withdrawn on the first postoperative day. In cases of accidental or intentional cystotomy, a longer period of catheter drainage is preferred. The device is left in a deactivated position for a period of 6 weeks.
COmPLICATIONS Complications associated with AUS implantation include intraoperative injury to the bladder, urethra or vaginal wall, device failure, erosion, and infection. When a number of risk factors for explantation were compared, including patient age, type and number of prior procedures, time lapsed between last procedure and AUS implantation, and perioperative injury, Costa et al. found the only significant factor to be perioperative injury. Of 49 patients who had perioperative injuries, eight explantations resulted, compared with only four in the 155 cases that did not have injuries.12 Major intraoperative complications can be minimized with meticulous surgical technique. Recognized injuries should be repaired primarily under direct visualization with the interposition of well-vascularized tissues if necessary. In many cases, inadvertent injury to the bladder, urethra, or vaginal wall should not preclude implantation of the device. Good surgical judgment should be utilized to determine the safety of completing the procedure. With improvements in the design and manufacture of the device, AUS malfunctions have decreased significantly. Potential pitfalls included fluid loss secondary to tubing fracture at connection sites, cuff leakage at 967
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stress points, and kinking of the tubing. Some problems have resulted from the cuff mechanism itself. Atrophy of the periurethral tissues decreases the compressive bulk within the cuff, not allowing for pressure to be dispersed evenly around the urethra, resulting in recurrent incontinence. Although newly designed cuff backing has addressed this issue, it must be considered in cases of failure.13 In cases of mechanical failure, the device may be revised. The surgeon’s judgment concerning replacement of a malfunctioning portion of the device rather than the whole device is critical. Clear indications for complete replacement of the device include fluid leakage, which may allow foreign material into the system, or a device that has been in place for more than 3 years.14 Device erosion has decreased since the introduction of modified cuffs; however, it remains a concern with any foreign body implantation. Significant risk factors for erosions include perioperative injury, incorrect implantation technique, history of prior procedures, and infection.12 Erosion of the sphincter cuff into the urethra is commonly associated with recurrent incontinence, although urinary tract infection may be the first and only symptom. Erosion of the cuff through the vaginal wall is associated with vaginal bleeding and discharge. Erosion of the pressure-regulating reservoir into the bladder is rare, and may present as a urinary tract infection or infection of the device. Pump erosion through the labium majus is diagnosed by direct examination. Infection or erosion should be treated with explantation of the entire device in the majority of cases. Reimplantation may be considered after 4–6 months. In cases of cuff erosion into the urethra, the placement of an omental flap between the cuff and urethra is recommended at reoperation. Experience with penile prosthesis implantation raises questions about the appropriateness of salvage procedures. In cases of erosion of the cuff into the urinary tract, salvage of the AUS is not recommended. In the isolated case of erosion of the sphincter tubing through the abdominal skin, or erosion of the pump through the labium, aggressive irrigation and debridement of the tissues may make replacement of certain AUS components and wound closure a possibility. When replacement of the pump is necessary, it should be moved to the opposite labium. The device with cuff erosion into the vaginal wall may be salvaged utilizing a Martius flap and vaginal wall closure. Before all salvage attempts, the patient should be counseled as to the high risk of eventual necessity for removal of the complete device.
RESULTS Published data on success rates for implantation of the AUS in female patients are shown in Table 66.1. The average success rate ranges from 68% in a series of 31 women by Donovan et al.15 to 100% in smaller series by Appell1 and Abbassian.9 In the largest series involving 207 patients, Costa et al. reported success rates of 88.7% and 81.8% in patients with non-neurogenic and neurogenic bladder, respectively.12 A study comparing AUS and pubovaginal sling in 77 patients with confirmed ISD revealed favorable results for both procedures (84% versus 91%, respectively).16 Table 66.1 also includes the published complications from the same series. Infection was seen in 3–7% of cases. Erosions represented the most common complications, occurring in 7–29% of cases. Reoperation for cuff malfunction or tubing problems has been as high as 21% in earlier series;17 however, there is a clear trend towards reduced numbers of device failures due to technologic advancements made over the years. Long-term follow-up data for the AUS in women are sparse. Existing reports indicate that revision of the AUS is likely to be necessary 10 years after implantation for either mechanical or non-mechanical reasons.3
CONCLUSION The use of the AUS in women is still rare compared to its use to treat male incontinence. The purpose of the AUS is to provide uniform circumferential compression of the bladder neck, without changing its position. The AUS is indicated in the subpopulation of incontinent women with proven ISD, and can be particularly useful in those patients who have undergone previous unsuccessful anti-incontinence procedures. In addition, in those women with ISD and a hypocontractile bladder, the AUS may be the initial treatment of choice over the sling due to its lower incidence of prolonged postoperative urinary retention. The AUS may be placed via either a transvaginal or a transabdominal approach. Advantages to the transvaginal approach include direct visualization of the difficult dissection of the urethrovaginal plane, and the ability to make a suprameatal incision to assist in the anterior dissection of the urethra. Advantages of the transabdominal approach include lack of a vaginal incision and improved exposure to the endopelvic fascia and anterior bladder neck dissection. Additionally, transabdominal exposure allows the opportunity to perform a deliberate cystotomy to assist in a particularly difficult dissection. Regardless of operative approach, emphasis should be placed on meticulous surgical approach as
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Table 66.1.
Success rates for implantation of the artificial urinary sphincter
Author 18
Scott
No. of patients
Success
Complications
139
84%
3 infxn (3%) 4 erosions (4%)
Revisions
Light & Scott19
39
87% dry 5% 2–3 ppd
1 infxn (2.5%) 3 erosions (7%)
Donovan15
31
68%
9 erosions (29%) 1 abuse (3%)
Diokno et al.17
32
94% dry 3% improved
1 dehiscence (3%) 1 abscess (3%)
7 revisions (4 cuff malf)
Abbassian9
21 revisions (11 cuff malf)
4
100% dry
0
0
Appell1
34
100% dry
0
3 revisions (2 cuff malf)
Duncan et al.20
29
52% improved
8 erosions (28%) 1 infxn (3.5%)
1 revision
Webster et al.2
25
92% dry 8% 1–2 ppd
1 postoperative death (4%)
4 revisions (3 cuff malf)
Costa et al.21
54
93% improved
3 erosions (6%) 1 infxn (2%)
Hadley et al.14
18
89% dry
2 erosions (11%)
22
Stone et al.
54
84% dry 12% improved
4 lost to follow-up 3 erosions (6%) 2 unable to use (4%)
Costa et al.12
190
88% dry 8% improved
12 explants (5.9%)
11 revisions
infxn, infection; malf, malfunction; ppd, pads per day.
intraoperative complications place the patient at risk for postoperative problems such as infection and erosion with eventual device explantation. The success of the AUS compares well to the success of more traditional procedures for urinary incontinence. The data suggest that placement of the AUS is a safe and effective treatment option for the carefully selected patient with ISD.
4. Wilson TS, Lemack GE, Zimmern PE. Management of intrinsic sphincteric deficiency in women. J Urol 2003;169(5):1662–9.
REFERENCES
8. Hadley R. Transvaginal placement of the artificial urinary sphincter in women. Neurourol Urodyn 1988;7:292–3.
1. Appell RA. Techniques and results in the implantation of the artificial urinary sphincter in women with type III stress urinary incontinence by a vaginal approach. Neurourol Urodyn 1988;7:613–9.
5. Appell RA. Sphincter insufficiency: testing and treatment. Curr Opin Urol 1997;7:197–204. 6. Fishman IJ, Scott FB. Pregnancy in patients with the artificial urinary sphincter. J Urol 1993;150:340–1. 7. Wang Y, Hadley HR. Artificial sphincter: transvaginal approach. In: Raz S (ed) Female Urology, vol. 1, 2nd ed. Philadelphia: Saunders, 1996; 428–34.
9. Abbassian A. A new operation for insertion of the artificial urinary sphincter. J Urol 1988;140:512–3.
2. Webster GD, Perez LM, Khoury JM et al. Management of type III stress urinary incontinence using artificial urinary sphincter. Urology 1992;39:499–503.
10. Salisz JA, Diokno AC. The management of injuries to the urethra, bladder or vagina encountered during difficult placement of the artificial urinary sphincter in the female patient. J Urol 1992;148:1528–30.
3. Fulford SC, Sutton C, Bales G et al. The fate of the ‘modern’ artificial urinary sphincter with a follow-up of more than 10 years. Br J Urol 1997;79:713–6.
11. Long RL, Barrett DM. Artificial sphincter: abdominal approach. In: Raz S (ed) Female Urology, vol. 1, 2nd ed. Philadelphia: Saunders, 1996; 419–27.
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12. Costa P, Mottet N, Rabut B et al. The use of an artificial urinary sphincter in women with type III incontinence and a negative Marshall test. J Urol 2001;165(4):1172–6. 13. Kowalczyk JJ, Mulcahy JJ. Use of the artificial urinary sphincter in women. Int Urogynecol J 2000;11:176–9. 14. Hadley R, Loisides P, Dickinson M. Long-term follow-up (2–5 years) of transvaginally placed artificial urinary sphincters by an experienced surgeon. J Urol 1995;153:432A [abstract 812]. 15. Donovan MG, Barrett DM, Furlow WL. Use of the artificial urinary sphincter in the management of severe incontinence in females. Surg Gynecol Obstet 1985;161: 17–20. 16. Mark SD, Webster GD. Stress urinary incontinence due primarily to intrinsic sphincteric deficiency: experience with artificial urinary sphincter and sling cystourethropexy. J Urol 1994;151(Suppl);420A [abstract 769]. 17. Diokno AC, Hollander JB, Alderson TP. Artificial urinary
sphincter for recurrent female urinary incontinence: indications and results. J Urol 1987;138:778–80. 18. Scott FB. The use of the artificial urinary sphincter in the treatment of urinary incontinence in the female patient. Urol Clin North Am 1985;12:305–15. 19. Light JK, Scott FB. Management of urinary incontinence in women with the artificial urinary sphincter. J Urol 1985;134:476–8. 20. Duncan HJ, Nurse DE, Mundy AR. Role of the artificial urinary sphincter in the treatment of stress incontinence in women. Br J Urol 1992;69:141–3. 21. Costa P, Mottet N, Le Pellec L et al. Artificial urinary sphincter AMS 800 in operated and unoperated women with type III incontinence. J Urol 1994;151(Part 2):477A [abstract 1000]. 22. Stone KT, Diokno AC, Mitchell BA. Just how effective is the AMS 800 artificial urinary sphincter? Results of longterm follow-up in females. J Urol 1995;153(Part 2):433A [abstract 817].
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67 New technologies for stress urinary incontinence Jay-James R Miller, Peter K Sand
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INTRODUCTION
pliable after its injection into soft tissues.1 It is easily injected, radiopaque, non-immunogenic, and noninflammatory.2 In an early study of 10 women with ISD who were treated with injection of 3.9 ml of calcium hydroxylapatite, three were cured and four were significantly improved at 1 year.3 Sand et al.2 recently reported on a multicenter prospective randomized trial comparing calcium hydroxylapatite to bovine collagen. The interim analysis showed that calcium hydroxylapatite was as easy to inject as bovine collagen, did not require antigenicity testing and provided greater improvement in Stamey grades, pad weight reduction, and leakage reduction (Table 67.1). Durability of treatment with calcium hydroxylapatite as compared to bovine collagen was demonstrated by the maintenance of the outcomes when the 6-month data were compared to the 12-month data. Long-term follow-up showed no evidence of ossification or interference with subsequent surgery, if required, with calcium hydroxylapatite. Autologous chondrocytes, harvested from ear cartilage, can be readily grown in cell culture and have been injected for childhood ureterovesical reflux with preliminary success and a favorable risk profile.4 Bent et al.5 used autologous chondrocytes harvested from auricular cartilage in the treatment of 32 women with type III incontinence. All patients received a single injection distal to the bladder neck. Incontinence severity grading indicated that 16 women were dry and 10 improved at 12 months postinjection. Eighty-one percent of the women were dry or improved. There was also significant improvement in pad weight tests and quality of life scores after treatment. In women who were dry post-treatment, the mean pad weight decreased from 22.4 to 0.1 g (p<0.001). The Urogenital Distress Inventory declined for all categories except bladder emptying and lower abdominal pain. One woman had prolonged urinary retention requiring selfcatheterization for 4 weeks but there were no serious adverse events. Periurethral injection of autologous chondrocytes appears to be safe, effective, and durable
New technologies in the treatment of stress urinary incontinence can be divided into two categories: revolutionary novel approaches and evolutionary improvements on existing therapies. Some evolutionary therapies are new bulking agents for periurethral injections, the prepubic tension-free vaginal tape, and the Remeex device; novel approaches include radiofrequency therapy and duloxetine pharmacotherapy.
EVOLUTIONARY THERAPIES Some longstanding treatments for stress urinary incontinence – urethral bulking and suburethral slings – are increasing in popularity with technologic advances. These advances have improved efficacy while simultaneously decreasing known complications. Recent evolutionary examples include carbon coated zirconium beads (Durasphere) and the transobturator tape procedures. Presented here are the newest evolutions in stress urinary incontinence treatment.
Urethral bulking materials Periurethral bulking to treat urinary incontinence is not new. It was first described more than 60 years ago to treat urinary incontinence. Current United States Medicare guidelines limit bulking agents to patients with intrinsic sphincter dysfunction (ISD). The ideal periurethral bulking agent would be non-reactive, permanent, nonmigratory, and treat incontinence with a single injection without complication. The search for such an ideal bulking agent continues. There are several urethral bulking materials currently under investigation with the aim of providing an effective, durable, biocompatible, and safe agent. These new agents include calcium hydroxylapatite, autologous chondrocytes, autologous stem cells, ethylene vinyl alcohol co-polymer, and dextranomer/ hyaluronic acid co-polymer. Perhaps the best-studied agent is calcium hydroxylapatite. It is a normal constituent in bone and remains Table 67.1.
Calcium hydroxylapatite versus collagen at 6 and 12 months after injection Improvement (%) (1 Stamey grade)
Improvement (%) (to Stamey grade 0)
No wet pads (%)
n
CaHA (6 months)
81*
49
49
45
Collagen (6 months)
62
48
48
43
CaHA (12 months)
80†
63
41
32
Collagen (12 months)
57
39
31
29
* p=0.0447; † p=0.0281; CaHA, calcium hydroxylapatite.
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with 50% of the patients dry at 12 months after one injection. Frauscher et al.6 recently treated five female patients who had stress urinary incontinence with ultrasoundguided injections of autologous myoblasts and fibroblasts. Skeletal muscle biopsies were taken from the left arm to obtain cultures of autologous myoblasts and fibroblasts. Both transurethral and three-dimensional ultrasound were used to investigate the lower urinary tract and direct the injections. The fibroblasts were mixed with collagen as a carrier for the cells and injected into the urethral submucosa to treat atrophy of the urothelium, while the myoblasts were injected directly into the striated urethral rhabdosphincter to reconstruct the muscle. Urinary incontinence was cured in all five patients 1 year after injection of autologous stem cells and quality of life was significantly improved postoperatively. Transurethral ultrasound showed a significantly increased thickness of the urethra and rhabdosphincter. Contractility of the rhabdosphincter was also improved as measured by electromyography after therapy. Uryx is an injectable solution of ethylene vinyl alcohol (EVOH) dissolved in dimethyl sulfoxide (DMSO). Upon contact with an aqueous environment the DMSO dissipates and the EVOH solidifies as a soft spongy mass which can be utilized as a bulking agent. The injected volume remains fixed and is equivalent to the final volume. The intraurethral bulking volume does not migrate or otherwise change with time. In one study,7 Uryx made more subjects continent than Contigen while injecting a lower mean volume (Table 67.2). There were no unanticipated or unique complications associated with EVOH injection. The three most prevalent complications in both treatment groups were delayed voiding, dysuria, and frequency. The majority of complications occurred early and resolved rapidly. Stenberg et al.8 originally reported on dextranomer/hyaluronic acid co-polymer as a biocompatible material for urethral injection in 1998. These authors subsequently reported 5-year follow-up data9 and now this material is being used in the novel Zuidex system Table 67.2.
(Fig. 67.1). This system allows for placement of the bulking agent without endoscopic guidance at four sites in the proximal urethra. Long-term follow-up was available for 16 of the 20 patients included in the original study (four were deceased from causes unrelated to the procedure). Three (15%) failed to respond to treatment and four (25%) others experienced recurrence of incontinence. A sustained response was noted
a
b
Figure 67.1. Zuidex system. (a) The patient is prepared as for cystoscopy and appropriate analgesia is administered. The length of the urethra is measured before introducing the implacer (with the tube covering the needles) so that top of tube is located at the level of the midurethra. The tube should not move backward during insertion, so pressure must be applied on rear end of the tube during insertion. (b) The tube is pulled back to release the needles within the urethra. A firm grip on the handpiece is maintained as one syringe is retracted 5–10 mm and then pushed forward to its bottom position in order to penetrate the mucosa. The contents of syringe are injected and the emptied syringe is left in place. The maneuver is repeated clockwise with the three remaining syringes. The syringes with needles are removed one by one and finally the implacer is removed. (Courtesy of Q-Med, Uppsala, Sweden.)
Uryx versus Contigen at 12 months after injection Improvement (%) (to Stamey grade 0)
Improvement (%) (>50% I-QoL scores)
Dry pad weights (%)
Uryx (all patients)
34
32
68
Contigen (all patients)
33
20
44
Uryx (1–2 injections)
45
–
72
Contigen (1–2 injections)
27
–
36
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in nine patients (57%), five (32%) of whom remained dry.9
Although the tension-free vaginal tape (TVT) procedure is a relatively safe and straightforward procedure, it is not without risk; for example, during the blind passage of the needle in the retropubic space, perforation of the bladder, vessels, nerves, or intestine may occur. Patients who have been operated on previously may have adhesions that increase the risk of visceral perforation. In an effort to avoid these potential complications the tran-
sobturator systems have been developed. A prepubic TVT alternative has also been developed10 in which the conventional TVT needles are placed superficial to the pubic bone (Fig. 67.2). After placing the needles, the procedure for tensioning the tape is slightly different from that used in conventional TVT operations. The plastic sheath covering the polypropylene mesh is first removed only on one side. Scissors or forceps are then placed between the urethra and the tape. The tape is then adjusted by pulling on the side where the plastic sheath has not been removed. It takes greater force to adjust the tape than with a conventional TVT operation because the axis of the tape is
a
b
Prepubic tension-free vaginal tape procedure
c
Figure 67.2. Prepubic sling. The surgical procedure is carried out under local, spinal or general anesthesia. The technique uses the conventional tension-free vaginal tape (TVT) kit, except that the handle is not attached to the TVT needles (i.e. it is hand-held). (a) The vaginal incision is made 0.5–1 cm more proximal to the midurethra than with the conventional TVT procedure. The paraurethral space is developed as with the conventional TVT, but then the dissection is directed more laterally toward the mid-ischiopubic bone. (b) When the bone is reached, the TVT trocar is introduced into the dissected periurethral space a. With the trocar tip aiming laterally, the ischiocavernosus muscle is perforated together with the superficial perineal fascia. This is done with the trocar tip in close contact with the pubic bone (see insert b). (c) When the muscle has been perforated, the trocar tip is angled straight up and the needle is passed under the vulva to the ipsilateral skin incision c. The suprapubic incision is the same as with the conventional TVT. The other trocar is then passed on the contralateral side of the urethra d. The ends of the tape are cut just as with the conventional TVT procedure. (Reproduced from ref. 10 with permission.)
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more horizontal and anterior. The final tension under the midurethra should be the same as the conventional TVT operation. The remaining plastic sheath can now be removed and the tape ends cut in the subcutaneous layer. The vaginal and abdominal incisions are then closed. Since the bladder cannot be perforated, cystoscopy is not necessary with the prepubic TVT procedure. The mean operative time is 18 minutes.10 The postoperative instructions are the same as those given to patients after a conventional TVT procedure. Daher and colleagues recently published their experience with 74 consecutive patients who underwent prepubic TVT.10 The mean postoperative follow-up was 5 months. Sixty (81%) of the patients were cured of stress urinary incontinence and another 10 patients (13%) were improved. There were four (6%) failures. Subjects who failed the procedure were incontinent within 2 months of surgery and there were no late recurrences. Postoperative retention was defined as post-void residual greater than 100 ml and was observed in three subjects. No patient suffered from de novo detrusor overactivity or had significant intraoperative bleeding defined as greater than 200 ml. Eleven patients complained of discomfort when sitting immediately after the procedure, but this symptom abated in all eleven within 7 days postoperatively. Some ecchymoses were noted in nine subjects after the procedure. The vaginal epithelium was perforated twice when introducing the needle tip lateral to the pubic bone. Both times it was noticed intraoperatively and the trocars were reinserted without any postoperative healing problems.10
Externally readjustable sling Some researchers have attempted to develop a device that would allow for adjustment of the suburethral tension of a sling with the aim of reducing postoperative urinary retention without decreasing its ability to treat stress urinary incontinence effectively. A Spanish group reported on a device and method that permits readjustment of sling tension, both intraoperatively and during the postoperative period.11 The method uses a device called Remeex, taken from the Spanish initials for mechanical external regulation – REgulación MEcánica EXterna (Fig. 67.3). The suburethral support is placed through a vaginal incision and the traction threads are guided through into the retropubic space where they are first passed through the varitensor. The sutures are passed through a previously made 4 cm suprapubic incision and are finally wound up by turning the manipulator clockwise. Tension-free placement is assured by placing two finger-
tips between the rectus fascia and the varitensor. The external manipulator is left protruding from the suprapubic incision as it is closed. After the operation, the device is tensioned by rotating the external manipulator until urinary leakage with increased intra-abdominal pressure disappears in the patient with a full bladder. The patient is then asked to urinate. If she has more than 100 ml of residual volume, then the external manipulator is rotated counterclockwise while simultaneously applying pressure to the suburethral support with either a urethral dilator or cystoscopy sheath. Suburethral pressure readjustment is repeated until the patient is able to void easily without urinary leakage. When stress urinary incontinence has disappeared and the post-void residual is less than 100 ml, a ‘disconnector’ is placed inside the external manipulator. Rotating the disconnector counterclockwise separates the external manipulator from the varitensor, and both the disconnector and the external manipulator can be removed. If either stress urinary incontinence or urinary retention reappears, then the external manipulator can be reattached to the varitensor under local anesthetic and the tension readjusted. The 113 subjects were followed for an average of 22 months after the Remeex procedure. Of these, 108 (95.5%) were objectively cured of their stress urinary incontinence. Fourteen subjects (12.3%) had either persistent or de novo urge urinary incontinence. Postoperative readjustment was required in 22 (19.4%) of the women: 15 (13.2%) because of slight persistence of stress urinary incontinence and seven (6.2%) because of voiding difficulty.11 Complications consisted of 15 women (13.2%) with bladder perforations, seven (6.1%) had wound seromas, four (3.5%) had wound infections, and one (0.8%) had a vaginal erosion. Five (4.4%) varitensors were removed in this series: four from the women with wound infections and one from an extremely thin patient who complained of suprapubic discomfort. In all of these cases the traction threads were tied one to the other. One (0.8%) suburethral component was removed for a vaginal erosion. There were no device malfunctions.11 Mantovani et al. reported a cure rate of 97% (31 of 32 subjects). Three subjects (9%) needed readjustment and one device (3%) was removed for infection.12 Early experience with the Remeex device has demonstrated success rates comparable to other synthetic slings but with a lower rate of urinary retention. The disadvantages are the complications of the varitensor: specifically, wound infection, seroma, and discomfort in thin subjects. 975
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stress urinary incontinence. Other treatment modalities as unique as the TVT are radiofrequency therapy and a new medication. Further research and greater clinical experience will be needed before it is known whether either treatment should be as widely accepted as the TVT.
Radiofrequency therapy
Figure 67.3. Remeex system. The device is made up of two parts: a mechanical regulation unit and a urethral support sling. The mechanical regulation component is a subcutaneous permanent implant with a ‘varitensor’ that permits adjustment of sling support from outside the body by means of an ‘external manipulator’, a disposable part of the set that is removed once the desired continence level is achieved. The urethral support portion of the device is made of a short (3 × 1.5 cm) suburethral polypropylene monofilament sling attached to two non-resorbable polypropylene monofilament traction threads used to elevate or lower the sling support. (Courtesy of Neomedic International, Barcelona, Spain.)
NOVEL APPROACHES Improving existing treatments is important for medicine, but every once in a while there comes along a treatment that not only improves existing technology but also changes the face of a disease. The most recent of these advances to gain wide acceptance for the treatment of stress urinary incontinence is the TVT midurethral sling. This procedure was more than an evolution of the traditional sling. It not only introduced a tensionfree and minimally invasive approach but also changed the sling position from the bladder neck to the midurethra. These departures from the traditional sling clearly made the TVT procedure a novel approach to treating
Radiofrequency energy is a form of electromagnetic energy that is reliable and highly controllable. This thermal therapy can produce well-defined areas of tissue heating. The technology has been used extensively in dermatologic and orthopedic surgery for tissue shrinkage and ablation. Radiofrequency thermal therapy is now being applied to the endopelvic connective tissue at the bladder neck and urethra for treating urethral hypermobility in patients with stress urinary incontinence with the Food and Drug Administration (FDA) approved SURx system. The mechanism of action is believed to be shrinkage of the collagenated tissue that supports the bladder neck and proximal urethra. Fulmer and coworkers13 reported using the SURx system via laparoscopy. The radiofrequency electrothermal probe is placed through a laparoscopic working trocar and positioned on the periurethral portion of the endopelvic connective tissue. Precisely controlled radiofrequency energy is applied to the endopelvic connective tissue, from an external generator, on either side of the urethra to heat and shrink the tissue. The average operative time was less than 60 minutes and 98% of the women were discharged home from the recovery room. Treatment surface area decreased an average of 17% in length and 21% in width. Preoperatively 41.2% of subjects reported using one pad or less daily, while at 1, 3, 6 and 12 months postoperatively 85.6%, 90.4%, 87.2%, and 86.9%, respectively, required one pad or less daily. Urodynamic evaluation at 12 months showed no leakage during the Valsalva maneuver in 78% of cases. There were no major postoperative complications and the minor complication rate was 5.3%.13 Dmochowski et al14 reported on transvaginal radiofrequency treatment as a new outpatient modality for genuine stress incontinence with urethral hypermobility. The SURx transvaginal system (Fig. 67.4) was used to apply radiofrequency energy to the endopelvic connective tissue to induce its shrinkage, thereby stabilizing the proximal urethra and bladder neck. In 120 subjects with more than 1-year follow-up at 10 institutions, the average operative time was less than 30 minutes and all women were treated as outpatients.14 Preoperatively 101 subjects (84%) averaged one or more episodes of urinary incon-
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Figure 67.4. Transvaginal SURx system. This system is composed of a small bipolar radiofrequency generator and a sterile, single-use disposable bipolar applicator that allows application of radiofrequency energy to the tissue. The applicator has a handle, trigger and a 270-degree rotational tip with microbipolar electrodes and a saline drip at the distal end of the probe to cool the tissue. There is a thermistor located between the electrodes for accurate monitoring of the treatment tissue temperatures. An electrode data collection device is used to collect automatically real-time device performance on 26 different treatment parameters during each procedure. Application of radiofrequency energy is accomplished by drawing the radiofrequency applicator tip over the connective tissue in a slow sweeping manner along the longitudinal axis, ensuring that both tines of the applicator tip are equally in contact with the connective tissue until all of the endopelvic connective tissue is treated. (Reproduced from ref. 14 with permission from Lippincott, Williams & Wilkins.) tinence per day. At 3, 6, and 12 months postoperatively 57%, 66%, and 59% of patients, respectively, averaged one or no daily episodes of incontinence. At 12 months, 79 of 109 (73%) women reported being continent or improved. A total of 30 cases were classified as failures and 11 women were lost to follow-up.14 There were no intraoperative complications, three (4%) minor postoperative complications occurred which resolved, and no device-related complications were reported.14 Another more minimally invasive application of radiofrequency technology is in the Novasys micro-remodeling system which is a non-incisional, transurethral application of radiofrequency technology. The device is placed in the urethra similar to the placement of a Foley catheter and requires no visualization of the treatment site (Fig. 67.5). The Novasys system utilizes microscopic suburothelial radiofrequency energy to heat submucosal tissue to collagen remodeling temperatures (as opposed to higher ablation temperatures, which produce gross
tissue shrinkage and cell destruction). Remodeling temperatures cause microscopic regions of the patient’s own submucosal collagen to denature without significant associated necrosis or small vessel thrombosis. Upon cooling and healing, these minute regions of collagen renature in a significantly more compact, less compliant architectural pattern. Creation of a limited number of these microscopic collagen remodeling sites in a helical pattern around the proximal urethra and bladder neck results in reduced dynamic compliance so there is less bladder neck and proximal urethral mobility in the face of increased intra-abdominal pressure. Since the remodeling is so limited, there is no gross luminal narrowing or significant effect on static compliance. Proven safe and effective for the treatment of fecal incontinence,15 anal fistula,16 and gastroesophageal reflux disease,17 radiofrequency tissue remodeling within the lower urinary tract may improve stress urinary incontinence. A 12-month pilot study was performed to demonstrate the safety, effect on quality of life, effectiveness, and durability of a Novasys treatment.18 The study enrolled 52 women with mild, moderate, or severe stress urinary incontinence and urethral hypermobility. There were no serious adverse events, no woman required catheterization at discharge, and recovery was rapid. At 6 and 12 months postoperatively, I-QoL scores had improved 78–82% and 70–82%, respectively, compared to baseline values. The proportion of ‘dry’ women at 12 months ranged from 22 to 67% in the different treatment groups.18 The results suggest that radiofrequency tissue remodeling may safely improve the quality of life for women with mild, moderate, and severe stress urinary incontinence, and may offer physicians and stress urinary incontinence patients a safe, rapid, and effective therapeutic option. Because this simple procedure does not require cystoscopic assistance, it may allow a larger number of physicians to provide treatment for this common disorder.
Medication for stress urinary incontinence New agents for the treatment of stress urinary incontinence are being sought worldwide. Most of the attention has focused on α-agonists with a high specificity for the urethral smooth muscle and selective serotonin–norepinephrine reuptake inhibitors. The serotonin–norepinephrine reuptake inhibitor class of antidepressants, and specifically duloxetine, have been shown to be beneficial in mild to moderate stress urinary incontinence when compared to placebo (Table 67.3). Cardozo and colleagues19 published a study showing duloxetine was superior to placebo for the treatment of 977
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a
b
Figure 67.5. Novasys Micro-Remodeling System. This catheter-based system uses radiofrequency energy to increase bladder outlet resistance without the need for surgery. (Courtesy of Novasys Medical, Inc., Newark, CA.)
severe stress incontinence in women with pure urodynamic stress incontinence between the ages of 35 and 75 who were scheduled to have surgery.19 At the conclusion of the 8-week study, ten women (22%) in the duloxetine group no longer wanted surgery, compared with none in the placebo group. Perhaps the most interesting finding
was that duloxetine was equally effective in women both with and without a low-pressure urethra.19 The effectiveness of duloxetine in the treatment of stress urinary incontinence in women both with and without a low-pressure urethra is linked to its mechanism of action. It inhibits the presynaptic reuptake of
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Table 67.3.
Median incontinence episode frequency decrease in duloxetine versus placebo Duloxetine
Placebo
Study
n
IEF (%)
n
IEF (%)
p-value
Millard et al.24
227
54
231
40
0.05
247
50
247
29
0.002
46
60
52
27
0.001
Dmochowski et al.
344
50
339
27.5
0.001
Norton et al.21
137
59
138
41
0.002
23
van Kerrebroeck et al. 19
Cardozo et al.
22
IEF, median incontinence episode frequency decrease.
CONCLUSION
O S NH • HCI CH3 Figure 67.6.
Molecular structure of duloxetine.
As the science of medicine continues to advance, so do the treatments for stress urinary incontinence. Some of these advancements will be major leaps like the TVT. Most, however, will be improvements like the transobturator tapes and Durasphere. It is important to study all of the new technologies presented in this chapter regardless of the long-term success of any because it is as important to be familiar with the failures as it is to know about the successes. Armed with this knowledge researchers will be less likely to revisit past mistakes and more likely to innovate successfully.
REFERENCES 1. Pettis GY, Kaban LB, Glowacki J. Tissue response to composite ceramic hydroxyapatite/demineralized bone implants. J Oral Maxillofac Surg 1990;48:1068–74.
serotonin and norepinephrine in the motor neurons of the pudendal nerve, thereby increasing the amount of these neurotransmitters in the synapse. Since these synapses are in the sacral spinal cord (Onuf’s nucleus), the effect is on the central nervous system. Animal studies have shown that increasing the serotonin and norepinephrine in the synapse led to increased pudendal stimulation of the urethral striated sphincter muscle.20 These studies measured an eight-fold increase in electromyographic activity during bladder storage. Human female subjects with stress urinary incontinence probably benefit from a similar mechanism. In addition to stimulating the striated urethral sphincter, animal studies have shown that duloxetine most likely decreases bladder overactivity.20 The most commonly reported adverse events with duloxetine use were nausea, fatigue, dry mouth, insomnia, constipation, dizziness, and somnolence. After 4 weeks of treatment the incidence of side effects was similar to that of placebo.21–24
2. Sand PK, Appell RA, Goldberg RP et al. Prospective randomized trial of calcium hydroxylapatite vs. bovine collagen for treatment of type III incontinence [abstract]. American Urogynecologic Society/Society of Gynecologic Surgeons Joint Scientific Meeting, San Diego, California, July 29–31, 2004. 3. Mayer R, Lightfoot M, Jung I. Preliminary evaluation of calcium hydroxylapatite as a transurethral bulking agent for stress urinary incontinence. Urology 2001;57:434–8. 4. Diamond DA, Caldamone AA. Endoscopic correction of vesicoureteral reflux in children using autologous ear chondrocytes: preliminary results. J Urol 1999;162: 1185–8. 5. Bent AE, Tutrone RT, McLennan MT et al. Treatment of intrinsic sphincter deficiency using autologous ear chondrocytes as a bulking agent. Neurourol Urodyn 2001;20:157–65. 6. Frauscher F, Klauser A, Zur Nedden D et al. Ultrasoundguided transurethral injection of adult stem cells for treatment of urinary incontinence: first clinical results [abstract]. 90th Scientific Assembly and Annual Meeting
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of The Radiological Society of North America, Chicago, Illinois, November 28–December 3, 2004. 7. Dmochowski RR, Herschorn S, Corcos J et al. Multicenter randomized controlled study to evaluate Uryx urethral bulking agent in treating female stress urinary incontinence [abstract]. 98th Annual Meeting of the American Urological Association, Chicago, Illinois, April 26–May 1, 2003. 8. Stenberg A, Larsson G, Johnson P et al. DiHA dextran copolymer, a new biocompatible material for endoscopic treatment of stress incontinent women: short term results. Acta Obstet Gynecol Scand 1999;78:436–42. 9. Stenberg A, Larsson G, Johnson P. Urethral injection for stress urinary incontinence: long-term results with dextranomer/hyaluronic acid copolymer. Int Urogynecol J Pelvic Floor Dysfunct 2003;14:335–8. 10. Daher N, Boulanger JC, Ulmsten U et al. Pre-pubic TVT: an alternative to classic TVT in selected patients with urinary incontinence. Eur J Obstet Gynecol Reprod Biol 2003;107:205–7. 11. Sousa-Escandon A, Lema-Grille J, Rodriguez-Gomez JI et al. Externally readjustable device to regulate sling tension in stress urinary incontinence: preliminary results. J Endourol 2003;17:515–21. 12. Mantovani F, Castelnuovo C, Bernardini P et al. ReMeEx device (External Mechanical Regulator) for incontinence implantation and regulation procedure, complications and results: 3 years follow up. Arch Ital Urol Androl 2004;76:49–50.
15. Takahashi T, Garcia-Osogobio S, Valdovinos MA et al. Extended two-year results of radio-frequency energy delivery for the treatment of fecal incontinence (the Secca procedure). Dis Colon Rectum 2003;46:711–5. 16. Filingeri V, Gravante G, Baldessari E et al. Radiofrequency fistulectomy vs. diathermic fistulotomy for submucosal fistulas: a randomized trial. Eur Rev Med Pharmacol Sci 2004;8:111–6. 17. Bergman JJ. Gastroesophageal reflux disease and Barrett’s esophagus. Endoscopy 2005;37:8–18. 18. Sotomayor M, Feria-Bernal G. Non-surgical, palpationbased outpatient treatment for stress urinary incontinence [abstract]. 33rd Annual Meeting of the International Continence Society, Florence, Italy, October 5–9, 2003. 19. Cardozo L, Drutz HP, Baygani SK et al. Pharmacological treatment of women awaiting surgery for stress urinary incontinence. Obstet Gynecol 2004;104:511–9. 20. Thor KB, Katofiasc MA. Effects of duloxetine, a combined serotonin and norepinephrine reuptake inhibitor, on central neural control of lower urinary tract function in the chloralose-anesthetized female cat. J Pharmacol Exp Ther 1995;274:1014–24. 21. Norton PA, Zinner NR, Yalcin I et al. Duloxetine versus placebo in the treatment of stress urinary incontinence. Am J Obstet Gynecol 2002;187:40–8. 22. Dmochowski RR, Miklos JR, Norton PA et al. Duloxetine versus placebo in the treatment of North American women with stress urinary incontinence. J Urol 2003;170:1259– 63.
13. Fulmer BR, Sakamoto K, Turk TM et al. Acute and longterm outcomes of radio frequency bladder neck suspension. J Urol 2002;167:141–5.
23. van Kerrebroeck PE, Abrams P, Lange R et al. Duloxetine versus placebo in the treatment of European and Canadian women with stress urinary incontinence. BJOG 2004;111:249–57.
14. Dmochowski RR, Avon M, Ross J et al. Transvaginal radio frequency treatment of the endopelvic fascia: a prospective evaluation for the treatment of genuine stress urinary incontinence. J Urol 2003;169:1028–32.
24. Millard RJ, Moore K, Reneken R et al. Duloxetine versus placebo in the treatment of stress urinary incontinence: a four-continent randomized clinical trial. BJU Int 2004;93:311–8.
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68 Diagnosis and treatment of obstruction following incontinence surgery – urethrolysis and other techniques Chad Huckabay, Victor W Nitti
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INTRODUCTION The increasing use of incontinence procedures to treat stress urinary incontinence (SUI) will lead to a rise in the number of patients having postoperative voiding problems. The physician treating incontinence and performing interventions will need to recognize voiding dysfunction and difficulties promptly. Furthermore, an expedient diagnosis must be made in some circumstances, especially now that synthetic slings such as the tension-free vaginal tape (TVT) are commonplace. The management alternatives for problems after TVT are unique from historical management options for pubovaginal slings, and retropubic and transvaginal suspension procedures. The most important factor in reducing obstruction has probably been the appreciation that operations for SUI work by restoring support, not by changing the position of the urethra. Obstruction will unavoidably occur in 1–2% of patients even with the most practiced surgeons. In this chapter we will explore the frequency of voiding dysfunction after incontinence surgery. The methods of diagnosis are delineated, but patient history remains the key. We will discuss diverse surgical techniques including urethrolysis by a variety of approaches, sling incision, and new less invasive methodologies applicable to midurethral synthetic slings.
INCIDENCE OF OBSTRUCTION AND VOIDING DYSFUNCTION AFTER STRESS INCONTINENCE SURGERY The true incidence of voiding dysfunction and iatrogenic obstruction after incontinence surgery is unknown and likely underestimated. Estimates of 2.5– 24% have been reported for various procedures.1–5 In a 1997 review, the incidence of postoperative urgency for patients with no urgency and no detrusor overactivity before incontinence surgery was 8–16% (median CI: 11%) for retropubic suspensions, 3–10% (median CI: 5%) for transvaginal suspensions, and 3–11% (median CI: 7%) for sling procedures. For the same procedures, urinary retention longer than 4 weeks occurred in 3–7% (median CI: 5%), 4–8% (median CI: 5%), and 6–11% (median CI: 8%), respectively. The incidence of permanent retention for all three procedures was thought to be less than 5%.6 Chaikin et al. found postoperative de novo urge incontinence in 3%, persistent urge incontinence in 23%, and unexpected permanent urinary retention in 2% of patients undergoing pubovaginal sling.7 For the same procedure, Morgan and colleagues reported de novo urgency in 23% and de novo urge incontinence in 7%; five women had reten-
tion after 3 months requiring urethrolysis. Interestingly, they reported a 74% resolution of urge incontinence (although concomitant anterior colporrhaphy may have contributed, p=0.07) and return to normal voiding in 92% at 1 month postoperatively.8 Reported rates of urinary retention after TVT have ranged from 1.4 to 9%.9–15 Others have described rates of voiding dysfunction after TVT as being 2–4%.16 Dunn et al. recently performed an extensive literature review to determine the incidence of ‘voiding dysfunction’ after incontinence procedures.17 They searched the Medline database from 1966 to 2001 for various procedures. All available data were retrospective collections, case reports or case cohort series. Rates of voiding dysfunction varied from 4 to 22% following Burch colposuspension, 5 to 20% following Marshall–Marchetti–Krantz (MMK) urethropexy, 4 to 10% following pubovaginal sling, 5 to 7% after needle suspension, and 2 to 4% following TVT. While it cannot be said that all patients with voiding dysfunction in these series were obstructed, it can be inferred that a number were. Postoperative urgency occurs more frequently in patients with pre-existing urgency symptoms. The large review sponsored by the American Urological Association in 1997 suggested postoperative urgency occurred in 36–66% of these patients after retropubic suspensions, 54% after transvaginal procedures, and 34–46% after slings.6
ETIOLOGY In general, voiding dysfunction after incontinence surgery is related to obstruction, detrusor overactivity, or impaired detrusor contractility. The risk of iatrogenic obstruction is usually related to technical factors. In a retropubic urethropexy, sutures placed too medial, close to the urethra, can cause urethral deviation or periurethral scarring. Sutures placed too distally can cause kinking with obstruction and an inadequately supported bladder neck/proximal urethra with potentially continued stress incontinence. If retropubic sutures are tied too tight, elevating the bladder neck toward the pubic bone excessively, this may result in overcorrection of the urethrovesical angle or ‘hypersuspension’. With suburethral sling procedures, excessive tension on the sling around or under the urethra is usually responsible for obstruction. Less commonly, displacement of the sling from its intended position may result in obstruction. The same holds true for bladder neck and midurethral slings. We have noticed that excessive tension on a midurethral synthetic sling can result in the rolling of the sling into a tight band.
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Kinking or angulation of the urethra, as well as external compression, may occur secondary to vaginal prolapse. This can result from prolapse that was not corrected (undiagnosed or ignored) at the time of incontinence surgery or from prolapse that occurred after (or as a result of) incontinence surgery. It is essential to examine and rule out apical, anterior or posterior prolapse as an etiology of urethral obstruction. Occasionally, postoperative voiding dysfunction is caused by a learned voiding dysfunction (also termed dysfunctional voiding) or failure of relaxation of the striated urethral sphincter.18 In these cases, patient education and sometimes biofeedback can be helpful. When the problem persists, botulinum A toxin injection into the urethral sphincter has been reported to be successful.19 Finally, impaired detrusor contractility may be responsible for a ‘relative obstruction’ after incontinence surgery. Sometimes this can be diagnosed preoperatively and the patient may be warned of the possibility of voiding dysfunction after surgery.
PRESENTATION The most obvious symptom/sign of obstruction is complete/partial urinary retention, and the inability to void continuously or the presence of a slow stream with or without intermittency. However, many women will present with predominate storage symptoms of frequency, urgency and urge incontinence, with or without voiding symptoms. The prevalence of various symptoms varies greatly according to different authors. While some authors report on cohorts with predominately obstructive symptoms or retention, others have shown the true variable nature by which obstruction presents. Carr and Webster reviewed the presenting symptoms in 51 women subsequently undergoing urethrolysis and found storage (irritative) symptoms (75%), voiding (obstructive) symptoms (61%), de novo urge incontinence (55%), need for intermittent catheterization (40%), persistent retention (24%), recurrent urinary tract infections (8%), and painful voiding (8%).20 Suffice to say that in any case of de novo voiding and/ or storage symptoms, the diagnosis of obstruction should at least be entertained.
IDENTIFYING RISKS FOR POSTOPERATIVE VOIDING DYSFUNCTION Ideally, the surgeon would like to know who is at risk for postoperative voiding dysfunction. As with other aspects of voiding dysfunction following incontinence surgery, this problem has no definitive answer. Urodynamic stud-
ies have been investigated to determine any factors that may be predictive. Miller et al. noted that women undergoing allograft pubovaginal sling who voided with no or minimal detrusor pressure had a significantly increased risk of postoperative retention. Of 21 women with no or minimal detrusor contraction, four developed retention whereas no patient with a detrusor contraction developed retention postoperatively. The presence of Valsalva voiding in this study did not affect the incidence of postoperative retention.21 Similarly, Weinberger and Ostergard in a study of 108 women undergoing synthetic suburethral slings found that the absence of detrusor contractions predicted delayed return to normal voiding. Valsalva voiding had no association with voiding dysfunction.22 Bhatia and Bergman, reporting on a series of Burch cystourethropexies, cited patients who void with Valsalva maneuver (intra-abdominal pressures greater than 10 cmH2O during voiding and detrusor pressures less than 15 cmH2O) being at 12 times greater risk of needing prolonged catheterization.23 Others have found that patients with preoperative Valsalva voiding or detrusor hypocontractility are more likely to report de novo urgency.24 Wang and Chen noted that patients with preoperative dysfunctional voiding – defined as maximum free flow (NIQmax) less than 12 ml/s and detrusor pressure at maximum flow (pdetQmax) of ≥20 cmH2O – were more likely to have a lower objective cure rate and lower quality of life scores after TVT than those with normal pressure–flow voiding dynamics.25 The association of low voiding detrusor pressures and Valsalva voiding with subsequent voiding dysfunction has not been found in several other studies.26,27 Pressure–flow studies are helpful in understanding the voiding dynamics of incontinent women; however, findings of low detrusor pressures or Valsalva voiding should not per se exclude patients from an anti-incontinence procedure.
DIAGNOSTIC EVALUATION Transient voiding dysfunction and urinary retention are frequent and expected after many types of anti-incontinence surgery. This is the rationale behind concomitant placement of suprapubic tubes or teaching clean intermittent catheterization preoperatively. TVT and transobturator slings are an exception to this as retention and obstruction should not persist beyond a few days. After traditional pubovaginal sling (and variants) or colposuspension, most women will begin voiding sufficiently on their own within a few days to weeks while others may take longer to resume normal voiding. Storage symptoms such as urgency, frequency, and urge incontinence are often more refractory than retention because they 983
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can be related to bladder changes. Such symptoms can sometimes take months to resolve. It has been common practice to delay evaluation of the patient with urinary retention or severe storage symptoms after pubovaginal sling, colposuspension or needle suspension for approximately 3 months postoperatively. Although this time frame is arbitrary, most data found in the literature are based on a waiting period of at least 3 months to allow adequate time for obstruction/ retention to resolve and to minimize the risk of recurrent stress incontinence. After 3 months, there is a very low probability that any persistent retention will resolve without intervention. More recently, some surgeons (including ourselves) have advocated earlier intervention in cases of complete retention; however, little data on outcomes and recurrence of stress incontinence are available. Few studies have focused on outcomes with respect to waiting a longer period before intervention. While it seems intuitive that longstanding symptoms (especially detrusor overactivity) will be less likely to respond to relief of obstruction the longer the patient is obstructed, this has not been proven conclusively. Leng et al. recently conducted a retrospective review of 15 women who underwent urethrolysis and found that patients with persistent symptoms postoperatively (n=8) had a significantly longer time from surgery to intervention than those who had no symptoms (n=7).28 Mean time to urethrolysis was 31.25 ± 21.94 months versus 9 ± 10.1 months respectively. The large overlap, small sample size, and the fact that more patients in the successful group had urinary retention (5/7 versus 3/8) make it difficult to come to definitive conclusions. We have not excluded obstructed patients from intervention based on duration of obstruction. The waiting period advocated for obstruction and retention for more traditional anti-incontinence procedures has been largely abandoned for TVT and TVTlike procedures. In theses cases quicker intervention is suggested when obstruction is suspected.9,11,29,30 Due to the immobility of the polypropylene mesh and the tremendous ingrowth of fibroblastic tissue at 1–2 weeks, patients with severe symptoms or urinary retention are less likely to improve after this time period.
History and physical examination The diagnostic evaluation of the patient with voiding dysfunction after incontinence surgery begins with a focused history and physical examination. Key points in the history are the patient’s preoperative voiding status and symptoms, and the temporal relationship of the lower urinary tract symptoms to the surgery. The type of
procedure performed and the number and type of other procedures done are also important. Urodynamic data such as uroflow and pressure–flow studies from before incontinence surgery are useful if available. If patients are straining to void (perhaps by habit), they should be instructed to stop this behavior, as incontinence procedures are designed to prevent the flow of urine with abdominal straining. Finally, it is important to determine if the symptom of stress incontinence persists. The most obvious presenting symptom of obstruction after incontinence surgery is inability to void or intermittent retention. Patients may also experience voiding (obstructive) symptoms including slow or interrupted stream and straining to void. Storage (irritative) symptoms of urinary frequency, urgency, and urge incontinence which persist after surgery may also be a sign of obstruction, even if emptying is complete. Physical examination may show overcorrection or hypersuspension where the urethra and urethral meatus appear to be pulled up toward the pubic bone and ‘fixed’. The angle of the urethra becomes more vertical than is normal. When severe, this is usually quite obvious, but can be confirmed by a Q-tip test. However, not all obstructed patients will appear to be overcorrected. It is important to assess for cystocele and other forms of prolapse which may cause obstruction (due to a kinking of the urethra). The patient should also be examined for persistent urethral hypermobility and stress incontinence.
Urodynamics Recent interest in female bladder outlet obstruction (BOO) has resulted in the publication of several unique proposals of urodynamic criteria for the diagnosis of female BOO. Chassagne et al. used the cut-off values of detrusor pressure at maximum flow rate (pdetQmax) of ≥20 cmH2O and maximum flow rate (Qmax) of <15 ml/s to define obstruction.31 In 2000, Lemack and Zimmern revised these values to a cut-off of Qmax of ≤11 ml/s and pdetQmax of ≥21 cmH2O.32 As a third update from this same group, new criteria were published in 2004, for the first time using a small group of asymptomatic controls, thus elevating the pdetQmax cut-off to 25 cmH2O.33 Nitti et al. used videourodynamic criteria, with less emphasis on pressure–flow dynamics, to diagnose BOO.34 In this study, obstruction was defined as radiographic evidence of an obstruction between the bladder neck and distal urethra in the presence of a sustained detrusor contraction of any magnitude during voiding. Blaivas and Groutz, realizing the possibility of test-induced catheter obstruction, designed a nomogram based on
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the maximum non-invasive flow rate (free Qmax) and the maximum detrusor pressure during voiding (pdetmax).35 Although each urodynamic definition for obstruction has merit, further investigation should provide a better understanding of when to use which criteria. The diagnosis of obstruction in women after incontinence surgery can be particularly difficult to make urodynamically. In cases of urinary retention and incomplete emptying, urodynamic studies may not be necessary before intervention, particularly if preoperative contractility and emptying are known to be normal. However, in cases of de novo or worsened storage symptoms, including urge incontinence without a significantly elevated post-void residual, a formal urodynamic evaluation is preferred. Classic high pressure, low flow voiding dynamics (or obstruction by any of the above criteria) will confirm the diagnosis of obstruction, but its absence does not always rule out obstruction. Many women with suspected obstruction after incontinence surgery do not generate a significant contraction on urodynamic studies but are obstructed nevertheless. Outcomes of surgical intervention in such cases are identical to those in women with classic high pressure, low flow dynamics. There appear to be no consistent preoperative parameters, urodynamic or otherwise, which predict success or failure of urethrolysis. For example, Foster and McGuire found that patients with detrusor overactivity had a higher rate of failure, but a later study, as well as others, found this not to be the case.36 Nitti and Raz found that, as the post-void residual increased, so did the rate of failure, but others have not confirmed this correlation.37 Carr and Webster found that the only parameter predictive of success was no prior urethrolysis.20 It is well established that urodynamics may fail to diagnose obstruction in a significant number of women obstructed as a result of anti-incontinence procedures. Additionally, patients with non-diagnostic urodynamic studies or who failed to produce a detrusor contraction have the same outcomes as those with urodynamic findings classic for obstruction, namely high pressure, low flow voiding. In the study by Nitti and Raz, four women who failed to generate a contraction during urodynamic testing had a successful urethrolysis.37 They also reported that the urodynamic findings in patients considered to be failures after transvaginal urethrolysis failed to elucidate the reason for their continued voiding dysfunction. Due to the limitations of urodynamics in these patients, the temporal relationship of the surgery to the onset of voiding and storage symptoms is relied upon as an indicator of obstruction. Likewise, if the patient fails to resume preoperative voiding or improve significantly, then continued obstruction is suspected.
Classic high pressure, low flow voiding dynamics do confirm the diagnosis of obstruction, but are a far from consistent finding. Urodynamics can also yield important information regarding instability, impaired compliance, bladder capacity, and voiding characteristics. Based on our experience, videourodynamics offers an advantage over simple urodynamics in this patient population, because of the ability to simultaneously image the bladder outlet. The utility of urodynamics may be considered as follows:
• For the patient in retention, urodynamics can
•
provide valuable information (e.g. detrusor overactivity or significantly impaired compliance, the latter being an absolute indication for intervention) and can confirm a diagnosis of obstruction, but should not exclude the patient from urethrolysis, even if there is no contraction or impaired contractility. Urodynamics may also identify learned voiding dysfunction. For the patient with storage symptoms with normal emptying, urodynamics can diagnose obstruction and – equally as important – rule out obstruction. It can help to provide a specific diagnosis that is useful in directing therapy, especially if obstruction can be excluded.
Endoscopy and imaging Endoscopic evaluation of the urethra may show scarring, narrowing, occlusion, kinking, or deviation of the urethra. These finding are especially helpful in cases where urodynamics are equivocal. The urethra and bladder should be carefully inspected for eroded sutures or sling material and the presence of a fistula. This is facilitated by the use of a rigid scope with a zero to 30-degree lens and little or no beak to allow for complete distension of the urethra. In cases where intervention is anticipated, endoscopy should be done routinely, either before surgery or at the time of surgery prior to incision. Radiographic imaging may be done independent of videourodynamics. A standing cystogram in the anteroposterior, oblique and lateral positions, with and without straining, assesses the degree of bladder and urethral prolapse and displacement or distortion of the bladder. A voiding cystourethrogram can assess the bladder, bladder neck, and urethra during voiding to determine narrowing, kinking or deviation (Fig. 68.1). While not mandatory, imaging can be extremely useful in equivocal cases. 985
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Figure 68.1. Obstruction at the midurethra by midurethral sling with proximal urethral and bladder neck dilation.
Summary In summary, the diagnosis of obstruction is made on the basis of clinical presentation (type and onset of symptoms), physical examination, and testing such as urodynamics, imaging or endoscopy, depending on the circumstances. A temporal relationship between surgery and the onset of symptoms is the most critical factor in diagnosis. Patients with normal emptying before incontinence surgery (especially if preoperative urodynamics showed normal voiding) who have significant retention or obstructive voiding symptoms after incontinence surgery, need little in the way of a diagnostic workup.
MANAGEMENT OF IATROGENIC OBSTRUCTION Conservative treatment Treatment of obstruction and its timing are usually dictated by the degree of bother of symptoms. In some cases an obstructed patient will opt for conservative management including clean intermittent catheterization (CIC) if necessary. In the woman who is not very bothered by catheterization and prefers this option to repeat surgery and a risk of recurrent stress urinary incontinence, CIC is a reasonable treatment plan. Although most women
ultimately choose definitive treatment, chronic CIC is an option in select cases. Patients who are emptying well but have significant storage symptoms secondary to iatrogenic obstruction may be treated initially with pharmacotherapy (anticholinergics) or pelvic floor physiotherapy. In our experience these measures are not usually successful when obstruction exists, but can be considered before surgery. The role for urethral dilation in cases of iatrogenic obstruction secondary to pubovaginal sling and colposuspension is not clear. While many practitioners report anecdotal success, no peer reviewed literature exists. It is our opinion that urethral dilation is of limited utility in these cases. Karram et al. reported an 82% cure or improved rate with urethral dilation using a Walther sound when performed within 2–6 weeks of TVT insertion for varying levels of voiding dysfunction in 28 women.29 There are concerns about the potentially traumatic nature of dilation which could induce scarring of the urethra. The cutting of suspension or sling sutures above the rectus has been described anecdotally with variable success. When conservative measures in a symptomatic patient fail, definitive surgical therapy by either formal urethrolysis (transvaginal or retropubic) or sling incision may be required. In addition, there is a limited but growing experience with manipulation of midurethral synthetic slings in the early postoperative period.
Surgical intervention When voiding dysfunction secondary to obstruction exists beyond a proper waiting period (see ‘Diagnostic evaluation’, above), surgical intervention is indicated. Success rates for various procedures range from 67 to 100% (Table 68.1) and appear to be independent of the particular procedure chosen, i.e. in general, one procedure is not superior to another, except perhaps under certain circumstances. To date, no consistent predictors for success have been identified. Individual series have cited certain factors which were associated with success or failure, but different series have not identified the same factors. For example, Carr and Webster found that the only predictors of success were no prior urethrolysis and omental interposition.20 Nitti and Raz found that as the post-void residual increased, so did the risk of failure.37 Foster and McGuire noted that patients with detrusor overactivity had a higher rate of failure.36 Others have not confirmed these findings.38 Certainly, high pressure, low flow voiding on urodynamics confirms obstruction; however, urodynamics often may be equivocal or non-specific.
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Table 68.1. Summary of series on urethrolysis and sling incision/loosening for the treatment of obstruction after incontinence surgery n
Type of urethrolysis
Success*
Recurrent SUI†
13
Transvaginal
92%
N/A
Foster & McGuire
48
Transvaginal
53%
0
Nitti & Raz37
42
Transvaginal
71%
0
39
Transvaginal
72%
3%
49
Zimmern et al.
36
38
Cross et al.
40
Goldman et al.
32
Transvaginal
84%
19%
47
23
Transvaginal with Martius flap
87%
16%
Petrou et al.48
32
Suprameatal
67%
3%
15
Retropubic
93%
13%
12
Retropubic
83%
25%
54
Mixed
78%
14%
Amundsen et al.
32
Transvaginal and sling incision
94% retention 67% urge symptoms
9%
Nitti et al.44
19
Sling incision
84%
17%
14
Sling incision
93%
21%
Klutke et al.
17
TVT incision and/or loosening
100%
6%
Rardin et al.11
23
TVT incision
100% retention 30% urge symptoms cured 70% urge symptoms improved
39% (two-thirds less SUI than pre-TVT)
Carey et al.
Webster & Kreder Petrou & Young Carr & Webster
39
50
20 43
45
Goldman
9
* Success is usually defined as cure or significant improvement in presenting symptoms (resumption of normal bladder emptying for patients in retention, and resolution of symptoms for patients with obstructive symptoms or frequency, urgency or urge incontinence). In some series success for specific symptoms is noted. † Recurrent stress urinary incontinence (SUI) is defined as percentage of patients without SUI before urethrolysis who experienced SUI after urethrolysis.
Several studies failed to show any correlation between urodynamic findings and the likelihood of successful voiding after urethrolysis.36,37,39 Furthermore, outcomes of urethrolysis in women without a demonstrable detrusor contraction on urodynamics (who voided normally prior to incontinence surgery) are equivalent to those women with classic findings of obstruction. With all surgical interventions for obstruction there is an inherent risk of recurrent stress incontinence. In general, this risk is approximately 15%, but reported rates vary from zero to 39% (see Table 68.1). While some have recommended concomitant anti-incontinence procedures at the same time as the procedure to relieve obstruction (e.g. urethrolysis and transvaginal needle suspension or sling), no significant benefit has been shown by others, and we do not routinely perform a repeat anti-incontinence procedure.36,37,40 In the majority of cases, patients are so disturbed by the symptoms caused by obstruction, that relieving them must be the primary goal. If stress incontinence does recur, it can be treated separately with a urethral bulking agent or even a repeat surgical procedure in the future.
Surgical techniques are usually tailored toward individual scenarios and previous surgeries. For example, in certain cases where the incontinence procedure causing obstruction was a retropubic suspension, a retropubic urethrolysis approach may be used to cut sutures and free retropubic adhesions. For transvaginal sling procedures, transvaginal sling lysis alone or formal urethrolysis can usually be performed successfully with less patient morbidity and quicker convalescence. Some have advocated a transvaginal suprameatal approach; however, we rarely perform this operation. With the much more common use of the TVT or synthetic midurethral slings, sling loosening techniques, urethral dilation, and sling incision alone are commonly performed in the clinic setting with local anesthesia within a shorter postoperative period before significant scarring occurs. In this section we will describe surgical techniques for the treatment of iatrogenic obstruction in order of invasiveness. This is not to imply that one technique should be chosen first over another; that decision depends upon multiple factors including the incontinence procedure 987
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performed, associated complications, surgeon comfort, and other factors.
Midurethral sling loosening or incision In women with postoperative urinary retention after midurethral synthetic sling procedures, some surgeons, including ourselves, advocate early intervention within 7–14 days. With midurethral synthetic slings, unlike traditional pubovaginal slings, the vast majority of patients are able to empty fairly normally within 72 hours. Early intervention allows one to perform a minimally invasive procedure, under local anesthesia in an office setting if preferred. The anterior vaginal wall is infiltrated with local anesthetic and the suture used to close the vaginal wall is opened. The synthetic sling is usually easily visualized. The sling is hooked with a right-angle clamp (or alternatively a Metzenbaum scissors or Hegar dilator). Spreading of the right-angle clamp or downward traction on the tape will usually loosen it (1–2 cm).9 This is usually possible if intervention is done by 10 days. Thereafter, tissue ingrowth may prevent loosening of the sling, in which case we recommend cutting it in the midline. The incision is suture closed, and the patient is allowed to attempt to void. Loosening or cutting of TVT has excellent results.9,11,29,30 In the two largest series of 17 and 23 patients, restoration of normal voiding and emptying occurred in all patients,9,11 storage symptoms were partially relieved in 70%, and completely relieved in 30%.11 Klutke et al. reported resolution of obstruction in all 17 patients while recurrent stress incontinence occurred in one patient.9 Rardin et al. found that impaired bladder emptying resolved in 100% of 23 patients, with 61% remaining continent, 26% with partial recurrence, and 13% with complete recurrence of stress incontinence.11 In cases of voiding difficulty or dysfunction beyond 4–6 weeks, the lysis of the TVT sling is better performed in the operating theatre. Scarring and patient discomfort are factors to consider as more extensive dissection may be needed to identify and cut the sling. The technique described below for sling incision is applicable to midurethral synthetic slings.
Transvaginal sling incision The transvaginal incision of the pubovaginal sling (autologous, allograft, xenograft or synthetic) rather than formal urethrolysis may limit morbidity, potential soft tissue and nerve injury, and fibrosis from surgical dissection. Notably, sling incision alone may effectively eliminate obstruction with results similar to formal urethrolysis. In 1995, Ghoniem and Elgamasy described a technique of incising the sling in the midline and using
a free vaginal epithelial interposition graft sutured to each cut end of the pubovaginal sling, keeping it intact to theoretically reduce the risk of postoperative stress incontinence. 41 Over time, the technique has evolved and interposition is no longer routinely used.42–45 Our technique starts with cystoscopy to assess the urethra and rule out erosion or urethral injury, followed by an inverted U or midline incision to expose the area of the bladder neck and proximal urethra.44 As the vaginal flap is dissected off, the sling should be identified above the periurethral fascia. The sling may be encased in scar tissue and thus require careful dissection of the scar to identify the sling. If the sling has significant tension on it, it may be especially difficult to identify. Insertion of a cystoscope or sound into the urethra with upward retraction, may help to expose the bladder neck and isolate the sling. Once the sling is isolated it should be separated from the underlying periurethral fascia with sharp or blunt dissection. The dissection may be facilitated by grasping the sling with an Allis clamp on either side of the midline and exerting downward pressure. Care should be taken to avoid injury to the bladder and urethra by beginning the dissection distally, identifying normal urethra then proceeding more proximally until the plane between the sling and urethra is identified. A right-angle clamp can be placed between the urethra and periurethral fascia and the sling, lifting the sling. The sling is then cut in the midline (Fig. 68.2a). Alternatively, if scarring is dense and the plane between the sling and periurethral fascia cannot be developed easily, the sling can be isolated lateral to the midline, off of the urethra. The edges of the sling are mobilized off the periurethral fascia to, but not through, the endopelvic fascia (Fig. 68.2b). In cases of extreme tension, the ends of the sling may retract back into the retropubic space after incision, but more often the sling stays secure to allow this mobilization. Lateral support is preserved because the retropubic space is not entered, and the urethra is not freed from the undersurface of the pubic bone. The ends of the sling can be left in situ or excised. We typically excise synthetic material and leave autografts and allografts in place. If there is any concern about urethral injury, cystourethroscopy should be carried out. In cases of autologous or biologic materials, if the sling cannot be clearly identified, then formal transvaginal urethrolysis (see below) should be performed. TVT and other midurethral synthetic slings can be isolated and incised in a similar manner. Unlike autologous and biologic slings, it is imperative to identify the sling and cut it. Conversion to urethrolysis without specifically cutting the sling may fail to relieve obstruction.
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a
b
Figure 68.2. (a) After an inverted U or midline incision, the sling is isolated in the midline and incised. A right-angle clamp may be placed between the sling and the periurethral fascia to avoid injury to the urethra. (b) The sling is freed from the undersurface of the urethra toward the endopelvic fascia. Ends may be excised or left in situ. (Reproduced from ref. 44 with permission.) Usually the sling is easily found, and identification can be aided by palpation of the sling (Fig. 68.3). However, sometimes this can be quite difficult, especially in cases where the sling has rolled onto itself and created a tight narrow band (Fig. 68.4). In such cases, patient and careful dissection to isolate the sling is required. In many cases after the midurethral sling is cut it retracts away from the urethra. At the surgeon’s discretion segmental resection of the suburethral portion of the sling may be performed. Our experience with sling incision has shown results equivalent to formal urethrolysis. The success rate for this procedure ranges from 84 to 93.5% with a 9–21% recurrent stress incontinence rate.43–45 If sling incision is not successful in relieving obstruction, formal urethrolysis may be carried out.
Transvaginal urethrolysis Formal urethrolysis may be accomplished through a retropubic or a transvaginal approach. Both methods have shown equivalent success rates and rates of recur-
rent stress urinary incontinence, although most of these series include patients who are obstructed as a result of a number of different anti-incontinence surgeries. The type of urethrolysis chosen will depend on several factors including patient presentation, type of incontinence procedure performed, failed prior urethrolysis, and surgeon preference. It has been our practice to perform transvaginal urethrolysis as a primary operation, and retropubic urethrolysis as a secondary operation (e.g. after failed transvaginal urethrolysis). We prefer the transvaginal technique because of its ease and the reduced morbidity and recovery time afforded by avoiding an abdominal procedure. However, there are times when a retropubic approach may be the best primary procedure, for example: when vaginal anatomy precludes a transvaginal approach; in cases where original incontinence surgery was associated with bladder perforation, fistula or other operative complication; when there is a synthetic sling which must be removed; or in cases where the patient wishes to avoid a vaginal incision. 989
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Figure 68.3. Isolated midurethral polypropylene sling causing obstruction 1 year after implantation. Note the ingrowth of tissue between the mesh (blue).
Figure 68.4. Obstructing midurethral polypropylene sling which has twisted into a 2 mm band. A right-angle clamp can be placed between the tension-free transvaginal tape (TVT) and the periurethral fascia and the TVT can be isolated and cut. All urethrolysis procedures begin with a thorough endoscopic examination of urethra, bladder neck, and bladder. Urethroscopy may show scarring, narrowing, occlusion, kinking or deviation of the urethra. Eroded sutures or sling material or evidence of a fistula should be excluded. A rigid scope with a zero to 30-degree lens and little or no beak to allow for complete distension of the urethra is ideal for female urethroscopy. It is common to find that the urethra and/or urethrovesical function are fixed and there is lack of mobility when moving the cystoscope up and down. After urethrolysis, mobility should be restored.
The most commonly used transvaginal technique was originally described by Leach and Raz.46 A midline or inverted U incision approximately 3 cm long is made in the anterior vaginal wall. A midline incision should extend from the midurethra to 1–2 cm proximal to the bladder neck. In the case of an inverted U, the apex should be located half way between the bladder neck and urethral meatus, with the lateral wing extending proximal to the bladder neck. With either incision, lateral dissection is performed along the glistening surface of the periurethral fascia to the pubic bone. The retropubic space is entered sharply by perforating the attachment of the endopelvic fascia to the obturator fascia (Fig. 68.5a). The urethra is dissected bluntly and sharply off the undersurface of the pubic bone and completely freed proximally to the bladder neck. Sharp dissection is usually required here (Fig. 68.5b). The urethra should be completely freed proximally to the bladder neck so that the index finger can be placed between the urethra and the symphysis pubis. Attachments to the undersurface of the pubic bone are sharply incised or swept down with the index finger retropubically. After initial mobilization, a right-angle clamp can be placed between the pubic bone and the urethra and a Penrose drain placed around the urethra. Downward traction on the Penrose drain further aids visualization and sharp dissection of all retropubic attachments (Fig. 68.6). The index finger may then be placed completely around the urethra between the pubic bone. When urethrolysis is complete there should be full mobility of the urethra which can be tested with up and down movement of an intraurethral sound or cystoscope. Once this is achieved, the vaginal wall is closed with absorbable sutures. Prior to closure, endoscopic examination is performed to rule out urethral or bladder injury. In cases of extensive urethrolysis it is good practice to assess ureteral integrity by giving intravenous indigo carmine prior to endoscopy and assessing ureteral efflux. Success rates with transvaginal urethrolysis vary from 53 to 93% (see Table 68.1). Carey et al. reported the use of a Martius labial fat pad flap with transvaginal urethrolysis with success in 87% of patients.47 The Martius flap may decrease the risk of recurrent fibrosis, provide some urethral support, and with any future surgery a sling may be placed outside the fat pad, thus decreasing the risk of urethral injury. We reserve it for select cases (e.g. repeat urethrolysis, extensive fibrosis) and usually divide the robust fat pad flap midway along its longitudinal axis and wrap the flap around the urethra, effectively supporting the undersurface and retropubic surface of the urethra. In select cases (e.g. extensive mobilization or stress incontinence coexisting with obstruction) it may be desir-
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a
Figure 68.6. Intraoperative photo after completed urethrolysis. A Penrose drain has been placed around the urethra, isolating it from the pubic bone.
b
Figure 68.5. Transvaginal urethrolysis. (a) An inverted U incision in the anterior vaginal wall and entrance into the retropubic space. (b) The urethra is sharply dissected off the undersurface of the pubic bone. The endopelvic fascia, periurethral fascia, and vaginal wall are retracted medially to expose the urethra in the retropubic space. (Reproduced from ref. 37 with permission.) able to resupport the urethra at the time of urethrolysis. Resuspension or pubovaginal sling may be carried out. Currently our practice is to consider a resuspension or
sling only if the patient has stress incontinence prior to urethrolysis or if support structures are severely compromised during urethrolysis. Resuspension does increase the risk of persistent obstruction and since most patients are distraught about obstruction, we feel it is best to take care of that problem and deal with recurrent SUI at a later time should it occur. Rates of recurrent SUI after resuspension vary between zero and 19%.20,36,38,40,47 Many of these patients may be salvaged with transurethral collagen injections should stress incontinence recur. Goldman et al. reported a 66% response rate to collagen in women with recurrent stress incontinence after transvaginal urethrolysis.40 In addition, the option for repeat surgery for SUI at a later date is preserved. It is important to discuss the pros and cons of resuspension and the treatment of recurrent stress incontinence with patients preoperatively, as this could affect the decision on whether or not to resuspend. A variant of transvaginal urethrolysis is the suprameatal approach described by Petrou et al.48 We have found this to have quite limited applicability. A theoretical advantage of this technique is that lateral perforation of 991
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the urethropelvic ligament is not required, minimizing the chance of recurrent urethral hypermobility and subsequent incontinence. An inverted U incision is made around the top of the urethral meatus (approximately 1 cm away) between the 3 and 9 o’clock positions. Using sharp dissection, a plane is developed above the urethra. Then, with a combination of sharp and blunt dissection, the urethra, vesical neck and bladder are freed from the pubic and pelvic attachments anteriorly and laterally. The index finger may then be passed into the retropubic space and, with a sweeping motion from medial to lateral, further freeing may be performed. If obstruction is caused by a pubovaginal sling, the lateral wings of the sling may be cut. Likewise, if the obstruction is caused by suspension sutures, these may be cut. As with transvaginal urethrolysis, a Martius flap may be placed. Petrou et al. reported a 65% success rate for retention and a 67% success for urgency symptoms, with a 3% recurrent stress incontinence rate.48 This approach may be beneficial if dissection between the urethra and pubic bone is excessively difficult. It may be particularly applicable for cases of repeat transvaginal urethrolysis (after a failed prior urethrolysis) or when scarring is particularly dense.
Retropubic urethrolysis Retropubic approaches to urethrolysis may be the preferred method under circumstances which include surgeon experience/familiarity with vaginal anatomy, inadequate vaginal access, original incontinence surgery or urethrolysis associated with bladder perforation, fistula, synthetic sling removal (Fig. 68.7), and when the patient desires to avoid another vaginal incision. Complicated cases that have failed prior extensive trans-
vaginal urethrolysis may also be performed retropubically. Previous retropubic surgery such as the MMK still may be managed transvaginally as shown by Zimmern et al.49 The technique of retropubic urethrolysis has been described by Webster and Kreder (Fig. 68.7).39 It may be accomplished through a Pfannensteil or low midline incision. The rectus fascia and muscle are opened in midline to the level of the pubic symphysis. After exposing the retropubic space, all prevesical and retropubic adhesions are sharply incised. Complications can be avoided by keeping the tips of the scissors against the pubic symphysis during sharp dissection. The objective is to restore complete mobility to the anterior vaginal wall allowing free movement of the vesicourethral unit. The urethra and urethrovesical junction are dissected off the pubic bone, without separating them from the anterior vaginal wall. The boundaries of the vagina in relation to the urethrovesical junction are identified by placement of the index finger of the surgeon’s nondominant hand into the vagina. Alternatively, a sponge stick or similar instrument may be used. Some degree of sharp dissection lateral to the urethra is usually required. In cases of severe scarring, it may be necessary to mobilize laterally as far as the ischial tuberosities. This often results in a paravaginal defect. In cases where a paravaginal defect is created as a consequence of urethral mobilization, the defect should be repaired by reapproximating the paravaginal fascia to the fascia of the obturator internus along the arcus tendineus. The paravaginal repair sutures are left untied. Finally, the peritoneum is opened with a small incision and an omental flap is mobilized. The flap is then placed
Bladder
Symph.
Paravaginal fascia
Paravaginal fascia
Sutures through fascia of obturator Paravaginal internus muscle fascia
Bladder
Symph.
Bladder
Peritoneum
Figure 68.7. Retropubic urethrolysis. The urethra and urethrovesical junction are dissected off the pubic bone, without separating them from the anterior vaginal wall. with sharp dissection. A paravaginal defect repair is then performed. Symph, symphysis pubis. (Reproduced from ref. 39 with permission.) 992
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between the pubic bone and the urethra and secured to the underside of the pubic bone with a 2-0 polyglycolic acid (PGA) suture. The omentum fills the dead space and helps to prevent recurrent adhesion.20 The paravaginal repair sutures are then tied and the abdomen is closed. Cystoscopy is performed to rule out urethral injury and confirm efflux of indigo carmine from the ureteral orifices. Webster and Kreder reported a successful outcome in 93% of 15 women undergoing retropubic urethrolysis and obturator shelf repair.39 In another series of 12 women, Petrou and Young reported resolution of obstruction in 10 patients, with new onset stress incontinence in 2 of 11 patients (18%).50 Carr and Webster reported complete or significant resolution of symptoms in 86% of patients with retropubic urethrolysis.20
Failed urethrolysis Failure of urethrolysis may be due to persistent or recurrent obstruction, detrusor overactivity, impaired detrusor contractility or learned voiding dysfunction. Recurrent obstruction may result from periurethral fibrosis and scarring, or intrinsic damage to the urethra that has occurred as a consequence of the urethrolysis surgery. We believe that inadequate dissection and lysis of the urethra probably represents the most common reason for failure of initial urethrolysis. When obstruction persists it is reasonable to attempt a repeat urethrolysis. We have found this to be effective in relieving urinary retention, but not as effective in treating persistent storage symptoms. We recently reported on the efficacy of repeat urethrolysis in 24 women who failed initial urethrolysis and remained in urinary retention.51 Both transvaginal and retropubic approaches were chosen depending on the clinical situation. Obstruction was cured in 92%, but storage symptoms completely resolved in only 12% and were improved and required medication in 69%. SUI recurred in 18%. These data clearly support aggressive repeat urethrolysis in the face of initial failure, at least for retention and incomplete emptying. In general, if an aggressive transvaginal urethrolysis fails, then a retropubic approach may be considered. In cases where the aggressiveness of the initial transvaginal procedure is unknown, or if only a sling incision was performed, then a repeat transvaginal approach may be appropriate.
CONCLUSION It is indeed a challenging prospect to treat the patient with significant irritative and obstructive features after performing an operation for incontinence. While keep-
ing in mind the patient’s symptoms and goals, the physician must use careful decision making when assessing, diagnosing, and treating obstruction. Fortunately, the various urethrolysis techniques are highly successful for restoring efficient voiding. We still seek improved methods of identifying those at risk for obstruction, diagnosing obstruction, and treating troublesome irritative voiding symptoms.
REFERENCES 1. Juma S, Sdrales L. Etiology of urinary retention after bladder neck suspension [abstract]. J Urol 1993;149:400A. 2. Spencer JR, O’Conor VJ Jr, Schaeffer AJ. A comparison of endoscopic suspension of the vesical neck with suprapubic vesicourethropexy for treatment of stress urinary incontinence. J Urol 1987;137:411–5. 3. Rost A, Fiedler U, Fester C. Comparative analysis of the results of suspension-urethroplasty according to Marshall–Marchetti–Krantz and of urethrovesicopexy with adhesive. Urol Int 1979;34:167–75. 4. Mundy AR. A trial comparing the Stamey bladder neck suspension procedure with colposuspension for the treatment of stress incontinence. Br J Urol 1983;55:687–90. 5. Cardozo LD, Stanton SL, Williams JE. Detrusor instability following surgery for genuine stress incontinence. Br J Urol 1979;51:204–7. 6. Leach GE, Dmochowski RR, Appell RA et al. Female Stress Urinary Incontinence Clinical Guidelines Panel summary report on surgical management of female stress urinary incontinence. The American Urological Association. J Urol 1997;158:875–80. 7. Chaikin DC, Rosenthal J, Blaivas JG. Pubovaginal fascial sling for all types of stress urinary incontinence: long-term analysis. J Urol 1998;160:1312–6. 8. Morgan TO Jr, Westney OL, McGuire EJ. Pubovaginal sling: 4-year outcome analysis and quality of life assessment. J Urol 2000;163:1845–8. 9. Klutke C, Siegel S, Carlin B, Paszkiewicz E, Kirkemo A, Klutke J. Urinary retention after tension-free vaginal tape procedure: incidence and treatment. Urology 2001;58:697–701. 10. Niemczyk P, Klutke JJ, Carlin BI, Klutke CG. United States experience with tension-free vaginal tape procedure for urinary stress incontinence: assessment of safety and tolerability. Tech Urol 2001;7:261–5. 11. Rardin CR, Rosenblatt PL, Kohli N, Miklos JR, Heit M, Lucente VR. Release of tension-free vaginal tape for the treatment of refractory postoperative voiding dysfunction. Obstet Gynecol 2002;100:898–902. 12. Sander P, Moller LM, Rudnicki PM, Lose G. Does the tension-free vaginal tape procedure affect the voiding phase?
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Pressure–flow studies before and 1 year after surgery. BJU Int 2002;89:694–8.
namic predictors of delayed voiding after fascia lata suburethral sling. Obstet Gynecol 1998;92:608–12.
13. Tamussino K, Hanzal E, Kolle D, Ralph G, Riss P. The Austrian tension-free vaginal tape registry. Int Urogynecol J Pelvic Floor Dysfunct 2001;12 (Suppl 2):S28–9.
28. Leng WW, Davies BJ, Tarin T et al. Delayed treatment of bladder outlet obstruction after sling surgery: association with irreversible bladder dysfunction. J Urol 2004;172:1379–81.
14. Kuuva N, Nilsson CG. A nationwide analysis of complications associated with the tension-free vaginal tape (TVT) procedure. Acta Obstet Gynecol Scand 2002;81:72–7. 15. Moran PA, Ward KL, Johnson D, Smirni WE, Hilton P, Bibby J. Tension-free vaginal tape for primary genuine stress incontinence: a two-centre follow-up study. BJU Int 2000;86:39–42. 16. Rackley RR, Abdelmalak JB, Tchetgen MB, Madjar S, Jones S Noble M. Tension-free vaginal tape and percutaneous vaginal tape sling procedures. Tech Urol 2001;7:90–100. 17. Dunn JS, Bent AE, Ellerkman RM, Nihira MA, Melick CF. Voiding dysfunction after surgery for stress incontinence: literature and survey results. Int Urogynecol J 2004;15:25–31. 18. FitzGerald MP, Brubaker L. The etiology of urinary retention after surgery for genuine stress incontinence. Neurourol Urodyn 2001;20:13–21. 19. Smith CP, O’Leary M, Erickson J, Somogyi GT, Chancellor MB. Botulinum toxin urethral sphincter injection resolves urinary retention after pubovaginal sling operation. Int Urogynecol J Pelvic Floor Dysfunct 2002;13:185–6.
29. Karram MM, Segal JL, Vassallo BJ, Kleeman SD. Complications and untoward effects of the tension-free vaginal tape procedure. Obstet Gynecol 2003;101:929–32. 30. Croak AJ, Schulte V, Peron S, Klingele C, Gebhart J, Lee R. Transvaginal tape lysis for urinary obstruction after tension-free vaginal tape placement. J Urol 2003;169:2238–41. 31. Chassagne S, Bernier PA, Haab F, Roehrborn CG, Reisch JS, Zimmern PE. Proposed cutoff values to define bladder outlet obstruction in women. Urology 1998;51:408–11. 32. Lemack GE, Zimmern PE. Pressure–flow analysis may aid in identifying women with outflow obstruction. J Urol 2000;163:1823–8. 33. Defreitas GA, Zimmern PE, Lemack GE, Shariat SF. Refining diagnosis of anatomic female bladder outlet obstruction: comparison of pressure–flow study parameters in clinically obstructed women with those of normal controls. Urology 2004;64:675–9; discussion 679–81. 34. Nitti VW, Tu LM, Gitlin J. Diagnosing bladder outlet obstruction in women. J Urol 1999;161:1535–40.
20. Carr LK, Webster GD. Voiding dysfunction following incontinence surgery: diagnosis and treatment with retropubic or vaginal urethrolysis. J Urol 1997;157:821–3.
35. Blaivas JG, Groutz A. Bladder outlet obstruction nomogram for women with lower urinary tract symptomatology. Neurourol Urodyn 2000;19:553–64.
21. Miller EA, Amundsen CL, Toh KL, Flynn BJ, Webster GD. Preoperative urodynamic evaluation may predict voiding dysfunction in women undergoing pubovaginal sling. J Urol 2003;169:2234–7.
36. Foster HE, McGuire EJ. Management of urethral obstruction with transvaginal urethrolysis. J Urol 1993;150:1448–51.
22. Weinberger MW, Ostergard DR. Postoperative catheterization, urinary retention, and permanent voiding dysfunction after polytetrafluoroethylene suburethral sling placement. Obstet Gynecol 1996;87:50–4. 23. Bhatia NN, Bergman A. Urodynamic predictability of voiding following incontinence surgery. Obstet Gynecol 1984;63:85–91. 24. Gateau T, Faramarzi-Roques R, Le Normand L, Glemain P, Buzelin JM, Ballanger P. Clinical and urodynamic repercussions after TVT procedure and how to diminish patient complaints. Eur Urol 2003;44:372–6; discussion 376. 25. Wang AC, Chen MC. The correlation between preoperative voiding mechanism and surgical outcome of the tension-free vaginal tape procedure, with reference to quality of life. BJU Int 2003;91:502–6. 26. Kobak WH, Walters MD, Piedmonte MR. Determinants of voiding after three types of incontinence surgery: a multivariable analysis. Obstet Gynecol 2001;97:86–91. 27. McLennan MT, Melick CF, Bent AE. Clinical and urody-
37. Nitti VW, Raz S. Obstruction following anti-incontinence procedures: diagnosis and treatment with transvaginal urethrolysis. J Urol 1994;152:93–8. 38. Cross CA, Cespedes RD, English SF, McGuire EJ. Transvaginal urethrolysis for urethral obstruction after antiincontinence surgery. J Urol 1998;159:1199–201. 39. Webster GD, Kreder KJ. Voiding dysfunction following cystourethropexy: its evaluation and management. J Urol 1990;144:670–3. 40. Goldman HB, Rackley RR, Appell RA. The efficacy of urethrolysis without re-suspension for iatrogenic urethral obstruction. J Urol 1999;161:196–8; discussion 198–9. 41. Ghoniem GM, Elgamasy AN. Simplified surgical approach to bladder outlet obstruction following pubovaginal sling. J Urol 1995;154:181–3. 42. Kusuda L. Simple release of pubovaginal sling. Urology 2001;57:358–9. 43. Amundsen CL, Guralnick ML, Webster GD. Variations in strategy for the treatment of urethral obstruction after a pubovaginal sling procedure. J Urol 2000;164:434–7.
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44. Nitti VW, Carlson KV, Blaivas JG, Dmochowski RR. Early results of pubovaginal sling lysis by midline sling incision. Urology 2002;59:47–51; discussion 51–2. 45. Goldman HB. Simple sling incision for the treatment of iatrogenic urethral obstruction. Urology 2003;62:714–8. 46. Leach GE, Raz S. Modified Pereyra bladder neck suspension after previously failed anti-incontinence surgery. Surgical technique and results with long-term follow-up. Urology 1984;23:359–62. 47. Carey JM, Chon JK, Leach GE. Urethrolysis with Martius labial fat pad graft for iatrogenic bladder outlet obstruction. Urology 2003;61:21–5.
48. Petrou SP, Brown JA, Blaivas JG. Suprameatal transvaginal urethrolysis. J Urol 1999;161:1268–71. 49. Zimmern PE, Hadley HR, Leach GE, Raz S. Female urethral obstruction after Marshall–Marchetti–Krantz operation. J Urol 1987;138:517–20. 50. Petrou SP, Young PR. Rate of recurrent stress urinary incontinence after retropubic urethrolysis. J Urol 2002;167:613–5. 51. Scarpero HM, Dmochowski RR, Nitti VW. Repeat urethrolysis after failed urethrolysis for iatrogenic obstruction. J Urol 2003;169:1013–6.
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69 Classification and epidemiology of pelvic organ prolapse Steven Swift
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INTRODUCTION
CLASSIFICATION OF PELVIC ORGAN SUPPORT
The study of pelvic organ prolapse is one area of medicine that seems so intuitive but in actuality is replete with anecdotal evidence, case series, and very little hard science. Most of this stems from the lack of a scientifically validated and universally agreed upon definition of the disease state of ‘pelvic organ prolapse’. A classification system to codify pelvic organ support has been defined and has gained international recognition. However, while it accurately describes the degree or stage of pelvic organ support, it does not classify it into normal versus abnormal or ‘prolapse’. This is akin to having a blood pressure cuff to measure blood pressure but no definition as to what represents normal versus hypertension. Until we can define the disease, we cannot properly identify its etiology or make any statements regarding therapy, prognosis or natural history. Therefore, all of the scientific literature regarding pelvic organ prolapse should be viewed with caution, paying particular attention to how pelvic organ prolapse is described and defined. Despite the current state of affairs, studies into the classification and epidemiology of pelvic organ prolapse are moving forward as the scientific community has recognized the problems and is addressing them via research protocols.
The above title specifically does not use the term ‘prolapse’ but instead uses ‘support’ as none of the current pelvic organ prolapse classification systems attempts to define ‘prolapse’. Instead, they only address where the vaginal walls or structures extend anatomically without making any reference as to what is normal versus abnormal or ‘prolapsed’. The history of classification systems for pelvic organ support extends back into the 19th century, with a new system appearing every generation or so, but with no system ever attaining widespread acceptance as the ‘gold standard’.1–7 Several of these systems are diagramed in Figure 69.1. Over the last decade, the pelvic organ prolapse quantification (POPQ) system has gained international recognition as the ‘gold standard’ for classifying pelvic organ support and it is the first and only system to gain recognition by most of the major societies that study pelvic organ support defects: the International Continence Society (ICS), the American Urogynecologic Society (AUGS), and the Society of Gynecologic Surgeons (SGS).8 It is also the only system to be extensively studied with several reports in the literature documenting excellent inter- and intraexaminer reliability.9–11 The only other system that has gained some widespread notoriety is the Baden and Walker
1963 Severity (Porges)
1972 Vaginal Profile (Baden)
1980 Grading System (Beecham) Midplane of vagina
Straining
Grade 1 Slight or 1st degree
Stage I
1st degree Grade 2
Introitus
Hymenal ring
(–) 1 cm
At rest
Straining
(+) 1 cm Moderate or 2nd degree
Grade 3
1996 Quantitative POP (ICS, AUGS, SGS)
2nd degree
Stage II
Stage III
Complete eversion
Marked or 3rd degree Grade 4
3rd degree
Stage IV
Figure 69.1. Comparison of the four most commonly used pelvic organ prolapse (POP) grading systems. AUGS, American Urogynecologic Society; ICS, International Continence Society; SGS, Society of Gynecologic Surgeons. 1000
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‘half-way’ system. In a recent survey of the literature on pelvic organ prolapse, it was the second most commonly employed classification system (with the POPQ being the first), and it is the only other system to be studied for interexaminer reliability.10,12 Currently, there is only one internationally recognized classification system for codifying pelvic organ support – the POPQ. It has proven itself to be a reliable system and it is the system that should be employed in research regarding pelvic organ support. The Baden and Walker ‘half-way’ system remains a common system in clinical practice and this may stem from its ease of use; however, it should not continue to supplant the POPQ in research studies and the scientific literature.10
THE PELVIC ORGAN PROLAPSE QUANTIFICATION SYSTEM While the POPQ system is recognized as the standard for describing pelvic organ support, it has not resolved all of the questions regarding pelvic organ prolapse. First, while it is a good system for codifying pelvic organ support, like its predecessors it does not establish any diagnostic criteria for pelvic organ prolapse. In addition, while it is the only universally recognized system, it has yet to gain universal acceptance in research or clinical practice. Despite being initially described and published in 1996, as of 2003, it still only appeared in about 30% of the literature regarding pelvic organ support defects, and, as of 2006, is only used clinically by about 40% of the members of the societies (ICS, AUGS) that acknowledge it as the recognized scientific standard for describing pelvic organ support.12,13 There are many reasons why the POPQ system has not gained widespread clinical use, but the most comTable 69.1.
monly cited reasons are: 1) not used by colleagues; 2) too time consuming; and 3) too confusing.13 There is some validity to these concerns, but there are also some misconceptions. If only 40% of the members of the ICS and AUGS use it their clinical practice, it would be surprising to find that other healthcare providers outside of these societies had embraced the POPQ in their clinical practice. While there is no literature on how the system is used outside of the field of urogynecology there is a study of 54 obstetrics and gynecology house officers and students who were trained to use the system. When specifically queried, only one of 54 reported seeing or using the system outside of their urogynecology rotation.14 Concerns about taking too much time to complete are unwarranted as it only takes 2–3 minutes to complete the examination, even in neophytes.9 Finally, while it may seem difficult to understand at first, when tested, obstetrics and gynecology house officers and medical students improved greatly on written understanding of the POPQ system after minimal instruction.14 Therefore, for all the concerns about the POPQ, only clinical use appears valid. Despite these barriers to its routine clinical use, it remains the only universally recognized pelvic organ prolapse classification system.
Performing the POPQ examination The POPQ examination takes nine measures of the position of midline vaginal structures (Table 69.1). All of the measurements are in centimeters relative to the hymeneal ring. The remnant of the hymeneal ring is used as the reference point because it is a fixed and easily identified landmark, as opposed to the introitus, which is a non-standardized anatomic structure (it is defined
Sites measure in the quantitative pelvic organ prolapse examination
Point
Description
A anterior (Aa)
A point on the anterior vaginal wall 3 cm above the hymeneal ring
B anterior (Ba)
Most dependent or distal point on the anterior vaginal wall segment between A anterior and point C or the cuff if subject is status posthysterectomy
C
Anterior lip of the cervix or the cuff if subject is status posthysterectomy
A posterior (Ap)
A point on the posterior vaginal wall 3 cm above the hymeneal ring
B posterior (Bp)
Most dependent or distal point on the posterior vaginal wall segment between A posterior and point D or the cuff if subject is status posthysterectomy
D
Posterior fornix (this space is left blank in the subject who is status posthysterectomy)
Genital hiatus (gh)
Middle of external urethral meatus to posterior hymeneal remnant
Perineal body (pb)
Posterior hymen to middle of anal opening
Total vaginal length (tvl)
Hymeneal ring to vaginal apex
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as ‘entrance into the vagina’). All of the points recorded during the examination, with the exception of total vaginal length, are measured with the subject performing a Valsalva maneuver or a deep cough. Structures that lie above the hymeneal ring are recorded as negative, whereas structures that prolapse beyond the hymeneal ring are recorded as positive (both recordings in centimeters) (Fig. 69.2). Any structure that descends to the level of the hymeneal ring is recorded as zero centimeters. Nine measurements are taken during the examination: two from the anterior vaginal wall, two from the apex of the vagina, two from the posterior vaginal wall, and one
each recording the genital hiatus, perineal body, and the total vaginal length at rest (see Table 69.1). These points are depicted diagrammatically in Figure 69.2; note also the two diagrams representing a large anterior segment defect with some apical descent (Profile A) and a large posterior defect (Profile B). The nine points may be recorded in a convenient manner using a three-by-three grid as noted in the figure. Any rigid measuring device – such as a marked wooden Pap smear spatula, ruler or engraved instrument – may be used. For descriptive purposes, an ordinal staging system is used whereby the prolapse stage is defined by the vaginal
C D 3 cm
Ba
Aa Bp tvl
Ap
gh
a
pb
Ba Aa s
s
s C
Aa
s
C Bp
ss
s Ba +3
s Ap Aa
4.5 gh –3
Ap
b
Table 69.2.
+6
Ba
1.5 pb –2
Bp
–2
Bp s
C
s
Ap –3
Aa
6 tvl
4.5 gh
–
+2
Ap
Profile A
–3
Ba
1 pb +5
Bp
Profile B
–6
C
8 tvl –
Figure 69.2. (a) The nine points recorded for the pelvic organ prolapse classification system. Terms are defined in Table 69.1. (b) Profile A represents a large anterior wall defect with some apical descent; Profile B represents a large posterior defect. Note the grid system used for recording the nine points.
Staging of pelvic organ prolapse
Stage
Description
0
No descensus of pelvic structures during straining
I
The leading surface of the prolapse does not descend below 1 cm above the hymeneal ring
II
The leading edge of the prolapse does not extend from 1 cm above the hymen to 1 cm through the hymeneal ring
III
The prolapse extends more than 1 cm beyond the hymeneal ring, but there is not complete vaginal eversion
IV
The vagina is completely everted
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structure that demonstrates the greatest degree of prolapse (Table 69.2). An easy method of remembering this staging system involves understanding stage II. Any vaginal structure that descends such that the leading edge is at or between 1 cm above and 1 cm past the hymeneal ring is stage II. If the vaginal structure or leading edge has some movement but remains above –1 cm it is stage I, and any structure or leading edge that descends beyond +1 cm is stage III up to complete eversion, which is stage IV. Stage 0 is no descent of any vaginal segment. At a practical level, an efficient method of performing the examination consists of placing a bivalved speculum in the vagina and measuring apical descent, using the posterior blade of the speculum to measure anterior and then posterior structures, and then measuring the perineal structures. Further information regarding the performance of the POPQ examination, including a videotape, is available at the AUGS website (www.augs. org). One aspect of this system that may be awkward, or even anathema, to adherents of prior systems is the strict avoidance of terms such as cystocele, rectocele or enterocele. The rationale behind this seemingly dogmatic practice is to avoid erroneous assumptions regarding the prolapsing organs. Since the vagina is relatively opaque it is not possible to identify which organ is on the other side of the epithelium. It is often difficult even for experienced observers to discriminate between a high rectocele and a pulsion enterocele. Furthermore, patients who have had prior reconstructive pelvic surgery may have gross alterations in their vaginal axis, which result in unusual patterns of prolapse (e.g. anterior enterocele after sacrospinous ligament suspension). Another change from previous systems is the avoidance of staging the individual vaginal segments, i.e. a patient having a stage II cystocele and stage III rectocele. Instead, the patient is given one overall stage; for example, the previously noted patient would be described as having a POPQ stage III examination.
symptoms relate to various degrees of support is paramount to defining the disease of pelvic organ prolapse. Currently there are several studies examining the distribution of pelvic organ support in various general female populations. These studies are being undertaken to determine the normal distribution of pelvic organ support.16–23 However, only three studies have looked at general populations of a significant age range employing the POPQ system.16–18 From the distribution of these three studies as plotted in Figure 69.3, it can be seen that POPQ stage II support represents between 30 and 50% of the populations studied. However, it is doubtful that pelvic organ prolapse is this prevalent; therefore the NIH definition may be too broad. Only 2–11% of subjects in these studies have stage 3 and 4 examinations, which is more consistent with current estimates on the percent of subjects undergoing surgical treatment for this condition. There is an 11% lifetime risk of undergoing surgical correction of pelvic organ prolapse and the incidence of surgery for pelvic organ prolapse is 22.7 per 10,000.24,25 Pelvic organ prolapse is a disease with essentially no mortality and only minimal morbidity; however, it is a condition that impacts greatly on quality of life. Therefore, symptoms play a central role in defining at what point a patient goes from ‘normal’ pelvic organ support to ‘abnormal’ pelvic organ prolapse. Despite the concerns involving a lack of data on symptoms and how they relate to anatomy, the NIH consensus conference did propose a definition of pelvic organ prolapse.15 They suggested that all POPQ stage II or greater pelvic organ support be considered ‘pelvic organ prolapse’, but felt that this definition would required scientific validation before it could be recommended as a clinical or research standard.
DEFINING PELVIC ORGAN PROLAPSE A recent National Institutes of Health (NIH) consensus conference recognized that without a standard validated definition of pelvic organ prolapse there could be little progress in studying the disease and its treatment. They noted that currently there are no clinically or scientifically validated definitions and felt that any proposed definition should take into account both a subject’s anatomy as well as their symptoms.15 Developing a knowledge base regarding the normal distribution of pelvic organ support in the female population and determining how
Figure 69.3. Percent of subjects in each POPQ stage in three studies of general female populations. n, the number of subjects examined in each study. 1003
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There are currently several studies investigating the correlation between symptoms and pelvic organ support. Most demonstrate that there is a very weak (if any) correlation between symptoms and advancing degrees of pelvic organ prolapse with the exception of the symptom of a bothersome vaginal bulge.26–30 In the few studies that correlated POPQ stage with symptoms it appears that symptoms begin to significantly increase once the leading edge of the vaginal wall extends to or just beyond the hymen.17,25 Therefore, a reasonable definition of pelvic organ prolapse may be protrusion of any vaginal segment to or beyond the hymen in symptomatic patients; however, this definition needs further study to document its validity.
The only universally accepted risk factor for pelvic organ prolapse is increasing age. Regardless of the definition used, this factor is always identified as an etiology and most estimates suggest that there is roughly a doubling in the risk of prolapse with every completed decade of life.16,17,23,31 The other proposed etiologies for pelvic organ prolapse are many but for the most part involve two types of insult: either the acute damage that occurs with pregnancy or the chronic insults from conditions that lead to continuous intermittent increases in intra-abdominal pressure. In addition, other areas that have been investigated include prior pelvic surgery and genetic factors.
EPIDEMIOLOGY OF PELVIC ORGAN PROLAPSE
The relationship between pregnancy and pelvic organ prolapse has been extensively studied and is mentioned in almost every treatise on this subject. It is assumed that as the fetal vertex passes through the birth canal there is direct damage to the nerves, fascia, and muscle that leads to eventual relaxation of the pelvic floor musculature and pelvic organ prolapse. While it is generally recognized that any parity is associated with an increased risk of prolapse, what role the delivery mode plays is more controversial.16–19,21,30–32,34 Specifically, can one delivery mode (i.e. cesarean section) provide protection against prolapse? The majority of the literature supports the notion that increasing parity increases the risk of pelvic organ prolapse.16,17,19,30,32 Studies suggest that anywhere from a four- to an 11-fold increase in the risk of prolapse is dependent on parity, with increasing parity imparting greater risk.17,19,31 However, the literature on the mode of delivery is mixed. When women who delivered only by cesarean section were compared to women who had any vaginal
As previously noted, there is no currently accepted definition of pelvic organ prolapse; therefore each study into its epidemiology is left to employ its own definition. Generally, the literature defines prolapse in one of two ways – either anatomically by examination or by surgical admission for corrective surgery. The concern regarding surgical admissions is that they miss those patients that manage their prolapse conservatively; the concern regarding anatomic descriptions is that no two studies use the same anatomic cutoffs.17,19,21,23,24,31–35 A list of the major epidemiologic studies and their definitions is provided in Table 69.3. This plethora of definitions makes it difficult to evaluate trends in the literature into the various etiologies and can lead to conflicting results. This portion of the chapter will examine the various proposed etiologies of pelvic organ prolapse, bearing in mind that the frequently conflicting results stem from the various definitions employed in each study. Table 69.3.
Effect of pregnancy
Definitions of pelvic organ prolapse from the various epidemiologic studies
Author
Definition 35
Jorgensen et al.
Surgical admission for surgery to correct prolapse
24
Olsen et al.
Surgical admission for surgery to correct prolapse
19
Mant et al.
Surgical admission for surgery to correct prolapse
Chiaffarino et al.32 33
Marchionni et al.
21
Samuelsson et al. 34
Gruel & Gruel 31
Baden and Walker stage 2 and greater Baden and Walker stage 2 and greater Presence of any cystocele, rectocele, uterine descent, or absence of the urethrovesical crease Any vaginal relaxation to the introitus (roughly equivalent to Baden and Walker stage 2 and greater)
Swift et al.
POPQ stage 3 prolapse
Hendrix et al.23
Stage 1 or greater prolapse by a unique system defined for this study (stage 1 is defined as in the vagina)
17
Swift et al.
Leading edge at –0.5 cm above the introitus or greater (some POPQ stage 2 and all stage 3 and 4)
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delivery, the data are inconclusive and do not suggest a protective effect.17 The data on instrumented vaginal delivery are sparse and in one study forceps delivery was not identified as a risk factor for the development of prolapse.32 In addition, there is one study suggesting that episiotomy protects against prolapse.33 The data regarding infant weight are more consistent, with most studies demonstrating an increase in prolapse with increasing fetal weight; delivery of a macrosomic infant carries the greatest risk.17,21,31,32 Pregnancy and macrosomia are consistently identified as risk factors for pelvic organ prolapse, but whether cesarean delivery or avoidance of an operative vaginal delivery can protect against pelvic organ prolapse remains a topic of debate with no clear evidence to support or refute this supposition.
Modifiable lifestyle risk factors There are several opinions regarding how to counsel patients in ways to prevent pelvic organ prolapse. Factors such as occupations that require a lot of lifting, together with obesity and smoking, all contribute to pelvic organ prolapse, and modifying or removing these insults will reduce the risk. The data on occupation as a risk for prolapse stem from an article published in 1994 on nursing assistants in Denmark. The investigators noted a 60% increased risk of surgery to correct pelvic organ prolapse and herniated lumbar disks in nursing assistants over the general population,35 and felt this was due to the excess heavy lifting of patients inherent in their job description. Since then, two large studies have incorporated job description into their data collection.17,32 Both found that manual workers and housewives had a slightly increased risk of prolapse over women who classified themselves as professionals. Obesity is another risk factor commonly quoted for pelvic organ prolapse. It is felt that the increasing weight from abdominal adipose tissue increases the pressure on the intra-abdominal organs, leading to pelvic floor weakness and prolapse. Here the literature is divided, with several studies suggesting it as a risk factor17,19,23,24,33 and several studies finding no association.21,31,33 Smoking is the final modifiable risk factor often associated with pelvic organ prolapse. Again the data are mixed, with several studies suggesting that current smokers are at risk,19,23,24 two showing no relationship,21,32 and one study suggesting smoking has some protection against pelvic organ prolapse.17 Among the lifestyle or modifiable etiologies, the only factor that demonstrates a consistent relationship with
an increased risk of pelvic organ prolapse is job description, with those individuals engaged in more manual labor having a greater risk of prolapse.
Medical illnesses Other areas that are commonly discussed and implicated as being etiologies of pelvic organ prolapse are chronic medical or congenital illnesses that result either in increased intra-abdominal pressure or in microvascular disease and poor quality collagen. The relationship between chronic illness and prolapse has been investigated in large epidemiologic studies with mixed results. It would seem intuitive that those illnesses associated with chronic recurrent increases in intra-abdominal pressure, constipation, and chronic obstructive pulmonary disease (COPD) would increase the risk of pelvic organ prolapse. Constipation is an illness that can be difficult to define; however – when evaluated – it appears consistently related to an increase in prolapse.23,36 Two studies evaluated COPD and neither noted it as a risk for prolapse.24,31 In one of these studies the number of subjects with COPD was very small and in the other the pelvic organ prolapse was defined by surgical admission so the data could be questioned. However, when taken with data on smoking, there does not appear to be a strong relationship between pulmonary disease and prolapse. Medical illnesses that lead to long-term damage to the microvasculature and peripheral neuropathies, such as hypertension and diabetes mellitus, have been suggested as a potential cause of pelvic organ prolapse. However, as with many etiologic studies, the results are mixed. In one large study the presence of any chronic illness was not associated with an increased incidence of prolapse;17 in another study, only hypertension was identified as a risk factor.31 There are also a few studies in women with collagen vascular diseases, such as Marfan and Ehlers–Danlos syndrome, which suggest that these patients are at an increased risk of prolapse.37,38 However, again the data are somewhat conflicting and this may stem from the lack of any definition of prolapse in these studies.
Race There is a long history of observational data to suggest that women of certain racial groups are at a greater or lesser risk of pelvic organ prolapse. There are early anecdotal reports of African–American and ‘Chinese’ women having a very low risk of pelvic organ prolapse in comparison to Caucasian women.39–41 While it can 1005
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be difficult to classify women into race (with the Tiger Woods phenomenon), it appears that African–American women having a slightly decreased risk of prolapse when compared to their Caucasian counterparts, and Hispanic women have an increased risk over Caucasian women.17,23,31 The data on Asian women in these trials are too sparse to draw any conclusions.
Menopausal status and hormone replacement therapy The association between menopausal status, hormonal therapy and pelvic organ prolapse is a very complicated issue. First, women who are menopausal tend to be older than their premenopausal counterparts and, as pointed out earlier, increasing age is probably the greatest risk factor for pelvic organ prolapse. In addition, women who take hormone replacement therapy (HRT) may not have taken it consistently since menopause and can be on any of a myriad of dosing schedules, further complicating any comparative studies. The majority of the studies suggest that postmenopausal women are at greater risk; however, when a multiple logistic regression analysis takes age into account, menopausal status becomes non-significant, suggesting that it may be the age factor more than the decreased estrogen levels that places the woman at risk for prolapse.17,23,31,32 In these same studies, when the role of HRT was evaluated in menopausal women, the results are even less clear. One study suggested that past use decreases risk but not current use, another suggested no difference between ever and never using HRT, and one suggested that postmenopausal women with current use had a risk equal to that of premenopausal women. It should be noted that, while HRT may not protect menopausal women from developing prolapse, it has never demonstrated a negative effect.
Prior pelvic surgery This is another area where it is difficult to determine if there are any significant relationships. First, it is known that up to 30% of women who undergo surgery for pelvic organ prolapse will require a second procedure to correct recurrent prolapse.24 Therefore, subjects who have had prior prolapse surgery have many of the underlying conditions that put them at risk for prolapse, and using this as a risk factor is similar to noting the increased risk of cancer in patients undergoing treatment for cancer. Conversely, many patients who have undergone a hysterectomy had it done to correct pelvic organ prolapse, as pelvic relaxation is the third
most common indication for hysterectomy in the US.42 Therefore, many of these patients have already been treated for prolapse and many will have been treated successfully. However, when hysterectomy is evaluated, most studies suggest that it does expose patients to an increased risk of pelvic organ prolapse.19,21,31,33 When the hysterectomy was done specifically for prolapse it increases the risk even more.33 The mechanism behind this phenomenon may be the disruption of the normal apical supports of the vagina in subjects with otherwise good support. This emphasizes the need to be ever mindful of providing strong attachment of the cardinal and uterosacral ligament complex to the vaginal cuff at the time of hysterectomy. In subjects who have undergone prior prolapse surgery there appears to be upwards of a five-fold increase in their risk of developing pelvic organ prolapse.31
Family history This is one area where we have almost no data; however, this may be of central importance when we counsel patients about other modifiable risk factors. There is one study where subjects who had undergone surgery for prolapse were asked about any family history of other relatives undergoing similar surgery.32 The authors noted that there was an increased risk of pelvic organ prolapse surgery if a patient’s mother or sister had undergone prolapse surgery.
SUMMARY While we are still in the infancy of understanding pelvic organ prolapse, we are moving forward. There is now a growing body of literature regarding the classification and epidemiology of pelvic organ prolapse incorporating the POPQ and well-described definitions of pelvic organ prolapse that are beginning to help us understand this complex disease. Currently, it is difficult to evaluate the various etiologies of pelvic organ prolapse because of the lack of a standard definition. This makes the plethora of emerging data difficult to interpret because often we are comparing apples and oranges. There are a few consistencies, with age and pregnancy being acknowledged risk factors for pelvic organ prolapse. Other factors that probably play a role include obesity, a job with a greater proportion of manual labor and lifting, lack of HRT, hysterectomy, and family history. However, before recommendations can be made regarding preventive strategies, more studies using a consistent definition are required.
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REFERENCES 1. Scanzoni FW. Senkung und Vorfall des uterus und der scheide. In: Scanzoni FW (ed) Lehrbuch der Krankheiten der Weiblichen Geschlechstorgane, 5th ed. Vienna: Braumueller, 1875; 654–64. 2. Kelly HA. Operative Gynecology. New York: Appleton & Co., 1898.
population of female subjects seen for routine gynecologic health care. Am J Obstet Gynecol 2000;183:277–85. 17. Swift SE, Woodman P, O’Boyle A et al. Pelvic Organ Support Study (POSST): the distribution, clinical definition and epidemiology of pelvic organ support defects. Am J Obstet Gynecol 2005 (in press).
3. Kuestner O. Prolapsus uteri et vaginea. In: Kuestner O, Bumm E, Doederlein A, Kroenig B, Menge C (eds) Kurzes Lehrbuch der Gynaekologie. Jena: G Fischers, 1912; 159–81.
18. Slieker-ten HMCP, Vierhout M, Bloembergen H, Schoenmaker G. Distribution of pelvic organ prolapse in a general population: prevalence, severity, etiology and relation with the function of pelvic floor muscles. Abstract presented at the Joint meeting of the ICS and IUGA, August 25–27, 2004, Paris, France.
4. Baden WF, Walker TA. Genesis of the vaginal profile: a correlated classification of vaginal relaxation. Clin Obstet Gynecol 1972;15:1048–54.
19. Mant J, Painter R, Vessey M. Epidemiology of genital prolapse: observations from the Oxford Family Planning Association study. Br J Obstet Gynaecol 1997;104:579–85.
5. Baden WF, Walker TA. Physical diagnosis in the evaluation of vaginal relaxation. Clin Obstet Gynecol 1972;15:1055–69.
20. Bland DR, Earle BB, Vitolins MZ, Burke G. Use of the pelvic organ prolapse staging system of the International Continence Society, American Urogynecologic Society, and the Society of Gynecologic Surgeons in perimenopausal women. Am J Obstet Gynecol 1999;181:1324–8.
6. Beechum CT. Classification of vaginal relaxation. Am J Obstet Gynecol 1980;136:957–8. 7. Porges RF. A practical system of diagnosis and classification of pelvic relaxations. Surg Gynecol Obstet 1963;117:761–73. 8. Bump RC, Mattiasson A, Bo K et al. The standardization of terminology of female pelvic floor dysfunction. Am J Obstet Gynecol 1996;175:10–7. 9. Hall AF, Theofrastous JP, Cundiff GC, Harris RL, Hamilton LF, Swift SE, Bump RC. Interobserver and intraobserver reliability of the proposed International Continence Society, Society of Gynecologic Surgeons, and American Urogynecologic Society pelvic organ prolapse classification system. Am J Obstet Gynecol 1996;175:1467–71. 10. Kobak WH, Rosenberger K, Walters MD. Interobserver variation in the assessment of pelvic organ prolapse. Int J Urogynecol Pelvic Floor Dysfunct 1996;7:121–4. 11. Prien-Larsen J, Mouritsen L. Pelvic organ prolapse: is ICSgrading without POP-Q measurement reliable? [abstract]. Int Urogynecol J 2001;12(Suppl 3):S45. 12. Muir T, Stepp K, Barber M. Adoption of the pelvic organ prolapse quantification system in peer-reviewed literature. Am J Obstet Gynecol 2003;189:1632–6. 13. Auwad W, Freeman R, Swift S. Is the pelvic organ prolapse quantification system (POPQ) being used? A survey of the members of the International Continence Society (ICS) and the American Urogynecology Society (AUGS). Int Urogynecol J 2004;15:324–7. 14. Steele A, Mallipeddi P, Welgloss J, Soled S, Kohli N, Karram M. Teaching the pelvic organ prolapse quantification system. Am J Obstet Gynecol 1998;179:1458–64. 15. Weber AM, Abrams P, Brubaker L et al. The standardization of terminology for researchers in female pelvic floor disorders. Int Urogynecol J 2001;12:178–86. 16. Swift SE. The distribution of pelvic organ support in a
21. Samuelsson EU, Victor FTA, Tibblin G, Svardsudd KF. Signs of genital prolapse in a Swedish population of women 20 to 59 years of age and possible related factors. Am J Obstet Gynecol 1999;180:299–305. 22. Versi E, Harvey M-A, Cardozo L, Brincat M, Studd WW. Urogenital prolapse and atrophy at menopause: a prevalence study. Int Urogynecol J 2001;12:107–10. 23. Hendrix SL, Clark A, Nygaard I, Aragki A, Barnabei V, McTiernan A. Pelvic organ prolapse in the Women’s Health Initiative. Am J Obstet Gynecol 2002;186:1160–6. 24. Olsen AL, Smith VJ, Bergstrom VO, Colling JC, Clark AL. Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 1997;89:501–6. 25. Rown JS, Waetjen LE, Subak LL, Thom DH, Van Den Eeden S, Vittinghoff E. Pelvic organ prolapse surgery in the United States, 1997. Am J Obstet Gynecol 2002;186:712–6. 26. Swift SE, Tate SB, Nichols J. Correlation of symptomatology with degree of pelvic organ support in a general population of women: what is pelvic organ prolapse? Am J Obstet Gynecol 2003;189:372–9. 27. Barber M, Walters M, Bump R. Association of the magnitude of pelvic organ prolapse and presence and severity of symptoms. Abstract presented at the 24th annual scientific meeting of the American Urgynecologic Society, September 11–13, 2003, Hollywood, FL. 28. Elkerman RM, Cundiff GW, Melik CF, Nihira M, Leffler K, Bent AE. Correlation of symptoms with location and severity of pelvic organ prolapse. Am J Obstet Gynecol 2001;185:1332–8. 29. Heit M, Culligan P, Rosenquist C, Shott S. Is pelvic organ prolapse a cause of pelvic or low back pain? Obstet Gynecol 2002;99:22–8.
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30. Burrows LJ, Meyn LA, Walters MD, Weber AM. Pelvic symptoms in women with pelvic organ prolapse. Am J Obstet Gynecol 2004;104:982–8. 31. Swift SE, Pound T, Dias JK. Case-control study of etiologic risk factors in the development of severe pelvic organ prolapse. Int Urogynecol J 2001;12:187–92. 32. Chiaffarino F, Chatenoud L, Dindelli M et al. Reproductive factors, family history, occupation and risk of urogenital prolapse. Eur J Obstet Gynecol Reprod Biol 1999;82:63–7. 33. Marchionni M, Luca Braco G, Checcucci V et al. True incidence of vaginal vault prolapse: thirteen years’ experience. J Reprod Med 1999;44:679–84.
prolapse and urinary stress incontinence. Br J Obstet Gynaecol 1994;101:147–52. 37. Carley ME, Schaffer J. Urinary incontinence and pelvic organ prolapse in women with Marfan and Ehlers–Danlos syndrome. Am J Obstet Gynecol 2000;182:1021–3. 38. McIntosh LJ, Stanitski DF, Mallett VT, Frahm JD, Richardson DA, Evans MI. Ehlers–Danlos syndrome: relationship between joint hypermobility, urinary incontinence and pelvic floor prolapse. Gynecol Obstet Invest 1996;41:135–9. 39. van Dongen L. The anatomy of genital prolapse. S Afr Med J 1981;60:357–9.
34. Gruel H, Gruel SA. Pelvic relaxation and associated risk factors: the results of logistic regression analysis. Acta Obstet Gynecol Scand 1999;78:290–3.
40. Zacharin RF. ‘A Chinese anatomy’ – the pelvic supporting tissues of the Chinese and Occidental female compared and contrasted. Aust N Z J Obstet Gynecol 1977;17:1–11.
35. Jorgensen S, Hein HO, Gyntelberg F. Heavy lifting at work and risk of genital prolapse and herniated lumbar disc in assistant nurses. Occup Med 1994;44:47–9.
41. Cox PSV, Webster D. Genital prolapse amongst the Pokot. East Afr Med J 1975;52:694–9.
36. Spence-Jones C, Kamm MA, Henery MM, Hudson CN. Bowel dysfunction: a pathologic factor in uterovaginal
42. Wilcox LS, Koonin LM, Pokras R, Struass LT, Xia Z, Peterson HB. Hysterectomy in the United States, 1988–1990. Obstet Gynecol 1994;83:549–55.
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70 Anterior vaginal wall prolapse Mark D Walters
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INTRODUCTION Anterior vaginal prolapse occurs commonly and may coexist with disorders of micturition. Mild anterior vaginal prolapse often occurs in parous women but usually presents few problems. As the prolapse progresses, symptoms may develop and worsen, and treatment becomes indicated. This chapter reviews the anatomy and pathology of anterior vaginal prolapse, with and without stress incontinence, and describes methods of vaginal repair.
ANATOMY AND PATHOLOGY Anterior vaginal prolapse (cystocele) is defined as pathologic descent of the anterior vaginal wall and overlying bladder base. According to the International Continence Society (ICS) standardized terminology for prolapse grading,1 the term ‘anterior vaginal prolapse’ is preferred to ‘cystocele’. This is because information obtained at the physical examination does not allow the exact identification of structures behind the anterior vaginal wall, although it usually is, in fact, the bladder. The ICS grading system for prolapse is discussed in detail in Chapter 69. The etiology of anterior vaginal prolapse is not completely understood, but it is probably multifactorial, with different factors implicated in prolapse in individual patients. Normal support for the vagina and adjacent pelvic organs is provided by the interaction of the pelvic muscles and connective tissue.2 The upper vagina rests on the levator plate and is stabilized by superior and lateral connective tissue attachments; the midvagina is attached to the arcus tendineus fasciae pelvis (white line) on each side.3 Pathologic loss of that support may occur with damage to the pelvic muscles, connective tissue attachments, or both. Nichols and Randall described two types of anterior vaginal prolapse: distension and displacement.4 Distension was thought to result from overstretching and attenuation of the anterior vaginal wall, caused by overdistension of the vagina associated with vaginal delivery or atrophic changes associated with aging and menopause. The distinguishing physical feature of this type was described as diminished or absent rugal folds of the anterior vaginal epithelium caused by thinning or loss of midline vaginal fascia. The other type of anterior vaginal prolapse – displacement – was attributed to pathologic detachment or elongation of the anterolateral vaginal supports to the arcus tendineus fasciae pelvis. It may occur unilaterally or bilaterally and often coexists with some degree of distension cystocele, with urethral hypermobility, or with apical prolapse. Rugal folds may or may not be preserved.
Another theory ascribes most cases of anterior vaginal prolapse to disruption or detachment of the lateral connective tissue attachments at the arcus tendineus fasciae pelvis, resulting in a paravaginal defect and corresponding to the displacement type discussed earlier. This was first described by White in 19095 and 1912,6 but disregarded until reported by Richardson in 1976.7 Richardson described transverse defects, midline defects, and defects involving isolated loss of integrity of pubourethral ligaments. Transverse defects were said to occur when the ‘pubocervical’ fascia separated from its insertion around the cervix, whereas midline defects represented an anteroposterior separation of the fascia between the bladder and vagina. A contemporary conceptual representation of vaginal and paravaginal defects is shown in Figure 70.1.8 There have been few systematic or comprehensive descriptions of anterior vaginal prolapse based on physical findings and correlated with findings at surgery to provide objective evidence for any of these theories of pathologic anatomy. In a study of 71 women with anterior vaginal wall prolapse and stress incontinence who underwent retropubic operations, DeLancey9 described
Figure 70.1. Three different defects can result in anterior vaginal wall prolapse. Lateral or paravaginal defects occur when there is a separation of the pubocervical fascia from the arcus tendineus fasciae pelvis, midline defects occur secondary to attenuation of fascia supporting the bladder base, and transverse defects occur when the pubocervical fascia separates from the vaginal cuff or uterosacral ligaments. (Reproduced from ref. 8 with permission.)
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paravaginal defects in 87% on the left and 89% on the right. The arcus tendineus fasciae pelvis were usually attached to the pubic bone but detached from the ischial spine for a variable distance. The pubococcygeal muscle was visibly abnormal with localized or generalized atrophy in over half of the women. Recent improvements in pelvic imaging are leading to a greater understanding of normal pelvic anatomy and the structural and functional abnormalities associated with prolapse. Magnetic resonance imaging (MRI) holds great promise, with its excellent ability to differentiate soft tissues and its capacity for multiplanar imaging. Further work is needed to correlate the different images with anatomy and histology under normal conditions and with pelvic support abnormalities. The pelvic organs, pelvic muscles, and connective tissues can be identified easily with MRI. Various measurements can be made that may be associated with anterior vaginal prolapse or urinary incontinence, such
as the urethrovesical angle, descent of the bladder base, the quality of the levator muscles, and the relationship between the vagina and its lateral connective tissue attachments. Aronson et al.10 used an endoluminal surface coil placed in the vagina to image pelvic anatomy with MRI, and compared four continent nulliparous women with four incontinent women with anterior vaginal prolapse. Lateral vaginal attachments were identified in all continent women. In Figure 70.2, the ‘posterior pubourethral ligaments’ (bilateral attachment of arcus tendineus fasciae pelvis to posterior aspect of the pubic symphyses) are clearly seen. In the two subjects with clinically apparent paravaginal defects, lateral detachments were evident (Fig. 70.3). Although this study involved only a small number of subjects, it provides the basis for further work in describing the anatomic abnormalities that accompany anterior vaginal prolapse and other abnormalities of pelvic support. This may ultimately guide the choice of surgical repair.
Figure 70.2. Axial T1-weighted image from a continent 38-year-old nulliparous woman, showing the connection of the anterior vaginal wall (v) to the posterior pubic symphysis (p) by the pubourethral ligaments (pul). The anterior vaginal wall and endopelvic fascia function as a sling or hammock for support of the urethra (u). o, Obturator internus muscle; r, rectum; l, levator ani musculature. (Reproduced from ref. 10 with permission.)
Figure 70.3. Axial T1-weighted image from a 57-yearold woman, para 5, with stress urinary incontinence. The paravaginal detachment (arrow) is seen at the level of the urethrovesical junction. v, anterior vaginal wall; p, posterior pubic symphysis; u, urethra; o, obturator internus muscle; c, endovaginal coil; r, rectum; l, levator ani musculature. (Reproduced from ref. 10 with permission.) 1011
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Anterior vaginal prolapse commonly coexists with urodynamic stress incontinence. Some features of pathophysiology may overlap, such as loss of anterior vaginal support with bladder-base descent and urethral hypermobility; other features, such as sphincteric dysfunction, may occur independent of vaginal and urethral support. The pathophysiology of stress incontinence is covered more fully in Chapter 11.
EVALUATION History When evaluating women with pelvic organ prolapse or urinary or fecal incontinence, attention should be paid to all aspects of pelvic organ support. The reconstructive surgeon must determine the specific sites of damage for each patient, with the ultimate goal of restoring both anatomy and function. Patients with anterior vaginal prolapse complain of symptoms directly related to vaginal protrusion or of associated symptoms such as urinary incontinence or voiding difficulty. Symptoms related to prolapse may include the sensation of a vaginal mass or bulge, pelvic pressure, low back pain, and sexual difficulty. Stress urinary incontinence commonly occurs in association with anterior vaginal prolapse. Voiding difficulty may result from advanced prolapse. Women may require vaginal pressure or manual replacement of the prolapse in order to accomplish voiding. Women may relate a history of urinary incontinence that has since resolved with worsening of their prolapse. This can occur with urethral kinking and obstruction to urinary flow; women in this situation are at risk for incomplete bladder emptying and recurrent or persistent urinary tract infections and for the development of de novo stress incontinence after the prolapse is repaired.
Physical examination The physical examination should be conducted with the patient in the lithotomy position, as for a routine pelvic examination. The examination is first performed with the patient supine. If physical findings do not correspond to symptoms or if the maximum extent of the prolapse cannot be confirmed, the woman is re-examined in the standing position. The genitalia are inspected, and if no displacement is apparent, the labia are gently spread to expose the vestibule and hymen. The integrity of the perineal body is evaluated, and the approximate size of all prolapsed
parts is assessed. A retractor or Sims speculum can be used to depress the posterior vagina to aid in visualizing the anterior vagina. After the resting examination, the patient is instructed to strain down forcefully or to cough vigorously. During this maneuver, the order of descent of the pelvic organs is noted, as is the relationship of the pelvic organs at the peak of straining. It may be possible to differentiate lateral defects, identified as detachment or effacement of the lateral vaginal sulci, from central defects, seen as midline protrusion but with preservation of the lateral sulci, by using a curved forcep placed in the anterolateral vaginal sulci directed towards the ischial spine. Bulging of the anterior vaginal wall in the midline between the forcep blades implies a midline defect; blunting or descent of the vaginal fornices on either side with straining suggest lateral paravaginal defects. Studies have shown that the physical examination technique to detect paravaginal defects is not particularly reliable or accurate. In a study by Barber et al.11 of 117 women with prolapse, the sensitivity of clinical examination to detect paravaginal defects was good (92%), yet the specificity was poor (52%) and, despite an unexpectly high prevalence of paravaginal defects, the positive predictive value was poor (61%). Less than two-thirds of women believed to have a paravaginal defect on physical examination were confirmed to possess the same at surgery. Another study by Whiteside et al.12 demonstrated poor reproducibility of clinical examination to detect anterior vaginal wall defects. Thus, the clinical value of determining the location of midline, apical, and lateral paravaginal defects remains unknown. Anterior vaginal wall descent usually represents bladder descent with or without concomitant urethral hypermobility. In 1.6% of women with anterior vaginal prolapse, an anterior enterocele mimics a cystocele on physical examination.13
Diagnostic tests After a careful history and physical examination, few diagnostic tests are needed to evaluate patients with anterior vaginal prolapse. A urinalysis should be performed to evaluate for urinary tract infection if the patient complains of any lower urinary tract dysfunction. If the patient’s estrogen status is unclear, a vaginal cytologic smear can be obtained to assess maturation index. Hydronephrosis occurs in a small proportion of women with prolapse; however, even if identified, it usually does not change management in women for whom surgical repair is planned.14 Therefore, routine imaging of the kidneys and ureters is not necessary.
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If urinary incontinence is present, further diagnostic testing is indicated to determine the cause of the incontinence. Urodynamic (simple or complex), endoscopic or radiologic assessments of filling and voiding function are generally indicated only when symptoms of incontinence or voiding dysfunction are present. Even if no urologic symptoms are noted, voiding function should be assessed to evaluate for completeness of bladder emptying. This procedure usually involves a timed, measured void, followed by urethral catheterization or bladder ultrasound to measure residual urine volume. In women with severe prolapse, it is important to check urethral function after the prolapse is repositioned. As demonstrated by Bump et al.,15 women with severe prolapse may be continent because of urethral kinking; when the prolapse is reduced, urethral dysfunction may be unmasked with occurrence of incontinence. A pessary, vaginal retractor or vaginal packing can be used to reduce the prolapse before office bladder filling or electronic urodynamic testing. If urinary leaking occurs with coughing or Valsalva maneuvers after reduction of the prolapse, the urethral sphincter is probably incompetent, even if the patient is normally continent. This is reported to occur in 17–69% of women with stage III or IV prolapse.15,16 In this situation, the surgeon should choose an anti-incontinence procedure in conjunction with anterior vaginal prolapse repair.16 If sphincteric incompetence is not present even after reduction of the prolapse, an anti-incontinence procedure is not indicated.
SURGICAL REPAIR TECHNIQUES Anterior colporrhaphy The objective of anterior colporrhaphy is to plicate the layers of vaginal muscularis and adventitia overlying the bladder (‘pubocervical fascia’) or to plicate and reattach the paravaginal tissue in such a way as to reduce the protrusion of the bladder and vagina. Modifications of the technique depend on how lateral the dissection is carried, where the plicating sutures are placed, and whether additional layers (natural or synthetic) are placed in the anterior vagina for extra support. The operative procedure begins with the patient supine, with the legs elevated and abducted and the buttocks placed just past the edge of the operating table. The chosen anesthetic has been administered, and one perioperative intravenous dose of an appropriate antibiotic may be given as prophylaxis against infection. The
abdomen, vagina, and perineum are sterilely prepped and draped, and a 16 Fr Foley catheter with a 5 ml balloon is inserted for easy identification of the bladder neck. If indicated, a suprapubic catheter is placed into the bladder. A weighted speculum is placed into the vagina. If a vaginal hysterectomy has been performed, the incised apex of the anterior vaginal wall is grasped transversely with two Allis clamps and elevated. Otherwise, a transverse or diamond-shaped incision is made in the vaginal mucosa near the apex. A third Allis clamp is placed about 1 cm below the posterior margin of the urethral meatus and pulled up. Additional Allis clamps may be placed in the midline between the urethra and apex. Hemostatic solutions (such as 0.5% lidocaine with 1:200,000 epinephrine) or saline may be injected submucosally, along the midline of the anterior vaginal wall, to decrease bleeding and to aid in dissection. The points of a pair of curved Mayo scissors are inserted between the vaginal epithelium and the vaginal muscularis, or between the layers of the vaginal muscularis, and gently forced upward while being kept half-opened/half-closed (Fig. 70.4). Countertraction during this maneuver is important to minimize the likelihood of perforation of the bladder. The vagina is then incised in the midline, and the incision is continued to the level of the midurethra. Alternatively, a scalpel can be used to make a midline anterior vaginal incision. As the vagina is incised, the edges are grasped with Allis or T-clamps and drawn laterally for further mobilization. Dissection of the vaginal flaps is then accomplished by turning the clamps back across the forefinger and incising the vaginal muscularis with a scalpel or Metzenbaum scissors, as shown in Figure 70.4c. An assistant maintains constant traction medially on the remaining vaginal muscularis and underlying vesicovaginal adventitia. This procedure is performed bilaterally until the entire extent of the anterior vaginal prolapse has been dissected; in general, the dissection should be carried further laterally with more advanced prolapse. The spaces lateral to the urethrovesical junction are sharply dissected toward the ischiopubic rami. It is also important to use sharp dissection to mobilize the bladder base from the vaginal apex as shown in Figure 70.5. In most cases, even if the patient does not suffer from urinary incontinence, plicating sutures at the urethrovesical junction should be placed to augment posterior urethral support and to ensure that stress incontinence, if not present at the time of operation, does not develop postoperatively. Vesical neck plication can also be used to treat mild stress urinary incontinence, but this is 1013
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a
b
Figure 70.5. Cystocele repair. Sharp dissection is used to mobilize the bladder base from the vaginal apex during anterior colporrhaphy.
c
d
Figure 70.4. Cystocele repair: (a) initial midline anterior vaginal wall incision; (b) the incision is extended to the level of the proximal urethra; (c) sharp dissection and traction on the bladder facilitate dissection of the bladder off the vaginal wall; (d) mobilization of the cystocele off the vaginal wall is completed. (Reproduced from ref. 8 with permission.)
probably only indicated in select women with very mild symptoms. Once the vaginal flaps have been completely developed, the urethrovesical junction can be identified visually or by pulling the Foley catheter downward until the bulb obstructs the vesical neck. Repair should begin at the urethrovesical junction, using No. 0 delayed absorbable or non-absorbable suture. The first plicating stitch is placed into the periurethral endopelvic fascia and tied (Fig. 70.6a). One or two additional stitches are placed to support the length of the urethra and urethrovesical junction.
After the stitches for vesical neck plication have been placed and tied, attention is turned to the anterior vaginal prolapse repair. In a standard anterior colporrhaphy, stitches using No. 2-0 or 0 delayed absorbable or nonabsorbable sutures are placed in the vaginal tissue (muscularis and adventitia) medial to the vaginal flaps and plicated in the midline without tension. Depending on the severity of the prolapse, one or two rows of plication sutures or a purse-string suture followed by plication sutures are placed (Fig. 70.6b). The vaginal epithelium is then trimmed from the flaps bilaterally, and the remaining anterior vaginal wall is closed with a running No. 3-0 subcuticular or locking suture. One modification of the standard repair is to extend the dissection and mobilization of the vaginal flaps laterally to the ischiopubic rami on each side. After the vesical neck plication has been performed, stitches are then placed laterally in the paravaginal tissue (lateral to the vaginal muscularis and adventitial layers, but not including the epithelium of the vaginal flaps). The paravaginal connective tissue is plicated in the midline under tension using No. 0 delayed absorbable or nonabsorbable sutures. This produces a firm bridge of tissue across the anterior vaginal space, but it also results in narrowing of the anterior vagina, which must be considered when planning a concomitant posterior colporrhaphy. The vaginal flaps are trimmed and closed as usual. Another modification involves the use of a prosthetic material to provide support in the anterior vagina. This can be done in several ways and the surgical techniques
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a
b
c
d
a
b
Figure 70.6. Cystocele repair. (a) Kelly plication sutures have been placed and tied, plicating the pubocervical fascia across the midline at the level of the bladder neck. (b) The bladder base has been plicated. Inset: Preferential support of the bladder neck when compared to the bladder base. (Reproduced from ref. 8 with permission.) continue to evolve. One modification is to place a piece of polyglactin 910 mesh into the fold of the imbricated bladder wall below the trigone and the apical portion of the anterior colporrhaphy. In a second modification, after the plication sutures have been placed and tied, the prosthetic layer is placed over the stitches and anchored in place at the lateral limit of the previous dissection, using interrupted stitches of No. 2-0 absorbable or non-absorbable suture. The anchor points are usually at or near the arcus tendineus fasciae pelvis or obturator fascia bilaterally, as shown in vure 70.7. Biologic materials that have been used include segments of rectus fascia, fascia lata, cadaveric fascia or other allograft or
Figure 70.7. Cystocele repair with mesh: (a) the bladder is dissected bilaterally and off the vaginal apex; (b) midline plication is completed; (c) after entering the left paravaginal space and exposing the arcus tendineus fasciae pelvis (white line), the prosthetic mesh is sewn to it; (d) the mesh is attached bilaterally and all sutures are tied, supporting the bladder. xenograft materials. Permanent (usually polypropylene) mesh may be used, although non-absorbable material carries a risk of infection or erosion, with need for subsequent revision or removal in 2–12% of cases (Table 70.1). A more recent innovative approach is to anchor an allograft, xenograft or polypropylene mesh without tension via strips placed through the obturator foramen with a special device (Perigee, American Medical Systems, Minneapolis, MN). This latter technique awaits study of safety and efficacy. Anti-incontinence operations are often performed at the same time as anterior vaginal prolapse repair to treat coexistent stress incontinence; sling placement may also improve the cure rate of the prolapse. Bladder neck suspension procedures (sling procedures or retropubic colposuspension) effectively treat mild anterior vaginal prolapse associated with urethral hypermobility and stress incontinence. More advanced anterior vaginal prolapse will not be treated adequately and, in these cases, anterior colporrhaphy should be performed, usually in conjunction with a midurethral sling. Surgical 1015
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Table 70.1.
Literature review of anterior vaginal wall prolapse repair with non-absorbable mesh*
Author (year)
Mesh
Nicita (1998)25
Polypropylene 23
Flood et al. (1998) 26
Julian (1996)
27
n
Follow-up (months)
Success rate (%)
Vaginal erosion
44
14
93.2
1 (2.3%)
Marlex
142
36
94.4
2 (2.1%)
Marlex
12
24
100
1 (8.3%)
100
1 (2.2%)
Mage (1999)
Mersuture
46
26
Migliari & Usai (1999)28
Mixed fiber†
15
23.4
93
0
Polypropylene
12
20.5
75
0
Polypropylene
18
1.5
100
Salvatore et al. (2002)
Polypropylene
32
17
87
4 (13%)
De Tayrac et al. (2005)31
Polypropylene
87
24
91.6
7 (8.3%)
29
Migliari et al. (2001)
30
Hardiman et al. (2000)
24
2 (11.1%)
* Definitions of success and surgical techniques vary. † 60% polyglactin 910 and 40% polyester.
judgment is required to perform the bladder plication tightly enough to reduce the anterior vaginal prolapse sufficiently, yet preserve enough mobility of the anterior vagina to allow adequate urethral suspension. If anterior colporrhaphy is combined with a sling procedure (midurethral or bladder neck), the cystocele should be repaired before the final tension is set for the sling. A midurethral sling, such as a tension-free vaginal tape (TVT) or transobturator sling, is best done through a separate midurethral incision after the cystocele repair is complete.
Vaginal paravaginal repair The aim of paravaginal defect repair for anterior vaginal prolapse is to reattach the detached lateral vagina to its normal place of attachment at the level of the arcus tendineus fasciae pelvis.17 This can be accomplished using a vaginal or retropubic approach. Retropubic paravaginal defect repair is discussed in Chapter 68, along with other retropubic procedures such as the Burch colposuspension. The preparation for vaginal paravaginal repair begins as for an anterior colporrhaphy. Marking sutures are placed on the anterior vaginal wall on each side of the urethrovesical junction, identified by the location of the Foley balloon after gentle traction is placed on the catheter (Fig. 70.8a). In patients who have had a hysterectomy, marking sutures are also placed at the vaginal apex. If a culdeplasty is being performed, the stitches are placed but not tied until completion of the paravaginal repair and closure of the anterior vaginal wall. As for anterior colporrhaphy, vaginal flaps are developed by incising the vagina in the midline and dissecting the vaginal mus-
cularis laterally. The dissection is performed bilaterally until a space is developed between the vaginal wall and retropubic space. Blunt dissection using the surgeon’s index finger is used to extend the space anteriorly along the ischiopubic rami, medially to the pubic symphysis, and laterally toward the ischial spine. If the defect is present and dissection is occurring in the appropriate plane, one should easily enter the retropubic space, visualizing retropubic adipose tissue. The ischial spine can then be palpated on each side. The arcus tendineus fasciae pelvis coming off the spine can be followed to the back of the symphysis pubis (Fig. 70.8b). After dissection is complete, midline plication of vaginal muscularis can be performed, either at this point or after placement and tying of the paravaginal sutures. On the lateral pelvic sidewall, the obturator internus muscle and the arcus tendineus fasciae pelvis are identified by palpation and then visualization. Retraction of the bladder and urethra medially is best accomplished with a Breisky–Navratil retractor, and posterior retraction is provided with a lighted right-angle retractor. Using No. 0 non-absorbable suture, the first stitch is placed around the tissue of the white line just anterior to the ischial spine. A Capio device works well to facilitate suture placement. If the white line is detached from the pelvic sidewall or clinically not felt to be durable, then the attachment should be to the fascia overlying the obturator internus muscle. The placement of subsequent sutures is aided by placing tension on the first suture. A series of four to six stitches are placed and held, working anteriorly along the white line from the ischial spine to the level of the urethrovesical junction (Fig. 70.8c). Starting with the most anterior stitch, the surgeon picks up the edge of the periurethral tissue
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(vaginal muscularis or pubocervical fascia) at the level of the urethrovesical junction and then tissue from the undersurface of the vaginal flap at the previously marked sites. Subsequent stitches move posteriorly until the last stitch closest to the ischial spine is attached to
the vagina nearest the apex, again using the previously placed marking sutures for guidance. Stitches in the vaginal wall must be placed carefully to allow adequate tissue for subsequent midline vaginal closure. After all the stitches are placed on one side, the same procedure
a b
c
d
Figure 70.8. Technique of vaginal paravaginal repair. (a) Marking sutures are placed at the bladder neck and vaginal apex. A midline anterior vaginal wall incision is made. (b) The bladder is dissected bilaterally and off the vaginal apex. Midline plication is performed. (c) Midline plication is completed; obvious bilateral paravaginal defects are present. (d) The bladder is retracted medially and numerous sutures are passed through the arcus tendineus fasciae pelvis (white line). 1017
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e
f
Figure 70.8. (e) Sutures are then passed through the detached pubocervical or endopelvic fascia. (f) Sutures are passed through the inside of the vaginal wall, thus completing the three-point closure. (Reproduced from ref. 8 with permission.) is carried out on the other side. The stitches are then tied in order from the urethra to the apex, alternating from one side to the other. This repair is a three-point closure involving the vaginal epithelium, vaginal muscularis and endopelvic fascia (pubocervical fascia), and lateral pelvic sidewall at the level of the arcus tendineus fasciae pelvis (Fig. 70.8d). There must be tissue-to-tissue approximation between these structures. Suture bridges must be avoided by careful planning of suture placement. Vaginal tissue should not be trimmed until all the stitches are tied. As previously stated, if not already performed, vaginal muscularis can then be plicated in the midline with several interrupted stitches using No. 0 delayed absorbable suture. The vaginal flaps are trimmed and closed with a running subcuticular or interlocking delayed absorbable suture.
the vagina is closed with running delayed absorbable suture. The vaginal cuff is then repaired according to the surgeon’s preference. This procedure has no effect on the bladder neck or urethral support, and care should be taken not to unmask latent stress incontinence by treating anterior vaginal prolapse without simultaneous urethral suspension.
Abdominal cystocele repair
RESULTS
Abdominal repair of mild anterior vaginal prolapse can be accomplished at the time of abdominal hysterectomy.18 After the cervix has been amputated from the vagina, the bladder is dissected off the anterior vaginal wall, nearly to the level of the ureters. A full-thickness midline wedge of anterior vaginal wall is excised, and
The main indication for surgical repair of anterior vaginal prolapse is to relieve symptoms when they exist, or as part of a comprehensive pelvic reconstructive procedure for multiple sites of pelvic organ prolapse with or without urinary incontinence. Few studies have addressed the long-term success of surgical treatments for anterior vaginal prolapse. Most published studies are uncontrolled
Cystoscopy Cystoscopy is usually performed after cystocele repair, especially if slings or apical suspension procedures are also being performed. The purpose is to ensure that no sutures or mesh have been placed in the bladder and to verify patency of both ureters.
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series. Definitions of recurrence vary and sometimes are not stated, and loss to follow-up is often not declared. In our review of surgical techniques for the correction of anterior vaginal prolapse,2 reported failure rates ranged from zero to 20% for anterior colporrhaphy and from 3 to 14% for paravaginal repair. Weber et al.19 studied three variations of anterior colporrhaphy using a prospective randomized study design and a very strict definition of success (Aa and Ba points at –3 or –2 cm; Stage 0 or I). Standard anterior colporrhaphy resulted in 30% of patients with a optimal or satisfactory anatomic result; anterior colporrhaphy with polyglactin 910 mesh overlay had 42% optimal or satisfactory result, and ultralateral plication under tension a 46% optimal or satisfactory result. No difference was seen in anatomic or functional outcomes and most patients reported satisfaction with their symptom improvement. In another randomized controlled trial using a different staging system, Sand et al.20 noted fewer recurrent cystoceles when polyglactin 910 mesh was incorporated into the imbrication of the repair. Prosthetic augmentation of cystocele repair is a promising though evolving innovation. There are many variations in techniques and materials used but there are few quality studies to date; one technique variation is shown in Figure 70.7. Biologic prosthetic materials placed over a midline cystocele plication as a simple overlay and anchored laterally has been carried out but does not appear to offer significant lasting improvement over standard repair.21 However, anchoring the mesh to the obturator fascia, the addition of suburethral slings,22 and anchoring of the prosthesis to the apical portion of the repair may significantly improve long-term results. Placement of non-absorbable mesh into an anterior vaginal prolapse repair is a promising, though more controversial, variation. Polypropylene mesh has limited foreign body reaction in general and is probably the best choice. Technique variations include mesh overlays, modified four-corner attachments, transobturator attachments, and anterior flaps as part of an apical mesh procedure. Cure rates appear high (see Table 70.1) but comparative trials with more traditional sutured repairs have not been undertaken. Vaginal mesh erosions continue to be a problem; they occur in 2.1–13% of cases,23,24 a significant number of which require re-operation for mesh removal. Creation of thicker vaginal flaps with an attached fibromuscularis may decrease the mesh erosion rate. Anterior colporrhaphy with bladder neck plication may be effective for treatment of mild stress incontinence associated with urethral hypermobility. However,
the cure rate after 1 year is only about 60% and it is less effective than Burch colposuspension and most slings.32 These findings hold irrespective of the coexistence of pelvic organ prolapse. However, suburethral plication may be satisfactory for some women with mild symptoms of stress incontinence who do not desire a sling or who have significant preoperative voiding dysfunction, or for elderly or medically compromised women in whom surgical risk must be minimized. For women with potential or occult stress incontinence in association with advanced prolapse, Meschia et al. reported that placement of a TVT results in significantly higher objective continence rates postoperatively compared to suburethral plication (92% versus 56%; p<0.01).16 Thus, placement of a TVT or a transobturator sling is recommended for all women with potential stress incontinence, excepting perhaps for very elderly patients and those with significant voiding dysfunction. Paravaginal defect repair using the transvaginal approach results in excellent anatomic cure of anterior vaginal prolapse.17 However, it has been used infrequently as an isolated procedure for treatment of stress urinary incontinence. Evidence suggests that it has less than satisfactory results when used in this capacity. In a report by Mallipeddi et al.,33 57% of subjects with anterior vaginal prolapse and stress incontinence treated with a vaginal paravaginal repair and bladder neck plication had persistent urinary incontinence after an average of 1.6 years of follow-up. Thus, while the vaginal paravaginal repair is safe and relatively effective for correction of anterior vaginal prolapse, it has limited applicability in the surgical correction of stress incontinence. Women with advanced anterior vaginal prolapse, with or without stress incontinence, often have other abnormal bladder symptoms such as urgency, urge incontinence, and voiding difficulty. In a study of surgical repair of large cystoceles by Gardy et al.,34 stress incontinence resolved in 94%, urge incontinence in 87%, and significant residual urine (>80 ml) in 92% of patients 3 months after needle suspension procedures and anterior colporrhaphy. Approximately 5% of patients developed a recurrent anterior vaginal prolapse, and 8% developed a recurrent enterocele after an average of 2 years of follow-up. Risk factors for failure of anterior vaginal prolapse repair have not been specifically studied. Vaginal prolapse recurs with increasing age and length of followup, but the actual frequency is unknown. Recurrence of anterior prolapse is more likely to occur with more severe initial prolapse35 and probably with transvaginal, compared to abdominal, repairs.36 Recurrence may represent a failure to identify and repair all support defects, 1019
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or weakening, stretching or breaking of patients’ tissues, as occurs with advancing age and after menopause. Sacrospinous ligament suspension of the vaginal apex, with exaggerated retrosuspension of the vagina, may predispose patients to recurrence of anterior vaginal prolapse. Other characteristics that may increase chances of recurrence are genetic predisposition, subsequent pregnancy, heavy lifting, chronic pulmonary disease, smoking, and obesity.
COMPLICATIONS Intraoperative complications are uncommon with anterior vaginal prolapse repair. Excessive blood loss may occur, requiring blood transfusion, or a hematoma may develop in the anterior vagina; this is probably more common after vaginal paravaginal repair than anterior colporrhaphy.37 The lumen of the bladder or urethra may be entered in the course of dissection. Accidental cystotomy should be repaired in layers at the time of the injury. After repair of cystotomy, the bladder is generally drained for 7–14 days to allow adequate healing. Ureteral damage or obstruction occurs rarely (0–2%),38 usually with very large cystoceles or with apical prolapse. Other rare complications include intravesical or urethral suture placement (and associated urologic problems) and fistulae, either urethrovaginal or vesicovaginal. If permanent sutures or mesh material are used in the repair, erosion, draining sinuses or chronic areas of vaginal granulation tissue can result. The incidence of these complications is unknown but may be as high as 13%.24 Urinary tract infections are common (especially with concurrent catheter usage), but other infections such as pelvic or vaginal abscesses are less common. Voiding difficulty can occur after anterior vaginal prolapse repair. In our hands, the average time to adequate voiding after cystocele repair with suburethral plication is 9 days.39 This problem may occur more often in women with subclinical preoperative voiding dysfunction. Treatment is bladder drainage or intermittent self-catheterization until spontaneous voiding resumes, usually within 6 weeks. Sexual function may be positively or negatively affected by vaginal operations for anterior vaginal prolapse. Haase and Skibsted40 studied 55 sexually active women who underwent a variety of operations for stress incontinence or genital prolapse. Postoperatively, 24% of the patients experienced improvement in their sexual satisfaction, 67% experienced no change, and 9% experienced deterioration. Improvement often resulted from cessation of urinary incontinence. Deterioration was always caused by dyspareunia after
posterior colporrhaphy. These authors concluded that the prognosis for an improved sexual life is good after surgery for stress incontinence, but that posterior colpoperineorrhaphy causes dyspareunia in some patients. The current popularity of synthetic or allograft mesh to augment vaginal prolapse repairs could improve sexual function if cure rates improve, or could worsen function if vaginal stiffness, mesh erosions or draining sinuses result. More data with careful follow-up after surgery are needed.
REFERENCES 1. Bump RC, Mattiasson A, Bø K et al. The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 1996;175:10–17. 2. Weber AM, Walters MD. Anterior vaginal prolapse: review of anatomy and techniques of surgical repair. Obstet Gynecol 1997;89:311–18. 3. DeLancey JOL. Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 1992;166:1717–28. 4. Nichols DH, Randall CL. Vaginal Surgery, 4th ed. Baltimore: Williams and Wilkins, 1996. 5. White GR. A radical cure by suturing lateral sulci of vagina to white line of pelvic fascia. JAMA 1909;21:1707–10. 6. White GR. An anatomical operation for the cure of cystocele. Am J Obstet Dis Women Child 1912;65:286–90. 7. Richardson AC, Lyon JB, Williams NL. A new look at pelvic relaxation. Am J Obstet Gynecol 1976;126:568–73. 8. Karram MM. Vaginal operations for prolapse. In: Baggish MS, Karram MM (eds) Atlas of Pelvic Anatomy and Gynecologic Surgery. Philadelphia: Saunders, 2001. 9. DeLancey JO. Fascial and muscular abnormalities in women with urethral hypermobility and anterior vaginal wall prolapse. Am J Obstet Gynecol 2002;187:93–8. 10. Aronson MP, Bates SM, Jacoby AF et al. Periurethral and paravaginal anatomy: an endovaginal magnetic resonance imaging study. Am J Obstet Gynecol 1995;173:1702–8. 11. Barber MD, Cundiff GW, Weidner AC et al. Accuracy of clinical assessment of paravaginal defects in women with anterior vaginal wall prolapse. Am J Obstet Gynecol 1999;181:87–90. 12. Whiteside JL, Barber MD, Paraiso MF et al. Clinical evaluation of anterior vaginal wall support defect: interexaminer and intraexaminer reliability. Am J Obstet Gynecol 2004;191:100–4. 13. Tulikangas PK, Lukban JC, Walters MD. Anterior enterocele: a report of three cases. Int Urogynecol J 2004;15:350–2. 14. Beverly CJ, Walters MD, Weber AM et al. Prevalence of hydronephrosis in women undergoing surgery for pelvic organ prolapse. Obstet Gynecol 1997;90:37–41.
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15. Bump RC, Fantl JA, Hurt WG. The mechanism of urinary continence in women with severe uterovaginal prolapse: results of barrier studies. Obstet Gynecol 1988;72:291–5. 16. Meschia M, Pifarotti P, Spennacchio M et al. A randomized comparison of tension-free vaginal tape and endopelvic fascia plication in women with genital prolapse and occult stress urinary incontinence. Am J Obstet Gynecol 2004;190:609–13. 17. Shull BL, Benn SJ, Kuehl TJ. Surgical management of prolapse of the anterior vaginal segment: an analysis of support defects, operative morbidity, and anatomic outcome. Am J Obstet Gynecol 1994;171:1429–39. 18. Macer GA. Transabdominal repair of cystocele, a 20year experience, compared with the traditional vaginal approach. Am J Obstet Gynecol 1978;131:203–6.
approach in the cure of genital prolapse.] Gynecol Obstet Biol Reprod (Paris) 1999;28:825. 28. Migliari R, Usai E. Treatment results using a mixed fiber mesh in patients with grade IV cystocele. J Urol 1999;161:1255–8. 29. Migliari R, De Angelis M, Madeddu G et al. Tension-free vaginal mesh repair for anterior vaginal wall prolapse. Eur Urol 200l;38:151–5. 30. Hardiman P, Oyawoye S, Browning J. Cystocele repair using polypropylene mesh [abstract]. Br J Obstet Gynaecol 2000;107:825. 31. de Tayrac R, Gerviase A, Chauveaud A et al. Tension-free polypropylene mesh for vaginal repair of anterior vaginal wall prolapse. J Reprod Med 2005;50:75–80.
19. Weber AM, Walters MD, Piedmonte MA et al. Anterior colporrhaphy: a randomized trial of three surgical techniques. Am J Obstet Gynecol 2001;185:1299–1306.
32. Glazener CMA, Cooper K. Anterior vaginal repair for urinary incontinence in women (Cochrane Review). In: The Cochrane Library, Issue 3, 2002. Oxford: Update Software.
20. Sand PK, Koduri S, Lobel RW et al. Prospective randomized trial of polyglactin 910 mesh to prevent recurrence of cystoceles and rectoceles. Am J Obstet Gynecol 2001;184:1357–62.
33. Mallipeddi PK, Steele AC, Hohli N et al. Anatomic and functional outcome of vaginal paravaginal repair in the correction of anterior vaginal prolapse. Int Urogynecol J 2001;12:83–8.
21. Gandhi S, Kwon C, Goldberg RP et al. A randomized controlled trial of fascia lata for the prevention of recurrent anterior vaginal wall prolapse [abstract]. Neurourol Urodyn 2004;23:558. 22. Goldberg RP, Koduri S, Lobel RW et al. Protective effect of suburethral slings on postoperative cystocele recurrence after reconstructive pelvic operation. Am J Obstet Gynecol 2001;185:1307–12. 23. Flood CG, Drutz HP, Waja L. Anterior colporrhaphy reinforced with Marlex mesh for the treatment of cystoceles. Int Urogynecol J 1998;9:200–4. 24. Salvatore S, Soligo M, Meschia M et al. Prosthetic surgery for genital prolapse: functional outcome [abstract]. Neurourol Urodyn 2002;21:296–7. 25. Nicita G. A new operation for genitourinary prolapse. J Urol 1998;160:741–5. 26. Julian TM. The efficacy of Marlex mesh in the repair of severe, recurrent vaginal prolapse of the anterior midvaginal wall. Am J Obstet Gynecol 1996;175:1472–5. 27. Mage P. [Interposition of a synthetic mesh by vaginal
34. Gardy M, Kozminski M, DeLancey J et al. Stress incontinence and cystoceles. J Urol 1991:145:1211–3. 35. Whiteside JL, Weber AM, Meyn LA et al. Risk factors for prolapse recurrence after vaginal repair. Am J Obstet Gynecol 2004;191:1533–8. 36. Maher CF, Qatawneh AM, Dwyer PL et al. Abdominal sacral colpopexy or vaginal sacrospinous colpopexy vaginal vault prolapse: a prospective randomized study. Am J Obstet Gynecol 2004;190:20–6. 37. Young SB, Daman JJ, Bony LG. Vaginal paravaginal repair: one-year outcomes. Am J Obstet Gynecol 2001;185:1360–6. 38. Kwon CH, Goldberg RP, Koduri S et al. The use of intraoperative cystoscopy in major vaginal and urogynecologic surgeries. Am J Obstet Gynecol 2002;187:1466–72. 39. Kobak WH, Walters MD, Piedmonte MR. Determinants of voiding after three types of incontinence surgery. Obstet Gynecol 2001;97:86–91. 40. Haase P, Skibsted L. Influence of operations for stress incontinence and/or genital descensus on sexual life. Acta Obstet Gynecol Scand 1988;67:659–61.
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71 Enterocele Kaven Baessler, Bernhard Schuessler
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Definition anD scope of an enterocele The term enterocele is derived form of enter (intestine) and cele (hernia), i.e. a herniation of the bowel or a hernial tumor containing bowel. In general, a hernia occurs when a rupture in the smooth muscle or connective tissue allows a bodily structure to protrude. An enterocele is usually referred to as a herniation through or into the vagina, typically as a posterior enterocele which develops in the rectovaginal space (pouch of Douglas, or cul-desac). The anterior enterocele in the vesicovaginal space is a rare entity. An enterocele is a form of pelvic organ prolapse: bowel is protruding into the vagina. Why and how this happens are etiologic and pathophysiologic issues which are illustrated in this chapter. Surgical treatment of an enterocele is often concurrent with, or identical to, operations for vaginal vault prolapse. Preventive and therapeutic procedures will be described.
anatomy, etiology, Defects anD pathophysiology normal anatomy The important anatomic structures with regard to enterocele formation are consistent with normal pelvic organ support mechanisms. An enterocele develops in the pouch of Douglas; therefore, the pouch of Douglas is an anatomic structure that plays an imperative and probably predisposing part. The pouch of Douglas is normally closed and does not contain intestine or omentum. In anatomy textbooks (e.g. Gray’s Anatomy), the extent of the pouch of Douglas has traditionally been described as 2–3 cm below the uterosacral ligaments. Histologic studies by Uhlenhuth and colleagues have demonstrated that, in the fetus, the pouch of Douglas 1 may extend to the perineal body. The consecutive fusion of the anterior and posterior peritoneum forms the rectovaginal septum and determines the depth of the pouch of Douglas.1–3 According to Uhlenhuth, the rectovaginal septum is distinguishable from the fascial capsule of the vagina and rectum. In contrast to anatomy textbooks, recent in vivo intra-abdominal measurements of the depth of the pouch of Douglas in young nulliparous women revealed considerable variations, with 25–75% of the posterior vaginal wall 4 covered with peritoneum. The mean depth of the pouch of Douglas was 49% of vaginal length in nulliparas, 46% in parous women and was significantly deeper (72%) in patients with posterior vaginal wall
prolapse. The mean vaginal length was 10 cm. Age and parity did not have an influence. It would appear that a deep pouch of Douglas is frequently present in young nulliparous women without pelvic organ prolapse, which implies a congenital variation and 4 predisposition. A sophisticated concept of normal pelvic organ support accentuates the imperative role of several factors, including integrity of the anterior and posterior endopelvic fasciae with intact attachments as well as normal tone, position, and functionality of the levator ani muscle. Normal pelvic floor muscle and fascial structures are required to hold the perineum in place and ensure normal bladder, bowel, and sexual function. It is apparent that fascial defects in the three levels of vaginal support and the posterior compartment may con56 tribute to pelvic organ prolapse including enteroceles. , Normal pelvic floor tone and position are essential for the nearly horizontal axis of the vagina which in turn is necessary to allow for a normal pelvic floor protecting intra-abdominal pressure distribution. These elements may well have an important role in keeping the pouch of Douglas closed.
the deep pouch of Douglas as a predisposing factor Principally, a posterior enterocele develops in the pouch of Douglas which is normally closed. Figure 71.1 illustrates the different characteristics in the development of enteroceles. Intra-abdominal measurements of the depth of the pouch of Douglas have shown that in women with posterior vaginal wall and anterior rectal wall prolapse the pouch of Douglas is significantly 4 deeper and may reach the level of the perineal body. In addition, the anatomy of the pouch of Douglas is considerably different, which is a recognized feature in some studies. In women with severe pelvic organ prolapse, a large or voluminous rectovaginal pouch was a consistent anatomic finding requiring obliteration during pelvic reconstructive surgery.7–9 Apart from a mobile vaginal axis and a dehiscence of the levator hiatus, French authors reported a ‘grande fosse pelvi-périnéale’ – a large pelvic pouch – to be a principal lesion in 10 women with enteroceles. Their anatomic observations included a deep and wide rectovaginal pouch and a rectosigmoid colon, which closely follows the sacral curve (Fig. 71.2). Although different positions and courses of 11 the sigmoid colon and its mesentery are known, systematic descriptions in women with pelvic organ prolapse are scarce. Baessler and Schuessler found 64% of women with enteroceles and all women with anterior
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Figure 71.1. The pouch of Douglas – ‘normal’ depth, deep, grande fosse pelvienne. (a) The ‘normal’ pouch of Douglas covers approximately one-third of the posterior vaginal wall and is closed. (b) Deep pouch of Douglas: peritoneum covers the posterior vaginal wall down to the level of the levator ani. Normal pelvic floor support prevents opening and exposure of the pouch of Douglas. (c) An enterocele has developed in the rectovaginal space displacing the posterior vaginal wall. The vaginal and rectal course is more vertical and the pelvic floor position is lower, leaving the pouch of Douglas unprotected. (d) Apical enterocele with separation of the anterior and posterior endopelvic fascia after hysterectomy. (e) Enterocele after Burch colposuspension with ventral displacement of anterior compartment; the pouch of Douglas was not protected. (f) Enterocele bulging primarily into the rectum; anterior rectal wall procidentia; intact posterior endopelvic fascia. rectal wall procidentia to have these features, termed a ‘grande fosse pelvienne’. A grande fosse pelvienne was also present in six of 43 women (14%) in the control group who did not have pelvic organ prolapse; three were nulliparous.12 Given these findings, it seems reasonable to regard a deep pouch of Douglas as a risk factor for enterocele formation. However, a deep pouch of Douglas does not necessarily result in an enterocele; an enterocele can only develop when other factors open and expose the (deep) pouch of Douglas.
the vaginal axis
Figure 71.2. Laparoscopic view of a grande fosse pelvienne: note the deep and wide pouch of Douglas, the lack of prominent uterosacral ligaments and the rectal course close to the sacrum with a short mesentery.
In a woman with normal pelvic organ support, the pouch of Douglas is closed, irrespective of its depth, and lies nearly horizontally between the levator plate and the vagina.13–15 A recent magnetic resonance imaging (MRI) study measured the mean levator–vaginal angle with a horizontal line at 35–53 degrees in different ethnic nulliparous populations.16 It is known that operations that change the vaginal axis can lead to increased prolapse in the ‘unprotected’ area. This is true for the higher inci1025
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dence of cystoceles after sacrospinous fixations where the position of the vagina is more posterior and also for the considerable rate of recto- and enteroceles after Burch colposuspensions or ventrofixations where the vagina is displaced anteriorly. A further process that changes the vaginal axis is excessive perineal descent (or descending perineum syndrome) which is often seen clinically in women with significant posterior vaginal wall prolapse (Fig. 71.3). A deep pouch of Douglas is likely to accentuate the process of enterocele development once the vaginal axis is changed.
some of which do not substantiate the concept of a fascia between rectum and vagina. However, it might simply be a question of definition: fascia is connective tissue, usually with smooth muscle cells, and it might also contain fatty or areolar tissue18 (Fig. 71.4). Whether the fascia is part of the vagina or rectum or whether it is a separate structure is of scientific but not clinical value. Fascia in the clinical sense means connective tissue that has tensile strength and is strong enough to hold sutures and support the underlying organs.
the endopelvic fascia
This syndrome has been described by colorectal surgeons as a ‘ballooning’ of the perineum during straining (see Fig. 71.3).19 Apart from bowel symptoms which can be similar to complaints of patients with rectoceles or enteroceles, excessive perineal descent of more than 2 cm (measured in relation to the ischial tuberosities) is seen more frequently in women with posterior vaginal wall prolapse.20 Solitary rectal ulcer, rectal prolapse, and intussusception are common concomitant findings.20,21 The etiology is unclear but reduced pelvic floor tone22 with insufficient perineal and endopelvic fascial attachment, as well as a deep pouch of Douglas and sigmoid colon elongation, have been discussed.
The integrity of the anterior and posterior endopelvic fasciae and their attachments is essential for normal pel6 vic organ support. A defect in the endopelvic fascia or insufficiency is necessary for an enterocele to protrude. However, an intact endopelvic fascia might prevent the enterocele bulging into the vagina, but not into the rectum where it causes anterior rectal wall procidentia. It is not entirely clear whether the endopelvic fascia is identical to the rectovaginal septum as the latter can be rather short, depending on the depth of the pouch of Douglas. Whole-thickness biopsies of the leading edge of radiologically proven enteroceles showed that in none of the examined 13 women was the vaginal epithelium in direct contact with the perineum and all had a well-defined vaginal wall muscularis.17 These findings add to the ongoing controversy on whether ‘fascia’ exists or not. It has been suggested that it is a structure that is artificially created during surgical dissection. This debate is complicated by inconsistent histologic studies,
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the descending perineum syndrome
pulsion, traction, sliding, true and congenital: concepts of enterocele development There are many different concepts and each one of them might be true in the individual patient. The idea to find a one-fits-all theory is probably in vain. Enteroceles may develop as a true hernia with a hernial sac and neck. A
Figure 71.3. Excessive perineal descent. Nearly normal position of the perineum at rest (a) but a ‘ballooning’ of the perineum on straining (b). This patient had a large rectoenterocele that did not protrude outside the introitus.
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rectal prolapse Colorectal surgeons view prolapse with a different attitude but have similar problems defining the etiology of rectal prolapse which might originate from the pouch of Douglas.25 Altemeier et al. described three types: type 1 is a false prolapse due to mucosal redundancy, type 2 is an intussusception without an association with the pouch of Douglas, and type 3 is a sliding hernia of the rectovaginal pouch.26 Enteroptosis and elongation of the rectosigmoid colon are considered contributing factors.27 Similar to vaginal enteroceles, type 3 rectal prolapse develops in the pouch of Douglas and basically is an enterocele bulging into the rectum, sometimes termed anterior rectal wall prolapse (see Fig. 71.1f). Figure 71.4. Mallory-trichrome stain of a biopsy taken from the tissue used in posterior vaginal wall repairs. The biopsy site was approximately 2 cm below the ischial spine. This stain is used to differentiate fibrous tissue (green) and smooth muscle (red). Note the amount of smooth muscle, organized connective tissue and areolar tissue. (With permission from Dr Christopher Maher, Auchenflower, Australia.) defect in the endopelvic fascia is then a prerequisite. It is argued that a traction enterocele is accompanied by loss of pelvic organ support14 and a greater vault descent with normal anatomic connections between the pouch of Douglas and vagina.23,24 In contrast, according to Nichols and Genadry,14 a pulsion enterocele is secondary to increased abdominal pressure whereas Zacharin states that a pulsion enterocele occurs as a late complication of pelvic surgery (e.g. hysterectomy) and is associated with a large rectovaginal pouch.23 However, Zacharin is convinced that the depth of the pouch of Douglas has no bearing on enterocele development. He considers levator incompetence and relaxation of the fascial support to be the primary defects. Nichols and Genadry describe iatrogenic enteroceles as a sequela of operations that alter the vaginal axis (e.g. Burch colposuspension) and congenital enteroceles which are associated with an ‘unusually’ deep pouch of Douglas (see Fig. 71.1e). In theory, an enterocele can only develop when important anatomic factors change: the vagina becomes more vertical and the (deep) pouch of Douglas opens, or the pubocervical and rectovaginal fasciae are separated. Whether a discrete defect in the endopelvic fascia is also required remains a topic for discussion. Therefore, Zacharin’s observation of a common deep pouch of Douglas in the Chinese female only corroborates the above: their pelvic floor status including tone and support prevents an exposure of the rectovaginal pouch.
further factors Old textbooks often quote other factors that might contribute to enterocele formation. Apart from established confounders for pelvic organ prolapse such as aging, obesity, constipation with excessive defecation straining, connective tissue diseases and parity, malnutrition – particularly in times of war – is mentioned.28
epiDemiology The prevalence of enteroceles is inseparable from the prevalence of other types of pelvic organ prolapse. Isolated enteroceles usually occur after pelvic surgery. The classic example is the development of enteroceles after Burch colposuspension in up to 32% of patients.29–31 It is also recognized that enteroceles and rectal prolapse frequently coexist with other defects of pelvic floor support.32–34 Specific data on enteroceles from women in the community are scarce. In a prevalence study of 639 women aged 45–85 years using the pelvic organ prolapse quantification of the International Continence Society, 22% had no prolapse at all, 37% had stage 1, 29% had stage 2, 9% had stage 3, and 3% had complete eversion.35
symptoms As with any other type of pelvic organ prolapse, an enterocele can cause prolapse symptoms, including the feeling of a bulge and a dragging sensation, and can interfere with bladder, bowel, and sexual function. Unlike a cystocele or rectocele, an enterocele does not appear to cause any stereotypical and pathognomonic symptoms, and very often symptoms cannot be distinguished from those of any coexisting pelvic organ prolapse. Some women primarily complain of rectal symptoms such as fullness 1027
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and incomplete or difficult bowel emptying; however, in others the prolapse symptoms are predominant.36 There might be dyschezia and a frequent, unproductive urge to defecate. Partial or complete obstruction of the urethra by the enterocele might result in voiding difficulties or reten37,37 tion. Dyspareunia, ‘slackness at intercourse’, vaginal dryness, and coital incontinence are frequently reported 38 by women with pelvic organ prolapse. Mainly a complication of previous pelvic floor surgery and hysterectomy, vaginal rupture and evisceration have been reported in women with enteroceles.40
clinical assessment anD investigations Vaginal and rectal examination with special attention to the endopelvic fascia is probably capable of identifying most enteroceles. Defects in the endopelvic fascia and their location with diminished vaginal rugae are a clue (Fig. 71.5). Simultaneous bimanual examination of the tissues between vagina and rectum under straining or in the standing position usually helps. An enterocele can be located in the anterior vaginal wall where it divides the pubocervical fascia or in the posterior vaginal wall, or it might separate the anterior and posterior endopelvic fasciae at the vaginal vault (apical enterocele). Occasionally peristalsis of the intestine bulging into the vagina establishes the diagnosis. If in doubt, and a diagnosis is necessary before an intraoperative evaluation to ascertain the presence or absence of an enterocele, radiologic assessment is the investigation of choice. Viscerography or fluoroscopic imaging includes the opacification of bladder, rectum, and vagina with con-
trast medium. An additional barium meal will show the small bowel. Ideally, the investigation is performed dynamically during straining or coughing and comprises defecography. The bowel evacuation gives room and is crucial for some enteroceles to descend. It will also give further information on bowel emptying, rectal prolapse or intussusception,41 although there are great variations of ‘normal’ findings. Shorvon et al. demonstrated that rectoceles and intussusception are frequently present in young and asymptomatic women.42 It is therefore most valuable when the clinician performs the radiologic investigations and interprets the findings in context with the symptoms. With the advance of dynamic defecation MRI, we now have an excellent method to evaluate pelvic floor dynamics. However, there are major disadvantages: it is expensive, not widely available and, at present, is performed in the supine position only. Defecation in this situation might be impossible for some patients. However, the images obtained are remarkable and usually provide an accurate diagnosis (Fig. 71.6).43 The improving three-dimensional (3D) ultrasound technology can also produce astounding images, especially when acquired as real-time sonography (4D). Although limited in the evaluation of structures located more proximally, it may provide information on fascial defects and also on pelvic floor dynamics. Even with conventional two-dimensional perineal ultrasound, it is still possible to identify an enterocele. Rectal ultrasound can also be helpful; sonographic diagnosis of an enterocele was confirmed intraoperatively in 27 of 29 cases.44
prevention of enteroceles Theoretically, obliteration of the pouch of Douglas and maintaining a normal vaginal axis should prevent enteroceles from developing. Controlled studies assessing prevention of enteroceles are scarce. Reattachment of the uterosacral ligaments to the vaginal vault during hysterectomy has long been advocated and several techniques are widely used. In a randomized controlled trial undertaken at the time of hysterectomy, Cruikshank and Kovac compared three available methods to prevent an enterocele:45
• Obliteration of the pouch of Douglas by suturing the • Figure 71.5. rugae.
A rectoenterocele with diminished vaginal
•
uterosacral ligaments in the midline, called a vaginal Moschcowitz-type operation; A McCall-type culdoplasty where the uterosacral ligaments are plicated and attached to the vaginal vault and the sutures externalized; Closing of the peritoneum with a purse-string suture.
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Up to 3 months postoperatively all procedures were equally successful (100%). After 3 years, the McCall-type method was found to be superior in terms of enterocele prevention; none of these 32 patients developed a symptomatic enterocele.45 The prevention of an enterocele after a Burch colposuspension, with or without additional pouch of Douglas obliteration, by either approximation of the uterosacral ligaments or Moschcowitz-type horizontal purse-string sutures, was reported recently.29 Without pouch of Douglas obliteration, postoperative enterocele formation after 3–16 years (mean 9 years) occurred in 19%, whereas after the additional Moschcowitz procedure the incidence was 11%, and 2% after uterosacral ligament plication. These differences were significant.29 Whether extensive distal preparation of the bladder during abdominal or laparoscopic hysterectomy with exposure of the pubocervical fascia might contribute to the development of anterior enteroceles is unclear. The utilization of intrafascial hysterectomy might be of value but this has not been assessed systematically. During intrafascial hysterectomy, parts of the endopelvic fascia are maintained in their normal position and plicated over the vaginal vault to prevent separation and subsequent enterocele formation.
conservative treatment Treatment of pelvic organ prolapse depends on associated symptoms, the extent of prolapse, the patient’s preferences for management, and whether the patient has completed her family. As subjective and objective success and durability of our current surgical prolapse repairs remain limited, and women’s longevity is increasing, more patients might ask for conservative options.
Figure 71.6. Enterocele, considerable pelvic floor and perineal descent, uterine and bladder prolapse: MRI pictures (a) at rest and (b) during straining.
Conservative treatment of pelvic organ prolapse in general includes the use of pessaries and pelvic floor training in early prolapse stages. Because of the enterocele etiology, pelvic floor muscle exercises are likely to be ineffective in isolated enteroceles. Vaginal pessaries might prevent deterioration of the prolapse, as well as alleviating symptoms of prolapse, and are especially useful if there is a long waiting list for surgery. There is an extensive range of mechanical devices available to reduce the prolapse but literature on success and complications is inadequate, especially if isolated enteroceles are considered. Pessaries are a viable option, and a trial of pessary fitting can easily be performed in clinics and be managed by specially trained nurses or continence advisers. In an observational study, 73 of 100 women with at least stage II pelvic organ prolapse had a successful pessary fitting trial. At assessment at 2 months, prolapse-related symptoms had disappeared in most women, in 50% urinary symptoms improved, and 92% were satisfied with their pessary. Dissatisfaction with the pessary treatment was associated with occult stress incontinence.46
surgical treatment There are procedures that obliterate only the pouch of Douglas by plicating the peritoneum (e.g. the Moschcowitz or Halban operation) or the uterosacral ligaments (e.g. the McCall procedure; Fig. 71.7). The failure rates are high if there is insufficient pelvic floor support present or if there has been a previous repair. Peritoneum alone is not a supportive structure. Therefore, best results might only be achieved when the pouch of Douglas obliteration is combined with surgery to support the vaginal vault or uterus. In the Cochrane Review of surgical management of pelvic organ prolapse, 1029
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Figure 71.7. McCall procedure. This is one of several different methods of vaginal suture placement through the uterosacral ligaments. the lack of randomized controlled trials for enterocele repair was apparent.47 There are few studies that address enteroceles directly. Current widely used procedures and their success rates are described below. As with other pelvic floor repairs, the patients’ goals should be kept in mind – they might diverge considerably from objective restoration of the anatomy.48
operations to obliterate the pouch of Douglas Several horizontal circular, purse-string type sutures, beginning at the most distal part of the pouch of Douglas/enterocele form the so-called Moschcowitz procedure which was described by Moschcowitz in 1912 after extensive anatomic studies of rectal prolapse.25 Although he found it a successful operation in his patients, it has subsequently been associated with a high failure rate and complications such as ureteral kinking and small bowel obstruction49 although there is a lack of controlled studies. Currently it tends to be used only as an adjunct to major pelvic floor surgery. Occlusion of the pouch of Douglas, as described by Halban in his 1912 textbook, includes several sagittal sutures positioned along the pouch in a vertical direction (Fig. 71.8).28 Although there is less risk for ureteral damage, the ureters should be checked carefully. As with the Moschcowitz operation, this approach has not been
Figure 71.8. Combination of a Halban-type pouch of Douglas obliteration with sagittal sutures and a McCall part with incorporation of the uterosacral ligaments after concomitant abdominal hysterectomy. Note that the anterior and posterior endopelvic fasciae are joined over the vaginal vault and incorporated in the pouch of Douglas obliteration. studied systematically and is currently performed concomitantly with other pelvic floor surgery. Both the Moschcowitz and Halban operations were initially described as abdominal procedures but can also be achieved transvaginally or laparoscopically.50,51 The McCall, Halban and Moschcowitz procedures and their extensive variations can be performed prophylactically to obliterate a deep pouch of Douglas or therapeutically to correct an enterocele. As described above in ‘Prevention’, there are several methods available to close the rectovaginal pouch, not only vaginally but also abdominally. A popular approach is the simple plication of the uterosacral ligaments in the midline and the McCall culdoplasty with its numerous modifications (see Figs 71.7, 71.8). The principal structure employed is the uterosacral ligaments which are sutured together in the midline with several interrupted stitches or one continuous stitch. Modifications include the incorporation of the vaginal vault or cervix into the sutures. During vaginal hysterectomy after the suture is passed through the uterosacral ligaments on either side, with or without inclusion of the rectosigmoid serosa, it is tied and the ends are passed through the medial aspect of the vaginal vault. Permanent or delayed absorbable sutures should be used although there are no controlled studies to corroborate this. Non-absorbable sutures should not be passed through the vagina to avoid any sinus formation or abscess. Given52 did not report any
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enterocele recurrences after an average follow-up of 7 years after McCall culdoplasty and pouch of Douglas obliteration with excision of peritoneum (Torpin wedge culdoplasty). Vaginal enterocele repair comprises identification, preparation, and opening of the enterocele sac, high closure of the peritoneum with a purse-string suture and excision of the sac if preferred. The failure rate with this repair was reported at 33% in one study, although 72% of women also received a posterior repair and 22% had a Burch colposuspension.53 A site-specific fascial defect repair with reattachment of the disruption might complete the vaginal repair.
the effect of pelvic organ prolapse operations on enterocele formation A surgical technique to suspend the vaginal vault and reattach the endopelvic fascia to the uterosacral ligaments has been studied by Shull et al.54 The concept of prolapse as a hernia is meticulously followed. Using one suture, the anterior and posterior endopelvic fasciae (usually after a concomitant repair) are connected to the uterosacral ligaments, thereby completely covering the vault with fascia. Two or three permanent stitches along the ligament might be passed; the more proximal sutures correspond with more lateral placements in the anterior and posterior fasciae. The success rate for vault prolapse and enteroceles was reported to be 99%. This method was originally described as a vaginal procedure; however, using these principal steps allows it to be performed (at least partly) laparoscopically as illustrated by Miklos et al.55 and Paraiso et al.51 Laparoscopically, the sutures are placed through the uterosacral ligaments which are later, during the vaginal part of the operation, passed through the anterior and posterior endopelvic fasciae. Early success rates were 100%; there were no recurrent enteroceles.55 Similar vaginal procedures that include some form of uterosacral ligament plication and address an enterocele have been described by Karram et al. with a 7% enterocele recurrence rate.56 There are two randomized controlled trials that compare the transvaginal and the transanal rectocele repair.57,58 The authors reported a higher incidence of enteroceles and rectoenteroceles in the transanal repair group. It was suggested that the transvaginal posterior repair with continuous plication of the fascia from the perineal body to the vaginal apex offers protection against enterocele formation.59 A posterior colporrhaphy augmented with vicryl mesh is not superior to a simple posterior repair in terms of recurrent enterocele according to one randomized controlled trial.60
combined operations for pelvic organ prolapse and concomitant enterocele There are several vaginal, abdominal and laparoscopic operations that address vaginal vault or uterine prolapse and concomitant enteroceles but there is a paucity of studies that assess long-term objective and subjective outcomes. Open abdominal61–63 and laparoscopic sacrocolpopexy51,64,65 may include pouch of Douglas obliteration. Obliteration of the pouch of Douglas with Moschcowitz or Halban sutures or rectovaginal mesh interposition as advocated by Villet et al.66 has been criticized by several authors because posterior enteroceles have been observed behind the mesh.62,67 However, on reviewing the available literature, there appears to be no considerably higher incidence of enteroceles in women who did not undergo any form of pouch of Douglas obliteration.62 There were 12 cases (2.2%) of recurrent vault prolapse or enterocele described out of 549 patients in whom the pouch of Douglas was obliterated. In 548 patients with no obliteration of the pouch of Douglas the failure rate of vault prolapse was 4.0% (22 of 548 cases).68 In a meta-analysis of two randomized controlled trials, the abdominal sacrocolpopexy with mesh and vaginal sacrospinous colpopexy were equally effective with regard to occurrence of postoperative enterocele (odds ratio = 0.77; 95% CI: 0.28–2.06).69,70 Non-randomized comparisons of sacrospinous and iliococcygeus colpopexy did not reveal any difference with respect to postoperative enteroceles.71 The same applies to fixation of the cervix/uterus or vaginal vault to the sacrospinous ligament.72
conclusion An isolated enterocele is rare and usually occurs after pelvic surgery that displaces the vaginal axis, leads to disruption of the anterior and posterior endopelvic fasciae or exposes the pouch of Douglas. A deep pouch of Douglas might predispose to enterocele formation. Enteroceles are frequently associated with pelvic organ prolapse in other compartments. Symptoms range widely and include prolapse sensation, disturbance of defecation and micturition, and dyspareunia. During careful clinical vaginal and rectal examination, enteroceles can usually be identified but imaging techniques such as viscerography and MRI are helpful. There are two procedures that close the peritoneum of the pouch of Douglas only: the Moschcowitz operation with horizontal sutures and the Halban method with vertical suture placement. Several other procedures and modifications utilize the uterosacral ligaments. These 1031
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repairs can be performed vaginally, open abdominally or laparoscopically, and are usually combined with other pelvic floor surgery. Operations that address vaginal vault prolapse might be necessary to accomplish a good anatomic and symptomatic result. To date there are no data available to recommend one particular procedure.
references 1. Uhlenhuth E, Wolfe WM, Smith EM et al. The rectogenital septum. Surg Gynecol Obstet 1948;86:148–63. 2. van Ophoven A, Roth S. The anatomy and embryological origins of the fascia of Denonvilliers: a medico-historical debate. J Urol 1997;157(1):3–9. 3. Holley RL. Enterocele: a review. Obstet Gynecol Surv 1994;49:284–93. 4. Baessler K, Schuessler B. The depth of the pouch of Douglas in nulliparous and parous women without genital prolapse and in patients with genital prolapse. Am J Obstet Gynecol 2000;182(3):540–4.
ing of normal levator ani anatomy and function. Obstet Gynecol 2002;99(3):433–8. 16. Rizk DE, Czechowski J, Ekelund L. Dynamic assessment of pelvic floor and bony pelvis morphologic condition with the use of magnetic resonance imaging in a multiethnic, nulliparous, and healthy female population. Am J Obstet Gynecol 2004;191:83–9. 17. Tulikangas PK, Walters MD, Brainard JA et al. Enterocele: is there a histologic defect? Obstet Gynecol 2001;98:634–7. 18. Weber AM, Walters MD. Anterior vaginal prolapse: review of anatomy and techniques of surgical repair. Obstet Gynecol 1997;89(2):311–8. 19. Henry MM, Parks AG, Swash M. The pelvic floor musculature in the descending perineum syndrome. Br J Surg 1982;69:470–2. 20. Fialkow MF, Gardella C, Melville J et al. Posterior vaginal wall defects and their relation to measures of pelvic floor neuromuscular function and posterior compartment symptoms. Am J Obstet Gynecol 2002;187(6):1443–8.
5. DeLancey JO. Structural anatomy of the posterior pelvic compartment as it relates to rectocele. Am J Obstet Gynecol 1999;180:815–23.
21. Harewood GC, Coulie B, Camilleri M et al. Descending perineum syndrome: audit of clinical and laboratory features and outcome of pelvic floor retraining. Am J Gastroenterol 1999;94:126–30.
6. DeLancey JO. Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 1992;166 (6 Part 1):1717–24.
22. Baessler K, Stanton SL. Symptomatic pelvic organ prolapse and perineal descent. Int Urogynecol J Pelvic Floor Dysfunct 2001:S24.
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8. Maloney JC, Dunton CJ, Smith K. Repair of vaginal vault prolapse with abdominal sacropexy. J Reprod Med 1990;35:6–10.
24. Zacharin RF, Hamilton NT. Pulsion enterocele: long-term results of an abdominoperineal technique. Obstet Gynecol 1980;55:141–8.
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25. Moschcowitz AV. The pathogenesis, anatomy, and cure of prolapse of the rectum. Surg Gynecol Obstet 1912;15:7–12.
10. Robert HG, Vayre P. Les élytrocèles. Considérations anatomique et thérapeutiques. A propos de 25 observations. Ann Chir 1964;18:1060–71.
26. Altemeier WA, Culbertson WR, Schowengerdt CJ, Hunt J. Nineteen years’ experience with the one stage perineal repair of rectal prolapse. Ann Surg 1971;173(6):993– 1006.
11. Anson BJ. An atlas of human anatomy. Philadelphia: WB Saunders, 1950. 12. Baessler K, Schuessler B. Anatomy of the sigmoid colon, rectum, and the rectovaginal pouch in women with enterocele and anterior rectal wall procidentia. Clin Anat 19, 2006 13. Berglas B, Rubin IC. Study of the supportive structures of the uterus by levator myography. Surg Gynecol Obstet 1953;97:677–92. 14. Nichols DH, Genadry RR. Pelvic relaxation of the posterior compartment. Curr Opin Obstet Gynecol 1993;5:458–64. 15. Singh K, Reid WM, Berger LA. Magnetic resonance imag-
27. Jorge JM, Yang YK, Wexner SD. Incidence and clinical significance of sigmoidoceles as determined by a new classification system. Dis Colon Rectum 1994;37:1112–7. 28. Halban J. Gynäkologische Operationslehre. Berlin: Urban and Schwarzenberg, 1912. 29. Langer R, Lipshitz Y, Halperin R et al. Prevention of genital prolapse following Burch colposuspension: comparison between two surgical procedures. Int Urogynecol J Pelvic Floor Dysfunct 2003;1:13–6. 30. Wiskind AK, Creighton SM, Stanton SL. The incidence of genital prolapse after the Burch colposuspension. Am J Obstet Gynecol 1992;167:399–404.
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31. Alcalay M, Monga A, Stanton SL. Burch colposuspension: a 10–20 year follow up. Br J Obstet Gynaecol 1995;102:740–5. 32. Peters WA 3rd, Smith MR, Drescher CW. Rectal prolapse in women with other defects of pelvic floor support. Am J Obstet Gynecol 2001;184(7):1488–94. 33. Thompson JR, Chen AH, Pettit PD et al. Incidence of occult rectal prolapse in patients with clinical rectoceles and defecatory dysfunction. Am J Obstet Gynecol 2002;187:1494–9. 34. Mellgren A, Schultz I, Johansson C et al. Internal rectal intussusception seldom develops into total rectal prolapse. Dis Colon Rectum 1997;40:817–20. 35. Slieker-ten Hover MCP, Vierhout M, Bloembergen H et al. Distribution of pelvic organ prolapse (POP) in the general population: prevalence, severity, etiology and relation with the function of the pelvic floor muscles. Neurourol Urodyn 2004:401–2. 36. Kinzel GE. Enterocele. 1961;81:1166–74.
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sary for pelvic organ prolapse. Am J Obstet Gynecol 2004;190(4):1025–9. 47. Maher CF, Baessler K, Glazener CMA, Adams EJ, Hagen S. Surgical management of pelvic organ prolapse in women (Cochrane Review). Cochrane Database Syst Rev 2004; Issue 4. 48. Hullfish KL, Bovbjerg VE, Steers WD. Patient-centered goals for pelvic floor dysfunction surgery: long-term follow-up. Am J Obstet Gynecol 2004;191:201–5. 49. Dicke JM. Small bowel obstruction secondary to a prior Moschcowitz procedure. Am J Obstet Gynecol 1985;152 (7 Pt 1):887–8. 50. Lyons TL. Minimally invasive treatment of urinary stress incontinence and laparoscopically directed repair of pelvic floor defects. Clin Obstet Gynecol 1995;32(2):380–91. 51. Paraiso MF, Falcone T, Walters MD. Laparoscopic surgery for enterocele, vaginal apex prolapse and rectocele. Int Urogynecol J Pelvic Floor Dysfunct 1999;10:223–9.
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52. Given FT Jr. ‘Posterior culdeplasty’: revisited. Am J Obstet Gynecol 1985;15320:135–9.
37. Marinkovic SP, Stanton SL. Incontinence and voiding difficulties associated with prolapse. J Urol 2004;171(3):1021–8.
53. Tulikangas PK, Piedmonte MR, Weber AM. Functional and anatomic follow-up of enterocele repairs. Obstet Gynecol 2001;98:265–8.
38. Haylen BT, Law MG, Frazer M et al. Urine flow rates and residual urine volumes in urogynecology patients. Int Urogynecol J Pelvic Floor Dysfunct 1999;10:378–83.
54. Shull BL, Bachofen C, Coates KW et al. A transvaginal approach to repair of apical and other associated sites of pelvic organ prolapse with uterosacral ligaments. Am J Obstet Gynecol 2000;183:1365–73.
39. Weber AM, Walters MD, Piedmonte MR. Sexual function and vaginal anatomy in women before and after surgery for pelvic organ prolapse and urinary incontinence. Am J Obstet Gynecol 2000;182(6):1610–5. 40. Croak AJ, Gebhart JB, Klingele CJ et al. Characteristics of patients with vaginal rupture and evisceration. Obstet Gynecol 2004;103(3):572–6. 41. Kelvin FM, Maglinte DD, Hornback JA et al. Pelvic prolapse: assessment with evacuation proctography (defecography). Radiology 1992;184:547–51. 42. Shorvon PJ, McHugh S, Diamant NE et al. Defecography in normal volunteers: results and implications. Gut 1989;30:1737–49. 43. Lienemann A, Anthuber C, Baron A et al. Diagnosing enteroceles using dynamic magnetic resonance imaging. Dis Colon Rectum 2000;43:205–12. 44. Vierhout ME, van PD. Diagnosis of posterior enterocele: comparison of rectal ultrasonography with intraoperative diagnosis. J Ultrasound Med 2002;21(4):383–7. 45. Cruikshank SH, Kovac SR. Randomized comparison of three surgical methods used at the time of vaginal hysterectomy to prevent posterior enterocele. Am J Obstet Gynecol 1999;180(4):859–65. 46. Clemons JL, Aguilar VC, Tillinghast TA et al. Patient satisfaction and changes in prolapse and urinary symptoms in women who were fitted successfully with a pes-
55. Miklos JR, Kohli N, Lucente V et al. Site-specific fascial defects in the diagnosis and surgical management of enterocele. Am J Obstet Gynecol 1998;179(6 Pt 1):1418– 22; discussion 1822–3. 56. Karram M, Goldwasser S, Kleeman S et al. High uterosacral vaginal vault suspension with fascial reconstruction for vaginal repair of enterocele and vaginal vault prolapse. Am J Obstet Gynecol 2001;185(6):1339–42; discussion 1342–3. 57. Kahn MA, Stanton SL, Kumar D et al. Posterior colporrhaphy is superior to the transanal repair for treatment of posterior vaginal wall prolapse. Neurourol Urodyn 1999;18:70–1. 58. Nieminen K, Hiltunen KM, Laitinen J et al. Transanal or vaginal approach to rectocele repair: a prospective, randomized pilot study. Dis Colon Rectum 2004;47(10):1636–42. 59. Nieminen K, Heinonen PK. Sacrospinous ligament fixation for massive genital prolapse in women aged over 80 years. BJOG 2001;108:817–21. 60. Sand PK, Koduri S, Lobel RW et al. Prospective randomized trial of polyglactin 910 mesh to prevent recurrence of cystoceles and rectoceles. Am J Obstet Gynecol 2001;184(7):1357–62; discussion 1362–4. 61. Baessler K, Schuessler B. Abdominal sacrocolpopexy and
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anatomy and function of the posterior compartment. Obstet Gynecol 2001;97:678–84. 62. Timmons MC, Addison WA, Addison SB et al. Abdominal sacral colpopexy in 163 women with posthysterectomy vaginal vault prolapse and enterocele. Evolution of operative techniques. J Reprod Med 1992;37(4):323–7. 63. van Lindert AC, Groenendijk AG, Scholten PC et al. Surgical support and suspension of genital prolapse, including preservation of the uterus, using the Gore-Tex soft tissue patch (a preliminary report). Eur J Obstet Gynecol Reprod Biol 1993;50(2):133–9. 64. Nezhat CH, Nezhat F, Nezhat C. Laparoscopic sacral colpopexy for vaginal vault prolapse. Obstet Gynecol 1994;84(5):885–8. 65. Ross JW. Techniques of laparoscopic repair of total vault eversion after hysterectomy. J Am Assoc Gynecol Laparosc 1997;4(2):173–83. 66. Villet R, Morice P, Bech A et al. Approache abdominale des rectoceles et des elytroceles. Ann Chir 1993:626–30. 67. Addison WA, Timmons MC, Wall LL et al. Failed abdominal sacral colpopexy: observations and recommendations. Obstet Gynecol 1989;74:480–3.
68. Baessler K, Leron E, Stanton SL. Sacrohysteropexy and sacrocolpopexy. In: Stanton SL, Zimmern PE (eds) Female Pelvic Reconstructive Surgery. Berlin: Springer, 2003; 184–91. 69. Maher CF, Qatawneh A, Dwyer PL et al. Abdominal sacral colpopexy or vaginal sacrospinous colpopexy for vaginal vault prolapse: a prospective randomized study. Am J Obstet Gynecol 2004;190(1):20–6. 70. Benson JT, Lucente V, McClellan E. Vaginal versus abdominal reconstructive surgery for the treatment of pelvic support defects: a prospective randomized study with long–term outcome evaluation. Am J Obstet Gynecol 1996;175(6):1418–21; discussion 1421–2. 71. Maher CF, Murray CJ, Carey MP et al. Iliococcygeus or sacrospinous fixation for vaginal vault prolapse. Obstet Gynecol 2001;98:40–4. 72. Maher CF, Cary MP, Slack MC et al. Uterine preservation or hysterectomy at sacrospinous colpopexy for uterovaginal prolapse? Int Urogynecol J Pelvic Floor Dysfunct 2001;12(6):381–4; discussion 384–5.
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INTRODUCTION Since the early 19th century, surgeons have performed posterior colporrhaphy to manage complete tears of the perineum. The supports of the genital organs were largely a mystery, and there was little distinction between prolapses of the rectum, bladder, and uterus. As anatomic concepts developed, surgeons ascertained that the main support of the uterus was the vagina, which in turn was supported by the insertion of the levator ani muscles into the perineum. This concept was the basis for the incorporation of plication of the levator ani muscles into posterior colpoperineorrhaphy, with the surgical goals of constriction of the vaginal tube, creation of a perineal shelf, and partial closure of the genital hiatus. Until recently, very little attention has been given to the functional derangements that are commonly associated with rectoceles. A rectocele is an outpocketing of the anterior rectal and the posterior vaginal wall into the lumen of the vagina.1 Some rectoceles may be asymptomatic, whereas others may cause such symptoms as incomplete bowel emptying, vaginal mass, pain, and pressure. The prevalence of rectoceles ranges from 20 to 80% in the general population.2 A rectocele is fundamentally a defect of the rectovaginal septum, not of the rectum. The size of the defect does not necessarily correlate with the amount of functional derangement. This chapter reviews the anatomy, pathophysiology, diagnosis, and management of rectoceles.
ANATOMY In 1839, Denonvilliers first described a layer of fascia found in males, which he named the ‘rectovesical septum’. Nichols and Milley later recorded the existence of this septum in surgical dissections and autopsies of fresh female cadavers.3 This layer of connective tissue is fused to the undersurface of the posterior vaginal wall. The rectovaginal fascia extends downwards from the posterior aspect of the cervix and the cardinal–uterosacral ligaments to its attachment on the upper margin of the perineal body and laterally to the fascia over the levator ani muscle. Richardson3 states that the rectovaginal septum and uterosacral ligaments provide suspensory support of the perineal body from the sacrum. Posterior to the rectovaginal septum lies the rectovaginal space, which provides a plane for dissection. In between the rectovaginal septum and the rectum is the pararectal fascia; inside this fibromuscular layer lie blood vessels, nerves, and lymph nodes, which supply the rectum. The pararectal fascia, originating from the pelvic sidewalls,
divides into fibrous anterior and posterior sheaths, which encompass the rectum. These layers provide additional support to the anterior rectal wall.4 Further support is provided by the levator ani, which are composed of paired iliococcygeus, puborectalis, and pubococcygeus muscles. These muscles function to maintain a constant basal tone and a closed urogenital hiatus. This constant basal tone prevents the urogenital hiatus from widening and the eventual descent of the pelvic viscera. These muscles also provide a contraction reflex to increased intra-abdominal pressures, preventing incontinence and prolapse. The anterior sacral nerve roots S2–S4, which innervate these muscles, cross the pelvic floor and are stretched and compressed during labor, increasing the risk of injury.4,5
ETIOLOGY Rectocele was once thought to be a condition affecting only multiparous females and resulting from obstetric damage or increased tissue laxity with aging and menopausal atrophy. However, recently, rectoceles and enteroceles have been noted to occur in approximately 40% of asymptomatic parous women.6 Shorvon et al. performed defecography on healthy, young, nulliparous, asymptomatic volunteers, noting that 17/21 women had small or moderately sized rectoceles.7 Rectoceles may thus have a wider prevalence than previously thought and may not be a result of parity. The most common causes of rectoceles are obstetric events. Traumatic obstetric events, which usually occur when the presenting part descends quickly in the second stage of labor, can predispose to rectocele formation. The forces of labor may separate, tear or distend the pelvic floor, altering the functional and anatomic position of the muscles, nerves, and connective tissues. The rectal fascia may separate from the perineal body, causing a transverse defect and low rectocele. Low rectoceles are isolated defects in the suprasphincteric portion of the rectovaginal fascia. They are usually caused by obstetric trauma that disrupts the attachments of the levator ani fascia and bulbocavernosus muscles. An eversion of the introitus will be noted on physical examination. This will aggravate constipation and will result in inefficient bowel movements and the need for stronger Valsalva maneuver.8–12 If mid or high rectoceles form, they may alter the vaginal axis.1,4,8,9 Laxity of the levator ani secondary to the levator detaching from the perineal body along the vaginal axis allows the pelvic organs to slide downwards, following the new altered axis. Women with an android pelvis are at increased risk because labor forces are directed
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towards the posterior vaginal wall and perineum, leaving the anterior vaginal wall relatively protected. Mid-vaginal rectoceles are most likely caused by obstetric trauma not involving the levator ani. The rectovaginal fascia is damaged by the stretching and laceration of the tissue, which results in the thinning of the fascia, leading to subsequent adhesion formation. This adhesion of the rectovaginal septum, vagina, and rectal capsule inhibits independent function. Symptoms may include incomplete bowel emptying, rectal pressure, and pain after bowel movements; they may also coexist with a high rectocele.12 High rectoceles often occur from pathologic overstretching of the posterior vaginal wall. The cardinal ligaments fuse with the vagina and cervix, causing the cervix to fuse with the anterior vaginal wall. The rectovaginal septum is absent from the posterior vaginal wall, causing loss of the anterior rectal wall support. High rectocele may also coexist with congenital deepness of the pouch of Douglas.12 Rectoceles may occur as a result of pathologic stretching of the pudendal nerves during descent of the fetal head, causing atrophy and denervation of the pelvic floor muscles. Sultan reported that most damage to the pelvic support occurs in the first vaginal delivery.13,14 Electromyographic studies demonstrate an 80% incidence of denervation of the perineal muscles after vaginal delivery.5,15,16 Denervation will probably recover after the postpartum period; however, it has been demonstrated that injury may be cumulative with increasing parity.5 Increased labor duration and weight of the baby directly influence the perineal damage and denervation of the pelvic floor. This neuropathy can lead to the weakening of pelvic floor muscles and development of a rectocele. Thus, shortening of the second stage of labor by episiotomy or forceps may decrease the risk of denervation and subsequent pelvic floor damage.8 Defecation disorders may account for a subgroup of rectoceles. They may lead to the weakening of the rectovaginal septum by continuous straining against an obstruction. One disorder, the perineal descent syndrome, is clinically diagnosed when the individual strains and the perineal plane descends past the ischial tuberosities;15 this disorder may be confused with a rectocele. Other conditions, such as paradoxical sphincter reaction (anismus), cause unconscious contraction of the voluntary striated muscles when attempting to defecate. This constant straining with bowel movements has been shown to cause or worsen a pre-existing rectocele and increasingly to weaken the rectovaginal septum by denervation injury.17 Anismus eventually leads to the accumulation of stool in the rectum, which may com-
plicate pelvic outlet obstruction and cause a progressive cycle, worsening the rectocele.18 Congenital absence of the perineum may mimic a rectocele. This pseudorectocele has its posterior vaginal wall exposed because of lack of inferior support; this may be corrected by surgical reconstruction of the perineum. Congenital absence allows for deepening of the cul-de-sac and weakening of the rectovaginal septum, leading to the development of a high rectocele and enterocele.6,12 Some studies have found differences in connective tissue strengths between races, which may contribute to rectoceles. Africans have been noted to have a decreased frequency of laceration after normal spontaneous deliveries and a subsequent decrease of uterine prolapse. This may be related to constitutional factors such as pelvis type, connective tissue, and ability to fibrose,12 whereas Hispanic, Filipino and Chinese women may have an increased risk of laxity of tissue.19
CLINICAL PRESENTATION The symptoms associated with a rectocele are summarized in Table 72.1. Clinical symptoms vary from being non-existent to severe bowel problems. A common complaint is constipation, which may occur in up to 75% of patients with rectoceles.2 Patients may also complain of incomplete rectal emptying, a sense of rectal pressure or a vaginal bulge.1,20,21 Patients may describe stool becoming trapped in the rectocele pocket itself. Vaginal digitation or perineal support is sometimes necessary to facilitate defecation.20 Constipation and straining may worsen the symptoms and lead to left lower quadrant abdominal pain if impaction occurs. Many non-specific symptoms, such as rectal pain, bleeding, fecal or gas incontinence, low back pain worsening throughout the day but relieved Table 72.1.
• • • • • • • • • • • •
Symptoms associated with a rectocele
Sensation of pelvic pressure Feeling that something is falling down or falling out from the pelvis Symptoms often worsened by standing up and eased by lying down Lower abdominal and/or back pain Bulging mass felt inside the vagina Painful or impossible vaginal intercourse Vaginal bleeding Constipation Problems with passage of stool as it becomes caught in the rectocele Sensation of incomplete bowel emptying Fecal incontinence Asymptomatic
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by lying down, and dyspareunia may occur, as well as many other defecatory disorders.6 The prevalence of fecal incontinence increases to 17% in populations with pelvic organ prolapse and urinary incontinence22 compared to 2–3% in the general population.23,24 The most common mechanisms are an incompetent sphincteric mechanism (secondary to a structural defect or pudendal nerve damage) and overflow incontinence. As previously mentioned, the majority of rectoceles are totally asymptomatic.
PHYSICAL EXAMINATION A rectocele is detected by observing the bulge in the posterior vaginal wall during maximum Valsalva or cough. The patient may be in the dorsal supine position (for the gynecologist) or in the left lateral decubitus position (for the colorectal surgeon). The use of the split blade of a Sims or Graves speculum to support the anterior segment can aid in visualization. A rectocele can be confirmed with a rectal examination during which anterior displacement of the vaginal wall adjacent to the rectum and the perineal body is noted. This can be differentiated from enterocele by noting bowel in the rectovaginal space: with the patient standing, the rectovaginal examination will reveal small bowel herniating into this space when an enterocele is present. Of women with rectoceles, 80% are asymptomatic and can be diagnosed only on physical examination.7,18 The current standardized system used for prolapse assessment is termed the pelvic organ prolapse quantification (POPQ) system, and was described by Bump et al. in 1996.25 The POPQ is a descriptive system that contains a series of site-specific measurements of a patient’s anterior, apical, and posterior pelvic organ support. This nomenclature has replaced the respective terms cystocele, enterocele, and rectocele as it is often uncertain which specific structures are contributing to prolapse at each segment. Prolapse is measured in centimeters relative to the hymeneal ring in relation to six defined points. Points proximal to the hymen are denoted as negative and points distal as positive. The other landmarks which complete the examination are the genital hiatus, perineal body, and total vaginal length. In the POPQ system, the posterior segment includes analogous points ascribed to the anterior segment. Point Ba corresponds to a point 3 cm proximal to the hymen in the midline of the posterior segment. Possible values range from –3 to +3 cm from the hymeneal ring. Point Bp represents the most distal portion of the posterior vaginal wall. The minimum value is –3 in the absence of
any posterior wall prolapse. In the presence of complete vaginal eversion, the maximum value equals the value of C. Richardson described site-specific defects in the rectovaginal septum that occur in various locations including the superior, inferior, right, left, and midline areas.3 These defects are often noted at the time of surgical intervention.26 One study has suggested that locating defects during clinical evaluation of the posterior vaginal wall is often inaccurate when compared to surgical assessment at the time of defect-specific repair.27
DIAGNOSTIC STUDIES Imaging studies Significant strides in the area of prolapse evaluation have occurred in the last decade, largely as a result of advanced technology in the field of radiology. However, the results of imaging studies are only useful when used in combination with other information, especially history, symptomatology, and physical examination, and should not be used alone to make treatment decisions. Potential uses of radiologic investigation include those situations in which: 1) symptomatology and physical findings do not correlate; 2) the pelvic anatomy is unusual or altered due to previous pelvic surgery or a congenital defect; and 3) the patient is unable to exert maximal straining during pelvic examination.
Dynamic proctography or defecography The use of contrast media in pelvic fluoroscopy allows the various prolapsed organs to be opacified and seen in real time. Traditionally, it has mainly been used in the study of anorectal dysfunction as evacuation proctography, which is also known as defecography. However, the addition of a cystogram (dynamic cystoproctography) to this modality allows further information to be gained during the assessment.28 The equipment required includes a thick barium paste, a radiolucent toilet, and video equipment. Images are taken at rest, during straining effort, and during and after evacuation. Currently, universally accepted radiologic criteria for defining pelvic organ prolapse are lacking.29 However, prolapse is usually radiologically defined in reference to the pubococcygeal line – a line extending from the inferior pubic ramus to the sacrococcygeal junction.30 This line is reproducible and includes the attachment sites for the levator muscle.
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A rectocele is seen radiologically as an anterior rectal bulge (Fig. 72.1).31–35 It is usually measured as the depth in relation to a line extended upward through the anterior anal wall. The cut-off value has not been universally agreed, but some authors consider a depth of greater than 3 cm to be abnormal (many asymptomatic women will be found to have a small rectocele 2 cm or less in depth).7,36 Proctography will also note the finding of postevacuation barium trapping which may help to explain any evacuation dysfunction.37 During testing, patients can be taught how to apply manual pressure in the vagina to obtain relief from the symptoms associated with incomplete emptying. Proctography may suggest the diagnosis of anismus, which may be the main contributor to a patient’s bowel dysfunction rather than a rectocele.38 This has important implications because anismus is treated with biofeedback therapy rather than with surgery. An enterocele is noted as a herniation of the small bowel into the cul-de-sac into the vagina, rectovaginal space, or both. The vagina and small bowel in the pelvis need to be opacified to obtain this diagnosis. They are most evident after evacuation as a full rectum may
obscure its visualization (Fig. 72.2). Sigmoidoceles are noted in approximately 5% of proctograms.39 However, there still may be false negatives with proctography due to insufficient filling of contrast media into the sigmoid. This finding is important in that a patient may require sigmoid resection or sigmoidopexy as treatment. Vaginal vault prolapse can also be assessed on postevacuation studies. Compared with physical examination, evacuation cystoproctography will detect many enteroceles and sigmoidoceles not seen on pelvic examination.31 Studies have shown that enteroceles are only identified approximately 50% of the time on physical examination, which is less than the rates of identifying rectoceles and cystoceles.32,39 This has been attributed to the failure of the patient to strain maximally during pelvic examination, an impediment that is removed during the evacuation phase of cystoproctography. One study by Altringer et al. found that patient diagnosis was changed in 75% of cases after dynamic cystoproctography.32 Another benefit is that fluoroscopy will identify the specific organs involved in the prolapse. However, it is difficult to correlate the degree of prolapse seen on imaging with that seen on physical examination as each has two separate reference points, the pubococcygeal line and hymen, respectively.29
Magnetic resonance imaging Magnetic resonance imaging (MRI) was first introduced as a diagnostic modality for pelvic organ prolapse by Yang et al.30 It has many advantages over dynamic cystoproctography:
• it is able to contrast soft tissue structures well; • it provides images in numerous different planes; • it can examine subtle pelvic floor changes such • • • •
Figure 72.1. A rectocele (r) with the classic ‘hockey puck’ appearance is shown to be trapping radiocontrast medium after the evacuation phase. (Reproduced from ref. 35 with permission.)
as superior rectovaginal, paravaginal, and uterine defects; it can assess pelvic floor musculature; bony landmarks are easier to identify; no catheterization is necessary; the patient is not exposed to ionizing radiation.
The main limitation is the supine position usually employed by this modality. As with dynamic proctocystography, the pubococcygeal line is used as the reference point radiographically (Fig. 72.3a). Pelvic organ prolapse is seen as an extension of the pelvic organ below the pubococcygeal line, and can be measured in the same way as with dynamic proctocystography (Fig. 72.3b).40 It also shares some of 1039
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a
b
Figure 72.2. (a, b) A full rectum (r) is partially obscuring complete visualization of the enterocele (sb). The enterocele is then noted to push contrast out of the rectocele, resulting in a better view of the enterocele. v, vagina. (Reproduced from ref. 35 with permission.)
a
b
Figure 72.3. (a) The pubococcygeal line used as a reference point radiographically is drawn from the inferior pubic symphysis to the sacrococcygeal junction (arrow = vaginal vault). (b) Compared to the normal examination in the first image, the second image shows prolapse of the bladder (b) and vaginal vault (long arrow) below the pubococcygeal line, compatible with a cystocele and vaginal vault prolapse. A rectocele is also seen as an anterior bulge (arrowhead) in relation to the anal canal (asterisk). (Reproduced from ref. 40 with permission.) the same advantages, including identifying prolapse not noted on physical examination. One study showed that the surgical plan was altered in 41% of cases after MRI and fluoroscopy were employed.41 Tunn et al. found that
rectoceles and enteroceles were easily identifiable with MRI in patients with posthysterectomy vault prolapse.42 There is evidence that MRI is equivalent or superior to proctocystography if evacuation studies are performed
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during the MRI investigation; it also enables an upright assessment to be undertaken.43,44 In addition, MRI defecography facilitates the diagnosis of anismus and intussusception. Another advantage is that the cervix and vaginal vault are often easier to see on MRI imaging than on fluoroscopy due to leakage of vaginal contrast in the latter. Fluoroscopy may not detect enteroceles in 20% of cases in which small portions of peritoneal fat enter the rectovaginal space.44 However, due to greater soft tissue contrast with MRI, the various tissue components can be seen with relative clarity. Disadvantages of MRI include:
• limited access to a vertical configuration magnet; • increased relative cost to fluoroscopy; • less physiologic modality than fluoroscopy if performed supine and without evacuation studies;
• lack of available MRI time due to demands from other specialties.
Ultrasonography Transperineal ultrasound has been described in the assessment of dynamic function of the pelvic floor.45 Dynamic anorectal endosonography has also been described and may detect the presence of enteroceles.46 The role of these alternate modalities has not been fully elucidated and needs further study.
Anal manometry Anal manometry measures rectal pressures by a transducer or balloon. Its measurement of rectal sensation evaluates the first feeling, urge, and discomfort; this information is used to distinguish causes of constipation. When an individual is able to tolerate increased volumes without signs of increased discomfort or the urge to defecate, overflow incontinence may occur. Careful consideration must be given to this evaluation process because individuals able to tolerate only small volumes in the rectum may have an irritable rectum, causing incontinence or urgency. Overflow incontinence and irritable bowel syndrome may mimic rectocele symptoms such as incontinence or incomplete emptying. If misdiagnosis of a rectocele is made, rectocele repair may exacerbate these disorders by causing a worsening of symptoms.16,17,47
Electromyography and nerve conduction studies Electromyography (EMG) and nerve conduction studies also have been used to evaluate defecation disorders.
Obstetric trauma denervates and causes atrophy of the pelvic floor muscles and tissue, which may lead to subsequent pelvic floor weakness. This denervation may be detected by EMG studies, and pudendal terminal motor latency can be used as a method to detect the causes of pelvic floor weakness.
Colonic transit studies For colonic transit studies, the patient ingests radiopaque markers, which are measured and counted in the right colon, left colon, sigmoid colon, and rectum. Clinically slow transit time is defined as less than two bowel movements per week over several years. The utility of this test in individuals with rectoceles is debatable; some have normal transit times whereas others have prolonged times.48 Patients whose symptoms did not improve after repair were found to have longer transit times preoperatively.20
MANAGEMENT Once the clinical diagnosis has been made and (if necessary) confirmed by ancillary studies, the decision to operate or to treat conservatively must be made. Most non-surgical treatments consist of proper bowel training, following an active lifestyle, and eating an appropriate amount of dietary fibre.49,50 These steps are most important when the main complaint is constipation. The only non-surgical therapy available for prolapse symptoms is estrogen replacement therapy in postmenopausal women in the setting of vaginal atrophy, and the use of a vaginal pessary. In our experience, pessaries have not been very effective in women with isolated symptomatic rectoceles. Indications for surgery should include being symptomatic, having an anatomic defect, or undergoing other pelvic reconstructive surgery with an asymptomatic rectocele.9 Symptoms that respond well to surgery include pelvic pressure and a vaginal bulge, vaginal digitalization or splinting (which occurs in 20–75% of symptomatic patients) and outlet obstruction constipation. Janssen and van Dijke noted that repair increased rectal sensitivity, causing the urge to defecate earlier as a positive predictor of a good outcome.47 In the colorectal literature it has been noted that defecography showing a rectocele ≥2 cm with symptoms is also a good indicator for surgery; however, this finding has not been conclusive in all studies.2 Sullivan et al.51 reported that anoscopic evidence of the rolling down of the anterior rectal wall will be present before surgical correction;20 however, this may not be valid for all female patients.47 1041
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Signs and symptoms that are predictive of a poor surgical outcome include a history of use of potent laxatives, incidence of preoperative pain and (possibly) large rectoceles in women who had previously undergone hysterectomy.20,21,47,52 A few studies in the colorectal literature have noted that hysterectomy disrupts parasympathetic nerves, causing decreased rectal sensation as well as increased rectal compliance, which may not be improved after anatomic correction.47,52 The persistence or development of dyspareunia after rectocele repair has been variable and is dependent on the surgical technique: levator plication and overnarrowing of the introitus may lead to increased dyspareunia, whereas defect-specific repair has been associated with disappearance or improvement of dyspareunia.26
SURGICAL REPAIR Indications for use of different approaches Traditionally, the vaginal and transrectal approaches have been used by gynecologists and colorectal surgeons, respectively, as a result of training and familiarity with each technique. Colorectal surgeons tend to focus on improving symptoms of rectal emptying and constipation and thus advocate transanal surgery in patients with defecation disorders. The transrectal approach is often used if perianal/ rectal pathology such as hemorrhoids, anterior rectal wall prolapse, or rectal mucosal redundancy is surgically treated concurrently with the rectocele. A vaginal approach is advocated when:
• other genital prolapse (i.e. enterocele, perineocele, • • •
apical or anterior vaginal wall prolapse) is to be repaired, thus avoiding a second incision; compromised anal function exists (a transanal retractor may further compromise function);53,54 an anal sphincteroplasty is also performed; a high rectocele exists (as the posterior fornix or vaginal apex is not reached through the transanal approach).55
Currently, there are no conclusive data to describe the proper indications for the use of graft material in posterior compartment repairs. Some authors advocate the use of mesh or graft in recurrent rectoceles, in patients with deficient rectovaginal fascia and weak tissue, in the presence of advanced prolapse, or with the coexistence of risk factors such as obesity and chronic constipation.56
Defect-specific rectocele repair According to Richardson, rectoceles are caused by a variety of breaks in the fascia.3 He described the most common break as being a transverse separation above the attachment to the perineal body, resulting in a low rectocele. Another common fascial break was considered to result from an obstetric tear or episiotomy that was incorrectly repaired. This midline vertical defect may involve the lower vagina and extend to the vaginal apex. Less common separations involving a lateral separation down one side of the fascia were also found to exist (Fig. 72.4). Richardson also stated that a U- or L-shaped tear in the fascia might occur. Since Richardson’s observation, there has been an increased movement among gynecologists towards site-specific rectocele repair. Richardson recommended performing the repair with a finger in the rectum, so that defects can be easily identified and fascia can be appropriately approximated with interrupted sutures (Fig. 72.5). Before starting any rectocele repair, the surgeon should approximate the introitus by using Allis clamps bilaterally to help determine how much perineal and vaginal tissue should be excised to correct a gaping introitus. The repaired opening should accommodate three fingerbreadths, taking into account that the levator ani and perineal muscles are relaxed from general anesthesia and may further constrict postoperatively and with postmenopausal atrophy. The next step is to place Allis clamps on the posterior perineum; a diamondshaped perineal incision is made and the overlying skin is removed (Fig. 72.6). The length and width of the perineal incision are dependent on the epithelium needed for restoration of the perineal body. Mayo scissors are used to make a plane in the rectovaginal space. As much fascia is left on the rectum as possible. Sharp dissection is usually required over the perineal body because of previous scarring from episiotomies. The surgeon performs blunt and sharp dissection to the apex of the vagina. This is continued laterally to the tendinous arch of the levator ani and extends inferiorly to the perineal body. If perineal lacerations are present, dissections are continued as follows. For grade 3 perineal lacerations, adequate exposure is needed to reapproximate the divided anal sphincter. In complete or grade 4 perineal lacerations, dissection continues to allow enough tissue exposure for the subsequent edge-to-edge anal mucosal suturing to be tension-free. Hemostasis is ensured and irrigation may be used to attain a clean operative field to allow inspection for defects. The rectovaginal fascia is inspected by the surgeon inserting a finger of the nondominant hand into the rectum (Fig. 72.7). The rectal
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Rectovaginal fascia Anterior rectal mucosa Edge of transverse defect
Figure 72.4. Representation of the various locations where breaks in the rectovaginal septum have been observed in patients with rectocele, as seen through a colporrhaphy incision. wall is brought forwards, distinguishing the uncovered muscularis (fascial defect) from the muscularis covered by the smooth semi-transparent rectovaginal septum. According to the plane of dissection and the location of the defect, frequently the rectovaginal fascia must be mobilized off the lateral vaginal epithelium (Fig. 72.8). After the defect has been identified, Allis clamps are used to grasp the connective tissue (perirectal or rectovaginal fascia), which is pulled over the bare area to facilitate repair (Fig. 72.9). The rectal finger is then used to determine if a defect has been corrected. Next, this area is sewn together with interrupted sutures, plicating the fascia over the rectal wall with a No.v 2-0 delayed absorbable suture (Fig. 72.10). The surgeon must continuously examine the vaginal caliber to ensure a smooth contour and a diameter of three fingerbreadths.3,4,6,57,58 Whereas rectocele repair is accomplished for identification of the fascial defect and reapproximation of the connective tissue, evaluation of the levator hiatus is an entirely different issue. In women who have an enlarged levator hiatus, it may be appropriate to place another set of interrupted sutures horizontally to narrow the levator hiatus. This portion of the operation is not necessary in all patients and is independent of rectocele repair. Perineorrhaphy is the next step in posterior segment reconstruction. The perineal body consists of the anal sphincter, the superficial and deep transverse perineal muscles, the bulbocavernosus muscles, and the junction of the rectovaginal fascia with the anal sphincter.
a
Rectovaginal fascia Anterior rectal mucosa Edge of midline defect
b
Figure 72.5. Transverse and midline defects detected on rectal examination. Inset demonstrates a site-specific defect closed with interrupted suture. Perineorrhaphy implies identification and reconstruction of these components. The first step in perineorrhaphy is to remove any old scar tissue to the point that fresh viable tissue is revealed. If a grade 4 laceration is present, the rectal mucosa is completely mobilized off 1043
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Figure 72.6. Rectocele demonstrated on rectal examination. Note that the perineal skin has been excised.
Figure 72.9. the defect.
Figure 72.7. Complete mobilization of the posterior vaginal wall from anterior rectal wall. Rectal examination demonstrates obvious rectocele, with minimal fascia on the anterior rectal wall.
Figure 72.10. The fascial edges have been sutured together and the defect closed.
Sufficient fascia has been mobilized to cover
the vaginal wall and reapproximated with interrupted sutures. The external anal sphincter is then reapproximated. After stepwise reapproximation of the transverse perineal muscles, the perineal body is sewn over the sphincter. Finally, the bulbocavernosus muscle ends are attached to the perineal body. This musculofascial complex is covered by suturing the overlying vulvar skin with a No. 3-0 suture in a running fashion. Vaginal packing is removed on postoperative day 1 and diet is advanced as tolerated.57,58
Traditional transvaginal repair
Figure 72.8. epithelium.
The fascia is being mobilized off the vaginal
The traditional rectocele approach has been described and illustrated by Nichols, Wheeless and others.59,60 The opening of the vagina is as previously described, via a midline incision or by removal of a triangular wedge of
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vaginal wall. Some surgeons will place an initial row of No. 2-0 interrupted sutures approximating the rectovaginal fascia. The rectocele is then depressed in the midline with the surgeon’s finger to reveal the margin of the puborectalis portion of the levator ani muscle. With the rectocele still depressed, a No. 1-0 absorbable suture is used to suture the margins of the levator ani muscles in an interrupted fashion. After all the sutures have been placed, they are tied. The posterior vaginal mucosa is appropriately trimmed and closed with either interrupted or continuous 3-0 absorbable suture. The perineal body is repaired as previously described.
Transrectal approach The transrectal approach was described by Sarles et al.11 In this method, all patients are treated preoperatively with oral laxatives and are given antibiotics: metronidazole (500 mg twice daily for 2 days prior to surgery) and cefuroxime (250 mg intravenously 1 hour before surgery). The anus and vagina are cleansed with povidone-iodine. A Park retractor is inserted into the anal canal to expose the anterior rectal surface. An incision of the anterior rectal mucosa is made 1 cm above the dentate line. The submucosal plane is sharply dissected 8–10 cm from the anal verge. Bleeding is controlled by diathermy. Dissection is performed anteriorly and laterally; the resulting bare areas are plicated using interrupted polyglycolic acid 2-0 sutures 0.5 cm apart; the suture includes the rectal muscle and the rectovaginal septum. If the vaginal mucosa is perforated, the stitch is removed. A mucosal flap at least 6 cm long is excised. A second layer of polyglycolic acid sutures 3-0 close the mucosal defect. Postoperative care includes delaying food by mouth for 48 hours after surgery and slowly advancing the diet over several days.
enterocele with attachment of the graft to the distal uterosacral ligaments (Fig. 72.11). A transperineal approach has been described that starts with a transverse incision over the perineum. A plane of dissection is created between the vaginal epithelium and external anal sphincter and continues apically until the cul-de-sac peritoneum is encountered, but not entered. A strip of mesh or graft is incorporated into the upper region of the dissection over which the levator ani muscles are plicated.61,62 During an abdominal approach for vault prolapse and enterocele, the accompanying rectocele may be corrected. For a high posterior defect, the posterior graft of a sacral colpopexy may be extended down the posterior wall.63,64 In the setting of additional perineal descent, a sacral colpoperineopexy may also be performed through an abdominal or combined abdominal/vaginal approach.65 In the abdominal approach, the rectovaginal space is entered and a series of sutures are placed along the posterior vaginal wall from the apex to the perineal body which will secure the posterior arm of the colpopexy graft. In the combined approach, the graft is brought into
Rectocele repair with mesh or graft Graft materials have been employed in both the traditional posterior colporrhaphy and the defect-specific technique in an attempt to strengthen the repair. In the latter variation, a site-specific repair is first performed (see Figs 72.6–72.10). A dermal allograft is then attached to the rectovaginal and pubocervical fasciae proximally, levator ani muscles laterally, and perineal body distally with a series of interrupted permanent sutures.56 The repair of a high rectocele can be challenging as there is commonly a deficiency of rectovaginal and pubocervical fasciae proximally. However, this repair can be facilitated by entry into an associated
Figure 72.11.
Graft augmentation of rectocele repair. 1045
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tion (18–27%) after levatorplasty.50 A study by Weber et al. reported an even higher dyspareunia rate of 26% after posterior repair only (except for one patient who had a levator plication) and 38% after a posterior repair with Burch colposuspension.67 The postoperative introital calibers in patients with or without dyspareunia were not different. The reasons for the unexpectedly high rate of dyspareunia in that study are unclear.
the vaginal field from the abdominal field (via the same posterior vaginal wall dissection used for a traditional or defect-specific repair) and sutured to the perineal body.
RESULTS AND COMPLICATIONS Posterior colporrhaphy without or with levatorplasty
Defect-specific rectocele repair
Anatomic cure rates after posterior colporrhaphy without or with levator plication range from 76 to 96% after a mean follow-up period of 12–42 months.1,48,66–68 One study revealed an 88% cure rate for constipation in 24 patients that were prospectively followed and evaluated pre- and postoperatively with standardized questionnaires, defecography, colon transit studies, anorectal manometry, and electrophysiology.1 In comparison, two studies showed a modest improvement (less than 50%)66 or an increase50 in constipation rate (from 22 to 33% after a mean follow-up of 52 months). Reasons suggested for these observations include: 1) unselective approach used in offering surgical treatment for persistent constipation;66 2) retrospective analysis of the data;1 and 3) the possibility that patients with a pathologic transit study might have a less favorable outcome with respect to constipation.1,68 In addition, the study by Kahn and Stanton showed an increase in rates of incomplete bowel emptying and fecal incontinence (4% preoperatively versus 11% postoperatively) after posterior colpoperineorrhaphy.50 De novo dyspareunia rates after levatorplasty have been reported to range from 12.5 to 16%. Several studies suggest that this is due to pressure atrophy of the included muscle and the resulting scarring.50,59 An additional study showed an increased rate of sexual dysfunc-
Table 72.2.
The surgical outcomes after defect-specific rectocele repair are summarized in Table 72.2.26,69–72 Anatomic cure rates range from 82 to 100% after a mean follow-up period of 3–18 months. Improvements in constipation were seen in 43–84% of patients26,69,70 with a de novo constipation rate of 3–4%;26,70 however, Kenton et al. found that the rate of constipation was not statistically significantly different after 1 year of follow-up and attributed this to the predominantly medical etiology for the disorder. In addition, the lack of a standardized definition of constipation contributes to the difference in constipation rates seen in the literature after rectocele repair.70 Improvements in the symptom of manual evacuation was noted in 36–63%,26,69,70 with a de novo rate of 7% in one study.26 Most studies report some improvement in dyspareunia after site-specific repair (35–92%)26,69–72 (see Table 72.2). The only study where site-specific rectocele repair was not combined with other prolapse or incontinence surgery followed 42 women for a period of 18 months. Improvement in sexual function was reported in 35% and there were no patients who developed de novo dyspareunia.72 Other studies report a de novo dyspareunia rate of zero to 8%.26,69–72
Results of defect-specific rectocele repair
Study
Cundiff et al.26
Porter et al.69
Kenton et al.70 Glavind & Madsen71 Singh et al.72
n
67
125
66
Mean follow-up (months)
12
6
Anatomic cure (%)
82
82
Improvement in vaginal protrusion (%)
–
Improvement in difficult defecation (%)
67
42
12
3
18
90
100
92
73
90
–
88
–
55
54
Improvement in constipation (%)
84
44
43
–
–
Improvement in manual evacuation (%)
63
65
36
–
–
Improvement in dyspareunia (%) de novo dyspareunia (%)
44/3
73/8
92/7
75/4
35/0
88
81
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Transanal approach The majority of studies are based on the experience of colorectal surgeons whose primary focus is defecatory dysfunction and anal incontinence. The results are summarized in Table 72.3.10,20,21,47,51,53,73–76 Anatomic cure rates range from 70 to 98% after a 12- to 52-month followup. Reported rates of symptomatic improvement are 58–100% after the transrectal approach. De novo anal incontinence may be a concern, especially in those with occult sphincter lacerations, as a transanal retractor may further compromise function. One study reported a 38% rate of new-onset fecal incontinence after this approach.66 In a combined transvaginal/transanal approach, van Dam et al. found an anatomic cure rate of 72% in 89 women after a mean follow-up period of 52 months. Rates of constipation were 63% preoperatively and 33% postoperatively, while difficulty in evacuation decreased
Table 72.3.
from 92% to 27%. However, rates of dyspareunia were found to be 28% preoperatively and 44% postoperatively which the authors attributed to the transvaginal portion of the operation.54 Studies comparing the transvaginal and transanal approaches have been mainly retrospective,49,66,77,78 or prospective and non-randomized.54 In a recent randomized controlled trial of 30 patients by Nieminen et al.,79 15 patients underwent transanal rectocele repair while the other 15 underwent vaginal posterior colporrhaphy. They excluded patients with other symptomatic prolapse or compromised anal sphincter function as evidenced by colon transit study. At 12 months follow-up, 14 (93%) patients in the vaginal group and 11 (73%) in the transanal group reported improvement in symptoms (p=0.08). The need to digitally assist rectal emptying decreased significantly in both groups, from 11 to 1 (73 to 7%) for the vaginal group and from 10 to 4 (66 to 27%) for the trans-
Results of transanal rectocele repair
Study
n
Mean follow-up (months)
Results
Complications
Sullivan et al.51
137
18
Anatomic cure 96% Difficult evacuation: 58% pre-op, 2% post-op Fecal incontinence: 39% pre-op, 3% post-op Dyspareunia 0%
1 RV fistula
Schapayak73
355
Anatomic cure 98% Constipation: 82% pre-op, 15% post-op
Infection 6% RV fistula 0.3%
Jansen & van Dijke47
64
12
Anatomic cure 70% Difficult evacuation: 72% pre-op, 16% post-op Fecal incontinence: 46% pre-op, 9% post-op Vaginal digitation: 26% pre-op, 4% post-op
None
Murthy et al.21
32
31
Constipation 84% improvement Vaginal bulge: 58% pre-op, 12% post-op
RV fistula 3%
34
10
Constipation 79% improvement
Bleeding 9%
123
38
82% improvement Reoperation 10%
Wound dehiscence 2.4% RV fistula 0.8%
Vaginal bulge: 72% pre-op, 14% post-op
None
Karlbom et al.20 Khubchandani et al.10 Rao et al.74 53
75
Ho et al.
21
37
100% improvement ↓ mean resting and maximum squeeze anal pressures
None
Tjandra et al.75
59
19
Improved evacuation without anismus 93% Improved evacuation with anismus 38% Vaginal bulge: 88% pre-op, 13% post-op
Bleeding 1.7%
Ayabaca et al.76
49
48
Anatomic cure 90% Constipation: 83% pre-op, 32% post-op Fecal incontinence: 71% pre-op, 27% post-op
1 infection 1 pyogenic granuloma 4 dehiscence 1 anal fissure
post-op; postoperatively; pre-op, preoperatively; RV, rectovaginal.
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anal group (p=0.17 between groups). Rectocele recurrence rates were 7% and 40%, respectively (p=0.04), and enterocele rates were zero and 27%, respectively (p=0.05). A 27% improvement rate in dyspareunia was noted; none of the patients developed de novo dyspareunia.79
Graft-augmented approach The ideal mesh or graft (allograft or autograft) material used to augment repairs of pelvic fascial defects remains elusive. It should be inexpensive and improve recurrence rates, it should not be rejected, and should cause no detriment to sexual and bowel function. Currently, there are few long-term data regarding the use of graft materials and mesh in the posterior segment. Results of graft augmentation are summarized in Table 72.4.56,61,68,80–84 Anatomic cure rates range from 92 Table 72.4.
to 100% (12–30 month follow-up) with the transvaginal approach, and 89–95% (12–29 month follow-up) with the transperineal approach. De novo dyspareunia rates range from 3 to 20%. Several studies show an improvement in bowel function.61,80,81 In a prospective, controlled trial, Sand et al. randomly assigned 160 patients to undergo anterior and posterior colporrhaphy with (80 patients) or without (80 patients) polyglactin 910 mesh reinforcement. Preoperatively, 91 women had a rectocele to the mid-vaginal plane, 31 to the hymeneal ring, and 22 beyond the introitus. In the treatment group, a strip of mesh was incorporated into the imbricating endopelvic fascia during the midline plication. Thirteen recurrent rectoceles were noted at 1 year follow-up, with no differences observed between the two groups (10% versus 8%).68 The use of non-synthetic grafts may have a lower erosion rate, although this has yet to be confirmed in
Results of graft augmentation in the posterior segment
Study
n
Graft
Osler & Astrup80
15
Sand et al.68
Mean follow-up (months)
Results
Complications
Dermis, autologous 30
Anatomic cure 100% Difficult evacuation: 58% pre-op, 2% post-op Vaginal bulge: 80% pre-op, 0% post-op
1 infection 3 de novo dyspareunia
73
Polyglactin
12
Anatomic cure 92%
None
43
Polypropylene
12
Anatomic cure 100%
1 RV fistula 3 erosions
43
Dermis, cadaveric
12
Anatomic cure 93%
None
Dell & O’Kelley
41
Dermis, porcine
12
Average Ap: 0.3 pre-op, –2.3 post-op Average Bp: 1.2 pre-op, –2.5 post-op 0% dyspareunia
6 vaginal dehiscence
Dwyer & O’Reilly84
50
Polypropylene
29
Anatomic cure 100% 0% erosion
1 RV fistula 1 de novo dyspareunia
9
Polypropylene
29
Anatomic cure 89% Difficult evacuation: 100% pre-op, 12% post-op Vaginal bulge: 100% pre-op, 0% post-op
1 de novo dyspareunia
14 polypropylene 8 polyvinyl
12
Anatomic cure 95% Constipation: 50% pre-op, 14% post-op Difficult evacuation: 95% pre-op, 32% post-op Vaginal bulge: 86% pre-op, 23% post-op
1 de novo dyspareunia
Transvaginal
82
Goh & Dwyer
Kohli & Miklos56 83
Transperineal Watson et al.61
Mercer-Jones et al.81
22
Ap/Bp, two points along the posterior vaginal wall; post-op; postoperatively; pre-op; preoperatively; RV, rectovaginal.
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randomized controlled trials. In a recent retrospective review by Dwyer and O’Reilly, polypropylene mesh was used as an overlay for repair of large or recurrent anterior and posterior compartment prolapse. Forty-seven patients had mesh placed under the bladder base with lateral extensions onto the pelvic sidewall, 33 women had a Y-shaped mesh placed from the sacrospinous ligaments to the perineal body, and 17 women had mesh placement in both compartments. Of the erosions that occurred in nine women (9%), six lesions were in the posterior segment. One woman required surgical repair of a rectovaginal fistula.84 In contrast, at 12 months of follow-up, Kohli and Miklos reported no complications (including erosion or fistula) in 43 women after placement of a cadaveric dermal graft.56 At 1-year follow-up of 35 women, Dell and O’Reilly noted no erosions after the use of a porcine collagen mesh that contained fenestrations in the graft material. They also described 6/41 patients that experienced wound separation and delayed vaginal healing when they previously employed the non-fenestrated form of the same material. The authors suggested that the fenestrations allowed immediate contact between the vaginal mucosa and underlying host tissues, thus facilitating appropriate tissue ingrowth.83
CONCLUSIONS The prevalence of surgical repair for urinary incontinence or genital prolapse has exceeded more than 10% of all women who reach the eighth decade of life.85 With society’s gradually aging population, there will be a large number of women suffering from rectoceles or defecation disorders. A thorough pelvic assessment is necessary prior to any planning regarding surgical or non-surgical intervention for pelvic organ prolapse. Patient history will direct the physician to look for appropriate findings on physical examination. The use of pelvic floor imaging may complement the clinical assessment of the pelvic floor, but its use needs to be further studied and defined prior to advocating its routine use. Ultimately, the goal of the evaluation is to fully appreciate the extent of the posterior vaginal wall prolapse and to relate that to any visceral or sexual dysfunction that may coexist.
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42. Tunn R, Paris S, Taupitz M et al. MR imaging in posthysterectomy vaginal prolapse. Int Urogynecol J Pelvic Floor Dysfunct 2000;11(2):87–92. 43. Kelvin FM, Maglinte DD. Radiologic investigation of prolapse. J Pelv Surg 2000;6:218–20.
27. Burrows LJ, Sewell C, Leffler KS et al. The accuracy of clinical evaluation of posterior vaginal wall defects. Int Urogynecol J Pelvic Floor Dysfunct 2003;14(3):160–3.
44. Lienemann A, Anthuber C, Baron A et al. Dynamic MR colpocystorectography assessing pelvic-floor descent. Eur Radiol 1997;7(8):1309–17.
28. Maglinte DD, Kelvin FM, Hale DS et al. Dynamic cystoproctography: a unifying diagnostic approach to pelvic floor and anorectal dysfunction. Am J Roentgenol 1997;169(3):759–67.
45. Beer-Gabel M, Teshler M, Barzilai N et al. Dynamic transperineal ultrasound in the diagnosis of pelvic floor disorders: pilot study. Dis Colon Rectum 2002;45(2):239–45.
29. Kelvin FM, Maglinte DD, Hale DS et al. Female pelvic organ prolapse: a comparison of triphasic dynamic MR imaging and triphasic fluoroscopic cystocolpoproctography. Am J Roentgenol 2000;174(1):81–8. 30. Yang A, Mostwin JL, Rosenshein NB et al. Pelvic floor descent in women: dynamic evaluation with fast MR imaging and cinematic display. Radiology 1991;179(1):25–33. 31. Kelvin FM, Maglinte DD, Hornback JA et al. Pelvic prolapse: assessment with evacuation proctography (defecography). Radiology 1992;184(2):547–51. 32. Altringer WE, Saclarides TJ, Dominguez JM et al. Fourcontrast defecography: pelvic ‘fluoroscopy’. Dis Colon Rectum 1995;38(7):695–9. 33. Halligan S. Commentary: imaging of anorectal function. Br J Radiol 1996;69(827):985–8. 34. Stoker J, Halligan S, Bartram CI. Pelvic floor imaging. Radiology 2001;218(3):621–41. 35. Kelvin FM, Maglinte DDT. Dynamic evaluation of female pelvic organ prolapse by extended proctography. Radiol Clin North Am 2003;41(2):395–407. 36. Bartram CI, Turnbull GK, Lennard-Jones JE. Evacuation proctography: an investigation of rectal expulsion in 20
46. Karaus M, Neuhaus P, Wiedenmann TB. Diagnosis of enteroceles by dynamic anorectal endosonography. Dis Colon Rectum 2000;43(12):1683–8. 47. Janssen LW, van Dijke CF. Selection criteria for anterior rectal wall repair in symptomatic rectocele and anterior rectal wall prolapse. Dis Colon Rectum 1994;37(11):1100–7. 48. Pucciani F, Rottoli ML, Bologna A et al. Anterior rectocele and anorectal dysfunction. Int J Colorectal Dis 1996;11:1–9. 49. Infantino A, Masin A, Melega E et al. Does surgery resolve outlet obstruction from rectocele? Int J Colorectal Dis 1995;10(2):97–100. 50. Kahn MA, Stanton SL. Posterior colporrhaphy: its effects on bowel and sexual function. Br J Obstet Gynaecol 1997;104(1):82–6. 51. Sullivan ES, Leaverton GH, Hardwick CE. Transrectal perineal repair: an adjunct to improved function after anorectal surgery. Dis Colon Rectum 1968;11(2):106–14. 52. Smith AN, Varma JS, Binnie NR, Papachrysostomou M. Disordered colorectal motility in intractable constipation following hysterectomy. Br J Surg 1990;77(12):1361–5. 53. Ho YH, Ang M, Nyam D et al. Transanal approach to rec-
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tocele repair may compromise anal sphincter pressures. Dis Colon Rectum 1998;41(3):354–8. 54. van Dam JH, Huisman WM, Hop WC et al. Fecal continence after rectocele repair: a prospective study. Int J Colorectal Dis 2000;15(1):54–7. 55. Goh JT, Tjandra JJ, Carey MP. How could management of rectoceles be optimized? Aust N Z J Surg 2002;72(12):896–901. 56. Kohli N, Miklos JR. Dermal graft-augmented rectocele repair. Int Urogynecol J Pelvic Floor Dysfunct 2003;14(2):146–9. 57. Baden W, Walker T. Evolution of the defect approach. In: Baden W, Walker T (eds) Surgical Repair of Vaginal Defects. New York: JB Lippincott, 1992; 1–7. 58. Baden W, Walker T. Vaginal approach to posterior vaginal defects: the rectal site. In: Baden W, Walker T (eds) Surgical Repair of Vaginal Defects. New York: JB Lippincott, 1992; 209–18. 59. Nichols DH, Randall CL. Posterior colporrhaphy and perineorrhaphy. In: Nichols DH, Randall CL (eds) Vaginal Surgery, 4th ed. Baltimore: Lippincott Williams and Wilkins, 1996; 257–89. 60. Wheeless CR. Posterior repair. In: Wheeless CR (ed) Atlas of Pelvic Surgery, 3rd ed. Baltimore: Williams and Wilkins, 1997; 46–9. 61. Watson SJ, Loder PB, Halligan S et al. Transperineal repair of symptomatic rectocele with Marlex mesh: a clinical, physiological and radiologic assessment of treatment. J Am Coll Surg 1996;183(3):257–61. 62. Parker MC, Phillips RK. Repair of rectocele using Marlex mesh. Ann R Coll Surg Engl 1993;75(3):193–4. 63. Addison WA, Cundiff GW, Bump RC, Harris RL. Sacral colpopexy is the preferred treatment for vaginal vault prolapse. J Gynecol Tech 1996;2:69–74. 64. Lyons TL, Winer WK. Laparoscopic rectocele repair using polyglactin mesh. J Am Assoc Gynecol Laparosc 1997;4(3):381–4. 65. Cundiff GW, Harris RL, Coates K et al. Abdominal sacral colpoperineopexy: a new approach for correction of posterior compartment defects and perineal descent associated with vaginal vault prolapse. Am J Obstet Gynecol 1997;177(6):1345–53. 66. Arnold MW, Stewart WR, Aguilar PS. Rectocele repair. Four years’ experience. Dis Colon Rectum 1990;33(8):684–7. 67. Weber AM, Walters MD, Piedmonte MR. Sexual function and vaginal anatomy in women before and after surgery for pelvic organ prolapse and urinary incontinence. Am J Obstet Gynecol 2000;182(6):1610–15. 68. Sand PK, Koduri S, Lobel RW et al. Prospective randomized trial of polyglactin 910 mesh to prevent recurrence of cystoceles and rectoceles. Am J Obstet Gynecol 2001;184:1357–62.
69. Porter WE, Steele A, Walsh P et al. The anatomic and functional outcomes of defect-specific rectocele repairs. Am J Obstet Gynecol 1999;181(6):1353–8. 70. Kenton K, Shott S, Brubaker L. Outcome after rectovaginal fascia reattachment for rectocele repair. Am J Obstet Gynecol 1999;181(6):1360–3. 71. Glavind K, Madsen H. A prospective study of the discrete fascial defect rectocele repair. Acta Obstet Gynecol Scand 2000;79(2):145–7. 72. Singh K, Cortes E, Reid WM. Evaluation of the fascial technique for surgical repair of isolated posterior vaginal wall prolapse. Obstet Gynecol 2003;101(2):320–4. 73. Schapayak S. Transrectal repair of rectocele: an extended armamentarium of colorectal surgeons. A report of 355 cases. Dis Colon Rectum 1985;28(6):422–33. 74. Rao GN, Carr ND, Beynon J et al. Endorectal repair of rectocoele revisited. Br J Surg 1997;84(7):1034. 75. Tjandra JJ, Ooi BS, Tang CL et al. Transanal repair of rectocele corrects obstructed defecation if it is not associated with anismus. Dis Colon Rectum 1999;42(12):1544–50. 76. Ayabaca SM, Zbar AP, Pescatori M. Anal continence after rectocele repair. Dis Colon Rectum 2002;45(1):63–9. 77. Van Laarhoven CJ, Kamm MA, Bartram CI et al. Relationship between anatomic and symptomatic long-term results after rectocele repair for impaired defecation. Dis Colon Rectum 1999;42(2):204–10. 78. Marti MC, Roche B, Déléaval J. Rectoceles: value of videodefaecography in selection of treatment policy. Colorectal Dis 1999;1:324–9. 79. Nieminen K, Hiltunen KM, Laitinen J et al. Transanal or vaginal approach to rectocele repair: a prospective, randomized pilot study. Dis Colon Rectum 2004;47(10):1636–42. 80. Oster S, Astrup A. A new vaginal operation for recurrent and large rectocele using dermis transplant. Acta Obstet Gynecol Scand 1981;60(5):493–5. 81. Mercer-Jones MA, Sprowson A, Varma JS. Outcome after transperineal mesh repair of rectocele: a case series. Dis Colon Rectum 2004;47(6):864–8. 82. Goh JW, Dwyer PL. Effectiveness and safety of polypropylene mesh in vaginal prolapse surgery. Int Urogynecol J 2001;12:S90. 83. Dell JR, O’Kelley KR. PelviSoft BioMesh augmentation of rectocele repair: the initial clinical experience in 35 patients. Int Urogynecol J Pelvic Floor Dysfunct 2005;16(1):44–7; discussion 47. 84. Dwyer PL, O’Reilly BA. Transvaginal repair of anterior and posterior compartment prolapse with Atrium polypropylene mesh. BJOG 2004;111(8):831–6. 85. Olsen AL, Smith VJ, Bergstrom JO et al. Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 1997;89(4):501–6.
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73 Vaginal approach to fixation of the vaginal apex May Alarab, Harold P Drutz
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IntroductIon Caring for women with pelvic floor disorders has become an increasingly important component of women’s health care. Pelvic organ prolapse is a major health issue for women; it affects almost half of all women over 50 years of age, with a lifetime prevalence of 30–50%.1 A 1997 study found that women with normal life expectancy will, by the age of 79 years, have an 11–12% chance of undergoing at least one operation for prolapse or incontinence, with a reoperation rate of 29%.2 With the current generation of women maintaining a more active lifestyle into an older age, it is likely that an increasing number of women will seek treatment for prolapse – a condition requiring increasing expertise on the part of the urogynecologist and pelvic reconstructive surgeon. It has been projected that over the next 30 years, the rate of women seeking care for pelvic floor disorders will double.3 Conservative management of pelvic organ prolapse using vaginal pessaries is a known and effective method of treating this problem; however, patients are increasingly inclined towards more permanent solutions to correct their symptoms while maintaining body image and coital function. Numerous surgical operations have been described for the support of the vaginal apex at the time of hysterectomy or for posthysterectomy vault prolapse, and are performed either abdominally or vaginally. In this chapter we will describe the different vaginal approaches for fixation of the vaginal apex.
HIstory Genital prolapse in antiquity finds its roots in the Ebers Papyrus (1500 BC).4 Soranus of Ephesus (AD 98–138) is commonly considered the foremost gynecologic authority of antiquity. He proposed vaginal hysterectomy for uterine prolapse in AD 120.5 The vaginal reconstructive approach was first described by Zweifel in 18926 and involved suspension of the prolapsed vagina to the sacrotuberous ligament. In 1909, White suspended the vaginal vault to the tendinous arch of the obturator fascia via a transvaginal approach.7 A transvaginal technique suspending the vaginal vault to the sacrouterine ligaments just below the sacral promontory was reported by Miller in 1927.8 In 1951, Amreich described a trasgluteal, and later a transvaginal, approach to attach an everted vagina to the sacrotuberous ligament.9 Sederl first tried the use of the sacrospinous ligament for this purpose in 1958.10 Richter introduced the sacrotuberous fixation in Europe in 1967, and one year later described the use of the sacrospinous ligament as an improved technique for the suspension
of the vaginal vault.11 This procedure was introduced in the United States by Randall and Nichols in 1971,12 and has been increasingly popular since then. Cruikshank and Cox have described the use of sacrospinous ligament fixation as an adjuvant to vaginal hysterectomy and colporrhaphy for marked uterovaginal prolapse in the presence of poor integrity of the endopelvic fascia.13
AnAtomIc consIderAtIon The normal support of the pelvic floor is based on three mechanical principles: 1. the uterus and vagina are attached to the walls of the pelvis by the endopelvic fascia that suspends the organs from the pelvic sidewalls; 2. the levator ani muscle constrict the lumens of these organs until they are closed, forming an occlusive layer on which the pelvic organs may rest;14 3. the flap valve, where the vagina is suspended in such a way that it rests against the supporting wall adjacent to it, controls increases in pressure which force the vagina against the wall, pinning it in place.15 The part of the pelvic fascia that attaches the uterus to the pelvic walls (i.e. the broad, cardinal, and uterosacral ligaments) is called the parametrium; similar tissue attaching the vagina to the pelvic walls is called the paracolpium. Unlike other ligaments in the body that are made of dense connective tissue, these ligaments contain blood vessels, nerves, and fibrous connective tissue (smooth muscle, collagen, and elastin), a composition that reflects their function as neurovascular and supportive structures. The paracolpium is attached to the upper two-thirds of the vagina, and consists of two portions: Level I (suspension, Fig. 73.1) consist of a relatively long sheet of tissue that converges from its broad origin on the lateral pelvic walls and sacrum to its attachment to the lateral walls of the vagina. Defective suspension at this level presents clinically as uterine or vaginal vault prolapse. At Level II (attachment) the mid-portion of the vagina is attached laterally and more directly to the pelvic walls, and stretches the vagina transversely between the bladder and the rectum. This part includes the pubocervical fascia anteriorly and the rectovaginal fascia posteriorly. At this level the vagina comes closer to the pelvic wall, and failure of level II support presents as cystocele or rectocele, or both. In the distal part of the vaginal wall (Level III: fusion) that extends from the introitus 2–3 cm above the hymeneal ring, the vagina is fused laterally to the levator ani muscle, posteriorly to the perineal body, and anteriorly it blends with the
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S1
S2
Hypogastric a.
S3
S4
Inf. gluteal a.
Pudendal n.
Int. pudendal a.
Sciatic n.
Coccygeal a. Sacrosp. lig. Sacrotub. lig.
Figure 73.1. At level I, paracolpium suspends the vagina from the lateral pelvic walls. Fibers of level I extend both vertically and posterior towards the sacrum. At level II, the vagina is attached to the arcus tendineus fasciae pelvis and superior fascia of the levator ani muscles. At level III, the vagina is fused to the medial surface of the levator ani muscles, urethra, and perineal body. (Reproduced from ref. 16 with permission from Elsevier.) urethra and is embedded in the connective tissue of the perineal membrane, with no intervening paracolpium. The attachments at this level are so dense that the vagina is left with no mobility, and displacement of the levator ani muscle, perineal body or the urethra will carry the vagina along with it.16
surgIcAl AnAtomy Pelvic fascia and ligaments have been used to suspend the prolapsed vagina; however, it should be borne in mind that the nerves and vessels surrounding these anchoring structures are susceptible to injury during surgical repair. In order to reduce hemorrhage and postoperative pain secondary to colpopexy operations, it is essential to understand the anatomic relations of the pelvic organs and their adjacent neurovascular structures. The pararectal space is filled with fat and loose areolar tissue, and the middle rectal artery and the nerve of the levator ani muscle course through this space.17 The sacrospinous ligament, located within the substance of the coccygeal muscle,18 extends from the lateral sacrum to the ischial spine (Fig. 73.2). The average length of the sacrospinous ligament is 43.04±6.58 mm;19 it divides the
Figure 73.2. Left hemipelvis. The sacrospinous ligament covered by the coccygeus muscle extends from the ischial spine to the sacrum. The pudendal neurovascular structures pass beneath the sacrospinous ligament at the ischial spine. The inferior gluteal artery passes between the sciatic nerve and the sacrospinous ligament. (Reproduced from ref. 20 with permission.) sciatic notch into the greater and lesser sciatic foramina. The inferior gluteal artery, after originating from the internal iliac artery, descends inferolaterally, passing through the greater sciatic foramen and leaves the pelvis by crossing the upper border of the sacrospinous ligament 8.54 mm from the ischial spine, accompanied by the inferior gluteal vein. After emerging from the sacral plexus, the inferior gluteal nerve passes close to the vessels and leaves the infrapiriform foramen by crossing the upper border of the sacrospinous ligament 13.82 mm from the ischial spine. Leaving the pelvis, the inferior gluteal complex crosses the sciatic nerve posteriorly, and branches inside the gluteus maximus muscle. The internal pudendal artery, after originating from the internal iliac artery (the anterior branch) and accompanied by the internal pudendal vein, reaches the upper border of the ligament and leaves the infrapiriform foramen accompanied by the pudendal nerve. The pudendal complex lies a maximum of 5.5 mm medial to the spine. The sciatic nerve is the most lateral of the structures emerging from the infrapiriform foramen, situated on average 25.14±3.94 mm lateral to the ischial spine.19 The coccygeal branch of the inferior gluteal artery passes 1055
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immediately behind the mid-portion of the sacrospinous ligament and pierces the sacrotuberous ligament at multiple sites. During the procedure of sacrospinous vault suspension, placing the sutures immediately medial and inferior to the ischial spine may cause injury to the pudendal vessels. However, placing the sutures superior to the midportion of the ligament may cause injury to the inferior gluteal artery. The coccygeal branches of the inferior gluteal artery may be injured if any deep suture traverses the full thickness of the ligament. Thompson et al. have shown that, by placing the sutures through the sacrospinous ligament 2.5 cm or more medially from the ischial spine along the superior border of the ligament and not through the full thickness, the risk of complications is minimal.20
etIology And pAtHopHysIology The opening in the levator ani muscle, through which the vagina and urethra pass, is called the urogenital hiatus of the levator ani (through which prolapse occurs). Although the rectum also passes through the opening, it is not included in the hiatus because the levator ani muscle attaches directly to the anus and the external anal sphincter. The hiatus is surrounded by the pubic bones anteriorly, the levator ani muscle laterally, and the perineal body and the external anal sphincter posteriorly. The levator ani muscle is always contracting, keeping the urogenital hiatus closed. It closes the vagina, urethra, and rectum by compressing them against the pubic bone, thus preventing any opening in the pelvic floor through which prolapse may occur. As long as the levator ani muscle functions normally, the pelvic floor is closed; the ligaments and fascia are under no tension. When the muscles relax or are damaged, the pelvic floor opens and the pelvic organs lie between the high abdominal pressure and the low atmospheric pressure; here the organs must be held in place by the ligaments, which can sustain the load for only a short period of time and eventually become damaged and fail to hold the vagina in place. This failure is due not only to acute damage, but also from the inability of the ligaments to self-repair. The injury to the connective tissue in the pelvis is due to rupture rather than stretching.21 Neuromuscular injuries to the pelvic floor are associated with the development of pelvic organ prolapse (POP).22 The health and function of the pelvic muscles provide significant protection to the ligaments to avoid POP. The neuromuscular damage to the pelvic floor that occurs during parturition plays a major role in the etiology of prolapse; however, the loads on the
pelvic floor resulting from increases in abdominal pressure also play a significant role in the development of this disorder – for example, continuous heavy lifting, chronic obstructive pulmonary disease, obesity, chronic constipation, large fibroids or tumors. Direct damage to the muscle may result from previous pelvic surgery, spinal cord conditions and injury, thinning of the muscle and fascia that occurs with postmenopausal atrophy and attenuation, and finally the collagen status of these groups of patients. It has been shown that women with Marfan or Ehlers–Danlos syndrome have high rates of urinary incontinence and POP. This finding supports the hypothesized etiologic role of connective tissue disorders as a factor in the pathogenesis of these conditions.23 These facts have been confirmed by recent studies showing decreased collagen and smooth muscle content in women with POP, with or without stress urinary incontinence (SUI), regardless of age, parity, body mass index or smoking,24 and increased collagen breakdown in the SUI and POP groups compared to controls.25
symptoms, presentAtIon And evAluAtIon Patients with vaginal apical prolapse can vary from being asymptomatic to presenting with various complaints of vaginal pressure, feeling something coming down, coital difficulties, urinary symptoms (urgency, frequency, incontinence or voiding dysfunction), and bowel emptying difficulties due to concomitant anterior and posterior vaginal wall defects. Burrows et al. investigated the correlation of symptoms with the severity of POP, and concluded that the more advanced the prolapse, the less likely the woman would have SUI, and the more likely to manually reduce prolapse to void; however, prolapse severity was not associated with sexual or bowel symptoms.26 Another study correlating symptoms in women with or without enterocele showed that women with enterocele were more likely to be older, postmenopausal, to have had posthysterectomy or vaginal prolapse repairs, and to have more advanced apical and posterior vaginal prolapse than women without enterocele, but not to differ from them in bowel function.27 A patient may present to a gynecologist, a urologist or a colorectal surgeon depending on their major complaint. A detailed history is taken, including a history of the chief complaint, urinary and bowel symptoms, obstetric and medical history, and current medication. A careful speculum and digital examination at rest and with straining is performed to quantify POP and SUI. By placing the Sim’s speculum along the posterior vaginal wall and asking the patient to bear down, we look for
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anterior compartment prolapse; the opposite is done to examine the posterior vaginal wall. A digital rectal–vaginal examination while the patient is straining is performed to differentiate between a high rectocele and an enterocele. There are numerous grading systems for prolapse.28–31 The pelvic organ prolapse quantification (POPQ) system31 produced by the International Continence Society has gained popularity among urogynecologists to describe, measure, and stage prolapse. Careful vaginal examination is vital to identify the site-specific vaginal wall prolapse present, and to identify patients at risk of developing SUI after their reconstructive surgery. SUI has been strongly associated with POP,32,33 and it has been shown that mild to moderate POP is often associated with SUI; however, women with severe POP rarely complain of urine leakage because of urethral kinking and increased urethral resistance with the urogenital prolapse in an unreduced state.34–36 In fact, these patients may complain of difficulty in voiding, with an elevated post-void residual volume and recurrent urinary tract infections.37 Liang et al. showed a 65.8% incidence of trabeculation in preoperative urethrocystoscopic evaluation in patients with marked prolapse; this can be attributed to the obstruction caused by the large prolape.38 The leakage problem manifests after correction of the prolapse in what is called occult or latent SUI, one of the common problems seen with complex vault prolapse.39 The incidence of occult SUI can vary from 22 to 80%, and can be quite distressing.40,41 Investigating abdominal leak point pressures (ALPPs) in patients with vaginal vault prolapse, Gallentine and Cespedes have shown a 50% incidence of occult SUI, with a mean decrease in ALPP of 59 cmH2O after prolapse reduction, a drop that is more marked than in patients with cystocele alone.42 Traditionally, the prolapse is reduced by inserting a pessary, and a recent study confirmed that continent patients suffering from severe POP, but with a positive pessary test and who did not undergo a concomitant SUI procedure, had a 64.7% risk of urinary leakage after their prolapse surgery.38 However, Bump et al., in an extensive study, showed that there was a high falsepositive rate of incontinence with barrier testing.43 If occult incontinence is not demonstrated, a concomitant incontinence procedure, with its associated morbidity, may be safely omitted.35 Investigations which may be required prior to any prolapse repair include accurate preoperative urodynamic studies (with the prolapse reduced to examine the expected outcome after repair), cystourethroscopy, and abdominal–pelvic ultrasound. In addition, transanal studies may be required if there is a history of fecal
incontinence. Other tests include defecography, anorectal motility studies, pudendal motor nerve latency studies, and magnetic resonance imaging of the pelvic floor.
surgIcAl tecHnIques In supportIng tHe vAgInAl Apex (vAgInAl ApproAcH) The vaginal approach to prolapse surgery carries significant low postoperative morbidity, and does not require additional skill or the cost of laparoscopy. It provides the option to perform the operation under regional or general anesthesia, and the ability to repair other pelvic defects simultaneously. Various techniques have been described for the treatment of vault prolapse: these include sacrospinous vault suspension, iliococcygeus muscle fixation, uterosacral ligament fixation, McCall culdoplasty, and posterior intravaginal slingoplasty. The different techniques of restoration of the vaginal apical defect are outlined as follows.
sacrospinous vault suspension Indications The main indication for sacrospinous ligament suspension is to correct total procidentia, or posthysterectomy vaginal vault prolapse with an associated weak cardinal uterosacral ligament complex, and in posthysterectomy enterocele.44,45 Bilateral sacrospinous ligament fixation has been described and recommended in patients with recurrent vault prolapse,46,47 or a desire to maintain a wide vaginal vault.48 The procedure has also been described as a prophylactic step at the time of vaginal hysterectomy against subsequent vaginal vault prolapse,13,49 as well as in patients with marked prolapse who wish to retain their uterus.50–52
Contraindications A short vagina, mainly attributed to previous repeated repairs, is considered the principal contraindication to performing sacrospinous colpopexy; the surgeon needs to ensure that there is an adequate vaginal depth to allow the attachment of the vault to the ligament without any tension. Surgical inexperience is another contraindication, and the procedure should only be performed by experienced reconstructive pelvic surgeons.
Surgical techniques Postmenopausal patients with vaginal atrophy usually benefit from preoperative local hormone treatment to improve the quality of the tissues, and to help improve the vascularity of the operative site. Preoperative intravenous prophylactic antibiotics as well as measures for 1057
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prophylaxis against venous thromboembolism (compression stockings and low dose subcutaneous heparin) are recommended. After the patient receives the appropriate anesthesia, bearing in mind the feasibility of regional anaesthesia with the vaginal approach, the surgery is performed with the patient in the dorsal lithotomy position. An intraoperative assessment allows the surgeon to identify the extent of the prolapse, and to confirm that the vault can reach the ligament without tension. In a marked uterovaginal prolapse, a vaginal hysterectomy is performed initially in the usual fashion; if a cystocele is present, this is dealt with next, usually with standard suburethral buttressing sutures.16,53 Some authors have suggested the addition of polyglactin mesh as an extra support to the anterior vaginal wall; however, a randomized trial by Weber et al. showed that this technique did not improve the cure rate compared to standard anterior colporrhaphy.54 Sand et al., in a similar caliber study, found the addition of mesh to be useful in the prevention of recurrent cystocele.55 Flood et al. have shown that reinforcing anterior colporrhaphy with Marlex mesh is highly effective in preventing recurrence of cystocele with minimal complications.56 When an enterocele is identified – usually noted as a distinct loss of the rectovaginal fascia with a sudden protrusion of the enterocele sac – it is demarcated by the pubocervical fascia anteriorly and the rectovaginal septum posteriorly. The sac is dissected free, opened, and a high ligation performed with a 2-0 type permanent purse-string suture.57 Sacrospinous ligament suspension is usually performed via the posterior approach. It starts with a longitudinal incision in the posterior vaginal wall after infiltration with a dilute solution of epinephrine
a
b
(1:200,000). The incision extends from the introitus to the vault, and the epithelium is dissected laterally on both sides, penetrating the right rectal pillar into the pararectal space near the ischial spine. The right ischial spine is palpated and, using a combination of sharp and blunt dissection, a window is created between the ligament and the rectovaginal space. It is important to split the fascia in front of the ligament that is palpated as a cord-like structure to ensure that the suture placement will involve the body of the ligament. The rectum is mobilized medially with the fingers and, with one retractor protecting the rectum medially, the Miya hook ligature carrier58 (Fig. 73.3a) – loaded with two delayed absorbable sutures and held in the right hand of the surgeon with the tip protected by the surgeon’s left index finger – is introduced into the vagina while an assistant retracts the rectum to the left with a Heaney retractor. The sutures are placed into the ligament at two fingerbreadths medial to the spine and just inferior to the superior border of the ligament, thus avoiding injury to the pudendal complex. Care must be taken not to penetrate the full thickness of the ligament to avoid injury to the inferior gluteal vessels and nerve. At the required location at the ligament, the hook is closed and the handle of the hook is lifted upwards, bringing the tip out of the ligament. A notched vaginal speculum is placed just below the tip of the hook (Fig. 73.3b) and the sutures retrieved with a nerve hook. Threading two sutures at the same time avoids the need to repeat the insertion. The two sutures are paired, loaded separately onto a Mayo needle, and passed through the angles of the vaginal epithelium at the level of the vault, 1–2 cm apart, and held for later tying.59 If bilateral suspension is to be performed, one suture will be placed per site.60
Figure 73.3. (a) Miya hook; (b) notched speculum.
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The anterior rectocele and the rectovaginal septum are repaired by interrupted absorbable sutures (Vicryl 2-0). The levator muscles are approximated separately with Vicryl No. 1 suture, but left untied at this stage; the ends are held. The bulbocavernosus muscle is approximated and held, and the vaginal skin is closed with a continuous locking suture until the level of the introitus. The sacrospinous sutures are tied, pulling the vault onto the ligament, ensuring a close approximation and avoiding the suture bridge between the vault and the ligament. Finally, the levator and bulbocavernousus muscle sutures are tied, and the vaginal skin is closed. A slight deviation of the vaginal apex to the right may be noted at the end of the procedure; this may be of benefit as the vault will no longer be subjected to intra-abdominal pressure after the operation.45 At the end of surgery, the bladder is drained transurethrally; a vaginal pack and hemovac drain are inserted if necessary in the reconstructed vagina, both to be removed in 24 hours. The earlier description of the procedure involves exposure of the ligament and placement of the sutures under direct vision.45,61 The ligament is grasped with an Allis forceps and a Deschamps ligature carrier is used to place the suture into the ligament; this technique requires more dissection in the pararectal space.61 Another modification is the Sharp technique, which uses the shut suture punch system.62 With its automatic suture retrieval, this method proved to be quick and easy, especially in obese patients; the downside, however, is that the sutures need to be of rigid material such as nylon or polypropylene. Watson has described using the Endo Stitch (a laparoscopic suturing instrument) to pass the suture through the sacrospinous ligament; advantages of this tool include a predictable penetration depth, without the need for a retrieval hook.63 The same advantages have been described with the Raz Anchoring System (RAS).64 On the other hand, Morley and DeLancey45 found that, with the help of traditional retractors, a straight or curved needle holder could position the suture with little difficulty. Their other modifications include creating a neovaginal apex via a circumscribing incision at the prolapse proper.45 Anterior sacrospinous vault suspension has been described, where the ligament is approached through an anterior vaginal incision. Goldberg et al. have shown that with this technique there will be a slight increase in vaginal length, with a decrease in recurrence of anterior vaginal wall prolapse.65 The choice of suture material remains controversial: some advocate the use of absorbable sutures;11,12,17,45,66
others used delayed absorbable or permanent sutures13,44– 46,58,59,67 to allow adequate time for fibrosis and scarring between the sacrospinous ligament and the vaginal apex. When absorbable sutures are used, they are passed through the full thickness of the vagina and tied over the vaginal mucosa, unlike the permanent sutures which should be passed submucosally in a double helix and tied beneath the vaginal mucosa.59,60
Results Thirty-six studies13,17,44–47,59–61,64–92 on sacrospinous colpopexy involving more than 2610 patients have been reported; these included women who underwent the procedure for posthysterectomy prolapse and procidentia. The lack of objective outcome measures and the variety of definitions of success made the data difficult to collate. Sze and Karram93 published a meta-analysis of the available literature, where 86% of patients were followed from 1 month to 11 years. Three investigators45,72,81 reported subjective or objective cure rates of 77–82%, while other studies did not specify the assessment method of the cure rate.12,58,61 The cure rate in general ranged between 879 and 97%.61 Based on the vault support alone as a final outcome, success was achieved in 80–90% of cases. The sacrospinous vault suspension distorts the vaginal axis, predisposing to future anterior compartment defects, with an incidence ranging between 20–33%83,94 and 92%.79 Goldberg et al. have shown in a retrospective analysis that anterior sacrospinous vault suspension showed a subtle but statistically significant decrease in anterior wall relaxation compared to the traditional posterior approach.65 Lovatsis and Drutz,60 in a 5-year case series study with a total of 293 cases, demonstrated a cure rate of 97% with a minimum of 1-year follow-up. The incidence of de novo SUI was 3.1% and anal incontinence 6%. However, 38 out of 43 patients who had preoperative anal incontinence denied any symptoms after surgery, giving a cure rate of 88.4%. The incidence of postoperative cystocele was 8.5%, and rectocele 3.5%. Nieminen and Heinonem investigated sacrospinous ligament fixation in women aged over 80 years with massive genital prolapse.68 They showed comparative results with younger women, and concluded that, in the absence of major vascular disease, this operation is as safe as the obliterative procedures; they noted, however, that intraoperative bleeding control is important in high risk patients.
Complications Hemorrhage Hemorrhage is the most commonly reported complication, the blood loss ranging from 75 to 839 ml. Sze and 1059
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Karram, in their review of 1229 cases of sacrospinous ligament suspension, found that only 27 (2%) cases required transfusion.93 Barksdale et al., in dissecting 10 female cadaveric pelves, concluded that the location of the inferior gluteal artery (because of its perpendicular course relative to the sacrospinous ligament, approximately mid-way between the ischial spine and the sacrum, and lying in a position immediately posterior to the most common location of suture placement) renders it more susceptible to injury. On the other hand, the pudendal neurovascular bundle was found to be relatively protected by the ischial spine, and therefore injury to the pudendal vessels would be uncommon and would respond to ligation of the internal iliac artery. Massive intraoperative bleeding should be dealt with by packing and vascular clips or packing and arterial embolozation.96 Other causes of bleeding are injury to the perirectal veins,13 sacral veins,44 and severe adhesions,76 mainly attributed to previous surgery. Nerve injury Nerve tissue was found in all parts of the sacrospinous ligament, with the highest concentration at the centre of the ligament.97 Postoperative sciatic neuralgia is induced by traction of the suture on the ligament, the tension being transmitted to the sciatic nerve. Usually the pain resolves in 2–3 weeks; if persistent, transvaginal infiltration of xylocaine may be helpful.97 Gluteal pain has been reported after sacrospinous fixation with an incidence of 3%93 and 6.1%,60 usually resolving spontaneously within 6 months. Immediate postoperative gluteal pain radiating to the posterior surface of the leg, accompanied by paresthesia, usually indicates posterior cutaneous, pudendal or sciatic nerve injury.61 The recommended treatment is immediate reoperation to remove the offending suture and to reposition the new suture in a more medial location on the same or the opposite sacrospinous ligament.61 Injury to pelvic organs Injury to pelvic organs such as the bladder and the rectum has been reported17,45,61,73,80 as a result of their close proximity to the sacrospinous ligament. These injuries should be immediately repaired using conventional techniques. The surgeon must be vigilant regarding this complication, and intraoperative cystoscopy and careful rectal examination after insertion of the suture into the ligament are mandatory. Dyspareunia Sexual function following sacrospinous ligament suspension has been evaluated in numerous stud-
ies.17,71,73,75,79,82 Clinically, the vaginal length is maintained after a sacrospinous suspension procedure. Richter and Albrich17 reported that eight of their patients were afraid to attempt coitus because of a narrowed vagina, while Given et al.95 found that the procedure did not interfere with coital function. Holley et al.79 compared pre- and postoperative sexual activity in 35 patients, and found a higher frequency of sexual intercourse postoperatively, with no associated dyspareunia. Postoperative SUI This complication may be a consequence of vesicourethral junction straightening that results from restoration of vaginal length and depth, or a significant reduction of urethral closure pressure when the vaginal vault is replaced intra-abdominally.61,98 It is recommended that all patients with a large prolapse be evaluated preoperatively to rule out the presence of occult SUI. Voiding dysfunction This problem has been highlighted in those cases where sacrospinous ligament fixation has been performed in conjunction with an incontinence procedure. This can be attributed to dislocation of the vesicourethral region from the right-sided vaginal vault, and ventral fixation in combination with colposuspension.97 Rare complications Other reported rare complications are death from postoperative coronary thrombosis (two patients)61,77 and pulmonary embolism (one patient).68 Evisceration through the vaginal incision has also been reported.99
Failures Failure to maintain the support of the vault after sacrospinous suspension may be attributed to a variety of reasons. Poor approximation of the vault to ligament may play a major role. The presence of the suture bridge will prevent fibrosis taking place between the ligament and the vault, leaving the support mainly dependent on the suture material (this is the main reason why this procedure is contraindicated in patients with short vagina). There is no supporting evidence in the literature that permanent sutures would reduce the incidence of recurrence. Additionally, although bilateral attachment offers better anatomic results with more surface area of attachment, it does not appear to contribute to a reduction in failure rate of the procedure.47 Nieminen et al. have shown that postoperative infection is an independent and most important individual risk factor for recurrence of prolapse, and the lack of intravenous antibiotic prophylaxis, preoperative vaginal
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ulcerations, and low age at operation were significantly associated with infectious complications.100 Prophylactic antibiotics are highly recommended and should be routine, and vaginal ulceration should always be treated preoperatively. If the sacrospinous procedure fails, it can be repeated on the opposite side. Bilateral sacrospinous fixation can also be performed in these circumstances, bearing in mind that fibrosis and scarring may make repeating the procedure on the same side extremely difficult.
vault prolapse repair: vaginal or abdominal route, and why? Both sacrospinous ligament vault suspension and abdominal sacrocolpopexy (laparoscopy or laparotomy) have their own indications with their separate advantages and disadvantages. Reconstructive pelvic surgeons require the surgical expertise and proficiency to do both, and to make an informed choice taking into consideration the patient’s age, weight, medical condition, coital activity, multiple previous laparotomies, and any history of previous failed surgery. The sacrospinous ligament vault suspension has the following advantages:
• It significantly reduces postoperative morbidity, • • •
and does not require the additional skills or cost of laparoscopy. The procedure can be performed under either local or regional anesthesia. It allows the simultaneous repair of other pelvic defects. It has a shorter operating time.
However, orthopedic deformities, coexisting intraabdominal pathology, and compromised vaginal length may favor the abdominal route. Furthermore, the abdominal route – whether open or laparoscopic – has its own complications of lumbosacral osteomyelitis101 and mesh erosion into the vagina,102 bladder,103 and rectum.104 In a retrospective review comparing vaginal sacrospinous colpopexy and abdominal sacral colpopexy, Hardiman and Drutz found the two procedures to be equally effective.59 Benson et al., in a prospective randomized study, found abdominal sacral colpopexy to be superior to the vaginal procedure (bilateral sacrospinous suspension) in the treatment of POP.67 However, in both studies, 50% of the women had uterovaginal prolapse, the results of which may be not relevant to women with posthysterectomy vault prolapse.
A recent prospective randomized study by Maher et al. found both the abdominal and the vaginal procedure to be highly effective in the treatment of vaginal vault prolapse. However, the abdominal route was associated with a longer operating time, a slower return to activities, and more cost. Both significantly improved the patients’ quality of life.105 There are no randomized trials comparing laparoscopic sacral colpopexy to sacrospinous ligament suspension. We would anticipate that the results with regard to the short hospital stay, intraoperative blood loss, preservation of vaginal length, and coital function will be comparable between the two; however, cost effectiveness and the additional skills of laparoscopy may favor the vaginal approach. There have been a few case series studying the laparoscopic approach,106,107 and well-designed randomized trials in this field are required.
different vaginal approaches for fixation of the vaginal apex Iliococcygeal fixation The suspension of the vaginal cuff to the iliococcygeal fascia was described by Inmon in 1963,108 and was popularized by Shull and colleagues,109 with the proposed advantages of decreasing neurovascular injury or further cystocele.109,110 Using this procedure, the vaginal vault is fixed to the iliococcygeus fascia on both sides, just anterior to the ischial spine, with the muscle being approached by either an anterior or a posterior vaginal incision. Usually no vaginal epithelium needs to be excised, as the upper vagina is attached bilaterally, resulting in good vaginal length and circumference. Meeks et al., in a case series of 110 patients undergoing iliococcygeal vault suspension, reported one bowel injury and one bladder injury, with eight recurrences of anterior wall relaxation.110 Maher et al., in a case-controlled study comparing sacrospinous vault suspension to iliococcygeal fixation of the vaginal vault,111 found the two procedures to be equally effective in treating vaginal vault prolapse, with similar rates of postoperative cystocele, buttock pain, and hemorrhage requiring transfusion. However, fixation of the vault to this more distal location may potentially foreshorten the vagina.
McCall culdoplasty In 1957, McCall described suspension of the vaginal vault from the origins of the uterosacral ligament along with obliteration of the pouch of Douglas.112 Elkins et al. described a high McCall culdoplasty technique to repair the prolapsed vault at hysterectomy, where the uterosacral ligaments are plicated close to the pelvic sidewall.82 1061
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Cruikshank and Kovac, in a randomized comparison of three surgical methods used at the time of vaginal hysterectomy, concluded that McCall culdoplasty is superior to a vaginal Moschcowitz-type procedure and to simple peritoneal closure in preventing recurrence of enterocele.113 Colombo and Milani, in a retrospective case-control study comparing the functional and anatomic outcome of sacrospinous vault suspension and McCall culdoplasty, found no statistical difference in recurrence of vault prolapse between the two procedures.114 Previous studies by Shull et al.115 and Karram et al.116 found that the uterosacral ligaments are durable structures in patients with advanced POP; however, all available data comparing this procedure to sacrospinous ligament suspension are retrospective reviews, and prospective randomized trials are needed.
Posterior intravaginal slingoplasty (IVS) Papa Petros was the first to describe posterior intravaginal slingoplasty when he reported 75 patients aged 40–70 years with vault prolapse.117 Seventy-one patients were followed up for between 1 and 4.5 years. Vault prolapse recurred in 6%, and the main complication was tape erosion (5.3%) The surgical technique (Fig. 73.4) includes level I repair that aims to insert a tape in the position of the
uterosacral ligament; this has a vaginal stage and a perineal stage. The vaginal stage starts with a 4–5 cm transverse incision in the posterior vaginal wall 1.5–2 cm below the hysterectomy scar and is opened anteroposteriorly. A rectal examination is performed to identify what is adherent to the vault. At the perineal stage, a tape as an inverted ‘U’ is passed around the rectum behind the posterior vaginal wall via the ischiorectal fossa. Level II repair aims to approximate the rectovaginal fascia towards the midline, and level III includes restoring the integrity of the perineal body. The total operating time varied between 30 and 60 minutes. Mean blood loss was 120 ml. Rectal perforation was reported in two patients with no serious consequences. All patients were discharged within 24 hours and were back to normal activities within 7–10 days. Farnsworth reported a larger series of 93 patients, and had a cure rate of 91%. Median followup was 12 months (range 2–24 months). There was one rectal perforation and one rectal erosion.118 These two papers showed that the IVS procedure had comparable results to other more established surgical techniques. However, it should not be undertaken without adequate training. It is suitable in patients with a short vagina, where sacrospinous fixation is not appropriate. Larger randomized trials comparing it to other known procedures are essential.
conclusIon
Figure 73.4. Tunneler insertion. Patient in lithotomy position. The tunneler is seen entering the ischiorectal fossa (IRF) by penetration of levator plate (LP) 2 cm lateral to the external anal sphincter. G, gluteal muscle; IRVs, inferior rectal nerves and veins; PC, pudendal canal. (Reproduced from ref. 117 with permission from Springer-Verlag.)
Appropriate management of vault prolapse is a known problem and, with an increasing aging and yet more active population, there will be an increased need to manage women with complex vaginal prolapse with procedures that restore anatomy, and maintain bladder, bowel, and sexual function. The reconstructive procedures for vaginal vault prolapse remain controversial, and with the availability of different routes and procedures, it is important to take into consideration the patient’s age, medical status, sexual activity, reproductive history, and previous surgery. Bowel and bladder function should also be taken into account in making the decision. It is therefore essential that every clinician dealing with complex vaginal prolapse be well versed in all surgical techniques, and management should be individually tailored for each patient. Well-designed prospective randomized trials should be undertaken to determine whether or not any of the procedures described truly deserves to be considered the ‘gold standard’.
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88. Meschia M, Bruschi F, Amicarelli F et al. The sacrospinous vaginal vault suspension: critical analysis of outcomes. Int Urogynecol J 1990;10:155–9.
74. Baker MH. Success with sacrospinous suspension of the prolapsed vaginal vault. J Gynecol Surg 1992;175:419–20. 75. Heinonen PK. Transvaginal sacrospinous colpopexy for vaginal vault and complete genital prolapse in aged women. Acta Obstet Gynecol Scand 1992;71:377–81. 76. Shull BT, Capen CV, Riggs MW, Kuch TJ. Preoperative and postoperative analysis of site-specific pelvic support defects in 81 women treated with sacrospinous ligament suspension and pelvic reconstruction. Am J Obstet Gynecol 1992;166:1764–71. 77. Kaminski PF, Sorosky JI, Pees RC, Rodczkski ES. Correction of massive vaginal prolapse in aged women. J Am Geriatr Soc 1993;41:42–4.
89. Vigano R, Ferrari A, Quellari P, Frigerio L. Sacrospinous ligament fixation: long term follow up. Int Urogynecol J 2000;11:i–ii. 90. Febbraro W, Beucher G, Von Theobold P et al. Feasibility of bilateral sacrospinous ligament vaginal suspension with a stapler. Prospective study with the first 34 cases. J Gynecol Obstet Biol Reprod 1997;26:815–21. 91. Brieger GM, MacGibbon AL, Atkinson KH. Sacrospinous colpopexy. Aust N Z J Obstet Gynecol 1995;35:86–7. 92. Hoffman MS, Harris MS, Bouis PJ. Sacrospinous colpopexy in the management of uterovaginal prolapse. J Reprod Med 1996;41:299–303. 93. Sze EH, Karram MM. Transvaginal repair of vault prolapse: a review. Obstet Gynecol 1997;89:466–75.
78. Porges RF, Smilen SW. Long-term analysis of the surgical management of pelvic support defects. Am J Obstet Gynecol 1994;171:1518–28.
94. Karram MM, Sze EH, Walters MD. Surgical treatment of vaginal vault prolapse. In: Walters MD, Karram MM (eds) Urogynecology and Reconstructive Pelvic Surgery, 2nd ed. St Louis: Mosby, 1999; 235–56.
79. Holley RJ, Varner RE, Gleason BP et al. Recurrent pelvic support defects after sacrospinous ligament fixation for vaginal vault prolapse. J Am Coll Surg 1995;180:444–8.
95. Given FY, Muhlendorf TK, Browning GM. Vaginal length and sexual function after colpopexy for complete uterovaginal eversion. Am J Obstet Gynecol 1993;169:284–8.
80. Sauer HA, Klutke CG. Transvaginal sacrospinous ligament fixation for treatment of vaginal prolapse. J Urol 1995;154:1008–12.
96. Barksdale PA, Elkins TE, Sanders CK et al. An anatomic approach to pelvic hemorrhage during sacrospinous ligament fixation of the vaginal vault. Obstet Gynecol 1998;91:715–18.
81. Peters WA, Christenson ML. Fixation of the vaginal apex to the coccygeal fascia during repair of vaginal vault eversion with enterocele. Am J Obstet Gynecol 1995;172:1894–1902. 82. Elkins TE, Hooper JB, Goodfellow K et al. Initial report of anatomic and clinical comparison of the sacrospinous ligament fixation to the high McCall culdoplasty for vagi-
97. Barksdale PA, Gasser RF, Gauthier CM, Elkins TE, Wall LL. Intraligamentous nerves as a potential source of pain after sacrospinous ligament fixation of the vaginal apex. Int Urogynecol J Pelvic Floor Dysfunct 1997;8:121–5. 98. Scotti RJ. Repair of genitourinary prolapse in women. Curr Opin Obstet Gynecol 1991;3:404–12.
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99. Farrell SA, Scotti RA, Osterrgard DR et al. Massive evisceration: a complication following sacrospinous vaginal vault fixation. Obstet Gynecol 1991;78:560–2. 100. Nieminen K, Huhtala H, Heinonen PK. Anatomic and functional assessment and risk factors of recurrent prolapse after vaginal sacrospinous fixation. Acta Obstet Gynecol Scand 2003;82:471–8. 101. Weidner AC, Cundiff GW, Harris RL et al. Sacral osteomyelitis: an unusual complication of abdominal sacral colpopexy. Obstet Gynecol 1997;90:689–91. 102. Kholi N, Walsh PM, Roat TW, Karram MM. Mesh erosion after abdominal sacrocolpopexy. Obstet Gynecol 1998;92:999–1004. 103. Patsner B. Mesh erosion into the bladder after abdominal sacral colpopexy. Obstet Gynecol 2000;95:1029. 104. Kenton KS, Woods MP, Brubaker L. Uncomplicated erosion of polytetrafluoroethylene grafts into the rectum. Am J Obstet Gynecol 2002;187:233–4. 105. Maher CF, Qatawneh AM, Dwyer PL et al. Abdominal sacral colpopexy or vaginal sacrospinous colpopexy for vaginal vault prolapse: a prospective randomized study. Am J Obstet Gynecol 2004;190:20–6. 106. Mahendran D, Prashar S, Smith ARB et al. Laparoscopic sacrocolpopexy in the management of vaginal vault prolapse. Gynecol Endosc 1996;5:217–22. 107. Cusson M, Bogaert E, Narducci F et al. Laparoscopic sacral colpopexy: short-term results and complications in 83 patients. J Gynecol Obstet Biol Reprod 2000;29:746–50.
110. Meeks GR, Wasshburne JF, McGehee RP, Wiser WL. Repair of vaginal vault prolapse by suspension of the vagina to iliococcygeus (prespinous) fascia. Am J Obstet Gynecol 1994;171(6):1444–52. 111. Maher CF, Murray CJ, Carey MP et al. Iliococcygeus or sacrospinous fixation for vaginal vault prolapse. Obstet Gynecol 2001;98:40–4. 112. McCall ML. Posterior culdoplasty: surgical correction of enterocele during vaginal hysterectomy: a preliminary report. Am J Obstet Gynecol 1957;10:595–602. 113. Cruikshank SH, Kovac SR. Randomized comparison of three surgical methods at the time of vaginal hysterectomy to prevent posterior enterocele. Am J Obstet Gynecol 1999;180:859–65. 114. Colombo M, Milani R. Sacrospinous ligament fixation and modified McCall culdoplasty during vaginal hysterectomy for advanced uterovaginal prolapse. Am J Obstet Gynecol 1998;179:13–20. 115. Shull BL, Bachofen C, Coates K et al. A transvaginal approach to repair of apical and other associated sites of pelvic organ prolapse with uterosacral ligaments. Am J Obstet Gynecol 2000;183:1365–74. 116. Karram M, Goldwasser S, Kleeman S et al. High uterosacral vaginal vault suspension with fascial reconstruction for vaginal repair of enterocele and vaginal vault prolapse. Am J Obstet Gynecol 2001;185:1339–43.
108. Inmon WB. Pelvic relaxation and repair including prolapse of the vagina following vaginal hysterectomy. South Med J 1963:56:577–82.
117. Papa Petros PE. Vault prolapse II. Restoration of dynamic vaginal supports by infracoccygeal sacropexy, an axial day-case vaginal procedure. Int Urogynecol J 2001;12:296–303.
109. Shull BL, Capen MD, Riggs MW et al. Bilateral attachment of the vaginal cuff to iliococcygeus fascia: an effective method of cuff suspension. Am J Obstet Gynecol 1993;168:1669–74.
118. Farnsworth BN. Posterior intravaginal slingoplasty (infracoccygeal sacropexy) for severe posthysterectomy vaginal vault prolapse – a preliminary report on efficacy and safety. Int Urogynecol J 2002;13:4–8.
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74 Abdominal approach to fixation of the vaginal apex Wesley Hilger, Jeffrey Cornella
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IntroductIon Pelvic organ prolapse is a common condition that can adversely affect a woman’s quality of life. A recent study found that in older women with an intact uterus, 25% had prolapse with the leading edge below the hymeneal ring.1 Up to 14% of all hysterectomies are performed for prolapse and the risk of requiring surgery for prolapse after a hysterectomy has been reported to be up to 5%.2,3 Each year in the United States approximately 200,000 women undergo surgery for pelvic prolapse or urinary incontinence.4 One-third of these women will experience recurrent prolapse and require additional surgery within 4 years.5 As the population in developed countries ages, pelvic organ prolapse will be a condition that all physicians caring for women will encounter with increasing frequency.6 A full understanding of the pathophysiology, evaluation, and treatment of prolapse will become increasingly important. There are many surgical approaches to vaginal prolapse. Lane first proposed the abdominal sacrocolpopexy in 1962.7 Since that time it has undergone several modifications but the basic concept of the procedure has remained the same: support of the vagina with a suspensory bridge connected to the anterior longitudinal ligament of the sacrum.8 Abdominal sacrocolpopexy has been studied extensively and has been shown to be reliable and durable.9 This chapter will discuss the pathophysiology of prolapse, the evaluation of the patient with prolapse, the surgical techniques of abdominal sacrocolpopexy, and possible complications of the procedure.
water holding up the boat while the moorings are the connective tissue. If the muscles do not function (or the water level is lowered in the dock) due to nerve damage or direct damage then more stress is placed on the connective tissue (moorings). Eventually, this stress can lead to connective tissue damage and prolapse. The connective tissue supporting the pelvic viscera includes the endopelvic fascia, the arcus tendineus fascia pelvis and the uterosacral and cardinal ligaments. DeLancey12 divided the connective tissue support in the pelvis into three interconnected levels (Fig. 74.1). Level I support occurs at the cervix or vaginal cuff and consists of the uterosacral and cardinal ligament complexes. These ligaments attach the uterus, cervix, and upper vagina to the pelvic walls. Level II support occurs at the mid-portion of the vagina. These supporting connective tissue layers aid in supporting and separating the bladder anteriorly and rectum posteriorly from the vagina. At level III the vagina fuses directly with the urethra anteriorly, perineal body posteriorly, and levator ani muscles laterally. Damage to or weakness of the support structures at each level will
PathoPhysIology The pathophysiology of vaginal vault prolapse is not fully understood. Support of the female pelvic viscera involves the complex interaction among pelvic floor muscles, nerves, and connective tissue. It is believed that abnormal anatomy and abnormal function of the pelvic viscera result from congenital or acquired weakness of one or more of the components that interact to support them. Risk factors thought to contribute to vaginal prolapse include obesity, chronic bronchitis, vaginal delivery, multiparity, age, and diseases of collagen metabolism.10 The levator ani muscles are the primary muscles of support in the pelvis. They are typically the main active source of support for the pelvic viscera. When the muscles relax during micturition or defecation, the connective tissue attachments of the pelvis bear the load of the intra-abdominal pressure. Norton11 used a ‘boat in a dry dock’ analogy to describe this relationship between muscle and connective tissue. The muscles act like the
Figure 74.1. At level I, paracolpium suspends the vagina from the lateral pelvic walls. Fibers of level I extend both vertically and posterior towards the sacrum. At level II, the vagina is attached to the arcus tendineus fasciae pelvis and superior fascia of the levator ani muscles. At level III, the vagina is fused to the medial surface of the levator ani muscles, urethra, and perineal body. (Reproduced from ref. 12 with permission from Elsevier.)
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lead to prolapse of the corresponding pelvic viscera: loss of anterior support can lead to cystocele or urethral hypermobility; deficiencies in the cardinal–uterosacral complex will lead to prolapse of the vaginal apex or uterus; and loss of posterior support can lead to enterocele or rectocele.
PatIent selectIon and PreoPeratIve evaluatIon Patients with vaginal apical prolapse are likely to have support defects in other compartments of the vagina (Fig. 74.2). Each patient should be assessed for symptoms related to the anterior, apical, and posterior compartments to help guide the physical examination and plan corrective surgery. Symptoms commonly associated with pelvic organ prolapse include vaginal bulge, low back pain, sense of pelvic pressure and fullness, constipation, urinary and/or fecal incontinence, and the inability to empty the bladder and/or rectum.13 Studies have shown that there are no symptoms typical of vaginal prolapse and that symptoms do not correlate with the severity of prolapse.14,15 As an example, as the prolapse increases in severity, symptoms of urinary incontinence may be masked if kinking of the urethra occurs.14 Patients with prolapse in general, and especially those who describe resolution of stress urinary incontinence symptoms, should be suspected of having occult incontinence. A thorough understanding of the patient’s symptoms should precede the physical examination but only
Figure 74.2. A patient with a massive vaginal vault prolapse and multicompartment defects. (Reproduced with permission from the Mayo Foundation for Medical Education and Research.)
a thorough physical examination will reveal the degree and site of vaginal support defects. The physical examination should be performed in a systematic fashion to evaluate all compartments. Standardized staging for pelvic organ prolapse has been described, and currently the International Continence Society advocates use of the pelvic organ prolapse quantification (POPQ) system.16 Evaluating subjects in the standing as well as the supine position may make a difference in the degree of prolapse noted and it is recommended that both examinations be performed.17 The anterior compartment should be assessed for paravaginal versus midline defects and urethral hypermobility. Specific findings on examination may indicate a paravaginal defect: persistent rugae in the prolapsed anterior wall or, if the prolapse does not occur with lateral support of the anterior vaginal wall, with ring forceps on examination. Apical or cervical descent should be assessed as should posterior wall and perineal descent. Levator ani tone, anal tone, and perineal reflexes should be tested for neurologic integrity of the pelvic floor. Stress incontinence can be unmasked after prolapse surgery in 8–60% of patients.18,19 Provocative maneuvers (i.e. straining or cough) with a full bladder should be performed with the prolapse evident and the prolapse reduced to try to detect occult stress incontinence. A large cotton swab or sponge stick elevating the prolapsed apex to its normal anatomic position is useful for this portion of the examination. Finally, a simple office bladder fill including a post-void residual volume can assess the sensation, capacity, and function of the bladder. Further evaluation and testing with urodynamics, magnetic resonance imaging (MRI) or defecography should be performed as indicated by the history, symptoms, and physical examination. Currently, urodynamic measures have not been validated in women with prolapse. MRI also lacks standardized protocols and its impact on identifying fascial defects and improving surgical outcomes is not known. At our institution we have found that, in most patients, these modalities add little to our assessment and treatment plan. The surgery for pelvic prolapse must be individualized for each patient. The patient’s medical history, symptoms, examination findings and expectations help to guide the surgeon’s decision-making process. In our practice, an abdominal sacrocolpopexy is performed in subjects who are medically stable, have failed prior vaginal suspension procedures, have a short vagina, or need further abdominal surgery. Currently, studies do not indicate who would benefit most from an abdominal sacrocolpopexy. In our practice, additional procedures 1069
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such as bilateral salpingo-oophorectomy, paravaginal defect repair, Burch procedure, or perineorrhaphy are added as needed. It is controversial whether a hysterectomy should be performed at the time of abdominal sacrocolpopexy. There is concern for increased risk of mesh erosion due to exposure to the vagina. Studies have noted a range of erosion rates from zero to 27% when the uterus is completely removed but there are no randomized trials.9 If a hysterectomy is to be carried out, any one of three procedures can be performed to decrease the risk of erosion: a supracervical hysterectomy can be undertaken; the cuff can be closed in two layers; or an intervening portion of biologic graft can be placed between the cuff and the mesh. Preoperative instructions for our patients include clear liquids the day before surgery, with bowel preparation the evening before surgery. Each patient also has a preoperative visit to discuss the proposed procedure, the risks and the benefits, and to answer any remaining questions.
abdomInal sacrocolPoPexy technIque All surgeons should have a standard technique for patient positioning, preparation, and procedure. To form this technique, a thorough understanding of the anatomy, surgical principles, and possible complications of the procedure is required. This knowledge will allow the surgeon to perform an abdominal sacrocolpopexy efficiently, make adjustments in technique as dictated by intraoperative findings, and minimize postoperative complications. Patients are given thromboembolic stockings and sequential compression devices as deep venous thrombus (DVT) prophylaxis. The patient is placed in a dorsal lithotomy position in Allen-type stirrups. This position allows for access to the vagina, perineum, and rectum during the procedure. The Allen stirrups also allow for elevation of the legs should an additional vaginal procedure need be performed. The abdomen and vagina are prepped with betadine and a single dose of preoperative antibiotics is given. The choice of entry incision depends on the patient. We have found that a Pfannenstiel incision gives adequate exposure in most patients. A midline incision may be used to gain greater exposure in an obese patient or it may be used if the patient has a prior midline scar. If there is a paravaginal defect that is to be repaired with an abdominal paravaginal repair, or if the patient has stress incontinence that will be repaired with a Burch procedure, we will enter the space of Retzius and per-
form the retropubic procedures prior to entering the peritoneal cavity. Once procedures in the space of Retzius are completed, the peritoneal cavity is entered. If there are adhesions of the bowel to the pelvis, these are lyzed and the small bowel is packed above the level of the sacral promontory. We use a Bookwalter retractor with a bladder blade, two side blades, and a malleable blade that retracts the packing. A device should be placed in the vagina to aid in identification and manipulation of the vagina. Such a device can be a Lucite rod, EEA sizer or sponge stick. We prefer to use the Lucite rod because it manipulates the vagina well, fills the entire cavity, and allows sutures to be easily placed through the entire thickness of the vagina. Once the vagina is identified, its overlying peritoneum is dissected away. Initially, stay sutures are placed at the apical corners to aid in orientation. Metzenbaum scissors are used to incise the peritoneum transversely. The posterior peritoneum is then dissected down to the rectovaginal septum of the pelvis. Care is taken to avoid the rectum. Another Lucite rod can be placed into the rectum for visualization if it is difficult to identify. Finally, the anterior peritoneum and bladder are dissected off the anterior vagina. Dissecting the peritoneum widely off the vagina provides a large surface area for attaching the mesh. If there are fascial defects noted at the apex of the vagina these are repaired with 2-0 Vicryl suture but no effort is made to excise the underlying vaginal mucosa. We feel that efforts to maintain the integrity of the vaginal mucosa will reduce the chance of mesh erosion. Once the vagina is dissected and exposed, the mesh is attached. Typically, a 4 × 18 cm strip of mesh is required. The mesh is cut in a Y-formation and the appropriate length for each patient is determined intraoperatively. The mesh is folded in half longitudinally and cut along this line to create the arms of the Y. Length required for the arms of the Y is determined by the length of attachment required for the anterior and posterior aspects of the vagina. The folded mesh is then sutured in place at the corners to maintain the fold for easier handling. Other options include using two strips of mesh for the anterior and posterior aspects of the vagina. If the vagina is noted to have significant thinning then an allograft of porcine dermis may be placed between the mesh and the vaginal wall to prevent mesh erosion. Suture placement is crucial for mesh security. Initially, the sutures are attached to the posterior vagina. We have found that this portion of the vagina can be difficult to visualize if an attempt is made to attach the mesh directly. We recommend a monofilament suture and use
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a No. 0 Prolene suture on a CT-1 needle. The first two sutures are placed bilaterally as caudad as possible on the posterior vaginal wall. Essentially, full thickness bites are taken with the suture and this can easily be felt as the needle encounters the vaginal rod. The sutures are tagged with curved Kelly clamps for orientation. A second row of bilateral sutures approximately 1–2 cm cephalad is placed in the posterior vagina. (Concerns have been raised regarding mesh erosion with full thickness bites; however, this has not been assessed in controlled studies and we feel our technique is sound based on our clinical outcomes.) If the position and orientation of the suture appears appropriate, the mesh is attached to the vagina. Sutures are placed through the mesh with the aid of a Mayo needle, the mesh is pushed down over the posterior vagina, and the sutures tied. After the posterior flap of mesh is fixed to the vagina the corresponding apical and anterior portions can easily be fixed. At this point sutures can be placed directly through the mesh and vagina using the Lucite rod as a backstop. The sutures are placed in a bilateral and midline fashion in 1–2 cm increments. The mesh is usually placed 4–5 cm along the anterior vaginal wall. The number of sutures required is typically 8–10 sutures for the posterior, apex, and anterior segments of the vagina. Once the two arms of the Y-segment of the mesh are applied to the vagina, attention is then turned to the sacral promontory. Important landmarks for the sacral promontory of the pelvis include bifurcation of the aorta at the level of L4– L5, the right ureter, right iliac vessels, the middle sacral vein, the sigmoid colon, and the left common iliac vein that crosses the midline over the sacral promontory. The peritoneum over the promontory is incised sharply and delicate blunt and sharp dissection is used to expose the anterior longitudinal ligament overlying the sacrum (Fig. 74.3). Care should be taken during this dissection to avoid damaging middle sacral vessels and presacral veins because life-threatening hemorrhage can occur.20 The peritoneal incision is extended to the posterior cul-de-sac with care taken to avoid the rectum to the left and the ureter to the right of the dissection. Two No. 0 Prolene sutures on a CT-2 needle are placed just below the level of the sacral promontory, approximately 1–2 cm apart (Fig. 74.4). Attachment at the upper third of the sacrum reduces the risk of bleeding from presacral vessels lower in the sacrum without compromising the angle of the vagina.21 The appropriate length of the graft is determined as one that avoids any tension on the graft and vagina (Fig. 74.5). The excess graft is cut and removed and the promontory sutures are then brought through the remaining graft and tied down.
Figure 74.3. Arial view of the pelvis showing a Lucite rod in the vagina. The peritoneum has been dissected off the apex of the vagina but the mesh has yet to be applied. The peritoneum at the sacral promontory has been incised and anatomic structures can be appreciated: right internal iliac artery, right ureter, right common iliac artery, left common iliac vein, sigmoid colon (retracted). (Reproduced with permission from the Mayo Foundation for Medical Education and Research.) Reperitonealization of the graft is performed with a running 2-0 delayed absorbable suture. Care should be taken to ensure that all areas of the graft material are covered with peritoneum. The packs are removed and the abdomen is closed in the usual fashion. Attention should then be turned to the vagina if needed. Cystoscopy is not routinely performed after abdominal sacrocolpopexy but is performed if indicated by another procedure (e.g. Burch procedure, paravaginal repair, etc.). Posterior colpoperineorrhaphy is performed at this time if a posterior vaginal defect not addressed by the mesh is suspected, or if the perineal body needs to be reconstructed. The hospital postoperative course is usually uneventful. Pain is controlled with intravenous medication until clear liquids are tolerated. Clear liquids are started as 1071
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soon as the patient desires and the diet is advanced as soon as liquids are tolerated. The patient has their Foley catheter removed the next day unless dictated otherwise by another procedure. The typical hospital stay is 2–3 days. Patients are discharged home with instructions to avoid excessively increasing intra-abdominal pressure (due to heavy lifting or straining) or having anything in the vagina for 6 weeks. Estrogen is not prescribed regularly but is used for symptoms like hot flashes or vaginal dryness. All patients are re-examined 6 weeks after surgery and treated as needed.
results and comPlIcatIons
Figure 74.4. Arial view of the pelvis with sutures noted at the vaginal apex and 1–2 cm below the sacral promontory (mesh not attached). Inset: sutures are placed through the mesh with a Mayo needle. (Reproduced with permission from the Mayo Foundation for Medical Education and Research.)
Figure 74.5. Sagittal view of the pelvis showing attached Y-shaped mesh extending posteriorly and anteriorly along the vagina and attached to the sacrum. The lack of tension on the mesh is noted. (Reproduced with permission from the Mayo Foundation for Medical Education and Research.)
Many studies have evaluated the success of abdominal sacrocolpopexy. These studies vary in their surgical technique, patient population, definition of success, and length of follow-up. When looking at anatomic success in terms of apical support, success ranges from 78 to 100%; those looking at satisfaction or complete relief of symptoms reported 85–100% success.9 Studies looking at the durability of the procedure found success rates of 74–91% an average 10–14 years after the procedure.22,23 Failures after abdominal sacrocolpopexy typically occur in other compartments. The failure rate in the posterior compartment has been noted in up to 57% of subjects in one study, even when attempts were made to extend the mesh along the posterior vagina.24 The anterior compartment can be equally problematic with one study noting anatomic failures in 29% of subjects.25 The surgeon should be aware that sacrocolpopexy is effective and durable for apical support but other compartments may require additional surgeries due to subsequent failure. Further studies are needed to address how to repair all compartment defects optimally at one time. Abdominal sacrocolpopexy appears to be more effective for vault prolapse when compared to vaginal sacrospinous suspension. Benson et al.26 were the first to compare sacrocolpopexy to bilateral sacrospinous vault suspension in a randomized trial consisting of 88 subjects. In this trial, with a mean 2.5-year follow-up, the vaginal group had a higher number of unsatisfactory outcomes than the abdominal group (33% versus 16%) and surgical failures were noted 11 months sooner in the vaginal group than the abdominal group (mean 11.2 versus 22.1 months). Lo and Wang27 randomized 138 women to unilateral sacrospinous ligament suspension or abdominal sacrocolpopexy. Patients were followed for 2.1 years after surgery and there were more optimal surgical results in the abdominal group (94.2%) than in the vaginal group (80.3%). Finally, Maher et al.28
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randomized 95 subjects to abdominal sacrocolpopexy versus sacrospinous ligament suspension. At the end of the 2-year follow-up period, patients’ symptoms and anatomic success were equivalent. However, the vaginal group had a higher percentage of failures extending to the introitus (17% versus 4%) and postoperative cystoceles (14% versus 7%). In addition to success and failure, it is important to discuss with patients the possible immediate and long-term postoperative complications associated with abdominal sacrocolpopexy. The intra- and postoperative complications as presented by Nygaard et al.9 in their thorough review of the literature on abdominal sacrocolpopexy are presented in Table 74.1. The incidence of mesh erosion varies depending on which mesh is used in the procedure and how it is placed. The overall rate of 3.4% has been reported in the literature.9 Typically, erosion occurs within the first 2 years after surgery but may occur many years later.29 The lowest rate of erosion is noted in autologous or cadaveric fascia (0%) and the highest rates are noted in Teflon and polyethylene mesh (5%).9 Placement of mesh via a combined vaginal–abdominal sacral colpoperineopexy has a prohibitively high rate (40%) of erosion.29 The ideal mesh should be biocompatible, inert, hypoallergenic, sterile, resistant to mechanical stress or shrinkage, convenient, and affordable30 – the ideal mesh is currently not available! Autologous fascia has no risk of erosion but takes longer to harvest and has associated morbidities with harvesting that make it unattractive. Freeze-dried cadaveric fascia has been found to have a high rate of failure (83%) due to autolysis.31 Of the synthetic mesh types available, we feel that a macroporous table 74.1.
Complication rates
Complication
Percentage
Intraoperative Cystotomy
3.1
Enterotomy or proctotomy
1.6
Ureteral injury
1.0
Hemorrhage or transfusion or both
4.4
Postoperative Urinary tract infection
10.9
Wound problems
4.6
Postoperative ileus
3.6
Deep venous thrombus or pulmonary embolus
3.3
Small bowel obstruction
1.1
Data from ref. 9.
polypropylene mesh is currently the best option. Studies have found that it has the lowest rate of erosion (0.5%) next to autologous fascia.9 The ability to reduce the risk of mesh erosion depends on preoperative planning and intraoperative technique.32 Vaginal health should be optimized as indicated by the vaginal skin prior to the procedure. Thin vaginal mucosa may require a period of estrogen cream to help increase tissue strength. Erosive lesions of vaginal epithelium secondary to pessary use should be allowed to heal prior to surgery. Proper technique of placement of the mesh includes using one that has a good track record of minimal mesh erosion. The mesh should be attached to a healthy fibromuscular layer of vaginal tissue; if this is not available then an intervening layer of dermal allograft should be considered to add strength to the tissue. Minimal tension should be placed on the mesh and reperitonealization should be performed. If mesh erosion occurs after abdominal sacrocolpopexy it can typically be dealt with conservatively. This includes trimming the visible mesh, cauterizing granulation tissue and applying estrogen cream. If resolution of the erosion does not occur, then surgical removal of the mesh can be accomplished via a vaginal, laparoscopic or abdominal route. Typically, the prolapse will not fail after the mesh has been removed. After mesh removal, allowing the sinus tract to drain into the vagina and heal by secondary intention may facilitate a better recovery.32
conclusIon Abdominal sacrocolpopexy is a procedure that has continued to evolve since Lane first proposed using a suspensory bridge to support the vaginal apex by attaching it to the sacrum. Surgeons have taken minimally invasive technologies and applied them to the technique of sacrocolpopexy. Nezhat et al.33 reported the first case series in 1994 and since that time several small case series have followed. The largest series of 83 patients noted that six subjects required a conversion to laparotomy, and at 12 months 62/63 (94%) noted no evidence of recurrent prolapse.34 The laparoscopic approach is reported to shorten hospitalization, decrease pain, and decrease time to return to normal activities. However, this approach requires advanced laparoscopic training, a skilled laparoscopic assistant, and increased operating room time. Recently, robotic laparoscopic surgery has been used in an effort to overcome the technical skill required for regular laparoscopic surgery.35 Although promising, the minimally invasive approach to sacrocolpopexy needs further exploration and study to compare its success and complication rate to the open approach. 1073
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Abdominal sacrocolpopexy is an effective and durable surgery for the treatment of vaginal vault prolapse. To perform this procedure safely and effectively, knowledge of pelvic anatomy and surgical technique are required. Possible complications after the procedure must be recognized and addressed to minimize the morbidity to the patient. As our understanding of the pathophysiology of prolapse increases and new surgical technologies arise, the technique of abdominal sacrocolpopexy will continue to evolve.
14. Ellerkamann RM, Cundiff GW, Melick CF et al. Correlation of symptoms with location and severity of pelvic organ prolapse. Am J Obstet Gynecol 2001;185:1332–8.
reFerences
18. Gallentine ML, Cespedes RD. Occult stress urinary incontinence and the effect of vaginal vault prolapse on abdominal leak point pressures. Urology 2001;57:40–4.
1. Nygaard I, Bradley C, Brandt D. Pelvic organ prolapse in older women: prevalence and risk factors. Obstet Gynecol 2004;104:489–97.
15. Burrows LJ, Meyn LA, Walters MD et al. Pelvic symptoms in women with pelvic organ prolapse. Obstet Gynecol 2004;104:982–8. 16. Bump RC, Mattiasson A, Bo K et al. The standardization of terminology of female pelvic organ prolapse and pelvic organ dysfunction. Am J Obstet Gynecol 1996;175:10–7. 17. Silva WA, Kleeman S, Segal J et al. Effects of a full bladder and patient positioning on pelvic organ prolapse assessment. Obstet Gynecol 2004;104:37–41.
2. Farquhar CM, Steinar CA. Hysterectomy rates in the United States 1990–1997. Obstet Gynecol 2002;99:229–34.
19. Bergman A, Koonings PP, Baddard CA. Predicting postoperative urinary incontinence development in women undergoing operation for genitourinary prolapse. Am J Obstet Gynecol 1988;158:1171–5.
3. Mant J, Painter R, Vessey M. Epidemiology of genital prolapse: observations from the Oxford Family Planning Association study. Br J Obstet Gynaecol 1997;104:579–85.
20. Sutton GP, Addison WA, Livengood CH III et al. Lifethreatening hemorrhage complicating sacral colpopexy. Am J Obstet Gynecol 1981;140:836–7.
4. Boyles SH, Weber AM, Meyn L. Procedures for pelvic organ prolapse in the United States, 1979–1997. Am J Obstet Gynecol 2003;188:108–15.
21. Addison WA, Livengood CH, Sutton GP et al. Abdominal sacral colpopexy with mersilene mesh in the retroperitoneal position in the management of posthysterectomy vaginal vault prolapse and enterocele. Am J Obstet Gynecol 1985;153:140–6.
5. Olsen AL, Smith VJ, Bergstrom JO et al. Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 1997;89:501–6. 6. Luber KM, Boero S, Choe JY. The demographics of pelvic floor disorders: current observations and future projections. Am J Obstet Gynecol 2001;184:1496–501; discussion 1501–3. 7. Lane FE. Repair of posthysterectomy vaginal-vault prolapse. Obstet Gynecol 1962;20:72–7. 8. Timmons MC, Addison WA, Addison SB et al. Abdominal sacral colpopexy in 163 women with posthysterectomy vaginal vault prolapse and enterocele: evolution of operative techniques. J Reprod Med 1992;37:323–7. 9. Nygaard IE, McCreery R, Burbaker L et al. Abdominal sacrocolpopexy: a comprehensive review. Obstet Gynecol 2004;104:805–23. 10. Fornell EU, Wingren G, Kjolhede P. Factors associated with pelvic floor dysfunction with emphasis on urinary and fecal incontinence and genital prolapse: an epidemiological study. Acta Obstet Gynecol Scand 2004;83:383–9. 11. Norton PA. Pelvic floor disorders: the role of fascia and ligaments. Clin Obstet Gynecol 1993;36:926–38. 12. DeLancey JO. Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 166:1992;1717–28. 13. American College of Obstetricians and Gynecologists. Pelvic organ prolapse. ACOG Technical Bulletin 214. Washington, DC: ACOG, 1995.
22. Hilger WS, Poulson M, Norton PA. Long-term results of abdominal sacrocolpopexy. Am J Obstet Gynecol 2003;189:1606–10. 23. Lefranc JP, Atallah D, Camatte S et al. Long-term follow-up of posthysterectomy vaginal vault prolapse abdominal repair: a report of 85 cases. J Am Coll Surg 2002;195:352–8. 24. Baessler K, Schuessler B. Abdominal sacrocolpopexy and anatomy and function of the posterior compartment. Obstet Gynecol 2001;97:678–84. 25. Brubaker L. Sacrocolpopexy and the anterior compartment: support and function. Am J Obstet Gynecol 1995;173:1690–6. 26. Benson JT, Lucente V, McClellan E. Vaginal versus abdominal reconstructive surgery for the treatment of pelvic support defects: a prospective randomized study with long-term outcome evaluation. Am J Obstet Gynecol 1996;175:1418–22. 27. Lo T-S, Wang AC. Abdominal colposacropexy and sacrospinous ligament suspension for severe uterovaginal prolapse: a comparison. J Gynecol Surg 1998;14:59–64. 28. Maher CF, Qatawneh AM, Dwyer PL et al. Abdominal sacrocolpopexy or vaginal sacrospinous colpopexy for vaginal vault prolapse: a prospective randomized study. Am J Obstet Gynecol 2004;190:20–6.
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29. Visco AG, Weidner AC, Barber MD et al. Vaginal mesh erosion after abdominal sacral colpopexy. Am J Obstet Gynecol 2001;184:297–302.
33. Nezhat CH, Nezhat F, Nezhat C. Laparoscopic sacral colpopexy for vaginal vault prolapse. Obstet Gynecol 1994;84:885–8.
30. Birch C, Fynes MM. The role of synthetic and biological prostheses in reconstructive pelvic floor surgery. Curr Opin Obstet Gynecol 2002;14:527–35.
34. Cosson M, Bogaert E, Narducci F et al. Laparoscopic sacral colpopexy: short-term results and complications in 83 patients. J Gynecol Obstet Biol Reprod 2000;29:746–50.
31. Fitzgerald MP, Edwards SR, Fenner D. Medium-term follow-up on use of freeze-dried, irradiated donor fascia for sacrocolpopexy and sling procedures. Int Urogynecol J Pelvic Floor Dysfunct 2004;15(4):238–42.
35. Elliott DS, Frank I, DiMarco DS et al. Gynecologic use of robotically assisted laparoscopy: sacrocolpopexy for the treatment of high-grade vaginal vault prolapse. Am J Surg 2004;188:52S–56S.
32. Hurt WG. Abdominal sacral colpopexies complicated by vaginal graft extrusion. Obstet Gynecol 2004;103:1033–4.
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75 Preservation of the prolapsed uterus Vasiliki Varela, Adam Magos
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IntroductIon
HIstory
Pelvic organ prolapse is a common condition and a major cause of gynecologic surgery. Women who reach 80 years of age have an 11% risk of undergoing at least one operation for this indication during their lifetime.1 It is projected that the rate of women seeking treatment for pelvic floor disorders will double over the next 30 years.2 The pathogenesis of uterine prolapse is thought to be related to weakness of the supporting connective tissues of the pelvic structures, but is not fully understood. Pelvic floor dysfunction is a possible result of many contributing factors such as pregnancy, multiparity, labor, vaginal birth, obstetric trauma, chronic increased abdominal pressure, and the aging process. Uterine prolapse can be managed in a number of different ways – some conservative, some radical. The choice of treatment is influenced by the age of the patient, the severity of the symptoms, the degree of prolapse, desire for maintenance (or not) of reproductive and sexual function, and general health. Therapeutic options range from observation, physiotherapy, and the use of vaginal pessaries to surgery, which often involves hysterectomy as part of the pelvic reconstructive process (Table 75.1). There is an increasing recognition that uterine-preserving procedures have an important role in management. Uterine prolapse does not just affect elderly, postmenopausal women who have completed their family and who are therefore prepared to undergo hysterectomy as part of their treatment. For instance, a recent Swedish study found the prevalence of uterine prolapse to be 5% in women aged 20–59 years.3 The successful surgical treatment of uterine prolapse when the uterus needs to be preserved is a challenging problem for the pelvic surgeon. This chapter describes the indications for, and techniques and results of, surgery of prolapse if the uterus is to be maintained.
Uterine prolapse was first recorded on the Kahuun papyri in 2000 BC. Hippocrates described numerous non-surgical treatments for this condition. In AD 98, Soranus of Rome first described the removal of the prolapsed uterus when it became black. The first successful vaginal hysterectomy for the cure of uterine prolapse was self-performed by a peasant woman named Faith Raworth, as described by Willouby in 1670. In 1861, Sammuel Choppin of New Orleans performed the first vaginal hysterectomy under anesthesia and antiseptic conditions. From the early 1800s, other successful surgical procedures were introduced for the treatment of this condition. By the beginning of the 20th century, European and American reports of hysterectomy, colporrhaphy, cervical amputation, transposition/interposition operations, cervical ligament plications, colpocleisis, ventral fixation of the uterus to the abdominal wall, and trachelorrhaphy for procidentia were being published. In the early 1900s, Bonney emphasized the passive role of the uterus in uterovaginal prolapse, and suggested uterine-preserving surgery.4 Ross later described the pericervical fascia as the cornerstone of pelvic reconstruction, which is not always addressed during vaginal hysterectomy with anterior–posterior colporrhaphy.5 Since then, many authors have reported their experiences with uterus-sparing pelvic reconstructive surgery.
table 75.1.
IndIcatIon The traditional procedure for uterovaginal prolapse has been vaginal hysterectomy together with an anterior and posterior colporrhaphy. Rationales for performing hysterectomy include the removal of a non-functional organ in postmenopausal women, the removal of any concomitant uterine or cervical pathology, as well as
Routes of surgery and procedures for uterine prolapse*
Route of surgery
Uterine sparing
Uterine non-sparing
Vaginal
Manchester procedure Uterosacral suspension/plication Sacrospinous fixation Le Fort and other colpocleisis
Vaginal hysterectomy ± culdoplasty ± sacrospinous fixation
Abdominal
Sacrohysteropexy/sacrocervicopexy Pectineal ligament suspension
Abdominal hysterectomy with sacrocolpopexy
Joint vaginal/abdominal
Retropubic suspension
–
Laparoscopic
Ventrosuspension Uterosacral ligament plication Hysteropexy with culdoplasty
Laparoscopic hysterectomy with sacrocolpopexy
* Can be combined with surgery for vaginal prolapse if indicated.
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the long-term success of the surgery which can theoretically be compromised by leaving the uterus in situ. However, there is no evidence that hysterectomy affects the efficacy of incontinence surgery with complete pelvic floor reconstruction, or the durability of the repair.6 In fact, it may increase the risk of pelvic neuropathy and disrupt natural support structures such as the uterosacral–cardinal ligament complex.7 Some studies suggest that women who undergo hysterectomy may be at increased risk for de novo urinary incontinence, bladder dysfunction and prolapse, as well as increased blood loss, morbidity, and operative and postoperative recovery times.8,9 Recent randomized trials comparing subtotal (supracervical) with total hysterectomy came to the same conclusions. For instance, Thakar et al. reported no difference in urinary function or in any measures of bowel function between the two types of hysterectomy.10 According to the authors, subtotal abdominal hysterectomy results in more rapid recovery and fewer short-term complications but neither subtotal nor total abdominal hysterectomy adversely affects pelvic organ function at 12 months postoperatively; however, it should be noted that patients with symptomatic uterine prolapse were not included in this study. Another area of debate relates to the effect of hysterectomy on sexual well-being. The traditional view according to Masters and Johnson states that removal of the uterus may affect the patient’s sexual and personal life as the uterus and cervix can have a significant role in orgasm and sexual function.11 Again, data from prospective randomized trials have refuted this. The UK study quoted above also looked at measures of sexual function, including frequency of intercourse and orgasm, and found no significant change in either group after surgery.10 Similarly, a recent randomized clinical trial conducted in Denmark, comparing total to subtotal abdominal hysterectomy regarding effects on sexuality, also showed that there were no statistically significant differences between the two operation methods.12 Considering all of the above, the aims of the surgical procedure should be to correct prolapse with the greatest efficacy, in both the short and long term, but with the least morbidity. Any intervention should have no adverse effect on sexual function and, especially in young women, preserve fertility. According to these criteria, uterine preservation warrants serious evaluation. A variety of surgical techniques have been described in an attempt to satisfactorily correct uterine prolapse while preserving the uterus, including vaginal, abdominal, laparoscopic, and combined procedures.
surgery Vaginal procedures The traditional approach to the surgical management of uterovaginal prolapse is via the vagina. This route is considered less invasive than the other routes, with lower morbidity and faster recovery.
Manchester procedure The Manchester procedure was originally described in 1888 by Archibald Donald of Manchester, England, and subsequently modified by Fothergill as an alternative to vaginal hysterectomy for the management of uterovaginal prolapse in patients with cervical elongation and intact, non-attenuated uterosacral–cardinal ligaments. The procedure consists of: 1. amputation of the elongated and descended cervix; 2. plication and fixation of the cardinal ligaments in front of the residual cervix; 3. anterior colporrhaphy (posterior colporrhaphy can also be performed if necessary). The operation begins with an anterior circumcision of the cervix at the level of the bladder sulcus. The anterior wall is divided and dissected off the bladder laterally, the supravaginal septum and the vesicouterine ligaments are divided, and the bladder is displaced upward. The cervix is then circumcised laterally and posteriorly, and the vagina is separated from the cervix. The entire bundle of tissue entering the cervix laterally, which includes the cardinal ligament and cervical branch of the uterine artery, is clamped, divided and suture ligated, and the cervix is amputated with a scalpel. The posterior cervix is covered with the vaginal wall with a Sturmdorf suture, and the cardinal ligaments are sewn to the anterior cervical stump using two Fothergill stitches (Fig. 75.1).13 Finally, the bladder fascia is plicated as at anterior colporrhaphy, and the vagina is closed. Many experts claim that the anatomic and functional results of the Manchester operation in suitable cases are good and comparable with those of hysterectomy, but with decreased morbidity and mortality. Studies in this area tend to be retrospective with all their inherent limitations. For instance, a report by Thomas et al. published in 1995 compared data from 88 consecutive Manchester procedures with 105 randomly selected vaginal hysterectomy patients;14 anterior and/or posterior repairs were performed as indicated. All patients undergoing Manchester procedure or vaginal hysterectomy had uterine prolapse as the pri1079
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Uterosacral suspension/plication
Figure 75.1. Approximation of cardinal ligaments and posterior Sturmdorf suture at Manchester repair. (Reproduced from ref. 13 with permission.) mary indication for surgery. The Manchester patients were older (66 versus 52 years), and more likely to be menopausal (median 14.5 years versus 4 years from last period) and to have advanced prolapse. The median operating time was 100 minutes for the Manchester procedure compared with 130 minutes for vaginal hysterectomy, and the estimated blood loss was lower with the former (200 versus 300 ml). Postoperative cuff abscess or cellulitis occurred in 5% of hysterectomy patients but was not seen after the Manchester procedure. No other differences in postoperative complications were noted. Questionnaire follow-up of 67 patients an average of 2.5 years after Manchester repair revealed that four (6%) experienced recurrent prolapse, the time to recurrence ranging from 8 weeks to 5.5 years. Similar follow-up data for vaginal hysterectomy patients were not recorded. A prior revue by Conger and Kettel in 1958 involving 960 Manchester procedures reported a prolapse recurrence rate of 4.3%;15 however, this study was based on a questionnaire sent to patients with a response rate of only 52%. The ability to conceive is preserved but reduced after the Manchester operation. Approximately one-third of women who desire children become pregnant after this procedure,16 but the risks of spontaneous abortion and premature delivery are significantly increased as a consequence of cervical incompetence. The rate of cesarean section after the Manchester procedure is 20–50%. The rate of recurrent prolapse after delivery, even after prophylactic cesarean section, is high.
In 1966, Williams described transvaginal uterosacral– cardinal ligament plication in 20 women ranging from 21 to 37 years of age with uterovaginal prolapse.17 Eleven patients had uterovaginal prolapse up to 3 cm beyond the introitus, and nine had prolapse beyond this point. The mean parity of the patients was 2.9. The peritoneal cavity was entered via a posterior colpotomy. The uterosacral ligaments were identified and divided from the cervix, plicated across the midline and reinserted into the cervix. A transverse incision was made through the peritoneum between the cervix and the bladder and the cardinal ligaments were plicated across the midline. The plicating sutures were tied tightly and the cervix was drawn upward. In four cases additional procedures for the correction of cystocele, rectocele, and enterocele were concurrently performed. Postoperative complications occurred in five patients and included genitourinary tract infection in one, pelvic cellulites in two, atonic bladder in one, and vaginal bleeding in one patient who subsequently underwent a subtotal vaginal hysterectomy. Three patients (15.5%) experienced a recurrence of uterine prolapse within 6 months of surgery and were all treated with vaginal hysterectomy. Six patients subsequently had full-term pregnancies with no recurrence of prolapse. Williams found this procedure to have low morbidity and high success in women without marked vaginal relaxation. However, the undefined duration of follow-up, the small sample size, and the lack of a control group limit this study. As far as we are aware, no further data are available about this procedure.
Sacrospinous uterosacral fixation (sacrospinous hysteropexy) Transvaginal sacrospinous ligament fixation is an established treatment for vaginal and uterovaginal prolapse, and is usually undertaken after or with vaginal hysterectomy.18,19 As a result, data concerning this procedure combined with uterine conservation are relatively scant. Richardson et al. described the use of this procedure in five women aged 24–31 years with uterine prolapse.20 The rectovaginal space was entered via a posterior colpotomy and the uterosacral ligaments were identified. The right sacrospinous ligament was then exposed and attached to the uterosacral ligaments and posterior colporrhaphy completed. A Stamey or Pereyra procedure was performed concurrently for stress incontinence in four of the five patients. The follow-up period was 6–24 months, during which there were no recurrences of prolapse and no pregnancies reported. There are no data on preoperative evaluation of degree of uterine prolapse and no comment regarding patient comfort or the
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development of postoperative dyspareunia. Although this case series supports the concept of uterine preservation in the management of uterine prolapse, it is limited by its very small sample size and its lack of a control group. Kovac and Cruikshank reported the results of transvaginal sacrospinous uterosacral ligament fixation in 19 women aged 17–37 years with uterovaginal prolapse.21 Mean patient parity was 1.31 vaginal births (0–4). Eight patients (four parous and four nulliparous) had symptomatic moderate uterovaginal prolapse, and 11 (nine parous and two nulliparous) had severe uterovaginal prolapse. All patients had markedly attenuated but identifiable uterosacral ligaments on pelvic examination and all desired fertility. Four of these procedures were performed unilaterally to the right sacrospinous–coccygeal complex and 15 were performed bilaterally. Ligament fixation was performed as follows: 1. The posterior vaginal wall was opened to the level of the cervix and the rectovaginal space entered. 2. The rectovaginal space was dissected bluntly to the level of the ischial spines. 3. The descending rectal septum was perforated, opening the pararectal space. 4. Further dissection exposed the uterosacral ligaments; these were grasped for identification, traction, and suture placement. 5. The right sacrospinous–coccygeus complex (for unilateral procedure) or both sacrospinous– coccygeal complexes (for bilateral procedures) were identified; sutures were placed to one side or to each sacrospinous ligament respectively, and then sewn to each uterosacral ligament to be tied (Figs 75.2, 75.3). The uterosacral sutures were tied within 1–2 cm of the cervical attachment of the uterosacral ligament. 6. Traction on the other end of the suture drew the uterosacral ligaments and cervix lateral and cephalad above the levator plate. A McCall culdoplasty was performed concurrently (Fig. 75.4). All sutures were left untied until additional adjunct procedures were completed; the sacrospinous uterosacral sutures were then tied. In this series, there were no injuries to the bladder or nerves. In one case an accidental rectal perforation occurred which was repaired without sequelae. The average time for sacrospinous uterosacral fixation was 15 minutes, with an average blood loss of 75 ml (200 ml with adjunct procedures). The average hospital stay was 2.4 days and mean follow-up for all 19 patients was 3.1
Figure 75.2. Miya hook with sutures is placed through the sacrospinous ligament. (Reproduced from ref. 21 with permission.)
Figure 75.3. Unilateral sacrospinous uterosacral fixation illustrating closure of the cul-de-sac. (Reproduced from ref. 21 with permission.) years with two patients lost to follow-up. Eleven of the 12 patients who failed to conceive had good objective results and have retained excellent uterovaginal support, vaginal depth, and displayed no defect recurrence during follow-up. One patient returned for her 6 weeks 1081
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Figure 75.4. Bilateral sacrospinous uterosacral fixation; uterosacral plication is also shown. (Reproduced from ref. 21 with permission.) postoperative visit with moderate uterovaginal prolapse and was cured after a second bilateral operation. Five patients became pregnant, and all were delivered vaginally without incident; one patient has been delivered twice since the operation. This patient had moderate uterovaginal prolapse after her first delivery, and subsequent to her second vaginal delivery she had a vaginal hysterectomy. Since the original report, eight additional sacrospinous uterosacral fixations with three resultant vaginal deliveries have been reported. The authors feel that this procedure may be used to treat uterovaginal prolapse in parous and nulliparous women desiring uterine preservation or further childbearing. The procedure is less time consuming and has less morbidity than major abdominal surgery, is associated with minimal intraabdominal manipulation, and avoids the longer recovery needed after a laparotomy. By performing uterosacral plication, enterocele formation is avoided, and vaginal depth, axis, and function are restored. However, pre- and postoperative assessments were not blinded, and subjective data were not routinely collected. In addition, this study is limited by its lack of a control group. In 2001, Maher et al. reported the results of a retrospective study comparing sacrospinous hysteropexy and vaginal hysterectomy with sacrospinous fixation for symptomatic uterine prolapse.22 Seventy women aged 23–87 years with symptomatic second or third degree uterovaginal prolapse were included in the study; 34 had a sacrospinous hysteropexy and 36 had a vaginal hysterectomy with sacrospinous vault fixation. All women underwent
independent review and examination. The groups were similar in age, parity, body mass index, menopausal status, prior pelvic reconstructive surgical history, presence of stress incontinence, and degree of cervical prolapse. Mean follow-up was 26 months in the hysteropexy group and 33 months in the hysterectomy group, with seven patients in each group being lost to follow up. The groups were assessed retrospectively for subjective outcomes via site-specific vaginal examinations. Women were independently evaluated by a non-surgical author blinded to the surgery performed. Data regarding operating time, intraoperative blood loss, transfusion requirement, thromboembolic events and full recovery time were also collected. The operating time in the hysteropexy group was 59 minutes compared to 91 minutes in the hysterectomy group (p<0.01). The mean intraoperative blood loss in the hysteropexy group was 198 ml compared to 402 ml in the hysterectomy group (p<0.01). No patients required blood transfusion or experienced thromboembolic events. The duration of hospitalization was also similar. In terms of the correction of prolapse, there was no statistically significant difference in either the subjective or the objective success of the surgery. For instance, the subjective success rates were 78% in hysteropexy group and 86% in the hysterectomy group (p=0.7). The objective success rates were 74% and 72%, respectively (p=1.0). The patient-determined satisfaction rates were 85% and 86%, respectively (p=1.0). The authors concluded that vaginal hysterectomy may not be necessary in the surgical treatment of uterine prolapse, and that sacrospinous hysteropexy is an effective alternative in treating uterovaginal prolapse, with a decrease in both mean operating time and intraoperative blood loss.
Neugebauer–Le Fort procedure For some patients, particularly elderly women who are not sexually active and/or suffer from severe medical illnesses, pelvic organ prolapse can be managed by surgically closing off the vagina, commonly referred to as the ‘Le Fort’ or ‘Neugebauer–Le Fort’ colpocleisis.23,24 The procedure is performed as follows: 1. A rectangular incision is made in the anterior vaginal wall, extending from 2 cm proximal to the tip of the cervix to 4–5 cm below the external urethral meatus. 2. The vaginal mucosa is undermined and freed with scissors in the area of the vesicovaginal tissue plane. 3. Plication of the bladder neck should be routinely performed because of the high incidence of postoperative stress incontinence.
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4. An analogous area of vaginal tissue is excised from the posterior vaginal wall. 5. With the cervix pushed back with a sponge stick, the congruent edges of the incisions at the anterior and posterior vaginal walls are approximated with interrupted absorbable sutures. 6. The vesicovaginal and rectovaginal fasciae are approximated in a second layer and the uterus and vaginal apex are gradually turned inward (Fig. 75.5). 7. After the vagina has been inverted, the superior and inferior margins of the original vaginal incisions are sutured. 8. An aggressive perineorrhaphy should be performed to narrow the introitus. The classic technique has been modified over the years:
• wider vaginal excision described by Wyatt in 1912;25
Figure 75.5. Approximation of vesicovaginal and rectovaginal fascia during Le Fort operation. (Reproduced from ref. 13 with permission.)
• pubocervical fascial plication before colpocleisis of •
• • •
Adair and DaSef in 1936;26 excision of a triangular vaginal mucosa, creating a canal permitting sexual intercourse and decreasing the incidence of iatrogenic stress urinary incontinence described by Goodall and Power in 1937 (Fig. 75.6);27 the conceptually similar Labhardt partial colpocleisis;28 circular amputation of the cervix preceding the Le Fort suggested by Mazer and Israel in 1948;29 the Doderlein crossbar colporrhaphy.28
In selected patients, total colpocleisis is an alternative to the other procedures which result in partial vaginal obliteration. The surgical procedure consists of stripping the vaginal mucosa from the underlying fascia, everting the uterovaginal prolapse up into the pelvis and suturing the vaginal cavity closed using either purse-string or interrupted anterior/posterior sutures in a stepwise fashion. This operation differs considerably from the Le Fort procedure, because complete vaginal obliteration is achieved.30–32
Figure 75.6. Completed Le Fort operation showing position of sutures. (Reproduced from ref. 13 with permission.) 1083
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Several recent studies have shown that the Le Fort colpocleisis and its modifications offer significant advantages in a select population of elderly, not sexually active or medically compromised patients, and represent a good treatment option when conservative management is not feasible.33,34 However, colpocleisis is an obliterative procedure which in the main does not allow maintenance of sexual function and leaves little if any access to the uterus should disease of the uterus develop after the operation. With the advances in anesthesia, surgical techniques and perioperative care, these operations are now only rarely performed.
abdominal procedures Although the vaginal route for the surgical treatment of prolapsed uterus is considered less invasive, the abdominal approach offers a better and easier access to the peritoneal cavity, the pelvic structures and, especially, the sacrum and sacrospinous ligaments.
Sacrohysteropexy/sacrocervicopexy The originators of this technique to support the vaginal vault and uterus include Stoesser35 and Arthure and Savage.36 Stoesser described the results of transabdominal sacrocervicopexy in 22 women aged 18–44 years with uterovaginal prolapse and attenuated uterine support ligaments. His technique included the following steps:
the treatment of uterovaginal prolapse but it is limited by its undefined duration of follow-up and its small sample size. Practice has changed through the years to the use of synthetic materials to support the vaginal vault with or without the uterus. Various meshes (Gore-Tex, Teflon, polypropylene) and Mersilene suture have all been tried. In 1997, Banu reported the results of sacrohysteropexy in 19 young women aged 17–27 years with uterine prolapse.37 Through an abdominal approach, a Mersilene tape was fixed on the posterior surface of the uterus and anchored to the anterior longitudinal ligament over the sacral promontory. There were no significant intra- or postoperative complications and no recurrence was reported during the 3–5 year follow-up period. Constantini et al. reported satisfactory results in seven patients with uterovaginal prolapse who underwent sacrohysteropexy with Gore-Tex mesh, although first degree cystocele recurred in three women during the 12–68 month follow-up period.38 In 2001, Leron and Stanton reported the results of sacrohysteropexy with Teflon mesh for the treatment of uterovaginal prolapse in 13 patients (mean age 38 years) who desired uterine preservation (Fig. 75.7).39 Twelve women had second degree uterine prolapse and one woman had third degree prolapse. Mean follow-up time was 16 months (range 4–49 months) and only one woman had a recurrence of first degree uterine prolapse during that period.
1. Through an abdominal incision, a strip of external oblique fascia was excised; Stoesser initially used rectus sheath or abdominal scar derivatives to create sacrocervical ligaments, but found that the external abdominal oblique aponeurosis was superior. 2. The retroperitoneal space was entered via the posterior cul-de-sac. The strip of fascia was then used as a de novo sacrocervical ligament to join the posterior cervix to the sacral periosteum, providing support to the uterus. Twenty-one of the 22 patients underwent concurrent surgical procedures, including myomectomy, resection of endometriosis, colporrhaphy, presacral neurotomy, and round ligament plication. Simultaneous round ligament plication was abandoned after the first 17 procedures as it was found to be insufficient. Stoesser reported ‘good’ operative outcomes with no postoperative failures. There are no data on the baseline degree of uterine prolapse or any details on the pre- and postoperative assessment of the patients. Stoesser’s case series supports the concept of uterine preservation in
Figure 75.7. Sacrohysteropexy using a synthetic mesh. (Reproduced from ref. 39 with permission.)
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Most recently, in 2003, Barranger et al. reported the results of abdominal hysteropexy carried out between 1987 and 1999 in 30 women of childbearing age with uterovaginal prolapse, who wanted uterine preservation.40 Mean age was 35.7 years (range 29–33 years) and mean parity was 2.3 (1–5). Thirteen women had grade 2 uterovaginal prolapse and 17 had grade 3 prolapse. All patients were healthy and active and all of them wished to conserve their uterus and preserve their fertility. Three patients had undergone previous surgery that included Burch colposuspension and periurethral Teflon injection, posterior colporrhaphy and salpingectomy for ectopic pregnancy. Eleven patients (36.6%) were urinary continent but the remainder had some type of urinary incontinence. Abdominal sacrohysteropexy was performed under general anesthesia. The peritoneal cavity was entered through a Pfannenstiel or midline infraumbilical incision. Thereafter, the technique was as follows: 1. A transverse incision was made through the peritoneum between the uterus and the bladder. 2. The bladder was mobilized and a polyester fiber mesh was attached to the anterior vaginal wall and passed through the right and the left broad ligaments next to the uterus. 3. After the rectum was mobilized from the vaginal wall, another polyester mesh was attached to the posterior vaginal wall. 4. An incision was made in the posterior peritoneum over the sacral promontory, which extended inferiorly along the right lateral aspect of the rectum. The anterior and posterior meshes were then attached to the ligaments with two nonabsorbable sutures in such a way that the vagina and the uterus were elevated without tension. 5. The peritoneal incision over the anterior vaginal wall was closed transversally. A Burch procedure and posterior colporrhaphy were performed in all cases of sacrohysteropexy. Intraoperative and early postoperative complications occurred in two (6.6%) and four patients (13.3%), respectively. The average hospital stay was 7 days (range 6–9 days). The mean objective and subjective followup periods were 44.5 months (range 2–156 months) and 94.6 months (range 8–160 months), respectively. Follow-up consisted of a history, physical examination, and urodynamic study. The same questions were asked before and after the operation to assess symptoms. To assess subjective results an independent party asked the patients by phone to answer a questionnaire about symp-
toms of recurrent uterovaginal prolapse, constipation, dyspareunia, symptoms of urinary incontinence, and reproductive performance. With regard to pregnancy, an assessment was made concerning their number and their outcome. The pelvic floor support was evaluated and categorized as cured (grade 0 or 1 uterovaginal prolapse, asymptomatic) or failed (grade 2–4 uterovaginal prolapse, symptoms of recurrent uterovaginal prolapse or recurrent prolapse surgery). At the time of the last physical examination, there were two cases of recurrent uterovaginal prolapse (6.6%) of which one was symptomatic and required repeat surgical treatment. At the time of the last questionnaire, apart from the patient who underwent repeat surgery, no patients had any uterovaginal prolapse symptoms. Three women had pregnancies that were conceived spontaneously, which led to three early legal abortions. The authors concluded that, although abdominal sacrohysteropexy is a more invasive procedure than the vaginal approach, it is safe and effective in the treatment of uterovaginal prolapse in women of childbearing age. The long-term results were excellent in the correction of prolapse without a time-dependent decrease in efficiency. It was, however, difficult to draw a conclusion about reproductive performance as well as continued uterovaginal support after pregnancy and delivery in this study.
Pectineal ligament suspension In 1993, Joshi described a new technique of uterine suspension to the pectineal ligaments as an alternative to traditional procedures in 20 women who averaged 27.5 years of age (range 17–32 years).41 Utilizing a wide Cherney incision, the procedure involved the following steps: 1. The abdomen and subsequently the retropubic space are entered. 2. The uterus is pulled up and the peritoneum incised transversely at the level of the internal cervical os. 3. A Mersilene tape measuring 30×0.5 cm is anchored at its midpoint to the anterior wall of the uterus, just above the level of the internal os. 4. The retropubic space is developed and the pectineal ligaments on either side are cleared of loose areolar tissue as laterally as possible. 5. A long artery forceps is passed subperitoneally from the retropubic space, just below the lateral end of the round ligament toward the lateral edge of the peritoneal incision over the uterus to grasp the lateral end of the Mersilene tape; the lateral end of the tape is drawn to the retropubic space and the procedure is repeated on the other side. 1085
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6. The visceral peritoneum is closed, keeping the tape outside the peritoneum. 7. The lateral end of the Mersilene tape is passed through an adequate thickness of the pectineal ligament on each side as laterally as possible. The two ends of the tape are drawn to elevate the uterus and are anchored to the pectineal ligaments using three to four firm knots of the tape. 8. The knots are fixed with sutures to prevent loosening, and the excess portion of the tape is cut off. A simultaneous Burch colposuspension was performed in five patients, posterior colporrhaphy in three, anterior colporrhaphy in one, and Moschcowitz culdoplasty in one case. There were no intra- or postoperative complications reported and no early or late morbidity during the follow-up period of 6–30 months. Of nine women desiring further childbearing, seven conceived within 6 months of surgery; at the time this case series was initially reported, five had an uneventful vaginal delivery at term and the other two had continuing normal gestations. There was no recurrence of prolapse at 6 weeks postpartum in any of the women. According to the author, suspension of the uterus from strong ligaments such as the pectineal ligaments minimizes the chance of prolapse recurrence and the procedure requires only minimal dissection in an area distant from important structures; therefore it may be considered a simple, safe and effective treatment for uterine prolapse in young women. However, it is acknowledged that the sample size of the study was small with limited duration of follow-up and, even now, further evaluation is awaited.
combined procedures Uterovaginal prolapse is often associated with stress urinary incontinence. A combined vaginoabdominal procedure may restore both the pelvic anatomy and urinary continence without the need for hysterectomy and extensive dissection and plications of the anterior vaginal wall.
1. First, the vesical neck, paraurethral tissues, uterine isthmus and uterosacral–cardinal ligament complex are mobilized transvaginally. 2. Sutures are placed at the uterosacral–cardinal ligaments bilaterally and the suture ends are left long and tagged. 3. The retropubic spaces are entered with gentle digital dissections. 4. Suspensory sutures are placed in the endopelvic fascia and vaginal wall lateral to the bladder neck, three on each side. 5. A Moschcowitz-type culdoplasty is performed. 6. The suspensory sutures are retrieved through a transverse suprapubic incision, and the paraurethral endopelvic fascia and the uterosacral–cardinal ligaments are suspended from Cooper’s ligaments. The operation was performed on 16 patients aged 30–80 years, seven of whom had previously undergone up to three anti-incontinence procedures. The followup period was 5 years or longer, during which time no significant postoperative complications or recurrences of symptomatic uterine prolapse or stress incontinence were reported. Although the results of the study are limited by the small sample size and the lack of controls, the author felt that this procedure was simple, conservative, and effective, and could safely be performed as an alternative to the traditional vaginal hysterectomy with anterior/posterior colporrhaphy.
Laparoscopic procedures With modern innovations in minimally invasive surgery, several laparoscopic procedures have been described for the treatment of uterine prolapse with uterine preservation and these are addressed later in the book. Suffice to say, that some very simple laparoscopic techniques have been tried as well as those that try to reproduce complex abdominal procedures. However successful some of these operations prove to be in the short term, even the keenest laparoscopic surgeon has to admit that longterm data are currently not available.
Retropubic suspension
concLusIon
In 1989, Nesbitt described a new operative approach designed to correct uterovaginal prolapse as well as stress urinary incontinence while preserving the uterus.42 It consisted of a combined vaginoabdominal retropubic ventral suspension of both the uterine isthmus and the vesical neck:
The traditional surgical treatment for uterovaginal prolapse has long been vaginal hysterectomy with an anterior/posterior colporrhaphy. However, women who wish to preserve their fertility may desire uterine preservation. Furthermore, hysterectomy may not be necessary in the surgical correction of uterovaginal prolapse and
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may serve to increase the morbidity of the surgical procedure and cause psychological misgivings. The idea of uterine preservation at prolapse surgery is not new. The Manchester procedure, one of the earlier surgical options for the treatment of uterovaginal prolapse, is an attractive option but is limited by the postoperative decrease in fertility and the high rates of pregnancy wastage and recurrence of prolapse. As a result, the search has continued for alternative uterinepreserving procedures and now the gynecologist has a choice of several vaginal, abdominal, combined vaginoabdominal, and laparoscopic techniques. These reconstructive operations aim to correct prolapse, maintain urinary and fecal continence, and preserve coital and childbearing function. As a result of our better understanding of the anatomy of the pelvis, its supports and attachments, modern surgical techniques have evolved to be site specific. The question remains as to which patients are suitable candidates for uterine preservation and which procedure is the ideal for a given patient. There is a paucity of information available on the efficacy of the uterussparing procedures and there are few if any comparative studies of pelvic floor reconstruction with and without hysterectomy. In order to routinely recommend uterine preservation at the time of uterovaginal prolapse surgery, studies with more patients, objective evaluation techniques, control subjects and longer follow-up are necessary. However, the current literature suggests that pelvic floor reconstruction with uterine preservation is feasible and safe and may be considered by the pelvic surgeon for selected women who desire it.
reFerences
simultaneous hysterectomy during Burch colposuspension for urinary stress incontinence. Obstet Gynecol 1988;72:866–9. 7. Nesbitt RE Jr. Uterine preservation in the surgical management of genuine stress urinary incontinence associated with uterovaginal prolapse. Surg Gynecol Obstet 1989;168:143–7. 8. Kjerluff KH, Langenberg PW, Greenaway L et al. Urinary incontinence and hysterectomy in a large prospective cohort study in American women. J Urol 2002;167:2088–92. 9. Petros PE. Influence of hysterectomy on pelvic-floor dysfunction. Lancet 2000;356:1275. 10. Thakar R, Ayers S, Clarkson P et al. Outcomes after total versus subtotal abdominal hysterectomy. N Engl J Med 2002;347:1318–25. 11. Masters WH, Johnson VE. Human Sexual Response. Boston: Little, Brown, 1966. 12. Zobbe V, Gimbel H, Andersen MA et al. Sexuality after total vs. subtotal hysterectomy. Acta Obstet Gynecol Scand 2004;83:191–6. 13. Hirsch HA, Kaser O, Ikle FA. Atlas of Gynecologic Surgery, 3rd ed. Stuttgart: Thieme, 1997. 14. Thomas AG, Brodman ML, Dottino PR et al. Manchester procedure vs. vaginal hysterectomy for uterine prolapse. J Reprod Med 1995;40:299–304. 15. Conger GT, Kettel WC. The Manchester–Fothergill operation: its place in gynecology. Am J Obstet Gynecol 1958;76:634–40. 16. Taylor RW. Pregnancy after pelvic floor repair. Am J Obstet Gynecol 1966;94:35–9. 17. Williams BF. Surgical treatment for uterine prolapse in young women. Am J Obstet Gynecol 1966;95:967–71. 18. Randall CL, Nichols DH. Surgical treatment of vaginal inversion. Obstet Gynecol 1971;38:327–32.
1. Olsen AL, Smith VJ, Bergstrom JO et al. Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 1997;89:501–6.
19. Cruikshank SH, Cox DW. Sacrospinous fixation at the time of transvaginal hysterectomy. Am J Obstet Gynecol 1990;162:1611–19.
2. Luber KM, Boero S, Choe JY. The demographics of pelvic floor disorders: current observations and future projections. Am J Obstet Gynecol 2001;184:1496–1501.
20. Richardson DA, Scotti RJ, Ostergard DR. Surgical management of uterine prolapse in young women. J Reprod Med 1989;34:388–92.
3. Samuelsson EC, Victor FTA, Tibblin G et al. Five-year incidence and remission rates of female urinary incontinence in a Swedish population less than 65 years old. Am J Obstet Gynecol 2000;183:568–74.
21. Kovac RS, Cruikshank SH. Successful pregnancies and vaginal deliveries after sacrospinous uterosacral fixation in five of nineteen patients. Am J Obstet Gynecol 1993;168:1778–86.
4. Bonney V. The principles that should underline all operations for prolapse. J Obstet Gynaecol Br Emp 1934;41:669–83.
22. Maher CF, Cary MP, Slack MC et al. Uterine preservation or hysterectomy at sacrospinous colpopexy for uterovaginal prolapse? Int Urogynecol J 2001;12:381–5.
5. Ross JW. Apical vault repair, the cornerstone of pelvic vault reconstruction. Int Urogynecol J 1997;8:146–52.
23. Le Fort L. Nouveau procede pour la guerison du prolapsus uterin. Bull Gen Ther 1887;92:337.
6. Langer R, Ron-El R, Neuman M et al. The value of
24. Neugebauer LA. Einige Worte uber die mediane Vaginal-
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naht als Mittel zur Beseitigung des Gebarmuttervorfalls. Zbl Gynakol 1881;5:25. 25. Wyatt J. Le Fort’s operation for prolapse with an account of eight cases. J Obstet Gynaecol Br Emp 1912;22:266. 26. Adair F, DaSef L. The Le Fort colpocleisis. Am J Obstet Gynecol 1936;32:218–26. 27. Goodall J, Power R. A modification of the Le Fort operation for increasing its scope. Am J Obstet Gynecol 1937;34:968–76. 28. Reiffenstuhl G, Platzer W, Knapstein PG. Vaginal Operations. Surgical Anatomy and Technique, 2nd ed. Baltimore: Williams and Wilkins, 1996; 161–75. 29. Mazer C, Israel S. The Le Fort colpocleisis: an analysis of 43 operations. Am J Obstet Gynecol 1948;56:944–9. 30. Nichols DH, Randall CL. Vaginal Surgery, 4th ed. Baltimore: Williams and Wilkins, 1996. 31. Adams HD. Total colpocleisis for pelvic eventeration. Surg Gynecol Obstet 1951;92:321–4. 32. Morley GW. Treatment of uterine and vaginal prolapse. Clin Obstet Gynecol 1996;39:959–69. 33. Neimark M, Davila GW, Kopka SL. Le Fort colpocleisis: a feasible treatment option for pelvic organ prolapse in the elderly woman. J Pelvic Med Surg 2003;9:83–9. 34. Denehy TR, Choe JY, Gregori CA et al. Modified Le Fort colpocleisis with Kelly urethral plication and posterior colpoperineoplasty in the medically compromised elderly:
a comparison with vaginal hysterectomy, anterior colporrhaphy, and posterior colpoperineoplasty. Am J Obstet Gynecol 1995;173:1697–1702. 35. Stoesser FG. Construction of a sacrocervical ligament for uterine suspension. Surg Gynecol Obstet 1955;101:638–41. 36. Arthure HGE, Savage D. Uterine prolapse and prolapse of the vaginal vault treated by sacral hysteropexy. J Obstet Gynaecol Br Emp 1957;64:355–60. 37. Banu LF. Synthetic sling for genital prolapse in young women. Int J Gynecol Obstet 1997;57:57–64. 38. Constantini E, Lombi R, Micheli C et al. Colposacropexy with Gore-tex mesh in marked vaginal and uterovaginal prolapse. Eur Urol 1998;34:111–17. 39. Leron E, Stanton SL. Sacrohysteropexy with synthetic mesh for the management of uterovaginal prolapse. Br J Obstet Gynaecol 2001;108:629–33. 40. Barranger E, Fritel X, Pigne A. Abdominal sacrohysteropexy in young women with uterovaginal prolapse: longterm follow-up. Am J Obstet Gynecol 2003;189:1245–50. 41. Joshi VM. A new technique of uterine suspension to pectineal ligaments in the management of uterovaginal prolapse. Obstet Gynecol 1993;81:790–3. 42. Nesbitt RE. Uterine preservation in the surgical management of genuine stress urinary incontinence associated with uterine prolapse. Surg Gynecol Obstet 1989;168:143–7.
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76 Urinary incontinence following prolapse surgery Brigitte Fatton, Bernard Jacquetin, Rufus Cartwright
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IntroductIon The development or persistence of urinary incontinence following surgery for urogenital prolapse remains a problem for all urogynecologists and female urologists. Although the quoted risk varies widely between different authors and different case series,1–7 recent publications have estimated rates of between 11%8 and 28%.3 A recent prospective epidemiologic study9 reported a 7.5% rate of surgery for stress urinary incontinence following ‘successful’ prolapse surgery at 5-year follow up. This is clearly an underestimate as few patients actually present for repeat surgery in these circumstances. Minimally invasive techniques such as midurethral tension-free slings may present a simple solution for postoperative stress urinary incontinence following prolapse surgery. However, even an appropriately counseled patient following skilled surgery will regard the original operation as being unsuccessful if they subsequently develop urinary incontinence which was not a pre-existing problem for them. It is therefore important to try to identify those patients who are at risk of stress urinary incontinence following surgery for urogenital prolapse and to evaluate any possible preventive measures. This type of screening is difficult and it is inappropriate to develop a wholesale preventive approach as this can cause unacceptable morbidity for uncertain benefit. Based on a review of the literature, the authors wish to propose a rational management pathway.
ing clinical examination. It represents true incontinence which has not been apparent because of the protective role of the prolapse maintaining continence because of outflow obstruction of the lower urinary tract. Potential stress urinary incontinence is identified in a woman who does not have preoperative urinary incontinence, either on history or on clinical examination, but who is predisposed to develop incontinence secondary to a procedure to correct her urogenital prolapse. This may occur because of inappropriate transmission of intra-abdominal pressure during stress or because of intrinsic urethral sphincter incompetence.
PathoPhysIologIc PrIncIPles Masked stress urinary incontinence can be explained by the mechanical prevention of urinary incontinence due to the position of the prolapse.4 The ‘ball effect’ can be caused by uterine prolapse or a large cystocele, kinking of the urethra or even a rectocele. All of these may prevent urinary leakage.4,10–12 However, it is important to distinguish between the two main mechanisms underlying masked incontinence: urethral compression and kinking of the urethra.
• Intrinsic urethral compression is due to significant
defInItIons The concepts of ‘masked’ and ‘potential’ in urinary incontinence are frequently confused. This explains the discrepancies between some studies. In the English literature the terms ‘potential’, ‘occult’, ‘masked’, ‘latent’, and ‘iatrogenic’ appear to be used interchangeably to describe stress urinary incontinence that develops following prolapse surgery in a previously continent patient. Classic ‘masked’ incontinence is labeled as ‘potential’ incontinence, even though it is impossible to predict the latter preoperatively. These two situations are completely different, with separate pathophysiologic mechanisms, and require different diagnostic techniques and management. Stress urinary incontinence can present in conjunction with urogenital prolapse. Even if the patient fails to mention it, it should become obvious by taking a thorough history. In such cases, a combined procedure to deal with both the prolapse and the stress incontinence should be undertaken. Masked stress urinary incontinence will not be revealed from the history alone but should be identified follow-
•
uterine descent or a large posterior vaginal prolapse. This can be corrected by a speculum preventing the protrusion of the posterior vaginal wall or the uterine descent. Many consider the use of reduction techniques to be fairly reliable and reproducible and therefore find them useful in screening for masked incontinence.10 Kinking of the urethra due to herniation of the anterior vaginal wall can be more difficult to correct. Reduction of the prolapse with excessive traction on the posterior vaginal wall may, in fact, open the bladder neck. This will lead to an overdiagnosis of ‘masked stress incontinence’.
The practical methods for reducing prolapse are variable. Some people prefer the pessary test, while others prefer an intravaginal tampon13,14 and/or a speculum blade.4 The pathophysiology of ‘potential urinary incontinence’ remains unknown, which partially explains the difficulty in preventing it, and several hypotheses have been suggested. In considering these theories, it is important to employ precise terminology. ‘Potential urinary incontinence’ should not be used to describe all types of postoperative incontinence occurring in previously dry women. In the authors’ opinion, potential urinary
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incontinence should only refer to stress urinary incontinence excluding de novo cases of overactive bladder. Detrusor overactivity has very different causes, notably surgical overcorrection. Overactive bladder is frequently found to coexist with severe urogenital prolapse, which may be exacerbated or alleviated by surgery.15
dIagnosIs Masked urinary incontinence is not identified in the history. It can be suspected if the patient gives a history of stress urinary incontinence which improves with the onset or exacerbation of a prolapse. This transitory stress urinary incontinence deserves attention. The diagnosis of masked stress urinary incontinence should only be made at clinical examination. Urinary leakage may be observed following reduction of the prolapse during a thorough clinical examination. It is important to know whether or not the woman’s bladder is full prior to the examination as clinical examination with an empty bladder is unhelpful, whereas examination with an overfull bladder may lead to overdiagnosis. Reduction of the prolapse is important. A forceps can be placed on the cervix to realign the cervix in its anatomic position and the anterior and posterior blades of a vaginal speculum can be used to correct a cystocele and a rectocele, respectively. The patient can then be asked to cough or strain. It is important to position the patient appropriately for the examination. Although it is usually most convenient to start the examination on a gynecologic couch, if this does not give conclusive results it may be necessary to examine the patient in the sitting or standing position. It is important to recognize that even these examination techniques cannot always replicate the anatomic correction produced by surgery. Some surgeons have suggested further intraoperative tests to improve the reliability of screening. These tests require the cooperation of the patient and can only be attempted under regional or local anesthesia. At the end of the procedure, the bladder is filled with 250–300 ml of fluid and the patient is asked to cough. If there is an objective leak under these circumstances, a preventive continence procedure is indicated. Other authors have suggested that this is not a physiologic stress test as anesthesia alters the angle of the urethrovesical junction and this serves local sanitation. Another alternative to a well-conducted clinical examination is the pessary test conducted over several days. It corrects prolapse and allows screening of masked incontinence during the patient’s normal daily life. There are, however, limitations to this procedure: either unwilling-
ness on the part of the patient or anatomic difficulties such as previous hysterectomy, discomfort from a ring, or local atrophy. A recent study evaluating patient satisfaction at 2 months following placement of a pessary reported a 21% rate of unmasked incontinence. 16 It is not possible to establish a diagnosis of potential urinary incontinence although certain risk factors may be identified in the assessment of a woman with urogenital prolapse. • history: Mild stress urinary incontinence, which affects 30–50% of women, is usually reasonably well tolerated and may not be mentioned during the course of a consultation. Severe constipation, chronic bronchitis or asthma may be causes of raised intraabdominal pressure with consequent deleterious effects on the pelvic floor. Some professional, sporting or domestic activities may also involve regular increases in intra-abdominal pressure. Although these factors may predispose to pelvic floor laxity, they do not in themselves predict postoperative stress urinary incontinence. • clinical examination: Hypermobility of the urethrovesical junction may be demonstrated with the Qtip test or observed with the naked eye. Obesity is known to have a negative impact on the pelvic floor. Abdominoperineal asynchronicity should be sought and, if present, may be treated with pelvic floor reeducation; however, this has not been shown to be of any particular value. • investigations: It is contentious whether or not urodynamic studies should be carried out on all women prior to prolapse surgery. However, the authors feel that such investigations are important and may reveal preoperative risk or provide objective evidence of postoperative complications. Despite this, the majority of authors consider that urodynamic studies have a low predictive value for potential urinary incontinence. However, urodynamics may reveal additional information such as urethral sphincter weakness or a low baseline Valsalva leak point pressure.13,17 Thus, the quality of the clinical assessment including a pessary test or other maneuvers to reduce the prolapse, together with controlled bladder filling, are most important. For women with prolapse who are to undergo surgery, conventional radiology18 such as cystourethrography does not distinguish between continent and incontinent women. Therefore, radiology does not help to screen for patients at risk of postoperative incontinence.3 Ultrasound may prove more useful19 as 1091
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it can help in the evaluation of urethral/bladder neck support preoperatively. In the future it may help to select those women who need to undergo a concomitant continence procedure; however, this has proved difficult to date. Even when the possible risk factors have been established it is not possible to give a precise estimation of the risk of developing urinary incontinence following surgery for urogenital prolapse. However, some operations for prolapse are more likely to cause problems than others. Richter’s sacrospinous fixation causes backward angulation of the vagina, so when there is overcorrection of the vaginal vault prolapse it tends to open the bladder neck, increasing the risk of incontinence. It is also important to consider the type of pelvic floor repair as a residual prolapse may be protective against the development of urinary incontinence.3
ManageMent Although it is difficult to reach a consensus, there are certain important questions that should be considered.
When should a combined prolapse and urinary incontinence procedure be carried out? If stress incontinence and prolapse are both known to be present, then it is important to treat both at the same time. A recent study by Liang et al.20 revealed that 64.7% of patients with a positive preoperative pessary test who were not offered a primary continence procedure developed incontinence after prolapse surgery. Some surgeons will always perform a continence procedure; however, this may be unnecessary for 35% of patients, thus justifying a delayed approach. Some pelvic floor surgeons who operate with patients under regional anesthesia employ a cough test at the end of the prolapse procedure.21,22 In a prospective study (personal communication), Pigné observed that of 70 patients with stress incontinence prior to prolapse surgery, only 60 had a positive cough test following the prolapse procedure, and of the remaining 10 only one developed postoperative stress incontinence requiring a later insertion of a tension-free vaginal tape (TVT). In the same study, of the 76 patients without stress incontinence prior to surgery, the cough test was positive in 18 (24%) which, in the author’s opinion, justified a combined continence procedure. Of the remaining 58 patients, six developed postoperative incontinence and four required further surgery. For patients with prolapse and stress incontinence an intraoperative cough test will avoid a continence procedure in 14% (10 out of 70), with an expected risk of requiring a secondary
procedure for incontinence (1 out of 10). For patients with prolapse but no stress incontinence carrying out a cough test, this still leaves a 10% rate of postoperative incontinence and necessitates a continence procedure in 24%. Some authorities would consider that, if there is no urinary leakage demonstrated preoperatively (after reduction of the prolapse), there is no reason to carry out a continence procedure. In such circumstances, several studies have shown that the risk of urinary incontinence after prolapse surgery is very small. In the case of mild stress incontinence, and depending on the preference of both the surgeon and the patient, the management choices are shown in Figure 76.1. In all other cases, a prophylactic continence procedure would appear unnecessary except for those surgeons who undertake an intraoperative cough test at the end of the prolapse procedure (Fig. 76.2). The reliability of the cough test during pelvic floor surgery is controversial. Some consider that it has only weak discriminative power. However, systematic use of the cough test under controlled intraoperative conditions (position on the operating table, method of anesthesia, disturbance of neuromuscular tone) can identify some false negatives and avoid overtreatment of other patients. This will only affect a small proportion of women. Those who support this method emphasize its advantages. It is the only useful intraoperative test carried out in an anatomic position. Preoperative tests cannot be undertaken in this position, and under- or overcorrection will distort the final outcome. It appears likely that, taking into account the views of different published case series, preoperative maneuvers to reduce prolapse tend to produce more false positives than false negatives.
Which continence procedure? This is based on the views and preferences of the surgeon but the reliability and low morbidity of suburethral slings (either retropubic or transobturator) are good choices.23 It is important to avoid procedures with unknown long-term reliability24 and to opt for the procedure which would be best for stress incontinence alone. Needle suspensions and Kelly bladder neck plication have been abandoned because of their poor results.24,25 Burch colposuspension26 is also being superseded by procedures which are as effective but with lower morbidity.
How can we prevent ‘potential urinary incontinence’? As our understanding of the pathophysiologic mechanism underlying potential stress incontinence is so poor, prevention therefore relies on good practice in urogynecologic surgery. Preventive efforts on their own may be
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Figure 76.1. Management of women with masked stress urinary incontinence (SUI).
Figure 76.2. Management of women with no preoperative urinary incontinence. SUI, stress urinary incontinence.
insufficient but by neglecting them there is an increased risk of postoperative complications. Excessive tension in a repair should be avoided, particularly at the level of the anterior vaginal wall and the vaginal vault. Many authors have emphasized the increased risk and additional problems associated with procedures such as sacrospinous fixation. In a retrospective study of 62 women,27 the results in terms of postoperative incontinence were significantly better for the group having a Pereyra suspension alone (34 patients, median follow-up 23 months, subjective cure of stress incontinence 91%, objective cure of stress incontinence 88%) compared to the group having a Pereyra suspension in addition to
a sacrospinous ligament fixation (28 patients, median follow-up 26 months, subjective cure of stress incontinence 68%, objective cure of stress incontinence 61%). The posterior angulation of the vaginal axis as a result of the sacrospinous fixation predisposes to opening of the bladder neck by a fraction on the posterior wall. This has been confirmed by Sze et al.28 in a retrospective comparison of abdominal sacrocolpopexy with Burch colposuspension versus sacrospinous fixation with needle suspension. The rate of recurrent incontinence in the former group was 4% but in the latter was 9%. The choice of continence procedure may have biased this study. 1093
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30
26
Groutz et al. (2000) Prospective
25
Masked SUI, n=30
Without SUI, n=70
Masked SUI, n=55
Stamey
8 m. (range 3–9)
3.5 y.
3.5 y.
Needle colposuspension, n=3 No surgery
3.5 y.
44 m. (range 12–96)
47 m. (range 12–108)
Burch, n=52
No surgery
Without SUI, n=10
Klutke & Ramos (2000) Retrospective
Pubovaginal sling
Masked SUI, n=14
Chaikin et al. (2000)32 Prospective
25.5 m.
>5 y.
33 Pereyra Kelly plication
>5 y.
>5 y.
21 Pereyra 40 Kelly Nichols
>5 y.
2.9±1.8 y.
Cystopexy + pubourethral ligaments plication, n=50
15 Kelly Nichols
2.6±1.7 y.
6 w. and 6 m.
Follow-up
Cystopexy, n=52
Masked SUI, n=30
Masked SUI
Patent SUI
Potential UI
Gordon et al. (1999)24 Prospective
Colombo et al. (1997)31 Randomized
Colombo et al. (1996) Randomized
Plication, n=5
Colposuspension, n=4
Colporrhaphy, n=10
Potential or masked, n=20 Transmission <90% or positive pessary test Without UI, n=9 (hypermobility only)
Surgery Transcutaneous needle colposuspension (Muzsnaï), n=10
Incontinence type
29
Bump et al. (1996) Prospective randomized
Urinary results according to incontinence type and surgical procedure
Author/year/trial
table 76.1.
Subjective and objective SUI: 23.3%
SUI: 0%
SUI: 4%
SUI: 4%
SUI: 0%
SUI: 14%
Subjective and objective SUI: 50% Objective SUI: 37%
SUI: 0%
SUI: 15%
SUI: 29%
SUI: 40%
SUI: 8% (n=4)
SUI: 8% (n=4)
Suburethral plication: SUI=21% at 6 w., 7% at 6 m.
Colposuspension: SUI=7% at 6 w., 14% at 6 m.
Results
–
De novo detrusor instability: 5%
–
De novo detrusor instability: 30%
De novo urge incontinence: 0%
1 de novo urge incontinence
–
Detrusor instability after Pereyra: 2%
Detrusor instability after Kelly Nichols: 4%
1 reoperation Long-term micturition difficulties: 10% Symptomatic detrusor instability: 2%
1 reoperation Long-term micturition difficulties: 0% Symptomatic detrusor instability: 2%
Plication – detrusor instability: 7%
Colposuspension – detrusor instability: 36%
Comments
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Masked SUI, n=38
34
Masked SUI
Masked SUI (positive pessary test), n=49
Meschia et al. (2004) Prospective randomized
Liang et al. (2004)20 Prospective
Subjective SUI: 0% Objective SUI: 10%
Results
Unknown Unknown Unknown
No TVT, n=17 No TVT, n=30
24 m.
Plication TVT, n=32
26 m.
27 m. (range 12–52)
No postoperative SUI
Subjective SUI: 64.7% Objective SUI: 52.9%
Subjective SUI : 9.4% Objective SUI: 0%
Idiopathic de novo overactivity: 0%
Idiopathic detrusor overactivity: 5.9%
Idiopathic detrusor overactivity: 16%
De novo urge incontinence: 4%
De novo urge incontinence: 12%
Subjective SUI: 4% Objective SUI: 8% Subjective SUI: 36% Objective SUI: 44%
De novo urge incontinence: 8%
De novo urge incontinence: 9.5% Permanent retention: 0%
De novo detrusor instability (without obstruction): 13.33%
Comments
Subjective and objective SUI at 1 year follow-up: 2%
15 m. (range 6–39) SUI: 5%
14.25 m. (range 12–24)
Follow-up
TVT
TVT
Pubovaginal sling
TVT
Surgery
SUI, stress urinary incontinence; TVT, tension-free vaginal tape; UI, urinary incontinence; w, week; m, month; y, year.
No masked SUI (negative pessary test), n=30
Masked SUI, n=100
Groutz et al. (2004)35 Prospective
Barnes et al. (2002) Retrospective
23
Masked SUI
Gordon et al. (2001) Prospective
33
Incontinence type
Urinary results according to incontinence type and surgical procedure (cont.)
Author/year/trial
table 76.1.
Urinary incontinence following prolapse surgery
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What information should we give to patients before surgery? It is important that patients understand the possibilities. They need to know that there is a de novo incidence of stress incontinence following correction of a prolapse. This varies with the type of prolapse and the surgical procedure chosen to repair the pelvic floor as well as the quality of repair. This can change over time; the literature suggests a rate of between 10 and 30%. The specific possible complications must be clearly explained as people often regard minimally invasive procedures as routine and complication-free. The most common urinary problems are dysuria and overactive bladder (Table 76.1). The complications and their management have been the subject of a recent literature review.36 Estimates of the rate of postoperative dysuria vary from 2 to 22% depending upon the operative technique employed36 (needle suspensions 5–7%,37 suburethral sling 4–10%,38 TVT 2–4%,22 Marshall–Marchetti–Kranz procedure 5– 20%,39,40 Burch colposuspension 4–22%41,42). Symptoms of overactive bladder are even more frequently encountered, varying from 6 to 25% depending upon the choice of technique36 (sling 8–25%,43 TVT 6–12%,44–46 retropubic urethropexies 6–16%41,47). Failure of the procedure is possible regardless of the choice of operation and the patient must be forewarned. For suburethral support techniques it is reasonable to suggest a figure of 10% when treating masked stress incontinence.20,23,33,35 The major risks of a preventive procedure are the morbidity associated with an initial operation that is poorly tolerated by patients who may regard a preventive procedure as pointless. They must also be informed about the possible treatment that would be available should stress incontinence occur following pelvic floor surgery. It is important to reassure patients that if postoperative complications do recur they will benefit from having had appropriate preoperative counseling.
references 1. Bergman A, Koonings PP, Ballard CA. Predicting postoperative urinary incontinence development in women undergoing operation for genitourinary prolapse. Am J Obstet Gynecol 1988;158:1171–5. 2. Borstad E, Rud T. The risk of developing urinary stressincontinence after vaginal repair in continent women: a clinical and urodynamic follow-up study. Acta Obstet Gynecol Scand 1989;68:545–9. 3. Borstad E, Skrede M, Rud T. Failure to predict and attempts to explain urinary stress incontinence following vaginal repair in continent women by using a modified
lateral urethrocystography. Acta Obstet Gynecol Scand 1991;70:501–6. 4. Bump RC, Fantl JA, Hurt WG. The mechanism of urinary continence in women with severe uterovaginal prolapse: results of barrier studies. Obstet Gynecol 1988;72:291–5. 5. Richardson DA, Bent AE, Ostergard DR. The effect of uterovaginal prolapse on urethrovesical pressure dynamics. Am J Obstet Gynecol 1983;15:901–5. 6. Rosenzweig BA, Pushkin S, Blumenfeld D, Bhatia NN. Prevalence of abnormal urodynamic test results in continent women with severe genitourinary prolapse. Obstet Gynecol 1992;79:539–42. 7. Scheepers HC, Wolterbeek JH, Gerretsen G, Venema P. [Inventory and follow-up of patients with surgery for (uterine) vaginal prolapse, combined with or without (masked) stress incontinence.] Ned Tijdschr Geneeskd 1998;142:79–83. 8. Beck RP, McCormick S, Nordstrom L. A 25-year experience with 519 anterior colporrhaphy procedures. Obstet Gynecol 1991;78:1011–18. 9. Clark AL, Gregory T, Smith VJ, Edwards R. Epidemiologic evaluation of reoperation for surgically treated pelvic organ prolapse and urinary incontinence. Am J Obstet Gynecol 2003;189:1261–7. 10. Karram MM. What is the optimal anti-incontinence procedure in women with advanced prolapse and ‘potential’ stress incontinence? Int Urogynecol J Pelvic Floor Dysfunct 1999;10:1–2. 11. Long CY, Hsu SC, Wu TP, Sun DJ, Su JH, Tsai EM. Urodynamic comparison of continent and incontinent women with severe uterovaginal prolapse. J Reprod Med 2004;49:33–7. 12. Romanzi LJ. Management of the urethral outlet in patients with severe prolapse. Curr Opin Urol 2002;12:339–44. 13. Gallentine M, Cespedes D. Occult stress urinary incontinence and the effect of vaginal vault prolapse on abdominal leak point pressures. Urology 2001;57:40–4. 14. Ghoneim GM, Walters F, Lewis V. The value of the vaginal pack test in large cystoceles. J Urol 1994;152:931–4. 15. Cardozo LD, Stanton SL, Williams JE. Detrusor instability following surgery for genuine stress incontinence. Br J Urol 1979;51:204–7. 16. Clemons JL, Aguilar VC, Tillinghast TA, Jackson ND, Myers DL. Patient satisfaction and changes in prolapse and urinary symptoms in women who were fitted successfully with a pessary for pelvic organ prolapse. Am J Obstet Gynecol 2004;190:1025–9. 17. Veronikis DK, Nichols DH, Wakamatsu MM. The incidence of low-pressure urethra as a function of prolapsereducing technique in patients with massive pelvic organ prolapse (maximum descent at all vaginal sites). Am J Obstet Gynecol 1997;177:1305–13.
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18. Bergman A, McKensie C, Ballard CA, Richmond J. Role of cystourethrography in the preoperative evaluation of stress urinary incontinence in women. J Reprod Med 1988;33:372–6.
30. Colombo M, Maggioni A, Scalambrino S, Zanetta G, Vignali M, Milani R. Prevention of postoperative urinary stress incontinence after surgery for genitourinary prolapse. Obstet Gynecol 1996;87:266–71.
19. Bergman A, Koonings PP, Ballard CA, Platt LD. Ultrasonic prediction of stress urinary incontinence development in surgery for severe pelvic relaxation. Gynecol Obstet Invest 1988;26:66–72.
31. Colombo M, Maggioni A, Scalambrino S, Vitobello D, Milani R. Surgery for genitourinary prolapse and stress incontinence: a randomized trial of posterior pubourethral ligament plication and Pereyra suspension. Am J Obstet Gynecol 1997;176:337–43.
20. Liang CC, Chang YL, Chang SD, Lo TS, Soong YK. Pessary test to predict postoperative urinary incontinence in women undergoing hysterectomy for prolapse. Obstet Gynecol 2004;104:795–800. 21. Bombieri L, Freeman RM. Recurrence of stress incontinence after vault suspension: can it be prevented? Int Urogynecol J Pelvic Dysfunct 1998;9:58–60. 22. Pigné A. Peut-on améliorer la continence des patients lors de la chirurgie du prolapsus. XXVII ème congrès de la Société Francophone d’UroDynamique, Bucarest; 3–5 Juin 2004 (unpublished data). 23. Meschia M, Pifarotti P, Spennacchio M, Buonaguidi A, Gattei U, Somigliana E. A randomized comparison of tension-free vaginal tape and endopelvic fascia plication in women with genital prolapse and occult stress urinary incontinence. Am J Obstet Gynecol 2004;190:609–13. 24. Gordon D, Groutz A, Wolman I, Lessing JB, David MP. Development of postoperative urinary stress incontinence in clinically continent patients undergoing prophylactic Kelly placation during genitourinary prolapse repair. Neurourol Urodyn 1999;18:193–7. 25. Groutz A, Gordon D, Wolman I, Jaffa AJ, Kupferminc MJ, David MP, Lessing JB. The use of prophylactic Stamey bladder neck suspension to prevent post-operative stress urinary incontinence in clinically continent women undergoing genitourinary prolapse repair. Neurourol Urodyn 2000;19:671–6. 26. Klutke JJ, Ramos S. Urodynamic outcome after surgery for severe prolapse and potential stress incontinence. Am J Obstet Gynecol 2000;182:1378–81. 27. Nguyen JK, Bhatia NN. Risk of recurrent stress incontinence in women undergoing the combined modified Pereyra procedure and transvaginal sacrospinous ligament vault suspension. Urology 2001;58:947–52. 28. Sze EHM, Kohli N, Miklos R, Roat T, Karram MM. A retrospective comparison of abdominal sacrocolpopexy with Burch colposuspension versus sacrospinous fixation with transvaginal needle suspension for the management of vaginal vault prolapse and coexisting stress incontinence. Int Urogynecol J 1999;10:390–3. 29. Bump RC, Hurt WG, Theofrastous JP et al. Randomized prospective comparison of needle colposuspension versus endopelvic fascia plication for potential stress incontinence prophylaxis in women undergoing vaginal reconstruction for stage III or IV pelvic organ prolapse. Am J Obstet Gynecol 1996;175:326–33.
32. Chaikin DC, Groutz A, Blaivas JG. Predicting the need for anti-incontinence surgery in continent women undergoing repair of severe urogenital prolapse. J Urol 2000;163:531–4. 33. Gordon D, Gold RS, Pauzner D, Lessing JB, Groutz A. Combined genitourinary prolapse repair and prophylactic tension-free vaginal tape in women with severe prolapse and occult stress urinary incontinence: preliminary results. Urology 2001;58:547–50. 34. Barnes NM, Dmochowski RR, Park R, Nitti VW. Pubovaginal sling and pelvic prolapse repair in women with occult stress urinary incontinence: effect on post-operative emptying and voiding symptoms. Urology 2002;59:856–60. 35. Groutz A, Gold R, Pauzner D, Lessing JB, Gordon D. Tension-free vaginal tape (TVT) for the treatment of occult stress urinary incontinence in women undergoing prolapse repair: a prospective study of 100 consecutive cases. Neurourol Urodyn 2004;23:632–5. 36. Dunn JS, Bent AE, Ellerkman RM, Nihira MA, Melick CF. Voiding dysfunction after surgery for stress incontinence: literature review and survey results. Int Urogynecol J 2004;15:25–31. 37. Spencer JR, O’Connor VJ Jr, Schaeffer AJ. A comparison of endoscopic suspension of the vesical neck with suprapubic vesicourethropexy for treatment of stress urinary incontinence. J Urol 1987;137:411–15. 38. Horbach NS. Suburethral sling procedures. In: Ostergard DR, Bent AE (eds) Urogynecology and Urodynamics: Theory and Practice, 4th ed. Baltimore: Williams and Wilkins, 1996; 569–79. 39. McDuffie RW Jr, Litin RB, Blundon KE. Urethrovesical suspension (Marshall–Marchetti–Krantz). Experience with 204 cases. Am J Surg 1981;141:297–8. 40. Zimmern PE, Hadley HR, Leach GE, Raz S. Female urethral obstruction after Marshall–Marchetti–Krantz operation. J Urol 1987;138:517–20. 41. Alcalay M, Monga A, Stanton SL. Burch colposuspension: a 10–20 year follow-up. Br J Obstet Gynecol 1995;102:740–5. 42. Maher C, Dwyer P, Carey M, Gilmour D. The Burch colposuspension for recurrent urinary stress incontinence following retropubic continence surgery. Br J Obstet Gynecol 1999;106:719–24. 43. Weinberger MW, Ostergard DR. Long term clinical and
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urodynamic evaluation of polytetrafluoroethylene suburethral sling for treatment of genuine stress incontinence. Obstet Gynecol 1995;86:92–6.
46. Rackley RR, Abdelmalak JB, Tchetgen MB, Madjar S, Jones S, Noble M. Tension-free vaginal tape and percutaneous vaginal tape sling procedures. Tech Urol 2001;7:90–100.
44. Karram MM, Segal JL, Vassallo BJ, Kleeman SD. Complications and untoward effects of the tension-free vaginal tape procedure. Obstet Gynecol 2003;101:929–32.
47. Langer R, Lipshitz Y, Halperin R, Pansky M, Bukovsky I, Sherman D. Long-term (10–15 years) follow-up after Burch colposuspensions for urinary stress incontinence. Int Urogynecol J 2001;12:323–6.
45. Kuuva N, Nilsson CG. A nationwide analysis of complications associated with the tension-free vaginal tape (TVT) procedure. Acta Obstet Gynecol Scand 2002;81:72–7.
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77 Episiotomy and perineal repair Ranee Thakar, Christine Kettle
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IntroductIon Perineal injury is inherent in childbirth and various methods and materials were used by accoucheurs in an attempt to restore perineal integrity. Surgical treatment in the form of a crossed or bootlace suture is first mentioned in Avicenna’s famous Arabic book. However, the first recorded perineal suture was that of Guillemeau in 1610.1 Perineal trauma resulting from childbirth remains a common problem2 that causes a significant increase in maternal morbidity and may also have devastating effects on family life and sexual relationships.3 More than 85% of women sustain perineal trauma after childbirth,4 and up to two-thirds need suturing.2 Perineal pain and discomfort affect up to 42% of women at 10 days postpartum and in 10% of women these problems persist at 18 months following childbirth.5 Moreover, up to 58% of women experience superficial dyspareunia at 3 months postpartum.6 This chapter covers management and repair of episiotomy and first and second degree tears. Preventive measures are also discussed.
ApplIed AnAtomy Anatomy of the perineum
versely between the ischial tuberosities. The anterior triangle, which contains the external urogenital organs, is known as the urogenital triangle and the posterior triangle, which contains the termination of the anal canal, is known as the anal triangle.
Urogenital triangle The muscles are classified into a superficial and a deep group relative to the perineal membrane (urogenital diaphragm). The bulbospongiosus, superficial transverse perineal, and the ischiocavernosus muscles lie in the superficial compartment (Fig. 77.1). The bulbospongiosus muscle encircles the vagina and inserts anteriorly into the corpora cavernosa clitoridis. Posteriorly, some of its fibers may merge with those of the superficial transverse perineal muscle and also with the external anal sphincter. Beneath the bulbospongiosus muscles lie the vestibular bulbs anteriorly and the Bartholin’s glands posteriorly. The Bartholin’s gland is a pea-shaped structure and its duct opens at the introitus just superficial to the hymen at the junction of the upper two-thirds and the lower third of the labia minora. The deep transverse perineal muscle lies below the perineal membrane. It is thin and difficult to delineate and hence some authors deny the existence of this muscle.7
Anal triangle The perineum corresponds to the outlet of the pelvis and is somewhat lozenge- shaped. The perineum can be divided into two triangular parts by drawing a line trans-
Clitoris Ischiopubic ramus
This area includes the anal sphincters and ischiorectal fossae. The external anal sphincter is subdivided into three parts – subcutaneous, superficial, and deep – and
Ischiocavernosus muscle Vestibular bulb Perineal membrane
Bulbospongiosus muscle Ischial tuberosity
Bartholin’s gland Superficial transverse perineal muscle Perineal body Levator ani muscle External anal sphincter
Coccyx
Figure 77.1.
The superficial muscles of the perineum.
Gluteus maximus muscle
Cardozo fig.77.1
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is inseparable from the puborectalis muscle posteriorly (Fig. 77.2). The internal anal sphincter is a thickened continuation of the circular smooth muscle of the bowel. It is separated from the external anal sphincter (striated muscle) by the conjoint longitudinal muscle which is a continuation of the longitudinal smooth muscle of the bowel but may receive contributions from the puborectalis muscle and the deep external sphincter8 (see Chapter 78).
Perineal body The perineal body is the central point between the urogenital and the anal triangles of the perineum. Its three-dimensional form has been likened to that of the cone of the red pine, with each ‘petal’ representing an interlocking structure, such as an insertion site of fascia or a muscle of the perineum.9 Within the perineal body there is interlacing of muscle fibers from the bulbospongiosus, superficial transverse perineal, and external anal sphincter muscles. Above this level there is a contribution from the longitudinal rectal muscle and the medial fibers of the puborectalis muscle.
defInItIon of perIneAl trAumA Perineal trauma may occur spontaneously during vaginal birth or when a surgical incision (episiotomy) is intentionally made to facilitate delivery. It is possible to have an episiotomy and a spontaneous tear (e.g. extension of an episiotomy). Anterior perineal trauma is defined as injury to the labia, anterior vagina, urethra or clitoris; posterior perineal trauma is defined as any injury to the posterior vaginal wall or peri-
Figure 77.2.
neal muscles and may include disruption of the anal sphincters.
Structures involved First degree perineal trauma is very superficial and may involve the skin and subcutaneous tissue of the anterior and posterior perineum, the vaginal mucosa, or a combination of these. Second degree tears or mediolateral episiotomy involves the superficial perineal muscles (bulbocavernosus, transverse perineal) or the perineal body if a midline episiotomy incision is made. If the trauma is very deep the pubococcygeus muscle may be disrupted. Rarely, more complex trauma can occur, whereby the tear extends in a circular direction, behind the hymeneal remnants, bilaterally upwards towards the clitoris, causing the lower third of the vagina to detach from the underlying structures.7
epISIotomy Episiotomy is a surgical incision made with scissors or a scalpel into the perineum in order to increase the diameter of the vulval outlet and facilitate delivery.10 The two main types of episiotomy incision are midline and mediolateral.11 When a midline episiotomy is undertaken, the incision is made from the midpoint of the introitus and is directed vertically towards the anus; with a mediolateral episiotomy, the incision begins in the midline but is directed directly away from the anal sphincter and rectum. Hudson et al.12 have suggested that the term ‘mediolateral’ is a misnomer and they call this type of incision a ‘posterolateral episiotomy’ as it commences in the midline and is aimed to one side of
The anal sphincter. 1101
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the perineum in order to avoid the anal sphincter. It is claimed that the midline incision is easier to repair and that it is associated with less blood loss, better healing, less pain, and earlier resumption of sexual intercourse. However, there is no reliable evidence to support these claims.5 Limited evidence from one quasi-randomized trial suggested that the midline incision may increase the risk of third and fourth degree tears compared with the mediolateral incision.13 However, these data should be interpreted with caution as there may be an increased risk of selection bias due to quasi-random treatment allocation; in addition, analysis was not by intention to treat.
Incidence There is a wide variation in the incidence of episiotomies performed in different countries. Clinicians’ experiences, practices, and preferences in terms of intrapartum interventions may influence the rate and severity of perineal trauma. Moreover, episiotomy rates may vary considerably according to individual practices and policies of staff and institutions.3 In the United Kingdom, it is estimated that over 85% of women who give birth will sustain some degree of perineal trauma and, of these, 60–70% will require suturing.14 However, episiotomy rates have reduced in English-speaking countries and Europe over the last 20 years, probably due to the accumulation of evidence supporting restrictive use of the procedure. Episiotomy is a common obstetrical procedure, yet statistics relating to prevalence are not always easily located. Figure 77.3 presents data graphically to illustrate the considerable variation in the use of episiotomy.15 Episiotomy rates that include both primiparous and multiparous women range from as low as 9.7% (Sweden) to 100% (Taiwan); rates for primiparous women range from 63.3% (South Africa) to 100% (Guatemala).15
Indications for episiotomy Episiotomy is still performed routinely in many parts of the world in the belief that it protects the pelvic floor. However, evidence from randomized controlled trials suggests that routine episiotomy does not prevent severe posterior perineal tears. Carroli and Belizan have conducted the most recent systematic review of randomized clinical trials using the Cochrane Collaboration methodology to determine the possible benefits and risks of restrictive episiotomy versus routine episiotomy. Mediolateral episiotomy was the method of incision for all six trials included in the review except for a North American trial where midline episiotomy was performed.
Figure 77.3. Graphical presentation of the considerable variation in the use of episiotomy: rates by country, 1995– 2003.* indicates primiparous data only. (Reproduced from ref. 15 with permission.)
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The review revealed that there is a lower risk of posterior perineal trauma, need for suturing and healing complications associated with the restrictive use of episiotomy at 7 days postpartum. However, there is no difference in the incidence of major outcomes such as severe vaginal or perineal trauma, pain, dyspareunia or urinary incontinence between the restrictive and routine/liberal use of episiotomy. The only disadvantage shown in restrictive use of episiotomy is an increased risk of anterior perineal trauma. This systematic review concluded that there is evidence to support the restrictive use of episiotomy compared to routine episiotomy (irrespective of the type of episiotomy performed). This finding applied to both primiparous and multiparous women.5 There is currently an absence of clear, evidence-based clinical indications for the use of episiotomy. However, it is reasonable to suggest that an episiotomy should be performed to accelerate vaginal delivery in cases of fetal distress, to facilitate safe delivery if shoulder dystocia occurs, to prevent severe perineal trauma during an instrumental delivery (forceps or ventouse), to aid vaginal delivery in cases where the perineal tissue is thick or rigid causing serious delay, and in cases in which prolonged ‘bearing down’ maybe harmful for the mother (e.g. severe hypertensive or cardiac disease). However, these indications are not absolute and clinical discretion should always be used.
episiotomy rate Although there is clear evidence to recommend restrictive use of episiotomy, there appears to be no consensus regarding the ideal episiotomy rate. Henriksen et al.16 performed an observational study involving 2188 pregnant women and found that those allocated to the group of midwives with the lowest rate of episiotomies were more likely to have an intact perineum, more spontaneous perineal tears, but no increased risk of having an anal sphincter tear. In a further publication17 the authors reported a relative decrease of 18% in episiotomy rates after distributing awareness profiles to the midwives, but the rate of anal sphincter tears did not change. There was a tendency towards an increased risk of tears if the midwives tried to reduce episiotomy rates below 20%. This supports the view that the overall ideal episiotomy rate should be between 20 and 30% but fails to indicate the ideal rate for nulliparae versus multiparae. The World Health Organization recommended that an episiotomy rate of 10% for spontaneous vaginal deliveries would be the ideal.18 Moreover, the figures on what is the appropriate episiotomy rate are not based on robust evidence.
mAnAgement of perIneAl trAumA For many centuries, there has been longstanding debate relating to suturing of perineal trauma following childbirth. Some accoucheurs believe that it is much better to leave perineal trauma unsutured to facilitate ‘ensuing’ deliveries, while others argue that the outcome for women and their partners is considerably improved if the trauma is sutured.
non-suturing of perineal trauma Non-suturing of perineal skin Results from two large randomized controlled trials carried out in Ipswich, UK (single center) and the other in Nigeria (multicenter)19,20 show that there are no major adverse effects associated with leaving the perineal skin unsutured. The trials compared leaving the skin unsutured but apposed (the vagina and perineal muscles were sutured) to the traditional repair whereby all three layers (vagina, perineal muscles and skin) were sutured. The trials showed conflicting results for perineal pain, with the UK trial showing no difference in short- and long-term perineal pain but the Nigerian trial showing that leaving the skin unsutured was associated with a reduction in perineal pain up to 3 months postpartum. Both trials reported lower rates of dyspareunia at 3 months and a significant increase in wound gaping at 2 days in the groups that had perineal skin unsutured. Wound gaping persisted up to 10 days in the UK trial but there was only a non-significant increase at 14 days postpartum in the Nigerian trial.
Non-suturing of perineal trauma There have been two small randomized controlled trials21,22 and two small retrospective studies23,24 carried out to compare the effects of non-suturing versus suturing of first and second degree tears. One of these trials (n=74 primiparous women) carried out in Scotland by Fleming and colleagues21 found no significant difference between non-suturing and suturing in terms of perineal pain but reported significantly more women in the sutured group had good wound approximation at 6 weeks postpartum. Perineal pain and healing were assessed using standardized measures at 1 day, 10 days and 6 weeks following birth. In the other small Swedish trial (n=78 primiparous women) carried out by Lundquist and colleagues22 that compared non-suturing to suturing of spontaneous tears which involved the labia, vagina, and perineum found a non-significant increase in short-term discomfort with non-suturing but no difference in wound healing between the groups. Data from this trial must be interpreted with caution, as the sample size was small, 1103
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it was unclear how healing was defined and measured, and most results did not reach statistical significance. The two small retrospective studies found no difference in short-term morbidity or wound healing rates.23,24 The practice of leaving first and second degree tears unsutured is associated with poorer wound healing and nonsignificant differences in short-term discomfort.3
Suture material A Cochrane systematic review of eight randomized controlled trials25 involving 3642 primiparous and multiparous women found that absorbable synthetic material (polyglycolic acid and polyglactin 910) when compared with catgut suture material was associated with less short-term morbidity. Although all the trials showed consistently lower rates of perineal pain, analgesia use, suture dehiscence, and resuturing in the polyglycolic acid and polyglactin 910 groups, two trials found that polyglycolic acid and polyglactin 910 were associated with an increased risk of suture removal up to 3 months postpartum. Standard polyglactin 910 is not totally absorbed from the wound until 60–90 days. However, a more rapidly absorbable form of material is now available. This material has the same chemical composition as polyglactin 910 but is sterilized by gamma irradiation, which causes loss in tensile strength at 10–14 days and complete absorption from the tissue by 42 days.26 Three randomized controlled trials2,27,28 comparing rapid-absorption polyglactin 910 to standard polyglactin 910 found no clear difference in short-term pain between the groups. However, two of the trials2,27 found a significant reduction in ‘pain when walking’ at 10–14 days postpartum.28 Only one of the trials reported a reduction in superficial dyspareunia at 3 months postpartum. All three trials found that rapid-absorption polyglactin 910 was associated with a significant reduction in the need for suture removal up to 3 months following childbirth. In light of current evidence, rapid-absorption polyglactin 910 is the most appropriate suture material for perineal repair.3
interrupted sutures. No differences were seen in the need for analgesia, resuturing of the wound or in dyspareunia. Based on one trial only, there was no difference in long-term pain and failure to resume pain-free intercourse within 3 months of the birth. The continuous technique was associated with less need for the removal of sutures. These results suggest that the continuous subcuticular technique for skin closure is associated with less short-term pain than techniques employing interrupted sutures.29
Continuous non-locking method Based on an observational study by Fleming,30 Kettle et al.2 conducted a large factorial randomized controlled trial (n=1542) comparing the loose non-locking continuous suture for all layers to the traditional interrupted method. The trial found a significant reduction in perineal pain at 10 days, which persisted up to 12 months after childbirth but did not reach statistical significance. There was no statistical difference in the rates of superficial dyspareunia between the groups at 3 months postpartum. Suture removal was significantly less in the continuous suturing group. The reason for the reduction in pain is probably due to the fact that the skin sutures are placed in the subcutaneous tissue, thus avoiding the profusion of nerve endings in the superficial skin surface. The rationale behind using the continuous technique is that stitch tension due to reactionary edema is transferred throughout the whole length of the single knotless suture in comparison to interrupted sutures which are placed transversely across the wound. Another advantage of the continuous suturing technique is that only one piece of suture material is required to complete the perineal repair as compared to two to three pieces for the interrupted method, thus reducing the overall expenditure. Based on the above evidence it can be concluded that perineal trauma should be repaired using the continuous non-locking technique to reapproximate all layers (vagina, perineal muscles, and skin) with rapid-absorption polyglactin 910.
method of repair
procedure for perineal repair
Skin closure
Assessment of perineal trauma
A Cochrane systematic review of four randomized controlled trials involving 1864 primiparous and multiparous women compared the continuous subcuticular suture technique of perineal skin closure to interrupted sutures. The subcuticular technique was associated with less pain for up to 10 days postpartum compared with
The person responsible for the woman’s care must inspect the perineum thoroughly as soon as possible following the birth, using good lighting. Prior to commencing suturing it is important that the health professional explains the procedure to the woman and her partner and obtains consent. The woman is placed in a
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comfortable position so that the trauma is easily visualized. It is not necessary to use lithotomy poles to support the woman’s legs during the procedure unless she has a working epidural or spinal anesthesia. Rectal examination should be carried out prior to commencement of repair. This helps in the identification of anal sphincter trauma. If the woman does not have an epidural, the woman should be asked to squeeze the anal sphincter. If the external anal sphincter is torn, the separated ends will retract towards the ischiorectal fossa.
and finishing with a terminal knot placed in the vagina beyond the hymeneal remnants.
The interrupted suturing method (Fig. 77.5)
The first stitch is inserted above the apex of the vaginal trauma to secure any bleeding points that may not be visible. Vaginal trauma, perineal muscles, and skin are approximated with a loose, continuous non-locking technique. The skin sutures are placed loosely and fairly deeply in the subcutaneous tissue, reversing back
The first stitch is inserted above the apex of the vaginal trauma to secure any bleeding points. Vaginal trauma is repaired with a continuous locking (blanket) stitch and the suture is tied at the fourchette with a loop knot. Interrupted sutures are inserted to close the perineal muscle (deep and superficial) and interrupted transcutaneous stitches are inserted to reapproximate the skin edges. A rectal examination should be performed after completing the repair to ensure that suture material has not been accidentally inserted through the rectal mucosa. Following completion of the repair, the extent of the injury sustained, the suture technique, and the materials used must be documented in the case notes in black
Figure 77.4. The continuous suturing technique. (a) Vaginal trauma is repaired using a loose, continuous nonlocking stitch to the vagina; (b) perineal muscle is repaired using a loose, continuous non-locking stitch; (c) skin is closed using a loose subcutaneous stitch. (Reproduced from ref. 31 with permission.)
Figure 77.5. Suturing the vagina using the interrupted suturing method. (a) Vaginal trauma is repaired with a continuous locking (blanket) stitch to the vaginal wall; (b) interrupted sutures are inserted to close the perineal muscles (deep and superficial); (c) interrupted transcutaneous stitches are inserted to reapproximate the skin edges.
The continuous suturing technique31 (Fig. 77.4)
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ink. It is also useful to include a diagram to illustrate the extent of the trauma.
prevention of perineal trauma Although the case for prevention of perineal trauma is compelling, how to accomplish this is less clear. Certain antenatal risk factors such as maternal nutritional status, body mass index, ethnicity, infant birth weight,32 race, and age33 cannot be altered at the time of delivery but awareness of them might prompt modifications in the care pathway.
Cesarean section Elective cesarean section is the only form of delivery that can totally ensure absence of perineal trauma. However, compared to vaginal delivery, cesarean section is associated with an increase in mortality and morbidity.34–36 Furthermore, the case for elective cesarean section to prevent perineal trauma cannot be substantiated.
Ventouse versus forceps delivery A recent Cochrane Review found that the use of the vacuum extractor for assisted vaginal delivery when compared to forceps is associated with significantly less maternal trauma and with less general and regional anesthesia. Overall there were more deliveries with vacuum extraction and fewer cesarean sections were carried out in the vacuum extractor group. However, the vacuum extractor was associated with an increase in neonatal cephalhematomata and retinal hemorrhages. Serious neonatal injury was uncommon with either instrument.37
Delivery positions It has been postulated that position at delivery (upright or lying down) may influence the risk of perineal trauma. One systematic review found that any upright position marginally reduced episiotomies compared with the supine or lithotomy positions for delivery but this was offset by an increase in second degree tears. Rates of assisted deliveries were slightly reduced in the upright group. The findings of this systematic review should be interpreted with caution because of the variable qualities of the trials and the diversity of the treatment interventions (squatting, kneeling, Gardosi cushion, birthing chair).38
Delivery techniques Traditionally, manual support of the perineum has been regarded as mandatory for protecting maternal tissue during delivery. It is widely believed that guarding the
perineum during delivery of the fetal head prevents or reduces perineal trauma. The National Perinatal Epidemiological Unit at Oxford conducted a randomized controlled trial of the hands-on or poised (HOOP) method of delivery.14 At the end of second stage of labor women were allocated to either ‘hands on’ (the midwife’s hands applied pressure on the baby’s head and supported the perineum; lateral flexion was then used to facilitate the delivery of the shoulders) or the ‘hands poised’ (the midwife kept her hands poised, not touching the head or perineum and allowing spontaneous delivery of the shoulders). The trialists found that a reduction in pain at 10 days was noted in the hands-on group (31.1% versus 34.1%, p=0.02), but the rate of episiotomy was significantly lower in the hands-poised group. However, analysis was based on intention to treat and it must be noted that following randomisation 30% of the hands-poised group converted to the hands-on method. Mayerhofer et al.,39 in a similar randomized study using perineal trauma as a primary outcome measure, found that women receiving hands-on care had a significantly higher rate of third degree perineal tears (2.7% versus 0.9%). Likewise, the episiotomy rate was significantly higher in the hands-on group (17.9% versus 10.1%), but there was no statistically significant difference in overall perineal trauma between the two groups.
Epidural analgesia There are conflicting data on the effect of epidural analgesia on perineal trauma. Robinson et al.40 showed that women who had epidural analgesia were more likely to have perineal trauma, but this was due to the increased risk of operative vaginal deliveries and episiotomies with epidurals. Poen et al.41 found an increased risk of anal sphincter injury due to epidurals and suggested that this could be due to blocking the pain, which normally functions as an alarm for perineal stretching. In contrast, others have found a significant increase in episiotomy rate during vaginal delivery associated with epidurals but without an increase in perineal tears.42 Overall it appears that the increased perineal trauma is related to the associated increase in instrumental delivery.43
Perineal massage Stretching and massaging of the perineum in the antenatal period and during the second stage of labor has been promoted as a means of increasing the elasticity of the perineum and reducing the need for episiotomy. The protective value of perineal massage during the antenatal period has been evaluated in two randomized studies. It involves digital perineal stretching with oil lubrication
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from 35 weeks’ gestation for about 10 minutes every day. In the United Kingdom, Shipman et al.44 randomized 861 nulliparous women and found a non-significant benefit of 6% in the prevalence of perineal trauma (75% versus 69%, p<0.07), but a secondary analysis by maternal age showed a much larger benefit (12.1%) with massage among those aged 30 years and over. In a larger randomized study, Labrecque et al.45 found that among participants without a previous vaginal birth, a significantly greater number of women in the experimental group (24%) delivered with an intact perineum compared to the control group (15%). A dose–response effect was observed. However, for women who had a previous vaginal delivery, there were no differences in intact perineum rates between the experimental and control groups. This effect means that for every 10 women doing perineal massage there will be one additional woman whose perineum remains intact after delivery. More importantly, pregnant women find perineal massage acceptable. This study is encouraging in demonstrating the effectiveness of a simple, womancontrolled intervention to maintain perineal integrity. At 3 months postpartum there was no difference in perineal function between women who had and those that had not received perineal massage.46 Perineal massage has also been advocated in the second stage of labor, which is provided by the midwife by inserting two fingers in the vagina, and using a sweeping motion to stretch the perineum with lubricating gel during each uterine contraction. In a randomized study, Stamp et al.47 found no benefit from massage in terms of an intact perineum or pain. Available evidence suggests that perineal massage may be beneficial to mothers if performed during the antenatal period, especially if they have not had a previous vaginal delivery. Although perineal massage in labor does not increase the likelihood of an intact perineum, it is a harmless practice and midwives can follow their usual practice while taking into account the preferences of the woman.
Water births Anecdotal reports suggest that the perineum is more pliable in water and can stretch more easily, resulting in less trauma. However, a recent Cochrane Review48 showed no difference in episiotomy or perineal tears after immersion in water during the first and second stages of labor. However, there is evidence that water immersion during the first stage of labor reduces maternal pain and the use of analgesia, without adverse outcomes on labor duration, operative delivery or neonatal outcomes.
Home delivery In a prospective observational study of 1068 women, Murphy and Feinland49 investigated perineal outcomes in a home birth setting. In this sample, 69.6% had an intact perineum, 1.4% had an episiotomy, 29% had a first or second degree tear, and 0.7% had obstetric anal sphincter injury. Logistic regression analysis showed that in multiparae, low socioeconomic status and higher parity were associated with an intact perineum, whereas increased age (≥40 years), previous episiotomy, weight gain over 40 pounds, prolonged second stage, and the use of oils and lubricants were associated with perineal trauma. Among nulliparas, low socioeconomic status, kneeling or hands-and-knees position at delivery, and manual support of the perineum at delivery were associated with an intact perineum, whereas perineal massage during delivery was associated with perineal trauma. The results of this study suggest that it is possible for midwives to achieve a high rate of intact perineums and a low rate of episiotomy in a selected setting and population group.
trAInIng Throughout the centuries, midwives have received very little formal training in the art of perineal suturing. In June 1967, midwives working in the United Kingdom were permitted by the Central Midwives Board (CMB) to perform episiotomies, but they were not allowed to suture perineal trauma.50,51 In June 1970 the Chairman of the CMB issued a statement that midwives who were working in ‘remote areas overseas’ may be authorized by the doctor concerned to repair episiotomies, provided they have been taught the technique and were judged to be competent, but the final responsibility lay with the doctor. However, it was not until 1983 that perineal repair was included in the midwifery curriculum in the UK when European Community Midwives Directives came into force and the CMB issued the following statement: ‘Midwives may undertake repair of the perineum provided they have received instruction and are competent in this procedure’. However, there has not been enough emphasis on training. In 1995, Sultan et al.52 carried out a survey in London to assess junior doctors’ and qualified midwives’ knowledge relating to perineal trauma and anatomy and to establish if they were satisfied with their training. Only 20% of junior doctors and 48% of midwives considered their training to be of a good standard when allowed to perform their first unsupervised perineal repair. Furthermore, many of the answers relating to anatomy and classification of tears were incorrect. To 1107
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improve training we have recently introduced a course using video presentations and specially designed models to demonstrate anatomy and techniques of repair (www. perineum.net) (Thakar, Kettle and Sultan, personal communication). In a questionnaire survey of 208 health professionals attending this course, 64% were dissatisfied with their training prior to performing their first unsupervised perineal repair. Evaluation of the course carried out by administration of questionnaires 8 weeks following the course showed a significant increase in the participant’s ability to classify degree of perineal trauma accurately. Participants changed their practice to evidence-based care after the course with significantly more performing the continuous suturing technique for repair of second degree tears and episiotomy. It has also been demonstrated that practitioners require more focused training relating to performing mediolateral episiotomies. Andrews et al.53 carried out a prospective study over a 12-month period of women having their first vaginal delivery to assess positioning of mediolateral episiotomies. The depth, length, distance from the midline, the shortest distance from the midpoint of the anal canal, and the angle subtended from the sagittal or parasagittal plane were measured following suturing of the episiotomy. Results of the study demonstrated that no midwives and only 13 (22%) doctors performed a truly mediolateral episiotomy and that the majority of the incisions were in fact directed closer to the midline.52
concluSIon Obstetric perineal trauma can have a devastating effect on a woman’s social life with associated psychological sequelae. Consequently, every attempt should be made to prevent such trauma, which may lead to shortterm problems such as pain and dyspareunia or more long-term effects such as prolapse and incontinence. Practitioners must base their care on current research evidence and be aware of the potential maternal morbidity that may occur as a result of perineal injury following childbirth. Furthermore, there is a need for more structured training programs and national guidelines to ensure practitioners are appropriately skilled to identify, correctly classify, and repair perineal trauma in order to minimize morbidity and associated problems. Reducing the adverse sequelae of perineal trauma may make vaginal birth more desirable and could possibly decrease the escalating interest in cesarean section.
referenceS 1. Magdi I. Obstetric injuries of the perineum. J Obstet Gynaecol Br Commw 1949;49:687–700. 2. Kettle C, Hills RK, Jones P et al. Continuous versus interrupted perineal repair with standard or rapidly absorbed sutures after spontaneous vaginal birth: a randomised controlled trial. Lancet 2002;359:2217–23. 3. Royal College of Obstetricians and Gynaecologists. Methods and materials used in perineal repair. RCOG Guideline No. 23. London: RCOG, 2004. 4. Sleep J, Grant A. Pelvic floor exercises in postnatal care. Br J Midwifery 1987;3:158–64. 5. Carroli G, Belizan J. Episiotomy for vaginal birth. Cochrane Database Syst Rev 2004;(1):CD000081. 6. Barrett G, Pendry E, Peacock J et al. Women’s sexuality after childbirth: a pilot study. Arch Sex Behav 1999;28:179–91. 7. Sultan AH, Kamm MA, Bartram CI. Perineal damage at delivery. Contemp Rev Obstet Gynaecol 1994;6:18–24. 8. Thakar R, Sultan AH. Management of obstetric anal sphincter injuries. Obstetrician Gynaecologist 2003;5:72–8. 9. Woodman P, Graney AO. Anatomy and physiology of the female perineal body with relevance to obstetrical injury and repair. Clin Anat 2002;15:321–34. 10. Thacker SB, Banta HD. Benefits and risks of episiotomy: an interpretative review of the English language literature, 1860–1980. Obstet Gynecol Surv 1983;38(6):322–38. 11. Cunningham F, Gant N, Leveno K, Gilstrap L, Hauth J, Wenstrom K (eds) Williams Obstetrics, 21st ed. New York: McGraw-Hill, 2001. 12. Hudson C, Sohaib S, Shulver HM et al. The anatomy of the perineal membrane: its relationship to injury in childbirth and episiotomy. Aust N Z J Obstet Gynaecol 2004;42:193–6. 13. Coats PM, Chan KK, Wilkins M, Beard RJ. A comparison between midline and mediolateral episiotomies. Br J Obstet Gynaecol 1980;87:408–12. 14. McCandlish R, Bowler U, Van Asten H et al. A randomised controlled trial of care of the perineum during second stage of normal labour. Br J Obstet Gynaecol 1998;105:1262–72. 15. Graham ID, Davies C. Episiotomy: the unkindest cut that persists. In: Henderson C, Bick D (eds) Perineal Care: An International Issue. Salisbury: Quay Books, 2004; 58–86. 16. Henriksen TB, Bek KM, Hedegaard M, Secher NJ. Episiotomy and perineal lesions in spontaneous vaginal deliveries. Br J Obstet Gynaecol 1992;99:950–4. 17. Henriksen TB, Bek KM, Hedegaard M, Secher NJ. Methods and consequences of changes in use of episiotomy. BMJ 1994;309:1255–8.
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18. World Health Organization Maternal and Newborn Health/Safe Motherhood Unit. Care in normal birth: a practical guide. Report of a Technical Working Group. Doc. No. WHO/FRH/MSM/96.24. Geneva: WHO, 1996; 29.
36. Clarke SL, Koonings PP, Phelan JP. Placenta praevia, baccreta and prior cesarean section. Obstet Gynecol 1985;89:89–92.
19. Gordon B, Mackrodt C, Fern E et al. The Ipswich Childbirth study: a randomised evaluation of two stage after birth perineal repair leaving the skin unsutured. Br J Obstet Gynaecol 1998;105:435–49.
37. Johanson RB, Menon V. Vacuum extraction versus forceps for assisted vaginal delivery. Cochrane Pregnancy and Childbirth Group. Cochrane Database Syst Rev 2004;(4): CD000224.
20. Oboro VO, Tabowei TO, Loto OM et al. A multicentre evaluation of the two layer repair of after birth perineal trauma. J Obstet Gynaecol 2003;1:5–8.
38. Gupta JK, Nikodem VC. Woman’s position during second stage of labour (Cochrane Review). In: The Cochrane Library, Issue 2. Chichester: Wiley, 2004.
21. Fleming EM, Hagen S, Niven C. Does perineal suturing make a difference? The SUNS Trial. Br J Obstet Gynaecol 2003;110:684–9.
39. Mayerhofer K, Bodner-Adler B, Bodner K et al. Traditional care of the perineum during birth: a prospective, randomized study of 1,076 women. J Reprod Med 2002;47:477–82.
22. Lundquist M, Olsson A, Nissen E et al. Is it necessary to suture all lacerations after vaginal birth? Birth 2000;27:79–85. 23. Head M. Dropping stitches. Nursing Times 1993;89:64–5. 24. Clement S, Reed B. To stitch or not to stitch? A long term follow-up study of women with unsutured perineal tears. Practicing Midwife 1999;2:20–8. 25. Kettle C, Johanson RB. Absorbable synthetic versus catgut suture material for perineal repair (Cochrane Review). In: Cochrane Library, Issue 1. Chichester: Wiley, 2004. 26. Ethicon. A unique product completes the family: Ethicon Vicryl Rapide. Edinburgh: Ethicon, 1991. 27. Gemymthe A, Langhoff-Roos J, Sahl S et al. New Vicryl formulation: an improved method of perineal repair? Br J Midwifery 1996;4:230–4. 28. McElhinney BR, Glen DRJ, Harper MA. Episiotomy repair: Vicryl versus Vicryl Rapide. Ulster Med J 2000;69:27–9. 29. Kettle C, Johanson RB. Continuous versus interrupted sutures for perineal repair (Cochrane Review). In: The Cochrane Library, Issue 1. Chichester: Wiley, 2004. 30. Fleming N. Can the suturing method make a difference in postpartum perineal pain. J Nurse-Midwifery 1990;35:19–25. 31. Kettle C. The management of perineal trauma. In: Henderson C, Bick D (eds) Perineal Care: An International Issue. Salisbury: Quay Books, 2004; 58–86. 32. Renfrew MJ, Hannah W, Albers L, Floyd E. Practices that minimize trauma to the genital tract in childbirth: a systematic review of the literature. Birth 1998;25:143–60. 33. Howard D, Davies PS, DeLancey JOL, Small Y. Differences in perineal lacerations in black and white primiparas. Obstet Gynecol 2000;96:622–4. 34. Hall MH, Bewley S. Maternal mortality and mode of delivery. Lancet 1999;354:776. 35. Sultan AH, Stanton SL. Preserving the pelvic floor and
perineum during childbirth – elective caesarean section? Br J Obstet Gynaecol 1996;103:731–4.
40. Robinson JN, Norwitz ER, Cohen AP et al. Epidural analgesia and third- or fourth-degree lacerations in nulliparas. Obstet Gynecol 1999;94:259–62. 41. Poen AC, Felt-Bersma RJF, Dekker GA et al. Third-degree obstetric perineal tear: risk factors and the preventative role of mediolateral episiotomy. Br J Obstet Gynaecol 1997;104:563–6. 42. Bodner-Adler B, Bodner K, Kimberger O et al. The effect of epidural analgesia on the occurrence of obstetric lacerations and on the neonatal outcome during spontaneous vaginal delivery. Arch Gynecol Obstet 2002;267:81–4. 43. Lieberman E, O’Donoghue C. Unintended effects of epidural analgesia during labor: a systematic review. Am J Obstet Gynecol 2002;186:S31–68. 44. Shipman MK, Boniface DR, Tefft ME, McGlohry FM. Antenatal perineal massage and subsequent perineal outcomes: a randomised controlled trial. Br J Obstet Gynaecol 1997;104:787–91. 45. Labrecque M, Eason E, Marcoux S et al. Randomised controlled trial of prevention of perineal trauma by perineal massage during pregnancy. Am J Obstet Gynecol 1999;180:593–600. 46. Labrecque M, Eason E, Marcoux S. Randomized controlled trial of prevention of perineal trauma by perineal massage during pregnancy. Am J Obstet Gynecol 2000;182:76–80. 47. Stamp G, Kruzins G, Crowther C. Perineal massage in labour and prevention of perineal trauma: randomised controlled trial. BMJ 2001;322:1277–80. 48. Cluett ER, Nikodem VC, McCandlish RE, Burns EE. Immersion in water in pregnancy, labour and birth. Cochrane Database Syst Rev 2004;(2):CD000111. 49. Murphy PA, Feinland JB. Perineal outcomes in a home birth setting. Birth 1998;25:226–33. 50. Myles MF. Textbook for Midwives, 7th ed. London: Churchill Livingstone, 1971.
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51. Silverton L. The Art and Science of Midwifery, 1st ed. London: Prentice Hall, 1993. 52. Sultan AH, Kamm MA, Hudson CN. Obstetric perineal trauma: an audit of training. J Obstet Gynaecol 1995;15:19–23.
53. Andrews V, Thakar R, Sultan AH, Jones PW. Are mediolateral episiotomies actually mediolateral? BJOG 2005;112(8):1156–8.
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78 Primary repair of obstetric anal sphincter injury Abdul H Sultan
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INTRODUCTION
CLASSIFICATION OF PERINEAL TEARS
Obstetric anal sphincter injuries (OASIS) are the major cause of anal incontinence and can have a devastating effect on a woman’s quality of life. Until the advent of anal endosonography the cause was attributed largely to pelvic neuropathy. However, despite identification and immediate repair of OASIS, the outcome is suboptimal as more than a third of women suffer from impaired continence. This chapter deals with acute OASIS and a description of the various repair techniques is given.
There is considerable inconsistency in the literature regarding the classification of perineal tears, especially relating to third and fourth degree tears.5 In order to standardize description of anal sphincter injury. Sultan6 modified the existing classification of perineal tears and the new classification has been accepted by the Royal College of Obstetricians and Gynaecologists7 as well as the International Consultation on Incontinence:8
DEFINITION To avoid confusion, the terms ‘primary’ and ‘secondary’ when referring to anal sphincter repair need to be clarified. Following OASIS, repair of the anal sphincter in the immediate postpartum period is usually performed by an obstetrician as a primary procedure. When a repair of the anal sphincter is performed to treat fecal incontinence (usually years after childbirth), it is regarded as a secondary sphincter repair even though a direct primary repair may or may not have been attempted in the postpartum period. Indeed, there is now considerable evidence to suggest that occult1,2 or missed3 mechanical trauma to the anal sphincter during childbirth is a major etiologic factor in the development of fecal incontinence.4 In the UK, primary repair is conducted by obstetricians while secondary repairs are predominantly performed by colorectal surgeons.
Longitudinal smooth muscle
1. First degree: laceration of the vaginal or perineal skin only. 2. Second degree: involvement of the vaginal/perineal skin, perineal muscles and fascia but not the anal sphincter. 3. Third degree: disruption of the vaginal/perineal skin, perineal body and anal sphincter muscles. This should be subdivided into (Fig. 78.1): • 3a: partial tear of the external sphincter involving less than 50% thickness. • 3b: more than 50% of external sphincter thickness torn. • 3c: internal sphincter also torn. 4. Fourth degree: a third degree tear with disruption of the anal epithelium Isolated tears of the rectal mucosa without involvement of the anal sphincter (Fig. 78.2) are a rare event and should not be included in the above classification.
Circular smooth muscle Rectum
3a
3b
3c
4 Internal anal sphincter External anal sphincter
Anus Fat
Fat
Figure 78.1. The anal sphincter demonstrating the new classification of anal sphincter injury (see text for full explanation).
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Figure 78.2. An isolated ‘button hole’ tear of the rectal mucosa (arrow) inferior to which can be seen an intact anal sphincter.
INCIDENCE OF OASIS AND OUTCOME OF REPAIR The reported incidence of OASIS varies from one unit to the next according to obstetric practice but appears to be more specifically related to the type of episiotomy practiced. OASIS is reported to occur between 0.5 and 2.5% of deliveries in centers where mediolateral episiotomy is practiced9–11 and 11%12 (19% in primiparae13) in centers where midline episiotomy is practiced. Midline episiotomies are favored in North American practice while mediolateral episiotomies are favoured in Europe. To date, 28 studies have evaluated outcome following anal sphincter rupture (Table 78.1). Apart from two studies22,23 all were performed in centers practicing mainly mediolateral episiotomy. On average, approximately 37% of women continue to suffer from anal incontinence despite primary sphincter repair (Table 78.1). The morbidity would be much higher if other symptoms such as fecal urgency,9 anal discomfort and dyspareunia35 are evaluated. The embarrassing symptom of anal incontinence during sexual intercourse is encountered in 72% of symptomatic women.35 Anal resting and squeeze pressures are consistently lower in women who previously sustained anal sphincter rupture.9,16,25,27,30,32,35 The anal canal is shorter after repair.9,19 The development of incontinence does not appear to be directly related to a pelvic neuropathy as demonstrated by EMG10,21 and pudendal nerve motor latency conduction studies.4,9,25 Tetzschner et al.10 reported that 3-month pudendal latency measurements are longer in women at risk for incontinence. However, these measurements were still within the normal range and no relationship was demonstrated between abnormal latency and incontinence. Although anal sphincter disruption and
repair are invariably associated with some degree of denervation and atrophy, current neurophysiologic tests available are not sensitive or specific enough to quantify pudendal neuropathy. There is, however, evidence to show that poor outcome following primary9,21,25 and secondary4 repair may be related more to persistent mechanical disruption as demonstrated by anal endosonography rather than ‘pudendal neuropathy’. Unsatisfactory outcome following primary sphincter repair may be attributed either to operator inexperience or to repair technique and subsequent management. Training and experience of clinicians performing perineal repair have been questioned,38,39 and hands-on training workshops have been shown to influence a change in clinical practice.40
TECHNIQUE OF PRIMARY REPAIR In 1930, Royston41 described a commonly practiced technique of repair following OASIS: the ends of the torn sphincter were approximated by inserting a deep catgut suture through the inner third of the sphincter muscle and a second set (mattress or interrupted) through the outer third of the sphincter. Subsequently, Ingraham et al.42 described a modification of the Royston technique41 such that the sutures were only inserted in the fascial sheath or capsule of the sphincter ani. Fulsher and Fearl43 also described this technique but emphasized that no sutures should pass through the sphincter muscle. More specifically, Cunningham and Pilkington44 inserted four interrupted sutures in the capsule of the external sphincter at the anterior, posterior, superior, and inferior points. In 1948, Kaltreider and Dixon45 described the end-to-end repair technique that had been used since 1935 in which one mattress or figure-of-eight suture was inserted to approximate the sphincter ends. Obstetricians have used the end-to-end repair technique for decades, using either interrupted or figure-ofeight sutures (Fig. 78.3).9,46 However, as shown in Table 78.1, despite repair, anal incontinence occurs in 37% of women (range 15 to 61%). In addition, fecal urgency can affect a further 69,36 to 28%.35 Frank fecal incontinence affected 9% (range 226 to 23%35). Persistent anal sphincter defects following repair have been reported in 3420 to 91%36 of women (Fig. 78.4). By contrast, when fecal incontinence is due to sphincter disruption, colorectal surgeons favor the ‘overlap technique’ of sphincter repair (secondary) as described by Parks and McPartlin.47 Jorge and Wexner48 reviewed the literature and reported on 21 studies using the overlap repair with good results ranging from 74 to 100%. Engel et al.4 prospectively studied 55 patients with fecal 1113
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Table 78.1.
Prevalence of anal incontinence following primary repair of obstetric anal sphincter rupture
Authors
Year
Country
n
Follow-up (months)
Anal incontinence (%)
2000
Switzerland
177
13 years
15
1998
Australia
84
31
17*
1996
UK
81
3
20
Sander et al.
1999
Denmark
48
1
21
Crawford et al.18
1993
USA
35
12
23
Sorensen et al.
1993
Denmark
38
3
24
20
2004
England
53
3
25
Nielsen et al.
1992
Denmark
24
12
29
Go & Dunselman22
1988
Netherlands
20
6
30
2003
USA
165
6
30
2001
Netherlands
125
14 years
31
2003
Sweden
186
4 years
33
Uustal Fornell et al.
1996
Sweden
Poen et al.25
1998
Netherlands
1994
Sangalli et al.14 Wood et al.
15
Walsh et al.
16 17
19
Mackenzie M
21
13
Fenner et al.
23
DeLeeuw et al.
Wagenius & Laurin
24 11
51
6
40
117
56
40
UK
34
2
41
1999
Sweden
46
9
41
Sorensen et al.
1988
Denmark
25
78
42
Tetzschner et al.10
1996
Denmark
72
24–48
42
2003
UK
?
42
1999
New Mexico
15
4
43
1988
Sweden
62
3
44
Bek & Laurberg
1992
Denmark
121
Davis et al.32
2003
UK
2000
Ireland
2003
Gjessing et al.
Goffeng et al.36
9
Sultan et al.
26
Zetterstrom et al. 27
28
Williams et al.
29
Kammerer-Doak et al. 30
Haadem et al.
31
33
Fitzpatrick et al. 34
Nazir et al.
35
37
Pinta et al.
124
?
50 3.6
50
154
3
53
Norway
100
18
54
1998
Norway
38
12–60
57
1998
Sweden
27
12
59
2004
Finland
52
15
61
Mean
52
37
* Includes two with secondary sphincter repair.
incontinence undergoing overlap anterior anal sphincter repair and reported a good clinical outcome in 80%. A poor result was found to be associated with an external anal sphincter (EAS) defect, while demonstration of an overlap by anal endosonography (Fig. 78.5) correlated with a favorable outcome. It is now known that – like other incontinence procedures – outcome can deteriorate with time, and one study has reported 50% continence at 5-year follow-up.49 However, a number of women in this study had more than one attempt at sphincter repair.49 Sultan et al.50 were the first to describe the EAS overlap technique
for acute OASIS and, in addition, advocated separate identification and repair (Fig. 78.6) of the internal anal sphincter (IAS). Despite scepticism from surgeons that overlapping friable torn muscle as a primary procedure is not possible, Sultan et al.50 evaluated the feasibility of this technique in 27 women and demonstrated that EAS overlap repair as well as identification and end-to-end repair of the IAS was possible following acute OASIS. They observed that, compared to matched historical controls51 who had an end-to-end repair, anal incontinence could be reduced from 41 to 8% using the overlap technique and separate repair of the internal
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–2.8
Figure 78.3. Conventional end-to-end approximation of the disrupted anal sphincter with two figure-of-eight sutures.
E
p
–2.3
–2.8 Figure 78.5. Anal endosonographic image demonstrating overlap of the two ends of the external sphincter. P, probe in anal canal with arrow showing its outer limit. Immediately adjacent to this is the anal epithelium. E, external sphincter; I, internal sphincter. The overlap can be seen between the open arrows. (Reproduced from ref. 50 with permission.)
–2.3 Figure 78.4. Anal endosonographic image demonstrating an external sphincter defect (between arrows) in a woman complaining of fecal incontinence following an end-to-end repair. The arrows overlie the two retracted ends of the muscle. (Reproduced from ref. 50 with permission.)
sphincter.50 Based on this they recommended a randomized trial between end-to-end and overlap repair. The only published randomized trial published to date is by Fitzpatrick et al. in Dublin33 who found no significant difference between the two methods of repair although there appeared to be a trend towards more symptoms in the end-to-end group. There were methodologic differences in that the torn IAS was not identified and repaired separately and they used a constipating agent for 3 days after the repair. Unfortunately, they included partial EAS tears in their randomized study. A true overlap is not possible if the sphincter ends are not completely divided. Nevertheless, as the authors concur, a better outcome would be expected with both techniques as a consequence of focused education and training in anal sphincter repair.
i
i
Figure 78.6. End-to-end approximation of the torn ends of the internal anal sphincter (i). (Reproduced from ref. 50 with permission.)
Fernando et al.52 performed a multicenter randomized trial of end-to-end versus overlap using the technique described by Sultan et al.50 At 1-year follow-up they found significantly more urge fecal incontinence in the end-to-end group (24% versus 0; p=0.006).52 1115
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PRINCIPLES AND TECHNIQUE OF REPAIR 1. OASIS should only be repaired by a doctor experienced in anal sphincter repair or by a trainee under supervision. 2. Repair should be conducted in the operating theater where there is access to good lighting, appropriate equipment, and aseptic conditions. In our unit we have a specially prepared instrument tray containing a Weislander self-retaining retractor, four Allis tissue forceps, McIndoe scissors, tooth forceps, four artery forceps, stitch scissors, and a needle holder (www.perineum.net). 3. General or regional (spinal, epidural, caudal) anesthesia is an important prerequisite, particularly for overlap repair as the inherent tone of the EAS can result in retraction of the torn muscle ends within its sheath. Muscle relaxation is necessary to retrieve the ends, especially if the intention is to overlap the muscles without tension. 4. The full extent of the injury should be evaluated by a careful vaginal and rectal examination in lithotomy and graded according to the classification above (see Fig. 78.1). If there is any uncertainty about the grading it should always be given the higher grade. 5. On rare occasions an isolated ‘button hole’ type tear (see Fig. 78.2) can occur in the rectum without disrupting the anal sphincter. This is best repaired transvaginally using interrupted Vicryl sutures. To minimize the risk of a persistent rectovaginal fistula, a second layer of tissue should be interposed between the rectum and vagina by approximating the rectovaginal fascia. A colostomy is rarely indicated unless there is a large tear extending above the pelvic floor or there is gross fecal contamination of the wound. 6. In the presence of a fourth degree tear, the torn anal epithelium is repaired with interrupted polyglactin (Vicryl) 3-0 sutures with the knots tied in the anal lumen. A subcuticular repair of the anal epithelium via the transvaginal approach has also been described.5 7. The sphincter muscles are repaired with polydioxanone (PDS) 3-0 dyed sutures (see Fig. 78.3). Compared to a braided suture these monofilamentous sutures are less likely to precipitate infection. Non-absorbable monofilament sutures such as nylon or polypropylene (Prolene) are preferred by some colorectal surgeons and can be equally effective. However, they can cause stitch abscesses and the sharp ends of the suture can cause discomfort,
necessitating removal. As complete absorption of PDS takes longer than Vicryl, to avoid suture migration care should be taken to cut suture ends short and ensure that they are covered by the overlying superficial perineal muscles. 8. The IAS should be identified and, if torn, repaired separately from the EAS. The IAS lies between the EAS and the anal epithelium. It is thinner and paler than the striated EAS. The appearance of the IAS can be described as being analogous to the flesh of raw fish as opposed to the red meat appearance of the EAS. The ends of the torn muscle are grasped with Allis forceps and an end-to-end repair is performed with interrupted or mattress PDS 3-0 sutures. A torn IAS should be approximated with interrupted sutures as overlapping can be technically difficult. There is some evidence that repair of isolated IAS defects is beneficial in patients with established anal incontinence.53 9. The torn ends of the EAS are identified and grasped with Allis tissue forceps (Fig. 78.7). In order to perform an overlap, the muscle may need mobilization by dissection with a pair of McIndoe scissors separating it from the ischioanal fat laterally. When performing an overlap repair, the EAS should be grasped with Allis forceps (Fig. 78.8) and pulled across to overlap in a ‘doublebreast’ fashion. The torn ends of the EAS can then be overlapped (Fig. 78.9) using PDS 3-0 sutures. A proper overlap is only possible when the full length of the torn ends of the EAS are identified; overlapping allows for a greater surface area of contact between muscles (see Fig. 78.9). By contrast, an end-to-end repair can be performed without identifying the full length of the EAS, giving rise to incomplete apposition (Fig. 78.10). Consequently, the woman may remain continent but would be at an increased risk of developing incontinence later in life. A shorter anal length has been reported following end-to-end primary repair of the external anal sphincter.9 It has also been shown that a shorter anal length is the best predictor of fecal incontinence following secondary sphincter surgery.54 Unlike end-to-end repair, if further retraction of the overlapped muscle ends were to occur, it is highly probable that muscle continuity would be maintained. However, if the operator is not familiar with the overlap technique or if the EAS is only partially torn (Grade 3b) then an end-to-end repair should be performed. Instead
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A
Figure 78.7. The torn ends of the external anal sphincter (arrows) being elevated by two pairs of Allis forceps. A, anal epithelium. (Reproduced from ref. 50 with permission.)
Figure 78.9. The technique of overlap repair of the external anal sphincter. The first suture is inserted approximately 1.5 cm from the torn edge of the muscle (open arrow) and carried through to within 0.5 cm of the edge of the other arm of the external sphincter. A second row of sutures (small arrows) is inserted to attach the loose end of the overlapped muscle.
Cardozo fig.78.10 Figure 78.10. Diagram showing how incomplete apposition can occur with the end-to-end repair of the external sphincter.
Figure 78.8. The full width of the external sphincter (arrows) after mobilization. (Reproduced from ref. 50 with permission.) of using hemostatic figure-of-eight sutures, two or three mattress sutures should be used (similar to IAS repair). 10. After repair of the sphincter, the perineal muscles should be sutured to reconstruct the perineal body. A short deficient perineum would make the anal sphincter more vulnerable to trauma during a subsequent vaginal delivery. Finally, the vaginal skin is sutured and the perineal skin is approximated with a Vicryl 3-0 subcuticular suture. 11. A rectovaginal examination should be performed to confirm complete repair and ensure that all tampons or swabs have been removed. 12. Intravenous broad spectrum antibiotics such as cefuroxime 1.5 g and metronidazole 500 mg
should be commenced intraoperatively and we prefer to continue this orally for 5–7 days. Although there are no randomized trials to substantiate benefit of this practice, the development of infection could jeopardize repair and lead to incontinence or fistula formation. 13. Severe perineal discomfort, particularly following instrumental delivery, is a known cause of urinary retention and following regional anesthesia it can take up to 12 hours before bladder sensation returns. A Foley catheter should be inserted for about 24 hours unless midwifery staff can ensure that spontaneous voiding occurs at least every 3 hours. 14. Detailed notes should be made of the findings and repair. A pictorial representation of the tears can prove very useful when notes are being reviewed following complications, audit or litigation. 15. As passage of a large bolus of hard stool may disrupt the repair, a stool softener (lactulose 15 ml bd) and a bulking agent such as Fybogel (ispaghula husk, 1 sachet bd) is prescribed 1117
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for at least 10–14 days postoperatively. Bowel confinement was practiced by some clinicians who were concerned that the passage of formed stool might disrupt a freshly repaired anal epithelium and sphincter muscle.52 However, a prospective, randomized, surgeon-blinded trial (n=54) revealed that outcome of reconstructive anorectal surgery was not adversely affected by omission of bowel confinement and was associated with fewer episodes of fecal impaction.55 16. It is important that the woman understands the implications of sustaining OASIS and should be told how to seek help if symptoms of infection or incontinence develop. 17. Ideally, these women should be followed up in a dedicated perineal clinic by a team with a special interest in OASIS. All women should be given advice on pelvic floor exercises while others with minimal sphincter contractility may need electrical stimulation.56 18. Women who sustain anal sphincter injury need careful counseling regarding their management in a subsequent pregnancy. It is known that the risk of recurrence of anal sphincter injury in centers that practice mediolateral episiotomy is only 4.4%.57 Therefore, asymptomatic women who have no evidence of compromised anal sphincter function (ideally confirmed by anal ultrasound and manometry) should be encouraged to have a vaginal delivery.5 As cesarean section is associated with increased morbidity and mortality,58 it should be reserved for those who are symptomatic and women who had undergone a secondary anal sphincter repair for fecal incontinence.
REFERENCES 1. Sultan AH, Kamm MA, Hudson CN. Anal sphincter disruption during vaginal delivery. N Engl J Med 1993:329;1905–11. 2. Donnelly V, Fynes M, Campbell D, Johnson H, O’Connell R, O’Herlihy C. Obstetric events leading to anal sphincter damage. Obstet Gynecol 1998;92:955–61. 3. Andrews V, Thakar R, Sultan AH. Occult anal sphincter injuries – myth or reality? Neurourol Urodyn 2004;23(5/6):442–4. 4. Engel AF, Kamm MA, Sultan AH, Bartram CI, Nicholls RJ. Anterior anal sphincter repair in patients with obstetric trauma. Br J Surg 1994:81:1231–4. 5. Sultan AH, Thakar R. Lower genital tract and anal sphincter trauma. Best Pract Res Clin Obstet Gynaecol 2002;16(1):99–116.
6. Sultan AH. Editorial: Obstetric perineal injury and anal incontinence. Clin Risk 1999;5(5):193–6. 7.
Royal College of Obstetricians and Gynaecologists. Management of third and fourth degree perineal tears following vaginal delivery. RCOG Guideline No. 29. London: RCOG Press, 2001.
8. Norton C, Christiansen J, Butler U et al. Anal incontinence. In: Abrams P, Cardozo L, Khoury S, Wein A (eds) Incontinence, 2nd ed. Plymouth: Health Publication, 2002; 985–1044. 9. Sultan AH, Kamm MA, Hudson CN, Bartram CI. Third degree obstetric anal sphincter tears: risk factors and outcome of primary repair. BMJ 1994;308:887–91. 10. Tetzschner T, Sorensen M, Lose G, Christiansen J. Anal and urinary incontinence in women with obstetric anal sphincter rupture. Br J Obstet Gynaecol 1996;103:1034–40. 11. Uustal Fornell EK, Berg G, Hallbook O, Matthiesen LS, Sjodahl R. Clinical consequences of anal sphincter rupture during vaginal delivery. J Am Coll Surg 1996;183:553–8. 12. Hueston WJ. Factors associated with the use of episiotomy during vaginal delivery. Obstet Gynecol 1996;87:1001–5. 13. Fenner DE, Becky-Genberg MPH, Brahma P, Marek L, DeLancey JOL. Fecal and urinary incontinence after vaginal delivery with anal sphincter disruption in an obstetrics unit in the United States. Am J Obstet Gynecol 2003;189:1543–50. 14. Sangalli MR, Floris L, Weil A. Anal incontinence in women with third or fourth degree perineal tears and subsequent vaginal deliveries. Aust N Z J Obstet Gynaecol 2000;40:244–8. 15. Wood J, Amos L, Rieger N. Third degree anal sphincter tears: risk factors and outcome. Aust N Z J Obstet Gynaecol 1998;38:414–17. 16. Walsh CJ, Mooney EF, Upton GJ, Motson RW. Incidence of third-degree perineal tears in labour and outcome after primary repair. Br J Surg 1996;83:218–21. 17. Sander P, Bjarnesen L, Mouritsen A, Fuglsang-Frederiksen A. Anal incontinence after third/fourth degree laceration. One-year follow-up after pelvic floor exercises. Int J Urogynecol 1999;10:177–81. 18. Crawford LA, Quint EH, Pearl ML, DeLancey JOL. Incontinence following rupture of the anal sphincter during delivery. Obstet Gynecol 1993;82:527–31. 19. Sorensen M, Tetzschner T, Rasmussen OO, Bjarnessen J, Christiansen J. Sphincter rupture in childbirth. Br J Surg 1993;80:392–4. 20. Mackenzie N, Parry L, Tasker M, Gowland MR, Michie MR, Hobbiss JH. Anal function following third degree tears. Colorect Dis 2004;6:92–6. 21. Nielsen MB, Hauge C, Rasmussen OO, Pedersen JF, Christiansen J. Anal endosonographic findings in the follow-
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up of primarily sutured sphincteric ruptures. Br J Surg 1992;79:104–6.
tears: outcome after primary repair. Acta Obstet Gynecol Scand 1998;77:736–40.
22. Go PMNYH, Dunselman GAJ. Anatomic and functional results of surgical repair after total perineal rupture at delivery. Surg Gynecol Obstet 1988;166:121–4.
36. Goffeng AR, Andersch B, Berndtsson I, Hulten L, Oresland T. Objective methods cannot predict anal incontinence after primary repair of extensive anal tears. Acta Obstet Gynecol Scand 1988;77:439–43.
23. DeLeeuw JW, Vierhout ME, Struuk PC, Hop WCJ, Wallenberg HCS. Anal sphincter damage after vaginal delivery: functional outcome and risk factors for fecal incontinence. Acta Obstet Gynecol Scand 2001;80:830–4.
37. Pinta TM, Kylanpaa M, Salmi TK. Primary sphincter repair: are the results of the operation good enough? Dis Colon Rectum 2004;47:18–23.
24. Wagenius J, Laurin J. Clinical symptoms after anal sphincter rupture: a retrospective study. Acta Obstet Gynecol Scand 2003;82:246–50.
38. Sultan AH, Kamm MA, Hudson CN. Obstetric perineal tears: an audit of training. J Obstet Gynaecol 1995;15:19–23.
25. Poen AC, Felt-Bersma RJF, Strijers RLM, Dekkers GA, Cuesta MA, Meuwissen SGM. Third-degree obstetric perineal tear: long-term clinical and functional results after primary repair. Br J Surg 1998;85:1433–8.
39. Fernando RJ, Sultan AH, Radley S, Jones PW, Johanson RB. Management of obstetric anal sphincter injury: a systematic review and national practice survey. BMC Health Services Research 2002;2:9.
26. Zetterstrom J, Lopez A, Anzen B, Norman M, Holmstrom B, Mellgren A. Anal sphincter tears at vaginal delivery: Risk factors and clinical outcome of primary repair. Obstet Gynecol 1999;24:21–8. 27. Sorensen SM, Bondesen H, Istre O, Vilmann P. Perineal rupture following vaginal delivery. Acta Obstet Gynecol Scand 1988;67:315–18.
40. Thakar R, Sultan AH, Fernando R, Monga A, Stanton S. Can workshops on obstetric anal sphincter rupture change practice? Int Urogynecol J 2001;12(3):S5. 41. Royston GD. Repair of complete perineal laceration. Am J Obstet Gynecol 1930;19:185–95. 42. Ingraham HA, Gardner MM, Heus GE. A report on 159 third degree tears. Am J Obstet Gynecol 1949;57:730–5.
28. Williams A, Adams EJ, Bolderson J, Tincello DG, Richmond D. Effect of new guideline on outcome following third degree perineal tears: results of a three-year audit. Int Urogynecol J 2003;14:385–9.
43. Fulsher RW, Fearl CL. The third-degree laceration in modern obstetrics. Am J Obstet Gynecol 1955;69:786–93.
29. Kammerer-Doak DN, Wesol AB, Rogers RG, Dominguez CE, Dorin MH. A prospective cohort study of women after primary repair of obstetric anal sphincter laceration. Am J Obstet Gynecol 1999;181(6):1317–23.
45. Kaltreider DF, Dixon McC. A study of 710 complete lacerations following central episiotomy. Southern Med J 1948;41:814–20.
30. Haadem K, Ohrlander S, Lingman G. Long-term ailments due to anal sphincter rupture caused by delivery – a hidden problem. Eur J Obstet Gynecol Reprod Biol 1988;27:27–32. 31. Bek KM, Laurberg S. Risks of anal incontinence from subsequent vaginal delivery after a complete obstetric anal sphincter tear. Br J Obstet Gynaecol 1992;99:724–7. 32. Davis I, Kumar D, Stanton SL, Thakar R, Fynes M, Bland J. Symptoms and anal sphincter morphology following primary repair of third degree tears. Br J Surg 2003;90:1573–9. 33. Fitzpatrick M, Behan M, O’Connell R, O’Herlihy C. A randomized clinical trial comparing primary overlap with approximation repair of third degree obstetric tears. Am J Obstet Gynecol 2000;183:1220–4. 34. Nazir M, Stien R, Carlsen E, Jacobsen AF, Nesheim B. Early evaluation of bowel symptoms after primary repair of obstetric perineal rupture. Dis Colon Rectum 2003;46:1245–50. 35. Gjessing H, Backe B, Sahlin Y. Third degree obstetric
44. Cunningham CB, Pilkington JW. Complete perineotomy. Am J Obstet Gynecol 1955;70:1225–31.
46. Hauth JC, Gilstrap LC III, Ward SC, Hankins CD. Early repair of an external sphincter ani muscle and rectal mucosal dehiscence. Obstet Gynecol 1986;67(6):806–9. 47. Parks AG, McPartlin JF. Late repairs of injuries of the anal sphincter. Proc R Soc Med 1971;64:1187–9. 48. Jorge JMN, Wexner SD. Etiology and management of fecal incontinence. Dis Colon Rectum 1993;36:77–97. 49. Malouf AJ, Norton CS, Engel AF, Nicholls RJ, Kamm MA. Long term results of overlapping anterior anal-sphincter repair for obstetric trauma. Lancet 2000;355:260–5. 50. Sultan AH, Monga AK, Kumar D, Stanton SL. Primary repair of obstetric anal sphincter rupture using the overlap technique. Br J Obstet Gynaecol 1999;106:318–23. 51. Sultan AH. Third degree tear repair. In: MacClean AB, Cardozo L (eds) Incontinence in Women. London: RCOG Press, 2002; 379–90. 52. Fernando RJ, Sultan AH, Kettle C, Jones P, O’Brien PMS. A randomised trial of overlap vs end-to-end primary repair of the anal sphincter. Neurourol Urodyn 2004;23:411–12. 53. Meyenberger C, Bertschinger P, Zala GF, Buchmann P. Anal sphincter defects in fecal incontinence: correla-
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tion between endosonography and surgery. Endoscopy 1996;28:217–24. 54. Hool GR, Lieber ML, Church JM. Postoperative anal canal length predicts outcome in patients having sphincter repair for fecal incontinence. Dis Colon Rectum 1999;42:313–18. 55. Nessim A, Wexner SD, Agachan F et al. Is bowel confinement necessary after anorectal reconstructive surgery? A prospective, randomized, surgeon-blinded trial. Dis Colon Rectum 1999;42:16–23.
56. Sultan AH, Nugent K. Pathophysiology and non-surgical treatment of anal incontinence. Br J Obstet Gynaecol 2004;111(Suppl 1):84–90. 57. Harkin R, Fitzpatrick M, O’Connell PR, O’Herlihy C. Anal sphincter disruption at vaginal delivery: is recurrence predictable? Eur J Obstet Gynecol Reprod Biol 2003;109:149–52. 58. Sultan AH, Stanton SL. Preserving the pelvic floor and perineum during childbirth – elective caesarean section? Br J Obstet Gynaecol 1996;103:731–4.
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79 Surgery for fecal incontinence Klaus E Matzel, Manuel Besendörfer
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IntroductIon The true prevalence of fecal incontinence is unknown. Approximately 2% of the general population suffers from the inability to control bowel emptying,1 but this rate rises with age, affecting up to 11% of men and 26% of women over the age of 50,2 and, in combination with urinary incontinence, up to 40% of nursing home patients.3 Recent advances in diagnostic methods have led to a better understanding of the physiology of the various components of the continence organ. Today, fecal continence is understood to be maintained by coordinated, synergistic, and organic functions of three organs: the reservoir system of the rectum, the outlet resistance of the sphincteric complex, and the sensory lining of the anal canal. Their functional interaction is attained by a convergence of somatomotor, somatosensory, and autonomic innervation. Rectal reservoir function can be addressed therapeutically with surgical resection, but most surgical procedures for fecal incontinence aim to improve, augment, or substitute sphincteric function.
dIagnostIc technIques and treatment consIderatIons Causes of fecal incontinence are multiple. To establish a meaningful therapeutic concept, it is important to identify morphologic and functional deficits of the various anatomic components contributing to anal continence. Endoanal ultrasound and magnetic resonance imaging (MRI) enable us to detect morphologic defects of the rectum and sphincteric complex. With anorectal manometry we can test and quantify the muscular function of the smooth muscle internal anal sphincter and the striated muscular external anal sphincter, the perception of rectal filling and distension, the compliance of the rectal reservoir, and the reflexive interaction of the rectum and anal sphincter. Electromyographic recording of the striated muscles of the external anal sphincter and the pelvic floor allows us to differentiate muscular from neurogenic defects and to estimate the extent of reinnervation. Peripheral latency recording (pudendal nerve terminal motor latency [PNTML]) helps to identify the location of neural damage. To a certain extent, isolated deficits within each functional component of the continence organ can be compensated for – indeed, most cases of incontinence can be sufficiently treated with relatively simple and pragmatic measures. Because comparable morphologic and functional lesions may result in clinical pictures of varying severity, the use of advanced diagnostic proce-
dures should be determined by the desired therapeutic consequence. The diagnosis of fecal incontinence is based on a standard anorectal examination (to exclude pathologic conditions that may result in secondary incontinence) and a focused history. Standardized questionnaires and general and disease-specific quality-of-life scores4,5 have become widely used in recent years to quantify the extent and severity of fecal incontinence and its impact on quality of life and to monitor therapeutic effects. If a muscular defect is suspected, endoanal ultrasound should be added. If sphincteric lesions amenable to direct repair are excluded, conservative treatment such as diet, medication and retrograde irrigation can – without further diagnostic steps – be initiated to improve stool consistency, delay colonic transit, and establish a normal periodicity to bowel emptying. If these fail or do not produce adequate results, further diagnostic procedures are indicated to differentiate muscular from neurogenic and combined lesions. Based on the diagnostic findings, two concepts of treatment can be discussed: functional rehabilitation and morphologic reconstruction. The former is indicated in patients with no morphologic defects, and aims to recruit residual function of the continence organ; the latter is indicated in patients with morphologic defects of functional relevance, and aims to re-establish morphologic integrity.
FunctIonal rehabIlItatIon Biofeedback is the first choice for functional rehabilitation. Based on the principle of operant conditioning, visual or acoustic signals are used to teach the patient awareness and use of specific physiologic functions and thus to recruit residual function. Success ranges widely, from 38 to 100%.6 Retrograde irrigation is intended to improve rectal reservoir function (by distension and improved perception through a defined stimulus) and to establish a rhythm for sufficient bowel emptying (to ensure time intervals free of fecal loss). If these conservative therapies fail to improve symptoms, surgical intervention should be considered.
sacral nerve stimulation Sacral nerve stimulation (SNS) is based on the concept of recruiting residual function of the continence organ by stimulation of its peripheral nerve supply. The sacral spinal nerves are the most distal common location of a dual peripheral nerve supply of the striated pelvic floor and anal sphincter muscles.7 Various physiologic func-
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tions contributing to continence are activated by low frequency electrostimulation of one or more sacral spinal nerves by a fully implantable neurostimulation device.8 The indication for the implantation of a permanent neuroprosthesis is based on the results of the following two-step test stimulation.9
Acute percutaneous/peripheral nerve evaluation (PNE) PNE10 determines whether, in the prospective patient, contraction of the striated pelvic floor muscles can be elicited by SNS (thus establishing the integrity of the sacral spinal nerves), and tests the individual relevance of each sacral spinal nerve to anal sphincteric contraction and anal canal closure (thus identifying the optimal site of stimulation).10 The procedure can be performed under general or local anesthesia. For acute PNE, needle electrodes are inserted into the dorsal sacral foramina of S2, S3, and S4. This positioning aims for placement close to the site where the sacral spinal nerves enter the pelvic cavity through the ventral opening of the sacral foramen and proximal to the sacral plexus. Stimulation can provoke contraction of the external anal sphincter, pelvic floor, and lower extremities.11 The concomitant reactions of the leg and foot are helpful to ensure adequate placement of the needle electrode. With different parameters applied during testing, these side effects will be eliminated during therapeutic stimulation. If this acute stimulation successfully elicits contraction of the pelvic floor, subchronic percutaneous stimulation is initiated.
(pulse width 210 µsec; frequency 15 Hz), except during voiding and defecation. The results of the test stimulation are highly predictive: most commonly a >50% reduction in incontinent episodes or in days with incontinence is generally accepted as the indication for the implantation of a permanent neurostimulation device.
chronic stimulation with a permanent implant Permanent stimulation with a fully implantable device aims to make use of the therapeutic effect achieved by subchronic PNE. The permanent system consists of the quadripolar foramen lead and the pulse generator: the electrode is placed close to the sacral spinal nerve successfully tested during subchronic stimulation,10 and the generator is positioned subcutaneously in the abdomen or gluteal area (Fig. 79.1). Placement is performed under general anesthesia. Recently, a less invasive technique that uses a foramen electrode with a modified anchoring device placed through a trocar has been proposed12 (Fig. 79.2). This technique can be used either for stage one of the twostage implant or for electrode placement after successful screening with wire electrodes. It can be performed under local anesthesia. The foramen electrode contains four contact electrodes. The combination most effective with regard to required voltage and the patient’s perception of muscle contraction of the perineum and anal sphincter is chosen for permanent low frequency stimulation (pulse width
Subchronic percutaneous/peripheral nerve evaluation The sacral spinal nerve(s) found in acute testing to be most effective with regard to muscular contraction (most commonly, but not consistently, S3) is/are stimulated continuously for a period of time sufficient to demonstrate a potential beneficial effect. The length of the observation period depends on the frequency and severity of the incontinence. Two technical options can be used for subchronic PNE: a temporary, percutaneously placed, test stimulation lead (or multiple leads) that will be removed at the end of this phase,10 or a surgically placed quadripolar lead, the so-called ‘foramen electrode’. Both types of lead are connected to an external pulse generator for screening. The latter electrode can be connected to an implanted pulse generator (so-called ‘two-stage implant’) if the test stimulation is effective. With both techniques the selected sacral spinal nerve is continuously stimulated
Figure 79.1. Sacral nerve stimulation: foramen electrode with impulse generator. 1123
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Figure 79.2.
Sacral nerve stimulation: placement of a so-called ‘tined lead’ electrode through a trocar.
210 µsec; frequency 15 Hz; on/off: 5 s/1 s or continuous stimulation; level of stimulation usually above the individual patient’s perception of muscular contraction, and adjusted if necessary). The pulse generator is activated by telemetry. Patients interrupt stimulation with a hand-held device only for defecation and urination. With the help of the acute and subchronic test stimulation, the spectrum of indications for SNS has been continuously expanded to patients suffering from fecal incontinence, owing to a wide variety of causes resulting in a lack of function, these being:
• weakness of the external anal sphincter13 with
concomitant urinary incontinence14 or a defect and/or deficit of the smooth muscle internal anal sphincter;15
• status following rectal resection;16 • limited structural defects of the external anal •
sphincter combined with limited defect of the internal anal sphincter;15 neurogenic incontinence.17
During the evolution of SNS as a treatment for fecal incontinence, a standard evaluation of outcome became broadly accepted. Not only is the effect on bowel control measured, but also the effect on quality of life. The short- and long-term effects of SNS have been demonstrated in multiple single and multicenter trials (Table 79.1). With chronic SNS the frequency of involuntary loss of bowel content is reduced, the ability to postpone defecation is improved,24 and a substantial percentage of patients gain full continence.10 Quality of
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table 79.1.
Results of sacral nerve stimulation
Reference
Year
Study
n
Pretreatment
PNE
Treatment*
Follow-up (months)
14 (11–14)†
–
0.5 (0–2)
14 (6–48)
3 (2–14)
0
0
14 (5–37)
Incontinent episodes: liquid or solid/1 week 18
2004
SC
14
19
2001
SC
5
20
2001
MC
16
5.5 (1–19)
–
0 (0–1)
10.5 (3–45)
2004
MC
46
7.5 (1–78)
–
1 (0–39)
12 (1–72)
2002
SC
15
11 (2–30)
0 (0–7)
0 (0–4)
24 (3–80)
6
2 (1–7)
0 (0–4)
0.5 (0–2)
9 (2–19)
1.5 (1–5)
0 (0–1)
59 (5–70)
8.3 (1.7–78.7)
–
0.75 (0–25)
23.9 (1–36)
–
2‡, §
24 15 (3–26)
Altomare et al. Ganio et al. Ganio et al.
21
Jarrett et al.
22
Kenefick et al. 14
2001
SC
23
2001
SC
6
24
2004
MC
34
25
2002
SC
4
17
2001
SC
16
2 (1–5)
–
0.7 (0–5)
2002
SC
27
8.7 (2–38)
0.7 (0–10)
0.5 (0.5–0.7)§
2004
SC
14
15 (12.5–17.5)
–
5.7 (2–6)§
14 (6–48)
2004
MC
27
14 (5–20)
–
6 (1–20)
–
2000
SC
5
16 (13–20)
–
2 (0–13)
16
2003
SC
16
16 (12–19)
–
2 (0–7)
32.5 (3–99)
2002
SC
10
19.5 (14–20)
–
5.5 (0–20)
4.5 (1–12)
2004
MC
37
16 (9–20)
–
6 (0–20)
6 (0–36)
Leroi et al.
Matzel et al. Matzel et al. Ripetti et al. Rosen et al.
26
Uludag et al.
12‡
6 (3–6)
6.0‡
Cleveland Clinic Score** 18
Altomare et al. 21
Jarrett et al.
15
Malouf et al.
13
Matzel et al.
27
Rasmussen & Christiansen 28
Rasmussen et al.
Data: median (range), if not noted otherwise. *Data at last follow-up; † Median value over 2 weeks; ‡ Mean (SD and range not available); § Follow-up value (median of values at published follow-up intervals); ** Cleveland Clinic Score: 0 continent, 20 incontinent. MC, multicenter; SC, single center; PNE, peripheral nerve evaluation.
life is improved postoperatively, both in subscales of general quality-of-life instruments15,22,24 and, significantly, in all categories of the disease-specific Fecal Incontinence Quality of Life Index.4,17,18,24 Complications are rare. In less than 5% of patients has device removal become necessary,10,29 mostly because of pain or infection. After removal because of infection, reimplanation can be performed successfully at a later date.8 The physiologic mode of action of SNS is not yet clearly understood. Its effect is complex and multifactorial, involving somatomotor, somatosensory, and autonomic functions of the anorectal continence organ.10,29
reconstructIve technIques Morphologic reconstruction is indicated if a defined, functionally relevant, sphincteric defect is diagnosed. Several techniques, such as direct overlapping sphincter repair, postanal repair, and total pelvic floor repair, have been advocated in the past, and sphincter repair is
now generally accepted as first line treatment for incontinence owing to sphincteric defects. Electromyography of the external sphincter may be helpful to estimate the functional outcome and to counsel the patient properly, as some studies suggest that the presence of pudendal neuropathy adversely affects results.6 Sphincter repair aims to re-establish function by reconstructing the morphologic defect; a muscular gap is closed by adaption of the dehiscent muscle. With a curved incision over the perineal body, the scar tissue is dissected until healthy muscle on either side can be identified. The scar can be used in the readaption of the muscular anal ring (Figs 79.3, 79.4). The muscle can be sutured either in an overlapping fashion or by adaption.30 Anterior plication of the levator muscles can be added. The results of sphincter repair are not reported uniformly and thus it is difficult to evaluate series and to compare the outcome of this technique with that of other procedures. Moreover, prospective outcome recording is rare; most reported results are based on patients’ recall 1125
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Figure 79.4. Firm (but not tight) tied sutures with overlapping muscle ends.
Figure 79.3. Mattress sutures placed through the mobilized external anal sphincter muscle to achieve an overlap sphincter repair.
table 79.2.
and are limited to functional issues without addressing the quality of life of the patient. Approximately twothirds of patients report a significant improvement in continence (Table 79.2). However, the long-term therapeutic effect of sphincter repair has recently been questioned as several studies have reported a deterioration in function over time.41–43 If sphincter repair – despite re-establishment of morphologic integrity – fails to achieve success, or if function deteriorates over time, patients can be considered for functional rehabilitation, such as biofeedback, irrigation, and sacral nerve stimulation.
Results of anterior overlapping sphincter repair*
Reference
Year
Study
n
Excellent/ good (%)
Fair (%)
Poor (%)
Follow-up (months)
2001
SC
158
62
26
12
43 (6–120)
1994
SC
55
79
17
4
15 (6–36)
Fleshman et al.
1991
SC
55
71
22
6
– (12–24)
34
Gibbs & Hook
1993
SC
16
73
15
12
na
Gilliland et al.35
1998
SC
100
60
19
21
24 (2–96)†
1990
SC
30
83
17
0
1994
SC
60
60
18
22
na
Nikiteas et al.
1996
SC
42
67
14
19
38 (12–66)†
Oliveira et al.39
1996
SC
55
71
9
20
29
1999
SC
38
68
13
18
3
Buie et al.31 32
Engel et al.
33
36
Jacobs et al.
37
Londono-Schimmer et al. 38
40
Rasmussen et al.
– (7–60)
Data: mean (range), if not noted otherwise. *Adapted from ref. 6; † Median (range). na, not applicable.
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sphincter replacement Sphincter replacement procedures are indicated if functional rehabilitation is not successful, if incontinence is the result of a substantial muscular defect that is not suitable for sphincter repair, or if a neurologic defect is present. Two techniques have gained broad acceptance: dynamic graciloplasty (DGP)44 and the artificial bowel sphincter (ABS).45
Dynamic graciloplasty DGP is a modification of the transposition of the gracilis muscle around the anus to function as a neosphincter, described in the early 1950s.46 The gracilis muscle is mobilized through an incision on the inner thigh and detached at its proximal attachment at the tuberositas tibiae. Only the proximal vascular pedicle and its neural supply are preserved (Fig. 79.5). With two perianal incisions the mobilized gracilis muscle is placed around the anus. The aim of this transposition is to encircle
A Sa
Gr
the anal canal completely with muscle tissue. Thus, the configuration of the muscle sling – the alpha, gamma, epsilon configuration – is determined by the length of the muscle and its tendon. This passive muscle wrap is rendered dynamic by the implantation of a neurostimulation device (Fig. 79.6). The system consists of two electrodes, placed intramuscularly, close to the nerve, connected to a pulse generator and positioned subcutaneously or beneath the fascia in the lower abdominal wall.44 The implantation can be performed either during the muscle transposition or with a timely delay.47 To adapt the muscle to prolonged contraction, the periods of stimulation are increased in a stepwise fashion. Chronic low frequency stimulation causes muscle fiber transformation. The gracilis muscle is predominately composed of fast-twitch, fatigue-prone, type II muscle fibers, which low frequency stimulation will convert to slow-twitch, fatigue-resistant type I fibers. The increase of type I fibers ensures an adequate physiologic condition for continuous contraction of the transposed muscle (induced by permanent stimulation without continuous conscious patient effort) with subsequent closure of the anal canal.48 The stimulator is deactivated by an external magnet. Thus, bowel emptying becomes a voluntary act. The short- and long-term efficacy of dynamic graciloplasty is reported in several single and multicenter trials (Table 79.3), but not uniformly. Data collection, outcome measurement, and criteria for success vary. Nevertheless, the therapeutic effect is not limited to an improvement in bowel emptying, but also to quality of life.44,57
Artificial bowel sphincter Figure 79.5 Gracilis (Gr) muscle with proximal neuromuscular pedicle and distal vascular pedicle. A: artery; Sa: sartorius muscle.
The artificial bowel sphincter (ABS) consists of three components (Fig. 79.7): an inflatable Silastic cuff placed
.ORMAL POSITION OF THE GRACILIS -AGNET .EUROSTIMULATOR
4IBIAL TUBEROSITY
%LECTRODES
)SCHIAL SPINE
.EOSPHINCTER TRANSPOSED GRACILIS MUSCLE
Figure 79.6. Dynamic graciloplasty (DGP): transposed gracilis muscle configured as a gamma loop with implanted neurostimulation device.
>À`âÊv}°Ç°äÈ
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2000 2001 1998 1998
50
Baeten et al.
51
52
2002 2004
MC
SC
MC
SC
SC
SC
SC
MC
SC
Study
2000 2004
57
MC
MC 15
–
61 76
–
–
–
69
–
64
85
76
63
18.4±9
18±4
19
16.4
100%
100%
100%
100%
100%
Level 4/5
Level 1/2 73
Pretreatment
Continent (%)
72
47
8
64
5
28
26
200
72
52
n
29%
24%
26%
23%
>50%: 57%, <50%: 10%, ø: 33%
>50%: 57%, <50%: 13%, ø: 30%
>50%: 63%, <50%: 11%, ø: 26%
5.5±4.6
18±12
6
5.4
7%
15%
11%
4%
Level 3, Level 4/5
Treatment
Data: median (range) if not noted otherwise. *Adapted from ref. 58; † Williams Score: 1 continent, 5 incontinent; ‡ Mean (range); § Cleveland Clinic Score: 0 continent, 20 incontinent. MC, multicenter; SC, single center; na, not applicable.
Wexner et al.
Baeten et al.
44
Percentage improvement in incontinence during therapy
Penninckx
Ortiz et al.
56
1999
55
Mander et al.
54
Altomare et al.
53
Cleveland Clinic Score§
Rosen et al.
Cavina et al.
1997
1995
44
Baeten et al.
Baeten et al.
49
Year
Results of dynamic graciloplasty*
Williams Score†
Reference
table 79.3.
24
18
12
48 (13–117)
Median 39
16 (15–67)
24 (6–58)
19.2 (3–53)
37.8 (4–68)‡
na
23 (1–52)‡
25 (3–89)
Follow-up (months)
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Figure 79.7. The artificial bowel sphincter consists of a cuff, a pump and a reservoir. around the anus via perianal tunnels; a liquid-filled, pressure-regulating balloon positioned in the preperitoneal fat; and a manual pump connecting these components, which is placed in either the right or left labium majus or the scrotum45 (Fig. 79.8). The anal canal is closed as the cuff fills with liquid. At the time for defecation the device is deactivated via the manual pump, the cuff empties, and the anus opens to pass stool. The cuff is refilled and the anus is closed after a few minutes.59 As with dynamic graciloplasty, opening of the ABS becomes a voluntary act and closure of the anal canal is maintained without conscious effort – mimicking the initiation of defecation in the healthy. Short- and long-term effects on the function and quality of life have been published in several studies (Table 79.4), both single and multicenter.58,62 Again, outcome
measurement is inconsistent and data must be interpreted cautiously. The indications for both procedures are similar: endstage incontinence in patients with a substantial muscular and/or neural defect of the anal sphincter complex. Both procedures represent an alternative to the creation of a stoma. Each has advantages and disadvantages in certain anatomic and morphologic conditions. The innervation of the gracilis muscle must be intact for DGP to be successful. If the Silastic cuff of the ABS cannot provide sufficient coverage, the risk of infection with this implanted artificial material is higher. Both sphincter replacement procedures are associated with substantial morbidity58,70 in virtually all reports. In larger multicenter trials the need for operative revision reached 42% for DGP71 and 46% for ABS;64 treatment had to be discontinued in 8% and 30% of cases, respectively. The most severe complications were infections,58,70 not surprising when the operation is performed in a naturally contaminated area.71,72 In most cases device removal is unavoidable. The functional complication most relevant clinically is outlet obstruction,70,71 caused either by a pre-existing obstruction not identifiable because of incontinence or by ‘hypercontinence’ subsequent to neosphincter creation. In most cases, this functional problem can be treated with regular enemas.70,73
stoma creation The creation of a diverting stoma should be considered as an alternative to surgery for end-stage incontinence, despite not addressing incontinence per se, if co-morbidity or intellectual or physical inability precludes the above-described sphincter replacements. Stoma creation carries its own risks, however, and patient counseling and performance of the procedure and postoperative management should be undertaken with great care.
Figure 79.8. Artificial bowel sphincter implanted; pump easily accessible. Cardozo fig.79.08
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table 79.4.
Results of artificial bowel sphincter*
Reference
Year
Study
n
Pretreatment
2001
MC
24
Treatment
Follow-up (months)
AMS Scale† 60
Altomare et al. 61
2000
SC
8
45
2000
MC
24
62
2002
SC
2004
SC
2002
Dodi et al.
Lehur et al. Lehur et al.
63
Parker et al. Wong et al.
64
98.5 (75–120)‡
5.5 (0–49)‡
95.0 (±120)
19 (7–41)
19.4 (±19.3)
10.5 (4–23)
106 (±13)
25 (±25)
20 (6–35)
16
105 (±14)
23 (±22)
25 (7–49)
28
103 (74–120)‡
59 (0–108)‡
12
MC
101
106 (71–120)‡
48 (0–108)‡
12
2001
MC
24
14.9 (11–20)‡
2.6 (0–6)‡
19 (7–41)
2002
SC
53
17 (±3)
4 (±3)
26.5 (7–55)
1998
SC
13
17 (±1.8)
4.5 (±3.4)
30 (5–76)
2000
SC
13
18.7 (±1.6)
2.1 (±2.6)
–
2002
SC
22
18 (14–20)‡
4 (0–14)‡
28 (6–48)
1998
SC
6
19.5 (0.8)
4.5 (4.9)
10 (5–13)
1999
SC
17
5.0 (0.0)
2.5 (0.9)
60 (60–120)
Cleveland Clinic Score§ 60
Altomare et al. 65
Devesa et al. 59
Lehur et al.
66
O’Brien & Skinner 67
Ortiz et al.
68
Vaizey et al.
Williams Score** 69
Christiansen et al.
Data: mean (SD) if not noted otherwise. *Adapted from ref. 70; † AMS: 0 continent, 120 incontinent; ‡ Median (range); § Cleveland Clinic Score: 0 continent, 20 incontinent; **Williams Score: 1 continent, 5 incontinent. MC, multicenter; SC, single center.
Diagnostics
Neutral deficit
Muscular deficit
Isolated defect EAS, IAS
Functional deficit EAS, IAS • without morphologic defect • with limited morphologic defect Neurogenic incontinence
Substantial muscular neural EAS defect
Diagnostic SNS (PNE)
Sphincter repair
Success
Failure
Thereapeutic SNS
Success
Failure
Sphincter replacement DGP, ABS
Success
Stoma
Failure
Figure 79.9. Surgery for fecal incontinence. ABS, artificial bowel sphincter; DGP, dynamic graciloplasty; EAS, external anal Cardozo fig.79.1 sphincter; IAS, internal anal sphincter; PNE, peripheral nerve evaluation; SNS, sacral nerve stimulation. 1130
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summary The surgical options for fecal incontinence have increased during recent years, and a new treatment algorithm has evolved (Fig. 79.9). Symptoms and quality of life can be improved if patient selection is appropriate. Although these procedures carry some morbidity, they may offer an alternative to the creation of a diverting stoma.
reFerences 1. Nelson R, Norton N, Cautley E, Furner S. Community based prevalence of anal incontinence. JAMA 1995;274:559–61. 2. Roberts RO, Jacobsen SJ, Reilly WT, Pemberton JH, Lieber MM, Talley NJ. Prevalence of combined fecal and urinary incontinence: a community-based study. J Am Geriatr Soc 1999;47:837–41. 3. Chiang L, Ouslander J, Schnelle J, Reuben DB. Dually incontinent nursing home residents: clinical characteristics and treatment differences. J Am Geriatr Soc 2000;48:673–6. 4. Rockwood TH, Church JM, Fleshman JW et al. Fecal Incontinence Quality of Life Scale: quality of life instrument for patients with fecal incontinence. Dis Colon Rectum 2000;43:9–16. 5. Brazier JE, Harper R, Jones NM et al. Validating the SF-36 health survey questionnaire: a new outcome measure for primary care. BMJ 1992;305:160–4. 6. Madoff RD, Parker SC, Varma MV, Lowry AC. Fecal incontinence in adults. Lancet 2004;364:621–32. 7. Matzel KE, Schmidt RA, Tanagho EA. Neuroanatomy of the striated muscular anal continence mechanism: implications for the use of neurostimulation. Dis Colon Rectum 1990;33:666–73.
tion has high initial success rate: preliminary results. Eur Urol 2002;208:1–5. 13. Matzel KE, Bittorf B, Stadelmaier U, Hohenberger W. Sakralnervstimulation in der Behandlung der Stuhlinkontinenz. Chirurg 2003;74:26–32. 14. Leroi AM, Michot F, Grise P, Denis P. Effect of sacral nerve stimulation in patients with fecal and urinary incontinence. Dis Colon Rectum 2001;44:779–89. 15. Malouf AJ, Vaizey CJ, Nicholls RJ, Kamm M. Permanent sacral nerve stimulation for fecal incontinence. Ann Surg 2000;232:143–8. 16. Matzel KE, Stadelmaier U, Bittorf B, Hohenfellner M, Hohenberger W. Bilateral sacral spinal nerve stimulation for fecal incontinence after low anterior resection. Int J Colorect Dis 2002;17:430–4. 17. Rosen HR, Urbarz C, Holzer B, Novi G, Schiessel R. Sacral nerve stimulation as a treatment for fecal incontinence. Gastroenterology 2001;121:536–41. 18. Altomare DF, Rinaldi M, Petrolino M et al. Permanent sacral nerve modulation for fecal incontinence and associated urinary disturbances. Int J Colorect Dis 2004;19:203–9. 19. Ganio E, Luc AR, Clerico G, Trompetto M. Sacral nerve stimulation for treatment of fecal incontinence. Dis Colon Rectum 2001;44:619–31. 20. Ganio E, Ratto C, Masin A et al. Neuromodulation for fecal incontinence: outcome in 16 patients with definitive implant. The Initial Italian Sacral Neuromodulation Group (GINS) experience. Dis Colon Rectum 2001;44:965–70. 21. Jarrett MED, Varma JS, Duthie GS, Nicholls RJ, Kamm MA. Sacral nerve stimulation for faecal incontinence in the UK. Br J Surg 2004;91:755–61. 22. Kenefick NJ, Vaizey CJ, Cohen CG, Nicolls RJ, Kamm MA. Medium-term results of permanent sacral nerve stimulation for faecal incontinence. Br J Surg 2002;89:896–901.
8. Matzel KE, Stadelmaier U, Hohenberger W. Innovations in fecal incontinence: sacral nerve stimulation. Dis Colon Rectum 2004;47:1720–8.
23. Matzel KE. Sacral spinal nerve stimulation in treatment of fecal incontinence. Semin Colon Rectal Surg 2001;12:121–30.
9. Matzel KE, Stadelmaier U, Hohenfellner M, Gall FP. Electrical stimulation for the treatment of faecal incontinence. Lancet 1995;346:1124–7.
24. Matzel KE, Kamm MA, Stösser M et al. Sacral nerve stimulation for fecal incontinence: a multicenter study. Lancet 2004;363:1270–6.
10. Hohenfellner M, Matzel KE, Schultz-Lampel D et al. Sacral neuromodulation for treatment of micturition disorders and fecal incontinence. In: Hohenfellner R, Fichtner J, Novick A (eds) Innovations in Urologic Surgery. Oxford: ISIS Medical Media, 1997; 129.
25. Ripetti V, Caputo D, Ausania F, Esposito E, Bruni R, Arullani A. Sacral nerve neuromodulation improves physical, psychological and social quality of life in patients with fecal incontinence. Tech Coloproctol 2002;6:147–52.
11. Matzel KE, Stadelmaier U, Gall FP. Direkte Elektrostimulation der sakralen Spinalnerven im Rahmen der anorektalen Funktionsdiagnostik. Langenbecks Arch Chir 1990;380:184–8. 12. Spinelli M, Giardiello G, Arduini A, van den Hombergh U. New percutaneous technique of sacral nerve stimula-
26. Uludag Ö, Darby M, Dejong CHC, Schouten WR, Baeten CGM. Sacrale neuromodulatie effectif bij fecale incontinentie en intacte kringsspieren; een perspectieve studie. Ned Tijdschr Geneeskd 2002;146:989–93. 27. Rasmussen O, Christiansen J. Sakralnervestimulation ved analinkontinens. Ugeskr Laeger 2002;164:3866–8. 28. Rasmussen OO, Buntzen S, Sorensen M, Laurberg S,
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Christiansen J. Sacral nerve stimulation in fecal incontinence. Dis Colon Rectum 2004;47:1158–62. 29. Tjandra JJ, Lim JF, Matzel KE. Sacral nerve stimulation – an emerging treatment for faecal incontinence. Aust N Z J Surg 2004;74:1098–106. 30. Tjandra JJ, Han WR, Goh J, Carey M, Dwyer P. Direct repair versus overlapping sphincter repair: a randomized controlled trial. Dis Colon Rectum 2003;46:937–43. 31. Buie WD, Lowry AC, Rothenberger DA, Madoff RD. Clinical rather than laboratory assessment predicts continence after anterior sphincteroplasty. Dis Colon Rectum 2001;44:1255–60. 32. Engel AF, Kamm MA, Sultan AH, Bartram CI, Nicholls RJ. Anterior anal sphincter repair in patients with obstetric trauma. Br J Surg 1994;81:1231–4. 33. Fleshman JW, Dreznik Z, Fry RD, Kodner IJ. Anal sphincter repair for obstetric injury: manometric evaluation of functional results. Dis Colon Rectum 1991;34:1061–7. 34. Gibbs DH, Hooks VH 3rd. Overlapping sphincteroplasty for acquired anal incontinence. South Med J 1993;86:1376–80. 35. Gilliland R, Altomare DF, Moreira H Jr, Oliveira L, Gilliland JE, Wexner SD. Pudendal neuropathy is predictive of failure following anterior overlapping sphincteroplasty. Dis Colon Rectum 1998;41:1516–22. 36. Jacobs PP, Scheuer M, Kuijpers JH, Vingerhoets MH. Obstetric fecal incontinence. Role of pelvic floor denervation and results of delayed sphincter repair. Dis Colon Rectum 1990;33:494–7. 37. Londono-Schimmer EE, Garcia-Duperly R, Nicholls RJ, Ritchie JK, Hawley PR, Thomson JP. Overlapping anal sphincter repair for faecal incontinence due to sphincter trauma: five year follow-up functional results. Int J Colorectal Dis 1994;9:110–3. 38. Nikiteas N, Korsgen S, Kumar D, Keighley MR. Audit of sphincter repair. Factors associated with poor outcome. Dis Colon Rectum 1996;39:1164–70. 39. Oliveira L, Pfeifer J, Wexner SD. Physiological and clinical outcome of anterior sphincteroplasty. Br J Surg 1996;83:502–5. 40. Rasmussen OO, Puggard L, Christiansen J. Anal sphincter repair in patients with obstetric trauma. Age affects outcome. Dis Colon Rectum 1999;42:193–5. 41. Malouf AF, Norton CS, Engel AF, Nicholls RJ, Kamm MA. Long-term results of overlapping anterior anal sphincter repair for obstetric trauma. Lancet 2000;366:260–5. 42. Karoui S, Leroi AM, Koning E, Menard JF, Michot F, Denis P. Results of sphincteroplasty in 86 patients with anal incontinence. Dis Col Rectum 2000;43:813–20. 43. Halverson AL, Hull TL. Long-term outcome of overlapping anal sphincter repair. Dis Colon Rectum 2002;45:345–8. 44. Baeten C, Bailey RA, Bakka A et al. Safety and efficacy
of dynamic graciloplasty for fecal incontinence: report of a prospective multicenter trial. Dis Colon Rectum 2000;43:743–51. 45. Lehur PA, Roig J, Duinslaeger M. Artificial anal sphincter: prospective clinical and manometric evaluation. Dis Colon Rectum 2000;43:1213–16. 46. Pickrell KL, Broadbent TR, Masters FW, Metzger JT. Construction of a rectal sphincter and restoration of anal continence by transplanting the gracilis muscle; a report of four cases in children. Ann Surg 1952;135:853–62. 47. Rongen MJ, Adang EM, van der Hoop AG, Baeten CGMI. One-step vs. two-step procedure in dynamic graciloplasty. Colorectal Dis 2001;3:51–7. 48. Baeten CG, Konsten J, Spaans F et al. Dynamic graciloplasty for treatment of fecal incontinence. Lancet 1991;338:1163–5. 49. Baeten CG, Geerdes BP, Adang EM et al. Anal dynamic graciloplasty in the treatment of intractable fecal incontinence. N Engl J Med 1995;332:1600–5. 50. Baeten CG, Uludag OO, Rongen MJ. Dynamic graciloplasty for fecal incontinence. Microsurgery 2001;21:230–14. 51. Cavina E, Seccia M, Banti P, Zocco G. Anorectal reconstruction after abdominoperineal resection. Experience with double-wrap graciloplasty supported by low-frequency electrostimulation. Dis Colon Rectum 1998;41:1010–16. 52. Rosen HR, Novi G, Zoech G, Feil W, Urbarz C, Schiessel R. Restoration of anal sphincter function by single-stage dynamic graciloplasty with a modified (split sling) technique. Am J Surg 1998;175:187–93. 53. Altomare DF, Rinaldi M, Pannarale OC, Memeo V. Electrostimulated gracilis neosphincter for faecal incontinence and in total anorectal reconstruction: still an experimental procedure? Int J Colorectal Dis 1997;12:308–12. 54. Mander BJ, Wexner SD, Williams NS et al. Preliminary results of a multicentre trial of the electrically stimulated gracilis neoanal sphincter. Br J Surg 1999;86:1543–8. 55. Ortiz H, Armendariz P, DeMiguel M, Solana A, Alos R, Roig JV. Prospective study of artificial anal sphincter and dynamic graciloplasty for severe anal incontinence. Int J Colorectal Dis 2003;18:349–54. 56. Penninckx F. Belgian Section of Colorectal Surgery. Belgian experience with dynamic graciloplasty for faecal incontinence. Br J Surg 2004;91:872–8. 57. Wexner S, Baeten C, Bailey R et al. Long term efficacy of dynamic graciloplasty for fecal incontinence. Dis Colon Rectum 2002;45:809–18. 58. Chapmann AE, Geerdes B, Hewett P, Young J, Eyers T, Kiroff G, Maddern GJ. Systematic review of dynamic graciloplasty in the treatment of faecal incontinence. Br J Surg 2002;89:138–53.
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59. Lehur PA, Glemain P, Bruley des Varannes S, Buzelin JM, Leborgne J. Outcome of patients with an implanted artificial anal sphincter for severe faecal incontinence. A single institution report. Int J Colorectal Dis 1998;13:88–92. 60. Altomare DF, Dodi G, La Torre F, Romano G, Melega E, Rinaldi M. Multicentre retrospective analysis of outcome of artificial anal sphincter implantation for severe fecal incontinence. Br J Surg 2001;88:1481–6. 61. Dodi G, Melega E, Masin A, Infantion A, Cavallari F, Lise M. Artificial bowel sphincter (ABS) for severe fecal incontinence: a clinical and manometric study. Colorectal Dis 2000;2:207–11. 62. Lehur PA, Zerbib F, Neunlist M, Gemain P, Bruley des Varannes S. Comparison of quality of life and anorectal function after artificial bowel sphincter implantation. Dis Colon Rectum 2002;45:508–13. 63. Parker SC, Spencer MP, Madoff RD, Jensen LL, Wong WD, Rothenberger DA. Artificial bowel sphincter. Longterm experience at a single institution. Dis Colon Rectum 2003;46:722–9. 64. Wong WD, Congliosi SM, Spencer MP et al. The safety and efficacy of the artificial bowel sphincter for fecal incontinence: results from a multicenter cohort study. Dis Colon Rectum 2002;45:1139–53. 65. Devesa JM, Rey A, Hervas PL, Halawa KS, Larranaga I, Svidler L, Abraira V, Muriel A. Artificial anal sphincter: complications and functional results of a large personal series. Dis Colon Rectum 2002;45:1154–63.
66. O’Brien PE, Skinner S. Restoring control: the Acticon Neosphincter artificial bowel sphincter in the treatment of anal incontinence. Dis Colon Rectum 2000;43:1213–16. 67. Ortiz H, Armendariz P, DeMiguel M, Ruiz MD, Alos R, Roig JV. Complications and functional outcome following artificial anal sphincter implantation. Br J Surg 2002;89:877–81. 68. Vaizey CJ, Kamm MA, Gold DM, Bartram CI, Halligan S, Nicholls RJ. Clinical, physiological and radiological study of a new purpose-designed artificial bowel sphincter. Lancet 1998;352:105–9. 69. Christiansen J, Rasmussen OO, Lindorff-Larsen K. Longterm results of artificial anal sphincter implantation for severe anal incontinence. Ann Surg 1999;230:45–8. 70. Mundy L, Merlin TL, Maddern GJ, Hiller JE. Systematic review of safety and effectiveness of an artificial bowel sphincter for faecal incontinence. Br J Surg 2004;91:665–72. 71. Matzel KE, Madoff R, LaFontaine LJ, Baeten CGMI, Buie WD, Christiansen J, Wexner S and the Dynamic Graciloplasty Therapy Study Group. Complications of dynamic graciloplasty: incidence, management and impact on outcome. Dis Colon Rectum 2001;44:1427–35. 72. Christiansen J. The artificial anal sphincter. Can J Gastroenterol 2000;14:152–4. 73. Rongen MJGM, Uludang Ö, El Naggar K, Geerdes BP, Konsten J, Baeten CGMI. Long-term follow-up of dynamic graciloplasty for fecal incontinence. Dis Colon Rectum 2003;46:716–21.
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80 Combined genital and rectal prolapse Vanessa Banz, Jürg Metzger, Bernhard Schuessler
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IntroductIon Pelvic floor dysfunction comprises a multitude of diagnoses and symptoms ranging from urinary and fecal incontinence to different forms of prolapse, chronic constipation, sexual dysfunction or pelvic heaviness and backache. The etiology of pelvic organ prolapse is complex and multifactorial with possible risk factors being pregnancy, childbirth, congenital or acquired connective tissue abnormalities, denervation or weakness of the pelvic floor. Additional causes may include aging, previous hysterectomy, menopause, and pathologies such as asthma and bronchitis which lead to chronically increased intra-abdominal pressure. As far as rectal prolapse and rectocele are concerned, chronic constipation is identified as a major contributor.1–3 This mixed bouquet of causes and effects requires well-differentiated diagnostic tools and an interdisciplinary approach. Today, prolapse of the anterior and middle compartment, i.e. bladder and uterus, as well as the anterior and posterior vaginal wall, is best managed by a urogynecologic pelvic surgeon. It is equally clear that prolapse of the rectum is the domain of the colorectal surgeon. Rectal prolapse disease is predominant in females; up to 85% of these patients are women.4 As its etiology is shared at least partly with the pathology of genital prolapse, incontinence, etc., it is to be expected that in many patients the problems are not confined to one anatomic compartment. This is supported by Peters et al. who found 52 out of 55 patients with rectal prolapse to suffer from other defects of pelvic floor support.5 If genital prolapse alone is addressed, more than one-third (34.3%) of patients with rectal prolapse also show signs of genital prolapse.6 In order to serve patients’ needs best, it is essential that there is cooperation between all disciplines involved (i.e. urogynecologist, colorectal surgeon, gastroenterologist and sometimes a neurologist), not only for optimizing surgical treatment but also for diagnosis and indication. As well as being an introduction to the understanding of rectal prolapse and the different types of surgical management available, this chapter aims to improve shared management of combined genital and rectal prolapse in the individual patient. As the evidence of knowledge in this field to date is poor, personal views and preferences could not be neglected in this chapter.
PathoPhysIology and EtIology Enterocele/sigmoidocele The descent of the peritoneum between the anterior rectal wall and the vagina into the pouch of Douglas is defined as an enterocele. In the enterocele sac (‘culde-sac syndrome’) one may find small intestine – the actual enterocele – or the sigmoid colon, the ‘sigmoidocele’. An elongated sigmoid colon may lead to an obstruction of the rectum upon defecation. Often the enterocele or sigmoidocele will be combined with other pathologic changes such as a rectocele or perineal descent (Fig. 80.1). Classification of a sigmoidocele according to Jorge et al.7 is based on the images obtained at defecography. This classification takes into account the lowest part of the sigmoidocele. Grade I sigmoidoceles have their deepest end above the pubococcygeal line. Grade II are below this line but above the ischiococcygeal line, and Grade III sigmoidoceles descend beyond.
Figure 80.1. MRI defecography during straining. A large sigmoidocele is present (SC) in combination with a rectocele (RC). 1136
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Enteroceles can bulge into the vagina or the rectum, a condition known as intussusception, or into both.
rectal prolapse Complete rectal prolapse (procidentia) is defined as the circumferential protrusion of all layers of the rectal wall through the anal sphincter (Fig. 80.2). Compared to this is the rectal intussusception, which may be seen as a telescope-like invagination of the rectal wall (commonly anterior rectal wall). Synonymously used to describe this condition are the terms ‘interior’, ‘incomplete’ or ‘occult’ rectal prolapse. It is sometimes regarded as an early manifestation of a complete prolapse. Although distinctly different from a complete rectal wall prolapse, anterior rectal wall intussusception can also protrude into and even through the anal canal (Fig. 80.3a). These two conditions are distinctly different from mucosal prolapse, which, as the name implies, is a prolapse solely of the rectal mucosa. Grade I prolapses are usually only diagnosed using a proctorectoscope or on contrast enema studies. Grade II prolapses can be seen upon pressing, and manifest themselves clinically as soiling of stool. A grade III prolapse is, in its maximal form, a permanent prolapse of
a
b
Figure 80.2. Full thickness, circumferential rectal prolapse – ‘rectal procidentia’.
Figure 80.3. A 38-year-old patient with four uncomplicated and fast vaginal deliveries complained about increasing obstructed defecation. (a) During forced Valsalva maneuver an anterior rectal wall prolapse was found to be the major source of the defecatory symptoms. (b) Vaginal inspection with Preisky speculum. Transanal digital examination revealed a rectocele. 1137
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the rectum, accompanied by varying degrees of incontinence for gas and liquid or stool of normal consistency. The prolapsed rectal wall may ulcerate and cause episodes of heavier bleeding. Rectal prolapse is seen either in the very young or in the elderly. In infants the as yet undeveloped sacral curve and the reduced resting tone predispose to rectal prolapse. In children it usually commences after episodes of violent diarrhea or after rapid and excessive weight loss. It is also associated with maldevelopment of the pelvis, neurologic defects or fibrocystic disease. A torn perineum predisposes in women, as does straining in men due to urethral obstruction. In older people, general atony of the sphincteric mechanism may be a risk factor. Although the etiology remains unclear, a series of accompanying or casual anatomic peculiarities appear to play a role. Prolapse patients often have a deep rectovaginal or rectovesical cul-de-sac, a loose attachment of the rectum to the presacral fascia or a general loosening of the mesorectal structures.8 Nearly all patients with complete rectal prolapse show signs of a weak sphincter, most certainly originating from constant constipation.
Pelvic floor dysfunction Although from an etiologic point of view the morphologic and functional pathologies may be quite different, the clinical symptoms may be very similar. Normally, the internal and external sphincters and the puborectal sling relax simultaneously. Together with the propulsive force of the rectum a coordinated defecation takes place. Patients with functional problems show a paradox reaction of the pelvic floor and external sphincter muscles, or failure to relax the internal sphincter, leading to obstruction upon defecation. Patients with pelvic floor dyssynergia with its involuntary, unconscious contraction of the pelvic floor muscles (anismus), with an involuntary contraction of the puborectal muscles – the so-called ‘paradoxical puborectalis syndrome’ – may thus present with symptoms identical to those seen in patients with pelvic organ prolapse. Differentiating between functional disorders (which in turn may also be combined with other anatomic pathologies) and purely mechanical–anatomic problems is often very challenging and is usually preceded by years of previous diagnostic steps and fruitless therapies. The distinction between the two entities is also of great importance as far as therapy strategies are concerned, as these will vary enormously – for example, biofeedback for pelvic floor dyssynergia rather than operative treatment options.9
dIagnostIc tools Even nowadays, with our extraordinarily high-tech, specific and exact diagnostic tools, a detailed history of the patient’s problems and symptoms is of enormous value. The complexity of pelvic floor dysfunction may become simpler as the patient unknowingly gives valuable hints, resulting in a narrowing down of the working hypothesis to a few probable causes. Irrespective of the specialism of the primarily consulted physician, it is important to obtain the best possible overview of the patient’s coloproctologic and urogynecologic problems. The subjective problems may then be transformed into objective, measurable data – for example, when using various scores such as the Rome criteria for constipation or the Faecal Incontinence Severity Index (FISI score) for fecal incontinence. An advantage of such scores is of course the opportunity to compare the results before and after the implemented therapy, thus indicating a certain measure of success, or failure.
Proctologic examination Every clinical examination should commence with a thorough proctologic check-up including inspection, palpation, and proctorectoscopy, The experienced examiner will often be able to make an accurate diagnosis solely on initial examination. However, considering the complexity of pelvic floor dysfunction, a clinical examination frequently does not suffice and further diagnostic imaging is required.
Endoanal sonography and anorectal manometry As stool incontinence/soiling is, along with obstructive defecation, the leading symptom in patients suffering from rectal prolapse, it is mandatory to rule out additional sphincter defects. Thus endoanal sonography and anorectal manometry serve best to identify whether incontinence may persist after rectal prolapse surgery. Anal manometry is a helpful diagnostic tool that allows accurate measurement of the sphincter complex. It can be used for measurement of the resting tone (as given by the function of the internal anal sphincter), the maximal contraction (as dominated by the external sphincter), and general functional coordination, as well as allowing estimation of the length of the anal canal. Endoanal sonography is the method of choice to identify muscular sphincter defects as well as providing a means of visualizing dynamic changes of accompanying pathologies such as entero- or rectoceles.10,11
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colonic transit time measurement In order to allow for differentiation between obstructed defecation and slow transit constipation one elegant and patient friendly method involves the swallowing of 10 markers per day over a time span of 6 or more days. A plain abdominal radiograph is taken the day after the last marker has been swallowed. Depending on the number of markers still seen, the transit time can be estimated, with a passage time of more than 72 hours being clearly pathologic.
conventional defecography versus dynamic pelvic floor MrI If the main problem of a patient with pelvic floor dysfunction is ‘obstructed defecation’, defecography is a highly sensitive and specific method for the detection of functional rectoceles, sigmoidoceles, and rectal prolapse, and also important for the detection of an intussusception.12,13 The addition of enteral and rectal contrast agent enhances the outcome of defecography.12,14 The main problem with defecography is its failure to optimally visualize the anterior and middle compartments. With many patients showing clinical involvement of more than one compartment, defecography is insufficient for understanding pathology within all three compartments. This is where dynamic pelvic floor magnetic resonance imaging (MRI) plays an important role. It allows complete visualization of the pelvic floor, inclusive of all organs, not only as a summary of images which conventional radiologic imaging provides but also in multiple slices and in different planes without the side effects of irradiation. As of yet, no true agreement exists regarding the exact indication for MRI defecography, whether or not rectal contrast should be applied, where the exact reference lines lie, and in what position the patient should be examined (lying or sitting; the latter technique with an important loss of image resolution). As the formation of prolapse – whether of rectal or urogenital origin – is often the result of dynamic changes, the sequence of images taken during a Valsalva maneuver gives further insight into the interaction of organs leading to the pathology responsible for the patient’s complaints. The additional information obtained by dynamic MRI as compared to defecography alone may influence and even change therapeutic strategies. Kaufmann et al. showed that, of 22 patients who underwent dynamic pelvic MRI, 41% had a modification of their planned operative procedure, which had been based on previous
clinical and conventional radiologic data.15 Diagnosis of levator hernias was only possible using pelvic MRI. In summary, one should – as with all potentially complex pathologies – start with a basic diagnosis. It cannot be overemphasized that detailed history taking and clinical examination are of primary importance for all further examinations. Whenever combined prolapse entities are suspected the patient should be examined in an interdisciplinary clinic combining colorectal, urogynecologic and, if necessary, gastroenterologic knowledge.
concoMItant rEctal ProlaPsE In gEnItal ProlaPsE PatIEnts Patients with genital prolapse of any type warrant careful history taking as well as clinical examination in order not to miss concomitant or combined rectoanal pathology. In particular, if a posterior enterocele is suspected, or if symptoms of bowel dysfunction are found which cannot otherwise be explained, colorectal investigation is mandatory. Not only is careful inspection of the vaginal and introital areas during rest and at maximal Valsalva necessary, but an overview of the complete posterior compartment including the anal region is also essential. If this is neglected – for example, in a patient complaining of stool outlet obstruction as shown in Figure 80.3 – anterior rectal prolapse could well be overlooked in favor of a simple rectocele. Also important is the fact that different entities often share many of the bowel symptoms (Fig. 80.4). Whenever a patient complains about obstructed defecation, stool incontinence or soiling, prolonged defecation time, rectal lump or fragmented defecation, it is mandatory that – as well as a careful digital transanal examination – proctoscopy, defecography (preferably by fast image MRI), and radiologic investigation of the colonic transit time be performed.
rEctal ProlaPsE Conservative methods of treatment rarely achieve the hoped-for success for adults with complex rectal prolapse in which the prolapse comprises the entire rectal wall. To date, there have been no randomized studies in which conservative treatment options were compared to operative management.16 Many different surgical techniques have already been proposed for the repair of rectal prolapse. The main difference lies with the surgical approach, for which there are two options: perianal and transabdominal (Fig. 80.5). 1139
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Rectocele
Mucosal prolapse
Constipation Obstructed defecation Slow transit constipation
Stool incontinence/ soiling
Enterocele
Rectal prolapse
Fragmental defecation
Prolonged defecation time
Anal lump
Hemorrhoids
Intussusception
Figure 80.4. Rectal pathologies in comparison to the spectrum of symptoms. Note that completely different diagnoses nearly always share the same symptoms.
Rectal prolapse
Perineal technique
Transabdominal technique
Anal encirclement (Thiersch)
Perineal resection
Open or laparoscopic
Delorme Altemeier
Rectopexy
Suture
Resection
Resection and rectopexy
Mesh
Frykman/ Goldberg
Anterior sling (Ripstein) Posterior Wells/Ivalon sponge
Perianal resection – for example, the operations according to Delorme and Altemeier – are nowadays usually only performed for the old and frail.16,17 One advantage of the perianal techniques is that they may be performed under regional or even local anesthesia. The transabdominal technique is usually used for the
Figure 80.5. Operative techniques for repair of rectal prolapse. younger, otherwise healthy patient. Transabdominal surgical techniques vary in the choice of approach (e.g. laparoscopy versus laparotomy), the extent to which the rectum is mobilized, the method of pexation of the rectum, and the option of combining rectopexy with resection.17 The primary goal of every surgical technique is to
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eliminate functional problems such as incontinence and constipation while aiming for the lowest recurrence rate and minimal morbidity and mortality. A Cochrane metaanalysis first published in 1999 included 10 studies with a total of 324 patients.16 The aim of this specific review was to answer the following four principal questions: 1. Is the abdominal approach more advantageous than the perianal approach? 2. Is one method of rectopexy superior to another? 3. Is laparoscopy better than laparotomy? 4. Should every rectopexy be combined with a resection? The authors of this particular study came to the conclusion that the small sample sizes of the included studies, some of which were methodically incorrect, make it difficult to publish practical guidelines. Overall, there does not appear to be a significant tendency towards an increased recurrence rate for either of the techniques. Postoperative fecal incontinence, however, was seen less frequently after an abdominal approach as compared to a perianal approach. No difference was seen between the various methods of fixation for rectopexy (mesh versus suture technique). The rate of postoperative constipation was lower for rectopexy, which had been combined with a resection as compared to rectopexy alone. An interesting study currently being conducted in England and Ireland was started in April 2000. The Association of Coloproctology launched a national study in which patients with full-thickness rectal prolapse were included. The aim is to collect data from 950 patients and to compare the abdominal approach with the perianal approach. The Delorme operation will be compared to the Altemeier, which in turn will be compared to suture rectopexy and resection rectopexy. Prolapse recurrence, defecography performance, and quality of life will be the measured outcomes. The study is likely to terminate in December 2005.16
Perianal operative techniques There is a wide spectrum of perianal operative techniques ranging from anal encirclement (according to Thiersch), rectal mucosectomy and muscle plicature according to Delorme, and transsphincteric and parasacral resection of the rectum. The operation of Delorme is widespread in England and is especially suitable for high-risk patients as it can be carried out under local anesthesia with slight sedation. First described in 1900, it combines the circular mucosectomy of the prolapsed rectum, followed by a pli-
cature of the underlying muscles (Fig. 80.6). Of utmost importance is that at least 10–12 cm of rectal mucosa is completely excised. Together with the plicature of the muscles by means of individual sutures, the prolapse is shortened and reduced back into the anal canal. The newly formed, circular muscle ring acts as a pessary. Recurrence rates of the Delorme technique are summarized in Table 80.1 and range from 14 to 30%. Another relatively frequently applied perianal operative technique is the rectum resection according to Altemeier.18 It involves the full thickness excision of the rectum and, if possible, the distal part of the sigma. Recurrence rates in the literature lie between 3 and 16% (Table 80.1). Postoperative convalescence is usually without any complications. However, potentially life-threatening complications such as pelvic sepsis have been described in the literature.19 Postoperative complications for both techniques are relatively common, those most frequently seen being constipation and incontinence. The Delorme technique reduces rectal capacity, compliance, and sensitivity20 whereas the Altemeier operation, with its coloanal anastomosis, often compromises the usually already existing sphincter defect. A levatorplasty is recommended to increase postoperative continence.21 A small trial, which included 10 patients per group, compared the abdominal with the perianal approach.22 Postoperative measurements of resting anal pressure, maximum squeeze pressure, and rectal compliance showed significantly better results for the abdominal group as compared to the perianal group.
abdominal operative techniques Many different abdominal techniques have been described in the literature comparing the extent of rectum mobilization, method of rectal fixation, and additional resection of the rectum or sigma. The simple suture rectopexy finds its roots back in the 1950s with complete mobilization of the rectum and proximal fixation. Postoperative fibrosis leads to a permanent fixation of the elevated rectum onto the presacral fascia.39 Various other materials such as non-resorbable mesh, polyvinyl alcohol (Ivalon) and Teflon have been used to increase the presence of scar tissue formation.17 Until the beginning of the 1990s the Ivalon sponge rectopexy, first described by Wells, was the method of choice. A rectangular piece of Ivalon sponge is fixed with a couple of sutures to the sacrum; the elongated rectum is then enclosed posteriorly in a semi-circular fashion and is fixed to the sponge. Some studies show that the implantation of Ivalon sponge has been associ1141
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ated with an increase in postoperative infection rates.40,41 Nowadays Ivalon sponge has been replaced by synthetic meshes, with the resorbable and the non-resorbable meshes achieving similar results.31,42,43 Anterior sling rectopexy was first described in 1952 by Ribstein.44 Here an anteriorly placed sling consisting of synthetic material is placed in front of the rectum, after having fully mobilized the latter, and is fixed to the sacral promontory. The concept behind this technique lies in the reconstruction of the posterior curvature of the rectum. Despite low mortality rates, frequent strictures at the point of fixation and a high recurrence rate led to this technique being abandoned very quickly. Results after posterior mesh rectopexy show that recurrence rates range between zero and 6%, although postoperative fecal incontinence or constipation is present in up to 60% of all patients, which is far too high a rate17 (see Table 80.1). A comparative study from Novell et al.32 showed that patients who had undergone Ivalon sponge rectopexy had more problems related to constipation than those operated on according to the suture rectopexy technique. As of yet, there have been no large, randomized
A
B
C
D
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trials comparing suture rectopexy and mesh rectopexy. However, there does appear reason to believe that the rate of infection and pelvic abscess formation, as well as postoperative constipation, is higher for the mesh group. Overall, there appears to be a slight advantage for the suture technique compared to mesh rectopexy.32,45,46 One important point to bear in mind is whether or not the lateral ligaments should be preserved when performing a rectopexy. Two trials47,48 with a total of 46 patients tried to answer this specific question. Postoperative constipation was significantly less common in those patients in whom the ligaments had been conserved (one patient versus seven), and postoperative continence and resting as well as squeeze pressure appeared to be positively influenced if the ligaments were preserved.
resection rectopexy Opposed to the simple suture and mesh rectopexies are the resection rectopexies. The currently preferred surgical technique was first described in 1969 by Frykman and Goldberg.36 While taking great care to spare the hypogastric nerves, the rectum is mobilized
Figure 80.6.
Delorme procedure.
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table 80.1.
Recurrence rates after surgical treatment of full-thickness rectal prolapse
Author Oliver et al.23 Tobin & Scott
24 25
Lechaux et al.
Watts & Thompson
26
Year
Technique
Patients (n)
Recurrence (%) Follow-up (months)
1994
Delorme
41
22
47
1994
Delorme
43
26
20
1995
Delorme
85
14
33
2000
Delorme
101
30
36
Altemeier et al.18
1971
Altemeier
106
3
228
Agachan et al.27
1997
Altemeier
21
5
30
1999
Altemeier
183
16
47
Keighley et al.
1983
Posterior mesh rectopexy
100
0
24
Aitola et al.30
1999
Posterior mesh rectopexy
96
6
78
Galili & Rabau31
1997
Posterior mesh rectopexy
37
3
44
1994
Suture rectopexy
32
3
47
1996
Suture rectopexy
65
0
65
Kessler et al.
1999
Laparoscopic suture rectopexy
32
6
48
Bruch et al.35
1999
Laparoscopic suture rectopexy
32
0
30
1969
Resection/rectopexy
80
0
1985
Resection/rectopexy
138
2
Kim et al.
1999
Resection/rectopexy
176
5
98
Stevenson et al.38
1998
Laparoscopic resection/rectopexy
34
0
18
28
Kim et al.
29
32
Novell et al.
33
Khanna et al.
34
36
Frykman & Goldberg Watts et al.
37
28
along the lines of the presacral fascia down to the pelvic floor. The anterior mobilization, which needs to be undertaken in order to allow optimal elongation of the rectum, is carried out in a similar fashion. After elongation of the rectum, the excessive colon is resected. The resection prevents the siphon effect and with it the problems of constipation. Fixation of the rectum occurs just below the sacral promontory onto the presacral fascia (Fig. 80.7). A new pouch of Douglas is then reconstructed at a higher level by means of peritoneal closure at promontory level. Long-term results demonstrate recurrence rates of 2–5%. This technique is particularly suitable for those patients with an elongated, redundant sigma and a long history of refractory constipation.49 Only two trials exist in which rectopexy alone is compared to rectopexy with resection.43,50 The only truly significant postoperative difference found was the rate of constipation. Whereas two out of 23 patients in the resection rectopexy group suffered from constipation, this problem was evident in 12 out of 23 patients in the simple rectopexy group without additional resection. More of these operations are performed laparoscopically.51–55 The postoperative results appear to be as good as those obtained from open surgery. Advantages of laparoscopic rectopexy are, of course,
– 48
as with any laparoscopic operation: less postoperative pain, shorter hospital stay, and shorter time off work. Disadvantages are the sometimes very long operating times with accordingly long anti-Trendelenburg positioning, which can be especially problematic for the older patient.56
laparoscopic methods Two small, randomized, single-center studies57,58 have so far compared laparoscopic mesh rectopexy with open mesh rectopexy. Both trials show a shorter hospital stay and fewer postoperative complications for the laparoscopic group with, however, notably longer operating times. Mortality for laparoscopic rectopexy is between zero and 3%, with recurrence rates lying between zero and 10% after a mean follow-up of 8–30 months.17 These results compare well with similar trials carried out for the open technique only. Recently, Benoist et al.46 published results of 14 patients who had undergone laparoscopic posterior mesh rectopexy compared with results from 18 patients with laparoscopic suture rectopexy with sigma resection, and a further 16 patients with suture rectopexy minus the resection. Mortality and morbidity were comparable for all three groups. On the other hand, postoperative 1143
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(a)
B
>À`âÊv}°nä°äÇL
(c)
Figure 80.7. Resection rectopexy according to Frykman and Goldberg.36
constipation was distinctly higher for rectopexy alone (62% with mesh and 64% without mesh) compared to laparoscopic rectopexy with resection (11%). Salkeld et al.59 recently published the economic aspects of laparoscopic rectopexy surgery compared to the open technique. A cost-efficiency analysis showed that although operating time is on average 51 minutes longer for laparoscopic surgery and the costs for oneway surgical instruments are £291 more per patient, the shorter hospital stay reduces the actual cost by £357 per patient as compared to the open technique.
summary/conclusion From a surgical point of view there is no single ideal operative technique for complete rectal prolapse. Different clinical criteria influence the choice of operation.60 Older patients with relevant co-morbidities who are unfit for abdominal surgery benefit from the perianal approach, which can be performed under regional or even local anesthesia. For all other patients we opt for the abdominal approach, as functional results regarding constipation and incontinence are better and the recur-
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rence rate definitively lower. In selected patients without any previous major abdominal surgery or relevant anesthesiologic contraindications for the long intraoperative anti-Trendelenburg positioning, we prefer laparoscopic operations. Patients with pre-existing constipation who had been preoperatively diagnosed with MRI defecography (outlet obstruction) or colon transit time (slow transit constipation), or patients with an intraoperatively diagnosed dolichosigma, are ideal candidates for laparoscopic resection rectopexy. We fix the mobilized rectum with sutures to the presacral fascia, as mesh implantation does not show any relevant advantages. As far as the perianal procedures are concerned, the choice of surgical treatment (Delorme versus perianal rectosigmoidectomy) should be chosen according to the experience and preference of the operating surgeon. Organ prolapse, which affects the middle as well as the posterior compartment, lies on the watershed of two specialties. This occurs if full-thickness rectal prolapse is combined with an entero- or rectocele. Here a combined diagnostic and therapeutic algorithm is important and will be discussed in the following section.
coMbInEd surgEry for gEnItal and rEctal ProlaPsE The literature on techniques and results of combined surgery for rectal and genital prolapse is scarce and consists of a few and mostly small case series. No data are yet available in a Medline research with regard to comparison of different methods. Based on logic and reason, however, it is obvious that single-step combined surgery offers the best solution for the patient and should be the primary aim. Even for a transvaginal repair of genital prolapse, together with a perineal approach for rectal prolapse – obviously a combination of two separate operations and two-step surgery – would add only a second anesthesia without beneficial effect. The only issue to debate is whether to perform the genital or the rectal operation first. To start with the correction of the genital prolapse is reasonable, provided a high peritonealization of the pouch of Douglas is planned. As is the case for rectal prolapse surgery, urogenital prolapse could also be repaired from below (transvaginal route) or above (laparotomy or laparoscopy). Which route is to be chosen for the individual patient is a matter of discussion between the urogynecologic and the colorectal surgeons. Choosing the perineal/transvaginal route is in favor of less invasive surgery against less successful outcome in the posterior compartment, i.e. risk of rectal prolapse recurrence and anal incontinence. As far as the vagina is concerned, cohabitation problems
are more likely to be expected. Based on that, it is obvious that these techniques are preferred if the patient is frail and elderly or carries other risk factors for major surgery. The abdominal (endoscopic) approach necessitates one-step surgery. Two-step surgery, independent of the remaining genital or rectal prolapse, is expected to bear more unnecessary risks for patients. This implies that one-step surgery needs sophisticated preoperative exploration of all compartments. Depending on the existing genital prolapse situation, concomitant surgery for genital prolapse consists of four steps: 1. 2. 3. 4.
Fixation of the vaginal cuff; Obliteration of the pouch of Douglas; Rectocele repair; Cystocele repair.
For the abdominal approach there is universal agreement to fix the vaginal cuff and close the pouch of Douglas from above.61–64 In one of the largest prospective case series of 89 hysterectomized patients, Collopy et al.62 preferred to repair the remaining vaginal descent from below following the abdominal procedure, whereas Sullivan et al.64 used a total mesh repair, extending the mesh lateral to the vagina and the bladder to the symphysis pubis. The high recurrence rate of more than 30% re-operations compared to nil in the series of Collopy, however, does not seem to favor this approach. Fixation of the vaginal cuff to the rectal ligament as used for mesh-free rectopexy has been shown to be successful in the hands of the authors, provided the vagina is long enough to be suspended without tension (Fig. 80.8). Routine fixation of the vaginal cuff or even the uterus, if still in place, because ‘there is genital prolapse present in 25% and if not yet present may occur later in life’ does not appear to be a meaningful prevention strategy but strongly supports preoperative interdisciplinary assessment63,65 (see the discussional remark in ref. 62). From the authors’ point of view, adequate cystocele repair is feasible with an extension of the mesh at the anterior vaginal wall,62,66 whereas for the effective recto-/ perineocele, extension and fixation of the posterior mesh down to the level of the perineum and fixation to the adjacent puborectalis sling appears to be necessary. The feasibility of this technique is simplified by the laparoscopic approach with a 30-degree optic. Techniques that introduce and fix the mesh from an introital incision have been shown to be burdened with a high mesh erosion rate. 1145
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Figure 80.8. Technique of mesh-free vaginal cuff fixation to the ventral ligament used for sacral rectopexy.
A large enterocele bulging into the vagina as well as causing the anterior rectal wall to intussuscept into the lumen of the rectum marks the ‘gray zone’ between the genital prolapse surgeon and the colorectal surgeon. Baessler and Schuessler have shown vaginal double pedicle fixation at the vaginal cuff concomitant with an obliteration of the pouch of Douglas to treat rectal intussusception successfully.62,66 However, contrary to the good anatomic results, symptoms of a high stool outlet obstruction developed after the surgery. It therefore seems reasonable to discuss concomitant rectal surgery if symptoms of stool outlet obstruction are found in conjunction with anterior rectal wall intussusception without overt rectal prolapse.
rEfErEncEs 1. Bump RC, Norton PA. Epidemiology and natural history of pelvic floor dysfunction. Obstet Gynecol Clin North Am 1998;25:723–46. 2. Gill EJ, Hurt WG. Pathophysiology of pelvic organ prolapse. Obstet Gynecol Clin North Am 1998;25:757–69. 3. MacLennan AH, Taylor AW, Wilson DH et al. The prevalence of pelvic floor disorders and their relationship to gender, age, parity and mode of delivery. BJOG 2000;107:1460–70. 4. Goligher JC. Prolapse of the rectum. In: Surgery of the Anus, Rectum and Colon. London: Baillière Tindall, 1980; 224–58. 5. Peters WA III, Smith MR, Drescher CW. Rectal prolapse
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in women with other defects of pelvic floor support. Am J Obstet Gynecol 2001;184:1488–94. 6. Gonzalez-Argente FX, Jain A, Nogueras JJ et al. Prevalence and severity of urinary incontinence and pelvic genital prolapse in females with anal incontinence or rectal prolapse. Dis Colon Rectum 2001;44:920–6. 7. Jorge JM, Yang YK, Wexner SD. Incidence and clinical significance of sigmoidoceles as determined by a new classification system. Dis Colon Rectum 1994;37:1112–17. 8. Heitland W. [Rectal prolapse in adults.] Chirurg 2004;75:882–9.
21. Williams JG, Rothenberger DA, Madoff RD et al. Treatment of rectal prolapse in the elderly by perineal rectosigmoidectomy. Dis Colon Rectum 1992;35:830–4. 22. Deen KI, Grant E, Billingham C et al. Abdominal resection rectopexy with pelvic floor repair versus perineal rectosigmoidectomy and pelvic floor repair for full-thickness rectal prolapse. Br J Surg 1994;81:302–4. 23. Oliver GC, Vachon D, Eisenstat TE et al. Delorme’s procedure for complete rectal prolapse in severely debilitated patients. An analysis of 41 cases. Dis Colon Rectum 1994;37:461–7.
9. Battaglia E, Serra AM, Buonafede G et al. Long-term study on the effects of visual biofeedback and muscle training as a therapeutic modality in pelvic floor dyssynergia and slow-transit constipation. Dis Colon Rectum 2004;47:90–5.
24. Tobin SA, Scott IH. Delorme operation for rectal prolapse. Br J Surg 1994;81:1681–4.
10. Barthet M, Portier F, Heyries L et al. Dynamic anal endosonography may challenge defecography for assessing dynamic anorectal disorders: results of a prospective pilot study. Endoscopy 2000;32:300–5.
26. Watts AM, Thompson MR. Evaluation of Delorme’s procedure as a treatment for full-thickness rectal prolapse. Br J Surg 2000;87:218–22.
11. Lohnert M, Doniec JM, Kovacs G et al. New method of radiotherapy for anal cancer with three-dimensional tumor reconstruction based on endoanal ultrasound and ultrasound-guided afterloading therapy. Dis Colon Rectum 1998;41:169–76. 12. Agachan F, Pfeifer J, Wexner SD. Defecography and proctography. Results of 744 patients. Dis Colon Rectum 1996;39:899–905. 13. Pfeifer J, Oliveira L, Park UC et al. Are interpretations of video defecographies reliable and reproducible? Int J Colorectal Dis 1997;12:67–72. 14. Herold A, Muller-Lobeck H, Jost WH et al. [Diagnostic evaluation of the rectum and pelvic floor in chronic constipation.] Zentralbl Chir 1999;124:784–95. 15. Kaufman HS, Buller JL, Thompson JR et al. Dynamic pelvic magnetic resonance imaging and cystocolpoproctography alter surgical management of pelvic floor disorders. Dis Colon Rectum 2001;44:1575–83. 16. Brazzelli M. Surgery for complete rectal prolapse in adults. Cochrane Database Syst Rev 2005; Issue 2. 17. Madiba TE, Baig MK, Wexner SD. Surgical management of rectal prolapse. Arch Surg 2005;140:63–73. 18. Altemeier WA, Culbertson WR, Schowengerdt C et al. Nineteen years’ experience with the one-stage perineal repair of rectal prolapse. Ann Surg 1971;173:993–1006. 19. Takesue Y, Yokoyama T, Murakami Y et al. The effectiveness of perineal rectosigmoidectomy for the treatment of rectal prolapse in elderly and high-risk patients. Surg Today 1999;29:290–3. 20. Penninckx F, D’Hoore A, Sohier S et al. Abdominal resection rectopexy versus Delorme’s procedure for rectal prolapse: a predictable outcome. Int J Colorectal Dis 1997;12:49–50.
25. Lechaux JP, Lechaux D, Perez M. Results of Delorme’s procedure for rectal prolapse. Advantages of a modified technique. Dis Colon Rectum 1995;38:301–7.
27. Agachan F, Reissman P, Pfeifer J et al. Comparison of three perineal procedures for the treatment of rectal prolapse. South Med J 1997;90:925–32. 28. Kim DS, Tsang CB, Wong WD et al. Complete rectal prolapse: evolution of management and results. Dis Colon Rectum 1999;42:460–6. 29. Keighley MR, Fielding JW, Alexander-Williams J. Results of Marlex mesh abdominal rectopexy for rectal prolapse in 100 consecutive patients. Br J Surg 1983;70:229–32. 30. Aitola PT, Hiltunen KM, Matikainen MJ. Functional results of operative treatment of rectal prolapse over an 11-year period: emphasis on transabdominal approach. Dis Colon Rectum 1999;42:655–60. 31. Galili Y, Rabau M. Comparison of polyglycolic acid and polypropylene mesh for rectopexy in the treatment of rectal prolapse. Eur J Surg 1997;163:445–8. 32. Novell JR, Osborne MJ, Winslet MC, Lewis AA. Prospective randomized trial of Ivalon sponge versus sutured rectopexy for full-thickness rectal prolapse. Br J Surg 1994;81:904–6. 33. Khanna AK, Misra MK, Kumar K. Simplified sutured sacral rectopexy for complete rectal prolapse in adults. Eur J Surg 1996;162:143–6. 34. Kessler H, Jerby BL, Milsom JW. Successful treatment of rectal prolapse by laparoscopic suture rectopexy. Surg Endosc 1999;13:858–61. 35. Bruch HP, Herold A, Schiedeck T et al. Laparoscopic surgery for rectal prolapse and outlet obstruction. Dis Colon Rectum 1999;42:1189–94. 36. Frykman HM, Goldberg SM. The surgical treatment of rectal procidentia. Surg Gynecol Obstet 1969;129:1225–30. 37. Watts JD, Rothenberger DA, Buls JG et al. The manage-
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ment of procidentia. 30 years’ experience. Dis Colon Rectum 1985;28:96–102.
procedure without a mesh prosthesis. Hepatogastroenterology 2002;49:1549–51.
38. Stevenson AR, Stitz RW, Lumley JW. Laparoscopic-assisted resection-rectopexy for rectal prolapse: early and medium follow-up. Dis Colon Rectum 1998;41:46–54.
53. Chiu HH, Chen JB, Wang HM et al. Surgical treatment for rectal prolapse. Zhonghua Yi Xue Za Zhi (Taipei) 2001;64:95–100.
39. Jacobs LK, Lin YJ, Orkin BA. The best operation for rectal prolapse. Surg Clin North Am 1997;77:49–70.
54. Zittel TT, Manncke K, Haug S et al. Functional results after laparoscopic rectopexy for rectal prolapse. J Gastrointest Surg 2000;4:632–41.
40. Lake SP, Hancock BD, Lewis AA. Management of pelvic sepsis after Ivalon rectopexy. Dis Colon Rectum 1984;27:589–90. 41. Ross AH, Thomson JP. Management of infection after prosthetic abdominal rectopexy (Wells’ procedure). Br J Surg 1989;76:610–2. 42. Winde G. Clinical and functional results of abdominal rectopexy with absorbable mesh-graft for treatment of complete rectal prolapse. Eur J Surg 1993;159:301–5. 43. Luukkonen P. Abdominal rectopexy with sigmoidectomy vs. rectopexy alone for rectal prolapse: a prospective, randomized study. Int J Colorectal Dis 1992;7:219–22. 44. Ribstein C. Treatment of massive rectal prolapse. Am J Surg 1952;83:68–71. 45. Madbouly KM, Senagore AJ, Delaney CP et al. Clinically based management of rectal prolapse. Surg Endosc 2003;17:99–103. 46. Benoist S, Taffinder N, Gould S et al. Functional results two years after laparoscopic rectopexy. Am J Surg 2001;182:168–73. 47. Selvaggi F. Surgical treatment of rectal prolapse: a randomized study. Br J Surg 1993;80:S89. 48. Speakman CT, Madden MV, Nicholls RJ et al. Lateral ligament division during rectopexy causes constipation but prevents recurrence: results of a prospective randomized study. Br J Surg 1991;78:1431–3. 49. Azimuddin K, Khubchandani IT, Rosen L et al. Rectal prolapse: a search for the ‘best’ operation. Am Surg 2001;67:622–7. 50. McKee RF, Lauder JC, Poon FW et al. A prospective randomized study of abdominal rectopexy with and without sigmoidectomy in rectal prolapse. Surg Gynecol Obstet 1992;174:145–8. 51. Kairaluoma MV, Viljakka MT, Kellokumpu IH. Open vs. laparoscopic surgery for rectal prolapse: a case-controlled study assessing short-term outcome. Dis Colon Rectum 2003;46:353–60. 52. Tsugawa K, Sue K, Koyanagi N et al. Laparoscopic rectopexy for recurrent rectal prolapse: a safe and simple
55. Heah SM, Hartley JE, Hurley J et al. Laparoscopic suture rectopexy without resection is effective treatment for full-thickness rectal prolapse. Dis Colon Rectum 2000;43:638–43. 56. Xynos E, Chrysos E, Tsiaoussis J et al. Resection rectopexy for rectal prolapse. The laparoscopic approach. Surg Endosc 1999;13:862–4. 57. Solomon MJ, Young CJ, Eyers AA, Roberts RA. Randomized clinical trial of laparoscopic versus open abdominal rectopexy for rectal prolapse. Br J Surg 2002;89:35–9. 58. Boccasanta P. Comparison of laparoscopic rectopexy with open technique in the treatment of complete rectal prolapse: clinical and functional results. Surg Laparosc Endosc 1998;8:460–5. 59. Salkeld G, Bagia M, Solomon M. Economic impact of laparoscopic versus open abdominal rectopexy. Br J Surg 2004;91:1188–91. 60. Brown AJ, Anderson JH, McKee RF et al. Strategy for selection of type of operation for rectal prolapse based on clinical criteria. Dis Colon Rectum 2004;47:103–7. 61. Barham K, Collopy BT. Posthysterectomy rectal and vaginal prolapse: a commonly overlooked problem. Aust N Z J Obstet Gynaecol 1993;33:300–3. 62. Collopy BT, Barham KA. Abdominal colporectopexy with pelvic cul-de-sac closure. Dis Colon Rectum 2002;45:522–6. 63. Kuijpers HC. Treatment of complete rectal prolapse: to narrow, to wrap, to suspend, to fix, to encircle, to plicate or to resect? World J Surg 1992;16:826–30. 64. Sullivan ES, Longaker CJ, Lee PY. Total pelvic mesh repair: a ten-year experience. Dis Colon Rectum 2001;44:857–63. 65. Mollen RM, Kuijpers JH, van Hoek F. Effects of rectal mobilization and lateral ligaments division on colonic and anorectal function. Dis Colon Rectum 2000;43:1283–7. 66. Baessler K, Schuessler B. Abdominal sacrocolpopexy and anatomy and function of the posterior compartment. Obstet Gynecol 2001;97:678–84.
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81 The role of laparoscopic surgery Anthony R B Smith
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IntroductIon The role of laparoscopic surgery in urogynecology/pelvic reconstructive surgery is not yet clear. This section identifies some of the issues that need to be addressed to clarify whether such surgery is merely a diversion to stimulate the whims of the gynecologic/urologic surgeon or a real advance in an area already clouded by uncertainty with respect to outcome and outcome assessment.
AdvAntAges Postoperative pain and recovery Laparoscopic surgery is frequently heralded as progress on the basis of smaller wounds leading to less postoperative pain and a faster recovery. While there is some evidence that postoperative pain is reduced, there are also randomized studies in which patients are blinded to the type of intervention (laparoscopic or open) and have been unaware, both in pain or speed of recovery, of which operation was performed. It is possible that factors other than wound size may influence postoperative pain in which case reconstructive procedures might be expected to gain more from the laparoscopic approach than ablative procedures such as hysterectomy. Furthermore, the avoidance of digital manipulation by gloved hands and abdominal packs should reduce the risk of ileus which is common following procedures such as open sacrocolpopexy. Small, fine instruments may produce less tissue trauma and reduce postoperative pain. It is also possible that less tissue trauma may induce less fibrosis which may be an important component of a successful repair procedure. These questions can only be answered by wellconducted, randomized trials. There have been very few performed to date.
visualization The view of the deep pelvis (including the pelvic floor) is better through the laparoscope than through either a low transverse or a longitudinal incision. Since a fundamental requirement of good surgery is clear visualization of the anatomy, surgery through the laparoscope should have an advantage. In addition, access to new areas with the clearer visualization provides the opportunity to develop pelvic floor reconstructive surgery. This area needs further study.
dIsAdvAntAges/Problems new skills training The learning of new laparoscopic surgical skills is a challenge for both the inexperienced and the experienced surgeon. Some surgeons are temperamentally happier with open surgery and should not be pushed into laparoscopic surgery unless there is clear evidence (as with laparoscopic surgery for ectopic pregnancy) that the open alternative is inferior. The surgeon is but one member of the theater team and it is equally important that all members of the theater staff receive training, particularly in the use of the complex range of new equipment that is often required. As with all surgery, medical staff must be appropriately accredited before they undertake laparoscopic procedures to minimize the influence of the learning curve on the outcome of the procedure. There is some evidence from the published series on laparoscopic colposuspension that surgical inexperience had a significant influence on the stress incontinence cure rate. Furthermore, established procedures should not be modified to accommodate surgical ineptitude while still attributing the same prognosis for the procedure; for example, a colposuspension performed with mesh and staples is not necessarily the same procedure as one performed with sutures. Anesthetic risks are also important and the use of high CO2 pressures and the steep Trendelenburg position for prolonged periods may cause additional problems for the patient. While obese patients may gain from laparoscopic surgery by a reduction in wound infections, they also provide additional challenges with ventilation.
managing complications The chapter in this section on complications and their management (Chapter 87) highlights the need to appraise patients of the potential hazards of laparoscopic surgery which include the risks peculiar to the laparoscopic approach in addition to the reconstructive procedure itself. Patient expectations of risk and prognosis may be different following ‘minimally invasive’ surgery and they must be advised that such surgery may result in significant complications including laparotomy and visceral injury. The mindset of patients and staff must be adjusted to recognize problems when they occur and to respond rapidly. The use of day case facilities and rapid discharge from hospital must include the easy provision of telephone advice and access to hospital for immediate review if required.
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82 Pelvic anatomy through the laparoscope Edmund Edi-Osagie
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INTRODUCTION Gynecologic surgeons have advanced the use of the laparoscope as both a diagnostic and a therapeutic tool over the last two decades. The reasons for this include the ease and relative safety with which a laparoscopy can be performed, facilitating diagnosis and treatment of pelvic pathology, and obviating the need for laparotomies with their higher risks and costs to both the patient and healthcare establishment. The modern laparoscope offers access to the pelvis that cannot be obtained by laparotomy, with unequalled and magnified views of the pelvic viscera. These magnified views make it easier to identify and operate on small structures, thereby reducing the overall risks of surgery. This has radically altered the gynecologic approach to pelvic surgery, previously the preserve of abdominal surgeons, allowing the safe laparoscopic accomplishment of sophisticated pelvic surgery such as hysterectomies (total and extended), myomectomies, reversals of tubal sterilization, excision of rectovaginal endometriotic disease, colposuspension, sacrocolpopexy, paravaginal repair, and pelvic lymphadenectomy, as well as resection and re-anastomosis of the ureters, sigmoid colon, and rectum. The safe performance of any, but especially laparoscopic, pelvic surgery is dependent on a comprehensive and thorough knowledge of pelvic anatomy. The effective placement of laparoscopic instruments such as the Veress needle, laparoscope trocar and ancillary ports depends on this knowledge to facilitate surgery and avoid damage to intra-abdominal and pelvic viscera, as well as to correct any damage that might occur. Gynecologic laparoscopic surgery does not necessarily entail totally new operations but rather the application of a new (minimal access) approach to the accomplishment of known gynecologic procedures. It is, however, peculiar in that the magnification it achieves, the pneumoperitoneum and the positioning of the patient can all affect the visualized image and alter the relationships of pelvic viscera. This knowledge is vital for the training and accreditation process for aspiring gynecologic laparoscopic surgeons. This chapter hopes to refresh and update readers’ knowledge of pelvic anatomy that is especially relevant to the safe performance of gynecologic laparoscopic surgery. It does not attempt a didactic description of all pelvic anatomy, as there are many notable published texts that do this perfectly, but will instead relate various pertinent aspects of pelvic anatomy to gynecologic laparoscopic surgery. It sets out by reviewing the anatomy of the anterior abdominal wall and then reviews the pelvic walls, peritoneum and viscera, relating them to gynecologic laparoscopic surgery and highlighting poten-
tial areas of difficulty and pitfalls that might befall the unwary during such surgery.
Anterior abdominal wall The anterior abdominal wall (Fig. 82.1) consists of several layers of tissue including, from outside in: 1. Skin – attaches loosely to the underlying subcutaneous connective tissue except at the umbilicus where it is firmly adherent; 2. Subcutaneous tissue – consists of two distinct layers, the superficial fatty layer (Camper’s fascia) and the deep membranous layer (Scarpa’s fascia); 3. Fatty layer; 4. Muscle layer – consists of the five muscles of the abdominal wall, i.e. the internal and external oblique, transversus and rectus abdominis, and pyramidalis muscles. The internal and external oblique and transversus abdominis muscles end anteriorly in a strong sheet-like aponeurosis (the rectus sheet) which interlaces with that from the opposite side at the linea alba (white line). All the layers of the linea alba fuse at the umbilicus to create a defect (the umbilical ring) directly underneath, making the umbilical site the thinnest part of the anterior abdominal wall and very amenable to laparoscope ports; 5. Deep fascia – consists essentially of the fascia investing the external oblique muscle as well as the transversalis fascia, a firm membranous sheet that lines most of the abdomen; 6. Endoabdominal fat and fascia – essentially a potential space (of Bogros); 7. Parietal peritoneum. The umbilicus overlies the fourth lumbar vertebra, the most anterior point of the lumbar lordosis, in 67% of people. However, the level of the umbilicus appears to descend with age and in the overweight, altering its relationship to the internal organs (such as the aorta and rectum) that remain fixed. Knowledge of this should help to ensure safe introduction of the Veress needle and other umbilical ports in these groups of patients.
Pelvic wall The pelvic wall consists of bony, ligamentous, and muscular components, and houses the pelvic cavity, which communicates superiorly with the abdominal cavity. The pelvic brim artificially divides the pelvic cavity into superior (the greater or false pelvis) and inferior (the
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a
b
lesser or true pelvis) compartments (Fig. 82.2). The pelvic girdle (bony pelvis) forms a protective wall around the pelvis and is made up of the two hipbones (each consisting of the pubis, ilium, and ischium), the sacrum, and the coccyx. The bodies and rami of the pubic bones and the pubic symphysis form the anterior pelvic wall, while the lateral pelvic walls are formed by the hipbones covered by the obturator internus muscle, the obtura-
Figure 82.1. Transverse section of the anterior abdominal wall: (a) at the level of the umbilicus; (b) below the level of the umbilicus.
tor nerves and vessels, and branches of the internal iliac vessels (Fig. 82.3). The posterior pelvic wall is formed by the sacrum and coccyx. The pelvic diaphragm, consisting of the levator ani and coccygeus muscles and their fascia, is stretched between the pubis anteriorly, the coccyx posteriorly and both lateral pelvic walls, and forms the inferior wall of the pelvic cavity. The levator ani muscles consist of the
Figure 82.2. Coronal section of the abdominopelvic cavity showing the greater (false) and lesser (true) pelvis separated by the pelvic brim. 1155
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Sacral promontory
Obturator nerve
Anterior sacroiliac ligament Psoas fascia Obturator internus fascia Greater sciatic foramen Sacrospinous ligament
Lesser sciatic foramen
Gluteus maximus Ischial tuberosity
Symphysis pubis
a
Inferior pubic ligament
Obturator membrane
Ureter
Lumbosacral trunk
Internal iliac artery Piriformis muscle
Inferior epigastric artery and vein Obturator nerve Obturator internus muscle
Coccygeus muscle Gluteus maximus
b
Pubococcygeus muscle
Perineal artery and nerve
pubococcygeus (which encircles and supports the urethra, vagina, and anal canal), the puborectalis (which forms a U-shaped muscular sling that passes posterior to the anorectal junction), and the iliococcygeus (the posterior-most part of the levators). The levator ani muscles and pelvic fascia are susceptible to damage by stretching or tearing during childbirth, often leading to an alteration of the position of the bladder neck and urethra and/or anorectal flexure, predisposing to urinary and/ or fecal incontinence.
Pelvic peritoneum, fascia, fossae and ligaments Peritoneum is a continuous, glistening, transparent serous membrane that lines the abdominal and pelvic cavities and invests their viscera. It consists of two layers, both made up of mesothelium: the parietal layer
Figure 82.3. Medial view of the structures which make up the walls and floor of the true pelvis: (a) the bony and ligamentous structures of the pelvic wall; (b) the muscular, nervous and vascular structures of the pelvic wall.
lines the internal surface of the abdominal and pelvic walls while the visceral layer invests the viscera. The peritoneal cavity is therefore a potential space between the parietal and visceral peritoneum that contains no organs and only a thin layer of fluid to keep its surfaces moist. A good understanding of the anatomy of this space is vital to safe performance of laparoscopy as the Veress needle, gas for insufflation, and all laparoscopic ports are inserted into this space. Peritoneum relates to abdominopelvic viscera in one of two ways: intraperitoneal where the viscus is completely covered by visceral peritoneum, or extraperitoneal (retroperitoneal) where the viscus is only partially covered by peritoneum. Viewed from anterior to posterior through the laparoscope (Fig. 82.4), pelvic peritoneum covers the: 1. retropubic space of Retzius – a potential space that lies behind the pubic symphysis and in front of the
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Suspensory ligament of ovary (infundibulopelvic ligament) Lateral umbilical ligament Medial umbilical ligament Fallopian tube Ovary Round ligament
Rectouterine fold
Vesicouterine pouch
Rectouterine pouch Levator ani
Pubic symphysis Anal canal
Urinary bladder
Uterus Vagina Pubovesical ligament
Urethra
Labium Labium minus majus
bladder, and is normally occupied only by venous plexuses; 2. transverse vesical fold on the bladder; 3. vesicouterine pouch between the bladder and the uterine isthmus; 4. opening of the vesicouterine pouch – leading to the vesicouterine septum that ends inferiorly in the fascia between the ureters and vagina; 5. body of the uterus and its appendages; 6. rectouterine pouch (of Douglas) – bordered anteriorly by the vagina and uterus, posteriorly by the rectum and its fascia, and laterally by the rectouterine folds that extend posteriorly towards the pararectal fossae; 7. opening of the rectouterine pouch – leading to the rectovaginal septum that ends at the union of the two uterosacral ligaments behind the cervix; 8. retrorectal space – situated between the rectal and retrorectal fascia. Laterally, pelvic peritoneum covers the lateral pelvic wall overlying the common iliac vessels and their continuations (the internal and external iliac vessels) and the obturator membrane and fascia. Peritoneal reflections over the pelvic organs give rise to five umbilical peritoneal folds, which in turn give rise to five peritoneal fossae (see Fig. 82.1):
Figure 82.4. Median section of the pelvis showing the pelvic organs and their peritoneal reflections.
1. Median umbilical fold – extending from the apex of the bladder to the umbilicus and covering the median umbilical ligament, which is the remnant of the urachus (reduced allantoic stalk) that joined the fetal bladder to the umbilicus; 2. Two medial umbilical folds – lying on either side of the midline lateral to the median folds and covering the medial umbilical ligaments, which contain the remnants of the occluded fetal umbilical arteries; 3. Two lateral umbilical folds – lying on either side of the midline lateral to the medial folds and covering the inferior epigastric vessels. These umbilical folds give rise to five peritoneal fossae: 1. Supravesical fossa – lying between the medial umbilical folds and bisected by the median umbilical fold; 2. Two medial inguinal fossae – lying on each side between the medial and lateral umbilical folds; 3. Two lateral inguinal fossae –lying on each side lateral to the lateral umbilical folds and containing the inguinal rings. Peritoneal relationships with the pelvic viscera give rise to specific mesenteries, ligaments, and fossae. The 1157
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broad ligament is a double layer of peritoneum extending from the uterus to the pelvic sidewalls and consisting of three peritoneal mesenteries: funicular (round ligament) meso, mesosalpinx and meso-ovarium (see Fig. 82.4). 1. The funicular meso (mesentery of the round ligament) extends from the uterine horn to the deep inguinal ring. Opening this mesentery provides access to the paravesical fossa which is bounded superiorly by the umbilical artery medially and iliac vascular pedicle laterally, and inferiorly by the levator ani muscles and Cooper’s ligament. The paravesical space contains the obturator nerve, the obturator and external iliac lymph nodes, and sometimes an accessory obturator vein. 2. The mesosalpinx (mesentery of the fallopian tube) is triangular when spread out and contains vascular archways (infratubal, infraovarian, and tubal branches of the ovarian vessels) and the infratubal nervous plexus. It is bordered superiorly by the fallopian tube and infundibulopelvic ligaments and laterally by the tubo-ovarian ligament and Richard’s fimbrial fringe. 3. The meso-ovarium (mesentery of the ovary) contains the ovarian vessels and nerves. The pre-ovarian fossa is triangle-shaped and lies between the funicular meso anteriorly, the mesosalpinx posteriorly, the external iliac vessels laterally, and the uterine horns medially. It overlies the obturator fossa and is opposite the appendix on the right and sigmoid colon on the left. The tubo-ovarian recess lies between the mesosalpinx and the meso-ovarium, while the ovarian fossa lies between the meso-ovarium anteriorly, the iliac vessels laterally, and the ureters and uterine vessels posteriorly, and overlies the obturator pedicle which contains the obturator nerves. The infundibulopelvic ligament contains the ovarian vessels and lies lateral to the ovary, crossing the external iliac vessels approximately 2 cm anterior to the ureter, and ending on the tubal extremity of the ovary. The ovarian ligament attaches the medial end of the ovary to the uterine horn below and behind the fallopian tube. The pararectal fossa opens superiorly into the sacroiliac sinus and is bordered anteriorly by the paracervix, medially by the rectum and uterosacral folds, laterally by the piriformis muscle, inferiorly by the levator ani muscle, and posteriorly by the lateral rectal ligament. The ureter runs across the pararectal fossa underneath peritoneum. There are two distinct types of pelvic cellular tissue: slack tissues (easily dissected) and dense tissues (fascia
and visceral ligaments). The slack tissues contain mostly areolar tissue and are predominant in the retropubic, paravesical, pararectal, and retrorectal spaces, and the vesicovaginal and rectovaginal septa. The dense tissues include the pelvic parietal and visceral fasciae. Pelvic fascia is a dense conjunctive lamina covering the pelvic wall (parietal pelvic fascia or urogenital diaphragm); it also forms the adventitia of the pelvic viscera (visceral pelvic fascia). Parietal pelvic fascia forms an effective support for the pelvic organs because of its continuity with the visceral pelvic fascia which invests the visceral subperitoneal surfaces of the organs. The density of the parietal pelvic fascia is variable and its deficiency in the midline leads to uterovaginal prolapse. Knowledge of the distribution and relationships of this fascia is therefore vital to successful repair of uterovaginal prolapse. The architecture of pelvic cellular tissue resembles a mesh, with traction at one point provoking shortening of the fibers and mesh densification: the greater the traction, the more pronounced the densification near the point of traction. The pelvic fasciae exchange fibers, making anatomic relationships tight and surgical dissection more difficult, thereby increasing the risks of visceral injury, particularly around the points of connection between parietal and visceral fasciae. Pelvic visceral ligaments arise from densifications of pelvic cellular tissue whose visceral insertions intermingle with the perivisceral fascia and are generally of two types: 1. lateral ligaments which relate to the internal iliac arteries and include the vesical, genital, and rectal ligaments; 2. sagittal ligaments which relate to the branches of the inferior hypogastric plexus and include the uterosacral, vesicouterine, and pubovesical ligaments. The vesical ligament is located around the anterior vesical arteries (branches of the umbilical artery) and attaches to the paracervix anteriorly. The genital ligament is the strongest of the pelvic ligaments, attaches the uterus to the pelvic sidewall, and provides its main support. It has three constituent parts: the parametrium, paracervix, and paravagina. The parametrium lies just above the ureters and contains the uterine vessels and lymphatics, while the paracervix lies beneath the ureters and contains the vaginal arteries and venous plexus and the uterovaginal lymph nodes. The rectal ligament is located around the middle rectal vessels, is thick and disposed almost transversely on each side of the rectum, separating the retrorectal from the pararectal space. The uterosacral ligaments arise from the posterolateral
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aspects of the cervix and vaginal fornix, the fibers from opposite sides intermingling at the point of origin from the uterus to form the torus uterinus. The ligament runs alongside the lateral aspects of the rectum to fan out into the sacral foramina of S2–S4. It contains few blood vessels but carries the inferior hypogastric nervous plexus of Lee and Frankenhauser. The vesicouterine ligaments extend from the uterine isthmus and cervix to the area around the urethral meatus in front of the parametrium. The pubovesical ligaments extend from the posterior wall of the symphysis pubis to the bladder neck.
peritoneum and relates anteriorly to the vesicouterine pouch and bladder, posteriorly to the rectouterine pouch and rectum, and laterally to the broad ligaments, transverse cervical ligaments, and ureters (see Fig. 82.4). The uterus gets its blood supply from the uterine arteries (Fig. 82.7) and nerve supply from the uterovaginal plexus, and has both passive (transverse cervical and uterosacral ligaments) and dynamic (pelvic diaphragm) supports. The fallopian tubes average 10 cm in length and extend laterally from the uterine horns along the free
Reproductive system The vagina averages 7–9 cm in length, links the cervix with the vestibule, and is bordered anteriorly by the bladder and urethra, posteriorly by the rectovaginal pouch, rectum and anal canal, and laterally by the ureters, visceral pelvic fascia, and levator ani (Fig. 82.5). It is normally collapsed so its anterior and posterior walls lie together except at its superior end where the cervix holds them apart. Innervation of the upper threequarters of the vagina is visceral from the uterovaginal plexus while the lower one-quarter is somatic from the pudendal nerve; hence only the lower end of the vagina is sensitive to touch and temperature. The uterus consists of a body (which includes the fundus and isthmus) that forms the upper two-thirds and a cervix that makes up the lower third; its position changes with the degree of fullness of the bladder and rectum (Fig. 82.6). It is covered anteriorly and posteriorly by
Ureter
Internal iliac artery and vein
Ureter crossing the pelvic brim Infundibulopelvic ligament Peritoneum Fallopian tube and ovary Uterus Uterosacral ligament Edge of broad ligament Bladder Vagina Anal canal
Figure 82.6. Sagittal section of the pelvis showing the relationships of the pelvic organs and peritoneum.
Sigmoid colon
Fallopian tube and ovary
External iliac artery and vein Round ligament of uterus
Broad ligament Uterine fundus
Uterine artery
Ureteric openings
Vaginal arteries
Trigone of bladder
Pubic bone
Obturator internus Vestibule
Figure 82.5. Anterior view of the lower abdominal and pelvic cavities showing coronal sections of the bladder and anterior pelvis. Part of the superior rami and bodies of the pubic bones, anterior aspect of the bladder, right adnexal structures, and peritoneum covering the right lateral pelvic wall are removed for illustration. 1159
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Uterus
Pampiniform plexus of veins Internal iliac artery
Fallopian tube
Ovarian artery and vein
Ovary Ligament of ovary Ureter
Uterine artery and vein
Uterine plexus
Vaginal artery and vein
Internal pudendal artery and vein
Vaginal plexus
Vagina
Figure 82.7. Posterior view of blood supply and venous drainage of the uterus, vagina, fallopian tubes and ovaries. edge of the mesosalpinx to open into the peritoneal cavity near the ovaries. They derive their blood supply from the tubal branches of the uterine and ovarian arteries and are innervated jointly by the uterine and ovarian nervous plexuses. The ovaries are located on the pelvic sidewalls suspended by the meso-ovarium and held in position by the ovarian ligaments medially and infundibulopelvic ligaments laterally, through which they receive the ovarian vessels and nervous plexuses.
Urinary system The lumbar ureter lies on the psoas muscle on each side of the rachis and is usually only of significance to gynecologic oncologists who perform lymphadenectomy. After descending into the pelvis, the right ureter crosses anterior to the external iliac artery near its origin while the left ureter crosses anterior to the distal end of the common iliac artery. The descending ureter maintains a close relationship with the infundibulopelvic ligament that crosses it and so it is liable to injury during surgery involving this ligament and/or the ovaries (see Fig. 82.6). Laterally, the ureter is adjacent to the internal iliac vein and in close proximity to the obturator nerve and vessels, as well as the umbilical, uterine and vaginal vessels. It is easy to identify in this position in slim patients because of its characteristic peristaltic motion under the peritoneum. The retroligamentary ureter runs forwards and medially along the posteromedial aspect of the uterine artery
towards the origin of the uterosacral ligament, where it is normally only 1–3 cm from the ligament. This relationship could be altered by endometriosis, cancer, infection or previous surgery, sometimes bringing the ureter into closer proximity to the uterosacral ligament and/or ovary. The intraligamentary ureter is not visible to the gynecologic surgeon and runs anteriorly across the transverse cervical ligament towards the bladder, crossing beneath the uterine artery at a point approximately 1.5 cm from the uterine isthmus and 1 cm from the lateral vaginal fornix. Diseases such as endometriosis can alter its relationships around this point, significantly increasing the risks of injury during procedures such as laparoscopic hysterectomy. The retrovesical ureter enters the vesical extremity of the vesicouterine ligament to reach the bladder. The ureter derives its blood supply from contributions from the renal, ovarian, common iliac and uterine arteries: these branches divide into a T-shape on reaching the ureter to form a rich surrounding adventitial network and anastomosis that compensate for vascular interruptions, thus allowing dissection of the ureter over long distances. In addition to knowledge of the course and relationships of both ureters, it is also important to appreciate the subtle differences between the right and left ureters, and to be able to identify, dissect, and protect the ureters from surgical injury (Fig. 82.8). Mobilizing the uterus anteriorly often helps to localize the ascending segment of the uterine artery correctly without altering the posi-
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• posteriorly by the inferolateral aspect of the bladder, the urethra, and pelvic vagina;
• laterally by the superior pubic ramus and pectineal ligament (of Cooper);
• inferiorly by the pelvic diaphragm.
Figure 82.8. Course of the pelvic ureter showing the three points where it is at most risk of surgical injury: (1) where it crosses the iliac vessels; (2) where it crosses the uterine artery; (3) at the level of the vaginal fornix. tion of the ureter. Transecting the correctly localized uterine artery at the level of the uterine isthmus, and pulling its proximal end laterally, helps to mobilize the ureter away from the uterus, further protecting it from injury. Similarly, opening the vesicouterine space to dissect out and mobilize the retrovesical ureter from the vesicouterine ligament can help to protect the ureter. The retropubic space (of Retzius) is an anterior preperitoneal space containing mostly loose fatty tissue; it is bordered:
• anteriorly by the pubic symphysis, pubovesical ligaments, tendinous arch of the parietal pelvic fascia, and retropubic branches of the obturator and pudendal nerves;
The vesical base of the retropubic space includes the trigone and retrotrigonal fossa; it increases in depth with age, a factor in the causation of postmicturition dribbling. The urethrovesical junction is situated approximately 2.5 cm from the pubic symphysis to which it is secured by the pubovesical ligaments to create an angle of 90–100 degrees between the urethra and bladder base, an angle that is crucial for urinary continence. The urethra descends inferiorly and anteriorly at an angle of 30 degrees from the vertical and is conventionally divided into three segments: supradiaphragmatic, diaphragmatic, and infradiaphragmatic. The pubovesical ligaments support the supradiaphragmatic urethra while the infradiaphragmatic urethra is supported by the pubourethral ligament and suspensory ligament of the clitoris. Urinary continence and micturition require cooperation and synergy between the bladder, urethra, and abdominopelvic pressure. During bladder filling, abdominopelvic pressure acts as a passive occlusive force on the supradiaphragmatic urethra, apposing the pelvic diaphragm against which the urethra pushes. During the micturition phase, the combined higher intravesical pressure and intraparietal tension caused by detrusor contractions are directed towards the urethrovesical junction, overcoming the urethral closure pressure and leading to opening of the urethra. Weakness or loss of the normal angle of the urethrovesical junction and shortening or increased horizontalization of the urethra predispose to urinary stress incontinence.
Intestinal system The common laparoscopic gynecologic operations do not involve the intestinal system but adequate knowledge of the pelvic part of this system is important for safe surgery. The rectum is at considerable risk of injury during certain procedures such as resection of rectovaginal endometriotic disease, surgery for pelvic cancer, and sacrocolpopexy. Placing a patient in the Trendelenburg position normally utilized for gynecologic laparoscopic surgery effectively moves most of the intestines out of the pelvis, leaving only the sigmoid colon and rectum. 1161
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The rectosigmoid junction overlies the S3 vertebra and is marked by discontinuation of the fatty omental appendices and a spreading out of the teniae of the sigmoid to form a continuous outer longitudinal layer of smooth muscle. The rectum follows the curve of the sacrum and coccyx (the sacral flexure) and ends anteroinferior to the tip of the coccyx by turning sharply posteroinferiorly (the anorectal flexure) as it perforates the pelvic diaphragm to become the anal canal. The anorectal flexure is maintained at an angle of approximately 80 degrees by the puborectalis muscle, a vital function for fecal continence. The dilated terminal end of the rectum (ampulla) lies directly above and is supported by the pelvic diaphragm and anococcygeal ligament, and acts as a reservoir for feces pending defecation. Peritoneum covers the anterior and lateral surfaces of the superior third of the rectum, only the anterior surface of the middle third, and none of the inferior third (the subperitoneal portion). Medially the visceral peritoneum over the rectum is reflected forward onto the vagina to form the rectouterine pouch (beneath which lies the rectovaginal septum) while laterally it is reflected onto the pelvic wall to form the pararectal fossae.
Pelvic vascular system The pelvis derives its vascular supply mainly from two paired (internal iliac and ovarian) and two unpaired (median sacral and superior rectal) arteries. The internal iliac artery arises from the bifurcation of the common iliac artery at the point where it is crossed by the ureter anterior to the sacroiliac joint, and descends posteriorly along the pelvic wall to the greater sciatic foramen (GSF). There, it divides into anterior (visceral) and posterior (parietal) branches to provide most of the blood supply to the pelvis. The visceral branch gives off the umbilical, uterine, vaginal, obturator, middle rectal, and internal pudendal arteries while the parietal branch gives off the iliolumbar, lateral sacral, and superior gluteal arteries. The umbilical artery runs along the superior aspect of the inferolateral part of the bladder to end as the superior vesical artery and constitutes a surgical landmark denoting the origin of the uterine artery. The uterine artery consists of three segments:
• from its origin, the parietal segment descends on the pelvic sidewall down to the ischial spine accompanied by the umbilical and obturator arteries anteriorly and the ureter medially;
• the parametrial segment runs medially beneath the •
parametrium and anterior to the ureter surrounded by lymph nodes and venous plexuses; the tortuous mesometrial segment runs alongside the lateral aspect of the uterus in the mesometrium accompanied by the uterine venous plexus, lymphatic vessels, and sometimes parauterine lymph nodes.
The uterine artery gives off several collateral branches including vesicovaginal, cervicovaginal, sinuous cervical, corporeal, and round ligament branches.
• The vaginal artery runs posterior to the uterine artery • • •
• • •
to supply the vagina. The obturator artery runs anteriorly towards the obturator foramen in between the obturator nerve above and obturator vein below. The middle rectal artery descends inferiorly and medially towards the lateral aspect of the rectum and into the lateral rectal fossa. The internal pudendal artery accompanies the pudendal nerve into the perineum, leaving the pelvis through the GSF and passing round the sciatic spine, penetrating the ischiorectal fascia and running along the pudendal canal to end in two branches – the deep and the dorsal arteries of the clitoris. The ovarian artery emerges from the abdominal aorta at the level of the L2 vertebra and descends to reach the ovary through the infundibulopelvic ligament. The superior rectal artery emerges from the inferior mesenteric artery to run in the superior rectal ligament to supply the rectum. The median sacral artery arises from the posterior aspect of the aorta just above its bifurcation and descends on the anterior aspect of the L4 and L5 vertebrae and the sacrum. This artery is exposed to significant risks of injury in this position during the tissue stripping and fixation that is undertaken for laparoscopic sacrocolpopexy or pelvic lymphadenectomy.
In the vast majority (80%) of people the umbilicus is situated at a level that is within 2 cm of the aortic bifurcation, and in slim people it often overlies the bifurcation or left common iliac vessels, placing them at significant risk of injury during umbilical port placement. This risk is further magnified in very slim women in whom the aorta could be less than 3 cm from the anterior abdominal wall. The lumbar lordosis sags on placing a patient in the modified lithotomy position that is normally utilized
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for gynecologic laparoscopic surgery, effectively moving the aorta further away from the anterior abdominal wall. Manually elevating the anterior abdominal wall and ensuring there is adequate pneumoperitoneum before trocar placement achieves the same objective.
Pelvic lymphatic system The pelvic lymphatic system consists of groups of lymph nodes organized around major pelvic blood vessels to drain the pelvic organs: 1. Lumbar (lateral aortic) nodes – drain the ureters, uterus, fallopian tubes, ovaries, and rectum; 2. Inferior mesenteric nodes – drain the rectum; 3. Common iliac nodes – drain the ureters, bladder, and vagina; 4. External iliac nodes – drain the ureters, bladder, vagina, and uterus; 5. Internal iliac nodes – drain the ureters, bladder, urethra, vagina, uterus, and rectum; 6. Superficial inguinal nodes – drain the urethra, vagina, and uterus; 7. Deep inguinal nodes – drain the urethra; 8. Sacral nodes – drain the bladder, urethra, vagina, and uterus; 9. Pararectal nodes – drain the rectum.
Pelvic nervous system The sacral and coccygeal nerves and the pelvic part of the autonomic nervous system form the main innervations of the pelvis.
Sacral plexus The sacral nervous plexus is located on the posterior wall of the lesser (true) pelvis, closely applied to the anterior surface of the piriformis muscle, and gives off two main nerves – the sciatic and pudendal. The sciatic nerve arises from the ventral rami of L4–S3 and leaves the pelvis through the GSF to supply the posterior aspects of the lower limbs. The pudendal nerve arises from the anterior divisions of the ventral rami of S2–S4, accompanies the internal pudendal artery out of the pelvis through the GSF, and hooks round the ischial spine and sacrospinous ligament to enter the perineum through the lesser sciatic foramen. It supplies the skin and muscles of the perineum and terminates as the dorsal nerve of the clitoris. The pudendal nerve also supplies visceral branches to the bladder, the reproductive organs, and the rectum, pro-
viding sensory innervation and the nervous control of micturition and defecation. The superior gluteal nerve arises from the posterior divisions of the ventral rami of L4–S1 and leaves the pelvis through the GSF to supply the gluteal muscles. The inferior gluteal nerve arises from the posterior divisions of the ventral rami of L5–S2 and leaves the pelvis through the GSF to supply the gluteus maximus muscle.
Obturator nerve The obturator nerve arises from the lumbar nervous plexus (L2–L4) in the greater pelvis and enters the lesser pelvis through the GSF to run in the extraperitoneal fat along the lateral wall to the obturator canal. It divides into anterior and posterior branches that leave the pelvis through this canal to supply the medial thigh muscles.
Coccygeal plexus The coccygeal plexus is a small network of nerve fibers formed by the ventral rami of S4 and S5, and the coccygeal nerves. It lies on the pelvic surface of the coccygeus muscle and supplies this muscle, part of the levator ani and the sacrococcygeal joint. It gives off the anococcygeal nerves, which pierce the sacrotuberous ligament to supply an area of skin in the coccygeal region.
Pelvic autonomic nerves The sacral sympathetic trunks are the inferior continuation of the lumbar sympathetic trunks and have the primary function of providing postsynaptic fibers to the sacral plexus for sympathetic (vasomotor, pilomotor, sudomotor) innervation of the lower limbs. They contain four sympathetic ganglia each, and descend on the pelvic surface of the sacrum medial to the sacral foramina to converge into the small ganglion impar (coccygeal ganglion) anterior to the coccyx. These send communicating branches to each of the ventral rami of the sacral and coccygeal nerves and small branches to the median sacral artery and inferior hypogastric plexus. The hypogastric plexuses consist of two networks of autonomic nerves – superior and inferior. The superior hypogastric plexus lies just inferior to the bifurcation of the aorta at the level of L5 and descends into the pelvis on either side anterior to the sacrum as the right and left hypogastric nerves. These descend within the hypogastric sheaths lateral to the rectum and then spread out in a fan-like fashion to merge with the pelvic splanchnic nerves and form the inferior hypogastric plexus. The 1163
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inferior hypogastric plexus (Lee and Frankenhauser’s ganglion) is a 4 cm long nervous quadrilateral lamina located in the lateral aspect of the uterosacral ligament. Extensions of this plexus (the pelvic plexus) pass to the cervix, lateral vaginal fornices, and the inferolateral surfaces of the bladder. Pelvic splanchnic nerves contain parasympathetic fibers from S2–S4 spinal cord segments, and visceral efferent fibers from cell bodies in the spinal ganglia of the corresponding spinal nerves. The inferior hypogastric and pelvic plexuses thus contain both sympathetic and parasympathetic fibers, which pass along the branches of the internal iliac arteries to form subplexuses (rectal, visceral, uterovaginal) on the pelvic viscera. The ovarian plexus originates from the aortic plexus to innervate the ovaries and distal half of the fallopian tubes and receives parasympathetic fibers from the pneumogastric nerve, explaining the vagal intestinal response to ovarian manipulation or torsion. The motor response to pelvic nociceptive stimuli correlates with pelvic innervation. For instance, the parietal pain of acute salpingitis is in fact pain from a viscus transmitted through the closest somatic nerve into the corresponding iliac fossa. The dyspareunia associated with rectovaginal endometriotic disease is accentuated by stimulation of the sympathetic fibers inside the rectovaginal septum causing the sympathetic motor cells to induce a reflex contraction of the pelvic diaphragm. Laparoscopic surgery, by avoiding large abdominal incisions, avoids transection of the anterior branches of the iliohypogastric and ilioinguinal nerves, which can lead to reversible cutaneous anesthesia of the pubic region, the insides of the upper thighs, and the labia majora, as well as weakness of the muscles of the anterior abdominal wall predisposing to hernia formation. Attention should therefore be paid to correct localization and closure of lateral ports to avoid nerve injury during port placement or nerve entrapment in a stitch during fascial closure of port sites that are placed too close to the anterior superior iliac spines. Such nerve entrapments could give rise to unexplained abdominal pain that only resolves with removal of the stitch. The obturator nerves may become affected by pelvic endometriotic disease or infection at the level of the obturator foramen, leading to obturator neuralgia on the superomedial aspect of the thighs and knees.
Acknowledgments I am grateful to Mr Harry Heyes of the Medical Illustration Department of Central Manchester and Manchester Children’s University Hospitals Trust for
meticulously producing the color images used throughout this chapter.
Bibliography 1. Abu-Rustum NR. Laparoscopy 2003: oncologic perspective. Clin Obstet Gynecol 2003;46:61–9. 2. Bradley WE. Neural control of urethrovesical function. Clin Obstet Gynecol 1978;21:653–67. 3. Cahill DR, Orland MJ, Miller G. Atlas of Human Crosssectional Anatomy, 3rd ed. New York: Wiley-Liss, 1996. 4. Dargent D. Laparoscopic surgery in gynaecologic oncology. J Gynecol Obstet Biol Reprod 2000;29:282–4. 5. Donnez J, Chantraine F, Nisolle M. Complications of laparoscopic surgery in gynecology. In: Donnez J, Nisolle M (eds) An Atlas of Operative Laparoscopy and Hysteroscopy, 2nd ed. New York: Parthenon, 2001; 373–87. 6. Ellis H. Clinical Anatomy. A Revision and Applied Anatomy for Clinical Students, 8th ed. Oxford: Blackwell Scientific, 1992. 7. Faucheron JL. Surgical anatomy of pelvic nerves. Ann Chir 1999;53:985–9. 8. Fauconnier A, Delmas V, Lassau JP et al. Ventral tethering of the vagina and its role in the kinetics of urethra and bladder neck straining. Surg Radiol Anat 1996;18:81–7. 9. Healy JE Jr, Hodge J. Surgical Anatomy, 2nd ed. Toronto: BC Decker, 1990. 10. Moore KL, Dalley AF. Clinically Oriented Anatomy, 4th ed. Baltimore: Lippincott, Williams and Wilkins, 1999. 11. Nezhat CH, Nezhat F, Brill AI et al. Normal variations of abdominal and pelvic anatomy evaluated at laparoscopy. Obstet Gynecol 1999;94:238–42. 12. Ploteau S, Donnez J. Anatomy in relation to gynecological endoscopy. In: Donnez J, Nisolle M (eds) An Atlas of Operative Laparoscopy and Hysteroscopy, 2nd ed. New York: Parthenon, 2001; 33–45. 13. Robert R, Brunet C, Faure A et al. Surgery of the pudendal nerve in various types of perineal pain: course and results. Chirurgie 1993–94;119:535–9. 14. Robert R, Prat-Pradal D, Labat JJ et al. Anatomic basis of chronic pelvic pain: role of the pudendal nerve. Surg Radiol Anat 1998;20:93–8. 15. Weber AM. New approaches to surgery for urinary incontinence and pelvic organ prolapse from the laparoscopic perspective. Clin Obstet Gynecol 2003;46:44–60. 16. Williams PL, Bannister LH, Berry MM, Collins P, Dussek JE, Ferguson MWJ (eds) Gray’s Anatomy, 38th ed. Edinburgh: Churchill Livingstone, 1995. 17. Woodburne RD, Burkel WE. Essentials of Human Anatomy, 9th ed. New York: Oxford University Press, 1994.
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83 Laparoscopic treatment of pelvic pain Christopher Sutton, Richard Dover
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INTRODUCTION Pelvic pain is a common symptom among women of reproductive age, and its diagnosis and management constitute a considerable part of a gynecologist’s workload. Women with acute pain usually present via the Accident and Emergency department. The pain is usually severe and of recent onset, and requires skilled assessment in order to distinguish gynecologic causes from diseases of adjacent organs or structures (Table 83.1). Pelvic pain of more than 6 months’ duration is usually labeled as chronic pelvic pain, and the differential diagnosis is usually more complex and requires careful evaluation of the physical, psychological, and emotional state of the patient1 (Table 83.2). Table 83.1.
Causes of acute pelvic pain
Gynecologic
Non-gynecologic
Uterus miscarriage acute degeneration of fibroid endometritis perforation (after insertion of IUCD/surgery) Fallopian tubes ectopic pregnancy acute salpingitis torsion (e.g. hydrosalpinx) Ovary cyst accident/ovulation torsion tubo-ovarian abscess metabolic idiopathic
Gastrointestinal appendicitis diverticulitis obstruction (adhesions/ volvulus) constipation ischemia gastroenteritis Urologic cystitis/pyelonephritis renal/ureteric colic retention Other musculoskeletal
IUCD, intrauterine contraceptive device.
Table 83.2.
Causes of chronic pelvic pain
Gynecologic
Non-gynecologic
Uterus primary dysmenorrhea adenomyosis fibroids Fallopian tube chronic salpingitis Ovary benign and malignant cysts endometriotic cysts entrapment by adhesions remnant syndrome General endometriosis venous congestion
Gastrointestinal adhesions constipation diverticular disease irritable bowel syndrome Urologica retention urethral syndrome interstitial cystitis Other musculoskeletal nerve entrapment idiopathic
If one overlooks the difficulties of defining the condition, and focuses on the patients themselves, the magnitude and importance of the problem become obvious. One author comments that chronic pelvic pain is responsible for approximately 5% of new gynecological referrals at his hospital,2 but unfortunately there is no community-based study from the UK that allows us to estimate the prevalence of chronic pelvic pain within the whole population. Such a study in the United States has been published, quoting a prevalence rate of 15%.3 This study also made an economic assessment of the problem: in addition to the medical costs associated with hospital attendance and treatments, 15% of the employed women reported time lost from work and 45% reported reduced productivity. Although there is no population-based UK study, a recent paper4 has reviewed all published work and quotes prevalence rates for dysmenorrhea of 45–97% and for abdominal pain of 23–29%. The authors make the valid point that the definitions used vary widely, and that the selection criteria in some cases may not have been truly representative of the population as a whole. The next step, once these patients have been identified, is to attempt to reach a diagnosis. The literature is replete with the potential difficulties of assessment in these women, and stresses the importance of the medical history as potentially the most important part of the process.2,5 The other issue that is constantly highlighted is the possibility of previous sexual abuse, which is more prevalent in women with chronic pelvic pain. This issue in the UK setting has been reviewed by Collett et al.6 Some clinicians have a special interest in this area and will take the time to explore all aspects of the history. However, it is most likely that the patient will undergo a diagnostic laparoscopy. Because of the number of patients who may suffer from pelvic pain it is not surprising that their investigation may account for more than 40% of all laparoscopic procedures in some units.7 The next area of interest is to consider the pathology encountered at the time of the diagnostic laparoscopy. In view of the confusion surrounding the definition of the condition under investigation, it should come as no surprise that the reported findings vary considerably from one unit to the next. It must be remembered, however, that these differences could also be explained in terms of different local referral practices, and the special interest and reputation of the clinician involved. With these reservations in mind, a superficial review of the published literature reveals that, at the time of diagnostic laparoscopy for chronic pelvic pain, the incidence of endometriosis is 16–33.3%, and the incidence of adhesions is 23.1–40%; negative findings may be encountered in 14.8–30% of cases.8–11 There appears
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to be considerable variation in these figures, and other papers quoting negative laparoscopy rates of 65%1 and 10–90%12 do little to clarify the issue. It is possible to discern some common themes from these confusing statements. While the exact proportions may vary considerably, it does appear that endometriosis and pelvic adhesions will be diagnosed in a large subgroup; however, the fact that pathology is demonstrable does not imply that the relationship between it and the symptoms is a causal one. There is also the indisputable fact that diagnostic laparoscopy will be negative in a percentage of patients. One of the reasons for the huge variability in these figures is that, even now, many gynecologists are unable to recognize the protean manifestations of the appearance of endometriosis (Figs 83.1–83.5). The classic appearance of hemosiderin (black powder burns – typical lesions) often represents old burnt-out disease whereas red telangiectases, flame-like lesions, yellow–brown peritoneum, subovarian adhesions, peritoneal defects, and neoangiogenesis (so-called subtle or atypical lesions) are often only recognized by experts in this condition. The rest of this chapter focuses on the various laparoscopic techniques that are available to treat endometriosis and pelvic adhesions and gives some measure of their success. The treatment of other pathologies such as chronic infection will not be covered, but options for laparoscopic treatment in cases where no pathology has been demonstrated are discussed briefly in the section on denervation.
LAPAROSCOPIC TREATMENT OF ENDOMETRIOSIS
rectovaginal septum deposits, and it has been suggested that these are in fact three separate conditions.13 The treatment of disease in each of these sites will be considered separately.
Peritoneal disease Endometriosis of the pelvic peritoneum may be superficial or deep. Indeed it has been suggested that deep deposits (3 mm) may be present in up to 60% of patients with this condition.14 The identification of deep disease
Figure 83.2. Endometriotic vesicular implant (sago-grain) with telangiectases and neoangiogenesis. Note the straight vessels of varying diameter.
Endometriosis may be present in the pelvis in three main areas: peritoneal deposits, ovarian endometriomas, and
Figure 83.1. Red flame-like lesions and telangiectases and marked neoangiogenesis.
Figure 83.3. Glandular tissue-like endometrium and hemorrhagic vesicles secreting large amounts of blood and other substances into a pool in the cul-de-sac. 1167
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Figure 83.4. Peritoneal pouches with endometriosis in the base (Allen–Masters syndrome).
between laser ablation and electrosurgical resection of focal disease is usually a matter of individual preference, but may be influenced by the range of equipment available and the location of the deposits concerned. The relative merits of these two techniques have been covered elsewhere.15 In our center we tend to use carbon dioxide laser vaporization through a second cannula placed laterally (Figs 83.6, 83.7) with a rotating mirror delivery system, employing the laser in super- or ultrapulse mode for more effective cutting. Although an electrosurgical needle is the most common method of treatment for peritoneal disease, on occasions we use excision, especially if the uterosacral ligaments are involved. While most clinicians are familiar with the use of lasers in the operating theater, and will have read papers describing the technique of laser ablation of endometriotic deposits, most would probably be surprised to learn that the first study subjecting this therapy to the rigors of
Figure 83.5. Subovarian adhesion between the interior surface of the ovary and typical deposits of hemosiderin (black lesions).
Figure 83.6. Laparoscopic laser surgery using television monitors on either side of the operating table.
is essential, since treatment – either vaporization or excision – needs to extend down to the level of normal tissue. Failure to appreciate the depth of a lesion may therefore lead to inadequate treatment and incomplete relief of symptoms. This is particularly true for deposits infiltrating deeply into the bladder, which may penetrate through the mucosa and give rise to cyclical hematuria. If this is the case, cure can be achieved only by complete excision of the lesion and laparoscopic suturing of the defect in the bladder, followed by catheter drainage for a ‘urologic week’. Most lesions do not penetrate the full thickness of the bladder wall, but it is important to remove all of the endometriotic implants and the vessels arising from neoangiogenesis that are supplying them. The choice
Figure 83.7. CO2 laser laparoscopy with the laser cannula inserted in the right or left iliac fossa.
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a prospective, randomized, double-blind study was not published until 1994. An earlier report described the use of laser ablation in the treatment of pelvic pain secondary to endometriosis followed up over 5 years by our unit at St Luke’s Hospital, Guildford.16 Of 228 consecutive patients treated for endometriosis, pelvic pain was improved in 126 of 181 women (69.6%) who suffered with it. Thirty-eight patients were no better and second look laparoscopy did not show any sign of endometriosis; however, most of these patients had other diagnoses such as irritable bowel syndrome. Only 17 had recurrent disease during the 5-year study and six were lost to followup (Fig. 83.8). The authors had some reservations about the design of this study because it was retrospective and therefore liable to all the biases inherent in this kind of study, particularly the ability of a surgeon to coerce the patient into saying she is better which often happens because of some innate wish to please the surgeon who performed the operation, whereas in reality she is really no better at all. Such biases can only be eliminated by a double-blind study where neither the patient nor the doctor or nurse following them up is aware of the treatment arm to which the patient had been allocated. Therefore, we consequently embarked on a prospective,
228 patients
Better
Symptoms
Pain and infertility 28
Pain alone 159
Infertility alone 41
Patients treated for Pain 187
Better 126
No better 38
Relapsed 17
Success rate
double-blind, randomized trial.17 Although the findings of this study have been well publicized, there are several interesting aspects that bear closer inspection. The study examined patients with symptoms suggestive of endometriosis who were recruited and then randomized to receive either a diagnostic laparoscopy only, or laparoscopy combined with laser ablation of all visible deposits of endometriosis and uterine nerve transection. Of the patients eligible for analysis, 62.5% of those who received laser therapy reported that symptoms were better or improved. This finding was statistically different from the 22.6% who had improved in the group that received laparoscopy alone (Figs 83.9–83.12). When the results were analyzed stage by stage, it was discovered that response rates were lowest amongst those with stage I disease; if these patients were excluded from the final analysis, then 73.7% of patients with mild or moderate disease obtained benefit. The authors suggested that endometriosis was in fact a chance finding in the group with minimal disease, and was not responsible for their symptoms. Some credence is given to this suggestion by the finding that three of the five women who did not derive benefit from laser ablation had no residual disease when they underwent a
Laser
18/32 (56%)
Expectant
15/32 (48%)
(Z=0.37, p=0.35)
Infertility 69
Lost to follow-up 6+6
Endometriosis alone 56
Pregnant 45
Other factors 7
Still infertile 11
70% pain free Pregnancy rate 80%
Successful outcome 69%
Figure 83.8. Results of laser laparoscopy in patients with Cardoza Fig 83.8 endometriosis.
Figure 83.9. Results of the Guildford trial of laser versus placebo showing very little difference at 3 months.
Better Laser
20/32 (62.5%)
Expectant
7/32 (22.6%)
(Z=2.92, p=<0.01) Figure 83.10. Results of the Guildford trial of laser versus placebo showing statistically different results at 6 months. 1169
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Percentage better
80
Laser Expectant
60 40 20 0
3 months
6 months
Figure 83.11. Guildford double-blind trial of laser versus placebo at 3 and 6 months. Proportion of patients with pain symptom alleviation – all stages.
Pain scores (with time)
9
Laser Expectant
8 7 6 5 4
Before
3 months
6 months
Figure 83.12. Guildford double-blind randomized controlled trial of laser versus placebo. Median visual analog pain scores (with time). Note difference at 6 months. second laparoscopy. This obviously raises doubts about the pathology responsible for their symptoms. It is suggested that, in cases of minimal disease, the diagnosis of endometriosis, which was invariably based on the interpretation of vascular patterns, may have been incorrect. It was suggested that the affected areas should be biopsied at the time of treatment so that a histologic diagnosis is available to help further treatment planning, should the response to laser ablation be suboptimal. This is of more than just academic interest because a diagnosis of endometriosis can have far-reaching consequences for a woman. The other aspect of the study that needs to be considered is that, in the two other patients who showed no improvement after laser laparoscopy, endometriosis had recurred but was not present at the site of previous laser treatment. This reminds us that endometriosis can be an aggressive and progressive condition, and that on some occasions laser surgery may need adjuvant medical therapy.
The patients were followed-up for 1 year after surgery and it is of some significance that, of those who responded initially, symptom relief was maintained in 90%.18 The main criticism directed at this study was that patients in the treatment arm received both laser ablation and uterine nerve transection, and it was therefore unclear which was responsible for the symptomatic benefit.19 To clarify this issue, a second prospective, doubleblind study was undertaken, in which patients were randomized to receive laser ablation either alone or in addition to uterine nerve transection. The results of this study were completely contrary to our expectations which shows the value of a double-blind study when the endpoint is improvement or otherwise of pelvic pain. The study showed that laparoscopic uterine nerve ablation (LUNA) did not add to the beneficial effects of ablation of the implants – in fact the results were almost identical to the earlier study.20 This not only validated the earlier study but also demonstrated that, where pathology is encountered, the addition of a denervation procedure does not provide additional symptomatic relief. These findings were similar to another study by Vercellini et al.,21 which was not double-blind but had larger numbers and a longer period of follow-up.
Ovarian endometriomas These lesions (Fig. 83.13) are readily treated using laparoscopic methods, which are as effective as treatment by laparotomy, but have the benefit of the shorter recovery time associated with endoscopic surgery.22 Therapeutic options are based on either vaporization of the lining of the structure, or stripping of the capsule. Whichever method is adopted, it is paramount that the whole of the internal aspect of the capsule is closely inspected before treatment in order to exclude the presence of an underlying malignancy. The use of multiple biopsies to allow subsequent histologic assessment is encouraged. In our department we aim to completely vaporize the cyst lining using a potassium titanyl phosphate (KTP/532) laser at the time of laparoscopy. Other centers use a carbon dioxide laser and adopt a three-stage approach.23 A retrospective review of all patients treated in this unit over a 10-year period revealed that 74% of patients reported improvement or resolution of their pain, and 57% of those trying for a pregnancy usually conceived in the few months following the operation.24 While this finding is encouraging, it is tempered by the fact that the recurrence rate was 19% during the study period and subsequent 2-year follow-up.25 Several facts need emphasizing, however:
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Figure 83.13. Bilateral ovarian endometriomas firmly adherent to the pelvic sidewall. 1. Not all the endometriomas occurred in the same site, nor indeed the same ovary;
Figure 83.14. Large nodule of deep infiltrating endometriosis (adenomyosis) on the anterior surface of the rectum going down into the rectovaginal septum.
2. This recurrence rate is in broad agreement with that of 11% quoted by others; 3. Lower rates of recurrence have also been quoted – 3.2% (1/31) – but follow-up extended to only 6 months in this study.26 The evidence therefore suggests that although laparoscopic treatment of ovarian endometriomas is possible, in common with peritoneal disease, there is a problem with recurrent disease. The incidence and delayed nature of recurrent disease should always be borne in mind when counseling patients prior to surgery, as well as those with a resurgence of symptoms.
Rectovaginal septum endometriosis The presence of endometriosis in the rectovaginal septum is not only particularly painful, but is also difficult to treat. In some cases a retroperitoneal nodule (Fig. 83.14) will be seen at the time of laparoscopy, lying in the posterior fornix of the vagina and extending down into the septum. Unfortunately, in many cases a deeply infiltrating septal lesion is almost impossible to see at the time of laparoscopic assessment and may be missed (Fig. 83.15). These nodules are, however, palpable on combined rectovaginal examination, particularly at the time of menstruation. Although these patients will constitute a minority of those presenting to a gynecologic clinic with chronic pelvic pain, there are some important points to raise. Most of these lesions are amenable to endoscopic laser or electrosurgery, as demonstrated in a series reported by Donnez et al.27 employing the carbon dioxide laser. The
Figure 83.15. The cul-de-sac may look normal to the inexperienced laparoscopist but closer inspection reveals a small dimple overlying a nodule in the rectovaginal septum and fibromuscular hyperplasia in the uterosacral ligaments and around the ureters. number of women with each of the presenting symptoms was not clearly defined, but it appears that most patients suffered from severe pelvic pain, severe dysmenorrhea, and severe dyspareunia. Of the 242 patients followed-up for more than 2 years, only 3.7% experienced recurrent severe dysmenorrhea and 1.2% dyspareunia. While the figures are not readily available, the impression is one of major symptomatic benefit. The second issue arising from this study is that, although the surgeons were among the most experienced in the world, four out of 497 patients treated by laparoscopy suffered a rectal perforation. It is therefore only too clear that any woman suffering from this condition should be referred to a suitably qualified surgeon. 1171
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PELVIC DENERVATION PROCEDURES As well as treating visible organic pathology at the time of laparoscopic assessment, the ability to interrupt several of the neural pathways responsible for the transmission of pain has also been used. Indeed, there are many who advocate the use of these methods when no pathology is demonstrable. There are two commonly used techniques: uterine nerve transection and presacral neurectomy (PSN).
Uterine nerve transection The idea is to disrupt the course of pain fibers as they leave the uterus in an effort to decrease dysmenorrhea; this is not a new idea, having previously been described over 40 years ago.28 The original paper reported that, by transecting the uterosacral ligaments close to their point of origin on the posterior aspect of the cervix (a technique that could be performed either abdominally or vaginally), it was possible to achieve complete pain relief in 86% of women with primary dysmenorrhea and 86.8% of women with secondary dysmenorrhea. The advent of non-steroidal anti-inflammatory agents and the combined contraceptive pill tended to focus attention on the medical management of these conditions, rather than the surgical, and the technique became almost forgotten. The emergence of laparoscopic surgery and the ability to divide these nerves (Fig. 83.16) without the need for open surgery generated much interest in resurrecting this technique, which had produced such good results. The technique is now a common procedure in our unit as well as many
Figure 83.16. Laparoscopic uterine nerve ablation dividing the uterosacral ligaments and the Lee–Frankenhauser plexus close to the point of insertion in the back of the cervix.
others around the world. Two recent review articles have described the history, anatomic rationale, and the various methods of dividing the nerves that are currently employed in this technique.29,30 It is of considerable relevance that in these times of evidence-based medicine, laser uterine nerve ablation (LUNA) has been subjected to the rigors of a prospective, randomized, double-blind study.31 Although the numbers in this report were small, and the surgeons used electrosurgery rather than laser, the results still warrant mention. In women with severe dysmenorrhea but no obvious pathology, 81% of those undergoing LUNA reported almost complete relief of pain at 3 months, although this fell to 45% at 12 months. None of those in the control group reported any benefit. Another study investigating the outcome of patients with primary dysmenorrhea reported an improvement rate of 73%, whereas in the 100 patients with endometriosis, 86% reported an improvement in symptoms, mainly dysmenorrhea.29 Other reported rates of improvement for primary dysmenorrhea range from 50 to 73%.11,32–34 These differences may be due to differing patient subgroups, and perhaps the degree of demarcation of the uterosacral ligaments, since if they are poorly developed an incomplete procedure is often performed.29 The group of patients who find that their dysmenorrhea worsens after this operation is of particular interest. Daniell and colleagues32–34 reported that 10% of their patients with primary dysmenorrhea experienced deterioration in symptoms after surgery. Because preoperative counseling includes an explanation of this potential development to the patient, it has been suggested that this may be a self-fulfilling prophecy, whereas it does not occur if you do not inform your patient of the possibility, as is the policy in our department.29 One publication35 has provided evidence suggesting that the benefits of a LUNA procedure could be due to an entirely different mechanism. Nisolle et al.35 demonstrated that, in patients with an apparently normal pelvis at the time of laparoscopy, histologic evidence of endometriosis may be found in biopsy samples of the uterosacral ligaments in 6% of cases. There is obviously considerable debate about the significance of this finding. If it transpires that these deposits are located laterally to the usual site of a LUNA procedure, this may help to explain why not all patients derive the same degree of benefit from this operation. The other explanation is that at second-look laparoscopy some of these LUNA procedures were very extensive, and may have removed much of the fibromuscular hyperplasia that is associated with deep infiltration of the uterosacral complex and is known to be associated with considerable pain.
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The last area to be considered is that of safety. Although widely performed, LUNA is not without risks since the rectum, ureter, and uterine artery are all within the immediate vicinity. Two deaths due to postoperative hemorrhage33 and two cases of severe uterine prolapse36 have been reported. However, when one considers the many thousands of LUNA procedures performed, this is a very low complication rate and we have had no serious complications in over 8000 cases.
Presacral neurectomy Interruption of the hypogastric plexus at the sacral promontory has been used for more than 60 years to provide relief from pelvic pain and dysmenorrhea. An early review of this topic showed that significant relief could be obtained from these symptoms in 80% of patients.37 This procedure has been well described in three recent reviews.30,38,39 Rather than performing a traditional excisional neurectomy, some workers recommend a divisional neurotomy, which is far quicker and, in the short term at least, appears to be just as effective.40 While there have been several publications considering the role of LUNA in patients with pelvic pain and a negative laparoscopy, most of the literature relating to PSN combines it with other therapeutic procedures. However, Candiani et al.41 have found that the addition of PSN made no difference to patient outcome. Seventyone patients with stage III or IV endometriosis and pelvic pain were assigned to conservative surgery alone, or with the addition of PSN. Postoperatively there was no significant difference in the reduction of dysmenorrhea, dyspareunia or intermenstrual pain between the two study groups. The findings of this paper are contradicted by those of Tjaden et al.42 which showed such overwhelming benefit from the addition of PSN that the trial was halted on the grounds that it would be unethical to continue because the response rate was so good. Unfortunately, the number of patients treated was hopelessly underpowered and merely demonstrated the folly of stopping a well-designed clinical trial far too early. Perry and Perez43 have raised the important issue of the reasons for failure of PSN. Although they reported a successful outcome in most of 103 women treated for pelvic pain or dysmenorrhea, the interest lies within a small subgroup. Of the patients in the study, 11 had previously undergone LUNA, without symptomatic benefit, yet all experienced alleviation of midline pain following PSN. The authors noted that the most common reason for PSN failing to improve midline pain was incomplete division of the presacral nerve. This is a reflection of
operator experience and confidence, and is reflected in our own practice where we see patients referred for assessment of their pelvic pain, having previously undergone a LUNA procedure, only to find little evidence of this at the time of surgery. We would suggest that the above observation could also be applied to LUNA. Several themes run through the literature on PSN, one being that patient assessment is paramount, especially with regard to the location of the pain. Reports have suggested that PSN is useful in the treatment of midline pain, but of no benefit when the pain is more lateral.44 This is supported by a report revealing that out of 27 women undergoing PSN, midline pain was relieved in 22 and reduced in a further four; however, lateral pain remained in three of 12 cases.45 Another theme common to most of these publications is that PSN should be reserved for patients with midline pain in whom previous attempts at medical therapy have failed. It should also be remembered that there are many potential complications associated with this procedure. Immediate complications include damage to major vessels,30,45 and long-term problems such as constipation are common. In view of the above evidence, it seems prudent that patients are carefully assessed and counseled prior to this procedure, and that it is performed by a competent and experienced endoscopic surgeon. Since transection of the uterosacral ligaments is easier to perform and less dangerous than division of the presacral nerve, the suggestion that PSN should be reserved for patients who have undergone an adequate transection of the uterosacral ligaments but still have persistent pelvic pain and dysmenorrhea seems wise.30
ADHESIOLYSIS Laparoscopic adhesiolysis crosses the boundary of gynecologic and general surgery. Adhesiolysis usually involves enterolysis – the release of adhesions involving the bowel – and a high degree of experience is required because of the risk of causing an intestinal perforation. Introduction of the trocar can be hazardous, and surgeons should be aware of the different methods by which this can be achieved and the various techniques available for enterolysis. These have been reviewed recently.30,46 As with the other causes of chronic pelvic pain, the relationship between adhesions and chronic pelvic pain is unclear, with several workers describing the presence of adhesions in 23–25% of patients with chronic pain, but also in 14–17% of women without pain.7,47 Coupled with this are the observations that, of women with adhesions, 50% have no risk factors for their development,30 1173
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and 66% have a completely normal abdominopelvic examination.48 While there appears to be little correlation between the degree of the adhesions and the severity of the symptoms,49 the pain does seem to be located at the site of the adhesions in most cases.49,50 If adhesions are relatively common in the asymptomatic population, what is it that makes certain adhesions painful, and does dividing them make any difference? Laparoscopic laser adhesiolysis was reported to produce pain relief in 76% of women;51 the authors noted that success was usual in patients who had a thick adhesive band limiting the mobility of the small intestine. This finding is corroborated by an important randomized trial in which 48 patients with stage II–IV adhesions either underwent adhesiolysis via a midline laparotomy, or were merely clinically observed.52 At 9–12 months follow-up there was no significant difference between the groups with regard to pelvic pain. More importantly, the improvement rate in the control group was 50%. A small subgroup of patients with severe, dense, vascular lesions involving the bowel did, however, show a significant improvement (89%) compared with the control group (17%). A review of the efficacy of adhesiolysis quotes improvement rates that vary between 63 and 89%.30 The design of these studies varied widely, however, and the period of review was only 1 month in some cases. Of interest is the fact that 4.7–23% of patients derive some initial benefit but then develop a recurrence of their symptoms; it has been suggested that this is due to reformation of adhesions.53 This makes it mandatory to scrutinize the length of follow-up, since good results at 1 month may have deteriorated dramatically by 12 months. The improvement rates should also be interpreted in light of the 50% response rate in the control group described above. Fayez and Clark50 appear to report much better results than other studies. In this study, 156 patients with chronic pelvic pain associated with postoperative adhesions were treated with laser adhesiolysis. Complete relief, defined as disappearance of symptoms and an ability to carry on with normal daily activity during the 12-month follow-up period, was reported in 137 (88%) patients. The remaining 19 (12%) improved, but to a lesser degree. However, five of these 19 (3% overall) patients – in all of whom severe, dense adhesions had been divided – presented with a recurrence of their symptoms after only 4–6 months. These women underwent repeat surgery, which confirmed the presence of adhesions at the site of pain, and subsequently rendered them pain-free. It is not clear why the results should be so much better in this study than in others. However, the prevention of de novo adhesions at the time of initial surgery and of rede-
velopment after adhesiolysis are areas that are attracting considerable interest. It is difficult to decide what recommendations can be made from the above data. However confusing the results may be, it seems sensible to attempt to prevent the initial formation of adhesions at the time of surgery. To this end, the use of laparoscopy for the initial surgery, which causes fewer postoperative adhesions than laparotomy, seems sensible.54 The main issue is the treatment that should be offered to patients with pelvic pain and adhesions. One study showed that adhesiolysis, combined with a second procedure in poor responders, gave excellent results,50 whereas others have shown that improvement can be achieved in the majority, but that this is often little better than can be achieved by a conservative approach. Taking an evidence-based approach, it could be argued that adhesiolysis should be offered only to women with stage IV adhesions involving the bowel, and should not be offered to those with lesser pathology. This approach may need to be modified in light of the development of conscious pain mapping (discussed below); however, if it can be demonstrated unequivocally that the adhesion is the source of the pain, rather than an incidental finding, then adhesiolysis becomes a far more attractive option. A more recent double-blind, randomized controlled trial involving surgical patients was reported by Swank and colleagues.55 Of 116 patients enrolled for diagnostic laparoscopy for chronic abdominal pain attributed to adhesions, 100 were randomly allocated to either laparoscopic adhesiolysis (52) or no treatment (48). Patients and assessors were unaware of treatment, and pain was assessed at 1 year by visual analog score (VAS; scale 0– 100), pain change score, use of analgesics, and quality of life score. Analysis was by intention to treat. Both groups reported substantial pain relief and a significantly improved quality of life, but there was no difference between the groups (mean change from baseline of VAS score at 12 months: difference 3 points, p=0.53; 95% CI: 7–13). This was an extremely well-designed study and a huge battery of investigations were performed to exclude other causes of chronic abdominal pain. Although this study concluded that laparoscopic adhesiolysis was no more effective than diagnostic laparoscopy alone, there was obvious improvement in both groups and similar studies have drawn attention to the enormous placebo effect in laparoscopy alone in diseases such as endometriosis.17 Additionally, of the 52 patients who underwent adhesiolysis, 14 (27%) had incomplete adhesiolysis, and although there were no complications in the diagnostic
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group there were six major complications in five (10%) individuals in the adhesiolysis group, which could have skewed the results. Nevertheless, this is the best evidence-based study in the literature and calls into question whether laparoscopic adhesiolysis with its attendant risk of complications has any advantage over diagnostic laparoscopy alone.
CONSCIOUS PAIN MAPPING Laparoscopy under general anesthesia allows a thorough evaluation of a patient’s pelvis but does not permit the surgeon to assess the significance of these findings. The concept of performing an interactive procedure where the surgeon is able to probe a lesion to see if it is responsible for the symptoms is obviously an attractive one. However, equipment manufacturers have only recently produced small-diameter laparoscopes with high-quality resolution that have made the widespread use of microlaparoscopy a feasible prospect. For this procedure, a laparoscopy is performed with a 2 mm laparoscope under local anesthesia and intravenous sedation. The lack of general anesthesia allows a degree of surgeon–patient interaction, and means that the surgeon can gently probe all the pelvic organs or demonstrate pathology to ascertain if any significant discomfort is produced. In theory this should enable the surgeon to differentiate between symptomatic and asymptomatic incidental findings and, therefore, to tailor patient care more appropriately. An early study on this subject compared the performance of office microlaparoscopy under local anesthetic (OLULA) in a group of patients with chronic pelvic pain, and a second group undergoing assessment for infertility.56 The operation was well tolerated by 20 of the 22 patients; two procedures were terminated, one because of benzodiazepine-induced disorientation in a non-English-speaking patient, and one because of an intraoperative anxiety attack in a patient with a history of severe anxiety disorders. These two cases obviously give some useful information as to the future selection criteria for this technique. This study produced two areas of interest in addition to the profound reduction in the cost of the procedure by avoiding expensive hospital charges. First, in three patients with chronic pelvic pain, an area of marked pain sensitivity was diagnosed. Two of these related to deposits of endometriosis but, importantly, both patients had other areas of endometriosis within the pelvis that did not produce increased pain sensitivity. In the third patient, the area of increased sensitivity related to a loop of bowel adherent to the anterior abdominal wall.
This is of considerable interest because, as mentioned earlier, while adhesions are found in many patients with chronic pelvic pain, they are also found in 14–17% of asymptomatic patients. The use of OLULA could therefore potentially allow surgeons to discriminate between symptomatic and asymptomatic adhesions in a patient with chronic pelvic pain, so that adhesiolysis, a potentially dangerous procedure, can be restricted to the areas where it would be expected to be of some benefit. The second interesting finding was that 10 of the 11 patients with chronic pelvic pain had a generalized visceral hypersensitivity to pain; this was not found in any of the patients being investigated for underlying infertility. The authors proposed several explanations for this finding and also suggest that, in the future, this may act as a marker for a certain subgroup of patients and may be of some prognostic significance. A second paper on this topic57 also demonstrated that this technique was highly acceptable to the patients, and reviewed the findings of 50 consecutive patients undergoing microlaparoscopy for chronic pelvic pain. Operative as well as diagnostic procedures were performed, and 14 of the 48 women who needed therapeutic procedures had these performed under local anesthesia. The incidence of significant adhesions was 62% (31 patients), and all of these were lyzed, irrespective of whether they were tender at the time of probing. Of these 31 women, 25 had pain on manipulation of their adhesions, but it is not clear whether their outcome was any better than that of the six women who had lysis of non-tender, perhaps asymptomatic, adhesions. This is obviously an important area of interest worthy of further work, a point noted by the authors. Thirteen of these women had a markedly tender appendix during their pain mapping, and all underwent appendicectomy, with subsequent symptomatic relief. Abnormal histologic findings were present in nine women, and seven women, including all those with normal histology, had severe periappendiceal adhesions. The authors made the critical point that although two of these appendices appeared distorted secondary to the presence of fecaliths, the others appeared macroscopically normal and would have been missed by performing a traditional laparoscopy on an unconscious patient; conscious pain mapping was the only technique capable of demonstrating this pathology. An interesting extension of this technique has been introduced by Demco58 who has shown that if conscious pain mapping is performed with a specially adapted xenon light source delivering blue light at a specific frequency, endometriotic lesions, particularly neoangiogenesis, can be seen (and confirmed by biopsy) in areas that appear visually normal when observed with 1175
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a conventional white light source. This would also add credence to the earlier finding of Nisolle et al.35 of biopsypositive endometriosis in visually normal endometrium.
SUMMARY At present it is not entirely clear what clinical features are required to make a diagnosis of chronic pelvic pain. Until that definitive statement is published and adhered to throughout the scientific and medical communities, it will continue to be difficult to compare one putative treatment with another. However, for the time-being, there are several aspects of this condition that can be critically reviewed.
• The investment of time with the patient during
•
•
•
•
the initial consultation may well pay dividends. A thorough history may suggest other pathology such as irritable bowel syndrome, or an underlying unrelated anxiety disorder that may manifest as pelvic pain, and needs addressing before more invasive investigation of the pelvis. This degree of assessment may well prevent many patients undergoing unnecessary laparoscopy. Diagnostic laparoscopy will reveal pathology in a variable percentage of cases, and the rationale for treating these findings laparoscopically has been discussed above. It should be remembered that this treatment can often be performed at the same time as the initial diagnostic laparoscopy, and that other treatments are available for conditions such as endometriosis, notably medical management, hysterectomy, and bilateral oophorectomy. That pathology can be demonstrated and treated does not necessarily imply that symptomatic relief will follow. Indeed, it should not be forgotten that these lesions may not be causal or may return rapidly following treatment, especially when dealing with endometriosis and adhesions. In cases where pain persists, there is the option of performing one of the pelvic denervation procedures. It cannot be stressed too firmly, however, that these techniques have their limitations and, if they have any role at all, it is in patients with midline, not lateral, pain. One should not forget that procedures such as PSN can be highly dangerous and should only be performed in adequately investigated and counseled patients, and by suitably experienced surgeons. Finally, a negative laparoscopy does not imply that there is no organic cause for the pain. The widespread use of OLULA and conscious pain
mapping in this subgroup of patients may lead to the demarcation of sensitive foci within the pelvis that may be of prognostic importance and amenable to treatment. Alternatively, it may indicate which areas of pathology are responsible for the symptoms when faced with multiple, possibly non-significant lesions. The possible benefits of this technique in assessing patients with chronic pelvic pain should not be underestimated, and it may be that this development is entirely responsible for a marked improvement in our comprehension of the pathophysiology of this poorly understood condition.
REFERENCES 1. Beard RW. Chronic pelvic pain. Br J Obstet Gynaecol 1998;105:8–10. 2. Stones RW. Chronic pelvic pain. Review 97/01. Personal Assessment in Continuing Education. London: Royal College of Obstetricians and Gynaecologists, 1997. 3. Mathias SD, Kupperman M, Liberman RF et al. Chronic pelvic pain: prevalence, health related quality of life and economic correlates. Obstet Gynecol 1996;87:321–7. 4. Zondervan KT, Yudkin PL, Vessey MP et al. The prevalence of chronic pelvic pain in women in the United Kingdom: a systematic review. Br J Obstet Gynaecol 1998;105:93–9. 5. Porpora MG, Gomel V. The role of laparoscopy in the management of pelvic pain in women of reproductive age. Fertil Steril 1997;68:765–79. 6. Collett BJ, Cordle CJ, Stewart CR. A comparative study of women with chronic pelvic pain, chronic nonpelvic pain and those with no history of pain attending general practitioners. Br J Obstet Gynaecol 1998;105:87–92. 7. Howard FM. The role of laparoscopy in the evaluation of chronic pelvic pain. Promises and pitfalls. Obstet Gynecol Surv 1993;48:117–18. 8. Kontoravdis A, Chryssikopoulos A, Hassiakos D et al. The diagnostic value of laparoscopy in 2365 patients with acute and chronic pelvic pain. Int J Gynaecol Obstet 1996;52:243–8. 9. Howard FM. Laparoscopic evaluation and treatment of women with chronic pelvic pain. J Am Assoc Gynecol Laparosc 1994;1:325–31. 10. Newham AP, van der Spuy ZM, Nugent F. Laparoscopic findings in women with chronic pelvic pain. S Afr Med J 1996;86:1200–3. 11. Wiborny R, Pichler B. Endoscopic dissection of the uterosacral ligaments for the treatment of chronic pelvic pain. Gynecol Endosc 1998;7:33–5. 12. Howard FM. The role of laparoscopy in the evaluation of chronic pelvic pain: pitfalls with a negative laparoscopy. J Am Assoc Gynecol Laparosc 1996;4:85–94.
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13. Donnez J, Nisolle M, Casanas-Roux F. Three-dimensional architectures of peritoneal endometriosis. Fertil Steril 1992;57:980–3. 14. Martin DC, Hubert GD, Levy BS. Depth of infiltration of endometriosis. J Gynecol Surg 1989;5:55–60.
29. Sutton C, Whitelaw N. Laparoscopic uterine nerve ablation for intractable dysmenorrhoea. In: Sutton C, Diamond M (eds) Endoscopic Surgery for Gynaecologists. London: WB Saunders, 1993; 159–68.
15. Redwine D. Non-laser resection of endometriosis. In: Sutton C, Diamond M (eds) Endoscopic Surgery for Gynaecologists. London: WB Saunders, 1993; 220–8.
30. Daniell JF, Lalonde CJ. Advanced laparoscopic procedures for pelvic pain and dysmenorrhoea. In: Sutton C (ed) Advanced Laparoscopic Surgery. London: Baillière Tindall, 1995; 795–808.
16. Sutton CJG, Hill D. Laser laparoscopy in the treatment of endometriosis. A 5-year study. Br J Obstet Gynaecol 1990;97:181–5.
31. Lichten EM, Bombard J. Surgical treatment of dysmenorrhoea with laparoscopic uterine ablation. J Reprod Med 1987;32:37–42.
17. Sutton CJG, Ewen SP, Whitelaw N, Haines P. Prospective, randomised, double-blind, controlled trial of laser laparoscopy in the treatment of pelvic pain associated with minimal, mild, and moderate endometriosis. Fertil Steril 1994;62:696–700.
32. Daniell JF, Feste J. Laser laparoscopy. In: Keye WR (ed) Laser Surgery in Gynaecology and Obstetrics. Boston: GK Hall, 1985; 147–65.
18. Sutton CJG, Pooley AP, Ewen SP et al. Follow-up report on a randomised controlled trial of laser laparoscopy in the treatment of pelvic pain associated with minimal to moderate endometriosis. Fertil Steril 1997;68:1070–4.
34. Daniell JF, Feste JR. Laser laparoscopy. In: Keye WR (ed) Laser Surgery in Gynecology and Obstetrics. Boston: GK Hall, 1985; 147–65.
19. Reiter RC. Letter 1995;3:1355–6.
to
the
editor.
Fertil
Steril
20. Sutton CJG, Dover RW, Pooley AP, Jones KD. Prospective, randomised, double-blind controlled trial of laparoscopic uterine nerve ablation in the treatment of pelvic pain associated with endometriosis. Gynecol Endosc 2001;10:217–22. 21. Vercellini P, Aimi G, Busacca M et al. Laparoscopic uterosacral ligament resection for dysmenorrhoea associated with endometriosis. Results of a randomised controlled trial. Fertil Steril 1997;68:3–5. 22. Bateman BG, Kolp LA, Mills S. Endoscopic versus laparotomy management of endometriomas. Fertil Steril 1994;62:690–5. 23. Donnez J, Nisolle M, Wayembergh M et al. CO2 laser laparoscopy in peritoneal endometriosis and in ovarian endometrial cysts. In: Donnez J (ed) Laser Operative Laparoscopy and Hysteroscopy. Louvain, Belgium: Nauwelaerts, 1989; 53–78. 24. Sutton CJ. Endometriosis. Infertil Reprod Med Clin North Am 1995;6:591–613.
33. Daniell JF. Fibreoptic laser laparoscopy. Baillières Clin Obstetr Gynecol Laparoscopic Surg 1989;3:545–62.
35. Nisolle M, Paindevine B, Bourdon A et al. Histologic study of peritoneal endometriosis in infertile women. Fertil Steril 1990;53:984–8. 36. Good MC, Copas PR, Doody MC. Uterine prolapse after laparoscopic uterosacral transection. A case report. J Reprod Med 1992;37:995–6. 37. Black WT. Use of presacral sympathectomy in the treatment of dysmenorrhoea: a second look after 25 years. Am J Obstet Gynecol 1964;89:16–32. 38. Daniell E, Dover RW. Laparoscopic use of the argon beam coagulator. In: Sutton C (ed) Endoscopic Surgery for Gynaecologists, 2nd ed. London: WB Saunders, 1998; 105–10. 39. Biggerstaff ED, Foster SN. Laparoscopic surgery for dysmenorrhoea: uterine nerve ablation and presacral neurectomy. In: Sutton C (ed) Gynecological Endoscopic Surgery. London: Chapman and Hall, 1997; 63–83. 40. Daniell W, Kurtz BR, Gurley LD et al. Laparoscopic presacral neurectomy vs. neurotomy: use of the argon beam coagulator compared to conventional technique. J Gynecol Surg 1993;9:169–73.
25. Sutton CJ, Ewen SP, Jacobs SA et al. Laser laparoscopic surgery in the treatment of ovarian endometriomas. J Am Assoc Gynecol Laparosc 1997;4:319–23.
41. Candiani G, Fedele L, Vercellini P et al. Presacral neurectomy for the treatment of pelvic pain associated with endometriosis: a controlled study. Am J Obstet Gynecol 1992;167:100–3.
26. Marrs RP. The use of potassium-titanyl-phosphate laser for laparoscopic removal of ovarian endometrioma. Am J Obstet Gynecol 1991;164:1622–8.
42. Tjaden B, Schlaff WD, Kimball A et al. The efficacy of presacral neurectomy for the relief of midline dysmenorrhoea. Obstet Gynecol 1990;76:89–91.
27. Donnez J, Nisolle M, Gillerot S et al. Rectovaginal septum adenomyotic nodules: a series of 500 cases. Br J Obstet Gynaecol 1997;104:1014–18.
43. Perry CP, Perez J. The role for laparoscopic presacral neurectomy. J Gynecol Surg 1993;9:165–8.
28. Doyle JB. Paracervical uterine denervation by transection of the cervical plexus for the relief of dysmenorrhoea. Am J Obstet Gynecol 1955;70:1–16.
44. Nezhat C, Nezhat F. A simplified method of laparoscopic presacral neurectomy for the treatment of central pelvic pain due to endometriosis. Br J Obstet Gynaecol 1992;99:659–63.
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45. Biggerstaff ED, Foster S. Presacral neurectomy for treatment of midline pelvic pain: laparoscopic approach with laparoscopic treatment of a single major complication. J Am Assoc Gynecol Laparosc 1994;1(S4):17.
52. Peters AAW, Trimbos-Kemper GCM, Admiraal C et al. A randomised clinical trial on the benefit of adhesiolysis in patients with intraperitoneal adhesions and chronic pelvic pain. Br J Obstet Gynaecol 1992;99:59–62.
46. Daniell JF, Dover RW. Laparoscopic enterolysis. In: Sutton C (ed) Endoscopic Surgery for Gynaecologists, 2nd ed. London: WB Saunders, 1998; 390–7.
53. Steege JF, Stout AL. Resolution of chronic pelvic pain after laparoscopic lysis of adhesions. Am J Obstet Gynecol 1991;165:278–83.
47. Trimbos JB, Trimbos-Kemper GCM, Peters AAW et al. Findings in 200 consecutive asymptomatic women having a laparoscopic sterilisation. Arch Gynecol Obstet 1990;247:121–4.
54. Lundorff P, Hahlin M, Kallfelt B et al. Adhesion formation after laparoscopic surgery in tubal pregnancy: a randomised study versus laparotomy. Fertil Steril 1991;55:911–15.
48. Cunanan RG, Courey NG, Lippes J. Laparoscopic findings in patients with pelvic pain. Am J Obstet Gynecol 1983;146:589–91. 49. Stout AL, Steege JF, Dodson WC et al. Relationship of laparoscopic findings to self-report of pelvic pain. Am J Obstet Gynecol 1991;164:73–9. 50. Fayez JA, Clark RR. Operative laparoscopy for the treatment of localised chronic pelvic–abdominal pain caused by postoperative adhesions. J Gynecol Surg 1994;10:79–83. 51. MacDonald R, Sutton CJG. Adhesions and laser laparoscopic adhesiolysis. In: Sutton CM (ed) Lasers in Gynaecology. London: Chapman and Hall, 1992; 95–113.
55. Swank DJ, Swank-Bordewizk SCG, Hop WCJ et al. Laparoscopic adhesiolysis in patients with chronic abdominal pain: a blinded randomised controlled multi-centre trial. Lancet 2003;361:1247-51. 56. Palter SF, Olive DL. Office microlaparoscopy under local anesthesia for chronic pelvic pain. J Am Assoc Gynecol Laparosc 1996;3:359–64. 57. Almeida OD, Val-Gallas M. Conscious pain mapping. J Am Assoc Gynecol Laparosc 1997;4:587–90. 58. Demco L. Laparoscopic spectral analysis of endometriosis [abstract]. 13th Congress of Gynecological Endocrinology (ISGE), Kuala-Lumpur, M1–2, 2004; 5.
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84 Laparoscopic colposuspension and paravaginal repair Rohna Kearney, Alfred Cutner
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IntroductIon Laparoscopic surgery should be considered the same as open surgery but carried out through smaller incisions with longer instruments. Although there is increased exposure and magnification deep in the pelvis, this is at the expense of less tactile feedback. Thus any discussion on laparoscopic colposuspension and paravaginal repair should be very similar to that of the open counterpart. However, the requirement to learn new surgical skills for the different operative environment results in a learning curve which has led some surgeons to develop ‘short cut’ surgery and hence new operations have been devised.1 These are often given the same name as the traditional counterpart but must be assessed in their own right and should not be considered the same. Most alterations to the traditional approach are due to the difficulty that surgeons have had in learning suturing techniques. Other problems in the early phase of laparoscopic surgery were in the limitations in the optical and instrumental technology. Advances in these areas enabled the surgeon to operate in a more dexterous manner. SynOptics launched the tube camera in 1978 and William Chang invented the first solid-state medical video camera in 1981. The first three-chip camera to be produced giving better clarity of vision arrived in 1989. The S-Video signal was developed in 1992 and the first digital zoom and digital enhancement capabilities were developed in 1999. This latest advancement in digital technology has been a further step forward in image clarity. Alongside this, instrumentation has advanced to be ergonomically more suitable, further aiding surgical movements. The development of robotic surgery may result in further advances (Fig. 84.1).
In this chapter we will first discuss colposuspension and then paravaginal repair. Techniques and outcomes, where available, will be discussed. The indications for the operation, as opposed to the route, will only be briefly mentioned as these are fully explained in the relevant other chapters of the book.
colposuspensIon Although the Burch colposuspension was first described in 1961,2 the Tanagho modification is now considered the standard method in which a colposuspension should be performed.3 However, colposuspension is taken to be synonymous with Burch colposuspension, which is neither the case semantically, nor in the reporting of the literature. Colposuspension merely means elevating the ‘colpos’, i.e. the vagina. The first report in the literature of a laparoscopic colposuspension was by Vancaille and Schuessler in 1991.4 This was not in fact a Burch but rather a modification of the Marshall–Marchetti–Kranz procedure.5 The authors suspended the vagina with two non-absorbable 2-0 sutures on either side to the pubic symphysis as they were unable to clearly visualize Cooper’s ligaments. The first actual report of a laparoscopic modified Burch colposuspension was in 1993 by Liu and Paek.6 They used two absorbable sutures to elevate the vaginal tissue to Cooper’s ligaments. The various methods of colposuspension described in the literature are shown in Table 84.1.
Mesh technique A technique using mesh to suspend the vagina to Cooper’s ligaments has been described by several authors.7,8 One or two pieces of Prolene mesh are inserted along the
Figure 84.1. The ‘da Vinci’ robotic surgical system. 1180
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table 84.1.
Different methods used to suspend the vagina
Author
Year
Method
1991
Non-absorbable sutures to pubic symphysis
1993
Absorbable sutures to Cooper’s ligaments
1996
Laparoscopic Stamey
1997
Mesh and staples
Breda et al.
1996
Hand-held needle
Das30
1998
Bone anchors
1995
Glue
1998
Teleoscopy
Vancaille & Schuessler
4
Liu & Paek6 10
Carter
8
Birken & Leggett 9
65
Kiilholma et al.
11
Shoemaker & Wilkinson El-Toukhy & Davies
48
2001
Tacks
Zullo et al.46
2001
Staples
12
2002
Bipolar electrochemical energy
Ross et al.
paravaginal fascia lengthwise, 2 cm lateral to the bladder neck on either side, and are fixed to Cooper’s ligaments with staples or tacks. A combined laparoscopic and vaginal approach using a hand-held needle has been described.9 This involves using one suprapubic port to create a pneumocavity in the space of Retzius. Two small suprapubic incisions are made on either side and a suture mounted on a specially designed handheld needle is passed through Cooper’s ligament and through the lateral fornix of the vagina. The needle is then withdrawn after taking a second bite of the vagina and the vagina is fixed to Cooper’s ligaments with an extracorporeal knot.
Laparoscopic needle suspension Carter described a laparoscopic Stamey procedure in 1996.10
Teleoscopy Shoemaker and Wilkinson proposed using laparoscopy to examine the bladder after colposuspension.11 They inserted a telescope through a 5 mm cannula into the dome of the bladder in 103 women following bladder neck suspension. They reported that sutures were found in the bladder in 8% of cases.
Bipolar electrochemical energy Ross et al. describe using bipolar electrochemical energy to induce shrinkage of the paravaginal tissue causing bladder neck elevation in 94 women.12 They found that this resulted in 30% shrinkage of the tissue.
Laparoscopy Von Theobald et al. proposed using laparoscopy to assess women with recurrent stress urinary inconti-
nence after previous colposuspension by laparotomy.13 They reported their findings in five cases and advocated repeating the colposuspension if there was evidence of anatomic failure.
technique of colposuspension Currently there are two methods for carrying out a modified laparoscopic Burch colposuspension. They differ in the method of entry into the cave of Retzius. There are other variations including number and size of ports, type of ports, methods used for dissection, type of sutures, and method of knot tying. We will first describe in detail the method of transperitoneal laparoscopic Burch colposuspension as carried out in our unit. Preoperative counseling includes a full explanation of the risks of the procedure and the advantages and disadvantages over the open procedure. The risks include those of laparoscopic entry and laparoscopic surgery, and those of the procedure itself. Preoperative bowel preparation is advised as it improves visualization of the operative field and reduces contamination in the event of a bowel injury.14 A single intravenous dose of prophylactic antibiotic is given. The patient is prepared for surgery, cleaned and draped. She is initially placed supine without any table tilt. The legs are placed in a lithotomy position at an angle of 30 degrees at the hips. A size 14 Foley catheter with 5 ml of water in the catheter balloon is placed in the bladder and left on free drainage. We normally use a Veress needle to obtain a pneumoperitoneum. An incision is made in the umbilical region, as it is at this point that the layers of the rectus sheath and peritoneum are fused. The patient is placed supine with no tilt and the needle is first directed towards the 1181
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sacral promontory and, when the characteristic clicks of passing through the layers are felt, the needle is then directed towards the pelvis. A water test is used to confirm entry into the correct space and the abdomen is insufflated. Insufflation ceases when the pre-set pressure of 20 mmHg is achieved. The main 11 mm trocar is then placed through the umbilical region.15 Where the patient is at high risk of bowel adhesions near the umbilicus from previous abdominal surgery, other sites are considered. We use Palmers point in highrisk cases (the left subcostal area in the mid-clavicular line)16,17 (Fig. 84.2). Palpation to identify the spleen is carried out prior to insertion of the Veress needle, and a nasogastric tube is inserted to reduce the chance of perforating an inflated stomach (Fig. 84.3). Where the
Figure 84.2.
Veress needle entry at Palmer’s point.
Figure 84.3. Dilated stomach visible in the left subcostal region. To prevent injury to the stomach when inserting the Veress needle subcostally, a nasogastric tube is inserted to deflate the stomach.
patient is very thin, a Hassan entry technique is used to reduce the risk of vascular injury.18 Once the laparoscope is inserted the abdominal contents are examined and the patient placed in a head-down tilt. The placement of additional ports is important. All additional ports must be placed under direct vision to avoid injury to viscera or vessels. Ports should be placed either very lateral or medial to avoid the inferior epigastric vessels.19,20 They should be placed so that adequate dexterity can be achieved during the operation. For laparoscopic colposuspension we place two lateral 5 mm ports and one suprapubic 11 mm port. We use 11 mm ports with a variable top for ease of placing sutures through the ports. The lateral ports are placed at least 8 cm from the midline and inserted at a 90-degree angle to avoid the epigastric vessels. We do not use large ports laterally as these need to be formally closed to reduce the incidence of incisional hernias.21,22 This closure increases postoperative discomfort. Prior to the colposuspension, the abdominal cavity is assessed. If any additional surgery is required (such as hysterectomy or removal of an adnexa), this is carried out prior to the colposuspension. However, some additional procedures are carried out after the colposuspension. The bladder is initially filled with 300 ml of blue saline to aid identification of the superior edge of the bladder dome. The obliterated median umbilical ligaments are used as markers for entry to the cave of Retzius. They are incised 2–4 cm cephalad to the bladder dome (Figs 84.4, 84.5). The cave of Retzius is dissected towards Cooper’s ligaments. The bladder is then drained to enable better access to the paravaginal tissues (Fig. 84.6). Dissection is performed with monopolar scissors on 60 Watts coagulation. This enables the tissues to be dissected without much bleeding. The dissection should avoid the urethra and the dorsal vein to the clitoris in the midline and the obturator neurovascular bundle laterally. This dissection will expose the pubic symphysis and bladder neck in the midline, and Cooper’s ligaments and the arcus tendineus fascia pelvis laterally. The bladder is retracted medially to allow the colposuspension to be performed. A pledget on a grasper with a marker thread is used for blunt dissection (Fig. 84.7). Non-absorbable No. 0 Ethibond® sutures are used for the colposuspension. One suture is placed on either side at the level of the bladder neck. A second suture is then placed on each side in a slightly more cephalad position (Figs 84.8, 84.9). A double bite of the vagina is taken with each suture and the suture is then placed through the ipsilateral Cooper’s ligament. Each suture is tied after insertion on limited tension using an extracorporeal surgical knot. A Redivac drain is left in the cave of Retzius
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Figure 84.4. The median umbilical ligament is grasped cephalad to the bladder dome after filling the bladder with 300 ml of saline.
Figure 84.5. An incision is made in the median umbilical ligaments cephalad to the bladder dome to gain access to the cave of Retzius. for 48 hours. If there has been any difficulty with the procedure, a cystoscopy is performed with a 120-degree scope to identify any sutures inadvertently placed in the bladder and to verify that the ureters are patent. If there appears to be a significant degree of uterine prolapse at the end of the procedure and the patient had not been considered for a hysterectomy, then a uterosacral plication is carried out at this stage. The uterosacral ligament is grasped medially and a lateral releasing peritoneal incision is performed to lateralize the ureter (Fig. 84.10). A 2-0 polydioxanone (PDS) suture is used to shorten each ligament and to approximate them in the midline (Fig. 84.11).23 Care is taken not to constrict the rectum. Where there is a greater degree of prolapse,
Figure 84.6. The cave of Retzius is dissected, clearly demonstrating the pubic symphysis and Cooper’s ligaments.
Figure 84.7. A pledget is used to dissect the bladder medially to allow suture placement. a suture hysteropexy using No. 0 Prolene to attach the right uterosacral ligament to the sacral promontory is performed. In addition, each ligament is shortened with a No. 0 Prolene suture. An indwelling urethral catheter is left for 72 hours. After the catheter is removed, the post-void residual is measured with a bladder scanner after the second void. If the residual is more than 100 ml, a urethral catheter is reinserted for a further week. The patient is then discharged home and reviewed in the outpatient clinic in one week.
Variations in technique The extraperitoneal approach involves accessing the preperitoneal space and dissecting into the cave of Retzius. Either a Veress needle can be placed in a suprapubic site 1183
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Figure 84.8. bladder neck.
The first suture is placed at the level of the
Figure 84.10. The ureter is dissected lateral to the uterosacral ligaments.
Figure 84.9. The second suture is placed cephalad to the previously placed suture.
Figure 84.11. Both uterosacral ligaments have been shortened and plicated together in the midline.
to reduce the risk of accidental peritoneal cavity entry, or a cut-down technique with dissecting balloons can be used. In addition, a gasless laparoscopic colposuspension procedure using extraperitoneal balloon dissection followed by a mechanical abdominal wall retractor, has also been described.24 Once a pneumo-Retzius has been obtained, the additional ports are inserted. Typically, two 11 mm trocars are used just above the hairline and close to either side of the midline. The colposuspension is then carried out in the same manner. The advantage of the pre-peritoneal approach is reduced risk of injury to intra-abdominal organs and quicker dissection time. In particular, the incidence of bladder injury is reduced. However, it is not possible to inspect the abdominal contents or to carry out additional intraperitoneal procedures at the same time.
In addition, the reduced access of this approach and the close port placement makes suturing more difficult. Thus some authors adopting this approach changed to using mesh and tacks rather than sutures to carry out the colposupension.25 Apart from the approach to the cave of Retzius, the other variations in the literature relate to the type and number of sutures used and whether mesh is used. In addition, there are variations in the type of knots used to elevate the vagina but these are never expanded upon as it is assumed that they are all similar. However, it has been demonstrated in in-vitro studies that different methods of knot tying result in different strengths.26,27 There are also reports of bone anchors, staples, and clips being used to attach the suture to Cooper’s ligaments or the pubic ramus.28–30
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evaluation of success of laparoscopic colposuspension The proposed advantages of the laparoscopic approach are better visualization of the anatomy, less postoperative pain, and an earlier return to normal activities.31 However, many authors have advised caution with the laparoscopic approach due to concerns of higher complication rates with poorer results.32,33 The Cochrane Database for Systemic Reviews was last updated on laparoscopic colposuspension in 2002 and includes eight studies up to April 2001.34 It concluded that the long-term performance of laparoscopic colposuspension is still uncertain and may be worse than the open procedure. A systematic review published by the same authors in 2003 found a similar subjective cure rate for laparoscopic and open colposuspension with a higher urodynamic objective cure rate for the open approach.35 However, the authors state that the evidence for the
table 84.2.
review is limited by small number of trials, low numbers of participants, and methodological problems. A review by Buller and Cundiff of laparoscopic surgeries for urinary incontinence evaluated 50 papers and found an 89% cure rate after 17 months with only 30% of papers reporting objective outcomes.36 Table 84.2 shows the reported success rates for laparoscopic colposuspension in the literature where sutures were used to elevate the vagina. When deciding what role laparoscopy has in the management of prolapse and incontinence, it is necessary to evaluate both the success rate and the complication rate of the laparoscopic approach. Previously many studies have compared laparoscopic colposuspension to open colposuspension with varying techniques and success rates reported. However, with the increasing use of tension-free vaginal tape (TVT) and other midurethral tapes, it is also necessary to compare laparoscopic colposuspension to these newer procedures.
Reported objective cure rates for laparoscopic colposuspension with sutures
Author
No. of patients
Langebrekke et al.66
8
67
Gunn et al.
15
68
Liu
132
Burton37 Su et al.39
Length of follow-up (months) 3 4–9 3–27
Cure rate (%) 88 100 97.2
30
12
73
46
12
80.4
45
78
12
58
45
Persson & Wolner-Hanssen (1 suture) Persson & Wolner-Hanssen (2 sutures)
83
12
83
69
Ross
32
12
94
Ross70
35
12
91
31
14.4
97
71
Kung et al.
72
Lam et al.
107
16
98
73
Liu & Paek
107
18
97.2
Liu & Paek 6
58
22
94.8
48
24
89
32
24
90.6
Lee et al.
48
26
93.8
Nezhat et al.76
40
30
91.9
30
36
60
74
18
87.9
23
18
82
82
12
89
30
12
89
47
12
85
74
Ross
75
Papasakelariou & Papasakelariou 76
41
Burton
38
Fatthy et al.
56
Üstün et al.
Huang & Yang Zullo et al.46 40
Cheon et al.
44
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laparoscopic colposuspension compared with open colposuspension Table 84.3 shows the methodology of studies comparing the laparoscopic approach to open colposuspension. Of these, only four are prospective randomized trials that compare the same operation, differing only in the mode of abdominal access.37–40 Burton randomized 60 women to laparoscopic or open colposuspension using two absorbable sutures on either side for both techniques. He reported a lower cure rate at 1 year with the laparoscopic approach compared to the open approach (60% versus 93%).41 Similarly at 3-year follow-up the results of the laparoscopic group continued to be worse than the open group.37 However, the author had only performed 10 laparoscopic procedures before the study and absorb-
table 84.3.
able sutures were used. In addition, in the laparoscopic arm a 12 mm needle was used and this may have resulted in an inadequate bite of tissue for suspension. Fatthy et al. showed a similar success rate for the two approaches, with the laparoscopic approach taking 17 minutes longer with 198 ml less blood loss, 40 hours less hospital stay, and return to light work 23 days earlier.38 Su et al. investigated 92 women randomly assigned to the laparoscopic or the open route.39 They included in the open group those patients who were unwilling to undergo the laparoscopic route after randomization. In addition, 14 women in the laparoscopic group had a laparotomy for hysterectomy immediately following colposuspension. They found less blood loss in the laparoscopy group, similar operating time but lower success rate at 1 year compared to the open group
Methodology of studies comparing laparoscopic colposuspension to open colposuspension
Author
Year
Study design
No. of patients
Laparoscopic technique
Open
Follow-up period
Ankardal et al.47
2004
Prospective, randomized
240
Transperitoneal mesh and staples
2 non-absorbable sutures
1 year
Huang & Yang44
2004
Cohort
157
Transperitoneal 2 nonabsorbable sutures
2 non-absorbable sutures
28 months laparoscopic group; 50 months open group
Cheon et al.40
2003
Prospective, randomized
90
Transperitoneal sutures
Fatthy et al.38
2001
Prospective, randomized
76
Extraperitoneal: n=34, 1 nonabsorbable suture
1 non-absorbable suture
18 months
El-Toukhy & Davies48
2001
Prospective, non-randomized
87
Extraperitoneal and transperitoneal: Prolene mesh and titanium tacks
2 non-absorbable sutures
32 months
Das30
1998
Prospective, non-randomized
20
Bone anchors
2 absorbable sutures
30 months
Saidi et al.43
1998
Retrospective
157
Extraperitoneal: 1 nonabsorbable suture
2 non-absorbable sutures
12.9 months laparoscopic group; 16.3 months open group
Miannay et al.42
1998
Retrospective
72
1 Non-absorbable suture
2 non-absorbable sutures
17 months laparoscopic group; 46 months open group
Burton37
1997
Prospective, randomized
60
2 Absorbable sutures
2 absorbable sutures
3 years
Su et al.39
1997
Prospective randomized
92
Transperitoneal: 1 or 2 nonabsorbable sutures (rarely 2) followed by laparotomy in 14 women
2–3 nonabsorbable sutures
3 months
1 year
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(80.4% versus 95.6%). The follow-up period was only 3 months and in the majority of cases only one suture was placed in the laparoscopic group compared to two or three sutures in the open group. The complication rate in the open group was higher than in the laparoscopic group (17.4% versus 10.8%). This study was included in the systematic review by Moehrer et al.; however, when a separate analysis was performed, excluding it due to methodologic flaws, the higher objective cure rate reported with the open approach was no longer significant.35 Cheon et al., in a randomized study of 90 women comparing open and laparoscopic colposuspension, reported similar objective cure rates at 1 year (86% versus 85%).40 Three further retrospective studies showed similar success rates at 1 year between the laparoscopic and open routes when non-absorbable sutures were used in both arms with less analgesia, shorter hospital stay, and earlier return to work seen in the laparoscopic group in two studies.42,43 The third study compared the anatomic result of the two procedures by assessing the bladder neck position with postoperative ultrasound and found no difference in resting, straining bladder neck position, and urethral mobility at 1 year postoperatively.44 Interestingly, one of these studies also showed a higher non-significant complication rate with the open procedure.43 McDougall reports a 30% success rate at 45 months for laparoscopic colposuspension with a nonabsorbable suture compared with 35% for needle suspension.28 However, the suture was attached to Cooper’s ligament by an absorbable clip. One randomized trial of 161 women undergoing laparoscopic colposuspension showed a higher objective success with two single-bite sutures on each side (83%) compared with one doublebite suture (58%).45 In the Medical Research Council colposuspension trial, 291 women were recruited in six centers in the UK. Of the 144 women allocated to laparoscopic surgery, 11 received open surgery and two had no operation. Of the 147 women allocated to open surgery, one had laparoscopic surgery and three had no operation. On intention-to-treat analysis at 2 years, the objective outcome (1-hour pad test) showed 80% cured in the laparoscopic group (85.4% data available), and 82% cured in the open group (79.6% data available); the subjective outcome (‘perfectly happy/pleased’ – Question 33 in the Bristol Female Urinary Tract Symptom Questionnaire) showed 55% cured in both the laparoscopic and the open group. These results demonstrate that, in the hands of experienced laparoscopic surgeons, laparoscopic surgery does not produce an inferior cure rate to open colposuspension.
success rates of non-suture colposuspension Table 84.1 demonstrated the different methods that have been used to carry out a colposuspension laparoscopically. Apart from the traditional suture method, the main method variation still adopted is the use of mesh and tacks to carry out the suspension. One randomized trial of 60 women compared the two laparoscopic methods. The authors demonstrated a higher objective failure rate at 1 year of 26.9% with the mesh technique compared to 11.1% with sutures.46 There are a further two studies in the literature that compare the laparoscopic route using mesh to the open procedure using sutures.47,48 Both studies reported a lower success rate with the laparoscopic approach. However, these studies are in fact comparing two entirely different operative procedures and the results cannot therefore be interpreted as outcome data for all laparoscopic colposuspension procedures.
complications Major complications reported following laparoscopic colposuspension include urinary tract injury, bowel injury, major vascular injury requiring transfusion, and abscess in the space of Retzius. In the longer term, failure of the procedure requiring repeat surgery, de novo detrusor overactivity, voiding difficulty, pain, ureteral obstruction, fistula, or posterior compartment prolapse may occur as for the open procedure. Buller and Cundiff, in their review of 1867 patients, report an overall complication rate of 10.3%.36 The bladder dome was the most commonly injured site and was repaired laparoscopically in the majority of cases. The lower urinary tract is injured in 2–3% of cases of laparoscopic colposuspension and paravaginal repairs.14,49 This is lower than the 10% reported with the open procedure.50 Intraoperative diagnosis of urinary tract injury is the main factor associated with decreased morbidity.51 Small bladder injuries can be managed by catheterization but if greater than 0.5 cm they should be closed laparoscopically in one or two layers with an absorbable suture. Where mesh has been substituted for sutures, different additional complications can occur. Kenton et al. have reported two cases of women who presented with complications following laparoscopic colposuspension with Prolene mesh and tacks. Both women had tacks removed retropubically from the bladder and retropubic space and no tacks were seen in Cooper’s ligament in either patient.52 In both cases, postoperative cystoscopy was not performed at the time of the colposuspension. 1187
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disadvantages The main disadvantage of the laparoscopic approach is that the surgeon must possess adequate minimal access skills to perform the procedure competently. It would appear that the modifications introduced, designed to overcome the difficulty of suturing in the cave of Retzius, result in lower success rates. There is a steep learning curve in laparoscopic surgery and this has resulted in fewer laparoscopic colposuspensions being performed. However, as the field of minimal access expands, there will be more competent laparoscopic surgeons available to mentor trainees.
cost The laparoscopic approach consistently requires longer operating time than the open colposuspension or TVT. The other cited factor against the laparoscopic approach is the increased cost associated with minimal access procedures. Kohli et al. reported a retrospective 2-year cost analysis of laparoscopic colposuspension with sutures compared with open colposuspension53. They found that the laparoscopic approach was more expensive than the open approach ($4960 versus $4079). This reflected the high hourly operative room charges in North America as the laparoscopic group took on average 44 minutes longer operating time. The postoperative care costs were lower in the laparoscopic group. Persson et al. reported that a laparoscopic colposuspension is cheaper than a TVT in Sweden (E1273.4 versus E1342.8) despite the TVT procedure being performed in less time.54 Differences in costs are difficult to assess as there is great variation in each country as to how long patients tend to stay in hospital following surgery and there are differing costs of operating time.
patient in the laparoscopic group required a laparotomy to remove the tacks inadvertently placed in the bladder, as they were too difficult to remove laparoscopically. However, 1-year data from the same study showed that the success rate of the TVT as defined by a negative stress test was 85.7% but the laparoscopic colposuspension group success rate had fallen to 56.9%.57 Of note, however, as discussed above, the mesh procedure is not synonymous with a standard colposuspension. A second study compared the laparoscopic approach using two absorbable sutures to the TVT in 46 women and reported similar outcomes with both procedures after 18 months.56 The TVT group required shorter operating time, shorter hospital stay, and less catheterization. Most recently an abstract publication has compared ‘re-do’ surgery where the patients were randomized to laparoscopic colposuspension or TVT and reported that the two procedures were equally effective in the medium term.58 Thus, overall, the data comparing a standard laparoscopic colposuspension with TVT would suggest that they are largely equivalent. However, the data available are too few to draw any firm conclusions.
paravagInal repaIr The aim of a paravaginal repair is to assess the integrity of the lateral attachment of the anterior vaginal wall from the pubic symphysis to the ischial spine and to repair any defects in this attachment (Fig. 84.12). This procedure can be completed at the same time as laparoscopic colposuspension.
laparoscopic colposuspension versus tensionfree vaginal tape procedures With the advent of midurethral tape procedures it is now pertinent to evaluate the performance of laparoscopic colposuspension compared with these newer minimally invasive procedures. The outcomes of two prospective randomized studies, comparing laparoscopic colposuspension to TVT, have been reported.55,56 One study comparing a laparoscopic colposuspension using Prolene mesh and tacks to the TVT in 121 women found similar cure rates at 6 weeks following surgery, with the TVT arm taking less operative time, shorter hospital stay, and earlier return to work.55 One
Figure 84.12. Sutures have been placed to complete the paravaginal repair.
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technique of paravaginal repair The anterior vaginal wall is elevated and the pubocervical fascia is reattached to the ipsilateral obturator internus muscle and fascia around the arcus tendineus with non-absorbable 2-0 sutures tied extracorporeally.14 A technique of stapling Prolene mesh to the vaginal margins and attaching it to Cooper’s ligament has also been described.59 The advantage of laparoscopic paravaginal repair compared with vaginal paravaginal is direct visualization of the anatomy.
complications Vaginal paravaginal repair is associated with a high complication rate with a transfusion rate reported as high as 16%.60 Mallipeddi et al. also reported a significant complication rate in 45 women undergoing vaginal paravaginal repair.61 Complications included one case of bilateral ureteric obstruction, one hematoma requiring drainage, two vaginal abscesses, and two women were transfused. A technique of vaginal paravaginal repair using Alloderm graft had an objective failure rate of 41% at 18 months postoperatively.62 Speights et al. reported no complications in 18 women who had a laparoscopic paravaginal repair.49
conclusIon Laparoscopic Burch colposuspension and paravaginal repair can be performed successfully with fewer complications than the open approaches. Current evidence suggests that laparoscopic colposuspension performed with sutures may be as effective as the open approach and the TVT procedures. The laparoscopic approach is associated with lower morbidity than the open procedures. It also avoids placing a permanent tape under the urethra, thereby reducing concern about the possibility of future tape erosion. However, the laparoscopic approach requires the surgeon to be competent in minimal access skills as well as urogynecology. The use of mesh and tacks or staples appears to reduce the success rate. Further studies are needed to evaluate the long-term outcome of the laparoscopic approach. As more surgeons become competent at operative laparoscopy, the long-term outcome of these procedures in more experienced hands will become evident.
reFerences 1. Gor M, McCloy R, Stone R, Smith A. Virtual reality laparoscopic simulator for assessment in gynaecology. Br J Obstet Gynaecol 2003;110:181–7. 2. Burch J. Urethrovaginal fixation to Cooper’s ligament for correction of stress incontinence, cystocele and prolapse. Am J Obstet Gynecol 1961;81:281–90. 3. Tanagho EA. Colpocystourethropexy: the way we do it. J Urol 1976;116:751–3. 4. Vancaille T, Schuessler W. Laparoscopic bladder-neck suspension. J Laparoendosc Surg 1991;1:169–73. 5. Marshall V, Marchetti A, Krantz K. The correction of stress incontinence by simple vesicourethral suspension. Surg Gynecol Obstet 1949;88:509–18. 6. Liu C, Paek W. Laparoscopic retropubic colposuspension (Burch procedure). J Am Assoc Gynecol Laparosc 1993;1:31–5. 7. Ou C, Presthus J, Beadle E. Laparoscopic bladder neck suspension using hernia mesh and surgical staples. J Laparoendosc Surg 1993;3:563–6. 8. Birken R, Leggett P. Laparoscopic colposuspension using mesh reinforcement. Surg Endosc 1997;11:1111–14. 9. Breda G, Silvestre P, Gherardi L, Xausa D, Tamai A, Giunta A. Correction of stress urinary incontinence: laparoscopy combined with vaginal suturing. J Endourol 1996;10:251–3. 10. Carter J. Laparoscopic Burch procedure for stress urinary incontinence: the Carter modification. Keio J Med 1996;45:168–71. 11. Shoemaker E, Wilkinson P. Teleoscopy after bladder neck suspension. J Am Assoc Gynecol Laparosc 1998;5:445–6. 12. Ross J, Galen D, Abbott K, Albala D, Presthus J, Su-Ou C, Turk T. A prospective multisite study of radiofrequency bipolar energy for treatment of genuine stress incontinence. J Am Assoc Gynecol Laparosc 2002;9:493–9. 13. Von Theobald P, Barjot P, Levy G. Feasibility of and interest in laparoscopic assessment in recurrent urinary stress incontinence after Burch procedure performed by laparotomy. Surg Endosc 1997;11:468–71. 14. Miklos J, Kohli N. Laparoscopic paravaginal repair plus Burch colposuspension: review and descriptive technique. Urology 2000;56:64–9. 15. A consensus document concerning laparoscopic entry techniques: Middlesbrough, March 19–20, 1999. Gynaecol Endosc 1999;8:403–6. 16. Childers J, Brzechffa P, Surwit E. Laparoscopy using the left upper quadrant as the primary trocar site. Gynecol Oncol 1993;50:221–5. 17. Pasic R, Levine R, Wolf W. Laparoscopy in morbidly obese patients. J Am Assoc Gynecol Laparosc 1999;6:307–12.
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18. Bowrey DJ, Blom D, Crookes PF et al. Risk factors and the prevalence of trocar site herniation after laparoscopic fundoplication. Surg Endosc 2001;15(7):663–6.
35. Moehrer B, Carey M, Wilson D. Laparoscopic colposuspension for urinary incontinence: a systematic review. Br J Obstet Gynaecol 2003;110:230–5.
19. Hurd W, Bude R, DeLancey J, Newman J. The location of abdominal wall blood vessels in relationship to abdominal landmarks apparent at laparoscopy. Am J Obstet Gynecol 1994;171:642–6.
36. Buller J, Cundiff G. Laparoscopic surgeries for urinary incontinence. Clin Obstet Gynecol 2000;43:604–18.
20. Balzer K, Witte H, Recknagel S, Kozianka J, Waleczek H. Anatomical guidelines for the prevention of abdominal wall haematoma induced by trocar placement. Surg Radiol Anat 1999;21:87–9.
37. Burton G. A three year prospective randomized urodynamic study comparing open and laparoscopic colposuspension. Neurourol Urodyn 1997;16:353–4. 38. Fatthy H, El Hao M, Samaha I, Abdallah K. Modified Burch colposuspension: laparoscopy versus laparotomy. J Am Assoc Gynecol Laparosc 2001;8:99–106.
21. Montz I, Holschneider C, Munro M. Incisional hernia following laparoscopy: a survey of American Association of Gynecological Laparoscopists. Obstet Gynecol 1994;84:881–4.
39. Su TH, Wang KG, Hsu CY, Wei HJ, Hong BK. Prospective comparison of laparoscopic and traditional colposuspension in the treatment of genuine stress incontinence. Acta Obstet Gynecol 1997;76:576–82.
22. Coda A, Bossotti M, Ferri F et al. Incisional hernia and fascial defect following laparoscopic surgery. Surg Laparosc Endosc Percut Tech 1999;9:348–52.
40. Cheon W, Mak J, Liu J. Prospective randomised controlled trial comparing laparoscopic and open colposuspension. Hong Kong Med J 2003;9:10–4.
23. Maher C, Carey M, Murray C. Laparoscopic suture hysteropexy for uterine prolapse. Obstet Gynecol 2001;97:1010–4.
41. Burton G. A randomised comparison of laparoscopic and open colposuspension. Neurourol Urodyn 1993;13:497–8.
24. Flax S. The gasless laparoscopic Burch bladder neck suspension: early experience. J Urol 1996;156:1105–7.
42. Miannay E, Cosson M, Lavvin D, Querleu D, Crepin G. Comparison of open retropubic and laparoscopic colposuspension for treatment of stress urinary incontinence. Eur J Obstet Gynecol Reprod Biol 1998;79:159–66.
25. Batislam E, Germiyanoglu C, Erol D. Simplification of laparoscopic extraperitoneal colposuspension: results of two-port technique. Int Urol Nephrol 2000;32:47–51. 26. Kadirkamanathan SS, Shelton JC, Hepworth CC, Laufer JG, Swain CP. A comparison of the strength of knots tied by hand and at laparoscopy. J Am Coll Surg 1996;182(1):46–54.
43. Saidi M, Gallagher S, Skop I, Saidi J, Sadler K, Diaz K. Extraperitoneal laparoscopic colposuspension: short-term cure rate, complications, and duration of hospital stay in comparison with Burch colposuspension. Obstet Gynecol 1998;92:619–21.
27. Shettko DL, Frisbie DD, Hendrickson DA. A comparison of knot security of commonly used hand-tied laparoscopic slipknots. Vet Surg 2004;33(5):521–4.
44. Huang W, Yang J. Anatomic comparison between laparoscopic and open Burch colposuspension for primary stress urinary incontinence. Urology 2004;63:676–81.
28. McDougall E. Laparoscopic management of female urinary incontinence. Urol Clin North Am 2001;28:145–9.
45. Persson J, Wolner-Hanssen P. Laparoscopic Burch colposuspension for stress urinary incontinence: a randomised comparison of one or two sutures on each side of the urethra. Obstet Gynecol 2000;95:151–5.
29. Henley C. The Henley suture-staple technique for laparoscopic Burch colposuspension. J Am Assoc Gynecol Laparosc 1995;2:441–4. 30. Das S. Comparative outcome analysis of laparoscopic colposuspension, abdominal colposuspension and vaginal needle suspension for female urinary incontinence. J Urol 1998;160:368–71.
46. Zullo F, Palomba S, Piccione F, Morelli M, Arduino B, Mastrantonio P. Laparoscopic Burch colposuspension: a randomised controlled trial comparing two transperitoneal surgical techniques. Obstet Gynecol 2001;98:783–8.
32. Bidmead J, Cardozo L. Short cut to incontinence? Lancet 2000;355:2183–4.
47. Ankardal M, Ekerydh E, Crafoord K, Milsom I, Stjerndahl JH, Engh ME. A randomised trial comparing open Burch colposuspension using sutures with laparoscopic colposuspension using mesh and staples in women with stress urinary incontinence. Br J Obstet Gynaecol 2004;111:974–81.
33. Das S. Laparoscopic surgery for female urinary incontinence: prudence shall prevail. J Soc Laparoendosc Surg 1999;3:273–7.
48. El-Toukhy T, Davies A. The efficacy of laparoscopic mesh colposuspension: results of a prospective controlled study. BJU Int 2001;88:361–6.
34. Moehrer B, Ellis G, Carey M, Wilson D. Laparoscopic colposuspension for urinary incontinence in women. Cochrane Database Syst Rev 2002;1:CD002239
49. Speights S, Moore R, Miklos J. Frequency of lower urinary tract injury at laparoscopic Burch and paravaginal repair. J Am Assoc Gynecol Laparosc 2000;7:515–18.
31. Cutner A, Rymer J. Patient recovery after laparoscopic colposuspension. Gynaecol Endosc 1998;7:307–8.
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50. Stevenson K, Cholhan H, Hartmann D, Buchsbaum G, Guzick D. Lower urinary tract injury during the Burch procedure. Is there a role for routine cystoscopy? Am J Obstet Gynecol 1999;181:35–8. 51. Sadik S, Onoglu S, Mendilcioglu I, Sehirali S, Sipahi C, Taskin O, Wheeler J. Urinary tract injuries during advanced gynaecologic laparoscopy. J Am Assoc Gynecol Laparosc 2000;7:569–72. 52. Kenton K, FitzGerald MP, Brubaker L. Multiple foreign body erosions after laparoscopic colposuspension with mesh. Am J Obstet Gynecol 2002;187:252–3. 53. Kohli N, Jacobs P, Sze E, Roat T, Karram M. Open compared with laparoscopic approach to Burch colposuspension: a cost analysis. Obstet Gynecol 1997;90:411–15. 54. Persson J, Teleman P, Eten-Bergquist C, Wolner-Hanssen P. Cost analyses based on a prospective randomised study comparing laparoscopic colposuspension with a tensionfree vaginal tape procedure. Acta Obstet Gynecol Scand 2002;81:1066–73. 55. Valpas A, Kivela A, Pentinnen J et al. Tension-free vaginal tape and laparoscopic mesh colposuspension for stress urinary incontinence. Obstet Gynecol 2004;104:42–9. 56. Üstün Y, Engin-Üstün Y, Gungor M, Tezcan S. Tensionfree vaginal tape compared with Burch urethropexy. J Am Assoc Gynecol Laparosc 2003;10:386–9. 57. Valpas A, Kivela A, Pentinnen J et al. Tension-free vaginal tape and laparoscopic mesh colposuspension in the treatment of stress urinary incontinence: immediate outcome and complications – a randomised clinical controlled trial. Acta Obstet Gynecol Scand 2003;82:665–71. 58. Maher C, Qatawneh A, Baessler K, Cropper M, Schluter P. Laparoscopic colposuspension or tension-free vaginal tape for recurrent stress urinary incontinence and or ISD: a randomised controlled trial. Neurourol Urodyn 2004;5/6:Abstract 25.
63. Liu C. Laparoscopic retropubic colposuspension (Burch procedure). A review of 58 cases. J Reprod Med 1993;38:526–30. 64. Das S, Palmer J. Laparoscopic colpo-suspension. J Urol 1995;154:1119–21. 65. Kiilholma P, Haarala M, Polvi H, Makinem J, Chancellor M. Sutureless colposuspension with fibrin sealant. Tech Urol 1995;1:81–3. 66. Langebrekke A, Dahlstrom B, Eraker R, Urnes A. The laparoscopic Burch procedure: a preliminary report. Acta Obstet Gynecol Scand 1995;74:153–5. 67. Gunn GC, Cooper RP, Gordon NS, Gragnon L. Use of a new device for endoscopic suturing in the laparoscopic Burch procedure. J Am Assoc Gynecol Laparosc 1994;2:65–70. 68. Liu C. Laparoscopic treatment of genuine urinary stress incontinence. Clin Obstet Gynecol 1994;8:789–98. 69. Ross JW. Laparoscopic Burch repair compared to laparotomy Burch for cure of urinary stress incontinence. Int Urogynecol 1995;6:323–8. 70. Ross JW. Two techniques of laparoscopic Burch repair for stress incontinence: a prospective randomized study. J Am Assoc Gynecol Laparosc 1996;3:351–7. 71. Kung R, Lie K, Lee P et al. The cost effectiveness of laparoscopic versus abdominal Burch procedures in women with urinary stress incontinence. J Am Assoc Gynecol Laparosc 1996;3:537–44. 72. Lam AM, Jenkins GJ, Hyslop RS. Laparoscopic Burch colposuspension for stress incontinence: preliminary results. Med J Aust 1995;162:18–22. 73. Liu C, Paek W. Laparoscopic retropubic colposuspension (Burch procedure). J Am Assoc Gynecol Laparosc 1993;1:31–5.
59. Washington J, Somers K. Laparoscopic paravaginal repair: a new technique using mesh and staples. JSJL 2003;7:301–3.
74. Ross J. Multichannel urodynamic evaluation of laparoscopic Burch colposuspension for genuine stress incontinence. Obstet Gynecol 1998;91:55–9.
60. Young S, Daman J, Bony L. Vaginal paravaginal repair: one year outcomes. Am J Obstet Gynecol 2001;185:1360–7.
75. Papasakelariou C, Papasakelariou B. Laparoscopic bladder neck suspension. J Am Assoc Gynecol Laparosc 1997;4:185–9.
61. Mallipeddi PK, Steele AC, Kohli N, Karram MM. Anatomic and functional outcome of vaginal paravaginal repair in the correction of anterior vaginal wall prolapse. Int Urogynecol J Pelvic Floor Dysfunct 2001;12(2):83–8. 62. Clemons J, Myers D, Aguilar V, Arya L. Vaginal paravaginal repair with an Alloderm graft. Am J Obstet Gynecol 2003;189:1612–18.
76. Lee C, Yen C, Wang C, Huang K, Soong Y. Extraperitoneoscopic colposuspension using CO2 distension method. Int Surg 1998;83:262–4. 77. Nezhat CH, Nezhat F, Nezhat CR et al. Laparoscopic retropubic cystocolposuspension. J Am Assoc Gynecol Laparosc 1994;1:339–49.
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INTRODUCTION The use of laparoscopy to treat pelvic organ prolapse has increased in recent years. In the United States the number of laparoscopic procedures performed for prolapse almost doubled in the period from 1979 to 1997 (1246 cases in 1979 and 2459 in 1997) against a small decline in the total number of operations performed for pelvic organ prolapse during this period.1 The main limitation of laparoscopy for the treatment of pelvic organ prolapse is the relatively small number of surgeons with sufficient laparoscopic and reconstructive pelvic surgical skills to perform these procedures safely and successfully. Approximately 200,000 women undergo surgery for pelvic organ prolapse in the United States each year.1 In a study of women from a large United States health maintenance organization it was reported that, by the age of 80 years, 11.1% of women had undergone surgery for pelvic organ prolapse or urinary incontinence, or both.2 Within 4 years of the primary surgical procedure, 29.2% of these women required repeat surgery for recurrent prolapse. Younger patients (age less than 60 years) and women with higher grades of prolapse (pelvic organ prolapse quantification [POPQ] stages 3 and 4) are more likely to experience recurrent prolapse after vaginal repair.3,4 The prevalence of vaginal vault prolapse following hysterectomy is approximately 10%.5 However, estimates of the prevalence of posthysterectomy vault prolapse vary markedly from 0.2% to 43%.5–7 Vault prolapse occurs in equal numbers following abdominal and vaginal hysterectomy.8,9 The high rate of failure with vaginal surgery to treat vaginal vault prolapse led to the development of the abdominal sacrocolpopexy (ASC) procedure. This approach employs the retroperitoneal interposition of a suspensory prosthesis (synthetic, autologous, allograft or xenograft) between the vaginal apex and the sacrum. ASC was originally described by Huguier in 1957 and later by Lane in 1962.10,11 Snyder and Krantz described attachment of the prosthesis along the full length of the rectovaginal septum.12 Addison et al. described the broad attachment of the prosthesis to both the upper anterior and posterior vaginal walls.13,14 Randomized trials comparing the ACS procedure with transvaginal sacrospinous ligament fixation to treat vaginal vault prolapse demonstrated a trend towards the ACS being the more effective procedure.15–17 In addition to the high success rate reported with the ACS procedure, other advantages include preservation of vaginal capacity resulting in maintenance of coital function, use of synthetic material resulting in durable support, and the use of the synthetic graft on both anterior and posterior vaginal aspects providing for balanced support of
the various vaginal sites and an acceptable vaginal axis. Significant problems associated with the ASC operation include de novo postoperative stress incontinence, intraoperative hemorrhage, dyspareunia, mesh erosion, and use of a laparotomy incision.11,12,14,18,19 Laparoscopic sacrocolpopexy (LSC) was first described by Nezhat et al. in 1994 although Wattiez et al. claim to have first performed this procedure in 1991.20,21 The proposed advantages of the LSC over the ASC include the avoidance of a major laparotomy incision, less postoperative pain, shorter time in hospital, and a quicker return to normal activities. The laparoscopic approach provides the surgeon with an enhanced view of the pelvic and intra-abdominal anatomy compared to the abdominal approach. The LSC takes advantage of the known high success rate of the traditional ASC combined with the benefits of laparoscopic surgery. The LSC should be performed in an identical manner to the ASC with the only difference being the smaller laparoscopic incisions.
ANATOMIC CONSIDERATIONS Following hysterectomy, the upper third of the vagina (including the vault) is supported by two mechanisms: 1. Direct support for the vaginal vault is provided by the parametrium (cardinal and uterosacral ligaments) and paracolpium fibers. These fibers act like suspensory ligaments and arise from the fascia of the piriformis muscle, sacroiliac joint and lateral sacrum, and insert into the lateral upper third of the vagina. 2. Indirect support for the vaginal vault is provided by the levator plate, formed by the fusion of the right and left levator ani muscles between the rectum and coccyx. Vaginal vault prolapse occurs as a consequence of failure of these direct and indirect supporting mechanisms. This is likely to involve weakness of the muscular pelvic floor and suspensory fibers of the parametrium and upper paracolpium.22,23 Recent work evaluating the fibromuscular composition of the vaginal wall in women with and without enterocele failed to demonstrate any focal ‘defect’ of the vaginal muscularis.24 Based on these anatomic considerations it is not surprising that a site-specific endopelvic fascial repair approach to the treatment of a vaginal apical defect is likely to carry an unacceptably high failure rate.25,26 For women with vaginal vault prolapse, surgical repair should generally be directed towards restoring vault sup-
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port and a normal vaginal axis. These anatomic considerations lend credibility to the concept of the ASC and LSC procedures.
Anatomy of the sacral promontory The presacral space is bounded superiorly by lumbosacral intervertebral disk and laterally by the right common iliac artery and left common iliac vein (Fig. 85.1). The right ureter is identified coursing in the right lateral aspect of the presacral space. The sacral promontory and presacral space are usually covered by the sigmoid colon. The sigmoid colon at this point is attached to the peritoneum, which is reflected over the left psoas major muscle and iliacus muscle. Once the sigmoid colon is retracted to the left side, the sacral promontory is easily identified. The presacral space and sacral promontory is accessed by gently lifting up the peritoneum directly over the sacral promontory and performing a midline longitudinal incision. This approach into the presacral space will avoid damage to the right common iliac artery and left common iliac vein. The middle sacral artery and vein are easily identified lying directly on the middle aspect of the sacrum. The middle sacral artery originates as a single branch from the posterior aspect of the aorta. The middle sacral vein arises from vessels emerging beneath the common iliac veins and drains into the inferior vena cava. Some women have an extensive venous plexus in the presacral space, and damage to these vessels can result in dramatic hemorrhage. The middle sacral artery gives off small branches that run laterally on the sacrum to either anastomose with the lateral sacral arteries or directly supply the ventral sacral nerve roots. Damage to these fine vessels can result in bleeding and ischemic injury to the ventral sacral nerve roots.
The hypogastric plexus of nerves descends into the pelvis anterior to the bifurcation of the aorta, enters the presacral space between the common iliac arteries, and is anterior to the middle sacral artery and vein. This plexus carries the autonomic nerves of the pelvic viscera. Extensive damage to this plexus of nerves may result in bladder, bowel, and sexual dysfunction. When performing a LSC procedure, meticulous dissection is recommended in order to reduce the risk of nerve damage. After entering the presacral space the anterior longitudinal ligament is exposed by gentle blunt dissection of the presacral tissues over the sacral promontory. Sharp dissection and the use of ablative techniques to access the anterior longitudinal sacral ligament should be avoided. When securing the prosthetic material to the sacral promontory the surgeon should avoid excessive use of sutures or stapling devices onto the sacral promontory. When performing a LSC procedure, the author uses only one or two sutures to secure the prosthesis onto the anterior longitudinal ligament on the sacral promontory, and has not encountered a case of mesh detachment from the sacral promontory with this approach.
CLINICAL ASSESSMENT AND PATIENT SELECTION Clinical assessment is undertaken in the usual fashion. This includes obtaining a detailed history with particular emphasis on any symptoms associated with the vaginal vault prolapse, especially urinary, bowel, and coital symptoms. A detailed general and pelvic examination is undertaken. It is important for the clinician to identify all the vaginal defects accurately so that they can be corrected at the time of surgery. The patient should be examined for signs of stress incontinence with the pro-
Figure 85.1. The presacral space is bounded by the lumbosacral intervertebral disk above and laterally by the right common iliac artery and left common iliac vein. The middle sacral artery and vein course over the anterior longitudinal ligament on the sacral promontory. 1195
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lapse present and reduced, and also for any anorectal pathology, including rectal prolapse. Urodynamic studies should be made available to patients with associated urinary symptoms. Imaging of the pelvic floor and anorectal physiologic testing are recommended as indicated.
Indications Currently, there is no consensus on the exact indications for both ASC and LSC procedures. The LSC is indicated for patients with symptomatic and significant prolapse of the vaginal vault who are considered appropriate candidates for an ASC. This approach is suitable for younger patients wishing to preserve coital function and in whom there are no contraindications to laparoscopic surgery. Gadonneix et al. reported that 89% of 46 consecutive patients presenting with multiple compartment prolapse could be treated by LSC.27 The LSC procedure should be made available to patients with significant vaginal vault prolapse with no contraindications to laparoscopy. Typically, these women have had a previous hysterectomy and an International Continence Society POPQ classification of stage 2 or greater prolapse at the vaginal vault site.4 Patients with significant stage 1 vault prolapse are sometimes offered this approach. LSC can also be used in conjunction with a hysterectomy to treat marked uterine prolapse of stage 2 or greater in younger women.10,26 LSC treats vaginal vault prolapse as well as high cystoceles and rectoceles when the mesh is extended onto the upper anterior and posterior vaginal walls.29 On occasion, the LSC procedure with extension of mesh anteriorly and in combination with a laparoscopic paravaginal repair is offered to women with a recurrent cystocele, as this combination of procedures is very effective in treating recurrent high cystoceles. LSC is a complex operation requiring both advanced laparoscopic and reconstructive pelvic surgery skills. Only surgeons competent in this operative technique should undertake this surgery.
Contraindications Vaginal operations may be more appropriate for frail women who do not wish to preserve coital function. LSC is not indicated for women with minor degrees of vault prolapse. This procedure is also not suitable for patients who otherwise have a contraindication to laparoscopic surgery. In these women an ASC or vaginal surgery to treat the vault prolapse should be offered.
SURGICAL TECHNIQUE A standardized technique for LSC does not exist. Surgery is performed under general anesthesia with muscle relaxation. A major challenge is the achievement and maintenance of adequate surgical exposure of the vaginal vault and sacral promontory. A steep Trendelenburg position, preoperative bowel preparation, avoidance of nitrous oxide anesthesia, and an adequate number of operating ports all facilitate good surgical exposure. Left lateral tilting of the patient can also be employed.30 Laparoscopic bowel retractors appear to be of limited benefit. Following induction with general anesthesia the woman is placed in a low lithotomy position using Allen stirrups. Use of Allen stirrups allows the patient to be repositioned during surgery without the need to redrape. Repositioning may be required when concomitant vaginal surgery is undertaken. Standard techniques are used to introduce a 10 mm operating laparoscope at the umbilicus. Under laparoscopic vision, two ports (for the right-handed surgeon a 10 mm port on the patient’s left and a 5 mm port on the patient’s right) are inserted through the anterior abdominal wall into the peritoneal cavity. In order to avoid injury to the inferior epigastric artery and vein and damage to the lateral cutaneous nerve to the thigh, these ports are sited two fingerbreadths above and two fingerbreadths medial to the anterior superior iliac spine. A further 5 mm port is introduced suprapubically in the midline under laparoscopic vision. A vaginal probe is inserted to identify the vaginal vault. With the vagina elevated cranially using the vaginal probe (Fig. 85.2), the peritoneum is opened transversely at the vaginal apex. This dissection continues posteriorly into the rectovaginal septum so that the peritoneum is dissected off the upper half of the posterior vaginal wall. At around this point the rectovaginal septum is entered and the rectum is dissected off the middle and lower posterior vaginal wall. On occasion, dissection can be facilitated by using a rectal probe. This dissection is carried out in the midline and extended laterally on both sides to the insertion of the uterosacral ligaments. The bladder is then dissected off the upper anterior vaginal wall. This dissection continues to approximately the midpoint of the anterior vaginal wall. Dissection is continued laterally towards both bladder pillars but generally dissection of the bladder pillars is avoided. This is to reduce intraoperative bleeding and injury to the autonomic nerves to the bladder. Once the peritoneum has been dissected off the upper vagina, along with dissection of the bladder and rectum, the sacral promontory is identified. Usually the sigmoid
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a
Figure 85.2. The vagina is elevated using a vaginal probe. This facilitates the dissection of peritoneum, bladder and rectum off the upper vagina. colon obscures the sacral promontory and needs to be reflected to the patient’s left. The sacral promontory is usually an easily recognizable and accessible structure (Fig. 85.3a). However, in obese patients the sacral promontory may be difficult to access. Prior to dissection in this region the right ureter should be carefully identified. The peritoneum over the sacral promontory is grasped and elevated. A vertical incision is made into the peritoneum in the midline to allow entry into the presacral space (Fig. 85.3b). The peritoneum is further dissected in a caudal direction on the right of the rectum and sigmoid colon and below the right ureter into the cul-de-sac to join the posterior vaginal peritoneal dissection. Once this dissection is completed, the tissues in the presacral space over the sacral promontory are carefully reflected laterally so that the glistening white fibers of the anterior longitudinal ligament are exposed (Fig. 85.4a). At this point it is important to carefully identify any vascular structures on the sacral promontory in the midline so that injury to these structures can be avoided when the prosthesis is attached to the sacral promontory. Two rectangular pieces of mesh (e.g. Gynecare Gynemesh PS, a type 1 polypropylene mesh)31 are then cut to size, the first being 15×3 cm and the second being 5×3 cm. The larger piece of mesh is used to support the posterior vaginal wall and vault and the smaller piece to support the anterior vaginal wall and vault. The larger mesh is introduced into the pelvis through the left 10 mm port. Using delayed absorbable monofilament sutures throughout, this mesh is attached to the posterior vaginal wall with four to six sutures. The smaller mesh is then introduced into the pelvis and attached to the upper anterior vaginal wall
b
Figure 85.3. (a) The sacral promontory is easily recognizable and accessible during laparoscopic sacral colpopexy. (b) The peritoneum over the sacral promontory is elevated and a vertical incision is made into the peritoneum in the midline to allow safe entry into the presacral space. with four sutures. Two sutures are placed at the vaginal vault and through both anterior and posterior pieces of mesh. The point of attachment of the mesh onto the sacral promontory is defined. The mesh is fixed to the sacral promontory without placing tension on the vagina. A permanent suture is passed in turn through the mesh and into the anterior longitudinal ligament in the middle of the sacral promontory, with care taken to avoid injury to any vessels at this site. Occasionally, a second bite into the anterior longitudinal ligament is taken (Fig. 85.4b). The suture is then passed again through the mesh and tied, anchoring the mesh onto the sacral promontory. Excess mesh above the knot is excised and removed from the abdomen (Fig. 85.5). The peritoneum is closed with a continuous delayed absorbable 1197
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monofilament suture starting at the sacral promontory. Closure of the peritoneum completely isolates the prosthesis from intra-abdominal viscera and contributes to the obliteration of the pouch of Douglas. Occasionally the pouch of Douglas may remain deep on the left side in which case a left-sided Moschcowitz and Halban procedure can be performed to reduce the possibility of enterocele formation.
Types of prosthesis
a
b
Figure 85.4. (a) The tissues in the presacral space are carefully reflected laterally exposing the glistening, white fibers of the anterior longitudinal ligament on the sacral promontory. (b) A suture is passed in turn through the mesh and into the anterior longitudinal ligament on the sacral promontory in the midline.
Ideally, the prosthesis used for LSC should be durable over a patient’s lifetime, user friendly, cost effective, and have a minimal risk of complications including erosion, infection, chronic inflammation, tissue contraction, pain, and dyspareunia. A variety of synthetic meshes and biologic grafts have been described for both ASC and LSC. There is insufficient research to provide surgeons with answers as to whether synthetic meshes are more durable than biologic grafts or whether specific meshes are superior to others with respect to clinical outcomes and complications. Surgeons should base their selection of synthetic mesh used for LSC on a thorough understanding of the important biomechanical and biocompatible properties of each available mesh. There is an emerging consensus that lightweight, open-weave, monofilament polypropylene meshes are the most suitable of the existing meshes for use in surgery for pelvic organ prolapse. New generation meshes specifically designed for pelvic organ prolapse surgery will require appropriate animal and clinical evaluation before being recommended for use in prolapse surgery.
Figure 85.5. Mesh is sutured to the vaginal vault with extension down the upper anterior and posterior vaginal walls. The mesh is then sutured to the sacral promontory with placing tension on the vaginal vault. 1198
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Although biologic grafts are unlikely to erode, poor durability remains a major concern. FitzGerald et al. reported a high prevalence of prolapse recurrence following ASC using freeze-dried, irradiated donor fascia.32 At 12-month median follow-up of 54 women after ASC, 43% experienced failure and this increased to 83% at 17 months. Of the 16 women who underwent repeat ASC with mesh, no graft material from initial ASC was identified in 13 (81%) cases, indicating a high rate of graft degradation and resorption. The authors concluded that the use of freeze-dried, irradiated donor fascia for ASC was associated with an unacceptably high failure rate. Until more clinical information becomes available on the use of biologic grafts such as donor fascia, porcine small intestine submucosa, and porcine dermis for ASC and LSC procedures, these grafts should be reserved for specific indications. These indications might include extremely thin vaginal epithelium, replacement for mesh that has required removal, prior pelvic irradiation, and situations of high risk for mesh infection (e.g. bowel resection during combined surgery for genital and rectal prolapse). However, there remains a lack of evidence to support the use of biologic prostheses over mesh in these circumstances.
Sacral promontory fixation Various methods of attaching the suspending prosthesis onto the sacral promontory at LSC have been reported. These include sutures, bone anchors, staples, and helical tacks.9,27,29,30,33,34 There is a lack of research comparing the various methods of fixation of the prosthesis onto the sacral promontory. Due to the technical difficulties involved in laparoscopic suturing with LSC, some surgeons have preferred bone anchors and staples to sutures. Surgeons have described attachment of the prosthesis to different points on the sacrum. Birnbaum advocated placement of the prosthesis at the level of S3–S4.35 Sutton et al. advocated placement of the prosthesis at the level of S1–S2 in order to reduce the risk of massive sacral bleeding.36 The author’s preference has been to use the anterior longitudinal ligament on the sacral promontory and to attach the mesh with sutures. The sacral promontory is the most accessible point on the sacrum and is particularly well visualized at laparoscopic surgery. Mesh should not be fixed to the lumbosacral intervertebral disk because of the risk of discitis, hemorrhage, and pain from damage to the sensory nerve supply.37 Superior visualization at the sacral promontory allows the surgeon to avoid damage to vascular
structures more easily and to control excessive sacral bleeding than does the hollow of the sacrum. Use of the sacral promontory has no detectable negative effect on the vaginal axis.36
Robotic assistance Elliot et al. reported on 20 patients treated by roboticassisted LSC.34 The mean operating time was 3.2 hours. The authors claim that robotic-assisted LSC is easier and quicker to perform than LSC using conventional laparoscopy. The major disadvantage of robotic-assisted LSC is the ‘prohibitive’ cost of the robotic system. No doubt robotic equipment will become cheaper and more widely available, and may eventually find an established role in LSC surgery.
Perioperative care It is the author’s practice that patients be administered a limited bowel preparation in the afternoon of the day prior to surgery. Patients should have an oral intake of clear fluids only during the 12-hour period prior to the commencement of fasting before surgery. Bowel preparation is used in order to improve surgical exposure rather than for anticipated bowel trauma. Intravenous broad-spectrum antibiotic therapy and subcutaneous thrombotic prophylaxis are administered with anesthesia induction and continued postoperatively. Handling of the mesh is kept to a minium. Maintaining hemostasis, liberal use of pelvic irrigation, evacuation of blood from the pelvis, and use of monofilament sutures to attach the mesh onto the vagina are all important measures undertaken to reduce the risk of mesh erosion. At the completion of surgery, cystoscopy may be undertaken to exclude ureteric or bladder injury. Digital rectal and vaginal examination should be performed to exclude the presence of perforating sutures. Following discharge from hospital, patients should avoid strenuous activity for 3–4 weeks. By this time the mesh will have become incorporated into the tissues and patients can then resume activities of normal daily living. Patients should avoid sexual intercourse for at least 6 weeks following surgery. Pelvic floor exercises may be recommenced any time after surgery.38
CONCOMITANT ANTI-INCONTINENCE SURGERY Urodynamic assessment is appropriate for women with symptomatic stress incontinence and vaginal vault prolapse. If urodynamic stress incontinence is demonstrated, then concomitant anti-incontinence surgery, in 1199
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addition to the LSC operation, is indicated. Laparoscopic colposuspension or a midurethral tape procedure – for example, the tension-free vaginal tape (TVT) operation – can be employed. Occasionally, a transurethral bulking agent is indicated for women with a rigid urethra and, typically, previous failed anti-incontinence surgery. The simplicity and demonstrated effectiveness of the TVT procedure makes this an attractive option over the laparoscopic colposuspension procedure. Paraiso et al., in a randomized trial of 72 women, found the TVT procedure to result in significantly greater objective and subjective cure rates for stress incontinence than laparoscopic Burch colposuspension.39 This finding was supported by Valpas et al.40 Furthermore, the opposing vector effect of combining LSC with laparoscopic colposuspension may result in persistence of postoperative stress incontinence. The role of anti-incontinence surgery for occult stress incontinence during surgery for pelvic organ prolapse remains the subject of ongoing debate. Nygaard et al. emphasized the clinical challenge of patients with occult stress incontinence and vault prolapse.18 A systematic review by Maher et al. was unable to determine whether or not ‘potential stress urinary incontinence detected on reduction of prolapse prior to surgery is best treated with formal continence surgery at the time of prolapse surgery, rather than being left untreated’.17 Based on current knowledge, the decision to offer concomitant anti-incontinence surgery during LSC is up to the clinical judgment of the surgeon after a careful discussion with the patient. The author gives patients the option of a concomitant TVT procedure or laparoscopic colposuspension during the LSC proTable 85.1.
cedure when occult stress incontinence is present. Patients should always be warned of the possibility of persisting or de novo urinary incontinence developing following LSC, whether or not anti-incontinence surgery is also performed. The prevalence of de novo postoperative urinary incontinence is approximately 15–18%.41
RESULTS To date, only a small number of studies on LSC have been reported (Table 85.1).9,10,20,21,27–29,33,34,42 All studies report high success rates and low morbidity with the LSC procedure. However, the different study methodologies employed make the outcome data difficult to collate. It is difficult to draw any conclusions about the long-term outcomes for LSC due to a lack of a standardized technique, wide variation in the definition of outcomes, and lack of control for potential confounders, especially concomitant surgery. In some series the majority of subjects underwent laparoscopic sacral hysteropexy (LSH) rather than LSC.10,27,29 However, the surgical outcomes in these studies did not differentiate between LSC and LSH. Higgs et al. reported on 140 consecutive cases treated by LSC of whom 103 were available for long-term followup.9 This is the largest case series of LSC reported to date with a median follow-up of 66 months. A prior vaginal hysterectomy had been performed in 48% of cases and prior abdominal hysterectomy in 52%. Prolene mesh was used in all cases and fixed to the sacrum by either sutures or staples. Concomitant surgeries included laparoscopic colposuspension (37.8%), paravaginal repair (19.4%),
Effectiveness of laparoscopic sacral colpopexy
Author
Year
Nezhat et al.20
1994
42
Ross
n
Follow-up (months)
Objective success (%)
Subjective success (%)
15
range 3–40
100
100
100
–
1997
19
12
21
2001
125
32
93.4
100
Cosson et al.28
2002
83
11
94
–
Wattiez et al.
29
Antiphon et al.
Comments
2004
108
17
96.3
83.5
40 LSC, 68 LSH
27
Gadonneix et al.
2004
46
24
83
95
7 LSC, 34 LSH, 5 conversions to open surgery
Sundaram et al.33
2004
10
16
Elliot et al.34
2004
20
5.1
10
2005
363
14.6
98.9
96
9
2005
140
66
92%
62%
Rozet et al. Higgs et al.
90 –
– 100 97 LSC, 266 LSH
LSC, laparoscopic sacral colpopexy; LSH, laparoscopic sacral hysteropexy.
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vaginal repair (19.4%), rectopexy (3.8%), anal sphincter repair (1.9%), and transurethral collagen injection (1%). The average age of the patients was 58 years and the mean duration of surgery was 145 minutes overall and 107 minutes if LSC was the only procedure. Review was conducted independent of the surgeon. Of the 140 women, 66 were available for follow-up examination and 92% (objective success rate) of these demonstrated good long-term vault support. A total of 103 women completed follow-up questionnaires and the subjective success rate was 62% with 64 of the 103 women reviewed reporting no ‘presence of a lump’. Rozet et al. reported on a large case series of 363 women treated by either LSC or LSH with mesh interposition between 1996 and 2002.10 Of the 363 cases, 97 (26.7%) underwent LSC (82 women had posthysterectomy vault prolapse and 12 underwent combined LSC and hysterectomy). The other 266 (73.3%) cases underwent LSH with mesh interposition. A polyester mesh, silicone coated on one side, was used with anterior and posterior mesh extensions. The mesh was sutured onto the sacral promontory and the peritoneum closed over the mesh. This study reported outcomes for the whole group and a subanalysis of patients who underwent LSC was not performed. A concomitant TVT procedure was performed in 163 (45%) cases, all of whom demonstrated the signs of stress incontinence preoperatively. The average age of the 363 subjects was 63 years and the average operating time 97 minutes. The prevalence of recurrent prolapse was only 4%.
COMPLICATIONS Just over 3.7 million women underwent surgery for pelvic organ prolapse from 1979 to 1997 in the United States; this included 31,387 women with laparoscopically performed prolapse surgery. Complications in association with all the various procedures used to treat prolapse occurred in only 5.5% of cases. In women who underwent laparoscopic surgery to manage pelvic organ prolapse, complications were identified in only 6.6% of patients, which is comparable with other prolapse operations. Women treated laparoscopically had a significantly higher risk of pulmonary edema but a lower risk of urinary complications.1 Higgs et al. reported that immediate and short-term complications were rare.9 However, the mesh erosion rate was high at 9%. When the mesh was introduced vaginally, the erosion rate was 20% but only 6% when introduced laparoscopically. The transvaginal introduction of the mesh was performed in 20 cases but abandoned
in favor of laparoscopic introduction after the authors noticed a high erosion rate with this technique. The main complications reported by Rozet et al. included eight conversions to ASC, three vaginal mesh erosions, two mesh infections, one bowel obstruction requiring bowel resection, and one case of spondylitis. No case of postoperative dyspareunia was reported.10 In the series reported by Cosson et al., conversion to ASC was required for six cases.28 One rectal and two bladder injuries were reported. Reoperation for hemorrhage or hematoma was required in three women.
CONCLUSION Posthysterectomy vaginal vault prolapse is a challenging clinical problem. The goals of surgery when treating vaginal vault prolapse are:
• the relief of patients’ symptoms; • the correction of vaginal vault prolapse by restoring the normal pelvic anatomy where feasible;
• the correction of coexisting urinary, coital, and • •
lower bowel dysfunction; the avoidance of the development of urinary, coital, and lower bowel dysfunction; the achievement of a durable result, which in some cases may require the use of prosthetic materials.
The ‘best’ operation for treating vaginal vault prolapse remains the subject of ongoing debate. In treating vaginal vault prolapse, vaginal, abdominal, and laparoscopic approaches should not be viewed as competing procedures.43 The choice of operation to treat vaginal vault prolapse depends on many factors: the surgeon’s training and experience will influence the choice of surgery, and a recommendation for a specific operation can only be made after careful clinical assessment and after taking into consideration the patient’s age, medical condition, coital activity, level of physical activity, and a history of failed prior surgery. Systematic review of the surgical management of prolapse has demonstrated the ASC procedure to be associated with a lower recurrence of vault prolapse and less dyspareunia than vaginal approaches.15–18 However, when compared to vaginal approaches, ASC required a longer operating time and patients were slower to return to activities of normal daily living. LSC should be performed in a similar fashion to ASC. Based on the reported experiences of many surgeons over the past 50 years,18 and upon personal experience of ASC and LSC procedures, the following important principles of ASC and LSC are proposed: 1201
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• Careful patient selection; • Appropriate level of surgical experience and • • • •
expertise; Use of a biocompatible prosthesis; A broad area of prosthesis attachment to the vaginal vault, and upper anterior and posterior vagina; Fixation of the prosthesis to the anterior longitudinal ligament on the sacral promontory rather than to the sacral hollow; Placement of the prosthesis without tension to reduce the risk of postoperative urinary incontinence.
From the limited available data, LSC appears to be a highly effective procedure for the treatment of vaginal vault and marked uterovaginal prolapse. The LSC procedure combines the accepted effectiveness of ASC over vaginal operations for vault prolapse with the significant benefits of laparoscopic surgery. These benefits include superior surgical visualization, less pain, and quicker return to activities of normal daily living. The major limitation of LSC is the high degree of laparoscopic and reconstructive pelvic surgical skills required to perform this operation effectively and safely. With continued advances in laparoscopic equipment (including robotics) and more widespread training in advanced laparoscopic surgery, LSC is likely to gain in popularity. Currently, there is a paucity of data on the effectiveness, functional outcome, and safety of LSC. Further prospective studies, including comparative studies, are required to evaluate the role of the LSC procedure.
REFERENCES
tomy enterocele and vaginal vault prolapse. Am J Obstet Gynecol 1981;140:852–9. 7. Toozs-Hobson P, Boos K, Cardozo L. Management of vaginal vault prolapse. Br J Obstet Gynaecol 1998;105:13–17. 8. Carey MP, Slack MC. Transvaginal sacrospinous colpopexy for vault and marked uterovaginal prolapse. Br J Obstet Gynaecol 1994;101:536–40. 9. Higgs PJ, Chua H-L, Smith ARB. Long term review of laparoscopic sacrocolpopexy. Br J Obstet Gynaecol 2005; in press. 10. Rozet F, Mandron E, Arroyo C et al. Laparoscopic sacral colpopexy approach for genito-urinary prolapse: experience with 363 cases. Eur Urol 2005;47:230–6. 11. Lane FE. Repair of posthysterectomy vaginal vault prolapse. Obstet Gynecol 1962;20:72–7. 12. Snyder TE, Krantz KE. Abdominal–retroperitoneal sacral colpopexy for the correction of vaginal prolapse. Obstet Gynecol 1991;77:944–9. 13. Addison WA, Livengood CH, Sutton GP, Parker RT. Abdominal sacral colpopexy with mersilene mesh in the retroperitoneal position in the management of posthysterectomy vaginal vault prolapse and enterocele. Obstet Gynecol 1985;153:140–6. 14. Addison WA, Timmons MC, Wall LL, Livengood CH. Failed abdominal sacral colpopexy: observations and recommendations. Obstet Gynecol 1989;74:480–3. 15. Bensen JT, Lucente V, McClellan E. Vaginal versus abdominal reconstructive surgery for the treatment of pelvic support defects: a prospective randomized study with long-term outcome evaluation. Am J Obstet Gynecol 1996;175:1418–22. 16. Maher CF, Qatawneh AM, Dwyer PL, Carey MP, Cornish A, Schluter PJ. Abdominal sacral colpopexy or vaginal sacrospinous colpopexy for vaginal vault prolapse: a prospective randomized study. Am J Obstet Gynecol 2004;190:20–6.
1. Boyles SH, Weber AM, Meyn L. Procedures for pelvic organ prolapse in the United States, 1979–1997. Am J Obstet Gynecol 2003;188:108–15.
17. Maher C, Baessler K, Glazener C, Adams E, Hagen S. Surgical management of pelvic organ prolapse in women. Cochrane Database Syst Rev 2004;4:CD004014.
2. Olsen AL, Smith VJ, Bergstrom JO, Colling JC, Clark AL. Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 1997;89:501–6.
18. Nygaard I, McCreey R, Brubaker L et al. Abdominal sacrocolpopexy: a comprehensive review. Obstet Gynecol 2004;104:805–23.
3. Whiteside JL, Weber AM, Meyn LA, Walters MD. Risk factors for prolapse recurrence after vaginal repair. Am J Obstet Gynecol 2004;19:1533–8. 4. Bump RC, Mattiasson A, Bo K et al. The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 1996;175:10–17. 5. Marchionni M, Bracco GL, Checcucci V et al. True incidence of vaginal vault prolapse: 13 years of experience. J Reprod Med 1999;44:679–84. 6. Symmonds R, Williams T, Lee R, Webb M. Post hysterec-
19. Visco AG, Weidner AC, Barber MD et al. Vaginal mesh erosion after abdominal sacral colpopexy. Am J Obstet Gynecol 2001;184:297–302. 20. Nezhat CH, Nezhat F, Nezhat C. Laparoscopic sacral colpopexy for vaginal vault prolapse. Obstet Gynecol 1994;84:885–8. 21. Wattiez A, Mashiach R, Donoso M. Laparoscopic repair of vaginal vault prolapse. Curr Opin Obstet Gynecol 2003;15:315–19. 22. DeLancey JOL. Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 1992:166;1717–28.
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23. Gosling JA. The structure of the bladder neck, urethra and pelvic floor in relation to female urinary incontinence. Int Urogynecol J 1996;7:177–8. 24. Tulikangas PK, Walters MD, Brainard JA, Weber AM. Enterocele: is there a histologic defect? Obstet Gynecol 2001;98:634–7. 25. Richardson AC. The anatomic defects in rectocele and enterocele. J Pelvic Surg 1995;1:214–21. 26. Miklos JR, Kohli N, Lucente V, Saye WB. Site-specific fascial defects in the diagnosis and surgical management of enterocele. Am J Obstet Gynecol 1998;179:1418–22. 27. Gadonneix P, Ercoli A, Salet-Lizee D et al. Laparoscopic sacrocolpopexy with two separate meshes along the anterior and posterior vaginal walls for multicompartment pelvic organ prolapse. J Am Assoc Gynecol Laparosc 2004;11:29–35. 28. Cosson M, Rajabally R, Bogaert E, Querleu D, Crepin G. Laparoscopic sacrocolpopexy, hysterectomy, and Burch colposuspension: feasibility and short-term complications of 77 procedures. J Soc Laparoendosc Surg 2002;6:115–19. 29. Antiphon P, Elard S, Benyoussef A et al. Laparoscopic promontory sacral colpopexy: is the posterior, rectovaginal, mesh mandatory? Eur Urol 2004;45:655–61. 30. Paraiso MFR, Falcone T, Walters MD. Laparoscopic surgery for enterocele, vaginal apex prolapse and rectocele. Int Urogynecol J 1999;10:223–9. 31. Amid PK. Classification of biomaterials and their related complications in abdominal wall hernia surgery. Hernia 1997;1:15–21. 32. FitzGerald M, Edwards SR, Fenner D. Medium-term follow-up on use of freeze-dried, irradiated donor fascia for sacrocolpopexy and sling procedures. Int Urogynecol J Pelvic Floor Dysfunct 2004;15:238–42. 33. Sundaram CP, Venkatesh R, Landman J, Klutke CG. Laparoscopic sacrocolpopexy for the correction of vaginal vault prolapse. J Endourol 2004;18:620–3.
34. Elliot DS, Frank I, DiMarco DS, Chow GK. Gynecologic use of robotically assisted laparoscopy: sacrocolpopexy for the treatment of high-grade vaginal vault prolapse. Am J Surg 2004;188 (Suppl):52–6. 35. Birnbaum SJ. Rational therapy for the prolapsed vagina. Am J Obstet Gynecol 1973;115:411–19. 36. Sutton GP, Addison WA, Livengood CH, Hammond CB. Life threatening hemorrhage complicating sacral colpopexy. Am J Obstet Gynecol 1981;140:836–7. 37. Kapoor B, Toms A, Hooper P, Fraser AM, Cox CW. Infective lumbar discitis following laparoscopic sacral colpopexy. J R Coll Surg Edinb 2002;47:709–10. 38. Kannus P, Parkkari J, Jarvinen TLN, Jarvinen TAH, Jarvinen M. Basic science and clinical studies coincide: active treatment approach is needed after a sports injury. Scand J Med Sci Sports 2003;13:150–4. 39. Paraiso MF, Walters MD, Karram MM, Barber MD. Laparoscopic Burch colposuspension versus tensionfree vaginal tape: a randomized trial. Obstet Gynecol 2004;104:1249–58. 40. Valpas A, Kivela A, Penttinen J et al. Tension-free vaginal tape and laparoscopic mesh colposuspension in the treatment of stress urinary incontinence: immediate outcome and complications – a randomised clinical trial. Acta Obstet Gynecol Scand 2003;82(7):665–71. 41. Bump RC, Hurt GW, Cotheofrastous JP et al. Randomized prospective comparison of needle colposuspension versus endopelvic fascia plication for potential stress incontinence prophylaxis in women undergoing vaginal reconstruction for stage 3 or 4 pelvic organ prolapse. Am J Obstet Gynecol 1996;175:326–35. 42. Ross JW. Techniques of laparoscopic repair of total vault eversion after hysterectomy. J Am Assoc Gynecol Laparosc 1997;4:173–83. 43. Carey MP, Dwyer PL. Genital prolapse: vaginal versus abdominal route of repair. Curr Opin Obstet Gynecol 2001;13:499–505.
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86 Other laparoscopic support procedures Peta Higgs
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IntroductIon Laparoscopic surgery has become popular in urogynecology and many treatments offered by the abdominal route have been described using the laparoscopic approach. There is, however, a paucity of data on this approach. The literature reveals descriptive techniques and case reports, often without results. There are no comparative studies between the laparoscopic and the abdominal or vaginal approach. Nevertheless, laparoscopy may offer an enhanced view of the pelvis and improve recovery times. The role of these support techniques needs to be assessed by comparison to conventional surgery in robust clinical trials.
ApIcAl support methods laparoscopic sacrocolpopexy
ligaments are then plicated proximally with non-absorbable sutures. Laterally, the vaginal fascia may be sutured to the cardinal ligaments. Anteriorly, the pubocervical fascia may be plicated to create a new ‘vaginal cuff’. The vaginal vault is then sutured to the plicated uterosacral ligaments for support (Fig. 86.1). At the end of the procedure the position of the ureters is checked. If there is excessive medial displacement, an incision into the pelvic peritoneum between the uterosacral ligament and the ureter is made. Proponents of this technique feel that it offers a sitespecific defect repair and anatomic alignment of the vaginal axis, without the use of synthetic materials. Results of these techniques are presented in small case series with short follow-up times and are summarized in Table 86.1. The largest series is by Cook et al.7 in which at least 71% of the women underwent concurrent prolapse repair at the time of surgery (see Table 86.1). The main apical support procedure was by enterocele
The best studied approach of laparoscopic apical support is laparoscopic sacrocolpopexy, discussed in Chapter 85. Other methods without the use of synthetic meshes and with uterine conservation are discussed here.
laparoscopic uterosacral-ligament vault suspension Vault suspension by the uterosacral ligaments has been described by a number of authors,1–8 often in combination with an enterocele repair. The technique involves peritoneal dissection to expose the vaginal apex. The uterosacral ligaments are then identified by elevating the vagina with a probe to stretch the ligaments. The course of the pelvic ureter must be identified to avoid damage. The uterosacral
table 86.1.
Figure 86.1. suspension.
Laparoscopic uterosacral ligament vault
Laparoscopic uterosacral ligament vault suspension
Author
No. of patients
Additional procedures
Follow-up (months)
Ostrzenski1
15
–
6–24
2
Ostrzenski
16 11
– Paravaginal repair
36+ Up to 42
Vancaillie & Butler8
17
Burch colposuspension, vaginal repair
3–12
0
Enterocele repair, ‘multiple other defect repairs’
6–12
0
17
Vaginal enterocele repair
6
12
10
Multiple*
8
0
44
Multiple*
Up to 36
7
Carter et al.3
8
5
Miklos et al.
6
Seman et al. 7
Cook et al.
Vault prolapse (%) 0 31 9
* Additional procedures included laparoscopic enterocele repair, laparoscopic supralevator repair, laparoscopic adhesiolysis, laparoscopic paravaginal repair, laparoscopic Burch colposuspension, posterior colporrhaphy and anterior colporrhaphy.
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repair with uterosacral ligament suspension. The followup time is not clearly stated. They found good vault support on pelvic organ prolapse quantification (POPQ) examination in 41 of 44 (93%) of women. Major surgical complications have been described in 4.4% of patients, including enterotomy, rectal perforation, conversion to laparotomy, and vesicovaginal fistula.6,7
laparoscopic vaginal suspension to anterior abdominal wall Fedele et al.9 describe a technique involving fixation of the vaginal vault with non-absorbable sutures to the anterior abdominal wall fascia. An initial enterocele repair is performed. The peritoneum over the vaginal vault is opened and two sutures placed in each corner of the vault. The sutures are passed subperitoneally and brought out of the trocars placed laterally 4–5 cm from the anterior iliac spine. The sutures are then fixed to the rectus sheath fascia. In their series of 12 women, all 12 underwent an enterocele repair incorporating the uterosacral ligaments as part of the procedure and 11 women had a concurrent vaginal repair. They found no recurrent vault prolapse at 9–28 months follow-up.9 Tsin et al.10 reported a similar technique using a synthetic mesh sutured to the cardinal ligament/uterosacral complex laparoscopically. Initial vaginal hysterectomy and McCall culdoplasty are performed. The mesh sling is tunneled from the round ligament insertion to the lateral pelvic wall to the skin incision. The mesh is then sutured to the rectus sheath fascia. At 12 months follow-up in this series of 10 women there was no recurrent vault prolapse. Reported complications included infection of the mesh at the anterior abdominal wall in one in 10 (10%) and suture extrusion at the vaginal vault in one in 10 (10%).10
uterIne prolApse laparoscopic sacro colpohysteropexy This technique is similar to sacrocolpopexy but allows for conservation of the uterus. It involves the use of synthetic mesh fixed from the cervix or uterosacral ligaments and the anterior vaginal wall to the sacral promontory for support.12,13 Rozet et al.13 describes dissection of the peritoneum from the uterosacral ligaments and pouch of Douglas to open the rectovaginal space down to the level of the levator ani muscles. The mesh is then fixed to the levator ani muscles using absorbable sutures. The bladder is dissected from the anterior vaginal wall and the vesicovaginal space is opened. A second mesh is fixed to the anterior vaginal wall. The anterior mesh is then passed through the broad ligament on the right side of the uterus only. The peritoneum over the sacral promontory is incised and both meshes are then fixed to the sacral promontory with a non-absorbable suture. The peritoneum is then closed to cover the mesh (Fig. 86.2). This technique can also be performed with the anterior mesh passed bilaterally through the broad ligaments and attached to either the posterior mesh or the
laparoscopic extraperitoneal sacrospinous suspension Lee et al.11 reported this technique of sacrospinous suspension. The vaginal vault is suspended to the sacrospinous ligament similar to the vaginal approach. The retropubic space and the pararectal spaces are opened to identify the sacrospinous ligament. A non-absorbable suture is then placed from the sacrospinous ligament to the vaginal vault. In their series of 12 women, one woman had recurrent vault prolapse at an average follow-up of 26 months. No surgical complications were reported.11
Figure 86.2.
Laparoscopic sacro colpohysteropexy. 1207
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sacral promontory directly.12 It can also be used with the mesh attached to the cervix alone if only level 1 support is required. Rozet et al.13 describes a series of 325 women, of whom 228 underwent laparoscopic sacro colpohysteropexy and 97 underwent laparoscopic sacrocolpopexy. Other procedures performed concurrently included Burch colposuspension, tension-free vaginal tape (TVT) and hysterectomy. Results include both the sacro colpohysteropexy and the sacrocolpopexy groups of women. They found prolapse recurrence in 13 of 325 (4%) of women with an average follow-up of 14.6 months. The prolapse recurred in the anterior compartment in 10 and in the posterior compartment in three. Excluded from analysis were eight women who were converted to laparotomy due to hypercapnia, extensive peritoneal adhesions, and bleeding. Late complications included de novo urge incontinence (19), de novo stress incontinence (19%), intestinal obstruction requiring laparotomy and bowel resection (1), sacral spondylitis (1), port site hernia (1), mesh infection (2), mesh erosion (3), and urinary retention following TVT (2). This technique offers a promising solution for women with apical support defects who wish to retain their uterus. Further pregnancies would be possible, although women should be warned of the likelihood of decreased fertility following surgery, recurrence of prolapse following a subsequent pregnancy, and the possible need for cesarean section in a future pregnancy. Many women, when given the option, choose to retain their uterus, even if future childbearing is not desired. The role of the cervix in sexual function is still debated and therefore it is preferable to allow women to choose between hysterectomy and uterine preservation. This technique offers this choice, without compromising the apical supports. Further longer term study will be required to ensure this support is lasting.
uterosacral ligament plication and shortening This technique has been described for women who desire uterine conservation. Ureters must be identified and peritoneal incisions are performed medial to the ureters to ensure there is no ureteric kinking after the plication. Non-absorbable sutures are used to plicate the uterosacral ligaments from their insertion at the cervix. Further sutures plicate the ligaments towards the sacrum and these close the pouch of Douglas. The uterosacral ligament is then shortened using a further suture placed from the cervical to the sacral end of the ligaments and tied14 (Fig. 86.3).
Figure 86.3. shortening.
Uterosacral ligament placation and
The largest series for this procedure has been reported by Maher et al.15 Forty-three women underwent the procedure, 41 of whom had concurrent procedures for prolapse including anterior and posterior vaginal repair, laparoscopic Burch colposuspension, and laparoscopic paravaginal repair. At an average follow-up of 12 months, nine (21%) women had recurrent uterine prolapse, with seven (16%) of the women having undergone further surgery for prolapse. The only surgical complication reported was one conversion to laparotomy for a uterine artery laceration. Two women had completed term pregnancies at the time of review.
laparoscopic uterine suspension with round ligaments The open technique is known to be unsuccessful when used for uterine prolapse. The round ligaments are suspended to or through the rectus sheath similar to the technique for a ventrosuspension. O’Brien and Ibrahim found this technique to be unsuccessful in eight of nine women who underwent the procedure.16 One case report has described this technique during pregnancy.17 Surgery was performed at 13 weeks’
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gestation. No uterine prolapse was seen at 3 months postpartum.
AnterIor compArtment support methods This is covered in Chapter 84.
posterIor compArtment support methods The posterior compartment is usually accessed via the vaginal route. Laparoscopic sacrocolpopexy may address posterior defects by extending the mesh down the posterior vaginal wall. This technique is discussed in Chapter 85. Laparoscopic surgeons find that this compartment is usually well visualized; however, there is no clinical evidence to support the use of laparoscopic rectocele repair.
laparoscopic enterocele repair Laparoscopic enterocele repair can be performed in a number of different ways. The pressure created with the pneumoperitoneum of the laparoscopy aids identification of the enterocele sac. The Moschcowitz procedure involves a purse-string non-absorbable suture to the peritoneum of the pouch of Douglas. The ureters must be observed after the procedure to ensure there is no kinking.18 The Halban procedure uses non-absorbable sutures placed in the sagittal plane from the posterior vagina to the inferior sigmoid serosa. Interrupted sutures are placed approximately 1 cm apart and tied as they are placed. Again the ureters must be identified at the end of the procedure.18 Alternatively, the enterocele is managed similar to a hernial sac. Upward traction with forceps in the vagina is used to identify the enterocele. The peritoneum is incised along the uterosacral ligaments and posterior vagina. The flap of excess peritoneum is then excised from the anterior rectum. The rectovaginal fascia is then plicated to close any fascial defects causing the enterocele. A synthetic mesh can be sutured over the posterior vaginal wall and uterosacral ligaments to close the fascial defect if required.14 Clinical results of the procedure alone are lacking as it is usually used in conjunction with other apical support procedures. Cadeddu et al.19 reported on three women using a modified Moschcowitz procedure and found no recurrent enterocele after a mean follow-up of 10 months. In prolapse surgery the Moschcowitz procedure has generally fallen out of
favor. In vaginal surgery, the McCall culdoplasty has been found to be superior to the Moschcowitz procedure in prevention of enterocele formation following vaginal hysterectomy. In a randomized study, after 3 years follow up, there were 0/32 enterocele formation in the McCall group compared to 6/33 in the Moschcowitz.20
laparoscopic rectocele repair This technique has been described using an absorbable mesh.21 The rectovaginal septum is opened to the level of the perineal body. The mesh is attached to the perineal body and posterior surface of the vaginal vault. If the cervix is present, the mesh is attached to the cervix and uterosacral ligaments; if not, the uterosacral ligaments are sutured to the anterior and posterior vaginal fascia and the mesh attached to this complex. Lyons and Winer21 described a series of 20 women in whom they used this technique. Enterocele repair was performed laparoscopically in all women. Other concurrent procedures included laparoscopic Burch colposuspension, paravaginal repair, subtotal hysterectomy, sacrocolpopexy, rectopexy and perineorrhaphy. They reported an 80% subjective improvement at 1 year. No follow-up clinical examination was performed.
conclusIon The evidence base for use of these laparoscopic support procedures is lacking. Studies to date are limited by small numbers, varied techniques, and short follow-up times. The best studied are the apical support methods, especially laparoscopic sacro colpohysteropexy. This technique is similar to laparoscopic sacrocolpopexy but allows for conservation of the uterus. It would appear that the technique offers good support without ‘shooting the messenger’ as the uterus itself is not the cause of prolapse, but its lack of suspensory support at the level of the uterosacral and cardinal ligaments. If these supports can be recreated, then the choice of uterine conservation can be offered. Further long-term data are still required. The nature of uterovaginal prolapse often requires that a number of the vaginal compartments need to be addressed simultaneously during surgery. This makes the analysis of one technique difficult. However, prospective trials with standardized examination techniques, such as the POPQ examination, with long-term follow-up would at least allow some comparison between different techniques. 1209
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Ultimately, clinical trials comparing the open and vaginal techniques with the laparoscopic approach are required to determine the best approach for women with prolapse.
10. Tsin D, Whang G, Sequeira R, Mahmood D, Granato R. Laparo-vaginal treatment of uterine procidentia. J Laparoendosc Surg 1995;5:145–9.
Acknowledgments Illustrations by Bill Reid, ERC, Royal Children’s Hospital, Melbourne, Australia.
12. Seracchioli R, Hourcabie J-A, Vianello F, Govoni F, Pollastri P, Venturoli S. Laparoscopic treatment of pelvic floor defects in women of reproductive age. J Am Assoc Gynecol Laparosc 2004;11:332–5.
reFerences
13. Rozet F, Mandron E, Arroyo C et al. Laparoscopic sacral colpopexy approach for genito-urinary prolapse: experience with 363 cases. Eur Urol 2005;47:230–6.
1. Ostrzenski A. Laser video-laparoscopic colpopexy. Ginkol Pol 1992;63:317–23. 2. Ostrzenski A. Laparoscopic colposuspension for total vaginal prolapse. Int J Gynecol Obstet 1996;55:147–52. 3. Carter J, Winter M, Mendehlsohn S, Saye W, Richardson A. Vaginal vault suspension and enterocele repair by Richardson-Saye laparoscopic technique: description of training technique and results. JSLS 2001;5:29–36. 4. Miklos J, Moore R, Kohli N. Laparoscopic surgery for pelvic support defects. Curr Opin Obstet Gynecol 2002;14:387–95. 5. Miklos J, Kohli N, Lucente V, Saye W. Site-specific fascial defects in the diagnosis and surgical management of enterocele. Am J Obstet Gynecol 1998;179:1418–23. 6. Seman E, Cook J, O’Shea R. Two-year experience with laparoscopic pelvic floor repair. J Am Assoc Gynecol Laparosc 2003;10:38–45. 7. Cook J, Seman E, O’Shea R. Laparoscopic treatment of enterocele: a 3-year evaluation. Aust N Z J Obstet Gynaecol 2004;44:107–10. 8. Vancaillie T, Butler D. Laparoscopic enterocele repair – description of a new technique. Gynecol Endosc 1993;2:211–6. 9. Fedele L, Garsia S, Bianchi S, Albiero A, Dorta M. A new laparoscopic procedure for the correction of vaginal vault prolapse. J Urol 1998;159:1179–82.
11. Lee C, Wang C, Yen C, Soong Y. Laparoscopic extraperitoneal sacrospinous suspension for vaginal vault prolapse. Chang Gung Med J 2000;23:87–91.
14. Margossian H, Walters M, Falcone T. Laparoscopic management of pelvic organ prolapse. Eur J Obstet Gynecol Reprod Biol 1999;85:57–62. 15. Maher C, Carey M, Murray C. Laparoscopic suture hysteropexy for uterine prolapse. Obstet Gynecol 2001;97:1010– 4. 16. O’Brien P, Ibrahim J. Failure of laparoscopic uterine suspension to provide a lasting cure for uterovaginal prolapse. Br J Obstet Gynaecol 1994;101:707–8. 17. Matsumoto T, Nishi M, Yokota M, Ito M. Laparoscopic treatment of uterine prolapse during pregnancy. Obstet Gynecol 1999;93:849. 18. Paraiso M, Falcone T, Walters M. Laparoscopic surgery for enterocele, vaginal apex prolapse and rectocele. Int Urogynecol J 1999;10:223–9. 19. Cadeddu J, Micali S, Moore R, Kavoussi L. Laparoscopic repair of enterocele. J Endourol 1996;10:367–9. 20. Cruikshank S, Kovac S. Randomized comparison of three surgical methods used at the time of vaginal hysterectomy to prevent posterior enterocele. Am J Obstet Gynecol 1999;180:859–65. 21. Lyons T, Winer W. Laparoscopic rectocele repair using polyglactin mesh. J Am Assoc Gynecol Laparosc 1997;4:381–4.
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87 Prevention, recognition, and treatment of complications in laparoscopic pelvic floor surgery Christopher Maher
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IntroductIon Gynecologists have led the surgical specialties in recognizing the benefits to our patients of reduced postoperative pain, fewer hospital admissions and the quicker return to normal activities associated with laparoscopy. Improved optics, lighting, instrumentation and technology over the last 15 years have seen an explosion in operative general gynecology surgery previously performed via laparotomy. Over the next decade, as laparoscopic suturing techniques are mastered, the laparoscope is likely to play an increasingly important role in female pelvic floor reconstructive surgery. It is vital while laparoscopic pelvic floor surgery is in its infancy that we are competent in the prevention, recognition, and treatment of complications associated with this mode of access to the abdomen and pelvis. In recent years the rate of complications from gynecologic laparoscopy has ranged from 4 to 8 per 10001–3 for diagnostic procedures and increased from 4 to 180 per 1000 operative gynecology surgeries.3–7 Risk analysis has revealed that the important factors leading to gynecologic laparoscopic complications include establishing laparoscopic access,5,6 concomitant laparoscopic hysterectomy3,8 and surgeon inexperience.4,9
Access complIcAtIons At least 50% of all reported complications at laparoscopic surgery occur at time of entry to the abdomen.5,6 The majority of gynecologists prefer the closed (Veress needle) technique to the open technique.1,10 The major complications related to entry include vascular and bowel injuries and associated hernia formation. Although entry-related complications using the closed approach are uncommon, they can be fatal and occur in 0.31–2.4/1000 procedures.1,4,8,9,11 Chapron et al.12 reported that major vascular injuries were reported five times more frequently following the closed technique as compared to the open approach. Of the 44 reported cases in the literature between 1982 and 1997, 82% followed the closed and 17% followed the open technique.12 A large Dutch review retrospectively compared open (12,444 patients) and closed (489,335 patients) access. They found the incidence of major vascular injury was 0.075% using the closed approach and 0% with the open approach (p<0.05). The incidence of visceral damage was 0.083% with the closed technique as compared to 0.048% with the open13 (p>0.05). In a randomized controlled trial (RCT), 150 subjects undergoing cholecystectomy were allocated to the open or the closed approach. Major complications were reported in 3/75 (4%) of the closed as compared to
1/75 (1.3%) of the open (p<0.05).14 The open approach was also significantly faster to perform. In a smaller RCT of 50 patients undergoing laparoscopic surgery, no difference in complications were observed but the open approach took half the time of the closed approach to obtain access.15 In contrast, in a more recent questionnaire review of Dutch gynecologists, the complication rate in those undergoing open laparoscopy was significantly higher compared to those undergoing closed laparoscopy.1 The complication rate amongst those undergoing open laparoscopy (579) was 1.38% as compared to 0.12% in the closed group (20,027) (p=0.001). While the rate of vascular injuries was the same in both groups, the rate of gastrointestinal injuries, wound infections and failed access was significantly greater in the open group. The rate of open laparoscopy among Dutch gynecologists was only 2% and was reserved for those with previous laparotomies, suspected adhesions, and the very obese or very thin. The authors concluded that the closed approach was safer than the open approach. An alternative message is that gynecologists should not perform procedures that they perform rarely in patients at high risk of complications. In my own tertiary referral urogynecology practice the open technique is used exclusively, but the literature only provides evidence that the risk of vascular injury is reduced with the open method. It has been demonstrated that 50% of those with previous midline vertical incisions and 20% with low transverse incisions have some degree of periumbilical adhesions.16 Studies have shown that employing counterpressure during gas insufflation of the peritoneal cavity produces a more consistent elevation of the anterior abdominal wall.17 Although not proven, firm elevation of the anterior abdominal wall should make for safer insertion of laparoscopic ports, including the first port. When there is concern regarding the safety of blindly introducing the insufflating needle at the umbilicus, an alternative site of placement is the left upper quadrant 3 cm below the costal margin in the mid-clavicular line (Palmers point; Fig. 87.1b). In retrospective audits no significant complications have been reported with this approach.18,19
trocAr-AssocIAted complIcAtIons primary trocars In an attempt to minimize the risk associated with accessing the abdominal cavity, increased attention has been focused on trocar design. The traditional pyrami-
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Superficial vessels:
Deep vessels:
Superficial epigastric artery
Interior epigastric artery
Superficial circumflex artery
Deep circumflex iliac artery
External iliac artery
Femoral artery a
1
1
2
2 3
4
b
c
3
4
1 2 3 4
Superficial epigastric artery Superficial circumflex iliac artery Interior epigastric artery Deep circumflex iliac artery
Figure 87.1. Coronal view: (a) anterior abdominal wall vasculature; (b) trocar placement sites. (c) Transverse view: trocar placement sites in relation to vessels, just below the level of the umbilicus. (© Maher/Francis.) dal trocar (Fig. 87.2) cuts through the tissue, and safety shields (Fig. 87.2) have been added to try to reduce the risk to the abdominal wall or of perforation of intraabdominal vessels or viscus. The cutting blade retracts into the plastic sleeve after the abdominal wall has been penetrated. Bhoyrul et al. reported that 87% of deaths from vascular injuries and 91% of bowel injuries at the time of entry involved trocars with safety shields.20 They concluded that, despite the blade retracting soon after entry into the peritoneum, the momentary presence of the blade in the abdominal cavity as seen in Figure 87.3 is all that is required for injuries to occur. Surgeons should not overestimate the level of safety associated with this device.
Conical or blunt tip trocars have been designed to reduce the risk associated with bladed trocars (see Fig. 87.2). They dilate the fascia and muscular tissues, thus decreasing the potential trauma as the trocar enters the abdominal cavity. Conical tips require a greater entry force to the abdomen than sharper pyramidal trocars21 and leave a defect approximately 50% narrower than the sharper pryamidal.22 Leibl et al., in a non-randomized study, demonstrated that the reduced wound defect following the use of conical trocars was clinically relevant, with incisional hernia being reported 10 times more frequently after the pyramidal as compared to the conical trocar.23 In a further study there were no reported injuries to blood vessels of the anterior abdominal wall 1213
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Figure 87.2. A variety of trocar designs. From left to right: pyramidal trocar (E.M.T. Warriewood, N.S.W.); shielded trocar (Versaport, Tyco, Norwalk, CT); conical trocar (Seperator, Applied Medical, Santa Margarita, CA); conical trocar and obturator (Step, Tyco, Norwalk, CT); optical access trocar (Optiview, Ethicon Endo-surgery, Cincinnati, OH).
Figure 87.3. The blade of a safety shield trocar, present momentarily prior to retracting, in an abdomen with adhesions. in the conical group as compared to 0.83% for the cutting trocar. In more recent RCTs the radially expanding conical trocar had less cannula site bleeding, reduced pain, fewer wound complications and higher patient satisfaction compared to the pyramidal trocar.24,25 Munro and Tarnay26 recently demonstrated that the fascial and muscular defect from a 12 mm blunt trocar resulted in a fascial defect similar to the 8 mm pyramidal trocar and suggested that the fascial defects from 12 mm blunt trocars do not need closing, a view supported by others.24,27
Optical access trocars (see Fig. 87.2) are designed to decrease the injury to vessels and viscera by allowing the surgeon to visualize abdominal wall placement during entry. Two optical access systems are available – one utilizes a bladed trocar that strikes the fascia and peritoneum under vision, and the other utilizes a nonbladed trocar where a clear conical tip that is rotated under laparoscopic vision as it rotates through the layers. Sharp et al. describe 79 serious complications following optical access trocars, four of which were fatal and reported to the American Food and Drug Administration.28 Only five of these were recorded in peer-reviewed literature. This report does not allow us to determine the incidence of these complications but more recent case series indicate an acceptable 0.3% entry-related complication rate using optical access trocars.29,30 An important advantage of laparoscopy over laparotomy is the lower rate of wound complications and hernias. In one study, the incidence of wound infection after open colposuspension was 11% as compared to 1% after the laparoscopic approach.31 Magrina estimated that the incidence of trocar hernias after laparoscopic gynecology surgery was 10–100 times lower than laparotomy.32 He found the incidence of hernia after laparoscopy ranged from 0.06 to 1% as compared to 13% 5 years after gynecologic laparotomy. The incidence of incisional hernia increases to 3% with the use of 12 mm trocars.33 It is largely accepted that while 5 mm trocars do not require fascial closure, when bladed trocars 10 mm or greater are utilized the defects should be closed to minimize the risk of bowel entrapment or incisional hernia. Preliminary studies have demonstrated that blunt trocars will significantly reduce the incidence of trocar site hernia22 and many believe they do not need to be closed.26,27
secondary trocars Secondary trocars are required for operative laparoscopic surgery. The correct positioning of these trocars is vital to minimize damage to the vasculature of the anterior abdominal wall (see Fig. 87.1) and to allow laparoscopic suturing in a safe and biomechanically friendly position for the surgical team. A thorough knowledge of the vasculature of the anterior abdominal wall is required to minimize and treat perforation of the vessels. The inferior epigastric artery arises from the external iliac artery and passes superior to the inguinal ligament, traveling superomedially just medial to the lateral edge of the rectus muscle. Its position deep to the rectus muscle and superior to the
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peritoneum allows for relatively easy laparoscopic localization (Fig. 87.4). The superficial epigastric artery arises from the femoral artery near the inguinal ring and courses medially above the rectus muscle towards the midline. The smallest branch of the femoral artery, the superficial circumflex iliac artery, runs laterally to supply the skin and superficial fascia. Perforation of the inferior epigastric artery will produce retroperitoneal or intraperitoneal bleeding; perforation of the superficial epigastric artery will result in intramuscular or subcutaneous bleeding. The deep circumflex iliac artery arises from the external iliac artery opposite the inferior epigastric artery and runs posterior to the inguinal canal to the anterior superior iliac spine where it anastomoses with a variety of vessels. Figure 87.1 demonstrates the course of the anterior abdominal wall vessels. The surgeon can use transillumination for locating superficial abdominal wall vessels but intraperitoneal identification is required for the inferior epigastric artery. When the inferior epigastric artery is difficult to visualize, intra-abdominal landmarks can be helpful. It usually arises from the inguinal canal medial to the round ligament and travels cranially lateral to the obliterated umbilical arteries. The lower ports are placed as in Figure 87.1b and 87.1c lateral to the inferior epigastric and medial to the deep circumflex vessels. If further trocars are required they can be sited in the midline suprapubically or at the level of the umbilicus lateral to the edge of the rectus muscle. If a 10 mm trocar or greater is required for introducing mesh, the harmonic scalpel or the removal of pathology, this is placed either
Figure 87.4. Laparoscopic localization of the left inferior epigastric artery lateral to the obliterated umbilical artery.
on the side of the surgeon or at the suprapubic site if utilized. Even after these preventive measures are employed, experienced laparoscopic surgeons may still be faced with arterial bleeding from the inferior epigastric artery. The offending trocar should not be removed as this denotes the location of the artery that may become difficult to visualize as the hematoma spreads. If the bleeding is recognized early and the inferior epigastric artery can be identified, both ends of the transected vessel can be diathermied with bipolar forceps (Fig. 87.5a). If this is unsuccessful, a No. 12 Foley catheter can be passed through the 5 mm trocar and the Foley balloon inflated to 10–15 cm3 with sterile water. The trocar is then removed over the catheter and firm traction secured with an umbilical cord clamp overnight (Fig. 87.5b). The following morning the clamp and catheter are removed. If this fails to secure the vessel, a CT-1 needle is passed through the abdominal wall into the abdomen and passed from inside the abdomen to the outside using laparoscopic needle holders and tied both cephalad and caudad to the trocar. The sutures are removed the following morning (Fig. 87.5c).
Bowel InjurIes The incidence of bowel injuries at gynecologic laparoscopy varies from zero to 5%.7,34 Approximately 50% of these injuries occur during entry,3,8,35 with the large and small bowel being equally involved.4,36 As there appears to be no significant difference in the rate of bowel injuries with either the closed or open approach to entry, little can be done to minimize the occurrence of injury, although some surgeons believe that the damage may be more readily detected intraoperatively with the open technique.37 After reviewing the literature, Magrina calculated that only 43% of bowel injuries at laparoscopic surgery were diagnosed intraoperatively.32 The mortality rate from bowel injuries in gynecologic laparoscopy ranges from 2.5 to 5%38 but this has been shown to increase to 21% in those with a delayed diagnosis of bowel injury.39 If there is a recognized Veress injury to the bowel at the time of surgery and there is no associated fecal spill, it is likely that the injury can be managed expectantly. Although no clear guidelines exist in nine cases of Veress injuries to the bowel treated expectantly, there were no complications.1,8,35 Trocar damage to the small bowel mandates careful inspection of the whole bowel to ensure no through-and-through injuries have occurred. Simple small injuries to the small and large bowel should be repaired in one or two layers of inter1215
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b
a
c
rupted sutures, the pelvis irrigated, and antibiotics commenced. Postoperatively, the patient is kept nil by mouth until flatus is passed. Electrosurgical injuries are more commonly seen in bowel injuries that are diagnosed postoperatively. Brosens et al. estimated that the average time to diagnosis after needle or trocar injury to bowel was 1.3 days as compared to 10.4 days for electrosurgical burns.39 Electrical injuries to the intestine are not always diagnosed intraoperatively or their appearance leads the surgeon towards conservative treatment.40 It is suggested that burns less than 5 mm in diameter can be treated expectantly.41 If the area of blanching exceeds 5 mm it is estimated that thermal damage may exceed up to
Figure 87.5. Bleeding inferior epigastric artery: (a) controlled with bipolar diathermy; (b) tamponaded with Foley catheter; (c) sutured. (© Maher/Francis.) 5 cm from the apparent injury, and resection should be considered.42 In patients returning after discharge with bowel damage or bowel obstruction, pre- and intraoperative evaluation by a general surgical colleague is advisable. Damaged bowel must be repaired or resected with or without a temporary colostomy. All necrotic tissue should be removed to minimize the risk of abscess formation. The most significant reduction in bowel complications during laparoscopic pelvic floor surgery will arise from preventing injury. The focus of attention should lie on careful adhesiolysis and enterolysis, and the detection of injuries intraoperatively rather than postoperatively. During adhesiolysis and enterolysis sharp dissection
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with minimal diathermy will be beneficial in preventing inadvertent bowel damage. Careful inspection of the bowel for hematoma or serosal damage that may suggest breaches of the mucosa, and the performance of the underwater test if there is any concern regarding the integrity of the bowel, are all useful in facilitating intraoperative rather than postoperative diagnosis of bowel damage. The underwater test involves holding any area of bowel suspected of damage under warmed saline to look for gas or bowel leakage. If the laparoscopic pelvic floor surgeon is faced with an abdomen of morbidly dense adhesions it may be prudent to remember that in a large prospective randomized controlled trial the vaginal approach to vault prolapse has been shown to be equally as effective as the abdominal route43 and the conversion to the vaginal approach may be the safest approach. At laparoscopic sacral colpopexy four (1.5%) bowel injuries in 261 cases were reported. A rectal44 and a colon45 injury were repaired laparoscopically without sequelae and two small bowel injuries were diagnosed postoperatively and underwent subsequent laparotomy.46 Bowel preparation prior to surgery was utilized: 1) to remove the bulky intraluminal contents to improve surgical field vision and bowel handling; and 2) to decrease the risk of peritoneal and wound contamination if the bowel was inadvertently opened. Neither of these beliefs has been confirmed in randomized controlled trials in elective operative gynecology47 or colorectal surgery.48 Finally, improving the laparoscopic experience of the surgeon may prove to be one of the simplest means of minimizing morbidity associated with bowel injuries at gynecologic laparoscopy. Brosens and Gordon reported that a gynecologist performing fewer than 100 laparoscopies a year had a five times higher rate of bowel injuries than those performing more than a 100 laparoscopies a year.35 Skills can be improved in a variety of ways including training programs, skills workshops, and operating with colleagues.
with the laparoscope in place, to ensure that there are no other unrecognized injuries and that the ureters are patent. After a watertight cystotomy repair the catheter can safely be removed at 4 days.46 If concomitant continence surgery is performed, nursing staff and the patient should be vigilant during the voiding trial to ensure that the bladder is not grossly overdistended. Some surgeons believe that postoperative cystoscopy is vital to minimize lower urinary tract complications following pelvic floor surgery so that unrecognized cystotomy may be repaired to prevent vesicovaginal fistula.50
InjurIes to the BlAdder
complIcAtIons relAted to pneumoperItoneum
Inadvertent cystotomy has been reported in 4% of laparoscopic colposuspensions.49 In 261 laparoscopic sacral colpopexies published, five (1.9%) inadvertent cystotomies were reported, all of which were repaired laparoscopically at the initial surgery without complication.44–46 A gas-filled urinary bag or blood in the urine indicates bladder trauma until proven otherwise; this warrants careful laparoscopic inspection of the bladder distended to 300 ml and cystoscopy. Cystotomies should be repaired in two layers so that the bladder is watertight at 300 ml. Post-repair cystoscopy should be performed
ureterIc InjurIes Ureteric injuries following pelvic floor surgery are reported in 3% of cases.51,52 The morbidity associated with ureteric injury can be dramatically reduced if identified intraoperatively using postoperative cystoscopy and intravenous indigo carmine.51,52 If indigo carmine is not clearly visible following laparoscopic pelvic floor repair, the injury is likely to be related to kinking of the ureter in the lateral retropubic space or in relation to the uterosacral/cardinal ligament sutures during sacral colpopexy or vault suspending procedures. Lateral retropubic or vault suspending sutures should be removed one at a time until ureteric patency is obtained. The sutures are then replaced at a lower level and ureteric patency again confirmed. If patency is not confirmed with the removal of the sutures, retrograde dye studies and intraoperative urologic consultation is required. Laparoscopic hysterectomy is associated with a 0.7– 1.4% risk of ureteric injury3,53 which is at least 10 times greater than at vaginal hysterectomy.8 Most of these injuries are related to clamping, incision or diathermy damage. Ureteric injuries related to concomitant laparoscopic hysterectomy usually require ureteric reimplantation by urologic colleagues.
Subcutaneous emphysema arises as carbon dioxide leaks into or is absorbed by subcutaneous tissue. Leaks to the extraperitoneal tissues can occur at entry, with opening of extraperitoneal spaces or through existing undetected herniae. The laparoscopic sacrocolpopexy involves significant retroperitoneal dissection, increasing the risk of subcutaneous emphysema that is usually quite innocuous. Significant or sudden subcutaneous emphysema around the face, neck, and chest must alert the physician to the possibility of mediastinal emphy1217
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sema. This usually arises from a congenital defect of the diaphragm but can also occur after trauma associated with upper abdominal surgery. Gas embolism can occur if gas enters the vascular system and usually occurs during or shortly after insufflation. The sudden development of hypotension, bradycardia or arrhythmias at this time should immediately raise the suspicion of gas embolism. While relatively rare, occurring in only 0.0014%,13 the mortality rate is as high as 28%.54 The pneumoperitoneum should be released and the procedure abandoned as soon as feasible.
AnethestIc complIcAtIons The gynecologist must be aware of the cardiovascular changes associated with operative laparoscopy. Most of the changes are due to establishment and maintenance of pneumoperitoneum or Trendelenburg positioning. Carbon dioxide remains the most widely used distension medium but is rapidly absorbed from the peritoneum and may cause hypercarbia and acidosis. Hypercarbia is associated with arrhythmias, increased cardiac output, and decreased systemic vascular resistance. Hyperventilation minimizes the impact of hypercarbia. Steep Trendelenburg may be required for posterior compartment or vault suspending procedures, and results in increased central venous pressure and decreased arterial pressure and cardiac output. Atelectasis and decreased pulmonary compliance can occur but are usually well controlled with general anesthesia, neuromuscular blockade, endotracheal intubation, and controlled ventilation. Both pneumoperitoneum and Trendelenburg positioning reduce femoral venous flow, increasing the risk of thrombotic complications.
conclusIon Laparoscopic pelvic floor surgery affords the surgeon and the patient significant advantages; however, complications related to obtaining access, surgeon inexperience, and associated laparoscopic hysterectomy can occur. The judicious use of the open approach or access via the left upper quadrant may be beneficial in minimizing access-related complications. Newer bladeless trocars may also act to decrease morbidity associated with access. Careful dissection during adhesiolysis and cautious and appropriate use of energy sources such as diathermy will decrease bowel injuries. Vigilance during surgery is required to detect and manage complications intraoperatively, rather than postoperatively.
Finally, experienced operating room staff – including assistants, scrub sisters, and anesthetists, who are well trained and enthusiastic in laparoscopic surgery – are vital to assist in avoiding complications associated with laparoscopic pelvic floor surgery.
reFerences 1. Jansen FW, Kolkman W, Bakkum EA et al. Complications of laparoscopy: an inquiry about closed- versus open-entry technique. Am J Obstet Gynecol 2004;190:634–8. 2. Miranda CS, Carvajal AR. Complications of operative gynecological laparoscopy. JSLS 2003;7:53–8. 3. Harkki Siren P, Sjoberg J, Kurki T. Major complications of laparoscopy: a follow-up Finnish study. Obstet Gynecol 1999;94:94–8. 4. Chapron C, Querleu D, Bruhat MA et al. Surgical complications of diagnostic and operative gynaecological laparoscopy: a series of 29,966 cases. Hum Reprod 1998;13:867–72. 5. Leonard F, Lecuru F, Rizk E, Chasset S, Robin F, Taurelle R. Perioperative morbidity of gynecological laparoscopy. A prospective monocenter observational study. Acta Obstet Gynecol Scand 2000;79:129–34. 6. MacCordick C, Lecuru F, Rizk E, Robin F, Boucaya V, Taurelle R. Morbidity in laparoscopic gynecological surgery: results of a prospective single-center study. Surg Endosc 1999;13:57–61. 7. Quasarano RT, Kashef M, Sherman SJ, Hagglund KH. Complications of gynecologic laparoscopy. J Am Assoc Gynecol Laparosc 1999;6:317–21. 8. Harkki Siren P, Kurki T. A nationwide analysis of laparoscopic complications. Obstet Gynecol 1997;89:108–12. 9. Jansen FW, Kapiteyn K, Trimbos Kemper T, Hermans J, Trimbos JB. Complications of laparoscopy: a prospective multicentre observational study. Br J Obstet Gynaecol 1997;104:595–600. 10. McMahon AJ, Baxter JN, O’Dwyer PJ. Preventing complications of laparoscopy. Br J Surg 1993;80:1593–4. 11. Tsaltas J, Healy DL, Lloyd D. Review of major complications of laparoscopy in a free standing gynaecologic day care hospital. Gynecol Endosc 1996;5:265–70. 12. Chapron CM, Pierre F, La Croix S, Querleu D, Lansac J, Dubuisson JB. Major vascular injuries during gynecologic laparoscopy. J Am Coll Surg 1997;185:461–5. 13. Bonjer HJ, Hazebroek EJ, Kazemier G, Giuffrida MC, Meijer WS, Lange JF. Open versus closed establishment of pneumoperitoneum in laparoscopic surgery. Br J Surg 1997;84:599–602. 14. Cogliandolo A, Manganaro T, Saitta FP, Micali B. Blind versus open approach to laparoscopic cholecystectomy: a randomized study. Surg Laparosc Endosc 1998;8:353–5.
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15. Peitgen K, Nimtz K, Hellinger A, Walz MK. Open approach or Veress needle in laparoscopic interventions. Results of a prospective randomized controlled trial. Chirurg 1997;68:910–3. 16. Audebert AJ, Gomel V. Role of microlaparoscopy in the diagnosis of peritoneal and visceral adhesions and in the prevention of bowel injury associated with blind trocar insertion. Fertil Steril 2000;73:631–5. 17. Phillips G, Whittaker M, Garry R. The depth of the pneumoperitoneum determines the safety of primary cannula insertion. J Am Assoc Gynecol Laparosc 1996;3(Suppl 4): S39–40. 18. Parker J, Reid G, Wong F. Microlaparoscopic left upper quadrant entry in patients at high risk of periumbilical adhesions. Aust N Z J Obstet Gynaecol 1999;39:88–92. 19. Patsner B. Laparoscopy using the left upper quadrant approach. J Am Assoc Gynecol Laparosc 1999;6:323–5. 20. Bhoyrul S, Vierra MA, Nezhat CR, Krummel TM, Way LW. Trocar injuries in laparoscopic surgery. J Am Coll Surg 2001;192:677–83. 21. Bohm B, Knigge M, Kraft M, Grundel K, Boenick U. Influence of different trocar tips on abdominal wall penetration during laparoscopy. Surg Endosc 1998;12:1434–8. 22. Bhoyrul S, Mori T, Way LW. Radially expanding dilatation. A superior method of laparoscopic trocar access. Surg Endosc 1996;10:775–8. 23. Leibl BJ, Schmedt CG, Schwarz J, Kraft K, Bittner R. Laparoscopic surgery complications associated with trocar tip design: review of literature and own results. J Laparoendosc Adv Surg Tech A 1999;9:135–40.
Siperstein AE. Use of the optical access trocar for safe and rapid entry in various laparoscopic procedures. Surg Endosc 2001;15:570–3. 31. Lavin JM, Lewis CJ, Foote AJ. Laparoscopic Burch colposuspension: a minimum 2-year follow-up and comparison with open colposuspension. Gynaecol Endosc 1998;7:251–8. 32. Magrina JF. Complications of laparoscopic surgery. Clin Obstet Gynecol 2002;45:469–80. 33. Kadar N, Reich H, Liu CY, Manko GF, Gimpelson R. Incisional hernias after major laparoscopic gynecologic procedures. Am J Obstet Gynecol 1993;168:1493–5. 34. Mirhashemi R, Harlow BL, Ginsburg ES, Signorello LB, Berkowitz R, Feldman S. Predicting risk of complications with gynecologic laparoscopic surgery. Obstet Gynecol 1998;92:327–31. 35. Brosens I, Gordon A. Bowel injuries during gynaecological laparoscopy. A multinational survey. Gynaecol Endosc 2001;10:141–5. 36. Chapron C, Pierre F, Harchaoui Y et al. Gastrointestinal injuries during gynaecological laparoscopy. Hum Reprod 1999;14:333–7. 37. Perone A. Laparoscopy using a simple open technique: a review of 585 cases. J Reprod Med 1985;30:660–3. 38. Champault G, Cazacu F, Taffinder N. Serious trocar accidents in laparoscopic surgery: a French survey of 103,852 operations. Surg Laparosc Endosc 1996;6(5):367–70. 39. Brosens I, Gordon A, Campo R, Gordts S. Bowel injury in gynecologic laparoscopy. J Am Assoc Gynecol Laparosc 2003;10:9–13.
24. Bhoyrul S, Payne J, Steffes B, Swanstrom L, Way LW. A randomized prospective study of radially expanding trocars in laparoscopic surgery. J Gastrointest Surg 2000;4:392–7.
40. Levy BS, Soderstrom RM, Dail DH. Bowel injuries during laparoscopy: Gross anatomy and histology. J Reprod Med 1985;30:168–72.
25. Yim SF, Yuen PM. Randomized double-masked comparison of radially expanding access device and conventional cutting tip trocar in laparoscopy. Obstet Gynecol 2001;97:435–8.
41. Nezhat C, Siegler AM, Nezhat FR, Nezhat C, Seidman DS, Luciano AA. Operative Gynecology Laparoscopy: Principles, Techniques and Complications. New York: McGrawHill, 2000.
26. Munro MG, Tarnay CM. The impact of trocar-cannula design and simulated operative manipulation on incisional characteristics: a randomized trial. Obstet Gynecol 2004;103:681–5.
42. Wheeless CR. Gastrointestinal injuries associated with laparoscopy. In: Phillips JM (ed) Endoscopy in Gynecology. Baltimore: Williams and Wilkins, 1978.
27. Liu CD, McFadden DW. Laparoscopic port sites do not require fascial closure when nonbladed trocars are used. Am Surg 2000;66:853–4.
43. Maher CF, Qatawneh AM, Dwyer PL, Carey MP, Cornish A, Schluter PJ. Abdominal sacral colpopexy or vaginal sacrospinous colpopexy for vaginal vault prolapse: a prospective randomized study. Am J Obstet Gynecol 2004;190:20–6.
28. Sharp HT, Dodson MK, Draper ML, Watts DA, Doucette RC, Hurd WW. Complications associated with optical-access laparoscopic trocars. Obstet Gynecol 2002;99:553–5.
44. Cosson M, Bogaert E, Narducci F, Querleu D, Crepin G. Promontofixation coelioscopique: resultats a court terme et complications chez 83 patientes. J Gynecol Obstet Biol Reprod (Paris) 2000;29:746–50.
29. Thomas MA, Rha KH, Ong AM et al. Optical access trocar injuries in urological laparoscopic surgery. J Urol 2003;170:61–3.
45. Bruyere F, Rozenberg H, Abdelkader T. La promonto-fixation sous coelioscopie: une voie d’abord seduisante pour la cure des prolapsus. Prog Urol 2001;11:1320–6.
30. String A, Berber E, Foroutani A, Macho JR, Pearl JM,
46. Antiphon P, Elard S, Benyoussef A et al. Laparoscopic
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promontory sacral colpopexy: is the posterior, recto-vaginal, mesh mandatory? Eur Urol 2004;45:655–61. 47. Muzii L, Angioli R, Zullo MA, Calcagno M, Panici PB. Bowel preparation for gynecological surgery. Crit Rev Oncol Hematol 2003;48:311–5. 48. Miettinen RP, Laitinen ST, Makela JT, Paakkonen ME. Bowel preparation with oral polyethylene glycol electrolyte solution vs. no preparation in elective open colorectal surgery: prospective, randomized study. Dis Colon Rectum 2000;43:669–75. 49. Smith AR, Stanton SL. Laparoscopic colposuspension. Br J Obstet Gynaecol 1998;105:383–4. 50. Cook JR, Seman EI, O’Shea RT. Laparoscopic treatment of enterocele: a 3-year evaluation. Aust N Z J Obstet Gynaecol 2004;44:107–10.
51. Harris RL, Cundiff GW, Theofrastous JP, Yoon H, Bump RC, Addison WA. The value of intraoperative cystoscopy in urogynecologic and reconstructive pelvic surgery. Am J Obstet Gynecol 1997;177:1367–9. 52. Jabs CF, Drutz HP. The role of intraoperative cystoscopy in prolapse and incontinence surgery. Am J Obstet Gynecol 2001;185:1368–71. 53. Garry R, Fountain J, Brown J et al. EVALUATE hysterectomy trial: a multicentre randomised trial comparing abdominal, vaginal and laparoscopic methods of hysterectomy. Health Technol Assess 2004;8:1–154. 54. Cottin V, Delafosse B, Viale JP. Gas embolism during laparoscopy. A report of seven cases in patients with previous abdominal surgical history. Surg Endosc 1996;10:166–9.
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Etiology and EpidEmiology Urogenital fistulae may occur congenitally, but are most often acquired from obstetric, surgical, radiation, malignant, and miscellaneous causes. In most third world countries over 90% of fistulae are of obstetric etiology,1–4 whereas in the UK and USA over 70% follow pelvic surgery5,6 (Table 88.1). Obstetric fistulae are covered in Chapter 89; this chapter deals primarily with surgical fistulae. Urogenital fistulae may occur following a wide range of surgical procedures within the pelvis (Fig. 88.1). It is often supposed that this complication results from direct injury to the lower urinary tract at the time of operation. Certainly on occasions this may be the case; careless, hurried, or rough surgical technique makes injury to the lower urinary tract much more likely. However, of 233 urogenital fistulae referred to the author over the last 17 years, 156 (66.9%) have been associated with pelvic surgery, and 118 (50.6%) followed hysterectomy; of these only five (4.2%) presented with leakage of urine on the first day postoperatively. In other cases it is presumed that tissue devascularization during dissection, inadvertent suture placement, infection or pelvic hematoma formation developing postoperatively results in tissue necrosis, with leakage developing most usually between 5 and 14 days later. Overdistension of the bladder postoperatively may be an additional factor in many of these latter cases. It has been shown that there is a high incidence of abnormalities of lower urinary tract function in fistula patients;7 whether these abnormalities antedate the surgery, or develop with or as a consequence of the fistula, is unclear. It is likely that patients with a habit of infrequent voiding, or those with inefficient detrusor contractility, may be at increased risk of postoperative urinary retention. If this is not recognized early and managed appropriately, the risk of fistula formation may be increased. Although it is important to remember that the majority of surgical fistulae follow apparently straightforward hysterectomy in skilled hands, several risk factors may be identified, making direct injury more likely (Table 88.2). Obviously anatomic distortion within the pelvis by ovarian tumor or fibroid will increase the surgical difficulty, and abnormal adhesions between bladder and uterus or cervix following previous surgery, or associated with previous sepsis, endometriosis or malignancy, may make fistula formation more likely. Preoperative or early radiotherapy may decrease vascularity, and make the tissues in general less forgiving of poor technique. Issues of training and surgical technique are also important. The ability to locate and if necessary dissect
out the ureter must be part of routine gynecologic training, as should the first aid management of lower urinary tract injury when it arises. The use of gauze swabs to separate the bladder from the cervix at cesarean section or hysterectomy should be discouraged; sharp dissection with knife or scissors does less harm, especially where the tissues are abnormally adherent.
prEvalEncE The prevalence of genital fistulae obviously varies from country to country and continent to continent as the main causative factors vary. Data from the Regional Health Authority Information Units in England and Wales suggests an average of 10 fistula repairs per health region per year over the last few years, and a national figure of approximately 152 repair procedures per year.8 The rate of fistula formation following hysterectomy in the UK has been variously estimated at between 1 in 640 operations5 and 1 in 1300 operations (Lawson J, 1990, personal communication). Using the above figure of 152 fistula repair procedures per year, of which 50% can be assumed to follow hysterectomy, at a time when approximately 72,000 hysterectomies were undertaken annually in England and Wales, would indicate a fistula rate of approximately 1 in 950 hysterectomies. This is comparable with the figure reported from health insurance data from Finland.9 Following laparoscopic assisted vaginal hysterectomy, the incidence of fistula development may approach 1%.10–12 Figures of between 1 and 4% fistulae have been reported following radical hysterectomy,13,14 with a similar incidence following radiation for gynecologic malignancies.15 The incidence of fistula formation following pelvic exenteration may be as high as 10%.16
classification Many different fistula classifications have been described in the literature on the basis of anatomical site; these may include urethral, bladder neck, subsymphysial (a complex form involving circumferential loss of the urethra with fixity to bone), midvaginal, juxtacervical or vault fistulae, massive fistulae extending from bladder neck to vault, and vesicouterine or vesicocervical fistulae. While over 60% of fistulae in the third world are midvaginal, juxtacervical or massive (reflecting their obstetric etiology), such cases are relatively rare in Western fistula practice; by contrast, 50% of the fistulae managed in the UK are situated in the vaginal vault (reflecting their surgical etiology).5 Cases are often subclassified into simple cases (where the tissues are healthy
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table 88.1.
Etiology of urogenital fistulae in two series, from north-east of England (Hilton, unpublished) and from south-east Nigeria* SE Nigeria (n=2389)†
NE England (n=233) Etiology
%
n
%
n
obstructed labor
7
1918
cesarean section
11
165
ruptured uterus
8
119
forceps/ventouse
4
breech extraction
1
symphysiotomy
1
placental abruption
1
Obstetric
14.2
33
abdominal hysterectomy
97
radical hysterectomy
13
vaginal hysterectomy
4
LAVH
3
cesarean hysterectomy
1
cervical stumpectomy
2
laparoscopic oophorectomy
1
colporrhaphy
5
cystoplasty
3
colposuspension
3
sling
1
needle suspension
1
urethral diverticulectomy
92.2
33 25
35
11
subtrigonal phenol injection
1
nephroureterectomy
2
lithoclast
1
colectomy
5
unknown surgery in childhood
1
suture to vaginal laceration Surgical
2202
12 66.9
156
4.4
105
Radiation
8.6
20
0.0
0
Malignancy
0.0
0
1.8
42
foreign body
6
uncertain
6
vaginal pessary
4
catheter associated
2
trauma
2
11
infection
1
7
congenital
3
coital injury Miscellaneous Total
22 10.3
24
1.7
40
100.0
233
100.0
2389
* Data from ref. 2. † 2389 patients for whom notes could be examined, out of a total series of 2484 patients. LAVH, laparoscopically assisted vaginal hysterectomy.
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a
Figure 88.1.
table 88.2.
b
Postoperative urogenital fistulae following: (a) anterior colporrhaphy; (b) urethral diverticulectomy.
Risk factors for postoperative fistulae
Risk factor
Pathology
Anatomical distortion Abnormal tissue adhesion
Specific example Fibroids Ovarian mass
Inflammation
Infection Endometriosis
Previous surgery
Cesarean section Cone biopsy Colporrhaphy
Malignancy Impaired vascularity
Ionizing radiation Metabolic abnormality Radical surgery
Preoperative radiotherapy Diabetes mellitus
Compromised healing
Anemia Nutritional deficiency
Abnormality of bladder function
Voiding dysfunction
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c
d
Figure 88.1. Postoperative urogenital fistulae following (cont.): (c) radical hysterectomy; (d) colposuspension (the fistula in the latter case was fixed retropubically in the midline at the bladder neck, and the photograph shows the patient prone, in the reverse lithotomy position). and access good) or complicated (where there is tissue loss, scarring, impaired access, involvement of the ureteric orifices, or the presence of coexistent rectovaginal fistula). An alternative classification, based on the extent of sphincter involvement in longitudinal and circumferential aspects, has been proposed by Waaldijk;17 this has the potential benefit of being more informative of both treatment and prognosis.
prEsEntation Fistulae between the urinary tract and the female genital tract are characteristically said to present with continuous urinary incontinence, with limited sensation of bladder fullness, and with infrequent voiding. Where there is extensive tissue loss, as in obstetric or radiation fistulae, this typical history is usually present, the clinical findings gross, and the diagnosis rarely in doubt. With postsurgi-
cal fistulae, however, the history may be atypical and the orifice small, elusive or occasionally completely invisible. Under these circumstances the diagnosis can be much more difficult, and a high index of clinical suspicion must be maintained. Occasionally a patient with an obvious fistula may deny incontinence, and this is presumed to reflect the ability of the levator ani muscles to occlude the vagina below the level of the fistula. Some patients with a vesicocervical or a vesicouterine fistula following cesarean section may maintain continence at the level of the uterine isthmus, and complain of cyclical hematuria at the time of menstruation, or menouria.18,19 In other cases patients may complain of little more than a watery vaginal discharge, or intermittent leakage which seems posturally related. Leakage may appear to occur specifically on standing or on lying supine, prone, or in left or right lateral positions, presumably reflecting the degree of 1227
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bladder distension and the position of the fistula within the bladder; such a pattern is most unlikely to be found with ureteric fistulae. Although in the case of direct surgical injury leakage may occur from day one, in most surgical and obstetric fistulae symptoms develop between 5 and 14 days after the causative injury; however, the time of presentation may be quite variable. This will depend to some extent on the severity of symptoms, but as far as obstetric fistulae in the third world are concerned, is determined more by access to health care. In a recent review of cases from Nigeria, the average time for presentation was over 5 years, and in some cases over 35 years, after the causative pregnancy.2 Urethrovaginal fistulae distal to the sphincter mechanism will often be asymptomatic, and require no specific treatment. Some may lead to obstruction, and are more likely to present with postmicturition dribbling than other types of incontinence; they can therefore be very difficult to recognize. More proximally situated urethral fistulae are perhaps most likely to present with stress incontinence, since bladder neck competence is frequently impaired.
dye studies Although other imaging techniques undoubtedly have a role (see below), carefully conducted dye studies remain the investigation of first choice. Phenazopyridine may be used orally, or indigo carmine intravenously, to stain the urine and hence confirm the presence of a fistula. The identification of the site of a fistula is best carried out by the instillation of colored dye (methylene blue or indigo carmine) into the bladder via a catheter with the patient in the lithotomy position. The traditional ‘three swab test’ has its limitations and is not recommended. The examination is best carried out with direct inspection, and multiple fistulae may be located in this way. If leakage of clear fluid continues after dye instillation, a ureteric fistula is likely, and this is most easily confirmed by a ‘two dye test’, using phenazopyridine to stain the renal urine, and methylene blue to stain bladder contents.20
imaging Excretion urography
invEstigations If there is suspicion of a fistula, but its presence is not easily confirmed by clinical examination with a Sims’ speculum, further investigation will be necessary to confirm or fully exclude the possibility. Even where the diagnosis is clinically obvious, additional investigation may be appropriate for full evaluation prior to deciding treatment. The main principles of investigation therefore are:
• to confirm that the discharge is urinary; • to establish that the leakage is extraurethral rather than urethral;
• to establish the site of leakage; • to exclude multiple fistulae. Biochemistry and microbiology Excessive vaginal discharge or the drainage of serum from a pelvic hematoma postoperatively may simulate a urinary fistula. If the fluid is in sufficient quantity to be collected, biochemical analysis of its urea content in comparison to that of urine and serum will confirm its origin. Urinary infection is surprisingly uncommon in fistula patients; however, especially where there have been previous attempts at surgery, urine culture should be undertaken and appropriate antibiotic therapy instituted.
Although intravenous urography is a particularly insensitive investigation in the diagnosis of vesicovaginal fistula, knowledge of upper urinary tract status may have a significant influence on treatment measures applied, and should therefore be looked on as an essential investigation for any suspected or confirmed urinary fistula. Compromise to ureteric function is a particularly common finding when a fistula occurs in relation to malignant disease or its treatment (by radiation or surgery). Dilation of the ureter is characteristic in ureteric fistula, and its finding in association with a known vesicovaginal fistula should raise suspicion of a complex ureterovesicovaginal lesion (Fig. 88.2). While essential for the diagnosis of ureteric fistula, intravenous urography is not completely sensitive; the presence of a periureteric flare is, however, highly suggestive of extravasation at this site.
Retrograde pyelography Retrograde pyelography is a more reliable way of identifying the exact site of a ureterovaginal fistula, and may be undertaken simultaneously with either retrograde or percutaneous catheterization for therapeutic stenting of the ureter.
Cystography Cystography is not particularly helpful in the basic diagnosis of vesicovaginal fistulae, and a dye test carried out
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tula, and is deemed by several authorities to be an essential preliminary to definitive surgical treatment.5,26–29 It is important at the time of examination to assess the available access for repair vaginally, and the mobility of the tissues. The decision between the vaginal and the abdominal approach to surgery is thus made: when the vaginal route is chosen, it may be appropriate to select between the more conventional supine lithotomy position with a head-down tilt, and the prone (reverse lithotomy) with head-up tilt. This may be particularly useful in allowing the operator to look down onto the bladder neck and subsymphysial fistulae; it is also of advantage in some massive fistulae in encouraging the reduction of the prolapsed bladder mucosa.30
Endoscopy cystoscopy
Figure 88.2. Intravenous urogram (with simultaneous cystogram) demonstrating a complex surgical fistula occurring after radical hysterectomy. After further investigation including cystourethroscopy, sigmoidoscopy, barium enema, and retrograde cannulation of the vaginal vault to perform fistulography, the lesion was defined as a ureterocolovesicovaginal fistula. under direct vision is likely to be more sensitive. It may, however, occasionally be useful in achieving a diagnosis in complex or vesicouterine fistulae.
Ultrasound, computed tomography, and magnetic resonance imaging Endoanal ultrasound and magnetic resonance imaging (MRI) are particularly useful in the investigation of anorectal and perineal fistulae. Although abdominal, vaginal, transperineal, and Doppler ultrasound have all been reported in known cases, the role of these techniques in the diagnosis or assessment of urogenital fistulae remains to be clarified.21–25
Examination under anesthesia Careful examination, if necessary under anesthetic, may be required to determine the presence of a fis-
Although some authorities suggest that endoscopy has little role in the evaluation of fistulae, it is the author’s practice to perform cystourethroscopy in all but the largest defects. In some obstetric and radiation fistulae the size of the defect and the extent of tissue loss and scarring may make it difficult to distend the bladder; nevertheless, much useful information is obtained. The exact level and position of the fistula should be determined, and its relationship to the ureteric orifices and bladder neck are particularly important. With urethral and bladder neck fistulae the failure to pass a cystoscope or sound may indicate that there has been circumferential loss of the proximal urethra, a circumstance which is of considerable importance in determining the appropriate surgical technique and the likelihood of subsequent urethral incompetence.3,7 The condition of the tissues must be carefully assessed. Persistence of substantial slough means that surgery should be deferred, and this is particularly important in obstetric and postradiation cases. Biopsy from the edge of a fistula should be taken in radiation fistulae if persistence of recurrent malignancy is suspected. Malignant change has been reported in a longstanding benign fistula, so where there is any doubt at all about the nature of the tissues, biopsy should be undertaken.30 In areas of endemicity, evidence of schistosomiasis, tuberculosis, and lymphogranuloma may become apparent in biopsy material, and again it is important that specific antimicrobial treatment is instituted prior to definitive surgery. 1229
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prEopErativE managEmEnt Before epithelialization is complete, an abnormal communication between viscera will tend to close spontaneously, provided that the natural outflow is unobstructed. Bypassing the sphincter mechanisms by urinary catheterization may encourage closure. The early management is of critical importance, and depends on the etiology and site of the lesion. If surgical trauma is recognized within the first 24 hours postoperatively, immediate repair may be appropriate, provided that extravasation of urine into the tissues has not been great. The majority of surgical fistulae are, however, recognized between 5 and 14 days postoperatively, and these should be treated with continuous bladder drainage. It is worth persisting with this line of management in vesicovaginal or urethrovaginal fistulae for 6–8 weeks, since spontaneous closure in both surgical and obstetric cases may occur within this period.31,32 It is important to appreciate that some fistulae may be associated with few or no symptoms, and even if persistent these do not require surgical treatment. Small distal urethrovaginal fistulae, uterovesical fistulae with menouria, and some low rectovaginal fistulae may fall into this category.
palliation and skin care During the waiting period from diagnosis to repair, incontinence pads should be provided in generous quantities so that patients can continue to function socially to some extent. Fistula patients usually leak very much greater quantities of urine than those with urethral incontinence from whatever cause, and this needs to be recognized in terms of provision of supplies. The vulval skin may be at considerable risk from urinary dermatitis, and liberal use of silicone barrier cream should be encouraged. Steroid therapy has been advocated in the past as a means of reducing tissue edema and fibrosis, although these benefits are refuted and there may be a risk of compromise to subsequent healing. Local estrogen has been recommended by some, and while empirically there may be benefit in postmenopausal women, or those obstetric fistula patients with prolonged amenorrhea, the evidence for this is lacking.
antimicrobial therapy Opinions differ on the desirability of prophylactic antibiotic cover for surgery, some avoiding their use other than in the treatment of specific infection, and some advocating broad spectrum treatment in all cases. The
only randomized trial in this area failed to demonstrate benefit from antibiotic prophylactic treatment in obstetric fistula patients,33 although the author’s current practice is for single dose prophylaxis in patients undergoing repair of surgical fistulae.
counseling As surgical fistula patients are usually previously healthy individuals who entered hospital for what was expected to be a routine procedure, and end up with symptoms infinitely worse than their initial complaint, they are invariably devastated by their situation. It is vital that they understand the nature of the problem, why it has arisen, and the plan for management at all stages. Confident but realistic counseling by the surgeon is essential and the involvement of nursing staff or counsellors with experience of fistula patients is also highly desirable. The support given by previously treated sufferers can also be of immense value in maintaining patient morale, especially where a delay prior to definitive treatment is required.
gEnEral principlEs of surgical trEatmEnt timing of repair The timing of surgical repair is perhaps the single most contentious aspect of fistula management. While shortening the waiting period is of both social and psychological benefit to what are always very distressed patients, these issues must not be traded for compromise to surgical success. The benefit of delay is to allow slough to separate and inflammatory change to resolve. In both obstetric and radiation fistulae there is considerable sloughing of tissues, and it is imperative that this should have settled before repair is undertaken. In radiation fistulae it may be necessary to wait 12 months or more. In obstetric cases most authorities suggest that a minimum of 3 months should be allowed to elapse, although others have advocated surgery as soon as slough is separated. With surgical fistulae the same principles should apply, and although the extent of sloughing is limited, extravasation of urine into the pelvic tissues inevitably sets up some inflammatory response. Although early repair is advocated by several authors, again most would agree that 10–12 weeks postoperatively is the earliest appropriate time for repair. Pressure from patients to undertake repair at the earliest opportunity is always understandably great, but
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is never more so than in the case of previous surgical failure. Such pressure must, however, be resisted, and 8 weeks is the minimum time that should be allowed between attempts at closure.
dissection
Many urologists advocate an abdominal approach for all fistula repairs, claiming the possibility of earlier intervention and higher success rates in justification. Others suggest that all fistulae can be successfully closed by the vaginal route. Surgeons involved in fistula management must be capable of both approaches, and have the versatility to modify their techniques to select that most appropriate to the individual case. Where access is good and the vaginal tissues sufficiently mobile, the vaginal route is usually most appropriate (Fig. 88.3a,b). Access for vaginal repair may be improved by the use of unilateral or bilateral episiotomy, although where even this proves inadequate and the fistula cannot be brought down, the abdominal approach should be considered. Overall, more surgical fistulae are likely to require an abdominal repair than obstetric fistulae, although in the author’s series of cases from the UK, and those reviewed from Nigeria, two-thirds of cases were satisfactorily treated by the vaginal route regardless of etiology.
Great care must be taken over the initial dissection of the fistula, and the surgeon should probably take as long over this as over the repair itself. The fistula should be circumcised in the most convenient orientation, depending on size and access. All things being equal, a longitudinal incision should be made around urethral or midvaginal fistulae; conversely, vault fistulae are better handled by a transverse elliptical incision (Fig. 88.3c). The tissue planes are often obliterated by scarring, and dissection close to a fistula should therefore be undertaken with a scalpel or scissors (Fig. 88.3d). It must be recognized that, in many cases, particularly of obstetric fistulae, the defect in the bladder may be considerably larger than the visible defect in the vagina, and circumcision must be undertaken well away from the fistula edges. Sharp dissection is easier with countertraction applied by skin hooks, tissue forceps or retraction sutures. Blunt dissection with small pledgets may be helpful once the planes are established, and provided one is away from the fistula edge. Wide mobilization should be performed so that tension on the repair is minimized (Fig. 88.3e). Bleeding is rarely troublesome with vaginal procedures, except occasionally with proximal urethrovaginal fistulae. Diathermy is best avoided, with pressure or underrunning sutures preferred.
instruments
suture materials
All operators have their own favored instruments, although those described in the treatise by Chassar Moir26 and Lawson30 are eminently suitable for repair by any route. The following are particularly useful:
Although a range of suture materials have been advocated over the years, and a range of opinion still exists, the author’s view is that absorbable sutures should be used throughout all urinary fistula repair procedures. Polyglactin (Vicryl) 2-0 suture on a 25 mm heavy tapercut needle is preferred for both the bladder and vagina, and polydioxanone (PDS) 4-0 on a 13 mm round-bodied needle is used for the ureter.
route of repair
• series of fine scalpel blades on the No. 7 handle, especially the curved No. 12 bistoury blade;
• Chassar Moir 30-degree angled-on-flat and 90-degree • • •
• •
curved-on-flat scissors; cleft palate forceps; Judd-Allis, Stiles, and Duval tissue forceps; Millin’s retractor for use in transvesical procedures, and Currie’s retractors for vaginal repairs. The Lone Star™ ring retractor may give considerable advantage, particularly for vaginal procedures; Skin hooks to put the tissues on tension during dissection; Turner-Warwick double curved needle holder is particularly useful in areas of awkward access, and has the advantage of allowing needle placement without the operator’s hand or the instrument obstructing the view.
spEcific rEpair tEchniquEs vaginal procedures Dissection and repair in layers There are two main types of closure technique applied to the repair of urinary fistulae: the classical saucerization technique described by Sims,34 and the much more commonly used dissection and repair in layers. Sutures must be placed with meticulous accuracy in the bladder wall, care being taken not to penetrate the mucosa which should be inverted as far as possible. The repair should 1231
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a
b
Figure 88.3. Simple posthysterectomy vault vesicovaginal fistula, and steps in vaginal repair procedure by dissection and closure in layers: (a) fistula visible in vaginal vault; (b) tissue forceps applied illustrating tissue mobility, and ease of access for repair per vaginam. be started at either end, working towards the midline, so that the least accessible aspects are sutured first (Fig. 88.3g). Interrupted sutures are preferred and should be placed approximately 3 mm apart, taking as large a bite of tissue as feasible. Stitches that are too close together, or the use of continuous or purse-string sutures, tend to impair blood supply and interfere with healing. Knots must be secure with at least three hitches, so that they can be cut short, leaving the minimum amount of material within the body of the repair. With dissection and repair in layers the first layer of sutures in the bladder should invert the edges; the second adds bulk to the repair by taking a wide bite of bladder wall, but also closes off dead space by catching the back of the vaginal flaps (Fig. 88.3h). After testing the repair (Fig. 88.3i) (see below), a third layer of interrupted mattress sutures is used to evert and close the vaginal wall, consolidating the repair by picking up the underlying bladder wall (Fig. 88.3j).
Saucerization The saucerization technique involves converting the track into a shallow crater, which is closed without dissection of bladder from vagina using a single row of interrupted sutures. The method is applicable only to small fistulae and perhaps to residual fistulae after closure of a larger defect; in other situations the technique does not allow secure closure without tension.
Vaginal repair procedures in specific circumstances The conventional dissection and repair in layers as described above is entirely appropriate for the majority of midvaginal fistulae, although modifications may be necessary in specific circumstances. In juxtacervical fistulae, or indeed vesicocervical fistulae, vaginal repair may be feasible if the cervix can be drawn down to provide access. Dissection should include mobilization of the bladder from the cervix. The repair should be
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c
d
Figure 88.3. Simple posthysterectomy vault vesicovaginal fistula, and steps in vaginal repair procedure by dissection and closure in layers (cont.): (c) fistula circumcised using No. 12 scalpel; (d) sharp dissection around fistula edge. undertaken transversely to reconstruct the underlying trigone and prevent distortion of the ureteric orifices. Vault fistulae, particularly those following hysterectomy, can again usually be managed vaginally. The vault is incised transversely and mobilization of the fistula is often aided by deliberate opening of the pouch of Douglas.35 The peritoneal opening does not require to be closed separately, but is incorporated into the vaginal closure. With subsymphysial fistulae involving the bladder neck and proximal urethra as a consequence of obstructed labor, tissue loss may be extensive, and fixity to underlying bone a common problem. The lateral aspects of the fistula require careful mobilization to overcome disproportion between the defect in the bladder and the urethral stump. A racquet shape extension of the incision facilitates exposure of the proximal urethra. Although transverse repair is often necessary, longitudinal closure gives better prospects for urethral competence.
Where there is substantial urethral loss, reconstruction may be undertaken using the method described by Chassar Moir26 or Hamlin and Nicholson.36 A strip of anterior vaginal wall is constructed into a tube over a catheter. Plication behind the bladder neck is probably important if continence is to be achieved. The interposition of a labial fat or muscle graft not only fills up the potential dead space, but also provides additional bladder neck support and improves continence by reducing scarring between bladder neck and vagina. With very large fistulae extending from bladder neck to vault, the extensive dissection required may produce considerable bleeding. The main surgical difficulty is to avoid the ureters. They are usually situated close to the superolateral angles of the fistula and, if they can be identified, they should be catheterized. Straight ureteric catheters passed transurethrally or double pigtail catheters may both be useful in directing the intramural 1233
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f
Figure 88.3. Simple posthysterectomy vault vesicovaginal fistula, and steps in vaginal repair procedure by dissection and closure in layers (cont.): (e) fistula fully mobilized; (f) vaginal scar edge trimmed. portion of the ureters internally; nevertheless great care must be taken during dissection.
abdominal procedures Transvesical repair Repair by the abdominal route is indicated when high fistulae are fixed in the vault and are inaccessible per vaginam. Transvesical repair has the advantage of being entirely extraperitoneal. It is often helpful to elevate the fistula site by a vaginal pack, and the ureters should be catheterized under direct vision. The technique of closure is similar to that of the transvaginal flap-splitting repair except that for hemostasis the bladder mucosa is closed with a continuous suture.
Transperitoneal repair It is often said that there is little place for a simple transperitoneal repair, although a combined transperitoneal and transvesical procedure is favored by urologists and
is particularly useful for vesicouterine fistulae following cesarean section. A midline split is made in the vault of the bladder and extended downwards in a racquet shape around the fistula. The fistulous track is excised and the vaginal or cervical defect closed in a single layer. The bladder is then closed in two layers.
interposition grafting Several techniques have been described to support fistula repair in different sites. In each case the interposed tissue serves to create an additional layer in the repair, to fill dead space, and to bring in new blood supply to the area. The tissues used include:
• Martius graft – labial fat and bulbocavernosus muscle passed subcutaneously to cover a vaginal repair; this is particularly appropriate to provide additional bulk in a colpocleisis and in urethral and bladder neck fistulae may help to maintain
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g
h
Figure 88.3. Simple posthysterectomy vault vesicovaginal fistula, and steps in vaginal repair procedure by dissection and closure in layers (cont.): (g) first two sutures of first layer of repair in place lateral to the angles of the repair; (h) second layer completed, sutures catching the back of the vaginal flaps to close off dead space.
• •
•
competence of closure mechanisms by reducing scarring;37 Gracilis muscle passed either via the obturator foramen or subcutaneously is used as above;36 Omental pedicle grafts may be dissected from the greater curve of the stomach and rotated down into the pelvis on the right gastroepiploic artery. This may be used at any transperitoneal procedure, but has its greatest advantage in postradiation fistulae;38,39 Peritoneal flap graft is an easier way of providing an additional layer at transperitoneal repair procedures, by taking a flap of peritoneum from any available surface, most usually the paravesical area.27
testing the repair The closure must be watertight and so should be tested at the end of vaginal repairs by the instillation of dye into the bladder under minimal pressure; a previously unsus-
pected second fistula is occasionally identified in this way. Testing after abdominal procedures is impractical.
postopErativE managEmEnt fluid balance Nursing care of patients who have undergone urogenital fistula repair is of critical importance, and obsessional postoperative management may do much to secure success. As a corollary, however, poor nursing may easily undermine what has been achieved by the surgeon. Strict fluid balance must be kept and a daily fluid intake of at least 3 liters, and output of 100 ml per hour, should be maintained until the urine is clear of blood. Hematuria is more persistent following abdominal than vaginal procedures, and intravenous fluid is therefore likely to be required for longer in this situation. 1235
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j
Figure 88.3. Simple posthysterectomy vault vesicovaginal fistula, and steps in vaginal repair procedure by dissection and closure in layers (cont.): (i) testing the repair with methylene blue dye instillation; (j) final layer of mattress sutures in the vaginal wall. (Reproduced from ref. 8 with permission.)
Bladder drainage Continuous bladder drainage in the postoperative period is crucial to success, and nursing staff should check catheters hourly throughout each day to confirm free drainage and check output. Bladder irrigation and suction drainage are not recommended. Views differ as to the ideal type of catheter. The caliber must be sufficient to prevent blockage, although whether the suprapubic or urethral route is used is to a large extent a matter of individual preference. The author’s usual practice is to use a ‘belt and braces’ approach of both urethral and suprapubic drainage initially, so that if one becomes blocked, free drainage is still maintained. The urethral catheter is removed first, and the suprapubic retained, and used to assess residual volume, until the patient is voiding normally.40
The duration of free drainage depends on the fistula type. Following repair of surgical fistulae, 12 days is adequate. With obstetric fistulae up to 21 days’ drainage may be appropriate, and following repair of radiation fistulae 21–42 days is required. Routine cystography is not advocated, although if there is any doubt about the integrity of the repair it is wise to carry out dye testing prior to catheter removal. Where a persistent leak is identified, free drainage should be maintained for 6 weeks.
mobility and thromboprophylaxis The biggest problem in ensuring free catheter drainage lies in preventing kinking or drag on the catheter. Restricting patient mobility in the postoperative period helps with this, and some advocate continuous bed rest during the period of catheter drainage. If this approach
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is chosen, patients should be looked on as being at moderate to high risk for thromboembolism, and prophylaxis must be employed.41 If patients are restricted to bed following urogenital fistula repair, a laxative should be administered to prevent excessive straining at stool.
subsequent management On removal of catheters most patients will feel the desire to void frequently, since the bladder capacity will be functionally reduced having been relatively empty for so long. In any case it is important that they do not become overdistended, and hourly voiding should be encouraged and fluid intake limited. It may also be necessary to wake them once or twice through the night for the same reason. After discharge from hospital patients should be advised to gradually increase the period between voiding, aiming to be back to a normal pattern by 4 weeks postoperatively. Tampons, pessaries, douching, and penetrative sex should be avoided until 3 months postoperatively.
prognosis It is difficult to compare the results of treatment in different series, since the lesions involved and the techniques of repair vary so greatly, and definitions of cure are inconsistent. Cure rates are perhaps best considered in terms of closure at first operation, and vary from 60 to 98%.2,5,6,36,42–48 Stress incontinence has long been recognized to persist following fistula closure,23 most commonly in obstetric fistula patients when the injury involves the sphincter mechanism, particularly if there is tissue loss,49 although persistence of this and other functional abnormalities of the lower urinary tract have also been reported in a proportion of surgical fistulae involving the urethra or bladder neck.7 We have recently investigated the persistence of urinary symptoms between 1 and 10 years following anatomically successful closure of surgical fistulae; while seriously bothersome symptoms were very uncommon, mild symptoms were reported in 75% of patients.50 Of the 233 patients in the author’s series managed in the UK, 19 (8.2%) healed without operation, 10 declined surgery for various reasons, 4 (1.7%) underwent primary urinary diversion, and 3 patients with radiotherapy fistulae died without being operated upon – 2 from recurrent disease and 1 from cachexia without recurrence. Of the 178 patients who have undergone repair surgery, 170 (95.5%) were cured by the first operation; of the 105 fistulae following simple hysterectomy, 103 (98.1%) were cured at their first operation.
A law of diminishing returns is evident in fistula surgery as in many other forms of surgery. Although repeat operations are certainly justified, the success rate decreases progressively with increasing numbers of previous unsuccessful procedures. Surgical series are rarely large enough for this to be evident; in a series of 2484 largely obstetric fistulae the success rate fell from 81.2% for first procedures to 65.0% for those requiring two or more procedures.2 It cannot be overemphasized that the best prospect for cure is at the first operation, and there is no place for the well-intentioned occasional fistula surgeon, be they gynecologist or urologist.8
rEfErEncEs 1. Danso K, Martey J, Wall L, Elkins T. The epidemiology of genitourinary fistulae in Kumasi, Ghana, 1977–1992. Int Urogynecol J Pelvic Floor Dysfunct 1996;7(3):117–20. 2. Hilton P, Ward A. Epidemiological and surgical aspects of urogenital fistulae: a review of 25 years experience in south-east Nigeria. Int Urogynecol J Pelvic Floor Dysfunct 1998;9:189–94. 3. Waaldijk K. The surgical management of bladder fistula in 775 women in Northern Nigeria. MD thesis, University of Utrecht, Nijmegen, 1989. 4. Zacharin R. Obstetric Fistula. Vienna: Springer-Verlag, 1988. 5. Hilton P. Urogenital fistulae. In: Maclean A, Cardozo L (eds) Incontinence in Women – Proceedings of the 42nd RCOG Study Group. London: RCOG, 2002; 163–81. 6. Lee R, Symmonds R, Williams T. Current status of genitourinary fistula. Obstet Gynecol 1988;71:313–9. 7. Hilton P. The urodynamic findings in patients with urogenital fistulae. Br J Urol 1998;81:539–42. 8. Hilton P. Debate: Post-operative urinary fistulae should be managed by gynaecologists in specialist centres. Br J Urol Int 1997;80(Suppl 1):35–42. 9. Harkki-Siren P, Sjoberg J, Tiitinen A. Urinary tract injuries after hysterectomy. Obstet Gynecol 1998;92:113–8. 10. Chapron CM, Dubuisson JB, Ansquer Y. Is total laparoscopic hysterectomy a safe surgical procedure? Hum Reprod 1996;11(11):2422–4. 11. Malik E, Schmidt M, Schneidel P. [Complications following 106 laparoscopic hysterectomies.] Zentralbl Gynakol 1997;119(12):611–5. 12. Price JH, Nassief SA. Laparoscopic-assisted vaginal hysterectomy: initial experience. Ulster Med J 1996;65(2):149–51. 13. Averette HE, Nguyen HN, Donato DM et al. Radical hysterectomy for invasive cervical cancer. A 25-year prospective experience with the Miami technique. Cancer 1993;71:1422–37.
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14. Emmert C, Köhler U. Management of genital fistulas in patients with cervical cancer. Arch Gynecol Obstet 1996;259:19–24.
32. Waaldijk K. Immediate indwelling bladder catheterisation at postpartum urine leakage: personal experience of 1200 patients. Tropical Doctor 1997;27:227–8.
15. White A, Buchsbaum H, Blythe J, Lifshitz S. Use of the bulbocavernosus muscle (Martius procedure) for repair of radiation-induced rectovaginal fistulas. Obstet Gynecol 1982;60(1):114–8.
33. Tomlinson AJ, Thornton JG. A randomised controlled trial of antibiotic prophylaxis for vesico-vaginal fistula repair. Br J Obstet Gynaecol 1998;105:397–9.
16. Bladou F, Houvenaeghel G, Delpero JR, Guerinel G. Incidence and management of major urinary complications after pelvic exenteration for gynecological malignancies. J Surg Oncol 1995;58:91–6. 17. Waaldijk K. Surgical classification of obstetric fistulas. Int J Gynaecol Obstet 1995;49(2):161–3. 18. Falk F, Tancer M. Management of vesical fistulas after Cesarean section. Am J Obstet Gynecol 1956;71:97–106. 19. Youssef A. ‘Menouria’ following lower segment Cesarean section: a syndrome. Am J Obstet Gynecol 1957;73:759–67. 20. Raghavaiah N. Double-dye test to diagnose various types of vaginal fistulas. J Urol 1974;112:811–2. 21. Abulafia O, Cohen HL, Zinn DL, Holcomb K, Sherer DM. Transperineal ultrasonographic diagnosis of vesicovaginal fistula. J Ultrasound Med 1998;17(5):333–5. 22. Adetiloye VA, Dare FO. Obstetric fistula: evaluation with ultrasonography. J Ultrasound Med 2000;19(4):243–9. 23. Huang WC, Zinman LN, Bihrle W 3rd. Surgical repair of vesicovaginal fistulas. Urol Clin North Am 2002;29(3):709–23. 24. Volkmer BG, Kuefer R, Nesslauer T, Loeffler M, Gottfried HW. Colour Doppler ultrasound in vesicovaginal fistulas. Ultrasound Med Biol 2000;26(5):771–5. 25. Yang JM, Su TH, Wang KG. Transvaginal sonographic findings in vesicovaginal fistula. J Clin Ultrasound 1994;22(3):201–3. 26. Chassar Moir J. The Vesico-vaginal Fistula, 2nd ed. London: Baillière, 1967. 27. Jonas U, Petri E. Genitourinary fistulae. In: Stanton S (ed) Clinical Gynecologic Urology. St Louis: Mosby, 1984; 238–55.
34. Sims J. On the treatment of vesico-vaginal fistula. Am J Med Sci 1852;XXIII:59–82. 35. Lawson J. Vesical fistulae into the vaginal vault. Br J Urol 1972;44:623–31. 36. Hamlin R, Nicholson E. Reconstruction of urethra totally destroyed in labour. Br Med J 1969;2:147–50. 37. Martius H. Die operative Wiederherstellung der vollkommen fehlenden Harnrohre und des Schiessmuskels derselben. Zentralbl Gynakol 1928;52:480. 38. Kiricuta I, Goldstein A. The repair of extensive vesicovaginal fistulas with pedicled omentum: a review of 27 cases. J Urol 1972;108:724–7. 39. Turner-Warwick R. The use of the omental pedicle graft in urinary tract reconstruction. J Urol 1976;116:341–7. 40. Hilton P. Bladder drainage. In: Stanton SL, Monga AK (eds) Clinical Urogynecology. London: Churchill Livingstone, 2000. 41. Thromboembolic Risk Factors (THRIFT) Consensus Group. Risk of and prophylaxis for venous thromboembolism in hospital patients. Br Med J 1992;305:567–74. 42. Chassar Moir J. Vesico-vaginal fistulae as seen in Britain. J Obstet Gynaecol Br Commonw 1973;80:598–602. 43. Elkins TE, Drescher C, Martey JO, Fort D. Vesicovaginal fistula revisited. Obstet Gynecol 1988;72:307–12. 44. Goodwin WE, Scardino PT. Vesicovaginal and ureterovaginal fistulas: a summary of 25 years of experience. Trans Am Assoc Genitour Surg 1979;71:123–9. 45. Hudson C, Hendrickse J, Ward A. An operation for restoration of urinary continence following total loss of the urethra. Br J Obstet Gynaecol 1975;82:501–4. 46. Kelly J. Vesicovaginal fistulae. Br J Urol 1979;51:208–10.
28. Lawson J. The management of genito-urinary fistulae. Clin Obstet Gynaecol 1978;6:209–36.
47. O’Conor VJ. Review of experience with vesicovaginal fistula repair. J Urol 1980;123:367–9.
29. Lawson L, Hudson C. The management of vesico-vaginal and urethral fistulae. In: Stanton S, Tanagho E (eds) Surgery for Female Urinary Incontinence. Berlin: SpringerVerlag, 1987;193–209.
48. Turner-Warwick RT, Wynne EJ, Handley-Ashken M. The use of the omental pedicle graft in the repair and reconstruction of the urinary tract. Br J Surg 1967;54:849–53.
30. Lawson J. Injuries to the urinary tract. In: Lawson J, Stewart D (eds) Obstetrics and Gynaecology in the Tropics and Developing Countries. London: Edward Arnold, 1967; 481–522. 31. Davits R, Miranda S. Conservative treatment of vesicovaginal fistulas by bladder drainage alone. Br J Urol 1991;68:155–6.
49. Waaldijk K. Step-by-Step Surgery for Vesico-vaginal Fistulas. Edinburgh: Campion, 1994. 50. Dolan L, Dixon W, Hilton P. Quality of life and urodynamic abnormality in patients following urogenital fistula repair [abstract]. Int Urogynecol J Pelvic Floor Dysfunct 2003;14:S42.
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IntroductIon The majority of women throughout the world still do not have access to medical attention for the delivery of their child. Maternal mortality is still unacceptably high throughout the developing world and paralleling this are high rates of maternal morbidity. One of the most feared consequences of a morbid delivery is the obstetric fistula – reducing a woman to a life of shame, isolation, and misery – a life which sometimes ends in suicide or at least the victim wishing she had died during that frightful labor.
EtIology and EpIdEmIology It is clear that the etiology of obstetric fistula is ischemic necrosis from an obstructed labor. The impacted presenting part compresses the pelvic tissues against the mother’s bony pelvis. This connection was made a thousand years ago. The early medical text Al Kanoun by Avicenna who died in 1037 gave the warning of labor causing a tear in the bladder – a condition ‘incurable and remains so until death’.1 This accounts for the vast number of obstetric vesicovaginal fistulae seen throughout the world. Less common causes of obstetric fistulae include those iatrogenic in origin: from trauma during cesarean section, forceps delivery or manipulations, and cuttings from poorly trained health attendants. Vesicovaginal fistulae have been recorded after almost every pelvic surgery. Less common causes include advanced cervical cancer, sexual trauma, and infections (e.g. tuberculosis of the bladder, schistosomiasis, and lymphogranuloma venereum). There have been numerous epidemiologic studies of obstetric fistula patients from various parts of the globe. Typically, the patient is primiparous (43–62.7%),2,3 but a significant number are multiparous (up to 20–25% having had four or more deliveries),2,4 presumably due to delivering larger children or malpresentations. Interestingly, a number of studies have shown these women to be short, often less than 150 cm tall, in Nigeria,4 India,5 Ethiopia,6 and Niger.7 Ampofo et al. showed them to be, on average, 7 cm shorter than the general female population.8 The women are largely uneducated, more than 92% having had no formal education.3,9,10 They are also young. Although it is difficult to get a true estimate of their age as it is often unknown, it is evident from their appearance that most are in their teens. If their age is asked and the answer relied upon, 42% are aged less than 20, with 65% being less than 25 years old.3 Other studies confirm this trend.9–11 The majority have had home deliveries with no skilled attendant present and typically more than 50% have
been divorced by their husbands due to their offences.3 It has been noted in Nigeria that if the woman is childless, she is more likely to be divorced, whereas those women who have live children are more likely to be attending those children and the husband has remained with her.10 What is unclear is the association of obstetric fistula and female genital cutting. The opinion of many fistula surgeons is that the obstructed labor occurs against the mother’s bony pelvis and not against the scarred tissues resulting from a circumcision at the outlet. From the experience in Addis Ababa, fistula can result from an infundibulation indirectly when a traditional health attendant may cut the circumcision open during labor, cutting anteriorly, damaging the urethra, bladder neck, and bladder base. The other factor that leads to some controversy is early or child marriage. It seems reasonable to assume that because adult height and sexual maturity are reached before the completion of pelvic growth, that early marriage and hence pregnancy may lead to an increase in obstructed labor and hence obstetric fistula.12–14 This has not been concretely confirmed by studies in the field. Unfortunately, early marriage can also result in traumatic fistula, if the husband needs to enlarge the young girl’s vagina to enable intercourse to take place. This is sometimes done, again by a traditional healer cutting open the vaginal tissues anteriorly and sometimes damaging the urethra and/or bladder in the process. This is similar to a ‘gishiri’ cut performed in some areas as a folk treatment for a variety of gynecologic ills.9
prEvalEncE There are no accurate figures for the true prevalence of obstetric fistula. There have been no population-based studies to determine the scope of the problem. A large hospital-based study of over 22,000 patients gave the incidence of obstetric fistula as 0.35% of deliveries.15 Knowing that the majority of women in the developing world deliver in their villages and not in a hospital, the true incidence is likely to be higher. That having been said, the World Health Organization (WHO) often quotes the incidence as 0.3%. Using this figure, throughout the world there are probably between 50,000 and 100,000 new cases of obstetric fistula each year and approximately 2 million women suffering from this condition.16 Others have taken further calculations equating the obstetric fistula rate with maternal mortality. Knowing that for every maternal death 30 women suffer some morbidity of which obstetric fistula is one, Danso and colleagues proposed that the obstetric fistula rate would approximate the materal mortality rate. If this
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is the case, there would be approximately 500,000 new cases worldwide each year.2
SymptomS and SIgnS The average length of labor that the patient has endured is 3.9 days and 98% end with a stillbirth. The woman is weak and shocked postdelivery and on average it takes a woman 26.1 days before she is strong enough to be able to walk unaided.3 The immediate course of the injury is that 3–10 days postdelivery a necrotic slough is extruded through the vagina and the vesicovaginal fistula is exposed, rendering her completely incontinent. If she has sustained similar injuries to the posterior vaginal wall she is also rendered incontinent of feces. It is easy to think of obstetric fistula just as a hole in the bladder and perhaps the rectum. However, unlike iatrogenic surgical fistula which is usually a discrete injury, the pathology of the obstetric fistula is broader and the term ‘field injury’ has been coined to refer to the range of injuries caused.17 The ischemic process not only affects the tissues of the bladder, vagina, and often the rectum and vagina, but also all the other tissues in the mother’s pelvis. This results in primary conditions, i.e. those associated with the etiology of obstetric fistula. There are also secondary conditions – delayed conditions that arise later as a result of incontinence or scarring within the pelvis.
Figure 89.1. Simple midvaginal vesicovaginal fistula.
primary conditions Vesicovaginal fistula (Figs 89.1, 89.2) The level of impaction during labor determines the site of injury. If the impaction occurs at the pelvic inlet, the vesicovaginal fistula may be juxta- or even intracervical.18 If impaction occurs lower the urethra may be involved. The urethra is injured in 28% of cases, with 5% of patients having the urethra completely destroyed.17 This has prognostic indications as the mechanisms for continence in the female have been destroyed.17–20
Figure 89.2. cross-section.
Simple midvaginal vesicovaginal fistula in
In a small number of obstetric fistula cases the lower part of the ureter can be involved. The whole ureterovesical junction is necrosed and sloughed away, leaving the vesicovaginal fistula with the ureter draining outside of the bladder straight into the vagina.
emic necrosis of the rectovaginal septum. It has various reported prevalence, ranging from 6% (Hancock B, personal communication) to 22%.3 If present, it usually occurs in conjunction with a vesicovaginal fistula; it rarely presents in isolation.3 The status of the anal sphincter should always be noted as there may be residual flatal or fecal incontinence even after repair.21 Neglected fourth degree tears are also common.
Rectovaginal injuries
Reproductive tract
A rectovaginal fistula occurs if the presenting part is impacted against the sacrum during labor, causing isch-
The tissues of the vagina are obviously injured, but in some cases the whole vagina has necrosed, leaving
Ureteric injury
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little or no identifiable remaining vaginal skin. Overall, approximately 28% of patients will need some form of vaginoplasty.17 The cervix is often torn or partly necrosed and fistula surgeons testify that it is rare to see an uninjured cervix. Vesicouterine fistulae, although more uncommon, do occur when the uterus is affected.
A recent series of mental health questionnaires revealed a 93% positive screening for depression (Goh JTW, unpublished work). In areas where there are almost no services to address mental health issues, this is a very pressing need indeed.
Limb contractures Muscles The muscles of the pelvic basin are often affected by a neuropathy, directly weakened by the ischemic process or even completely destroyed.
There are often stories of patients being shut away in huts for months if not years. It is thought that, with time, disuse can cause limb contractures. This is seen in roughly 1–2% of patients in Ethiopia. It is occasionally so severe that the woman’s legs are locked in the fetal position.
Bones A series by Cockshott performed x-rays on 312 women with obstetric fistula and found that 32% had some radiographic abnormality, including bony resorption, bony spurs, obliteration or separation of the symphysis pubis.22
Nerves It has been quoted that between 20 and 65% of obstetric fistula patients will have some form of peroneal neuropathy manifesting as bilateral or unilateral foot drop.17,23 There are currently three theories as to its etiology: a prolapsed intervertebral disk, direct compression of the fetus on the lumbosacral trunk during labor, or impingement of the common peroneal nerve during prolonged squatting in labor as it transverses the head of fibula.24,25 Waaldjik and Elkins commented that most patients do improve with time, although 13% still show some signs at 2 years.23
Secondary conditions Social consequences The consequences of complete incontinence for a woman in the developing world, where the status of women is usually low, is far reaching. Over half are divorced, because the husband realizes that his wife is now unable to fulfill her marital duties and is unable to bear children.3 Her incontinence has other consequences, as she is now in urine-soaked clothes, unable to clean herself or her attire. She is unable to interact socially, as others find her presence unacceptable. She cannot go to church to worship, to the market, or go to the well to draw water. She lives in isolation stripped of her dignity and place in society.
Mental health Little has been researched into the mental health status of fistula sufferers although suicide has been reported.
Malnutrition Malnutrition results from isolation as the patient may be fed and cared for inadequately by a relative in a small room or hut. The average body mass index (BMI) from a small unpublished series from Ethiopia was 19 (Browning A, unpublished work). Cases of severe malnutrition with hypoproteinemia are not uncommon.
Upper renal tract damage One study from Nigeria investigating intravenous pylorograms in women with fistula revealed 49% of patients sustained upper renal tract damage. The commonest damage was hydronephrosis (34%) but the damage extended all the way to non-functioning kidneys.26 This is presumably due to scarring partially or totally occluding the lower ureter causing obstructive uropathy and partly due to repeated ascending infections.
Bladder stones The constant leakage of urine leads many women to drink less water and hence pass less urine. The concentrated urine might collect in pockets of scar, vagina or bladder and, with time, form calculi, causing pain, infection, and increased odor. Occasionally the woman herself or perhaps a local healer will insert foreign bodies into the vagina to try to stem the flow. Such foreign bodies have included stones, rags or plant material, acting as a nidus for calculi formation.
Urine dermatitis (Fig. 89.3) The leakage of urine, often concentrated, affects the skin. The ammonias and phosphates can encrust on the skin, causing excoriations, secondary infections, and areas of tender hyperkeratosis. Much thought has gone into how to treat this condition – coined ‘urine dermatitis’ – but the most expedient way is to ensure that the urine is not in contact with the skin, either by applying barrier ointments such as Vaseline or (better) by closing the fistula, rendering the patient continent.
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After fistula occurrence, up to 44–63% of women may suffer from amenorrhoea.17,27 This has a multifactorial causality, most of which have not been clearly delineated. Surely some are due to stresses of the delivery and the resulting social isolation. Some patients do have their menses return following repair.27 A low BMI is often found to be the cause. In addition, it is thought that some women will have focal anterior pituitary necrosis from shock during the long labor.28 A small unpublished series by Dosu Ojengbede from Nigeria investigating the use of hysteroscopy showed that intrauterine scarring is common (Asherman’s syndrome) (Wall LL, personal communication). Others will have cryptomenorrhea from an obstructed outflow tract which, with time, can cause a large hematometra. If the patient does receive treatment, remarries or returns to her husband, the subsequent fertility rates are quite despondent. A number of studies have shown that as few as 19% achieve pregnancy27,29,30 with perhaps a higher rate of prematurity and infant mortality.31 Subsequent deliveries are hazardous. One small series following the pregnancies in women delivering post fistula repair showed an alarming 27% fistula recurrence rate with a supervised vaginal delivery.29 It is commonly recommended that any further deliveries should be performed by cesarean section.
The majority of obstetric fistula patients can be confidently diagnosed by history and examination alone – a history of a long labor (more than 1 day) with a stillborn child and complete incontinence of urine is the rule. Most obstetric fistulae can be diagnosed on simple vaginal examination – noting the site, size, and amount of scarring. Some very small vesicovaginal fistulae can give symptoms of stress urinary incontinence and in these circumstances a dye test must be performed. The classical teaching for this is to place three clean swabs into the vagina and insert 50–100 ml of gentian violet diluted with distilled water or saline via a catheter into the bladder. The swabs are left in the vagina for some minutes and then removed. A fistula is confirmed by the presence of dye on the gauze, and – depending on which of the three gauzes is stained – reveals the approximate site of the fistula. However, it is common in many centers to visualize the fistula directly by examining the patient with the aid of a Sims speculum, retracting on the posterior vaginal wall to expose the anterior wall, instilling the dye and seeing where the dye leaks into the vagina. In some very small fistulae and some vesicouterine or vesicocervical fistulae the dye may take some minutes to find its way into the vagina. In these circumstances, it is best to insert a gauze into the vagina, instill 50–100 ml of dye into the bladder, remove the catheter and ask the patient to walk about for 15–30 minutes. It is surprising how many gauzes are stained with dye at the end of this time when the initial examination showed a negative test. The posterior vaginal wall is examined digitally, again noting the site, size, and any scarring associated with a rectovaginal fistula. The status of the anal sphincter is noted as is the distance of the fistula margin to the sphincter. A small number of patients will complain of flatal incontinence with or without incontinence of diarrhea through the vagina, hinting that a small fistula, unrecognizable to the physician’s palpation, is present. A dye test can also be performed by the instillation of dilute colored fluid into the rectum via a Foley catheter. Routine urine tests, renal function tests or intravenous urography are not warranted as the results do not often influence management. Furthermore, not only are these tests very expensive, they are also unavailable in most units where fistula surgery is performed.
InvEStIgatIonS
claSSIfIcatIon
The investigations of the fistula are kept simple, merely because most patients with obstetric fistulae present in areas where resources are limited.
There are no standardized classifications for obstetric fistula. However, at a recent meeting of fistula surgeons hosted by the WHO, it was agreed that a classification
Figure 89.3. Urine dermatitis. Note the reddened transitional epithelia of the bladder fundus inverting through the introitus.
Reproductive outcomes
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system should include the main factors of site, size, and scarring. A three-tiered classification system with this in mind has been proposed by Goh and colleagues.32 It is still awaiting validation, but holds promise for a reliable and useful tool for the future (Table 89.1).
tImIng of rEpaIr It has been commonly taught that a surgeon should wait for roughly 3 months after the insult before attempting repair.33 The rationale behind this is to allow the necrotic tissue to slough away and the often suboptimal tissue that remains to recover before attempting to operate. There has been one compelling paper advocating earlier repair – to repair as soon as the dead tissue has come away, with active debridement while waiting. This affords a good success rate and enables the woman to regain health more quickly, before she is made an outcast.16 However, the tissues are much more difficult to handle at this stage, with the tissues tearing and sutures cutting out. This series was done by an extremely experienced fistula surgeon and the results
are yet to be replicated in other units and with more inexperienced surgeons. It would be prudent for the inexperience fistula surgeon to rely on the traditional teaching of waiting.
ImmEdIatE managEmEnt If a patient presents within the first few weeks of injury, while the tissues are still raw, a large gauge catheter should be inserted and kept on free drainage for up to 4 weeks. With this management, up to 20–40% of vesicovaginal fistulae will heal.16 Greater success is usually seen with smaller fistulae.
routE of rEpaIr The route of repair – vaginal or abdominal – traditionally depends on the experience and training of the surgeon. Those with gynecologic training often favor the vaginal route while those with urologic training tend to favor the abdominal route. The abdominal route might be found easier with high vault, juxtacervical or vesico-
table 89.1.
Proposed classification system for female genital fistula
Type
Classification
Genitourinary fistula 1
Distal edge of fistula >3.5 cm from the external urinary meatus
2
Distal edge of fistula 2.5–3.5 cm from the external urinary meatus
3
Distal edge of fistula 1.5–<2.5 cm from the external urinary meatus
4
Distal edge of fistula <1.5 cm from the external urinary meatus
a
Size <1.5 cm in the largest diameter
b
Size 1.5–3 cm in the largest diameter
c
Size >3 cm in the largest diameter
(i)
None or only mild fibrosis (around fistula and/or vagina) and/or vaginal length >6 cm, normal capacity
(ii)
Moderate or severe fibrosis (around fistula and/or vagina) and/or reduced vaginal length and/or normal capacity
(iii)
Special considerations, e.g. postradiation, ureteric involvement, circumferential fistula, previous repair
Genitoanorectal fistula 1
Distal edge of fistula >3 cm from hymen
2
Distal edge of fistula 2.5–3 cm from hymen
3
Distal edge of fistula 1.5–<2.5 cm from hymen
4
Distal edge of fistula <1.5 cm from hymen
a
Size <1.5 cm in the largest diameter
b
Size 1.5–3 cm in the largest diameter
c
Size >3 cm in the largest diameter
(i)
None or only mild fibrosis around the fistula and/or vagina
(ii)
Moderate or severe fibrosis
(iii)
Special considerations, e.g. postradiation, inflammatory disease, malignancy, previous repair
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vaginal/vesicouterine fistulae. Even these cases can be confidently managed vaginally with experience. This has obvious benefits postoperatively.
SurgIcal trEatmEnt Many surgical techniques have been described, including the open transvesical and transperitoneal or combined techniques, fibrin glue, laparoscopic techniques, partial colpocleisis, and cauterization. The most popular ‘flap splitting’ technique will be described here. At a recent meeting of fistula surgery experts hosted by the WHO it was agreed that the flap splitting technique should follow the principles of: 1. exposure of the fistula and protection of the ureters; 2. wide mobilization of the bladder off the vagina/ cervix/uterus and surrounding tissues; 3. tension-free closure of the bladder (single or double layer to the bladder); 4. dye test to confirm watertight closure of the bladder.
Exposure of the fistula and protection of the ureters The patient is placed in the exaggerated lithotomy position with the patient’s buttocks over the end of the operating table. The table is placed in steep Trendelenburg which will bring the anterior vaginal wall perpendicular to the surgeon’s gaze. In up to 28% of patients there is significant vaginal scarring that renders it impossible to insert a speculum. Lateral relaxing incisions are necessary to release the scar, expose the fistula and enable the speculum to be inserted for adequate exposure. In all trigonal and supratrigonal fistulae except the very small, the ureters should be identified and catheterized (Fig. 89.4). This can be done through the fistula and the catheter ends advanced through the urethra. This is to prevent inadvertent injury during dissection and inadvertent suturing of the ureter during repair.
Figure 89.4. fistula.
Ureters catheterized through the vesicovaginal
suture line, it runs the risk of disruption. The initial sutures secure the angles of the fistula. The bladder is closed with interrupted sutures (2-0 Vicryl) approximately 4 mm apart. Some surgeons place a second layer of sutures to the bladder. Wider mobilization may be necessary to achieve this but usually a one-layer closure of healthy bladder tissue should suffice.
Dye test to confirm watertight closure of the bladder Between 50 and 100 ml of dilute colored fluid (gentian violet; some surgeons use milk if no dye is available) is instilled into the bladder to ensure that a watertight closure has been achieved (Fig. 89.5).
Wide mobilization of the bladder off the vagina/ cervix/uterus and surrounding tissues The secret of successful vesicovaginal fistula surgery is wide mobilization of the bladder, releasing it from scarred attachments to the surrounding structures and excision of scar tissue from the bladder and surrounds so that good viable tissue is approximated in the repair.
Tension-free closure of the bladder Once successfully mobilized, the bladder is sutured together under no tension. If tension remains on the
Figure 89.5. fistula.
Dye test ensuring a watertight closure of the 1245
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Interpositional graft A contentious issue in fistula surgery is whether to use an interpositional graft. It has been traditionally taught that this aids healing by bringing a fresh blood supply to these compromised tissues. It may also plug any undetected microleaks. One small study did show an increased success rate using this graft.34 More experienced fistula surgeons now use grafts less often with no difference in rates of success; however, this is after accumulating experience with some thousands of vesicovaginal fistula repairs. Until further studies show otherwise, it is best to err on the side of caution and use a graft. The most common graft used is the Martius fibrofatty graft harvested from the labia majora. Other grafts of gracilis muscle, peritoneum, omentum, and broad ligament have been described. To form a Martius graft, an incision is made longitudinally along the bulge of the labia majora. The fat underneath is exposed and a flap of fat developed from anterior to posterior with the pedicle still being attached posteriorly. A tunnel is created into the vagina superficial to the inferior pubic ramus, beneath the bulbocavernosus and vaginal skin. The fat is introduced into the vagina and placed over the fistula repair with anchoring sutures. The vaginal and labial skins are repaired, taking precautions to prevent hematoma formation.
Figure 89.6.
Absent urethra. Incisions for creation of the new urethra
Bladder epithelia and entry into bladder Gauze
Specific surgical problems Sims speculum
Absent urethra About 5% of obstetric fistulae have the entire urethra sloughed, which poses one of the most difficult problems for the fistula surgeon17,35 (Fig. 89.6). An anatomic closure may be quite possible, but a functioning closure is very difficult. Two methods are commonly used: 1. A new urethra may be created from the remaining paraurethral tissues. Initial incisions are made about 2.5–3 cm apart on either side of where the new urethra will lie (Fig. 89.7). Flaps are then created and sewn over a Foley catheter and this delicate structure is anastomosed to the bladder. A graft is placed to help support and nourish this frail construction. Although a gracilis graft has been described, the Martius graft is more commonly used.36 The vaginal epithelia are drawn over the repair. 2. A new urethra may be created from an anterior flap of bladder tissue. A longitudinal flap is created after dissecting the bladder off the symphysis pubis and
Figure 89.7. urethra.
Initial incisions for the creation of a new
this is then advanced towards the urethral meatus. The flap is sewn into a tube over a Foley catheter, a graft placed and the vagina repaired.37 However, this is often not possible with obstetric fistulae as these types of fistula often result in much loss of bladder tissue; this procedure will thus decrease the size of an already small bladder. When a new urethra is created from the remaining paraurethral tissues, urethral strictures may form in the long term, resulting in urinary retention and voiding disorders. There is also a high rate of residual incontinence after repair – presumably stress urinary inconti-
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nence. To help reduce this, a sling of levator muscle can be used to support the repair, taking a flap of levator from the right and left (or scar tissue if there is no other tissue remaining) and sewing this in the midline.20
Circumferential fistula A circumferential fistula occurs against the posterior pubic symphysis. In these cases, the bladder is completely detached from the remaining urethra (Figs 89.8, 89.9). The bladder needs to be mobilized not only off the vagina and surrounding structures, but also off the pubic symphysis, dissecting high into the cave of Retzius.
The bladder is then advanced en masse to the urethra and anastomosed to it. Again there is a high rate of residual urinary incontinence, presumably stress urinary incontinence. This can be improved by the use of a levator muscle sling employed at the time of repair.20
Rectovaginal fistula The technique for repair is similar to that of the vesicovaginal fistula: flap splitting with wide mobilization, excision of scar tissue, repair of the fistula under no tension, and repair of vaginal epithelia. Grafts are rarely used for rectovaginal fistulae, but the Martius graft may be employed if a long enough pedicle is developed for it to reach the operative site. Rectovaginal fistulae can be comfortably repaired per vaginum but some surgeons may prefer to use the abdominal route for the high fistula adhered to the sacral promontory.
No vaginal tissue remaining
Figure 89.8. Small circumferential fistula. The urethra has been detached from the bladder neck.
Approximately 28% of cases will need some form of vaginoplasty due to vaginal skin loss; after repair, dyspareunia and apareunia can result.29 Vaginoplasty may be anything from a simple Fenton type procedure to release vaginal scarring to reconstruction of a new vagina from tissue flaps, anteriorly from the labia minora and majora and posteriorly with rotational flaps of gluteal skin. This does result in a scarred vagina. Other options are a neurovascular flap of tissue from the groin crease or a sigmoid neovagina.
poStopEratIvE carE Circumferential fistula
Figure 89.9.
Circumferential fistula in cross-section.
The ureteric catheters can be removed upon completion of the operation if the ureteric orifices were far from the fistula margin. If they were close to or on the margin, they remain for 5–7 days to ensure that the ureters do not obstruct with postsurgical swelling. Occasionally, the ureters will need reimplanting; if so, the catheters remain in place for 10–14 days. The Foley catheter remains on free drainage for 14 days postoperatively. This takes meticulous nursing as a full bladder will put pressure on the repair site and may even disrupt it. A vaginal pack is usually placed at the end of the operation. This reduces the operative dead space and is removed 24–72 hours later. The patient should mobilize as soon as she is able; however, it is important that the indwelling catheter be secured with either strong tape or a suture so that the balloon of the catheter does not pull on the fistula repair site while the patient is mobile. 1247
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A high fluid intake is encouraged to keep the bladder irrigated and a normal diet is encouraged. The stools should be kept loose in cases of rectovaginal fistula.
rESultS The fistula can be closed in up to 94% of cases with their first operation.3 If a fistula is not closed successfully, repeat operations prove difficult. With the second operation, the success rate drops to 79% and, with the third, to 53% (Browning A, unpublished work). Successful closure, however, does not necessarily equate to a functional cure. Rates of postoperative incontinence, largely stress urinary incontinence, vary between 5.6 and 33%.20,38 This rate reflects short-term follow-up, within the first few days of catheter removal. With time and with bladder retraining and strengthening of the pelvic floor muscles, this may improve. In northern Nigeria patients have been followed up over a period of 6 months and 15% of closed fistula patients still have some incontinence at time of final follow-up (Waaldjik K, personal communication). At the Addis Ababa Fistula Hospital patients are asked to return in 6 months if they are still experiencing leakage; 8% of patients do so (Browning A, unpublished work). Rectovaginal fistula repair appears to have a lower initial success rate of 73%.17 However, with subsequent operations it is almost always possible to get a successful closure although the patient may have some remaining anal flatal and/or stool incontinence from a poorly functioning sphincter.21
poStopEratIvE complIcatIonS The most concerning complication of fistula surgery is residual incontinence. This is thought mainly to be stress urinary incontinence in type, but detrusor instability must also play a role. One study of 22 women with severe incontinence following fistula closure underwent urodynamic assessment and 41% had genuine stress incontinence (GSI), 14% had GSI and poor compliance, 41% had GSI and detrusor overactivity, and 4% had voiding disorder and overflow incontinence.39 There have been several corrective methods proposed, but the most successful to date is a sling described by Carey and colleagues in which urodynamically selected patients have a tension-free sling of rectus sheath inserted beneath the midurethra. This is performed with open dissection into the cave of Retzius and the sling inserted under direct vision. The open step is necessary due to the often dense retropubic scarring and high risk of
bladder perforation if carried out as closed procedure with use of a trocar to pass the sling retropubically. A flap of omentum is inserted between the freed urethra and symphysis pubis to try to prevent further scarring. This procedure has a 66% cure rate at 14 months.39
faIlEd rEpaIrS One study examined 71 failed repairs. All 71 cases had a fistula described as complicated, meaning that one or more of the following was present: excessive scarring, total destruction of the urethra, ureteric orifices outside the bladder or at the edge of the fistula, a small bladder, both recto- and vesicovaginal fistulae in conjunction, or the presence of bladder stones. There was a statistically significant association for a failed repair as compared to a cured patient if the patient had a ruptured uterus at the time of labor, if they had a previous failed repair, if they presented with limb contractures, presented malnourished or in poor health, if the fistula was described as complicated, and if a blood transfusion was required.38
the irreparable fistula The term ‘irreparable fistula’ may be misleading, but some injuries are so severe that no bladder remains to be repaired. The only option for these women to have any quality of life is either to have a bladder augmentation or a urinary diversion operation. Bladder augmentations are not without their problems. In patients with such severe injuries the urethra is often affected, so even with a good reservoir, they are still unable to hold their urine. If the urethra is intact, then self-catheterization may be needed to effect full drainage of the bladder. This may be unmanageable for a woman living in the developing world, far from a supply of catheters and clean equipment. The diversional operations commonly used are direct ureterosigmoidostomy, Mainz II pouch or ileal conduit. The former two options require an intact anal sphincter and the woman to agree to pass urine through the anus. The Mainz II shows promise for women in developing nations as there are perhaps fewer long-term complications following this procedure.40–42 The ileal conduit restricts a patient to living near a service that can supply the conduit bags, which are often rare in the developing world. The patient also needs to be close to a health center that knows how to deal with any complications. The ureters and kidneys in these women are often dilated and compromised, and ascending infections can be common.
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thE futurE Obstetric fistula, like many morbidities suffered by women during labor, is preventable. This should be an attainable dream in the 21st century and this suffering placed in medical texts of yesteryear. The task, however, is immense, with up to 75,000 new obstetric units being required for Africa alone to supply adequate maternity care.43 In tandem with this, roads need to be built, transport systems put in place and, most importantly, men and women educated. Until all this is achieved, the obstetric fistula patient will still need our caring attention.
rEfErEncES 1. Zacharin RF. Obstetric Fistula. New York: Springer-Verlag, 1988. 2. Danso KA, Martley JO, Wall LL. The epidemiology of genitourinary fistulae in Kumasi, Ghana 1977–1992. Int Urogynecol J 1996;7:117–20. 3. Kelly J, Kwast BE. Epidemiological study of vesico-vaginal fistulas in Ethiopia. Int Urol J 1993;4:278–81. 4. Wall LL, Karshima JA, Kirschner C et al. The obstetric vesicovaginal fistula: characteristics of 899 patients from Jos, Nigeria. Am J Obstet Gynecol 2004;190:1011–19. 5. Bhasker Rao K. Genital fistula. J Obstet Gynaecol India 1975;25:58–65.
Northern Nigeria. Br J Obstet Gynaecol 1985;92(Suppl 5):1–119. 16. Waaldjik K. The immediate management of fresh obstetric fistulas with catheter and/or early closure. Int J Gynecol Obstet 1994;45:11–16. 17. Arrowsmith S, Hamlin EC, Wall LL. Obstructed labour injury complex: obstetric fistula formation and the multifaceted morbidity of maternal birth trauma in the developing world. Obstet Gynecol Surv 1996;51:568–74. 18. Mafouz N. Urinary fistula in women. J Obstet Gynaecol Br Emp 1957;64:23–34. 19. Hassim AM, Lucas C. Reduction in the incidence of stress urinary incontinence complicating a fistula repair. Br J Surg 1974;51:461–5. 20. Browning A. Prevention of residual urinary stress incontinence following successful repair of obstetric vesicovaginal fistula using a fibro-muscular sling. Br J Obstet Gynaecol 2004;111:357–61. 21. Murray C, Goh JT, Fynes M et al. Urinary and faecal incontinence following delayed primary repair of obstetric genital fistula. Br J Obstet Gynaecol 2002;109:828–32. 22. Cockshott WP. Pubic changes associated with obstetric vesico-vaginal fistulae. Clin Radiol 1973;24:241–7. 23. Waaldjik K, Elkins TE. The obstetric fistula and peroneal nerve injury: an analysis of 974 consecutive patients. Int Urogynecol J 1994;5:12–14.
6. Bal JS. The vesico-vaginal and allied fistulae – a report on 40 cases. Med J Zambia 1975;9:69–71.
24. Reif ME. Bilateral common peroneal nerve palsy secondary to prolonged squatting in natural childbirth. Birth 1988;15:100–2.
7. Docquier J, Sako A. Fistules recto-vaginales d’origine obstetricale. Med d’Afrique Noire 1983;30:213–15.
25. Sinclair RSC. Maternal obstetric palsy. South Afr Med J 1952;26:708–14.
8. Ampofo K, Out T, Uchebo G. Epidemiology of vesicovaginal fistulae in northern Nigeria. West Afr J Med 1990;9:98–102.
26. Langundoye SB, Bell D, Gill G et al. Urinary changes in obstetric vesico-vaginal fistulae: a report of 216 cases studied by intravenous urography. Clin Radiol 1976;27:531–9.
9. Tahzib F. Epidemiological determinants of vesicovaginal fistulas. Br J Obstet Gynaecol 1983;90:387–91.
27. Aimaku VE. Reproductive functions after the repair of obstetric vesicovaginal fistulae. Fertil Steril 1974;25:586– 91.
10. Murphy M. Social consequences of vesico-vaginal fistula in Northern Nigeria. J Biosoc Sci 1981;13:139–50. 11. Ibrahim T, Sadiq AU, Daniel SO. Characteristics of VVF patients as seen in the specialist hospital, Sokoto, Nigeria. West Afr Med J 2000;19:59–63. 12. Moerman ML. Growth of the birth canal in adolescent girls. Am J Obstet Gynecol 1982;143:528–32. 13. Wall LL. Dead mothers and injured wives: the social context of maternal morbidity and mortality among the Hausa of Northern Nigeria. Stud Family Planning 1998;29:341–59. 14. Ampofo EK, Omotara BA, Out T et al. Rick factors of vesico-vaginal fistulae in Maiduguri, Nigeria: a casecontrol study. Tropical Doctor 1990;20:138–9. 15. Harrison KA. Childbearing, health and social priorities: a survey of 22,774 consecutive hospital births in Zaria,
28. Bieler RW, Schnabel T. Pituitary and ovarian function in women with vesicovaginal fistula after obstructed and prolonged labour. South Afr Med J 1976;50:257–66. 29. Evoh NJ, Akinia O. Reproductive performance after the repair of obstetric vesico-vaginal fistulae. Ann Clin Res 1978;10:303–6. 30. Bhasker Rao K. Vesicovaginal fistula – a study of 269 cases. J Obstet Gynaecol India 1972;22:536–41. 31. Naidu PM, Krishna S. Vesico-vaginal fistulae and certain problems arising subsequent to repair. J Obstet Gynaecol Br Emp 1963;70:473–5. 32. Goh JTW. New classification for female genital tract fistula. Aust N Z J Obstet Gynaecol 2004;44:502–4. 33. Moir JC. The Vesico-vaginal Fistula. London: Baillière Tindall, 1967.
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34. Rangnekar NP, Imdad AN, Kaul SA. Role of the Martius procedure in the management of urinary–vaginal fistulas. J Am Coll Surg 2000;191:259–63.
tinence after delayed primary closure of genitourinary fistula: a technique for surgical management. Am J Obstet Gynecol 2002;186:948–53.
35. Ward A. Genito-urinary fistulae: a report on 1787 cases. Second International Congress on Obstetrics and Gynaecology, Lagos, Nigeria.
40. Koo HP, Avolio L, Dickett JW Jr. Long-term results of ureterosigmoidostomy in children with exstrophy. J Urol 1996;156:2037–40.
36. Hamlin RHJ, Nicholson EC. Reconstruction of urethra totally destroyed in labour. Br Med J 1969;1:147–50. 37. Elkins TE, Ghosh TS, Tagoe GA. Transvaginal mobilization and utilization of the anterior bladder wall to repair the vesicovaginal fistulas involving the urethra. Obstet Gynaecol 1992;79:455–60. 38. Kelly J, Kwast BE. Obstetric fistulas: evaluation of failed repairs. Int Urogynecol J 1993;4:271–3. 39. Carey MP, Goh JT, Fynes MM et al. Stress urinary incon-
41. Venn SN, Mundy AR. Continent urinary diversion using the Mainz-type ureterosigmoidostomy – a valuable salvage procedure. Eur Urol 1999;36:247–51. 42. D’elia G, Paherhink S, Fisch M et al. Mainz pouch II technique: 10 years’ experience. BJU Int 2004;93:1037–42. 43. Waaldik K. Evaluation report XIV on VVF projects in Northern Nigeria and Niger. Katsin, Nigeria: Babbar Ruga Fistula Hospital; 1998.
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Urethral DiverticUlUm introDUction Female urethral diverticulum (UD) has been a historically underdiagnosed condition. Novak1 stated, ‘This is a relatively rare condition and no gynecologist will see more than a few in a lifetime’. However, with higher clinical suspicion and improved diagnostic techniques, the frequency of diagnosis has increased.
history The existence of UD has been known since at least the early 19th century, when Hey reported the first case in 1805.2 In 1938, Hunner3 reported three cases associated with calculi and commented on the rarity of the condition. In 1956, Davis and Cian4 reported 50 cases, more than had been reported previously in the entire history of the Johns Hopkins Hospital. They also developed a double-balloon catheter to be used in conjunction with positive-pressure profilometry to facilitate diagnosis of UD.
incidence and patient profile The incidence of female UD is reported in the urologic literature as 0.6–6%5,6 and in the gynecologic literature as 5%.7 However, these numbers are probably an underestimate and, with increasing clinical suspicion, the true incidence may prove to be higher.8 Patients typically present in the third to sixth decades of life, with a mean age of 45 years.9 Rarely, UD has been diagnosed in neonates and children.10,11 A racial predilection has been suggested, with diagnosis in African– American women being two to six times that in white women;12 however, Ganabathi et al.9 found no racial differences. A concomitant UD13 has been found in 1.4% of women diagnosed with stress urinary incontinence (SUI).
etiology and pathophysiology There are two main schools of thought regarding the etiology of UD: acquired and congenital. The most widely accepted theory is UD formation due to infection of the periurethral gland. The periurethral glands are tuboalveolar structures located posterolaterally beneath the periurethral fascia. They are found in the proximal two-thirds of the urethra and drain into the distal third.14 Infection leads to obstruction of the glands, local abscess formation, and eventual rupture into the urethral lumen, as first described by Routh15 in 1890.
Trauma secondary to childbirth or forceps delivery16 remains a problem in developing countries, possibly contributing to UD formation.17 However, with current obstetric technology, traumatic delivery is no longer a prevalent factor in developed nations. In fact, 15–20% of patients diagnosed with UD are nulliparous, thereby completely refuting this etiologic theory.11 A congenital etiology is doubtful, although there has been some evidence supporting this theory.10 Faulty union of primordial folds, genesis from cell rests or Gartner’s duct remnants, and müllerian remnants causing vaginal cysts have all been suggested as possible etiologies.17 The discovery of mesonephric adenoma and adenocarcinoma has implicated Gartner’s duct remnants. Paneth cell metaplasia lining a UD also supports a congenital basis.18 Blind-ending ureters resulting from an aborted ureteral duplication may rarely lead to an anterior UD.19 Other suggested etiologies of UD include high-pressure voiding against outlet obstruction, urethral calculi, instrumentation, and complications of previous anterior vaginal surgery.17 Recently, a UD has been described following transurethral collagen injection therapy for stress urinary incontinence.20 The authors hypothesize that the collagen injections caused obstruction of the periurethral glands, resulting in the gradual accumulation of glandular secretions and subsequent development of a non-communicating diverticulum.
associated complications Complications associated with UD include incontinence, infection, stones, and malignancy. Urinary incontinence is common in patients with UD. In fact, Ganabathi et al.9 reported a 65% incidence of SUI among patients with UD (57% with SUI as the presenting complaint). These patients may also suffer from urge incontinence or ‘paradoxical incontinence’, in which urine stored in the UD is lost during stress.5 About 25–33% of patients present with recurrent urinary tract infections, including some who suffer from systemic infections. The most common infecting organisms of UD are Escherichia coli, Chlamydia and gonococcus; however, multiple organisms have been cultured.17,21 Up to 13% of patients present with calculi in the UD, and this can be confirmed by plain radiograph.22,23 Stones form secondary to stasis, infection and chronic inflammation in the UD.6 Stones can be multiple and, in some cases, quite large. A 5 × 6 cm stone was discovered in the urethral diverticulum of an elderly woman during workup for a firm vaginal mass. Urethrovaginal fistula secondary to rupture of a UD is another potential complication.24,25
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Approximately 200 cases of neoplasm within a UD have been reported in the world literature.26–29,37–43 There have also been reports of 16 cases of nephrogenic adenoma, a benign metaplastic condition.30–35 Malignancy must be considered whenever a UD is diagnosed, particularly when accompanied by hematuria, induration or firmness of a UD on physical examination, non-calcified filling defects within the UD on radiography, or a visible lesion on cystoscopic examination. Despite the fact that squamous epithelium lines most of the urethra, adenocarcinoma is by far the most common histopathologic condition demonstrated within UD.31 This lends further support to the theory that urethral diverticula develop from glandular origins. More than 80% of the diverticular cancers seen are either adenocarcinoma (61%) or transitional cell carcinoma (27%).36 Squamous cell carcinoma is rare, comprising only 12% of UD malignancies.36 When identified within a urethral diverticulum, squamous cell carcinoma appears to be very aggressive, with a mortality rate of 78% at 3 years.37 Treatment of diverticular carcinoma includes wide local excision for localized disease.28 Adjuvant radiation therapy or chemotherapy may also be indicated for extensive malignancy or for non-surgical candidates.38,39 Survival is a function of stage39 and grade38 of the disease. Squamous cell carcinomas are typically diagnosed at an advanced stage, with all reported cases presenting at stage T2 or higher, and require a more aggressive treatment approach.38,40–43 Because of the relative rarity of carcinoma in urethral diverticula, it has been difficult to develop a common definitive treatment strategy (Table 90.1). Among the 79 patients reviewed with variable lengths of follow-up between 6 months and 10 years, anterior pelvic exenteration appeared to offer the highest likelihood of prolonged disease-free interval (73%) and the lowest rate of local recurrence (4%).37 Rates of death and metastasis were similar between the treatment modalities.37
PreSentation clinical symptoms Patients found to have UD present with a variety of symptoms ranging from irritative voiding complaints to pelvic pain and dyspareunia (Table 90.2).5 The classic triad of UD is known as the ‘3 Ds’ – dysuria, dyspareunia, and dribbling. However, many patients are asymptomatic. Urinary urgency, frequency, and hematuria may also be associated with UD.44 The diagnosis is often not straightforward and UD may mimic other pelvic floor disorders, resulting in diagnostic delay.45 In a review of 46 consecutive cases of UD, the mean interval between onset of symptoms to diagnosis was 5.2 years.45 Frequently, patients are given an initial, erroneous diagnosis for which a variety of treatments are attempted (Table 90.3). A high index of suspicion is required in order to diagnose UD because many patients may not be overtly symptomatic upon initial evaluation. In cases
table 90.2.
Presenting symptoms in 627 women with urethral diverticula from published reports
Symptom
n (%)
Frequency
351 (56)
Dysuria
345 (55)
Recurrent infection
251 (40)
Tender mass
219 (35)
Stress incontinence
201 (32)
Post-void dribbling
160 (26)
Urge incontinence
157 (25)
Hematuria
107 (17)
Dyspareunia
376 (16)
Pus per urethram
75 (12)
Retention
25 (4)
Asymptomatic
38 (6)
Data from ref. 5.
table 90.1.
Frequency and outcome for treatment modalities used for carcinoma in a urethral diverticulum
Treatment
Patients (n)
Diverticulectomy
27
Radiation
Disease-free (%)
Local recurrence (%)
Death/metastasis (%)
Follow-up
9 (33)
13 (48)
5 (19)
9 months–7 years
10
2 (20)
5 (50)
2 (20)
2–5 years
Diverticulectomy + radiation
16
8 (50)
5 (31)
3 (19)
1–10 years
Anterior exenteration
26
19 (73)
1 (4)
6 (23)
6 months–3 years
Data from ref. 37.
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table 90.3.
Most common initial diagnoses and subsequent treatments given to patients before identification of a urethral diverticulum
Diagnosis
Treatment
Chronic cystitis trigonitis
Long- or short-term antibiotics
Stress urinary incontinence
Anti-incontinence surgery
Urge incontinence
Anticholinergics
Interstitial cystitis
Hydrodistension
Idiopathic pelvic pain syndrome
DMSO instillation Tricyclic antidepressants
Urethral syndrome
Urethral dilation
Vulvovestibulitis
Vaginal creams (antifungal/antibiotic)
Cystocele
Surgery
Sensory urgency
Anticholinergics
Psychosomatic disorder
Psychotherapy
Data from ref. 44.
of persistent irritative voiding symptoms, pelvic pain, and urinary incontinence unresponsive to therapy, UD should be kept in mind and excluded.45
Physical examination Patients with UD most commonly have anterior vaginal wall tenderness, with or without a concomitant palpable suburethral mass.45 Pressure on the mass may demonstrate expressible purulence or blood from the UD (Fig. 90.1), and firmness of the area may indicate a diverticular stone or neoplasm. Rarely, some patients are without any pertinent physical findings and workup is based only on clinical suspicion established by the patient’s history. Importantly, the clinician must also examine patients for urethral hypermobility with or without SUI, which can be addressed at the time of repair of the UD if deemed necessary.
Figure 90.1. Urethral diverticulum presenting as an anterior vaginal mass. (Reproduced from ref. 9 with permission.)
classification system Leach and co-workers51 created a system for classification of female UD known as the L/N/S/C3 system. This acronym represents Location, Number, Size, Configuration, Communication, and Continence. This system facilitates preoperative assessment of UD and standardizes the classification, thereby simplifying comparison between series. Table 90.6 illustrates the classification of 63 patients.
Differential diagnosis
DiaGnoSiS
The differential diagnosis of urethral and meatal/ perimeatal masses (Figs 90.2, 90.3) is illustrated in Tables 90.4 and 90.5 respectively. Note that Table 90.5 includes conditions that occur in locations distal to the majority of UD; however, they should be considered in the differential diagnosis.46
endoscopic examination A blunt-tip female urethroscope with a 0 or 30-degree lens is used. The anterior vaginal wall is compressed with a finger in the vagina, and the urethral lumen is inspected for any expression of pus from the floor or
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Cervix
Vagina
Gartner's duct Urethral diverticulum
Vaginal wall inclusion cyst
a
b
Gartner's duct cyst c
Figure 90.2. Differential diagnosis of urethral and anterior vaginal wall masses: (a) urethral diverticulum; (b) vaginal wall inclusion cyst; (c) Gartner’s duct cyst.
Caruncle
a
Ureter
b
Mucosal prolapse
c
Skene's gland cyst
Ureterocele d Ectopic ureteral orifice
roof of the urethra (Fig. 90.4). In 50% of patients there will be multiple diverticula and more than half of the UD will communicate with the middle third of the urethra.7 Cystoscopy is the only diagnostic tool that allows direct inspection of the urethra and bladder. In some cases, neoplasm or bladder stones may also be diagnosed; however, its value as a diagnostic tool has recently been questioned.52 Often the diverticular neck is hidden between collapsed urethral folds, and non-communicating diverticula will not have a visible orifice.53,54 Cystoscopy does not reveal any information regarding size, shape, or appearance of the diverticular wall.54 In addition, cys-
Figure 90.3. Differential diagnosis of meatal and perimeatal lesions: (a) caruncle; (b) mucosal prolapse; (c) Skene’s gland (or duct) cyst; (d) ureterocele.
toscopy is invasive and carries the risk of urinary tract infection. A negative finding on cystoscopy does not rule out the presence of a UD. Further evaluation including urodynamics or imaging studies should be performed as cystoscopy will frequently fail to diagnose UD.
Urodynamic evaluation Urodynamic studies are not always required in the evaluation of all patients with UD. The indications include patients with symptoms of SUI or bladder dysfunction.55–57 These symptoms may include urinary leakage with 1255
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table 90.4.
Differential diagnosis of urethral and anterior vaginal wall lesions Location
Symptoms/ physical exam
Cystoscopy/radiography
Comments
Urethral diverticulum Anterior vaginal wall, midline
UTI, dysuria, dyspareunia, post-void dribbling, cystic mass
Orifice of diverticulum visible on urethral floor, VCUG opacifies lesion
May be multilocular
Vaginal wall cyst
Anterior vaginal wall, midline or eccentric
Cystic mass; may be loculated
None or extrinsic compression
–
Gartner’s duct cyst
Anterolateral vaginal wall
Cystic mass
None or extrinsic compression; IVP may indicate ectopic ureteral drainage
Rule out ectopic ureter prior to excision
Müllerian remnant cyst
Midline
Cystic mass
None
–
Ectopic ureterocele48
Anywhere in bladder, urethra, vagina (upper third), uterus, fallopian tubes
Cystic mass
May be seen on IVP, US or cystoscopy
–
Leiomyoma, hamartoma
Vaginal wall
Solid mass
None or extrinsic compression
Rule out malignancy
Malignant urethral or vaginal neoplasms
Urethral or vaginal wall or hematuria
Solid mass; may have pain, may be seen on cystoscopy
None or extrinsic compression; ± adjuvant therapy, erythema, obvious lesion or tumor growing from the diverticulum into the urethral lumen
Wide local excision, radiation, combination, anterior pelvic exenteration
Lesion
IVP, intravenous pyelography; US, ultrasonography; UTI, urinary tract infection; VCUG, voiding cystourethrogram. Adapted from ref. 47.
table 90.5.
Differential diagnosis of meatal and perimeatal lesions
Lesion
Location
Presentation
Comments
Caruncle
Inferior to meatus
Asymptomatic or dysuria/pain with atrophic or ischemic mucosal changes
Postmenopausal age group
Skene’s gland cyst or abscess49
Inferior and lateral to meatus
Painful, orifice of duct visible at urethral meatus
Mucosal prolapse
Circumferential mucosal prolapse with central meatus
Pain and dysuria, atrophic or ischemic mucosal changes
Young girls or postmenopausal women
Prolapsed ureterocele50
Submeatal, prolapsed through meatus
Glistening mucosa, may be fluid filled, may be ischemic, may be asymptomatic
IVP to evaluate upper tract status
IVP, intravenous pyelography. Adapted from ref. 47.
increased intra-abdominal pressure, urge incontinence, or spontaneous loss of urine, which may represent intrinsic sphincter deficiency, paradoxical incontinence (i.e. loss of urine that has ‘pooled’ in the UD), or detrusor instability. Identification of these problems is critical in proper surgical planning. If a patient has a workup indicative of SUI, appropriate correctional surgery can be considered at the time of diverticulectomy. The uro-
dynamic findings in 55 women studied by Leach and Ganabathi55 are noted in Table 90.7.
radiologic studies Voiding cystourethrogram The voiding cystourethrogram (VCUG) is performed under fluoroscopic visualization with the patient stand-
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table 90.6.
L/N/S/C3 Classification system applied to 63 patients with urethral diverticula
Location (L)
Number (N)
Size (S)
Configuration (C1)
Communication (C2)
Continence (C3)
Proximal, beneath bladder neck (9)
Single
0.2 × 0.2 cm to 6.0 × 4.5 cm
Multiloculated (22)
Proximal urethra (16)
Complete (26)
Proximal urethra (7)
Multiple
Single (41)
Midurethra (35)
SUI only (30)
Saddle-shaped (14)*
Distal urethra (12)
Urge incontinence only (3)
Midurethra (36) Distal urethra (11)
SUI and urge incontinence (4)
* These patients are also included in the ‘simple’ or ‘multiloculated’ groups. SUI, stress urinary incontinence. Adapted from ref. 51.
ing (Fig. 90.5). Assessment of the bladder neck and proximal urethra as well as bladder neck competency is imperative to document incontinence that may be treated at the time of diverticulectomy. Filling defects
Symphysis
Diverticulum Finger closes urethrovesical junction
Figure 90.4. The technique of endoscopic examination of the urethra while ‘milking’ the anterior vaginal wall and urethral roof.
table 90.7. Urodynamic findings in 55 women with urethral diverticula Urodynamic finding
n (%)
Normal
22 (40)
SUI alone
18 (32.7)
SUI + DI
8 (14.5)
DI alone
5 (9)
Sensory urgency
1 (2)
Myogenic decompensation
1 (2)
DI, detrusor instability; SUI, stress urinary incontinence. Data from ref. 55.
Figure 90.5. A voiding cystourethrogram demonstrating a multiloculated diverticulum. (Reproduced from ref. 51 with permission.) 1257
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within a UD may represent tumor or stones5 (Fig. 90.6). An air–fluid level in the UD may indicate a UD that is much larger than it appears radiographically. In 50% of patients there will be multiple UD. Correct identification is critical to ensure complete excision of all components of the UD. Although VCUG has historically been considered the study of choice for the diagnosis of UD (Fig. 90.5), recent studies have begun to question the ability of VCUG to diagnose UD. A 3-year experience comparing VCUG to positive-pressure urethrography (PPUG) in the evaluation of UD found that the positive predictive value of VCUG after PPUG was only 60%.53 VCUG will also fail to identify UD in up to 56% of cases.58,59 Once considered the gold standard for diagnostic evaluation, VCUG is now used by many mainly as a screening test. Should it fail to adequately characterize or identify UD and there is still high suspicion that
the entity exists, other imaging modalities should be applied.53
Ultrasonography Ultrasonography is used in the evaluation of the upper tracts or, occasionally, in conjunction with VCUG to confirm the number and size of diverticula, especially in those not completely filled during urethrography23,60,61 (Fig. 90.7). Vargas-Serrano et al.61 advocate transrectal ultrasonography (TRUS) as the most sensitive tool in the diagnosis of female UD. Keefe et al.60 support transperineal or transvaginal sonography, stating 100% sensitivity in their small series and stressing the non-invasive nature of the technique. Multiple approaches to ultrasonography have been employed, including transvaginal,62,63 translabial,64 suprapubic,60 perineal,60 and TRUS.61 Intraoperative endoluminal ultrasonography has been described for localization of the UD;65,66 however, this is very difficult to perform. One limitation is that the modality is dependent on the technical skills of the operator. Advantages include real-time evaluation and the ability to clarify the spatial relationships between the diverticulum and the urethra.52 Compared to other diagnostic tools including VCUG, magnetic resonance imaging, and cystoscopy, ultrasound is less expensive.52
BL B
D
C D CU
Figure 90.6. A post-void film demonstrating filling defects within a urethral diverticulum suggestive of stones or tumor. (Reproduced from ref. 57 with permission.)
Figure 90.7. Transvaginal ultrasonography demonstrating a multiloculated urethral diverticulum opening into the proximal urethra. B, Foley catheter balloon; BL, bladder; C, diverticular communication; CU, intraurethral Foley catheter; D, diverticulum. (Reproduced from ref. 9 with permission.)
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Intravenous pyelography Intravenous pyelography (IVP) can be useful to evaluate the upper tracts and rule out an ectopic ureterocele.67–69 Ectopic ureterocele may be considered when there is an abnormal protrusion into the urethra or from the meatus. It is important to obtain a low pelvic view in order to visualize the urethra completely (Fig. 90.8).
Magnetic resonance imaging Magnetic resonance imaging (MRI) has recently been found to be a useful diagnostic tool with a high sensitivity for identifying fluid-filled cavities.30,70–73 Endorectal and endovaginal coil MRI techniques differ from surface or body coil MRI because the coil is placed within the body cavity adjacent to the tissue of interest. This results in improved signal-to-noise ratio and higher resolution imaging of the urethra.74 Kim et al.75 reported 100% sensitivity of MRI in the detection of UD. The signal intensity of fluid is high on T2-weighted images and isointense on T1-weighted images (Fig. 90.9). MRI is being advocated as helpful in defining the extent of a UD and differentiating it from other urethral or vaginal masses, such as malignancy, paraurethral cysts, and Gartner’s duct cysts. Endorectal coil MRI can also be useful in the diagnosis of periurethral fibrosis and other periurethral pathology.76 When compared to VCUG, MRI has been touted to have higher sensitivity and better characterization of size, location, and complexity of the diverticulum.74 The superior imaging may also impact surgical planning by more accurately delineating the extent of the diverticulum. The high cost
Figure 90.8. Intravenous pyelogram demonstrates the urethral diverticulum and the upper tracts.
BL P A
P
a
b
Figure 90.9. T2-weighted magnetic resonance imaging illustrates a multiloculated diverticulum (arrow) posterolateral to the urethra; (a) sagittal view; (b) axial view. A, anterior; BL, bladder; P, posterior. (Reproduced from ref. 72 with permission.) 1259
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of MRI is a detraction compared to other modalities. Endovaginal coil MRI may also be uncomfortable for the patient, but probably not any more so than VCUG or PPUG. The superior anatomic delineation provided by MRI makes it the present-day gold standard for imaging of UD.
Retrograde positive-pressure urethrography Retrograde positive-pressure urethrography (PPUG) is reported by Robertson7 to have a 90% accuracy. Additional studies have reported superior sensitivity of PPUG over VCUG for diagnosis of UD.58,59 However, the authors rarely use this technique and, in urologic practice today, it is employed only as a last resort, when high-quality VCUG or MRI is not available. It is a painful procedure for patients, often necessitating anesthesia; it is also technically difficult to obtain an adequate study, requiring a special catheter known as the Davis or Tratner catheter7,77 (Fig. 90.10). This catheter has a double balloon: one balloon is placed in the bladder; the distal (wedge-shaped) balloon slides to occlude the external meatus during injection of contrast via ports located between the balloons (Fig. 90.10).
theraPy history Numerous techniques for identification and repair of UD have been described. Intradiverticular placement of
a sound,3,78 a Foley catheter,79 a Fogarty catheter,80 gauze,81 silicone, or blood products82 have been used to facilitate identification of the defect. Repair has been performed endoscopically and transvaginally by incision of the urethral floor with layered reconstruction,34 marsupialization,83,84 packing of the UD with various materials to obliterate the cavity,85,86 and transvaginal flap creation with layered closure.55,79,87,88
observation Surgical resection and reconstruction are frequently necessary in the treatment of UD. However, observation is an option in the asymptomatic or very small UD. Marshall89 reported that UD in young girls might regress spontaneously; therefore, in this rare situation, observation may be a reasonable option.
endoscopic treatment Endoscopic treatment should be utilized only for distal UD to avoid injury to the proximally located continence mechanism. Transurethral saucerization with incision of the urethral floor90,91 or of the anterior urethra overlying the UD92 with a Collins’ knife through a pediatric resectoscope can be performed with minimal risk of complication. The major risk is incontinence and can be avoided by limiting this technique to distal UD.5 This risk also applies to transvaginal marsupialization (Fig. 90.11), an outpatient procedure often referred to as the Spence procedure.7 One blade of the scissors is placed in the vagina, the other in the urethra to marsupialize the cavity.
Symphysis Bladder
excision with vaginal flap technique
External meatus Diverticulum Vagina
The authors prefer the transvaginal flap technique for all midurethral or proximal UD. This technique allows complete resection of the UD with a three-layer closure and no overlapping suture lines. Simultaneous needle bladder neck suspension (BNS) can easily be performed when deemed necessary (in cases of SUI or bladder neck/proximal urethral hypermobility).
Preoperative preparation
Figure 90.10. Placement of a Tratner/Davis double-balloon catheter for positive-pressure retrograde urethrography.
Preoperatively, the risks of diverticulectomy – including bleeding, infection, recurrence, urethrovaginal fistula formation, and incontinence – are explained to the patient in detail. Patients may benefit from a short course of oral antibiotics, and all receive perioperative intravenous antibiotics.
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Diverticulum
a
b
c Urethra
Running stitch Urethra
Vagina
d
e
Figure 90.11. The Spence technique for marsupialization of distal urethral diverticula (UD): (a) lateral and (b) surgical views of UD; (c) one blade of the scissors is inserted into the UD and the other into the vagina and a full thickness cut of the diverticular septum is performed; (d) a running absorbable suture promotes hemostasis; (e) and (f) the new urethral meatus is created.
f
Cardozo Fig.90.11
Surgical technique The patient is placed in the lithotomy position, and a suprapubic tube (SPT) is placed. A 14 Fr urethral Foley catheter is passed and a weighted vaginal speculum and a Scott ring retractor facilitate exposure. The anterior vaginal wall (Fig. 90.12) is infiltrated with saline to facilitate dissection in the proper plane. A U-shaped incision is made with the apex located distal to the UD (Fig. 90.13). If concomitant BNS is performed, the vaginal dissection is extended laterally beneath the vaginal wall to the pubic bone on each side. The suspension sutures should be placed prior to manipulation or decompression of the UD to avoid postoperative infection. The endopelvic fascia is perforated with the bladder completely emptied and the retropubic space is developed. Helical 1-0 Prolene
Diverticulum
Figure 90.12. Anterior vaginal wall and urethral diverticulum. (Reproduced from ref. 55 with permission.) 1261
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Periurethral fascia
Anterior vaginal wall
Figure 90.13. An inverted U-incision is made in the anterior vaginal wall, and the vaginal wall is dissected off the underlying periurethral fascia. sutures are placed in the vaginal wall and directed with a Pereyra needle into the suprapubic incision. Cystoscopy is performed to ensure that no suture has passed into the bladder or urethra. Care must be taken to avoid entry into the UD during suture placement. If the UD is large and/or proximally located, it may be difficult to avoid; in this situation, the BNS should be postponed. The use of bone anchors for the BNS has been described;87 however, the authors do not advocate this when diverticulectomy is being performed in view of the risk of infection. Additionally, Swierzewski and McGuire93 have recommended a concomitant pubovaginal sling with diverticulectomy; however, the authors avoid the use of a concomitant sling procedure because of concerns of urethral erosion of the sling and breakdown of the reconstruction site. The diverticulectomy is continued with creation of a vaginal flap with sharp dissection directly on the shiny white layer of the vaginal wall. Dissection in the wrong plane can result in significant bleeding or inadvertent entry into the periurethral fascia or the UD, thereby rendering the remainder of the dissection very difficult. Mobilization of the vaginal flap towards the bladder neck, followed by a transverse incision in the periurethral fascia (Fig. 90.14) exposes
Figure 90.14. transversely.
The periurethral fascia is incised
the UD, which lies directly beneath this layer. The periurethral fascia is then sharply dissected off the UD (Fig. 90.15), which is then exposed circumferentially until the diverticular neck is encountered (Fig. 90.16). Difficulty in identification of the urethral communication site can result in incomplete resection of the UD and subsequent recurrence. Identification can be facilitated by insertion of a pediatric sound into the UD. Complete excision of both the UD and its neck can create a significant urethral defect (Fig. 90.17). Incomplete resection of the diverticulum can lead to recurrence. However, when the UD is large, extensive dissection beneath the trigone can endanger the ureters and bladder base, sometimes necessitating leaving the most proximal portion of the UD behind. In these cases, cautery to the inner epithelial surface will obliterate the cavity. The urethral defect is closed vertically over a 14 Fr catheter without tension using a fullthickness 4-0 Vicryl stitch, incorporating both urethral mucosa and the urethral wall (Fig. 90.18). The periurethral fascia is closed transversely with running 3-0 Vicryl (Fig. 90.19). Dead space should be obliterated beneath this layer. In cases in which there is insufficient tissue for closure of a second layer, or when the vaginal tis-
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sue is tenuous or fibrotic (such as secondary to previous surgery or radiation), a well-vascularized 8–12 cm Martius fat-pad graft may be placed between the vagina and urethra. The third and final layer is the vaginal wall,
which is closed with 2-0 absorbable suture. The three layers of closure include the urethral wall vertically, the periurethral fascia transversely, and the vaginal U-inci-
Urethral diverticulum
Figure 90.15. diverticulum.
The periurethral tissue is dissected from the
Urethra
Figure 90.17. The diverticulum is amputated at its communication site, thereby exposing the urethral Foley catheter and leaving a urethral defect.
Anterior flap Periurethral fascia Posterior flap
Figure 90.16. The diverticulum is isolated and carefully dissected until the communication is identified.
Figure 90.18. The urethra is reapproximated longitudinally with 4-0 absorbable suture. 1263
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Periurethral fascia Vaginal wall suture Periurethral fascia suture
Urethral suture
Figure 90.19. The periurethral tissue is closed transversely with 3-0 absorbable suture. sion. The goal is to avoid overlapping suture lines (Fig. 90.20). Antibiotic- or estrogen-soaked vaginal packing is inserted, and the SPT and Foley catheter are placed to gravity drainage. Anterior or dorsally located horseshoe-shaped and circumferential urethral diverticula present unique challenges to the pelvic surgeon. Because of their complexity, they frequently present as recurrent diverticula that have been operated on previously. The tissue planes may be obscured, complicating the dissection. The anterior location is also not easily accessed transvaginally. Anterior UD can become large, leading to difficulty filling the dead space created after excision. The subsequent urethral defect can be sizeable (>2 cm). Clyne and Flood have recently described an approach to anterior horseshoe-shaped UD using a suprameatal incision.94 In addition, they utilize double wrapped porcine xenograft to aid in filling of dead space. Retropubic approaches have also been described;95 however, for circumferential diverticula, a separate vaginal incision would also be necessary to excise the ventral portion of the diverticulum. A parasagittal vaginal incision with detachment of the urethra from the inferior pubic ramus laterally to facilitate anterior dissection has recently been outlined.96 Rovner and Wein have introduced a novel technique for excision and reconstruction of dorsal or circumferential UD by dividing the urethra to access the anterior portion of the diverticulum. Once
Figure 90.20. The vaginal wall flap is closed, resulting in a three-layer closure with no overlapping suture lines. excised, end-to-end urethroplasty or diverticular sac urethroplasty is performed.97 Martius flap interposition was performed in nearly all patients to help with closure of dead space.
Postoperative management The vaginal packing is removed on postoperative day 1. All patients receive 24 hours of intravenous antibiotics followed by oral antibiotics until the catheters are removed. Anticholinergics are given to relieve bladder spasms but are discontinued 24 hours prior to the VCUG, which is performed 7–10 days postoperatively. At the time of this first VCUG, approximately 50% of patients have some extravasation from the urethral reconstruction site.5 When extravasation is evident, the SPT is left in place, but the urethral catheter is not reinserted. A follow-up VCUG is obtained in a week’s time. When there is no extravasation, the SPT is clamped and a postvoid residual (PVR) is checked. If the PVR is 100 ml or less, the SPT is removed; if the PVR exceeds 100 ml, the SPT is left in place until this volume decreases.
reSUltS anD comPlicationS Potential complications following a urethral diverticulectomy include incontinence, UD recurrence,
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table 90.8.
Complications of urethral diverticulectomy
Complication
Possible causes
Incontinence
Failure to identify SUI preoperatively New onset SUI DI Recurrent diverticulum leading to ‘paradoxical incontinence’ Urethrovaginal fistula
Recurrent diverticulum
Failure to identify multiple diverticula preoperatively Incomplete excision Faulty closure
Urethrovaginal fistula
Closure under tension Tenuous, unhealthy tissue Failure to close in layers Overlapping suture lines
Irritative symptoms
Urinary tract infection Bladder dysfunction (DI) Outlet obstruction
Urethral stricture
Extensive urethral wall excision Closure under tension
DI, detrusor instability; SUI, stress urinary incontinence.
table 90.9.
Treatment modalities for 63 patients
Operative treatment
56 (88.9%)
Diverticulectomy alone
29 (51.8%)
Diverticulectomy + BNS
27 (48.2%)
Martius fat-pad graft No operative treatment
7 (11.1%) 7* (11.1%)
* In three cases surgery was refused; there were four cases of small asymptomatic diverticula not requiring surgery. BNS, bladder neck suspension. Reproduced, with modifications, from ref. 9 with permission.
table 90.10.
urethrovaginal fistula, irritative symptoms, urethral stricture, and general postoperative complications (Table 90.8).98 Ganabathi et al.9 evaluated 63 women who had been treated for UD between 1982 and 1992: 56 were treated operatively and seven were observed. The specific treatment modalities employed are shown in Table 90.9. Patients were followed-up for a mean of 70 months, with a range of 10–124 months. Table 90.10 reports the complications encountered. The two recurrences of the UD occurred distal to the initial repair site. Overall continence status, shown in Table 90.11, indicates that the majority of patients were totally continent. A greater percentage of the patients who underwent diverticulectomy alone were reported as continent, than were those who underwent diverticulectomy with concomitant BNS (Table 90.12). It was reported that incontinence was more frequently secondary to SUI than to detrusor instability, despite the presumed increase in bladder neck support. Incontinence may be secondary to persistent SUI that was present preoperatively. This situation can be avoided by a comprehensive preoperative evaluation so that it can be addressed at the time of diverticulectomy.9,99,100 Incontinence can also be a result of urethrovaginal fistula, recurrent diverticulum with paradoxical loss of urine with stress, infection, persistent detrusor instability or new-onset SUI. The first two conditions may
table 90.11. Incontinence
n (%)
Nil or moderate (dry or 0 pads/day)
45 (80.4)
Moderate (1–2 minipads/day)
10 (17.9)
Severe (several pads/day)
table 90.12.
2
Suprapubic tenderness*
1
Early urinary tract infection (none recurrent)
6
Urethrovaginal fistula†
1
Wound infection/urethral stricture
0
* Patient had concomitant bladder neck suspension. † Required subsequent surgical repair.
1 (1.8)
Continence status of 56 patients with mean follow-up of 70 months Diverticulectomy alone (n=29)
Diverticulectomy and BNS (n=27)
25 (86.2%)
20 (74%)
Incontinent
4 (13.8%)
7 (26%)
DI
1 (3.4%)
1 (3.7%)
SUI
3 (10.3%)
6 (22.2%)
Complications
Recurrence (distal repair site)
Overall continence of 56 patients with mean follow-up of 70 months
Continent
BNS, bladder-neck support; DI, detrusor instability; SUI, stress urinary incontinence. Reproduced, with modifications, from ref. 9 with permission.
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require surgical intervention. New-onset SUI may be a result of the urethral dissection, which may compromise urethral support, or secondary to dissection beneath the proximal urethra and bladder neck, which is often necessary when removing a large UD. Detrusor instability can be treated successfully in some cases with behavioral therapy, anticholinergic therapy or the addition of a tricyclic antidepressant such as imipramine; this not only increases bladder outlet tone but also decreases detrusor contractility. Recurrent UD is often a result of failure to identify multiple UD preoperatively, secondary to lack of either suspicion or proper high-quality studies.9,100 Incomplete excision of the diverticular neck, as well as faulty closure of the urethral defect, are also possible causes. This problem can be managed with interposition of a Martius fat-pad graft between the vagina and urethra.9 For small, distal recurrences, endoscopic saucerization or Spence marsupialization may suffice;5 however, caution must be exercised not to injure the proximally located continence mechanism. Urethrovaginal fistulae (UVF) formation, another potential complication, is managed in much the same manner and may be prevented by intraoperative Martius flap if tissues appear tenuous or under tension. UVF is discussed in more detail in the next section. Finally, urethral stricture resulting from extensive excision of the urethral wall at the time of diverticulectomy can be prevented by a tension-free urethral closure over a 14 Fr catheter. If this is not possible, reconstruction using vaginal wall can be contemplated, again with consideration of a Martius labial fat-pad graft.
UrethrovaGinal FiStUla introDUction Urethrovaginal fistula (UVF) is a rare condition. Fistulae range from small communications between the urethra and the vagina to total loss of the urethra and bladder neck.5,101–103 A distal fistula may present with vaginal voiding or a splayed urinary stream. Midurethral or proximal fistulae can present with varying degrees of continence, depending upon fistulae location and bladder neck competence.104,105 Urethral fistulae are most commonly caused by complications of previous surgery, such as anterior colporrhaphy or urethral diverticulectomy (see previous section). Urethral erosion of synthetic pubovaginal slings leading to fistulae formation is a relatively recent phenomenon. Its increased fre-
quency is most likely due to the increased popularity of the procedure over the past few years.106 A urethrovaginal fistula has also been reported following periurethral collagen injection.107 Other causes include radiation therapy and birth trauma, although this is rare with modern obstetric techniques. Obstructed labor remains the most common cause of urethral injury in developing countries.16
DiaGnoSiS The differential diagnosis of UVF includes SUI, intrinsic sphincter deficiency (ISD), or vaginal voiding due to other conditions. A careful history and physical examination can help to differentiate between the above conditions. Careful history taking may reveal previous vaginal or pelvic surgery or symptoms of stress versus urge incontinence. Physical examination is important to assess urethral loss, location and size of the fistula, urethral and bladder neck mobility, and quality of vaginal tissue, including scarring and atrophy. Studies that may aid in the diagnosis include cystourethroscopy, IVP to evaluate the upper tracts, renal ultrasonography, VCUG, and urodynamic studies. Cystoscopy is performed with a 20 Fr female urethroscope with a 0-degree lens. It is essential to examine the urethra, bladder neck, trigone, and quality of the tissue. A concomitant vesicovaginal fistula must be excluded. If identification of the UVF is difficult, simultaneous vaginal examination with a speculum may identify fluid spraying into the vagina through the communication. Upper tract evaluation is essential when the trigone is involved and may be accomplished with IVP or renal ultrasonography. A standing fluoroscopic VCUG is often helpful in identification of the urethral defect and in excluding a vesicovaginal fistula. VCUG also aids in assessment of urethral hypermobility and/or leakage of urine across the bladder neck during stress. Finally, urodynamic studies may be of benefit in evaluation of bladder function and sphincter integrity when the UVF is in the distal third of the vagina.
treatment The goal of treatment of urethral fistulae is to create a competent neourethra of adequate length to permit unobstructed passage of urine while preserving urinary continence.102 Additionally, urethrovaginal repair must be tension free. Distal fistulae may be managed with an extended meatotomy.5 The postoperative incontinence rate may be as high as 50% if SUI is not considered at
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the time of fistula repair.5 Some authors have suggested concomitant sling at the time of fistula repair.102 Because of concerns about the risks of erosion of the sling at the time of mid- or proximal UVF repair, the authors avoid performing a sling simultaneously with UVF repair.
operative technique Preoperative preparation is similar to that for urethral diverticulectomy (see previous section). Estrogen is administered preoperatively, if indicated, to treat atrophic vaginitis. Urine culture is performed to ensure that the urine is sterile preoperatively. If necessary, a short course of oral antibiotics is given. All patients receive perioperative intravenous ampicillin and gentamicin, unless contraindicated. Essentially, all types of urethral and bladder neck defects can be approached transvaginally, often in conjunction with a Martius fat-pad graft.104,105,108 This includes simple fistula repair and vaginal flap total urethral reconstruction. Our preferred approach for transvaginal fistulae closure and vaginal flap urethral reconstruction requires
Figure 90.21. An inverted U-incision is made in the vaginal wall with the apex just proximal to the fistula.
placement of the patient in the lithotomy position (Fig. 90.21). A 20–24 Fr SPT is placed and a 14 Fr urethral catheter is inserted. Postoperative self-catheterization of the neourethra must be avoided, hence the necessity of the SPT. The SPT also serves as a ‘safety valve’ if the urethral catheter becomes obstructed. The vaginal wall is infiltrated with saline to develop the proper plane, and an inverted U-incision is made. The apex of the incision is located just proximal to the fistula for fistulectomy and at the meatus for total urethral reconstruction. Dissection in the avascular plane exposes the shiny white surface of the interior vaginal wall. Excessive bleeding and bladder perforation are risks if dissection is too deep. When concomitant BNS is necessary, lateral dissection and perforation of the endopelvic fascia is performed. The suspension sutures in the anterior vaginal wall and periurethral tissue are placed but not tied. The authors tend not to advocate routine simultaneous sling procedures, owing to the risk of erosion through the reconstructed urethra. However, if the decision to proceed with a concomitant sling is made, the authors
Figure 90.22. The fistula is circumscribed but not excised. The avascular plane beneath the lateral vaginal wall is developed. 1267
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would certainly recommend the use of autologous or allograft tissue. Flisser and Blaivas have reported good success using autologous fascia slings with Martius labial fat-pad graft in patients at risk of postoperative incontinence with few complications.106 Leng et al. also endorse use of the autologous fascia sling in cases of urethrovaginal fistulae with type III SUI as it offers the advantage of dual function as a reinforcing layer and continence procedure.109 The fistula is circumscribed but not excised (Fig. 90.22). Scarred tissue margins are freed to allow a tension-free closure of the tract. A portion of the vaginal wall just distal to the fistula is then mobilized to create a flap. The fistula is closed with running locking absorbable suture (Fig. 90.23). For total reconstruction of the urethra, two vaginal wall incisions are made parallel to and on either side of the urethra to create medially based flaps (Fig. 90.24). The flaps are tubularized around a 14 Fr urethral catheter and approximated at the midline with 4-0 absorbable sutures (Fig. 90.25). For fistula repair, a second layer of running Lembert stitch with 3-0 absorbable suture is placed to complete a watertight closure. The third layer is the closure of the vaginal flap with a locked running stitch using absorbable suture. In this manner, overlapping suture lines are avoided (Fig. 90.26).
Figure 90.23.
The fistula is closed with absorbable suture.
Figure 90.24. Two longitudinal incisions are made to create medially based flaps.
Figure 90.25. catheter.
The flaps are rolled over a 14 Fr urethral
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Labial fat pad
Figure 90.26. The vaginal flap is closed with a running, locking absorbable suture. If the tissues are tenuous or inadequate, a Martius fatpad graft may be interposed between the urethra and the vagina. The labium majus is incised to expose the underlying fat pad. The flap is mobilized, preserving the pudendal vessels, located posteriorly (Fig. 90.27). The fat pad is passed through a subcutaneous tunnel from the labium majus to the vagina and secured over the fistula repair site with absorbable sutures (Fig. 90.28). A ¼-inch Penrose drain is placed deep into the labial wound, and the labial incision is closed in layers. The vaginal flap (described above) is closed over the Martius flap (Fig. 90.29). When a Martius fat-pad graft is not feasible, a meatalbased vaginal flap can be rotated distally (Fig. 90.30)102 or a neourethra can be created from a cutaneous portion of the gracilis muscle or a perineal artery-based myocutaneous flap.102 Finally, in selected cases, one may resort to closure of the bladder neck with creation of a catheterizable stoma or placement of a suprapubic catheter.110 The urethral Foley catheter and SPT are placed to gravity drainage, and an antibiotic- or estrogen-soaked vaginal pack is placed. Patients receive perioperative intravenous antibiotics, which are converted to oral medication on postoperative day 1. Anticholinergics are administered to prevent bladder spasm, and are dis-
Figure 90.27. The labium majus is incised, and the Martius fat-pad graft is mobilized with care to preserve the posteriorly located pudendal vessels.
Labial fat pad
Figure 90.28. The labial fat pad is passed through a medial tunnel and secured over the fistula repair site. 1269
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continued at least 24 hours prior to the VCUG, which is performed between postoperative days 7 and 10. If extravasation is noted, the SPT is left to gravity and the urethral catheter is not replaced. The VCUG is repeated after 1–2 weeks and the SPT is removed when there is no extravasation and PVRs are minimal (<100 ml).
Fistula site Labial fat pad
Figure 90.29. The vaginal wall flap is advanced over the fat-pad graft, resulting in closure with no overlapping suture lines.
reSUltS Few series in the literature report the results of UVF repair. Most series include 10 or fewer patients, and continence rates range from 30 to 87%, including patients who underwent a single operation or multiple repairs. Flisser and Blaivas106 reported on their experience with 74 women with urethral pathology requiring surgical reconstruction. The patients ranged from 22 to 80 years of age and were followed-up for 1–15 years (median 1.5 years). Autologous rectus fascia pubovaginal sling was performed in 56, modified Pereyra procedure in five, and Kelly plication in one. The authors abandoned needle suspension in favor of pubovaginal sling after observing high postoperative incontinence rates. Martius flaps were used in 58 cases. Preoperative incontinence was the indication for vaginal flap reconstruction in 62 patients. Postoperatively 54 (87%) considered their incontinence cured or improved. The symptomatic obstruction rate was 1.3% and recurrent fistulae were reported in two patients (3%). Flap necrosis occurred in three patients, leading to continent urinary diversion in two patients and use of a gracilis flap in one patient. Intermittent catheterization was required in one woman for 6 months and less than 6 weeks in three others. The symptomatic obstruction rate was 1.3%. Postoperatively, 12 patients (16%) reported severe urinary urgency or urge incontinence. Goodwin and Scardino111 similarly reported a 70% success rate following one operation in 24 patients treated for vesicovaginal or urethrovaginal fistula. Their success rate was 92% following a second operation. Keetel et al.112 reviewed their results in 24 patients with UVF and reported an overall success rate of 87.5%. Lee105 claimed
Figure 90.30. A meatus-based vaginal flap is rotated distally. 1270
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a 92% correction rate of UVF in 50 patients after one surgery and 100% success rate with two operations. Each of the series favored the vaginal approach over the abdominal approach: the vaginal approach generally involves a lower blood loss, shorter hospital stay and shorter operating time.111,112
comPlicationS Postoperative complications following urethral fistula repair may include urinary retention and urinary incontinence. High PVRs are not uncommon following urethral reconstruction, especially when performed with a simultaneous anti-incontinence procedure. Urinary retention usually resolves within a few weeks and can be managed by keeping the SPT in place until the PVRs reduce to 100 ml or less. If retention persists, the patient may be instructed on how to perform clean intermittent self-catheterization, which should not be initiated until the urethra has healed completely. Urinary incontinence may be secondary to undetected preoperative SUI, new-onset SUI if extensive dissection has been performed, or urge incontinence due to detrusor instability. SUI may be managed with concomitant needle suspension or sling procedure following adequate healing of the urethra. Periurethral collagen may also be considered if hypermobility is not a major concern. Anticholinergic medications may be helpful in the treatment of detrusor instability.
conclUSion Urethral diverticula in women represent a relatively rare entity that presents with a wide variety of symptoms. A high index of suspicion is necessary to establish the correct diagnosis, especially in patients with persistent lower urinary tract symptoms that have been refractory to conventional therapy. Advances in imaging techniques, including endoluminal MRI and transvaginal ultrasound, are capable of providing better characterization of the extent of some complex urethral diverticula. The goals of surgery include complete excision of the diverticulum with reconstruction of the resultant urethral defect. Patients with preoperative incontinence are potential candidates for a concomitant pubovaginal sling procedure. A Martius flap interpositional graft should be considered in cases where the tissues appear tenuous or fibrotic from previous surgery or radiation. Because of the risk of postoperative complications, including recurrent diverticula, stricture, or urethrovaginal fistula, surgical intervention must be individualized to each patient.
In the modern era, with appropriate preoperative planning and strict adherence to the basic surgical principles of a tension-free, multilayered repair, urethral diverticula and urethrovaginal fistulae can be treated with excellent anatomic and functional outcomes.
reFerenceS 1. Novak R. Editorial comment. Obstet Gynecol Surv 1953;8:423. 2. Hey W. Practical Observations in Surgery. Philadelphia: J. Humphries, 1805. 3. Hunner GL. Calculus formation in a urethral diverticulum in women. Urol Cutan Rev 1938;42:336. 4. Davis HJ, Cian LG. Positive pressure urethrography: a new diagnostic method. J Urol 1956;75:753–7. 5. Leach GE, Trockman BA. In: Walsh PC, Retik AB, Vaughan ED, Wein AJ (eds) Campbell’s Urology, 7th ed. Philadelphia: Saunders, 1997; 1141–51. 6. Wittich AC. Excision of urethral diverticulum calculi in a pregnant patient on an outpatient basis. J Am Osteopath Assoc 1997;97:461–2. 7. Robertson JR. Urethral diverticula. In: Ostergard DR (ed) Gynecologic Urology and Urodynamics: Theory and Practice, 2nd ed. Baltimore: Williams and Wilkins, 1985; 329–38. 8. Levinson ED, Spackman TJ, Henken EM. Diagnosis of urethral diverticula in females. Urol Radiol 1979– 80;1:165–7. 9. Ganabathi K, Leach GE, Zimmern PE, Dmochowski RR. Experience with the management of urethral diverticulum in 63 women. J Urol 1994;152:1445–52. 10. Hesserdorfer E, Kuhn R, Sigel A. [Pathogenetic synopsis of diverticular disease of the female urethra] (abstract). Urologe 1988;27:343–7. 11. Lee RA. Diverticulum of the urethra: clinical presentation, diagnosis, and management. Clin Obstet Gynecol 1984;27:490–8. 12. Davis BL, Robinson DG. Diverticula of the female urethra: assay of 120 cases. J Urol 1970;104:850–3. 13. Aldridge CW, Beaton JH, Nanzig RP. A review of office urethroscopy and cystometry. Am J Obstet Gynecol 1978;131:432–7. 14. Huffman AB. The detailed anatomy of the paraurethral ducts in the adult human female. Am J Obstet Gynecol 1948;55:86–101. 15. Routh A. Urethral diverticula. Br J Urol 1890;1:361. 16. McNally A. Diverticula of the female urethra. Am J Surg 1935;28:177. 17. Raz S, Little NA, Juma S. Female urology. In: Walsh, PC, Retick AB, Stamey TA, Vaughan ED (eds) Campbell’s Urology, 6th ed. Philadelphia: Saunders, 1992; 2782–8.
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18. Niemic TR, Mercer LJ, Stephens JK et al. Unusual urethral diverticulum lined with colonic epithelium with Paneth cell metaplasia. Am J Obstet Gynecol 1989;260:186–8. 19. Silk MR, Lebowitz JM. Anterior urethral diverticulum. J Urol 1969;101:66–7. 20. Clemens JQ, Bushman W. Urethral diverticulum following transurethral collagen injection. J Urol 2001;166:626. 21. Peters WH, Vaughan ED. Urethral diverticulum in the female. Obstet Gynecol 1976;47:549–52. 22. Aragona F, Mangano M, Artibani W, Passerini GG. Stone formation in a female urethral diverticulum. Review of the literature. Int Urol Nephrol 1989;21:621–5. 23. Pavlica P, Viglietta F, Losinno F et al. [Diverticula of the female urethra. A radiological and ultrasound study] (abstract). Radiol Med 1988;75:521–7. 24. Ginsberg S, Genandry R. Suburethral diverticulum: classification and therapeutic considerations. Obstet Gynecol 1983;61:685–8. 25. Nielsen VM, Nielsen KK, Vedel P. Spontaneous rupture of a diverticulum of the female urethra presenting with a fistula to the vagina. Acta Obstet Gynecol Scand 1987;66:87–8. 26. Evans KJ, McCarthy MP, Sands JP. Adenocarcinoma of a female urethral diverticulum: case report and review of the literature. J Urol 1981;126:124–6. 27. Okubo Y, Fukui I, Sakano Y et al. [Mesonephric adenocarcinoma arising in the female urethral diverticulum] (abstract). Nippon Hinyokika Gakkai Zasshi 1996;87:1138–41. 28. Seballos RM, Rich RR. Clear cell adenocarcinoma arising from a urethral diverticulum. J Urol 1995;153:1914–5. 29. Srinivas V, Dow D. Transitional cell carcinoma in a urethral diverticulum with a calculus. J Urol 1983;129: 372–3. 30. Klutke CG, Akdmna EI, Brown JJ. Nephrogenic adenoma arising from a urethral diverticulum: magnetic resonance features. Urology 1995;45:323–5. 31. Materne R, Dardenne AN, Opsomer RJ et al. [Apropos of a case of nephrogenic adenoma in a urethral diverticulum in a woman] (abstract). Acta Urol Belg 1995;63: 13–8. 32. Medeiros LJ, Young RH. Nephrogenic adenoma arising in urethral diverticula. A report of five cases. Arch Pathol Lab Med 1989;113:125–8. 33. Paik SS, Lee JD. Nephrogenic adenoma arising in an urethral diverticulum. Br J Urol 1997;80:150. 34. Parks J. Section of the urethral wall for correction of urethrovaginal fistula and urethral diverticula. Am J Obstet Gynecol 1965;93:683–92. 35. Summit RL, Murrmann SG, Flax SD. Nephrogenic adenoma in a urethral diverticulum: a case report. J Reprod Med 1994;39:473–6.
36. Poore RE, McCullough DL. Urethral carcinoma. In: Gillenwater JY, Grayhack JT, Howards SS, Duckett JW (eds) Adult and Pediatric Urology, 3rd ed. Salem, MA: Mosby, 1996; 1846–7. 37. Shalev M, Mistry S, Kernen K, Miles BJ. Squamous cell carcinoma in a female urethral diverticulum. Urol 2002;59:773iii–773v. 38. Gonzalez MO, Harrison ML, Boileau MA. Carcinoma in diverticulum of female urethra. Urology 1985;26: 328–32. 39. Jimenez de Leon J, Luz Picazo M, Mora MM et al. [Intradiverticular adenocarcinoma of the urethra in women] (abstract). Arch Exp Urol 1989;42:L931–5. 40. Wishard WN, Nourse MH, Mertz J. Carcinoma in a diverticulum of a female urethra. J Urol 1960;104:409–13. 41. Huvos AG, Muggia FM, Markewitz M. Carcinoma of the female urethra. N Y State J Med 1970;69:2042–5. 42. Torres SA, Quattlebaus RB. Carcinoma in a urethral diverticulum. South Med J 1972;65:1374–6. 43. Olivia E, Young RH. Clear cell adenocarcinoma of the urethra: a clinicopathologic analysis of 19 cases. Mod Pathol 1996;9:513–20. 44. Aspera AM, Rackley RR, Vasavada SP. Contemporary evaluation and management of the female urethral diverticulum. Urol Clin North Am 2002;29:617–24. 45. Romanzi LJ, Groutz A, Blaivas JG. Urethral diverticulum in women: diverse presentations resulting in diagnostic delay and mismanagement. J Urol 2000;164:428–33. 46. Jensen LM, Aabech J, Lundvall F, Iversen HG. Female urethral diverticulum. Clinical aspects and a presentation of 15 cases. Acta Obstet Gynecol Scand 1996;75:748–52. 47. Dmochowski RR, Ganabathi K, Zimmern PE, Leach GE. Benign female periurethral masses. J Urol 1994;152: 1943–51. 48. Curry NS. Ectopic ureteral orifice masquerading as a urethral diverticulum. Am J Roentgenol 1983;41:1325–6. 49. Dias P, Hillard P, Rauh J. Skene’s gland abscess with suburethral diverticulum in an adolescent. J Adolesc Health Care 1987;8:372–5. 50. Konami T, Wakabayashi Y, Takeuchi J, Tomoyoshi T. Female wide urethra masquerading as a urethral diverticulum in association with ectopic ureterocele. Hinyokika Kiyo 1988;34:1437–41. 51. Leach GE, Sirls LT, Ganabathi K et al. LNSC3: a proposed classification system for female urethral diverticula. Neurourol Urodyn 1993;12:523–31. 52. Gerrard ER, Lloyd LK, Kubricht WS, Koettis PN. Transvaginal ultrasound for the diagnosis of urethral diverticulum. J Urol 2003;169:1395–7. 53. Wang AC, Wang CR. Radiologic diagnosis and surgical treatment of urethral diverticulum in women. A reap-
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praisal of voiding cystourethrography and positive pressure urethrography. J Reprod Med 2000;45:377–82. 54. Siegel CL, Middleton WD, Teefey SA, Wainstein MA, McDougall EM, Klutke CG. Sonography of the female urethra. Am J Roentgenol 1998;170:1269–74. 55. Leach GE, Ganabathi K. Urethral diverticulectomy. Atlas Urol Clin North Am 1994;2:73–85. 56. Leach GE, Bavenden TG. Female urethral diverticula. Urology 1987;30:407–15. 57. Reid RE, Gill B, Laor E et al. Role of urodynamics in management of urethral diverticulum in females. Urology 1986;28:342–6. 58. Jacoby K, Rowbotham RK. Double balloon positive pressure urethrography is a more sensitive test than voiding cystourethrography for diagnosing urethral diverticulum in women. J Urol 1999;162:2066–9. 59. Golomb J, Leibovitch I, Mor Y, Morag B, Ramon J. Comparison of voiding cystourethrography and double-balloon urethrography in the diagnosis of complex female urethral diverticula. Eur Radiol 2003;13:536–42. 60. Keefe B, Warshauer DM, Tucker MS, Mittelstaedt CA. Diverticula of the female urethra: diagnosis by endovaginal and transperineal sonography. Am J Roentgenol 1991;156:1195–7. 61. Vargas-Serrano B, Cortina-Moreno B, Rodriguez-Romero R, Ferreiro-Arguees I. Transrectal ultrasonography in the diagnosis of urethral diverticula in women. J Clin Ultrasound 1997;25:21–8. 62. Iula G, Stefano ML, Castaldi L, del Vecchio E. Post irradiation female urethral diverticula: diagnosis by voiding endovaginal sonography. J Clin Ultrasound 1995;23: 63–5. 63. Mouritsen L, Bernstein I. Vaginal ultrasonography: a diagnostic tool for urethral diverticulum. Acta Obstet Gynecol Scand 1996;75:188–90. 64. Martensson O, Duchek M. Translabial ultrasonography with pulsed colour Doppler in the diagnosis of female urethral diverticulum. Scan J Urol Nephrol 1994;28: 101–4. 65. Chancellor MB, Liu JB, Rivas DA et al. Intraoperative endo-luminal ultrasound evaluation of urethral diverticula. J Urol 1995;153:72–5. 66. Lopez Rasines G, Rico Guttierez M, Abascal F, Calbia de Diego A. Female urethral diverticula: value of transrectal ultrasound. J Clin Ultrasound 1996;24:90–2. 67. Blacklock ARE, Shaw RE, Geddes JR. Late presentation of ectopic ureter. Br J Urol 1982;54:106–10.
70. Debaere C, Rigauts H, Steyaert L et al. MR imaging of a diverticulum in a female urethra. J Belg Radiol 1995;78:345–6. 71. Hricak H, Secaf E, Buckley DW et al. Female urethra: MR imaging. Radiology 1991;178:527–35. 72. Neitlich JD, Foster HE, Glickman MG, Smith RC. Detection of urethral diverticula in women: comparison of a high resolution fast spin echo technique with double balloon urethrography. J Urol 1998;159:408–10. 73. Siegelman ES, Banner MP, Ramchandani P, Schneall MD. Multicoil MR imaging of symptomatic female urethral and periurethral disease. Radiographics 1997;17: 349–65. 74. Blander DS, Rovner ES, Schnall MD et al. Endoluminal magnetic resonance imaging in evaluation of urethral diverticula in women. Urology 2001;57:660–5. 75. Kim B, Hricak H, Tanagho EA. Diagnosis of urethral diverticula in women: value of MR imaging. Am J Roentgenol 1993;161:809–15. 76. Lorenzo AJ, Zimmern P, Lemack GE, Nureberg P. Endorectal coil magnetic resonance imaging for diagnosis of urethral and periurethral pathologic findings in women. Urology 2003;61:1129–34. 77. Greenberg M, Stone D, Cochran ST et al. Female urethral diverticula: double-balloon catheter study. Am J Roentgenol 1981;136:259–64. 78. Young HH. Treatment of urethral diverticulum. South Am J 1938;31:1043–7. 79. Moore TD. Diverticulum of the female urethra. An improved technique of surgical excision. J Urol 1952;68:611–6. 80. Wear JB. Urethral diverticulectomy in females. Urol Times 1976;4:2–3. 81. Hyams JA, Hyams MN. New operative procedures for treatment of diverticulum of female urethra. Urol Cutan Rev 1939;43:573–7. 82. Feldstein MS. Cryoprecipitate coagulum as an adjunct to surgery for diverticula of the female urethra. J Urol 1981;126:698–9. 83. Downs RA. Urethral diverticula in females: alternative surgical treatment. Urology 1987:2:201–3. 84. Spence HM, Duckett JW. Diverticulum of the female urethra: clinical aspects and presentation of a simple operative technique for cure. J Urol 1970;14:432–7. 85. Ellik M. Diverticulum of the female urethra: a new method of ablation. J Urol 1957;77:243–6.
68. Boyd SD, Raz S. Ectopic ureter presenting in midline urethral diverticulum. Urology 1993;41:571–4.
86. Mizrahi S, Bitterman W. Transvaginal, periurethral injection of polytetrafluoroethylene (polytef) in the treatment of urethral diverticula. Br J Urol 1988;62:280.
69. Goldfarb S, Mieza M, Leiter E. Postvoid film of intravenous pyelogram in diagnosis of urethral diverticulum. Urology 1981;17:390–2.
87. Fall M. Vaginal wall bipedicled flap and other techniques in complicated urethral diverticulum and urethrovaginal fistula. J Am Coll Surg 1995;180:150–6.
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88. Leach GE, Schmidbauer CP, Hadley HR et al. Surgical treatment of female urethral diverticulum. Semin Urol 1986;4:33–42. 89. Marshall S. Urethral diverticula in young girls. Urology 1981;17:243–5. 90. Lapides J. Transurethral treatment of urethral diverticula in women. J Urol 1979;121:736–8. 91. Vergunst H, Blom JH, De Spiegeleer AH, Miranda SI. Management of female urethral diverticula by transurethral incision. Br J Urol 1996;77:745–6. 92. Spencer WF, Streem SB. Diverticula of the female urethra roof managed endoscopically. J Urol 1987;138:157–8. 93. Swierzewski SJ, McGuire EJ. Pubovaginal sling for treatment of female stress urinary incontinence complicated by urethral diverticulum. J Urol 1993;149:1012–4.
alternative to the bladder flap neourethra. J Urol 1989;141:542–5. 102. Blaivas JG. Treatment of female incontinence secondary to urethral damage or loss. Urol Clin North Am 1991;18:355–63. 103. Robertson JR. Urinary fistulas. In: Ostergard DR (ed) Gynecologic Urology and Urodynamics: Theory and Practice, 2nd ed. Baltimore: Williams and Wilkins, 1985; 323–8. 104. Leach GE. Urethrovaginal fistula repair with Martius labial fat pad graft. Urol Clin North Am 1991;18: 409–13. 105. Lee RA. Current status of genitourinary fistula. Obstet Gynecol 1988;72:313–9.
94. Clyne OJ, Flood HD. Giant urethral diverticulum: a novel approach to repair. J Urol 2002;167:1796.
106. Flisser AJ, Blaivas JG. Outcome of urethral reconstructive surgery in a series of 74 women. J Urol 2003;169: 2246–9.
95. Gilbert D, Cintron F. Urethral diverticula in the female: review of the subject and introduction of a different surgical approach. Am J Obstet Gynecol 1954;67:616.
107. Carlin BI, Klutke CG. Development of urethrovaginal fistula following periurethral collagen injection. J Urol 2000;164:124.
96. Vakili B, Wai C, Nihira M. Anterior urethral diverticulum in the female: diagnosis and surgical approach. Obstet Gynecol 2003;102:1179–83.
108. Chassagne S, Haav F, Zimmern PE. [The Martius flap in vaginal surgery: technique and indications] (abstract). Prog Urol 1997;7:120–5.
97. Rovner ES, Wein AJ. Diagnosis and reconstruction of the dorsal or circumferential urethral diverticulum. J Urol 2003;170:82–6.
109. Leng WW, Amundsen CL, McGuire EJ. Management of female genitourinary fistulas: transvesical or transvaginal approach. J Urol 1998;160(6 Pt 1):1995–9.
98. Coddington CC, Knab DR. Urethral diverticulum: a review. Obstet Gynecol Surv 1983;38:357–64.
110. Zimmern PE, Hadley HR, Leach GE et al. Transvaginal closure of the bladder neck and placement of a suprapubic catheter for destroyed urethra after long-term indwelling catheter. J Urol 1985;134:554–7.
99. Bass JS, Leach GE. Surgical treatment of concomitant urethral diverticulum and stress urinary incontinence. Urol Clin North Am 1991;18:365–73. 100. Ganabathi K, Sirls L, Zimmern PE, Leach GE. Operative management of female urethral diverticulum. In: McGuire E (ed) Advances in Urology. Chicago: Mosby, 1994; 199–228. 101. Blaivas JG. Vaginal flap urethral reconstruction: an
111. Goodwin WE, Scardino PT. Vesicovaginal and urethrovaginal fistulas: a summary of 25 years of experience. Trans Am Assoc GU Surg 1979;71:123–9. 112. Keetel WC, Schring FG, deProsse CA, Scott JR. Surgical management of urethrovaginal and vesicovaginal fistulas. Am J Obstet Gynecol 1978;131:425–31.
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91 Electrical stimulation of the lower urinary tract Firouz Daneshgari
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INTRODUCTION The first attempt at electrical stimulation of the lower urinary tract (LUT) may date back to 1878, when the Danish surgeon Saxtorph treated patients with urinary retention by intravesical stimulation,1 in which he inserted a special catheter with a metal electrode transurethrally. In 1811 Bell was the first to conduct experiments on the spinal nerve roots.2 His anatomic studies showed that manipulation of the intradural anterior fasciculus led to muscle convulsions of the back, whereas cutting across the posterior fasciculus of nerves resulted in no contractions.3 However, Bell drew the conclusion that the anterior nerve roots, connected to the cerebrum, conduct sensory and motor impulses. In his concept, the posterior nerve roots were connected to the cerebellum and accounted for the vital functions. Magendie was the first to conduct a physiologic investigation of spinal nerve roots.2 In radiculotomy studies on young puppies he found that cutting the posterior root extinguished sensation, although movement was still present,4 whereas cutting the anterior root abolished movement, but sensation was still present. Hence, he postulated that nerve roots consist of an anterior, efferent motor portion and a posterior, afferent sensory portion. It was not until 1833 that Hall uncovered a distinct function of the spinal cord and medulla oblongata – that of reflex action.5 These first perceptions formed the basis for further examinations of organ innervation by the autonomic nervous system. However, it was not until the 1940s that further efforts were undertaken. The central question was: Which part of the neuromuscular pathway for micturition should be chosen to initiate voiding in urinary retention or to prevent voiding in incontinence? Numerous techniques were developed and may be classified according to the location of electrical stimulation as follows: transurethral bladder stimulation, direct detrusor stimulation, pelvic nerve stimulation, pelvic floor stimulation, spinal cord stimulation, and sacral root stimulation.6 After experimentation with various methods of simulating the bladder through the transurethral approach, direct detrusor stimulation,7 pelvic nerve stimulation,8 pelvic floor stimulation,9 spinal cord stimulation,10 with pioneering work of Tanagho and later Schmidt,11–14 it was demonstrated that the stimulation of sacral root S3 generally induces detrusor and sphincter action.15 Following two decades of experimentation with various approaches to sacral root stimulation, finally, in October 1997, sacral neuromodulation for treatment of refractory urge incontinence
was approved by the Food and Drug Administration (FDA) in the United States. Since then and at the time of this writing, more than 20,000 Medtronic InterStim® systems have been implanted for three approved indications of sacral nerve stimulation (SNS) of the lower urinary tract. In this chapter we will review the various aspects of the electrical stimulation of the bladder and its application in managementv of LUT dysfunctions.
MeChaNIsMs Of aCTION Neuromodulation of LUT function can be explained by relatively simple spinal circuits mediating somatovisceral interactions within the sacral spinal cord. It is proposed that SNS activates or ‘resets’ the somatic afferent inputs that play a pivotal role in the modulation of sensory processing and micturition reflex pathways in the spinal cord (Fig. 91.1).16 Urinary retention and dysfunctional voiding can be resolved by inhibition of the guarding reflexes. Detrusor hyperreflexia and the overactive bladder syndrome can be suppressed by one or more pathways, i.e. direct inhibition of bladder preganglionic neurons, as well as inhibition of interneuronal transmission in the afferent limb of the micturition reflex (Figs 91.2–91.4).
PaTIeNT seleCTION The selection of patients for SNS begins with a careful history, physical examination, routine tests such as urinalysis and urine culture, and – most importantly – use
Infection, inflammation, anatomic abnormalities
Voluntary micturition control
Involuntary reflex mechanisms SNS therapy
Neurologic diseases
Figure 91.1. The concept of sacral nerve stimulation (SNS) is to modulate the abnormal involuntary reflexes of the lower urinary tract and restore voluntary control. (Reproduced from ref. 16 with permission.)
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Brain
Bladder C-fiber afferent
Bladder
Brain
(–)
SNS Bladder afferent (+)
Pudendal afferent
(+) (+)
SNS
(–) (+)
Figure 91.2. Pudendal afferent nerve stimulation can inhibit the micturition reflex. (Reproduced from ref. 16 with permission.)
(+)
Somatic efferent
Figure 91.4. The spinal guarding reflexes can be turned off by the brain to urinate. In neurologic disease, the brain cannot turn off the guarding reflex and retention can occur. However, SNS is capable of restoring voluntary micturition in cases of voiding dysfunction and urinary retention by inhibiting the spinal guarding reflex. (Reproduced from ref. 16 with permission.)
Brain
history Bladder afferent
(+) (+) (–)
(+)
(+)
Somatic efferent
Figure 91.3. The guarding reflex prevents urinary incontinence. When there is a sudden increase in intravesical pressure, such as during a cough, the urinary sphincter contracts via the spinal guarding reflex to prevent urinary incontinence. The spinal guarding reflex is turned off by the brain to urinate. (Reproduced from ref. 16 with permission.)
The important elements of history focuses on the primary voiding variables such as the frequency and severity of urge incontinent episodes and the number of pads used per 24-hour period. For patients with refractory urgency frequency, the number of voids, the voided volumes and the degree of urgency are assessed; in patients who experience inefficient voiding or urinary retention, the amount voided versus catheterized volumes per 24 hours and the patient’s sense of completeness of evacuation are fathomed. Associated symptoms such as pelvic pain and bowel and sexual symptoms are also assessed. As an extension of the history, a voiding diary is invaluable in order to document the patient’s voiding habits and complaints objectively.
Physical examination of bladder diaries to objectively record voiding variables. Urodynamic examination is commonly used to identify patients with detrusor overactivity (DO) with or without urinary leakage or urinary retention. Some reports suggest the utility of urodynamics in identification of proper candidates to SNS.
The physical examination should start with a neurourologic examination, checking for saddle sensation, sphincter tone, and bulbocavernosus reflex. Some investigators put emphasis on high pelvic tone noticed during the vaginal examination.17 In addition to examination of the bladder, urethra, perineum and vagina, rectal exam1277
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ination is a key aspect of the physical examination of any patient with voiding dysfunction.
aNaTOMIC laNDMaRk aND sURgICal TeChNIqUes Of saCRal NeUROMODUlaTION The S3 foramen is the desired anatomic landmark for placement of the leads for sacral neuromodulation. The techniques for S3 localization have included manual or fluoroscopic methods. The manual approach includes palpation of the sciatic notch, observation for the least curved portion of the sacrum, and measurement of approximately 11 cm from the caudal tip of the coccyx (Fig. 91.5). The manual method is more difficult with obese patients or in those without palpable landmarks, and in 2001 Chai et al. introduced the use of the ‘cross-hair’ fluoroscopic technique for S3 localization.18 The intent of fluoroscopy was not meant to ‘see’ the S3 foramen, but rather to help the surgeon identify a specific region to start percutaneous access of the S3 foramen (Fig. 91.6). More importantly, the use of lateral imaging helped determine the depth required for implanting the S3 lead (Fig. 91.7). As surgeons, particularly urologists, were familiar with the use of fluoroscopy due to their work in stone surgery, the application of fluoroscopy to sacral neuromodulation surgery was quickly accepted. The widespread use of fluoroscopic localization of S3 later allowed the introduction of the tined S3 lead19 and transformed the placement of a lead from an open procedure20 to a completely percutaneous one.21 The widely adopted
Figure 91.6. Localization of the S3 foramen by the crosshair technique. (Reproduced from ref. 16 with permission.)
Figure 91.7. Site of percutaneous placement of needle stimulations and stage I lead.
Figure 91.5. landmarks.
Localization of the S3 foramen by anatomic
percutaneous use of the tined lead approach superseded the need for fixation of the lead by methods such as bone anchors. The original method of SNS – entitled percutaneous nerve examination (PNE) – followed two steps: testing of the patient’s bladder response to sacral neurostimulation via a temporary lead placed into the S3 foramen, followed by possible simultaneous implantation of the chronic lead and the generator if the patient responded positively to the first step. Janknegt et al.22 first described the staged implantation approach in which an implanted S3 lead, rather than the temporary lead, was used for initial testing. The staged technique bypassed the problems with PNE which included a high risk of lead migration and the fact the original response of the patient obtained by the temporary wire may not be reproduced
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by the permanent lead. Several reports later confirmed a higher positive response rate, and a lesser rate of lead migration obtained by the staged approach. After placement of the lead, the following sensory and motor responses related to stimulation of the specific sacral root may be observed:
• S2: − clamp movement or twisting and pinching of the anal sphincter (pulling down the coccyx);
− plantar flexion of the entire foot, lateral rotation.
• S3: − bellows movement of the pelvic floor; − plantar flexion of the great toe(s); − paresthesia in the rectum, perineum, scrotum or vagina.
• S4: − bellows motion of the pelvic floor; − no lower extremity activity; − sensing pulling in the rectum only.
Stage I can be performed while the patient is under local anesthesia with conscious sedation (Fig. 91.8). After localization of the S3 foramen, the patient’s sensory and motor response is elicited. The proper position of the needle stimulator could also be checked by fluoroscopy. It is not uncommon for two different needle stimulators to lodge into the same foramen despite their distance on the skin (Fig. 91.9). After confirmation of the proper placement of the needle, a nick is made in the skin to allow for easier passage of the wider introducer. In addition to the foramen needle, the set-up for stage I includes the directional guide and the introducer assembly (Fig. 91.10). The introducer, with the obturator in place, is inserted coaxially over the directional guide wire (Fig. 91.11). Lateral fluoroscopy is required to determine the depth to which to insert the introducer. Once at the correct depth, the obturator is removed, leaving the introducer sheath within the S3 foraminal canal. The tined lead, with four plastic collapsible projections, is inserted into the sheath under lateral fluoroscopic guidance
The desired response and localization for electrical stimulation of the LUT should include S3 responses.
surgical approach Implantation of SNS consists of two steps: stage I and stage II. Stage I – or the trial step – involves the placement of a stimulation lead next to the dorsal root of S3 for a test period of between 1 and 4 weeks. If the patient’s symptoms under the existing indications for SNS improve more than 50%, then the patient is a candidate to undergo stage II (or permanent step) in which the permanent implantable pulse generator (IPG) unit is implanted in the soft tissue of the patient’s buttock. There is no consensus as to whether one or two implanted S3 leads should be performed as in stage I. Bilateral implantation allows for testing for both the left and right S3 nerve roots. At the time of stage II, the lead that is less efficacious can be removed or remain implanted for possible ‘backup’ in case the lead on the other side fails. Currently, there is no evidence that bilateral simultaneous stimulation has any added benefits to unilateral stimulation. Furthermore, it is not possible to stimulate both wires with one IPG because the IPG is not a dual channel stimulator. One would need to implant two IPGs for bilateral simultaneous stimulation. Nevertheless, bilateral implantation allows for a more complete evaluation and possibly offers the patient a higher chance of responding to sacral neurostimulation.
Figure 91.8. Lateral fluoroscopy view shows the proper site of needle stimulation in the S3 and S4 foramen.
Figure 91.9. Lateral fluoroscopy view shows convergence of two needles into the S3 foramen. 1279
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Figure 91.10. Set-up for stage I sacral neuromodulation, including directional guide, tined lead, foramen needle, and introducer assembly.
Figure 91.12. Placement of quadripole chronic lead through the introducer sheet. (Reproduced from ref. 21 with permission.)
Figure 91.11. Placement of introducer sheet over the directional guide. (Reproduced from ref. 21 with permission.)
Figure 91.13. The tined lead is in the proper position: two to three contact plates of the quadripole lead are resting on the S3 dorsal nerve root.
(Fig. 91.12). The lead has four quadripolar contact points. The position for the lead is such that lead position 1 is ‘straddling’ the ventral S3 foramen, i.e. half of lead position 1 is anterior and the other half is posterior to the ventral sacral cortex (Fig. 91.13). To test for proper motor and sensory responses in the patient, the sheath will be moved back to a white line marked on the lead by the manufacturer to expose all quadripolar contact points, but without engaging the plastic projections. Once stimulation confirms proper sensory and motor responses, the sheath is removed completely, allowing the plastic projections to engage the soft tissues and thus anchor the lead. Using a tunneler device supplied in the manufacturer’s kit, the tunneler is passed from the exit point of the tined lead to the right upper buttock incision, and the
proximal tip of the lead is connected to an extension cable. The connection is covered with a boot. The proximal tip of the extension cable is then passed subcutaneously to the contralateral buttock and is exited via a stab incision. Passing the extension wire to the contralateral side is performed in order to minimize the risk of infection. The incision sites are closed appropriately. Over the next 1–4 weeks, the patient is sequentially stimulated (one S3 at a time in case of bilateral implantation) via an external stimulator connected to the external extension to determine optimum bladder response (Fig. 91.14). The lead on the side giving the best response will be connected to the IPG during stage II surgery. In this step, the existing extension cable is removed and the proximal tip of the quadripole lead is connected to the IPG unit which is buried in the existing subcutaneous pocket
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Future pocket site
Percutaneous extension exit site
Connection of lead and percutaneous extension
Lead
Lead extension
Connection of lead and lead extension
Lead
Anchor
Figure 91.14. Stage I sacral neuromodulation: the external stimulator is connected to the chronic lead for the test period.
Figure 91.15. Stage II sacral neuromodulation: the implantable pulse generator unit is placed in the subcutaneous pocket.
(Fig. 91.15). The programming of the IPG unit can be done extracorporeally. A hand-held device also allows the patient to adjust the intensity of the IPG stimulation or control its on/off function (Fig. 91.16).
ClINICal ResUlTs The reported outcomes of SNS usually include the response of patients to stage I (test stage) and to stage II (permanent implantation). The evidence reported in the medical literature is limited to data reported in clinical trials, specifically excluding expert opinion. The International Consultation on Incontinence has adopted the Oxford level of evidence as the following categories: 1. Level 1 – usually involves meta-analysis of randomized clinical trials (RCTs). 2. Level 2 – includes ‘low’ quality RCTs or meta-analysis of good quality prospective ‘cohort studies’. These may include a single group when individuals who develop the condition are compared with others from within the original cohort group. There can be parallel cohorts, where those with the condition in the first group are compared with those in the second group. 3. Level 3 – evidence includes: • good quality retrospective ‘case-control studies’ where a group of patients who have a condition are matched appropriately (e.g. for age, sex, etc.)
Figure 91.16. The programming equipment for the implantable pulse generator unit. with control individuals who do not have the condition; • good quality ‘case series’ where a group of patients, all with the same condition/disease/ therapeutic intervention, are described, without a comparison control group. 4. Level 4 – evidence includes expert opinion where the opinion is based not on evidence but on ‘first principles’ (e.g. physiologic or anatomic) bench research. The process can be used to give ‘expert opinion’ or greater authority. 1281
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Reports of clinical trials on three indications of urge incontinence, urgency frequency, and urinary retention Currently, SNS has been approved by the FDA for three indications: urge incontinence, urgency frequency, and non-obstructive urinary retention. However, SNS has also been reported to be used for other ‘off label’ indications, such as neurogenic bladders in multiple sclerosis, interstitial cystitis, and chronic pelvic pain. There are also reports regarding the possible benefits of bilateral SNS. The majority of the reports on the non-formally indicated usages of SNS appear in the form of abstracts or case series. The initial report on the efficacy of SNS in the treatment of refractory urinary urge incontinence was published in 199923 (Level 2, as no placebo or sham control was used). This study reported on the treatment of 76 patients with refractory urinary urge incontinence from 16 contributing worldwide centers. The patients were randomized either to immediate implantation or to a control group with delayed implantation for a 6-month period. At 6 months, the number of daily incontinence episodes, severity of episodes, and absorbent pads or diapers replaced daily due to incontinence was significantly reduced in the stimulation group compared to the delayed group. Of the 34 stimulation group patients, 16 (47%) were completely dry, and an additional 10 (29%) demonstrated a greater than 50% reduction in incontinence episodes. The interesting finding was that during the therapy evaluation, the group returned to the baseline level of incontinence when the stimulation was inactivated. Complications were site pain of the stimulator implantation in 16%, implant infection in 19%, and leak migration in 7%. The use of SNS in urgency frequency was first reported in 2000.24 Similar to the previous design, 51 patients from 12 centers were randomized into either an immediate stimulation group or a control group (25 and 26 patients, respectively) (Level 2, as no placebo or sham control was used). Patients were followed for 1, 2 and 6 months, and afterwards at 6-month intervals for up to 2 years. At the 6-month evaluation, the stimulation group showed improvement in the number of voiding dailies (16.9 ± 9.7 to 9.3 ± 5.1), volume per void (118 ± 74 to 226 ± 124 ml), and degree of urgency (rank 2.2 ± 0.6 to 1.6 ± 0.9). In addition, significant improvement in quality of life was demonstrated, as measured by the SF-36 questionnaire. The first report on the use of SNS in urinary retention was published in 2001.25 In this study 177 patients with urinary retention refractory to conservative ther-
apy were enrolled from 13 worldwide centers between 1993 and 1998 (Level 2, as no placebo or sham control was used). Thirty-seven patients were assigned to treatment and 31 to the control group, with follow-up at 1, 2, 6, 12, and 18 months. The treatment group showed 69% elimination of catheterization at 6 months and an additional 14% with greater than 50% reduction in catheter volume per catheterization. Temporary inactivation of SNS therapy resulted in significant increases in residual volume, but the effectiveness of central nervous stimulation was sustained for 18 months after implantation. In 2000, a follow-up report on some of these patients was published26 (Level 3). This report showed follow-up results after 3 years in all the improved indications. Of 41 patients, 59% had urinary urge incontinence. Patients showed greater than 50% improvement, with 46% of patients being completely dry. After 2 years, 56% of the urgency frequency patients showed greater than 50% reduction in voids per day, and after 1–1.5 years, 70% of 42 retention patients showed greater than 50% reduction of catheter volume per catheterization. Other studies, generally case series, have published results on the use of SNS following its initial approval (Table 91.1). The results of the use of SNS in the US population were published in 200227 (Level 3). This publication showed the data collected from the US Patient Registry. The report included the use of SNS in 81 patients with all three indications: 27 for urgent continence, 10 with urgency frequency and 10 with urinary retention. In this report, 27 out of 43 patients with urge incontinence, 10 out of 19 with urgency frequency and 10 out of 19 with urinary retention showed improvement of more than 50%. The results of an Italian registry were published in 200128 (Level 3). This report included the details of 196 patients – 46 males and 150 females – for idiopathic urinary retention. Fifty percent of patients stopped catheterization and another 13% catheterized once a day at 1 year after implantation. At 12-month follow-up, 50% of patients with hyperreflexia had less than one incontinence episode daily and the problem was completely solved in 66 patients. Of the patients with urge incontinence, 39% were completely dry and 23% had less than one incontinence episode daily. In Norway, the results of users of this modality were published in 200229 (Level 3). The authors reported the first 3 years’ experience with 53 patients: 45 women and 8 men. This study showed similar results to previous studies.
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Table 91.1.
Published reports of use of SNS in various conditions of lower urinary tract dysfunction Patients with UI
Study
Total
Cured
>50%
Improved
US National Patient Register
81
27/43
Amundsen & Webster40
12
12/12
Hedlund et al.
14
13/14
8/14
Bosch & Groen41
45
27/45
18/45
Shaker & Hassouna42
18
12/18
8/18
112
21/41
19/41
10/34
26/34
29
26
Siegel et al.
23
Schmidt et al.
34
Grunewald et al.37
39
25
Jonas et al.
16/34
Patients with U/F
Patients with UR
>50%
>50%
Hassouna et al. 30
Aboseif et al.
Improved
Follow-up
10/19
2/12
16/29
13/18
25
5/29
29/42
24/42
16/34
18 m
18/21
29 24
Improved
10/19
20/29
18 m
14/25
32
12 m 18/20
2/20
24 m
UI, urinary incontinence; U/F, urgency frequency; UR, urinary retention.
Urinary retention Aboseif et al.30 reported on the use of SNS in functional urinary retention (Level 3). Thirty-two patients were evaluated and underwent temporary PNE. Those that had at least a 50% improvement in symptoms during the test period underwent permanent generator placement. All patients who went to permanent generator placement were able to void spontaneously. There was both an increase in voided volume (48–198 ml) and a decrease in post-void residual (315 to 60 ml), and 18 of 20 patients reported a greater than 50% improvement in quality of life.
been FDA approved for use in refractory overactive bladder (Fig. 91.17).
Method A 34-gauge stainless steel needle is placed about 5 cm cephalad to the medial malleolus and the needle is advanced posterior to the tibia. Once in place, a ground pad is placed on the calcaneus. A stimulator is then
Other indications Use of SNS for other off-labeled applications has been reported for treatment of refractory interstitial cystitis, chronic pelvic pain, pediatric voiding dysfunction, and neurogenic lower urinary dysfunction seen in multiple sclerosis.31 None of the reported case series (level 4) has led to new approved indications for SNS at the time of writing.
Peripheral nerve stimulation In 1987, Stoller et al. reported that stimulation of the peripheral tibial nerve in pig-tailed monkeys was able to inhibit bladder instability32 (Level 3). This initial work led to its use in patients with refractory overactive bladder. The Stoller afferent nerve stimulator (SANS) has
Figure 91.17. SANS device for percutaneous neurostimulation. 1283
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connected to the needle and the ground pad. With the stimulator on, flexion of the great toe indicates the correct needle position. Thirty-minute treatments then take place once a week for 10–12 weeks.
Results In 2000, Klinger et al. performed a prospective trial on 15 patients with urgency frequency syndrome.33 They underwent 12 stimulations with the SANS device (Level 3). Ten patients responded with a reduction in voiding frequency per day (16 to 4) and daily leakage episodes (4 to 2.4). The single complication was a hematoma at the puncture site. Govier et al.,34 in a multicenter study (Level 3), reported on the efficacy of SANS in 53 patients. All patients had refractory overactive bladder and were seen at five different sites in the US. After a 12-week stimulation, 71% of patients had at least a 25% decrease in daytime or night-time frequency. No adverse effects were noted.
COMPlICaTIONs A number of reports have been published on the complications of SNS.23,25,26,35 The earlier reports describe the complications with PNE which is no longer used in the majority of centers in the US. Siegel et al. summarized the complications in patients with refractory urge incontinence, urgency frequency and urinary retention that were included in the original trials of SNS.26 The complications were divided into those that were percutaneous test stimulation related and those that were post-implant related. Of the 914 test stimulation procedures performed on the 581 patients, 181 adverse events occurred in 166 of these procedures (18.2% of the 914 procedures). The vast majority of complications were related to lead migration (108 events, 11.8% of procedures). Technical problems and pain represented 2.6% and 2.1% of the adverse events. For the 219 patients who underwent implantation of the InterStim® system (lead and generator), pain at the neurostimulator site was the most commonly observed adverse effect at 12 months (15.3%). Surgical revisions of the implanted neurostimulator or lead system were performed in 33.3% of cases (73 of 219 patients) to resolve an adverse event. These included relocation of the neurostimulator because of pain at the subcutaneous pocket site and revision of the lead for suspected migration. Explant of the system was performed in 10.5% for lack of efficacy.1 Everaert et al. reported on complications related to SNS itself. Among the 53 patients who had undergone implantation of the quadripolar electrode (InterStim®
Model 3886 or 3080) and subcutaneous pulse generator in the abdominal site (InterStim® Itrel 2, IPG) between 1994 and 1998, device-related pain was the most frequent problem, occurring in 18 of the 53 patients (34%), and occurred equally at all implantation sites (sacral, flank or abdominal).36 Pain responded to physiotherapy in eight patients; no explantation was given for this pain. Current-related complications occurred in 11%. Fifteen revisions were performed in 12 patients. Revisions for prosthesis-related pain (n=3) and for late failures (n=6) were not successful. Grunewald et al. reported their results after 4 years of use of SNS.37 Complications requiring surgical revisions occurred in 11 of the 37 implanted patients (29.7%). They included infections in three cases (8.1%), lead migration in two cases (5.4%), pain at the site of the implanted pulse generator in three cases (8.1%), and a lead fracture, an electrode insulation defect and skin erosion at the site of the impulse generator in one case (2.7%). Hijaz and Vasavada reported the complications of our group at the Cleveland Clinic Foundation (CCF).35 Of the 180 stage I procedures performed for indications of refractory overactive bladder, idiopathic and neurogenic urinary retention, and interstitial cystitis, 130 (72.2%) proceeded to stage II implantation of the implantable pulse generator. In this group, 59 stage I leads were explanted (27.8%). The majority of lead explants were performed for unsatisfactory or poor clinical response (46/50; 92%), with the remainder being carried for infection (4/50; 8%). Stage I revisions comprised 22 of the 180 stage I (12.2%) procedures. Revisions were done for marginal response (13/22), frayed subcutaneous extension wire (6/22), lead infection (3/22) and improper localization of stimulus (1/22). Eleven (50%) of the revisions proceeded for stage II generator implant. When the revision was done for a marginal response (13/22), the response was ultimately clinically satisfactory in 5/13 (38.5%) and they proceeded to generator implant. For stage II complications, explants were performed in 16/130 (12.3%) of the CCF group. Explants were carried out for infection and failure to maintain response in 56.3% and 43.7% of cases, respectively. Revisions were performed for infection, and mechanical (generator related) and response causes. The revision rate with stage II was 20% (26/130). In summary, stage I complications can lead to either explants or revision of the tined lead. The reasons for either cause could be related to patient response, mechanical failure or infection. Explants for response reasons should not truly be considered a complication as much as it is an integral part of the procedure. Stage
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II complications are also seen for decay of response, mechanical or infection reasons. Table 91.2 summarizes the common complications of SNS reported in several series. Hijaz and Vasavada have also presented algorithms for trouble-shooting of SNS problems.35 When infection at the generator site is diagnosed, the best management would be explanation of the whole system. Despite attempts to salvage some of these patients, follow-up revealed that the infection persisted in all and eventual explant was inevitable. Trouble-shooting algorithms include search for causes of: 1) pocket (IPG site) discomfort; 2) recurrent symptoms; 3) stimulation occurring in the incorrect pelvic area; 4) no stimulation; and 5) intermittent stimulation.
fUTURe DIReCTIONs The initial success of SNS in treatment of some of the most bothersome conditions of the bladder has entered the electrical stimulation of the LUT into the therapeutic armamentarium of physicians dealing with those conditions. Subsequently, entry of this therapy has introduced new lines of research to enable us to answer many open and unresolved questions related to various issues of SNS in clinical practice. Daneshgari and Abrams compiled a list of the pertinent research questions that, in the opinion of several experts in the area of SNS, need to be addressed. These research questions include the following:
• Clinical predictors of responders: It is highly desirable to predict, with a reasonable level of accuracy, the potential response of patients to SNS, thus avoiding the test trial.
The BION® DevICe In search for a smaller, less invasive, and more selective electrical stimulation of the bladder, use of the BION® device in two forms – radiofrequency-activated BION® (RF BION®) and rechargeable BION® (BION-R®) – have been reported. The BION® device is a self-contained, battery-powered, telemetrically programmable, current-controlled mini-neurostimulator with an integrated electrode. It has a size of 27 × 3.3 mm and weighs only 0.7 g. It can be implanted adjacent to the pudendal nerve at Alcock’s canal (Fig. 91.18).38,39 The results of the BION® pilot studies indicate that a considerable reduction in the degree of detrusor overactivity incontinence can be obtained in severely refractory cases, including women who had failed sacral nerve neuromodulation. The described technique is well tolerated by the patients. It is minimally invasive and relatively simple. Clinical trials of the BION-R® device involving larger numbers of patients are currently underway in the US and Europe.
Table 91.2.
Figure 91.18. BION® device. (Reproduced from ref. 16 with permission.)
Summary of common complications of SNS
Number of patients PNE – Overall
Siegel et al.26
Everaert et al.36
Grunewald et al.37
Hijaz & Vasavada35
581
53
37
167
N/A
N/A
N/A
18.02%
Stage I – Overall
N/A
N/A
N/A
12.2%
Stage II – Overall
N/A
N/A
29.7%
20%
15.3%
34%
8.1%
N/A
8.4%
N/A
5.4%
N/A
6.1%
N/A
8.1%
33.3%
23%
29.7%
Pain at neurostimulator site Suspected lead migration Infection Revision of permanent SNS
10.7% 20%
N/A, not applicable; PNE, peripheral nerve stimulation; SNS, sacral nerve stimulation.
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• A comparison between the effects of continuous
• • • • •
versus intermittent stimulation with the aim of improving the percentage of patients benefiting from SNS. Whether a unilateral versus a bilateral stimulation in either category of the current indications would lead to an improved and more durable response. Comparing the effects of direct pudendal nerve stimulation versus SNS in patients with refractory overactive bladder. Functional brain imaging of responders and failures after implant of SNS to study possible differences in CNS effects of SNS in these two groups. Animal models to better delineate mechanisms of action for neuromodulation (i.e. neurotransmitters). Longitudinal studies to better understand the interaction between genitourinary, gastrointestinal and gynecologic complaints.
As in other areas in medicine, we are looking for those sparks of success that will lead to creative fires of expanding knowledge. But we also need to respect the well-established integrity of our field by being true to our clinician-investigative tools such as properly designed clinical trials as we protect and explore the increasing territory of electrical stimulation of the lower urinary tract.
RefeReNCes 1. Madersbacher H. [Conservative therapy of neurogenic disorders of micturition]. Urologe A 1999;38:24–9. 2. Cranefield P. Bibliography. Mount Kisco: Futura Publishing, 1974; 30. 3. Bell C. Idea of a new anatomy of the brain; submitted for the observations of his friends. London: Strahan and Preston, 1811; 136. 4. Magendie F. Expériences sur les fonctions des racines des nerfs rachidiens. Journal de Physiologie Expérimentale et Pathologique 1822;2:276. 5. Hall M. On the reflex function of the medulla oblongata and medulla spinalis. Phil Trans 1833; 635.
9. Caldwell KP. The electrical control of sphincter incompetence. Lancet 1963;2:174–5. 10. Nashold BS Jr, Friedman H, Boyarsky S. Electrical activation of micturition by spinal cord stimulation. J Surg Res 1971;11:144–7. 11. Nashold BS Jr, Friedman H, Glenn JF et al. Electromicturition in paraplegia. Implantation of a spinal neuroprosthesis. Arch Surg 1972;104:195–202. 12. Schmidt RA, Bruschini H, Tanagho EA. Sacral root stimulation in controlled micturition. Peripheral somatic neurotomy and stimulated voiding. Invest Urol 1979;17:130–4. 13. Tanagho EA, Schmidt RA. Bladder pacemaker: scientific basis and clinical future. Urology 1982;20:614–9. 14. Tanagho EA, Schmidt RA. Electrical stimulation in the clinical management of the neurogenic bladder. J Urol 1988;140:1331–9. 15. Tanagho EA, Schmidt RA, Orvis BR. Neural stimulation for control of voiding dysfunction: a preliminary report in 22 patients with serious neuropathic voiding disorders. J Urol 1989;142:340–5. 16. Leng WL, Chancellor MB. How sacral nerve stimulation neuromodulation works. Urol Clin North Am 2005;32:11–18. 17. Siegel SW. Selecting patients for sacral nerve stimulation. Urol Clin North Am 2005;32:19. 18. Chai TC, Mamo GJ. Modified techniques of S3 foramen localization and lead implantation in S3 neuromodulation. Urology 2001;58:786–90. 19. Spinelli M, Giardiello G, Gerber M et al. New sacral neuromodulation lead for percutaneous implantation using local anesthesia: description and first experience. J Urol 2003;170:1905–7. 20. Hohenfellner M, Schultz-Lampel D, Dahms S et al. Bilateral chronic sacral neuromodulation for treatment of lower urinary tract dysfunction. J Urol 1998;160:821–4. 21. Chai TC. Surgical techniques of sacral implantation. Urol Clin North Am 2005;32:27–35. 22. Janknegt RA, Hassouna MM, Siegel SW et al. Long-term effectiveness of sacral nerve stimulation for refractory urge incontinence. Eur Urol 2001;39:101–6.
6. Fandel T, Tanagho EA. Neuromodulation in voiding dysfunction: a historical overview of neurostimulation and its application. Urol Clin North Am 2005;32:1–10.
23. Schmidt RA, Jonas U, Oleson KA et al. Sacral nerve stimulation for treatment of refractory urinary urge incontinence. Sacral Nerve Stimulation Study Group. J Urol 1999;162:352–7.
7. Boyce WH, Lathem JE, Hunt LD. Research related to the development of an artificial electrical stimulator for the paralyzed human bladder: a review. J Urol 1964;91:41–51.
24. Hassouna MM, Siegel SW, Nyeholt AA et al. Sacral neuromodulation in the treatment of urgency-frequency symptoms: a multicenter study on efficacy and safety. J Urol 2000;163:1849–54.
8. Dees JE. Contraction of the urinary bladder produced by electric stimulation. Preliminary report. Invest Urol 1965;15:539–47.
25. Jonas U, Fowler CJ, Chancellor MB et al. Efficacy of sacral nerve stimulation for urinary retention: results 18 months after implantation. J Urol 2001;165:15–9.
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26. Siegel SW, Catanzaro F, Dijkema HE et al. Long-term results of a multicenter study on sacral nerve stimulation for treatment of urinary urge incontinence, urgency-frequency, and retention. Urology 2000;56:87–91.
35. Hijaz A, Vasavada S. Complications and trouble shooting of sacral neuromodulation therapy. Urol Clin North Am 2005;32:65–9.
27. Pettit PD, Thompson JR, Chen AH. Sacral neuromodulation: new applications in the treatment of female pelvic floor dysfunction. Curr Opin Obstet Gynecol 2002;14:521–5.
36. Everaert K, De Ridder D, Baert L et al. Patient satisfaction and complications following sacral nerve stimulation for urinary retention, urge incontinence and perineal pain: a multicenter evaluation. Int Urogynecol J Pelvic Floor Dysfunct 2000;11:231–5.
28. Spinelli M, Bertapelle P, Cappellano F et al. Chronic sacral neuromodulation in patients with lower urinary tract symptoms: results from a national register. J Urol 2001;166:541–5.
37. Grunewald V, Hofner K, Thon WF et al. Sacral electrical neuromodulation as an alternative treatment option for lower urinary tract dysfunction. Restor Neurol Neurosci 1999;14:189–93.
29. Hedlund H, Schultz A, Talseth T et al. Sacral neuromodulation in Norway: clinical experience of the first three years. Scand J Urol Nephrol Suppl 2002;210:87–95.
38. Bosch R. Treatment of refractory urge urinary incontinence by a novel minimally invasive implantable pudendal nerve mini-stimulator. J Pelvic Med Surg 2003;9:310.
30. Aboseif K, Tamaddon K, Chalfin S et al. Sacral neuromodulation in functional urinary retention: an effective way to restore voiding. BJU Int 2002;90:662–5.
39. Grill WM, Craggs MD, Foreman RD et al. Emerging clinical applications of electrical stimulation: opportunities for restoration of function. J Rehabil Res Dev 2001;38:641–53.
31. Bernstein AJ, Peters K. Expanding indications for neuromodulation. Urol Clin North Am 2005;32:59–63. 32. Stoller M, Copeland S, Millard R. The efficacy of acupuncture in reversing the unstable bladder in pig-tailed monkeys [abstract]. J Urol 1987;137:104A. 33. Klinger H, Pycha A, Schmidbauer J, Marberger M. Use of peripheral neuromodulation for treatment of detrusor overactivity: a urodynamic-based study. Urology 2000;56:766. 34. Govier FE, Litwiller S, Nitti V et al. Percutaneous afferent neuromodulation for the refractory overactive bladder: results of a multicenter study. J Urol 2001;165:1193–8.
40. Amundsen CL, Webster GD. Sacral neuromodulation in an older, urge-incontinent population. Am J Obstet Gynecol 2002;187(6):1462–5; discussion 1465. 41. Bosch JLHR, Groen J. Sacral nerve neuromodulation in the treatment of patients with refractory motor urge incontinence: long-term results of a prospective longitudinal study. J Urol 2000;163:1219–22. 42. Shaker HS, Hassouna M. Sacral nerve root neuromodulation: an effective treatment for refractory urge incontinence. J Urol 1998;159(5):1516–9.
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92 Complex reconstructive surgery Christopher R Chapple, Richard T Turner-Warwick
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INTRODUCTION Complex reconstructive surgery may be more appropriately considered as surgical restoration of lower urinary tract function. Preoperative evaluation relies upon accurate functional assessment and hence knowledge and understanding of the principles and practice of urodynamic investigation. An appreciation of lower urinary tract anatomy and pelvic surgery with some understanding of both gynecologic and urologic pathology is essential. The basic surgical principles are those underlying any form of successful surgical reconstruction, namely an understanding of anatomy and function with attention to excision of ischemic tissue, obliteration of dead space, interposition of vascularized tissue, avoidance of infection and hematoma, and tension-free anastomosis. The term ‘reconstructive surgery’ inspires images of difficult and esoteric surgical practice best confined to specialist centers. While there is no doubt that subspecialization increases the success of such surgery, the basic underlying principles are fundamental to the practice of all surgery, namely: 1. a detailed knowledge of normal anatomy and a clear definition of abnormal radiology; 2. comprehensive and appropriate assessment of upper and lower urinary tract function; 3. good surgical technique, with good access and exposure, and a full appreciation of available surgical techniques. In this brief exposition on the subject, it is the intention to consider areas in urogynecologic practice where functional and anatomic reconstruction is important; for example, where there is damage to the ureter, the bladder or urethra, and the important area of surgical resolution of severe detrusor overactivity which has proved resistant to conventional therapy.
URETERIC INJURY The ureter is an elastic and well-protected structure lying in the retroperitoneal space. Injury from external trauma is therefore uncommon, the majority of injuries being iatrogenic in origin. Although ureteral injuries account for only a small proportion of all urologic pathology, being the sole conduit from the kidney, ureteric integrity is essential for normal renal function. Such injuries therefore demand careful appraisal and timely intervention.
Iatrogenic ureteric injury As a number of iatrogenic ureteric injuries may never
become clinically apparent, the true incidence of injury is therefore difficult to estimate. The incidence of clinical ureteric injury in routine gynecologic surgery has been reported to vary from 0.2 to 1.5% in retrospective studies.1–5 This rises to 2.5% for prospective studies where postoperative urograms are carried out and up to 30–35% when radical pelvic surgery is involved.6–10 In a large study by Goodna et al., the incidence of ureteric injuries involving 4665 surgical operations was noted to be 0.4%, a figure which has not changed significantly over the years.2,11 In most series, gynecologic surgery accounts for about two-thirds of iatrogenic ureteral injuries. Most are related to abdominal, radical or vaginal hysterectomy, ovarian tumor surgery, and incontinence surgery. Non-gynecologic causes of iatrogenic injuries include colorectal surgery (15%), ureteroscopic surgery (2–17%), vascular surgery (6%), laminectomy/spinal fusion (1%), bladder neck suspension procedures (3%), appendicectomy (1%), and cesarean section (1%).12 Rare causes of ureteral injury following procedures such as open herniorrhaphy, CT-guided chemical sympathectomy, termination of pregnancy, and Kirschner wire application for hip dislocation in a child have also been reported.13–16 In recent years, with the development and proliferation of new laparoscopic techniques, there has been a significant increase in associated injuries, especially in gynecology, where laparoscopy now accounts for 25% of all gynecologic injuries to the ureter.17 This rise parallels the rise of ureteral injuries associated with a similar expansion in endoscopic approaches to complex ureteric problems in urologic practice. In a recent review by Selzman and Spirnak of 165 ureteric injuries, urologic surgery accounted for 42% of the total compared with 34% for gynecologic surgery and 24% for general surgery. The bulk of injuries to the ureter in this series followed endoscopic urologic surgery (79%) compared to gynecologic surgery and general surgery where the majority of ureteral injuries occurred during open procedures.18
Risk factors for iatrogenic ureteric injuries Previous surgery, bulky or invasive tumors, ureteric duplication and ectopic ureters, endometriosis, retroperitoneal fibrosis and inflammatory conditions such as chronic pelvic infection all predispose to iatrogenic ureteric injury. Situations when life is threatened due to hemorrhage, or during emergency cesarean section when speed becomes critical, can also predispose to iatrogenic ureteric injury.
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Types of iatrogenic injury 1. Avulsion: Avulsion occurs when forceful retraction is used, especially when tissues are soft as a result of infection or necrosis. 2. Transection: This is caused by the scissors or scalpel, especially when the ureters are enveloped within tumor or fibrous tissue. Common sites of such injuries during gynecologic surgery include: • the pelvic brim where the vascular pedicle to the ovary is in close proximity to the ureter; • the broad ligament where the ureter is crossed by the uterine artery; • the ureteric canal in the cardinal ligament, 1 cm lateral to the supravaginal cervix and 1 cm above the lateral vaginal fornix. In surgery of the rectum and sigmoid colon, the left ureter is more commonly involved in iatrogenic ureteric injury. Invasive tumor, dense fibrosis, and inflammatory conditions all contribute to ureteric trauma, even in the hands of experienced surgeons. Retrocecal appendicitis has been known to result in similar iatrogenic ureteric injuries on the right. During vascular surgery, ureteric injury can occur with aortoiliac and aortofemoral bypass. Predisposing factors include retroperitoneal fibrosis, radiation exposure, long-term ureteral stents, graft infections or graft dilation. 3. Ligation: This occurs when the ureters are mistaken for bleeding vessels. It can also occur during vaginal hysterectomy when the uterine arteries are being ligated, and in procidentia when the ureters prolapse with the uterus. 4. Crushing: This may occur when clamps are used blindly to control hemorrhage and is seen at sites similar to transection injury, especially during radical hysterectomy for cancer. Necrosis and ultimately stricture or fistula formation can result. 5. Devascularization: This occurs when extensive or overenthusiastic dissection of the ureter is performed. The ureter is supplied in 80% of individuals by a single artery along its entire length with anastomotic feeding vessels at each end and in the middle. Devascularization results in ischemic necrosis which ultimately leads to fistula or stricture. 6. Perforation: This is commonly caused by ureteroscopy and associated endoscopic manipulation for ureteric stones. Edematous tissue surrounding the stone and tissue traumatized by lithotripsy are predisposing factors. Needle injury during open surgery may result in perforation but is rarely a cause of problems in healthy tissues.
7. Fulguration: This can occur during transurethral resection of bladder cancers resected close to the ureteric orifices and then extensively diathermied. Laparoscopic diathermy and laser treatment of endometriotic lesions are an increasingly important cause of thermal injury to the urinary tract that has seen an increase in parallel with the rise of laparoscopic surgery in gynecology. 8. Fistula formation: This can follow transection, ischemic necrosis or perforation if the distal end of the ureter is not in continuity or is obstructed. Urine will then discharge from the vagina, operative wound or drain site, or into the peritoneal cavity or retroperitoneal space. 9. Stricture formation: This can follow any of the above injuries and ultimately lead to obstruction of the ureters, hydronephrosis, and renal damage.
Non-iatrogenic ureteric injury Non-iatrogenic ureteric injuries are uncommon, but are found in 2.3–17% of cases of penetrating abdominal trauma, most commonly gunshot or stab wounds.19 Associated injuries to the colon, duodenum, pancreas, and great vessels make such injuries potentially life threatening. Blunt or avulsion injuries are very rare, most commonly occurring after a fall from a height or being thrown from a car. Severe compression injuries such as those related to the steering wheel and seat belts can also cause ureteric injuries which may even present with a soft non-tender abdomen. Most blunt trauma involves the pelviureteric junction and often presents late with a ureteric fistula or urinoma as a result of an avulsion injury.20,21 Radiation injury to the ureters is rare and can occur in radiotherapy for cervical, bladder, rectal, and other pelvic tumors. Most post-irradiation ureteric strictures, however, are due to recurrent tumor. Presentation may be from 3 months up to 10 years, usually with a long thread-like stenotic lesion or a localized constriction about 4–6 cm from the bladder. These are thought to be due to endarteritis obliterans resulting from radiotherapy. Subsequent surgery on such poor quality tissues also predisposes to a higher complication rate involving the ureters.22
Presentation Approximately 15–25% of iatrogenic ureteric injuries during open surgery are discovered intraoperatively. The majority present postoperatively, delays in diagno1291
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sis being the rule rather than the exception. Delays can vary from 2 days to 12 years.23–27 Early signs of ureteral injuries are subtle and usually missed, the injury being discovered several days or weeks later when a complication occurs. In urologic surgery, however, where injury is most commonly associated with ureteroscopic procedures for stone disease, 77% are diagnosed intraoperatively. Of these ureteric injuries, 91% occur in the lower third, 7% in the middle third and 2% in the upper third. Penetrating injuries involving the ureter usually present with associated injuries and in most cases are identified intraoperatively during exploration of the wound. Gross hematuria is present in approximately one-third of the patients, whereas about another third do not have any blood on urinalysis at all.20,21,28,29
Diagnosis Ureteric injuries recognized intraoperatively and repaired immediately carry a better prognosis of cure than those which become manifest postoperatively as a result of complications.18,23,25,30 In a recent review of 165 ureteral injuries by Selzman and Spirnak, the number of procedures required to repair urologic injuries was 1.2 for those diagnosed intraoperatively compared to 1.6 for those diagnosed postoperatively.18 Seventy-seven percent of urologic injuries were diagnosed intraoperatively compared to 16% in gynecologic surgery and 56% in general surgery. This difference is due mainly to the different procedures that cause such injuries in these specialties in addition to the greater familiarity with ureteric anatomy amongst urologists. A high index of suspicion is required for the diagnosis of iatrogenic ureteric injury in the immediate postoperative period, especially in non-urologic operations. Fever is a common feature after any surgery; however, if persistent, it may be a sign of urinary sepsis which occurs in 10% of those with ureteric obstruction. Flank pain occurs in 36–90% of cases of hydronephrosis.25,27,31 Fistulae of the vagina and skin tend to present 7–10 days after surgery with urinary leakage.23–25,27,31 Those involving the peritoneum may leak urine from the wound or drains. An abdominal and pelvic mass, urinoma or pelvic abscess may also result. Malaise and gastrointestinal upset or ileus are often accompanying features. These do not settle spontaneously and an abdomen distended as a consequence of ileus and supposed ‘ascites’ should raise the suspicion of urinary leakage. Excessive wound drainage or leakage per vaginam may be collected, analyzed, and its electrolytes compared with those in the patient’s urine to establish the likely origin of this fluid.
Inevitably, ureteric injuries must first be suspected if they are to be detected. An intravenous urogram (IVU) is mandatory whenever ureteric injury is suspected. This will usually demonstrate the site of injury as well as associated pathology such as hydronephrosis and ureteric fistulation. Should an IVU be inconclusive, cystoscopy and retrograde pyelogram or antegrade nephrostogram is often useful; higher concentrations of contrast in these studies allow demonstration of leakage and establish the diagnosis in most cases. Following penetrating trauma, the ureters should be explored if injury is suspected. IVUs using high doses of contrast have not been helpful and, in a series of 12 patients with penetrating injuries of the ureter, only 25% were diagnosed on IVU.19 Features such as extravasation of contrast, ureteral obstruction, deviation, dilation or non-visualization are diagnostic. In 75% of such cases, IVU demonstrated only kidney presence and function.19–21 Conversely, direct exploration of the ureter and the use of indigo carmine dye intraoperatively provided the diagnosis in 83% of cases.19 CT scans are of limited value in demonstrating ureteral injuries per se but may be helpful when extravasation is seen or when urinomas have developed. The primary role of CT remains in the assessment of other associated abdominal and pelvic injuries. The absence of hematuria in a third of ureteral injuries and a negative IVU in about three-quarters of penetrating ureteral injuries implies that, in such cases – even in the presence of a negative preoperative diagnostic radiology – the suspicion of ureteric injury warrants exploration.20,21,28 Following blunt trauma, delays in diagnosis are relatively common due to the lack of early characteristic features and the association of other severe life-threatening injuries warranting more immediate attention.
Prevention Iatrogenic injuries are best managed by preventive rather than corrective measures. Avoidance of ureteric injury is invariably the principle of all good surgical practice and begins with a thorough knowledge of the course of the ureters, the nature and site of potential ureteric injuries, and adequate preoperative evaluation. This may include an IVU or contrast-enhanced CT scans to define anatomy if major pelvic or retroperitoneal surgery is planned. A preoperative IVU allows for comparative studies should a postoperative IVU become necessary. However, preoperative IVUs have not been shown to be of value prior to routine hysterectomy and cannot sub-
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stitute for good surgical technique and identification of anatomic landmarks.32,33 Congenital anomalies, ectopic ureters, and ureteric duplications should be recognized in advance and may be defined on preoperative imaging. Where radical surgery is being carried out and the ureters are involved or displaced by the pathology, their course should be mapped and the necessary precautions taken. Preoperative, or more commonly intraoperative placement of ureteric catheters may facilitate their identification during difficult anatomic dissection. Such maneuvers should not induce complacency since injuries are known to occur despite the presence of a ureteric catheter.34 Nevertheless, identification of the length of ureter within the operative field should significantly reduce the risk of damage. The ureters are recognized by the glistening appearance of their sheaths, peristalsis on stimulation, and characteristic feel on palpation. Dissection of the ureters may be necessary, especially when in close proximity to resection margins. Sharp dissection along the line of the ureter, incorporating a generous cuff of periureteric adventitia, should reduce the risk of ischemic injury. The close relationship of the uterine artery and the last 3 cm of the ureter makes it vulnerable to injury when mass ligature and blind clamping of an injured artery occurs. Proper identification and isolation of the uterine artery before ligation and digital compression of the internal iliac artery to control hemorrhage can avoid the need for blind clamping. Most unexpected hemorrhage can be controlled by suitable compression of the bleeding point until the ureter is identified. If ureteric injury is suspected during open surgery, indigo carmine dye may be useful in identifying the presence and site of the lesion. Contrast solution with intraoperative imaging is more useful during ureteroscopic procedures. Most ureteroscopic injuries occur during stone extraction and fragmentation. The experience of the urologist has also been shown to be an important risk factor.35 Other important principles in the prevention of ureteroscopic injuries include careful patient selection, availability of good endoscopic instrumentation and the use of intraoperative fluoroscopy. Large and high stones may be better managed by open surgery.
Management of ureteric injury The management of a ureteral injury depends on its extent and location, its etiology, associated injuries, and the time of its discovery.
Timing of surgery Ureteral injuries discovered intraoperatively and repaired immediately have excellent results, probably due to the absence of sequelae following urine leak and complications such as infection.18,36 If the injury is incurred during a ureteroscopic procedure, an internal stent placed retrogradely across the defect may be all that is required. Small perforations usually heal within 1–2 weeks, whereas larger defects and thermal injuries require up to 6 weeks of internal stenting. If immediate stenting is impossible, initial percutaneous nephrostomy and subsequent antegrade placement of the ureteral stent is indicated.17 Injuries diagnosed postoperatively may initially be managed conservatively using nephrostomy drainage and/or subsequent ureteric stenting if the ureteric defect is short (<2.5 cm) and a stent can be passed across the defect, either retrogradely or antegradely.26 About half of all ureteric injuries can be treated by such endoscopic stenting whereas the remainder will require an open procedure for definitive repair. In a series of 165 iatrogenic ureteric injuries, 49% were treated with 6 weeks of internal stenting, 89% showing no evidence of obstruction on follow-up lasting 1–20 years (mean of 8.5 years).18 A further series of 50 ureteric injuries found that endoscopic treatment performed for defects of less than 2 cm required less operating time, had fewer complications, and shorter hospital stays compared with those undergoing open surgery.37 No recurrences were noted over a 2-year follow-up period. However, 14 of the 30 patients selected for endoscopic treatment failed ureteric catheterization and subsequently required open repair (all were ureteric injuries diagnosed after 3 weeks). The authors concluded that endoscopic management of ureteric injuries should be carried out only in those with defects less than 2 cm in length diagnosed within 3 weeks of injury. In a further series of 27 patients, it was reported that percutaneous nephrostomy alone or in conjunction with ureteral stenting was successful in treating 11 (65%) of the 17 ureteral injuries considered suitable for endoscopic stenting.24 As reported by Cormio et al.,37 only one of 20 attempted retrograde ureteric catheterizations was successful in those with delayed diagnoses. All ureteric fistulae required ureteric stenting for healing and percutaneous nephrostomy was successful only in those with demonstrable ureteric obstruction. These cases presumably represent ligation or crush injuries requiring time for dissolution of sutures and tissue healing. Ureteric obstruction persisting after 8 weeks of percutaneous drainage will require open exploration and repair.24 In a series of 20 patients with 1293
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ureteric injuries who had percutaneous nephrostomy with or without a stent as a primary procedure, 80% had spontaneous recovery of the injured ureter without further intervention. Morbidity and re-operation rates were reduced compared with 24 ureteric injuries treated by immediate open ureteric repair.38 For those that require open surgical correction, immediate repair is increasingly shown to have similar if not better results compared with the traditional approach of waiting for 6 weeks to 3 months before definitive repair. A number of series support early surgical intervention within 3 weeks.23,25,26,29,30,39,40 Selzman and Spirnak also found that complications were five times higher in the group treated by delayed compared with immediate repair for urologically injured ureters.18
Open surgical management Ureteral transection is best repaired by immediate spatulated ureteroureterostomy. This should be carried out with a tension-free anastomosis using interrupted absorbable sutures. Sutures should not be too close together in an attempt to achieve a watertight anastomosis, as ischemia and subsequent stricture formation may result. A double ‘J’ stent is often used as a splint and removed between 2 and 6 weeks. Ligation injuries are simply de-ligated but crush injuries may be of greater extent due to ischemia and must be handled carefully.31 If doubt exists as to the viability of the ureter, partial excision and spatulated re-anastomosis may be required (Fig. 92.1). For injuries at or below the pelvic brim, an antireflux ureteroneocystostomy is the treatment of choice, for which various methods have been described. In the event of a gap between the end of the ureter and bladder, extra length can be obtained with a psoas hitch.41 Alternatively a Boari flap may be employed to achieve a tension-free anastomosis42,43 (Fig. 92.2). A graft length to width ratio of 3:2 is necessary, using a vascular pedicle based on the superior vesical artery. As the tubularized flap has no functional activity, the tube should be open-mouthed for adequate drainage.44 The theoretical advantage of the psoas hitch is the better preservation of the blood supply which may be more precarious in the Boari flap. Other practical advantages include the relative ease of closure of the incision in thick-walled bladders. The incision is relatively smaller to produce an equivalent length of tube, thereby facilitating a nonrefluxing reimplantation, and the subsequent ureteric positioning facilitates ureteroscopy. For ureteric defects above the pelvic brim, additional length of ureter of a few centimeters can be obtained by
Figure 92.1. The principle of end-to-end spatulated anastomosis of the ureter with omental wrap around to provide support to the repair. mobilization of the kidney, allowing spatulated ureteroureterostomy. Other options to foreshorten the ureteric course include calicoureterostomy, transureterostomy, and autotransplantation.45–47 If all else fails, nephrectomy is a final resort which, although previously an acceptable form of management for such injuries, is now less acceptable given the other available options. A number of non-biologic ureteral substitutes have been investigated with limited and generally short-lived success. The ileal ureter has proved the most reliable ureteric replacement to date.48,49 The main drawbacks to the use of bowel, as in other bowel replacement surgery, relates to the production of mucus (which can cause obstruction), inadequate peristalsis, anastomotic stricture, and reabsorption of excretory waste products. Consequently, contraindications to ileoureteric substitution include uncorrected bladder outlet obstruction and impaired renal function. Recurrent urinary tract infection and subsequent renal impairment are potential
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Figure 92.2. (a) With the formation of a Boari flap, a flap of bladder is raised; note the ischemic nature of the apex. (b) The ureter is anastomosed. (c, d) The flap is completed. (e) Forming a bladder elongation flap. complications.44 The appendix is an alternative biologic substitute but is of limited length.50 The fallopian tube has been employed but is limited by its relatively small caliber.
Postoperative care and follow-up Postoperative care following surgery for ureteric injuries requires close monitoring of renal function with appro1295
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priate fluid and electrolyte replacement, especially in the presence of postobstruction diuresis. Adequate antibiotic cover, wound care, and prophylaxis against deep vein thrombosis follow standard surgical practice. Meticulous care of catheters and drains is critical, given the dependence of renal function and uneventful postoperative recovery on these devices. Common complications include urinary leakage, infection and hematoma, and complications related to
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Figure 92.2. (cont’d) (f) Mobilizing the flap. (g) The bladder elongation flap easily reaches the pelvic brim, allowing ureteric reimplantation and is well vascularized. It is secured to the psoas muscle. (h) Postoperative cystogram.
drains and catheters. Percutaneous nephrostomy tubes may kink or become displaced due to their awkward locations in the flank. Proper anchoring techniques and after-care are therefore essential. Chronic and recurrent infections can also result from the use of long-term nephrostomy drainage. Alternatively, the use of internal stents may avoid such complications but often causes irritative symptoms and, in the long term, may become encrusted if not changed every 4–6 months. Vesicoureteric reflux
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may occur following reimplantation and may present with recurrent infection and dilation of the pelvicalyceal system. Monitoring of wound drainage and contrast radiography immediately after placement of stents or drains is essential. Tube nephrostograms are useful for diagnostic purposes. A repeat IVU following stent removal and long-term follow-up (including IVU at 6 weeks, and possibly longer) are recommended
Conclusions It is evident that it is important to diagnose ureteral injury as soon as possible and, if identified at the time of surgery, to carry out ureteral stenting (if possible) during endoscopic surgery or direct repair during open surgery. Failing this, a number of open surgical options to foreshorten the course of the ureter are available. If this is not possible, either ureteral substitution or autotransplantation should be considered. Definitive management of ureteric injury diagnosed postoperatively depends on the level and the extent of ureteric loss, its etiology, associated injuries or complications, and time to discovery. The functional status of the kidneys, and the age, condition, and prognosis of the patient are similarly important. Most injuries below the pelvic brim can be treated with a neoureterocystostomy employing a bladder elongation procedure. Mid and upper ureteric injuries above the pelvic brim, however, are more challenging. Small defects above the pelvic brim can be repaired with a spatulated ureteroureterostomy. In cases of extensive ureteral loss, measures such as mobilizing the kidney, transureteroureterostomy, renal autotransplantation, and ureteral substitution using small bowel may be required. Although reconstruction should be attempted whenever possible, in rare situations, based on the general condition of the patient, the function of both kidneys, and the degree of damage to the ureter, nephrectomy may represent the most appropriate management.
LOWER URINARY TRACT FISTULAE Fistulous communications between the bladder or urethra and adjacent structures can be a cause of great distress to the patient. Few patients are more anxious to be cured of their affliction, or are more grateful when this has been accomplished. The vast majority of such fistulae occur in women and follow gynecologic or obstetric trauma – most commonly urinary vaginal fistulae involving the bladder, ureter and, rarely, the urethra. Vesicointestinal communications usually occur as a com-
plication of inflammatory or malignant bowel disease, with the exception of the rare case of the radiation-damaged ‘frozen-pelvis’ following treatment of gynecologic malignancy. Urethrorectal and urethrocutaneous fistulae are the only group that occurs most commonly in men. The subdivision of fistulae into ‘simple’ and ‘complex’ introduces further nomenclature. At first sight this might be considered to unnecessarily complicate matters – but serves a useful purpose in defining the most appropriate surgical approach. Simple fistulae can usually be resolved by a simple closure in layers. More complex cases with associated tissue devascularization, previous failed surgical repair attempts or irradiation, extensive tissue loss or persistence of a focus of infection or malignancy, may require the use of adjunctive procedures. Fistulae arising from a diverse range of etiologies – whether traumatic, surgical, inflammatory, neoplastic or radiation-induced – are almost invariably amenable to surgical repair.
Urinary vaginal fistulae Whatever may be the cause of this distressing affection, it is a matter of serious importance to both surgeon and patient that it be rendered susceptible of cure. Sims 1852.51
Fistulae involving the vagina in undeveloped societies are most commonly associated with obstetric trauma and, as such, have from ancient times represented an important cause of severe morbidity and mortality in young women. In developed countries urinary vaginal fistulae occur most commonly between the bladder and vagina, sometimes involve the ureter, and usually follow gynecologic surgery, occasionally complicating the management of gynecologic malignancy.
Diagnosis The classic symptom of a urinary vaginal fistula is continuous involuntary incontinence following a hysterectomy or other pelvic operation. Nevertheless, where the fistula is small, the presentation may be far less florid, comprising no more than a watery vaginal discharge accompanied by normal voiding. Definition of the precise anatomic abnormality is of paramount importance when planning the most appropriate management of a fistula. The combined use of imaging modalities and a careful examination under anesthetic are essential elements of this process, since in many cases more than one 1297
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structure (e.g. both the bladder and ureter) is involved. In addition, the demonstration of associated functional abnormalities and the presence of malignant disease are important contributory factors which must be considered and investigated prior to undertaking definitive surgery. All patients should have an IVU to assess the number of ureters and to look for the presence of dilation or extravasation from a ureter which would be suggestive of its involvement in the fistula (Fig. 92.3). A voiding cystourethrogram may demonstrate the presence of a fistula and will document any associated vesicoureteric reflux, bladder base prolapse, and stress incontinence which may either relate to the patient’s symptomatology or could be usefully corrected at the time of surgical repair of the fistula. The ‘three-swab test’ (Fig. 92.4) can be helpful in the preoperative assessment. The identification of individual swabs is facilitated by the use of identifying sutures on their ‘tails’. Aqueous methylene blue dye is instilled into the bladder: the demonstration of dye staining of only the swab placed high in the vagina occurs with a vesicovaginal fistula; staining of the lowermost swab alone occurs with urethral leakage, either stress incontinence or a urethrovaginal fistula. Conversely if the uppermost swab is wet but not stained by dye and the lower two are dry, a ureteric fistula is likely. Obviously this test will not delineate the presence of a ureteric fistula in association with a vesical fistula. Cystoscopy, vaginoscopy, and examination under anesthesia (EUA) are essential in all cases and will often
demonstrate small fistulae not demonstrated using other modalities. Where doubt remains as to the exact diagnosis, even at the time of an EUA, the synchronous use of the three-swab test can again provide helpful additional information. Similarly, CO2 insufflation of the vagina in the presence of a fistula produces a stream of air bubbles which can be seen at cystoscopy. A biopsy should be taken from the edges of the fistula in all cases where there is any history of pelvic malignancy. If ureteric damage is suspected, ascending bulb ureterograms can be carried out, and this can be followed by the insertion of double ‘J’ stents.
Conservative management What are the indications for surgery versus conservative treatment? In a proportion of patients with small ‘simple’ vesicovaginal and ureterovaginal fistulae, conservative therapy may result in resolution of the fistula. In such patients the use of continuous drainage with a urethral catheter or internal splintage with a double ‘J’ stent, respectively, may be considered. It must be borne in mind that there is a low incidence of spontaneous closure in many series; Marshall reported only one case in a series of 92 patients.52 Following all nonsurgical management it should be remembered that the majority of fistulae will fail to heal spontaneously, a fact which must be balanced against the near certainty of surgical success, particularly if there is an iatrogenic etiology. A number of adjunctive measures can be used in addition to drainage:
• • • •
Local or systemic estrogen therapy;53 Antibiotic prophylaxis;54 Cystoscopic fulguration of the fistula;55 Corticosteroid therapy.56
Both estrogen therapy in the postmenopausal patient and antibiotic prophylaxis are likely to be helpful by improving the quality of the tissues and aiding subsequent surgery. Cauterization of fistulae was described as of limited benefit except in small fistulae by Sims,51 a sentiment reiterated by O’Conor who reported success with six patients.55 It seems unlikely that corticosteroid therapy has much to recommend it since, although it will reduce edema, it will also impair healing.
Timing of surgery Figure 92.3. Cystogram demonstrating leakage at the bladder base due to vesicovaginal fistula.
It is an essential requirement prior to surgery to have accurate knowledge of the patient’s vaginal and urinary
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Figure 92.4. Three-swab test showing the importance of identifying individual swabs, and the way in which this can localize a site of leakage. Bottom right: false-positive result due to reflux up the ureter and leakage from a ureterovaginal fistula. tract bacteriology, so that any pathogens can be eradicated by appropriate antimicrobial therapy; antibiotic prophylaxis should be used routinely. It is difficult to generalize as to the appropriate timing of surgical intervention for every case, since this will depend upon the systemic and local factors influencing the healing potential of the local tissues in the individual case. In the otherwise uncomplicated simple postoperative fistula, it is almost invariably possible to resolve the problem by early exploration within a few weeks, before the processes of inflammation and repair render surgery difficult. The majority of evidence suggests that if this window of opportunity is missed it is wise to defer surgery for at least 3 months.52,57 It is clearly inappropriate to carry out a surgical procedure which would potentially be rendered more complex and extensive and where morbidity is likely to be higher. In more complex fistulae where tissue healing is dependent on the interposition of a pedicled flap of vascularized tissue such as omentum, this timing is less critical to healing of the fistula. Although some workers have advocated repair between 3 and 12 weeks, it must be remembered that these cases all included interposed flaps of peritoneum or omentum.58,59 It is salutary to note that in a reported series of 11 ‘early’ repairs of vesicovaginal fistulae, 10 were successfully treated before 3 weeks
had elapsed after injury; the remaining case, however, repaired by simple layered closure at 35 days, recurred on the fifth postoperative day.60
Choice of approach The decision as to the best surgical approach for an individual case will be considerably biased by an individual surgeon’s preference and training. It will also depend upon the etiology, position, and size of the vesical fistula and the coexistence of associated ureteric or urethral damage. Adequate surgical access is crucial, not only for direct repair of the fistula itself, but also to allow additional procedures such as urethral repair, ureteric reimplantation or the interposition of pedicle flaps, essential to a successful outcome, to be undertaken. These requirements should be the most important factor in the selection of surgical approach. A vaginal approach provides limited access but avoids the morbidity associated with abdominal procedures; it is ideally suited to closure of the low simple fistula, and can be combined with the use of an interposed pedicled flap of labial/scrotal tissue or gracilis muscle for more complex fistulae. The abdominal approach is more invasive but is indicated for the repair of high or complex fistulae and lends itself to 1299
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the concomitant interposition of a pedicled omental flap in the repair. The most logical approach is to have the available expertise to utilize all of these procedures as necessary;61,62 preparing the patient for a synchronous perineoabdominal procedure at the outset of an operation, thereby facilitating the progression from one to the other if required.57
Repair technique The plethora of reports and techniques reported in the literature bear witness not only to the variation in the success of the different surgical methods in the hands of individual surgeons, but also to the diversity of available procedures. Surgical repair will succeed provided that it removes any predisposing etiologic cause for a fistula and reconstitutes the defect by the approximation of healthy, well-vascularized tissue. These criteria are easily achieved in simple fistulae by the trimming and tension-free approximation of adjacent wound edges. In more complex cases where the fistulous defect is large or fibrosis (resulting from infection, surgery or irradiation) compromises tissue healing, the interposition of a pedicled flap of well-vascularized tissue markedly increases the chances of success. In these cases it must be remembered that if the tension-free apposition of an epithelial defect is not possible, migration of epithelial cells will occur over an interposed vascularized pedicled flap. It is therefore acceptable to leave such defects provided that they are adequately covered by the flap.
Vaginal repair of vesicovaginal fistula Exposure The patient is placed on the operating table in the prone position slightly head-down, hips flexed to 30 degrees and legs widely abducted. The use of the prone position has the disadvantage that should vaginal repair prove difficult, progression to a synchronous abdominal approach is difficult or impossible. This is more than compensated for by the principal advantage of the position which places the fistula on the ‘floor’ of the vagina, in front of the operating surgeon. Optimal exposure to the fistula is achieved by the use of a Parkes anal retractor (Fig. 92.5), often combined with a ring retractor. In the presence of a narrowed introitus, exposure can be improved by a posterolateral episiotomy prior to insertion of the retractor. Dissection The vaginal epithelial margin of the fistula is circumcised. This can be facilitated by upward retraction on a
Figure 92.5. Use of a Parkes self-retaining retractor for fistula surgery. Foley catheter passed through the fistula into the bladder. In the uncomplicated case, excision of the fistulous tract is usually contraindicated since it will enlarge the size of the fistula, thereby making the repair more difficult. The tissue plane between vagina and bladder is developed and these structures are separated. These steps are important, since the success of any fistula repair depends upon the excision of damaged and devascularized tissues and tension-free closure in layers with meticulous attention to the integrity and positioning of the subcutaneous tissues.
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Closure It is important that the tissues used in the closure should be well vascularized and, wherever possible, suture lines which are in contact should be offset or placed at 180 degrees to each other. Absorbable sutures of interrupted 3-0 Vicryl/Monocryl are recommended. A rim of vaginal epithelium may be excised from around the fistula allowing repair by colpocleisis using a double or triple layer closure of the subcutaneous tissues.63 A modification reported by Twombly and Marshall64 involves the preservation of a flap of vaginal epithelium which is then used as the first layer closure of the defect. These techniques do produce some shortening of the vagina but are reported to produce little interference with sexual activity.63,65 They are most suitable for the postmenopausal patient, particularly if there is a deep vagina and a vault fistula and can, in experienced hands, be applicable to a wide range of different fistulae.66 Postoperative care It is important to provide a postoperative milieu that promotes satisfactory healing of the surgical repair. Careful review of urine bacteriology should be undertaken. The urinary tract should be drained continuously under low pressure. The synchronous use of both urethral and suprapubic drainage of adequate caliber (18 Fr) reduces the likelihood that blockage of a single catheter will result in overdistension and disruption of the surgical repair. Catheters should be left on free drainage for at least 10 days and the integrity of the repair confirmed at this juncture by the use of contrast studies; if there is any contrast leakage, the catheters should be left on drainage for a further week and radiologic re-evaluation repeated at that time.
Vaginal repair of the complex fistula In some cases the local vaginal tissues are damaged to the extent that a simple layered closure of the vagina is felt to be potentially precarious; such a situation may result from tissue loss or fibrosis produced by infection, radiation or previous surgery. In this situation it is necessary to augment the operation by the interposition of a vascularized flap between the two layers of the repair, filling dead space and bringing in a much needed blood and lymphatic supply. Many of these fistulae can be repaired using a vaginal procedure. A number of techniques have been described for the mobilization and deployment of adjacent soft tissue structures. These include the transposition of the medial fibers of the levator ani, the use of a gracilis muscle flap or a gracilis myocutaneous flap, and the use
of a pedicle flap of vulval fat and bulbocavernosus muscle.67–72 While the use of procedures utilizing the gracilis may be invaluable for the repair of extensive defects, the majority of cases can be satisfactorily resolved by the use of a Martius flap72 and hence this procedure will be described in detail here. A vertical incision is made in either labium majus allowing a posteriorly based pedicled vascularized flap of labial tissue to be raised. The size of the flap is determined by the size of the fistula and can be increased by anterior extension of the incision into the mons. The flap is mobilized, taking care not to damage the blood supply from the inferior hemorrhoidal vessels which enter posteriorly. Next a tunnel is made beneath a vulval skin bridge to the site of fistula closure. The labial flap is secured in position as part of the final layer closure (Fig. 92.6). A less common problem is that of a urethrovaginal fistula. The majority of patients with a distal urethrovaginal fistula are continent and asymptomatic provided that the bladder neck mechanism is competent.73 Vaginal repair of such a fistula is easily carried out. An associated urethral mucosal defect can be replaced by a suitable flap of adjacent vaginal mucosa supported by a Martius flap. Alternatively, a modification of the Martius procedure can be used whereby the urethral repair is facilitated by a suitably positioned skin island left on the labial pedicle.74 If the fistula is more proximal and a more extensive repair of urethra is likely to be necessary, or if it is associated with a vesicovaginal fistula, then a combined transvesical and abdominal approach is preferable.
Abdominal repair of urinary tract fistulae Exposure The patient is placed in the lithotomy position. A midline incision should always be used for the abdominal approach to a fistula repair because it is often necessary to extend this up to the xiphisternum to provide the necessary access for mobilization of the omentum. A more cosmetic result can be achieved, particularly in those patients who have recently undergone a gynecologic procedure via a Pfannenstiel incision, by reopening the transverse skin incision and making a vertical incision through the abdominal wall musculature. An additional upper midline incision may be necessary to aid omental mobilization (Fig. 92.7). Dissection A combined transperitoneal transvesical approach to a vesicovaginal fistula is to be preferred over the conventional anterior transvesical approach first described by 1301
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Figure 92.6. (a) Sound through a vesicovaginal fistula. (b) Having catheterized the ureters, the fibrotic margins of the fistula are excised. (c) Operative view of Figure 92.6d showing the importance of stay sutures. (d) Having closed the fistula, the deployment of a Martius flap.
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completed in the plane between bladder and vagina. It is important to create adequate space to allow the tension-free interposition of a suitable bulk of omentum. In difficult cases, in particular those where previous surgery has been attempted, the abdominal dissection can be combined with a subsequent vaginal dissection to produce an abdominoperineal tunnel, thereby allowing linear deployment of the omentum along the whole length of the vagina77,78 (Fig. 92.8b–e). Closure The vagina is closed with an absorbable 3-0 suture. The bladder is closed with a similar absorbable suture and adequate drainage ensured by the use of combined urethral and suprapubic drainage, the repair being wrapped in omentum. This surgical technique is applicable to a wide variety of fistulae and provides virtually guaranteed success.79 At the end of the procedure a colposuspension may be carried out if necessary, to reposition the proximal urethra and bladder neck, optimizing the transmission of intra-abdominal pressure and thereby mitigating against the development of stress incontinence.80
The use of pedicled interposition flaps
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Figure 92.6. (e) showing the importance of the deployed tissue as a sandwich between the two closure layers. (f) Final closure. Trendelenburg in 189075 and subsequently modified.76 This allows good access to the area of the fistula and facilitates separation of the bladder from the vagina with the formation of an abdominoperineal tunnel and good extravesical exposure of the terminal ureters.77 An initial incision is made in the vesicovaginal peritoneal fold and the posterior wall of the bladder opened in the midline down to the fistula. Separation of the vaginal vault from the bladder is facilitated by an orientating finger placed within the vagina (Fig. 92.8a). A three fingerbreadths space is
The interposition of well-vascularized tissue, such as omentum as described above, brings in a good blood supply and fills dead space. While this acts as an added safeguard for a successful result in simple fistulae, it is essential to the closure of complex fistulae. A number of techniques have been described in the literature. These include the use of peritoneal interposition, first described by Bardescu in 1900,81,82 the use of island myocutaneous and fasciocutaneous flaps,83,84 bladder mucosa,85 and omentum, first reported by Walters in 193578 and popularized in the last three decades.86,87 The omentum should be the tissue of first choice, as it is readily available and easy to mobilize, reaching down to the perineum in most cases. It has a good blood and lymphatic supply, and sufficient bulk to fill dead space without producing marked fibrosis during healing, which may compromise lower urinary tract function and render subsequent surgery more difficult. In contrast, peritoneum – while being readily available – does not possess these other properties and is commonly involved in local pathology or in the irradiated field. Bladder mucosal grafts can be used in a manner analogous to the techniques using vaginal epithelium, but carry the same potential disadvantages as suggested for peritoneum. Other flap procedures are an important part of the armamentarium but require particular expertise. 1303
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Figure 92.7. (a) A midline incision via a Pfannenstiel skin incision. (b) Retractors in place allowing access to the abdomen as per a midline incision. (c, d) Occasionally, to allow full mobilization of the omentum, an upper midline incision may be necessary. 1304
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Figure 92.8. (a) Demonstrating the correct plane for dissection between the vagina and bladder. (b) The plane is followed down behind the trigone. (c) If necessary, a perineal incision can be made to allow a full abdominoperineal tunnel to be developed. (d, e) Showing the fistula closed and omentum interposed. 1305
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The omentum should always be separated from its attachment to the transverse colon and mesocolon since postoperative distension of the bowel may otherwise disrupt its relationship with the repair. The lower margin of the omental apron will reach the perineum without additional mobilization in 30% of cases. In a further 30%, some degree of mobilization of the omentum by division of part of its vascular pedicle is necessary. While Kiricuta and Goldstein suggested that the omentum should be mobilized on the left gastroepiploic pedicle,86 Turner-Warwick et al. raised the important technical point that the gastroepiploic arch becomes increasingly small towards its left extremity and suggested that the omental flap should be based on the right gastroepiploic pedicle for a more reliable blood supply.87 In approximately 30% of cases, sufficient elongation is achieved by division of the left gastroepiploic pedicle and those of the direct left lateral vessels to the omentum. In the remaining cases, full mobilization of the omentum is required, based on the right gastroepiploic vessel as far as its gastroduodenal origin to prevent undue traction on individual short gastric vessels which might result in shearing and postoperative hemorrhage. Individual ligation of short gastric vessels is necessary using an absorbable suture. The resultant slender pedicle of this omental flap is protected by relocating it behind the mobilized descending colon. Mobilization of the omentum from the stomach does result in a mild ileus and it is therefore appropriate to institute gastric suction for a few days postoperatively. Insertion of a gastrostomy tube is a humane alternative to a nasogastric tube, particularly as the stomach is suitably exposed.
Repair of complex fistulae In our experience, the repair of complex vesicovaginal fistulae is most satisfactorily tackled via the abdominoperineal approach with omental interposition as described above.79 Certain additional points are, however, worthy of comment. If radiotherapy is implicated in the etiology of the fistula, the wall of the bladder is usually rendered more rigid and inflexible than is normally the case. In this situation, an oblique incision in the bladder wall is often preferable to one in the midline as this facilitates subsequent bladder closure by the rotation of a broad-based bladder flap. In those patients with radiation-induced fibrosis and necrosis the surgical procedure must be considered to consist of two separate stages. It is first necessary to excise all macroscopically abnormal tissue. If residual malignancy is suspected, this can be confirmed by frozen section. The presence of malignancy per se, unless extensive, should not preclude a reconstructive
procedure, but will clearly lead to more radical excision. The second stage of this operation involves a functional restoration of the integrity of the rectum, bladder, and vagina as far as this is feasible, filling the dead space within the inevitably ischemic pelvis with omentum and/or a cecolovaginoplasty.80 If there is an extensive defect then it may not be possible to obtain satisfactory apposition of the edges of the bladder wall without compromising its functional capacity. Closure of the bladder defect can be carried out with the additional use of an augmentation cystoplasty. Alternatively, the bladder defect can be left and the omentum used to patch it; animal studies have demonstrated that such a defect is covered within 2–3 weeks by new transitional epithelium, with the subsequent formation of a new smooth muscle layer within the omentoplasty, in continuity with the detrusor muscle at the margins of the defect.88,89 Clinical experience over the last 25 years has confirmed the efficacy of this technique 87,90,91 in the clinical setting.
SURGERY FOR DETRUSOR OVERACTIVITY Detrusor overactivity can result in considerable morbidity in patients with idiopathic detrusor overactivity (DO) and also those with neurogenic detrusor overactivity (NDO). In patients with DO, marked bladder overactivity leads to disabling frequency and incontinence, whereas in NDO, renal impairment may result from voiding dysfunction and back pressure on the upper tracts in association with high pressure phasic detrusor contractions and detrusor sphincter dyssynergia. In both conditions the cornerstone of the pharmacotherapy is still anticholinergic agents, often combined with bladder retraining. In the context of neurogenic bladder dysfunction, the clinical picture is complicated by an admixture of other functional problems associated with the bladder overactivity including uncoordinated detrusor contraction and varying degrees of bladder outflow obstruction. The aim of surgical therapy directed at the detrusor in both these conditions is to increase functional bladder capacity and decrease the amplitude of detrusor contractions, thereby preventing incontinence and protecting the upper tracts in patients with NDO. In recent years the mainstay of contemporary therapy for bladder overactivity has been augmentation cystoplasty, most usually using the ‘clam’ technique.92 Two further options have been recently explored: bladder autoaugmentation93 and sacral neuromodulation.94 While a number of surgical techniques for the treatment of detrusor overactivity have been described, it is now widely accepted that procedures such as detrusor
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transection and transtrigonal phenol injection produce unpredictable and temporary improvement with potentially serious side effects. Their routine use can therefore no longer be supported. More recently, botulinum toxin injection therapy into the bladder has become more popular and is being increasingly used. Definitive comments as to its efficacy will, however, await the results of adequately conducted long-term studies.95
Augmentation cystoplasty The principle underlying augmentation cystoplasty is that by bivalving a functionally overactive bladder and introducing a segment of detubularized intestine a low pressure bladder with an increased functional capacity will result. The two commonly used intestinal segments are ileum and sigmoid colon. The sigmoid is usually used in patients where a short small bowel mesentery renders the use of ileum difficult. Ileum is preferred as it produces lower reservoir pressures and better compliance. The original technique described for clam cystoplasty is still widely used but modifications to this include opening the bladder in the sagittal plane which appears to be equally effective, or opening the bladder as a ‘star’.96 This specific modification can be particularly useful in patients with NDO where the bladder is small and thick walled. An alternative surgical technique popularized by McGuire is his modification of the hemi-Koch procedure. This utilizes a transverse ‘smile’ incision (looking posteriorly) which is fashioned 3 cm above the ureteral orifices, creating an anteriorly based detrusor flap.97 Most workers find coronal or sagittal bivalving of the bladder to be effective and acceptable, provided that adequate opening of the bladder is performed right down to the ureteral orifices, both to adequately open the bladder and to prevent ‘diverticulation’ of the cystoplasty segment. A number of studies attest to the efficacy of augmentation cystoplasty in children, adolescents, and adults with DO and NDO:98–103
• Mundy and Stephenson reported a series of 40
•
cases in whom 90% were cured at a mean follow-up of 1 year.98 Mean functional bladder capacity was increased from 280 to 440 ml, reduced compliance was improved in 70% of patients, and detrusor overactivity abolished in 50%, the remainder having low pressure detrusor overactivity. In a series of 26 adolescents undergoing enterocystoplasty, of whom 19 had a ‘clam’ cystoplasty, results were satisfactory in all three males
•
•
•
•
but poor in five out of the 16 females. In three patients, difficulty was experienced with intermittent self-catheterization.99 In a series of 39 children with spina bifida, bladder capacity at safe storage pressures of less than 29 cm of saline was achieved in all patients with a reduction in upper tract distension in 91.7% of kidneys.100 A satisfactory result was achieved in all but one patient. Singh and Thomas reviewed 67 patients who underwent augmentation cystoplasty.101 Of these, 47 had an ileal segment and 20 a sigmoid segment. These data are presented in combination with a further 11 patients who had an ileocecal cystoplasty. Fifty-two patients had an artificial sphincter, nine had a colposuspension and one had both. Acceptable continence was achieved in 93.6% of patients. Hasan et al. reported on 48 patients who underwent augmentation cystoplasty for DO (n=35) or NDO 102 (n=13). Mean follow-up was 38 months, with 83% achieving a good outcome, 15% a moderate outcome, and 2% an unsatisfactory result. Flood et al. reported on 122 augmentation cystoplasties.103 It must, however, be borne in mind that the ‘McGuire’ technique used was different from the standard clam procedure reported for all the other series described above, and this was a very mixed group of patients: 67% had an ileal augmentation, 30% a detubularized cecocystoplasty, and 3% sigmoid. In 19 patients this procedure was related to undiversion and 17% had interstitial cystitis, 7% radiation cystitis, 13% miscellaneous conditions and the remainder were either NDO or DO. Mean follow-up was 37 months. Bladder capacity was increased from a preoperative mean of 108 ml to 438 ml and, of 106 successful patients, 75% had an excellent result, 20% were improved and 5% had major, persistent problems.
The above literature would support augmentation cystoplasty as being an effective therapy with a low operative morbidity and satisfactory long-term results, although most of the reported series have a follow-up of less than 5 years. It must be remembered that this is major surgery and despite adequate preoperative counseling, many patients take some months to adapt to their new bladder and to learn to void effectively by abdominal straining. It is important to monitor postoperative residual urine volumes. Intermittent self-catheterization (ISC) is necessary for a number of these patients, particularly those with NDO. Interestingly, the reported incidence of ISC varies from 15% up to 85% of cases.98 It is evident that a 1307
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number of factors contribute to the need for ISC. These include the level of residual deemed acceptable by the supervising urologist and the concomitant use of procedures directed at the bladder outflow – either urethral dilation (rebalancing) or treatments for stress incontinence. A particular debate centers on the treatment of coexisting stress incontinence at the time of clam cystoplasty; contemporary opinion remains divided on this matter since measures designed to treat stress incontinence will generally increase the need for ISC. Other problems encountered with augmentation cystoplasty include persistent mucus production, recurrent or persistent urinary tract infections, and metabolic disorders which are usually mild and subclinical. Provided that patients are counseled preoperatively, this is rarely a problem. Persistent urinary infection can be troublesome, particularly in female patients, and has been reported in up to 30% of cases, often requiring long-term antibiotic therapy. Long-term bowel dysfunction occurs in up to a third of patients and is thought to be related to the interruption of the normal enterohepatic circulation.101,102,104 Bladder perforations have been reported in up to 10% of patients.100 At present, lifelong follow-up of these patients is recommended, not only because of the above complications, but also in view of the suggestion that augmentation cystoplasty predisposes to the subsequent development of malignancy.105 However, there remains no convincing evidence to support an association with tumor in the absence of other predisposing factors such as previous tuberculosis or chronic urinary stasis such as that associated with paraplegia. Augmentation cystoplasty is an effective management option in contemporary practice in patients with intractable DO or NDO resistant to conventional therapy. In addition, cystoplasty can be used as part of an undiversion procedure. Although a proportion of patients are not significantly improved by this procedure, one series found a ‘good to moderate’ outcome in only 58% of patients with DO.102 It must be borne in mind that up to 30% of patients experience increased frequency and looseness of bowel motions and a tendency to incontinent episodes, with a significant number of patients requiring long-term ISC. With these observations in mind, alternative therapies have been explored, in particular bladder autoaugmentation.93
Bladder autoaugmentation In 1989, Snow and Cartwright initially reported a technique which they named bladder autoaugmentation.106 This procedure involves the excision of the detrusor muscle over the entire dome of the bladder, leaving the
underlying bladder urothelium intact. A large epithelial ‘bulge’ is created which functions by augmenting the storage capacity of the bladder and this is referred to as autoaugmentation. Following initial studies in six dogs, this technique was extended to seven patients aged 4–17 years, all of whom had poorly compliant bladders documented on pressure flow urodynamics. Following excision of the dome detrusor muscle, the lateral margins of the detrusor were fixed bilaterally to the psoas muscles. Patient follow-up was short. A subsequent report by these workers after studying a total of 19 patients concluded that, with a follow-up of between 3 months and 4 years, 80% of patients were continent and another 10% were significantly improved. A significant increase in bladder capacity of greater than 50 cc occurred in only 40% of patients, with minimal change in 35%; 25% actually had a decrease in capacity. The procedure was, however, accompanied by improved continence and reduced 106 rates of hydronephrosis. In 12 pediatric patients with low capacity bladders and demonstrable detrusor overactivity (aged 4–14 years, 10 with NDO), 6 months following autoaugmentation the mean increase in bladder capacity was 40% with a 33% decrease in mean leak point pressure.107 Postoperative complications were minor. A modification of the previous technique was used whereby a vesicomyotomy was used rather than vesicomyectomy with no fixation of the bladder laterally to the psoas muscles. A subsequent preliminary report in five adult patients, with the follow-up ranging from 12 to 82 weeks, reported an increase in bladder capacity which varied from 40% up to 310%; this was measured at an intravesical pressure of 40 cmH2O. Stohrer et al. reported a series of 29 patients aged 14–64 years with an average age of 35 years. Of these patients, 24 were felt likely to have NDO.108,109 All patients underwent preoperative urodynamic evaluation. The technique reported by these authors is based on the original one described by Snow and Cartwright with an extraperitoneal approach filling the bladder to 200–250 ml. A 7–8 cm diameter section of the detrusor around the urachus is dissected completely and removed leaving the mucosa intact. The detrusor is not fixed to the psoas muscle and all bands of detrusor overlying the urothelium are removed. The authors now have followup to 7 years and while they find that 50% of patients can void without significant residuals, up to half require ISC. They found an improved compliance and increasing capacity of 130–600 ml. An alternative surgical approach which has been explored in case reports is laparoscopic-assisted autoaugmentation but comment on this cannot be made
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in the absence of adequate numbers of patients and no significant follow-up.110 It is recognized that spontaneous perforation of an augmentation cystoplasty bladder is a potential risk, occurring in up to 10% of cases. This may be due to high intravesical pressure111 and can usually be managed successfully by conservative measures.112 Patients may be at even greater risk of perforation following autoaugmentation because of the thinness of the mucosa in the bulging ‘diverticulum’ produced by the operation. Evidence in support of this is provided by animal studies where autoaugmentation resulted in higher risk of perforation at lower pressures than augmentation cystoplasty.113 To date this complication has yet to be reported in clinical series, possibly because of ingrowth of fibrous tissue around the mucosal diverticulum with time, which may also account for the limited increase in capacity seen following the procedure. This phenomenon, if progressive, may limit the durability of this operation. At present, while autoaugmentation has a number of attractive features, it is clear that the resultant increase in bladder capacity and reduction in detrusor overactivity are far less pronounced than following augmentation cystoplasty. The number of cases reported in the literature is small with relatively short follow-up. It is questionable whether the associated benefits adequately compensate for the limited long-term efficacy of the procedure. The search for less invasive techniques therefore continues.
URINARY DIVERSION Urinary diversion may be either temporary or permanent. All surface diversions are simple surgical endeavors to correct the urinary waste disposal problems of patients who are unfortunate enough to have either lost, or never to have actually achieved, normal bladder function. While clearly ‘diversion is diversion’ and ‘cystoplasty is cystoplasty’ the development of so-called ‘continent diversion’ has confused this distinction – the surgical principles and the procedures that are used to create the urinary reservoir of this diversion are identical to those for a total cystoplasty. Because the only difference between these is the mechanism of their emptying, we would suggest a more rational terminological distinction, i.e. ‘stoma-cystoplasty’ and ‘sphincter-cystoplasty’. The two key components of the creation, or recreation, of a naturally functioning bladder are bladder-base sensation and a sufficiency of functional sphincter muscle. These are irreplaceable but, all too often, one or both are sacrificed at the time of a urinary diversion.
Even a small area of urothelium that has normal sensation can make all the difference when it is available for inclusion in a functional reconstruction because the sensation of bladder fullness avoids the need to time its emptying. Similarly, the remnants of an incompetent sphincter mechanism can sometimes be made to function satisfactorily. Thus it is important to preserve every bit of the functional tissue that might be important to a future reconstruction – even if one cannot envisage either the possibility of an undiversion or that it could subserve a useful purpose. The opportunity of restoration of sphincteric function ‘today’ has often been denied by the excisions of ‘yesterday’. Similar considerations apply to rectal sensation and the sphincteric control of defecation. An anal mechanism, or even its apparently useless remnants, should never be excised needlessly – many patients have lost their chance of anorectal continence as a result of an unnecessarily extensive routine abdominoperineal resection.
The options for urinary tract diversion and reconstruction A consideration of the range of procedure options available for urinary diversion, some of which are no longer advocated, summarizes the practical experience upon which the evolution of current preferences are based. These options can be conveniently considered in four distinct categories. 1. Free-draining surface diversion of the upper urinary tract: This naturally requires the collection of continuously draining urine. The need for this may be temporary; however, it may be permanent if the surgical retrieval of the reservoir function of the lower urinary tract is not possible. 2. Incontinence surface diversion of the lower tract: This is often required for the management of voiding difficulties; when these are irremediable this may be a long-term arrangement. An indwelling urethral catheter may be either drained continuously into a bag or intermittently released. Intermittent emptying of the natural bladder reservoir can also be achieved by intermittent catheterization of the urethra or a leak-proof suprapubic conduit (Fig. 92.9). 3. ‘Cystoplastic reconstruction’ of a urinary reservoir that is emptied either by sphincter control or by stomal catheterization: A total substitution cystoplasty may be appropriate when the whole bladder has to be removed; however, many bladder abnormalities 1309
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‘Cystoplasty’, ‘stoma-cystoplasty’ and ‘sphinctercystoplasty’ – a perspective of urinary reservoirs that are emptied intermittently
a
b
Figure 92.9. (a) An ileal conduit. (b) Formation of the ileal conduit.
require only a readjustment or a partial cystoplastic substitution. A reconstructed cystoplastic reservoir, partial or total, may be controlled by the sphincter mechanism – ‘sphincter-cystoplasty’ – or it may be emptied by intermittent catheterization of a leakproof conduit –‘stoma-cystoplasty’ (Fig. 92.10) 4. Internal urinary diversion controlled by the anal sphincter – ureterosigmoidoscopy: For some patients a rectosigmoid urinary diversion is a preferable alternative to surface diversion when the circumstances are appropriate. For nephrologic and carcinogenic reasons this procedure fell into disrepute for a number of years but procedural developments have addressed some of the potential problems: these include the limitation of renal damage and the early detection of malignant change (Fig. 92.11). When satisfactory sphincteric control of a cystoplasty is irretrievable, many alternative procedures such as catheterizable stoma cystoplasty reservoirs enable patients to achieve a reasonably acceptable quality of urologic life.
The surgical procedures of ‘cystoplasty’ and of ‘continent diversion’ have evolved as a result of the great endeavors and contributions of numerous colleagues over the years — whole textbooks have been written about them. However, the value of the terminological distinction between ‘cystoplasty’ and ‘continent diversion’ is questionable because the functional requirements and the surgical principles of creating their reservoirs are essentially similar. ‘Cystoplasty’ is a generic term for a reconstructive procedure (plasty) to recreate the functional capacity of a bladder reservoir (cysto). Like the term ‘urodynamics’, ‘cystoplasty’ is commonly used, understood, and misunderstood to mean different things. This adds additional confusion to the already complex field of the retrieval and the construction of functional urinary reservoirs. Some ‘simple’ cystoplasty operations restore the natural functional reservoir capacity of the bladder without involving any substitution procedure and not all substitution procedures involve the use of bowel. However, the term ‘cystoplasty’ is commonly used somewhat loosely, as a ‘semi-specific shorthand’ to denote the substitution of the bladder reservoir, partial or total, generally with the tacit assumption that bowel is used for the substitution and also that the functional control of the outlet is the natural urethral sphincter mechanism. Developments in the surgical retrieval of the natural bodily function of ‘intermittent urinary waste disposal’ often involve the creation of catheterizable leak-proof abdominal stoma conduits that are used for the intermittent emptying, either of normal bladders when the urethra is irremediably dysfunctional, or of substitution urinary reservoirs that are either partially or totally reconstructed. Thus an integrated reconsideration of the practical principles of cystoplasty and diversion seems appropriate, together with an integrated reconsideration of terminology. In this section, we use simple descriptive terminological exactitudes. A urethra-cystoplasty is a reconstructed urinary reservoir, the outlet of which is the urethra. When this is controlled by the sphincter it is a sphincter-cystoplasty; if it is emptied by self-catheterization it is a simple urethracystoplasty. The reservoir of a sphincter-cystoplasty may be either a partial or a total substitution of the bladder. If bowel is used for the substitution it can be optionally identified as an ‘ileal sphincter-cystoplasty’ or a ‘colonic sphincter-cystoplasty’ – as opposed to an ‘omental ure-
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Figure 92.10. Formation of a pouch with a catheterizable stoma. thra-cystoplasty’. A urethro-cystoplasty is a different entity because it denotes reconstruction of both the bladder and the urethra. A stoma-cystoplasty is a urinary reservoir with an abdominal stoma-conduit outlet. Its ‘continence’ is usually maintained by a valved leak-proof conduit that can be catheterized intermittently. The reservoir may be the native bladder – a partial substitution in situ – or a total substitution that is either in situ or ex situ. Alternatively, a stoma-cystoplasty can be less precisely described as a ‘continent diversion’. The functional characteristics and the principles involved in the construction of the bowel substitution urinary reservoirs of both a stoma-cystoplasty and a sphincter-cystoplasty are essentially similar, the difference is simply the mechanism of their evacuation. A leak-proof stoma conduit is a mechanistic construction specifically designed for emptying the reservoir by catheterization. The reliable sphincteric control of a sphincter-cystoplasty is often dependent upon a careful urodynamic assessment and appropriate surgical adjust-
ment and management: this requires quite separate consideration. Whether or not this terminology will be generally adopted, time will tell; it seems preferable to the illdefined ‘continent diversion’. A particular advantage is that it facilitates an independent analytical consideration of the three separate component procedure principles of cystoplastic reconstruction: 1. The creation of a urinary reservoir that has low pressure and reflux-proof ureteric implantations – these requirements are common to the reservoirs of both a sphinctercystoplasty and a stoma-cystoplasty. 2. The intricate mechanistic construction of a valved leak-proof stoma conduit that is required for the evacuation of the reservoir of a stoma-cystoplasty by self-catheterization. 3. A functionally orientated urodynamically controlled adjustment is often required to ensure the voiding efficiency and sphincteric control of a sphinctercystoplasty. 1311
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Figure 92.11. Formation of a ureterosigmoid pouch of the Mainz 2 type.
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72. Martius H. Die Operative Wiederherstellung der volkommen fehlenden Harnrohre und der Schliessmuskels derselben. Zentbl Gynak 1928;52:480–6.
53. Collins CG, Pent D, Jones FB. Results of early repair of vesicovaginal fistula with preliminary cortisone treatment. Am J Obstet Gynecol 1960;80:1005–12. 54. Lawson J. The management of genitourinary fistulae. Clin Obstet Gynecol North Am 1978;5:209–36. 55. O’Conor VJ. Review of experience with vesicovaginal fistula repair. Trans Am Assoc Genitourin Surg 1979;71:120–2. 56. Jonas U, Petri E. Genitourinary fistulae. In: Stanton SL (ed) Clinical Gynaecologic Urology. St Louis: Mosby, 1984.
73. Spence HM, Duckett JW. Diverticulum of the female urethra: clinical aspects and presentation of a simple operative technique for cure. J Urol 1970;104:432–7. 74. Turner-Warwick RT. The use of pedicle grafts in the repair of urinary tract fistulae. Br J Urol 1972;44:644–56. 75. Zacharin RF. Grafting as a principle in the surgical management of vesico-vaginal and recto-vaginal fistulae. Aust N Z J Obstet Gynaecol 1980;20:10–17. 76. O’Conor VJ, Sokol JK, Bulkley GJ, Nanninga JB. Suprapubic closure of vesicovaginal fistula. J Urol 1973;109:51–4.
57. Turner-Warwick RT. Repair of urinary vaginal fistulae. In: Rob C, Smith R (eds) Operative Surgery, 3rd ed. London: Butterworths, 1977; 206–18.
77. Turner-Warwick RT. Urinary fistula in the female. In: Harrison ED, Gittes RF, Perlmutter AD (eds) Campbell’s Urology. Philadelphia: Saunders, 1979; Ch. 85.
58. Persky L, Herman G, Guerrier K. Non-delay in vesicovaginal fistula repair. Urology 1979;13:273–5.
78. Walters W. Transperitoneal repair of a vesico-vaginal fistula. Proc Staff Meetings Mayo Clin 1935; 375–7.
59. Badenoch DF, Tiptaft RC, Thakar DR, Fowler CG, Blandy JP. Early repair of accidental injury to the ureter or bladder following gynaecological surgery. Br J Urol 1987;59:516–8.
79. Chapple CR, Turner-Warwick RT. Traumatic lower urinary tract fistulae – abdominoperineal repair with pedicled omental interposition. J Urol 1990;143:328A.
60. Cruikshank SH. Early closure of posthysterectomy vesicovaginal fistulas. South Med J 1988;81:1525–8. 61. Roen PR. Combined vaginal and transvesical approach in successful repair of vesicovaginal fistula. Arch Surg 1960;80:628–33. 62. Weyrauch HW, Rous SN. Transvesical–transvaginal approach for surgical repair of vesicovaginal fistulae. Surg Gynecol Obstet 1966;123:121–5. 63. Latzko W. Post-operative vesicovaginal fistulas. Am J Surg 1942;58:211–28. 64. Twombly GH, Marshall VF. Repair of vesico-vaginal fistula caused by radiation. Surg Gynec Obstet 1946;83:348. 65. Rader ES. Post-hysterectomy vesicovaginal fistula: treatment by partial colpocleisis. J Urol 1975;112:811–2. 66. Blaikley JB. Colpocleisis for difficult vaginal fistulae of bladder and rectum. Proc R Soc Med 1965;58:581–6. 67. Douglass M. Operative treatment of urinary incontinence. Am J Obstet Gynecol 1936;31:268–79. 68. Garlock JH. The cure of an intractable vesico-vaginal fistula by the use of a pedicled muscle flap. Surg Gynec Obstet 1928;47:255–60. 69. Ingleman-Sundberg A. In: Meigs JV (ed) Surgical Treatment of Carcinoma of the Cervix. London: Heinemann, 1954; 419.
80. Turner-Warwick RT. The omental repair of complex urinary fistulae. In: Gingell C, Abrams P (eds) Controversies and Innovations in Urological Surgery. London: Springer-Verlag, 1988; Ch. 26. 81. Bardescu N. Ein neues verfahren fur die operation der tiefen blasen-uterus-scheidenfisteln. Centralbl f Gynak 1900;24:170. 82. Eisen M, Jurkovic K, Altwein JE, Schreiter F, Hohenfellner R. Management of vesicovaginal fistulas with peritoneal flap interposition. J Urol 1974;112:195–8. 83. Robertson CN, Riefkohl R, Webster GN. Use of the rectus abdominis muscle in urological reconstructive procedures. J Urol 1986;135:963–5. 84. McCraw JB, Arnold PG. Atlas of Muscle and Myocutaneous Flaps. Norfolk, VA: Hampton Press, 1986. 85. Coleman JW, Albanese C, Marion D et al. Experimental use of free grafts of bladder mucosa in canine bladders: successful closure of recurrent vesicovaginal fistula utilising bladder mucosa. Urology 1985;25:515–7. 86. Kiricuta I, Goldstein AMB. Epiplooplastia vezicala, metoda de tratament curativ al fistulelor vezico-vaginale. Obstetrica si Ginecologia Buceresti 1956;2:163. 87. Turner-Warwick RT, Wynne EJC, Handley-Ashken M. The use of the omental pedicle graft in the repair and reconstruction of the urinary tract. Br J Surg 1967;54:849–53.
70. Hamlin RHJ, Nicholson EC. Reconstruction of urethra totally destroyed in labour. Br Med J 1969;2:147–150.
88. Goldstein MB, Dearden LC. Histology of omentoplasty of the urinary bladder in the rabbit. Invest Urol 1966;3:460–9.
71. McCraw JB, Massey FM, Shanklin KD, Horton CE. Vagi-
89. Helmbrecht LJ, Goldstein AMB, Morrow JW. The use of
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pedicled omentum in the repair of large vesicovaginal fistulas. Invest Urol 1975;13:104–7. 90. Kiricuta I, Goldstein AMB. The repair of extensive vesicovaginal fistulas with pedicled omentum. J Urol 1972;108:724–7. 91. Chapple CR, Turner-Warwick RT. Surgical salvage of radiation induced fibrosis – the ‘frozen pelvis’. J Urol 1990;143:349A. 92. Bramble FJ. The treatment of adult enuresis and urge incontinence by enterocystoplasty. Br J Urol 1992;54:693–6.
come and quality of life following enterocystoplasty for idiopathic detrusor instability and neurogenic bladder dysfunction. Br J Urol 1995;76:551–7. 103. Flood HD, Malhotra SJ, O’Connell HE et al. Long-term results and complications using augmentation cystoplasty in reconstructive urology. Neurourol Urodyn 1995;14:297–309. 104. Barrington JW, Fern-Davies H, Adams RJ et al. Bile acid dysfunction after clam enterocystoplasty. Br J Urol 1995;76:169–71.
93. Cartwright PC, Snow BW. Bladder autoaugmentation: early clinical experience. J Urol 1989;142:505–7.
105. Barrington JW, Fulford S, Griffiths D, Stephenson TP. Tumors in bladder remnant after augmentation enterocystoplasty. J Urol 1997;157(2):482–6.
94. Schmidt RA. Advances in genitourinary neurostimulation. Neurosurgery 1986;18:1041–4.
106. Snow BW, Cartwright PC. Bladder autoaugmentation. Urol Clin North Am 1996;23(2):323–31.
95. Reitz A, Stohrer M, Kramer G et al. European experience of 200 cases treated with botulinum-A toxin injections into the detrusor muscle for urinary incontinence due to neurogenic detrusor overactivity. Eur Urol 2004;45(4):510–5.
107. Stothers L, Johnson H, Arnold W et al. Bladder autoaugmentation by vesicomyotomy in the pediatric neurogenic bladder. Urology 1994;44(1):110–3.
96. Keating MA, Ludlow JK, Rich MA. Enterocystoplasty: the star modification. J Urol 1996;155:1723–5. 97. Weinberg AC, Boyd SD, Lieskovsky G et al. The hemiKoch ileocystoplasty: a low pressure anti-refluxing system. J Urol 1988;140:1380–4. 98. Mundy AR, Stephenson TP. ‘Clam’ ileocystoplasty for the treatment of refractory urge incontinence. Br J Urol 1985;57:641–6. 99. Woodhouse CRJ. Reconstruction of the lower urinary tract for neurogenic bladder: lessons from the adolescent age group. Br J Urol 1992;69:589–93. 100. Krishna A, Gough DC, Fishwick J, Bruce J. Ileocystoplasty in children: assessing safety and success. Eur Urol 1995;27:62–6. 101. Singh G, Thomas DG. Enteroplasty in neuropathic bladder. Neurourol Urodyn 1995;14:5–10. 102. Hasan ST, Marshall C, Robson WA, Neal DE. Clinical out-
108. Stohrer M, Kramer A, Goepel M et al. Bladder auto-augmentation – an alternative for enterocystoplasty: preliminary results. Neurourol Urodyn 1995;14:11–23. 109. Kramer G, Stoher M. Neurourology. Curr Opin Urol 1996;6(4):176–83. 110. McDougall EM, Clayman RV, Figenshau RS, Pearle MS. Laparoscopic retropubic auto-augmentation of the bladder. J Urol 1995;153:123–6. 111. Anderson PAM, Rickwood AMK. Detrusor hyperreflexia as factor in spontaneous perforation of augmentation cystoplasty for neuropathic bladder. Br J Urol 1991;67:210–2. 112. Slaton JW, Kropp KA. Conservative management of suspected bladder rupture after augmentation enterocystoplasty. J Urol 1994;152:713–5. 113. Rivas DA, Chancellor MB, Huang B, Epple A, Figueroa TE. Comparison of bladder rupture pressure after intestinal bladder augmentation (ileocystoplasty) and myomyotomy (autoaugmentation). Urology 1996;48:40–6.
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93 Gynecologic developmental abnormalities Melissa C Davies, Sarah M Creighton
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IntroductIon The müllerian system develops from the sixth week of life and it is estimated that the prevalence of congenital abnormalities, both major and minor, is approximately 5%.1–3 These anomalies may occur in isolation or in conjunction with other congenital malformations or as part of a syndrome. Many patients with simple anomalies will remain asymptomatic and may be diagnosed incidentally while being investigated for other problems or undergoing routine gynecologic/obstetric procedures. The others will present in a variety of ways depending upon the abnormality present. The most common presentations are primary amenorrhea, obstructed uterus or vagina, dyspareunia, and on investigation for infertility or recurrent miscarriage. Those diagnosed as neonates will usually be patients in whom there are associated major anomalies of the genitourinary and alimentary tracts such as persistent cloacal anomalies and anorectal malformations, or when urgent life-saving treatment is required (e.g. saltwasting congenital adrenal hyperplasia).
development of the müllerIan tract An understanding of the embryologic development of the urogenital system is essential to the diagnosis and management of developmental abnormalities. This subject is covered in detail in Chapter 00. What follows is a brief summary. Primordial gonads (genital ridges) appear during the sixth week of embryogenesis. Associated ducts – the müllerian or wolffian ducts – also develop. The fate of these undifferentiated ducts depends upon the genetic sex of the embryo. In XY embryos, the SRY gene (sex determining region of the Y chromosome) stimulates testicular differentiation. The developing testes produce androgens and anti-müllerian hormone (AMH), which
cause virilization and regression of müllerian structures. Therefore, in XX individuals, absence of the SRY gene allows the gonads to develop into ovaries, and the subsequent lack of AMH allows the müllerian ducts to develop into a uterus, fallopian tubes and vagina. The müllerian ducts grow in a caudal and medial direction and fuse in the midline to form the primitive uterus. These ducts form the right and left fallopian tubes, and midline fusion of these structures produces the uterus, cervix, and proximal two-thirds of the vagina. This rudimentary vagina fuses with the posterior urethra at week 7 to form the urogenital sinus. Fusion of the müllerian ducts also brings together the lateral peritoneal folds that form the broad ligaments. The vagina develops from a combination of the müllerian tubercles and the urogenital sinus. Cells proliferate from the upper portion of the urogenital sinus to form structures called the sinovaginal bulbs. These fuse to form the vaginal plate which extends from the müllerian ducts to the urogenital sinus. This plate begins to canalize, starting at the hymen, and proceeds upwards to the cervix (Fig. 93.1). This process is not complete until 21 weeks of gestation.4 The external genitalia in females consist of the genital tubercle, the urogenital sinus, and the urethral and labioscrotal folds.5 The genital tubercle becomes the clitoris, the urethral folds develop into the labia minora, and the labioscrotal folds become the labia majora. By week 12 of development these structures are recognizably female. These structures are sensitive to androgens and form the penis and scrotum in normal male development.
Imaging Accurate imaging is pivotal to the diagnosis of many of the conditions described below. Ultrasound is routinely
Figure 93.1. Embryologic development of the müllerian system. 1318
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used as the primary mode of investigation. Recent developments in this field have allowed better assessment of uterine anomalies, particularly with the introduction of high-resolution transvaginal ultrasound probes. Unfortunately, this may not be appropriate in children or young teenagers or in those whose problem is vaginal absence. More recently, three-dimensional (3-D) ultrasound has been employed in the diagnosis of uterine anomalies. Its benefits include the fact that it is non-invasive and allows for more accurate diagnosis compared with conventional ultrasound.6 Ultrasound has the benefit of being safe in pregnancy which is useful given that the subjects are nearly all young fertile women; it also allows concomitant assessment of neighboring structures such as the urinary tract. Magnetic resonance imaging (MRI) is an extremely useful tool in assessing these complex malformations,7,8 particularly where there is no vaginal cavity in which to put an ultrasound probe, or in children or adolescents who have not engaged in sexual activity (Fig. 93.2). There are no studies as yet comparing the accuracy of MRI with 3-D ultrasound.
Other imaging information:
modalities
may
give
useful
• Hysterosalpingography (HSG) gives information about
•
the internal contour of the uterus, and allows an assessment of the size and extent of uterine septa. However, it does not provide sufficient information to discern between a septate and a bicornuate uterus. It has two main drawbacks: 1) many patients consider it to be an uncomfortable procedure; and 2) it may be complicated by pelvic inflammatory disease. Hysteroscopy is of particular use in diagnosing uterine anomalies and has the benefit of allowing treatment in some cases, particularly in septate and arcuate uterus.9 As hysteroscopy does not provide any information on the outer surface of the uterus, it may be difficult to distinguish between a septate and a bicornuate uterus.
Investigative laparoscopy should be undertaken only in cases where all other imagining modalities have failed, and the potential for combining this with laparoscopic treatment should also be considered. Nevertheless, it is considered to be the gold standard in the investigation of gynecologic anomalies.10
SImple/ISolated anomalIeS Imperforate hymen
Figure 93.2. with cloaca.
MRI of an obstructed uterus in a young girl
The hymen is the embryologic septum between the sinovaginal bulbs above and the urogenital sinuses below. The incidence of imperforate hymen is estimated to be 1 in 1000 live female births.11 Hymen malformations are not usually associated with other müllerian or uterine anomalies. Failure of this septum to perforate in the embryo or in early childhood may present at adolescence with obstructed menstrual flow. The history is usually of several months of cyclical abdominal pain in an adolescent without menstruation. A pelvic mass may be palpated or found on ultrasound scan. On inspection of the vulva it is sometimes possible to see a bulging vaginal membrane. The treatment for these patients is a simple cruciate incision with excision of a quadrate of hymeneal tissue to allow drainage of the vagina and uterus. Wide excision of the hymen too close to the vaginal mucosa may result in stenosis at the introitus.12 There have been reports of familial cases of imperforate hymen, usually between siblings, suggesting a recessive mode of inheritance.13 There has also been a 1319
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report of imperforate hymen in two generations of the same family,14 which suggests a possible dominant mode of transmission. There may be a case for assessing all female family members of affected individuals.
transverse vaginal septum This uncommon condition occurs in approximately 1 in 70,000 females15 due to a failure of the müllerian ducts and urogenital sinus to canalize. These septa are most commonly found at the junction of the middle to upper two-thirds of the vagina. In cases of a complete transverse septum, associated uterine anomalies are common; one series reports the rate to be as high as 95%.16 Most presentations of this condition are in young girls after the menarche with cyclical pelvic pain as a result of hematocolpos, which may be complicated by hematometra, bilateral hematosalpinges and possibly endometriosis. It can rarely occur before puberty when the presentation is with pelvic pain, the obstruction in this case thought to be due to a build-up of mucous secretions from the cervical glands. In one interesting case expectant management was employed, where the thickness of the septum and volume of the dilated vagina were monitored regularly using ultrasonography. The thickness of the vaginal septum decreased from 26 to 8 mm over a period of 5 years, thus allowing a less complicated surgical procedure in a more mature patient.17 The thinning of the septum was felt to be due to a pressure effect of the hematocolpos. However, in the majority of cases the treatment is surgical excision without delay. If the septum is thin and low it may be possible to remove it using a vaginal approach.18 Care must be taken to ensure that the septum is entirely removed as vaginal stenosis may result if the procedure is incomplete. Thick transverse septa or those located higher up in the vagina will require an abdominoperineal approach. In those cases where the distance between the margins is too great, then some form of skin or intestinal graft may be required.
usually surgical resection if symptomatic. Care must be taken to resect the septum right up to the cervix or dyspareunia will continue. Rarely, one hemivagina is obstructed, with the other functioning normally. This may cause an unusual clinical picture of apparently normal menstruation from the unaffected side associated with pelvic pain. Vaginal examination may reveal a unilateral swelling due to hematocolpos. As menstruation appears initially normal, this results in delayed diagnosis of obstruction which would normally be made much quicker in the absence of any menstrual flow. Also, as this is an uncommon condition presenting in young females, the patient may attend a pediatrician rather than a gynecologist, especially as she is having what appear to be normal periods. Further investigation of these patients may demonstrate uterine anomalies. The imaging modality of choice in these cases would normally be MRI.8 One large study of 20 women found that 87.8% of cases had an associated uterine malformation, the commonest of which was a complete uterine septum.16 These more complex müllerian anomalies will be discussed in more detail later. Surgical treatment of simple vaginal longitudinal septa is generally uncomplicated and is approached vaginally. As the vagina is a vascular structure, care should be taken with hemostasis. As with transverse septa and imperforate hymen, postoperative vaginal stenosis should be looked for and treated if necessary.
uterine anomalies
longitudinal vaginal septum
Uterine anomalies are present in 0.5–2.0% of women;20,21 this rate is higher in women who are infertile and who have had repeated miscarriages.20 Attempts have been made to classify uterine anomalies. Perhaps the most widely accepted classification system for uterine anomalies is from the American Fertility Society.22 This classification organizes the anomalies into six major uterine anatomic types (Fig. 93.3). The resulting anomalies can be considered to be due to one of four events:23
Longitudinal septa are often asymptomatic and may not be apparent until the patient is sexually active (when it presents with dyspareunia) or in some cases during labor, where there may be a delay in the second stage.19 They result as a failure of reabsorption of the vaginal septum during embryogenesis. The septum may be complete, and extend from the cervix to the introitus, or partial, which may be of any length along the course of the vagina. Management for the majority of these is
1. Failure of one or more of the müllerian ducts to develop – agenesis, unicornuate uterus without rudimentary horn; 2. Failure of the ducts to canalize – unicornuate uterus with rudimentary horn; 3. Failure of or abnormal fusion of the ducts – uterus didelphys, bicornuate uterus; 4. Failure of the reabsorption of the midline uterine septum – septate uterus, arcuate uterus.
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Figure 93.3. The American Fertility Society classification of müllerian anomalies.
Septate uterus
Bicornuate uterus
The commonest of these anomalies appears to be septate uterus which accounts for approximately 35% of all uterine anomalies.23 The extent of the septum varies and may be partial or complete. It is known to result in early pregnancy loss and infertility, and this is how the majority of these patients present. However, septa can also be found by chance in women with an uncomplicated obstetric past history and so the decision on treatment can be complex. If treatment is recommended, then the most appropriate treatment for septate and arcuate uterus is resection of the septum; this can be achieved via hysteroscopic metroplasty, thus avoiding the need for a laparotomy and an incision in the uterus. It is known that metroplasty improves reproductive outcomes in these women.24
Bicornuate uterus accounts for 25% of uterine anomalies.23 These patients also have recurrent miscarriage, premature delivery, and infertility. There have also been reported neonatal risks, including low Apgar scores and small-for-date infants. Surgical options for these patients are limited. Pregnancies do occur and these women should be carefully monitored throughout. This is complicated further if there are multiple pregnancies, and twin pregnancies in bicornuate uteri have been reported.25,26
Unicornuate uterus Unicornuate uterus results from normal differentiation of only one müllerian duct. This may present with miscarriage or preterm delivery. One study 1321
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demonstrated a preterm delivery rate of 25% and early miscarriage rate of 37.5%.27 Non-communicating rudimentary horns with functional endometrium usually present with pain; this necessitates the removal of the horn, which may be carried out laparoscopically (Fig. 93.4).28 Removal of the horn is essential as pregnancy may occur within the horn.29 There have been reports of removal of pregnant uterine horns, and in this situation the risks are greater as the pregnant uterus is a more vascular structure. It is essential to obtain renal imaging such a preoperative intravenous pyelogram (IVP) as up to 30% will have associated renal tract anomalies.30 It is suggested that the standard treatment of these cases should include feticide and methotrexate as this, in addition to gonadotrophin-releasing hormone, would allow a safer approach to the laparoscopic removal of the uterine horn. The obstetric outcomes in subsequent pregnancies in this group of patients are largely unknown, although it is likely that they would result in premature labor. There have been case reports of full term labor after laparoscopic removal of a rudimentary horn with an ectopic pregnancy.31 In those cases where there is no functional endometrium in the uterine horn, the issue of removal is debatable as there is no risk of pregnancy and its consequences.
Didelphic uterus Didelphic uterus is often associated with a hemivagina, or a vaginal septum of varying degree, and possible duplicated kidneys or renal agenesis. It is thought to account for 10% of all uterine anomalies.
absent cervix Congenital absence of the cervix is a rare condition and occurs in 1 in 80,000 to 100,000 births.32 It is known to be associated with vaginal aplasia, both partial and complete, and renal anomalies. In a recent retrospective review of 18 patients, 39% had associated vaginal aplasia.33 Presentation is usually with primary amenorrhea and cyclical lower abdominal pain. Endometriosis or pelvic infection may result from the chronic hematometra. The differential diagnosis includes high transverse vaginal septum and in some cases the actual diagnosis may not be clear until surgery. The management of this condition has changed in recent years with the advances in reproductive technology. Previously, patients with cervical atresia were offered a total hysterectomy as complications of recanalizing the cervix were common and a viable pregnancy was unlikely.19,34 Now the recommended treatment options consist of either suppression of menses with preservation of the uterus for pregnancy with reproductive assistance, or uterovaginal anastomosis. There are very few data on outcomes following uterovaginal anastomosis, the largest study published stating that the postoperative complication rate was low with only 22% requiring further surgery. Furthermore, they report six spontaneous pregnancies in four of their patients.33 Despite these encouraging results it is important to realize that the possibility of serious complications exists and postoperative sepsis after uterovaginal anastomosis has resulted in septic shock and death.35 Reproductive technology has advanced to allow these patients an opportunity to become pregnant with the assistance of in vitro fertilization. There have been case reports of implanting embryos transmyometrially which have resulted in a viable pregnancy.36,37 In the latter case report the patient underwent uterovaginal canalization using amniotic membrane at the time of cesarean section.37 One of the difficulties of these techniques is the management of miscarriage should it occur. Cervical dilation and curettage is often not an option as there may be no obvious cervix, or a small scarred cervix. Therefore most cases would require a laparoscopic or open removal of the remnants of pregnancy. One case report has used a conservative approach of observation where the patient’s β-human chorionic gonadotropin levels were monitored with ultrasound examination of the uterus.32
complex anomalIeS Figure 93.4. horn.
Laparoscopic view of an obstructed uterine
Complex anomalies can be considered in two groups: anatomic and endocrine. This allows distinction based
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on the underlying cause rather than the system affected. Complex anatomic anomalies include the Mayer– Rokitansky–Kuster–Hauser syndrome.
congenital absence of the vagina Agenesis of the vagina occurs in approximately 1 in 5000 to 30,000 live female births.38,39 It is commonly referred to as Mayer–Rokitansky–Kuster–Hauser syndrome (MRKH). In the majority of suffers there is no discernable vagina present, whereas approximately 25% will have a short blind-ending pouch. This is almost always associated with an absent or rudimentary uterus. There are normal ovaries and 46,XX karyotype. Anomalies of the urinary tract are present in an estimated 34% of patients, and spinal anomalies are found in 12%.40 There is thought to be a genetic basis for this syndrome and currently possible implicated genes include HNF1b and members of the Wnt gene family.41,42 Treatment usually involves formation of a vagina. The preferred method for this is non-surgical with the use of pressure dilation therapy.43 This involves the use of graded dilators applied to the perineum at the point where the vagina would normally be sited (Fig. 93.5). In most patients, while there is no vagina, there is often a vaginal ‘pit’ which acts as a guide to the site where the patient should apply pressure. Success of this treatment is limited to motivated patients and it is recommended that they are seen regularly during this treatment and offered psychological support to improve outcomes. For those in whom dilation has not worked, or is not possible, then surgical construction is necessary. The
Figure 93.5.
Amielle dilators.
timing of this procedure should be carefully considered, as many of those who have surgery will need to use some form of pressure dilation to maintain the vagina. Numerous forms of vaginoplasty have been employed in the treatment of these patients. They range from simple skin grafting to more complex intestinal vaginoplasties, The use of bowel segments for vaginoplasty was reported in the literature as early as 1907;44 segments of rectum, ileum and sigmoid colon may be employed. Stenosis (apart from at the introitus) is rare, and the vagina remains moist and of appropriate caliber. However, a vagina constructed from intestine will be relatively insensitive, and may have excess mucus production requiring the patient to wear pads permanently. There have been reports of diversion colitis with colovaginoplasty and this can be difficult to treat.45 This seems to be less common with ileal vaginoplasty. Vaginal malignancy has also been reported following both intestinal and skin graft vaginoplasty,46 with a mean length of time to diagnosis of carcinoma of approximately 17 years.47 More recent reports of laparoscopic techniques that have become available include laparoscopic Davydov and Vecchietti procedures48,49 (Fig. 93.6). Psychological preparation is essential both before and after surgery. The maintenance of the neovagina postoperatively often requires regular dilation until regular sexual intercourse occurs. This is of particular importance in skin graft vaginas. The patient should be emotionally well adjusted and mature.50 Fertility options for these patients are limited, but as they have normal functioning ovaries then surrogacy is an option. There have been reports of successful surrogacy treatment in patients with Rokitansky syndrome.51–53
Figure 93.6.
Laparoscopic Vecchietti. 1323
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congenital adrenal hyperplasia Congenital adrenal hyperplasia (CAH) is the most common cause of ambiguous genitalia and occurs in approximately 1 in 14,000 births in the UK. The pathogenesis in the majority of cases is 21-hydroxylase deficiency. The lack of this enzyme leads to a decrease in the level of cortisol, which in turn causes an increase in adrenocorticotropic hormone (ACTH) secretion. This causes an increase in the levels of cortisol precursors which are forced along the androgen pathway. In its most severe form, aldosterone levels will also be low, which may lead to salt wasting, volume depletion, hypotension, reduced renal blood flow, and raised renin activity. The aim of treatment in these patients is to replace the aldosterone with fludrocortisone and replace glucocorticoid to suppress the ACTH overactivity Presentation differs depending upon the form of disease, and ranges from neonatal salt wasting crisis to adult onset of virilization. The majority of cases are diagnosed in children or neonates who are noted to have ambiguous or masculinized genitalia at birth. Virilization of the female genitalia occurs to a varying degree, causing labial fusion, clitoromegaly, and a confluence of the vagina and distal urethra (Fig. 93.7).54 Current standard practice includes corrective genital surgery to separate the labia, reduce the size of the clitoris and separate vagina and urethra.55 The aims of this are to create a feminine appearance, allow passage of menses, preserve sexual function, and prevent subsequent urinary tract complications.56 This is usually performed as a ‘one-stage’ procedure in infancy, although many patients require further surgery in adolescence to facilitate menstrual flow and allow penetrative sexual intercourse. There has been increasing recent controversy amongst clinicians and patient peer support
Figure 93.7.
Newborn with congenital adrenal hyperplasia.
groups as to the need for and timing of feminizing genital surgery. Genital surgery is associated with damage to sensory innervation of the clitoris and is associated with loss of sexual sensation and an increased risk of sexual dysfunction.57 Long-term data are, however, scanty and at present no consensus has been reached.
androgen insensitivity – complete and partial Androgen insensitivity syndrome, due to a defect in the androgen receptor (AR), has an incidence thought to be somewhere in the region of 1 in 13,000 to 40,000 live births.39,58 It is an X-linked recessive disorder where affected individuals have a normal male karyotype (XY) with a spectrum of clinical manifestations, and is generally subdivided into complete and partial. All patients have testes and normal testosterone production and metabolism, with either a female or ambiguous phenotype. There are usually no müllerian structures present. Patients with partial androgen insensitivity are diagnosed at birth, as there is ambiguity of the genitalia, and a decision regarding the sex of rearing needs to be made. This is a difficult and sensitive issue and should be handled in a specialist centre with a full multidisciplinary team of experts available, including a psychologist, pediatric urologist and endocrinologist. Those with complete androgen insensitivity (CAIS) may present later in life with primary amenorrhea or in some cases with inguinal hernia. The incidence of CAIS in females presenting with inguinal hernia is estimated to be in the region of 0.8–2.4%,59 and some would suggest that all girls presenting with inguinal herniae should be investigated for androgen insensitivity.60 Recommended treatment for these patients includes removal of gonads, as there is a potential for malignant change, and lengthening of the vagina if necessary. Gonadectomy may be delayed until after puberty, which allows the young female to undergo puberty spontaneously and minimizes disruption to schooling for hospital appointments and surgery. The gonadectomy should ideally be carried out laparoscopically, and a preoperative scan is required to locate the gonads accurately. After removal of the gonads, patients will require some form of hormone replacement, typically until 50 years of age, when most women would experience a natural decline in hormone levels. Patients should also undergo regular monitoring of bone mineral density. Vaginal lengthening may be undertaken at any time, and the patient should be counseled appropriately before. The treatment options for vaginal lengthening are as for MRKH, with dilation therapy as the first line choice of treatment.
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aSSocIated wIth other anomalIeS or aS part of a Syndrome anorectal malformation and cloaca Many patients with gynecologic developmental abnormalities may have other anomalies and the converse is also true. Females born with a persistent common cloacal channel will not only require reconstruction to separate the common cavity into three distinct structures (vagina, urethra and rectum) but there are also a significant percentage of these patients with associated gynecologic anomalies. The commonest of these is a duplicate vagina.61 In patients with a persistent cloaca the rate is quoted as being as high as 50%.62 Yet many of these patients are not routinely investigated for gynecologic developmental anomalies. In one recent study, 36% of female patients born with a cloacal anomaly presented with an obstructed uterus in puberty, all of whom required surgery.63 Any surgery required is more difficult in these patients as they have often undergone multiple surgical procedures as young children. Furthermore, fertility issues are also complicated by the fact that these women, once pregnant, will need to deliver via cesarean section with an experienced surgeon present.
turner’s syndrome Turner’s syndrome (TS) is the most common sex chromosome disorder in females, and occurs in 1 in 2000 live female births.64 It is the result of a complete or partial X chromosome monosomy. The syndrome is phenotypically characterized by short stature, webbed neck, wide carrying angle, and low posterior hair line. Ovarian dysgenesis is documented as occurring in 95% of TS sufferers.65 Ovarian failure occurs in the first few months or years of life. Therefore, these patients are not able to undergo a spontaneous puberty, and amenorrhea and minimal breast development are the norm, though not inevitable. One study has shown 16% of its Turner’s population to have undergone spontaneous puberty.66 However, few patients with Turner’s syndrome are fertile and spontaneous pregnancy occurs in approximately 5%,66 usually in patients who have mosaicism. Furthermore, those who mange to become pregnant have documented poor outcomes, with a 29% miscarriage rate, 7% perinatal death rate, and a 20% chance of having offspring with a chromosomal abnormality (e.g. Down’s syndrome, Turner’s syndrome).67 Initial management of these patients includes an echocardiogram and renal tract ultrasound as there are a significant percentage of associated cardiac and
renal anomalies. Growth hormone therapy should be considered in childhood to try to increase final height. Estrogen replacement is also necessary to induce a normal puberty. After puberty nearly all TS patients will require long-term hormone replacement to prevent the onset of osteoporosis and atherosclerosis.68 Due to the complex nature of this disease it is best managed by a multidisciplinary team where appropriate advice and counseling can be given.
concluSIon As these conditions are rare, the diagnosis is often missed or delayed, causing much anxiety for both the patient and her family. The key to managing these patients is thoroughness and attention to detail, and it is imperative to provide as accurate a diagnosis as possible. Many of these conditions have adverse implications for fertility or sexual function. Psychological input is crucial and should be offered to the family as a whole. Support will need to be ongoing in many cases through childhood and adolescence. Full information about the diagnosis and its implications must be made available to the family and should be explained clearly so that the patients and their parents can fully appreciate what the problem is and what the future holds for them. Other helpful resources that are available to these patients include patient support groups which exist for some of the conditions discussed above. These can provide useful additional information for the patients, often of a more practical nature, and also reinforce the idea that the patient is not alone in her suffering. Details of such organizations should be available in the clinics where these patients are seen. Another useful tool in aiding patients’ understanding of what are often quite difficult concepts is written literature, which should be in clear, easy-to-understand terms, and up to date. Such complex and rare conditions need the input of a multidisciplinary team comprising at the very least a psychological, surgical, and endocrinologic component. Specialized back-up services such as imaging, biochemistry, and genetics are also essential. Patients with complex developmental anomalies should be referred to specialized clinics which can provide the services required.
referenceS 1. Cooper JM, Houck RM, Rigberg HS. The incidence of intrauterine abnormalities found at hysteroscopy in patients undergoing elective hysteroscopic sterilization. J Reprod Med 1983;28(10):659–61. 2. Jurkovic D, Gruboeck K, Tailor A, Nicolaides KH. Ultra-
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sound screening for congenital uterine anomalies. Br J Obstet Gynaecol 1997;104(11):1320–1. 3. Simon C, Martinez L, Pardo F, Tortajada M, Pellicer A. Müllerian defects in women with normal reproductive outcome. Fertil Steril 1991;56(6):1192–3. 4. Kim HH, Laufer MR. Developmental abnormalities of the female reproductive tract. Curr Opin Obstet Gynecol 1994;6(6):518–25. 5. Cameron F, Smith C. Embryology of the female genital tract. In: Balen AH (ed) Paediatric and Adolescent Gynaecology. Cambridge: Cambridge University Press, 2004; 3–8. 6. Woelfer B, Salim R, Banerjee S, Elson J, Regan L, Jurkovic D. Reproductive outcomes in women with congenital uterine anomalies detected by three-dimensional ultrasound screening. Obstet Gynecol 2001;98(6):1099–103. 7. Troiano RN, McCarthy SM. Mullerian duct anomalies: imaging and clinical issues. Radiology 2004;233(1):19–34.
18. MacDougall J, Creighton SM. Surgical correction of vaginal and other anomalies: a multidisciplinary approach. In: Balen AH (ed) Paediatric and Adolescent Gynaecology. Cambridge: Cambridge University Press, 2004; 120–30. 19. Hampton HL. Role of the gynecologic surgeon in the management of urogenital anomalies in adolescents. Curr Opin Obstet Gynecol 1990;2(6):812–18. 20. Acien P. Incidence of Müllerian defects in fertile and infertile women. Hum Reprod 1997;12(7):1372–6. 21. Heinonen PK. Clinical implications of the didelphic uterus: long-term follow-up of 49 cases. Eur J Obstet Gynecol Reprod Biol 2000;1(2):183–90. 22. The American Fertility Society. Classifications of adnexal adhesions, distal tubal occlusion, tubal occlusion secondary to tubal ligation, tubal pregnancies, mullerian anomalies and intrauterine adhesions. Fertil Steril 1988;49(6):944–55.
8. Minto CL, Hollings N, Hall-Craggs M, Creighton S. Magnetic resonance imaging in the assessment of complex Müllerian anomalies. BJOG 2001;108(8):791–7.
23. Grimbizis GF, Camus M, Tarlatzis BC, Bontis JN, Devroey P. Clinical implications of uterine malformations and hysteroscopic treatment results. Hum Reprod Update 2001;7(2):161–74.
9. Grimbizis G, Camus M, Clasen K, Tournaye H, De Munck L, Devroey P. Hysteroscopic septum resection in patients with recurrent abortions or infertility. Hum Reprod 1998;13(5):1188–93.
24. Pabuccu R, Gomel V. Reproductive outcome after hysteroscopic metroplasty in women with septate uterus and otherwise unexplained infertility. Fertil Steril 2004;81(6):1675–8.
10. Pellerito JS, McCarthy SM, Doyle MB, Glickman MG, DeCherney AH. Diagnosis of uterine anomalies: relative accuracy of MR imaging, endovaginal sonography, and hysterosalpingography. Radiology 1992;183(3):795–800. 11. Stelling JR, Gray MR, Reindollar RH. Endocrinology and molecular biology of the female genital tract in utero to puberty. In: Gidwani G, Falcone T (eds) Congenital Malformations of the Female Genital Tract: Diagnosis and Management. Philadelphia: Lippincott, Williams and Wilkins, 1999; 21–40. 12. Joki-Erkkila MM, Heinonen PK. Presenting and longterm clinical implications and fecundity in females with obstructing vaginal malformations. J Pediatr Adolesc Gynecol 2003;16(5):307–12. 13. Usta IM, Awwad JT, Usta JA, Makarem MM, Karam KS. Imperforate hymen: report of an unusual familial occurrence. Obstet Gynecol 1993;82:655–6. 14. Stelling JR, Gray MR, Davis AJ, Cowan JM, Reindollar RH. Dominant transmission of imperforate hymen. Fertil Steril 2000;74(6):1241–4. 15. Banerjee R, Laufer MR. Reproductive disorders associated with pelvic pain. Semin Pediatr Surg 1998;7(1):52–61. 16. Haddad B, Louis-Sylvestre C, Poitout P, Paniel BJ. Longitudinal vaginal septum: a retrospective study of 202 cases. Eur J Obstet Gynecol Reprod Biol 1997;74(2):197–9. 17. Beyth Y, Klein Z, Weinstein S, Tepper R. Thick transverse vaginal septum: expectant management followed by surgery. J Pediatr Adolesc Gynecol 2004;17(6):379–81.
25. Barmat LI, Damario MA, Kowalik A, Kligman I, Davis OK, Rosenwaks Z. Twin gestation occupying separate horns of a bicornuate uterus after in-vitro fertilization and embryo transfer. Hum Reprod 1996;11(10):2316–18. 26. Narlawar RS, Chavhan GB, Bhatgadde VL, Shah JR. Twin gestation in one horn of a bicornuate uterus. J Clin Ultrasound 2003;31(3):167–9. 27. Raga F, Bauset C, Remohi J, Bonilla-Musoles F, Simon C, Pellicer A. Reproductive impact of congenital Müllerian anomalies. Hum Reprod 1997;12(10):2277–81. 28. Nezhat F, Nezhat C, Bess O, Nezhat CH. Laparoscopic amputation of a noncommunicating rudimentary horn after a hysteroscopic diagnosis: a case study. Surg Laparosc Endosc 1994;4(2):155–6. 29. Falcone T, Gidwani G, Paraiso M, Beverly C, Goldberg J. Anatomical variation in the rudimentary horns of a unicornuate uterus: implications for laparoscopic surgery. Hum Reprod 1997;12(2):263–5. 30. Cutner A, Saridogan E, Hart R, Pandya P, Creighton S. Laparoscopic management of pregnancies occurring in non-communicating accessory uterine horns. Eur J Obstet Gynecol Reproductive Biology 2004;113(1):106–9. 31. Adolph AJ, Gilliland GB. Fertility following laparoscopic removal of rudimentary horn with an ectopic pregnancy. J Obstet Gynaecol Can 2002;24(7):575–6. 32. Suganuma N, Furuhashi M, Moriwaki T, Tsukahara S, Ando T, Ishihara Y. Management of missed abortion in
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a patient with congenital cervical atresia. Fertil Steril 2002;77(5):1071–3. 33. Deffarges JV, Haddad B, Musset R, Paniel BJ. Utero-vaginal anastomosis in women with uterine cervix atresia: longterm follow-up and reproductive performance. A study of 18 cases. Hum Reprod 2001;16(8):1722–5. 34. Rock JA, Schlaff WD, Zacur HA, Jones HW Jr. The clinical management of congenital absence of the uterine cervix. Int J Gynaecol Obstet 1984;22(3):231–5. 35. Casey AC, Laufer MR. Cervical agenesis: septic death after surgery. Obstet Gynecol 1997;90(4 Pt 2):706–7. 36. Anttila L, Penttila TA, Suikkari AM. Successful pregnancy after in-vitro fertilization and transmyometrial embryo transfer in a patient with congenital atresia of cervix: case report. Hum Reprod 1999;14(6):1647–9. 37. Lai TH, Wu MH, Hung KH, Cheng YC, Chang FM. Successful pregnancy by transmyometrial and transtubal embryo transfer after IVF in a patient with congenital cervical atresia who underwent uterovaginal canalization during Caesarean section: case report. Hum Reprod 2001;16(2):268–71. 38. Aittomaki K, Eroila H, Kajanoja P. A population-based study of the incidence of müllerian aplasia in Finland. Fertil Steril 2001;76(3):624–5. 39. Blackless M, Charuvastra A, Derryck A, Fausto-Sterling A, Lauzanne K, Lee E. How sexually dimorphic are we? Review and synthesis. Am J Human Biol 2000;12(2):151–66. 40. Griffin JE, Edwards C, Madden JD, Harrod MJ, Wilson JD. Congenital absence of the vagina. The Mayer–Rokitansky–Kuster–Hauser syndrome. Ann Intern Med 1976;85(2):224–36. 41. Lindner TH, Njolstad PR, Horikawa Y, Bostad L, Bell GI, Sovik O. A novel syndrome of diabetes mellitus, renal dysfunction and genital malformation associated with a partial deletion of the pseudo-POU domain of hepatocyte nuclear factor-1β. Hum Mol Genet 1999;8(11):2001–8. 42. Biason-Lauber A, Konrad D, Navratil F, Schoenle EJ. A WNT4 mutation associated with Müllerian-duct regression and virilization in a 46,XX woman. N Engl J Med 2004;351(8):792–8. 43. ACOG committee opinion. Nonsurgical diagnosis and management of vaginal agenesis. Number 274, July 2002. Committee on Adolescent Health Care. American College of Obstetrics and Gynecology. Int J Gynaecol Obstet 2002;79(2):167–70. 44. Baldwin JF. Formation of an artificial vagina by intestinal transplantation. Ann Surg 1907;40:398–403. 45. Syed HA, Malone PS, Hitchcock RJ. Diversion colitis in children with colovaginoplasty. BJU Int 2001;87(9):857–60. 46. Lawrence AA. Vaginal neoplasia in a male-to-female transsexual: case report, review of the literature, and recommendations for cytological screening. Int J Transgenderism 2001;5(1). (Online.)
47. Steiner E, Woernle F, Kuhn W et al. Carcinoma of the neovagina: case report and review of the literature. Gynecol Oncol 2002;84(1):171–5. 48. Langebrekke A, Istre O, Busund B, Sponland G, Gjonnaess H. Laparoscopic assisted colpoiesis according to Davydov. Acta Obstet Gynecol Scand 1998;77(10):1027–8. 49. Veronikis DK, McClure GB, Nichols DH. The Vecchietti operation for constructing a neovagina: indications, instrumentation, and techniques. Obstet Gynecol 1997;90(2):301–4. 50. Templeman C, Hertweck SP. Vaginal agenesis: an opinion on the surgical management. J Pediatr Adolesc Gynecol 2000;13(3):143–4. 51. Beski S, Gorgy A, Venkat G, Craft IL, Edmonds K. Gestational surrogacy: a feasible option for patients with Rokitansky syndrome. Hum Reprod 2000;15(11):2326–8. 52. Van Waart J, Kruger TF. Surrogate pregnancies in patients with Mayer–Rokitansky–Kustner–Hauser syndrome and severe teratozoospermia. Arch Androl 2000;45(2):95–7. 53. Esfandiari N, Claessens EA, O’Brien A, Gotlieb L, Casper RF. Gestational carrier is an optimal method for pregnancy in patients with vaginal agenesis (Rokitansky syndrome). Int J Fertil Womens Med 2004;49(2):79–82. 54. Hughes IA. Management of congenital adrenal hyperplasia. Arch Dis Child 1988;63(11):1399–404. 55. de Jong TP, Boemers TM. Neonatal management of female intersex by clitorovaginoplasty. J Urol 1995;154(2 Pt 2):830–2. 56. Consensus statement on 21-hydroxylase deficiency from the Lawson Wilkins Pediatric Endocrine Society and the European Society for Pediatric Endocrinology. J Clin Endocrinol Metab 2002;87(9):4048–53. 57. Crouch NS, Minto CL, Laio LM, Woodhouse CR, Creighton SM. Genital sensation after feminizing genitoplasty for congenital adrenal hyperplasia: a pilot study. BJU Int 2004;93(1):135–8. 58. Bangsboll S, Qvist I, Lebech PE, Lewinsky M. Testicular feminization syndrome and associated gonadal tumors in Denmark. Acta Obstet Gynecol Scand 1992;71(1):63–6. 59. Gans SL, Rubin CL. Apparent female infants with hernias and testes. Am J Dis Child 1962;104:82–6. 60. Viner RM, Teoh Y, Williams DM, Patterson MN, Hughes IA. Androgen insensitivity syndrome: a survey of diagnostic procedures and management in the UK. Arch Dis Child 1997;77(4):305–9. 61. Metts JC III, Kotkin L, Kasper S, Shyr Y, Adams MC, Brock JW III. Genital malformations and coexistent urinary tract or spinal anomalies in patients with imperforate anus. J Urol 1997;158(3 Pt 2):1298–300. 62. Pena A. The surgical management of persistent cloaca: results in 54 patients treated with a posterior sagittal approach. J Pediatr Surg 1989;24(6):590–8.
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63. Warne SA, Wilcox DT, Creighton S, Ransley PG. Longterm gynecological outcome of patients with persistent cloaca. J Urol 2003;170(4 Pt 2):1493–6.
G. Spontaneous pubertal development in Turner’s syndrome. Italian Study Group for Turner’s Syndrome. J Clin Endocrinol Metab 1997;82(6):1810–13.
64. Gravholt CH, Juul S, Naeraa RW, Hansen J. Prenatal and postnatal prevalence of Turner’s syndrome: a registry study. BMJ 1996;312(7022):16–21.
67. Tarani L, Lampariello S, Raguso G et al. Pregnancy in patients with Turner’s syndrome: six new cases and review of literature. Gynecol Endocrinol 1998;12(2):83–7.
65. Saenger P, Wikland KA, Conway GS et al. Recommendations for the diagnosis and management of Turner syndrome. J Clin Endocrinol Metab 2001;86(7):3061–9.
68. Elsheikh M, Bird R, Casadei B, Conway GS, Wass JA. The effect of hormone replacement therapy on cardiovascular hemodynamics in women with Turner’s syndrome. J Clin Endocrinol Metab 2000;85(2):614–18.
66. Pasquino AM, Passeri F, Pucarelli I, Segni M, Municchi
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94 Pediatric urogynecology Andrew J Kirsch, Howard M Snyder
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IntroductIon
Female embryology
The wide spectrum of anomalies of female embryogen esis results in problems related to the development of the urinary and genital tracts. Many of the clinical disorders seen in girls and young women that appear to involve the genitalia alone may be the harbinger of related urinary tract disorders. Abnormalities present ing in infancy may be easy to recognize secondary to an abnormal antenatal ultrasonographic or physical exami nation in the newborn period. Many urogenital malfor mations, however, are elusive and may become evident only when a clinical problem arises. The most common urogynecologic disorders prompt ing childhood evaluation focus on problems of urinary continence and introital abnormalities. Interlabial masses, often included in the differential diagnosis of urinary incontinence, as well as difficulties with appro priate gender identification in genetic and phenotypic females, are discussed in this chapter. As congenital abnormalities result from abnormal embryogenesis, it is appropriate to begin with a brief overview of normal female embryology (see also Chapter 9).
Congenital abnormalities commonly involve both the urinary and genital tracts. An understanding of nor mal embryogenesis is a prerequisite for understanding congenital abnormalities. A detailed discussion of the embryology of the lower urinary tract is provided by Marshall1 and by Stephens et al.2 The divergence of normal sexual differential into male and female phenotypes begins in week 9 of gestation. If no Y chromosome is present, the ovaries develop whereas the testes and Sertoli cells do not. As a result, the wolffian system regresses (absence of andro gen production) and the müllerian ducts form the fallopian tubes, uterus, and proximal part of the vagina (absence of müllerian inhibiting factor). The embryo logic origins and adult counterparts of the female genital tract are shown in Figure 94.1 and described in Table 94.1.
Ovary (before descent) Epoophoron Paroophoron Uterine tube Urinary bladder Ureter
Uterus
Urethra Paraurethral glands a Ovary (after descent) Uterine tube
Tract of mesonephric duct Vaginal plate Greater vestibular gland Hydatid (of Morgagni) Epoophoron Paroophoron
Gartner's duct Gartner's duct cysts Vagina Hymen b
Labium majus
Figure 94.1. Embryology and development of the female genital tracts: (a) a 12-week fetus; (b) a newborn female ( urogenital sinus; mesonephric duct; paramesonephric duct).
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table 94.1.
Female embryology
Weeks of gestation
Embryonic structure/event
Adult counterpart
7–8
Genital ridge transformed
Ovary
9–10
Müllerian ducts fuse distally
Fallopian tubes, uterus, cervix, proximal vagina
12–20
Sinovaginal bulbs elongate, form vaginal plate; canalization of plate at urogenital sinus
Distal vagina
Genital tubercle elongates Urethral folds do not fuse Labial swellings enlarge Urogenital groove remains
Clitoris, hymen Labia minora Labia majora Introitus
Mesonephric ducts
Ureters
Vestigial structures: Mesonephric duct Proximal end Distal end
urInary IncontInence In gIrls etiology Urinary incontinence in females may have functional or neurogenic causes, or may be secondary to con genital abnormalities of the lower urinary tract. The most common cause of severe urinary incontinence in children is related to a neurologic deficit. The leading causes of neurogenic incontinence include myelome ningocele (spina bifida), sacral agenesis, and vertebral or spinal cord lesions. In these conditions, changes within the spinal cord may occur over time, making careful evaluation and close followup essential. In all children presenting with urinary incontinence, urinalysis should be performed to assess the presence of infection, hematuria, proteinuria, glucosuria or renal concentrating defect (early morning specific gravity, 1.022). Chronic nighttime wetting, polyuria or nocturia may indicate renal failure or diabetes and requires thor ough medical evaluation. Incontinence can be broadly divided between that requiring surgical intervention and that requiring medi cal or behavioral therapies. In general, incontinence related to primary nocturnal enuresis or infrequent voiding tends to resolve with time and does not require surgery. The following sections address the clinical pre sentation, evaluation, and treatment of lower urinary tract abnormalities associated with urinary incontinence in girls.
Appendix vesiculosa, paroöphoron and epoöphoron Gartner’s duct/cysts
FunctIonal causes oF urInary IncontInence Functional causes of urinary incontinence include pri mary nocturnal enuresis, dysfunctional voiding, and pseudoincontinence (e.g. vaginal voiding).
nocturnal enuresis Primary nocturnal enuresis is defined as persistent night time wetting past the age of 5 years. Nocturnal enuresis occurs in approximately 20% of 5yearold children and is more common in boys than girls.3 Daytime wetting, urinary urgency and frequency are more common in girls. Diagnosis and treatment of nocturnal enuresis is multifactorial, relying on both the pathophysiology and psychological analysis of the patient. Treatment using desmopressin, bedwetting alarm or combination therapy is often successful. Daytime symptoms such as enuresis, urgency and frequency may be treated with anticholin ergic medications.
dysfunctional voiding Children with dysfunctional voiding have difficulty relaxing their pelvic floor musculature, which com prises the external urethral sphincter and which is tra versed by the rectum. As a result, day and nighttime wetting, urinary frequency or infrequency, urgency, uri nary tract infections, and constipation or encopresis are common. 1331
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It is helpful if patients and their families keep an elimination diary to ascertain the child’s specific toilet ing habits. For example, many parents are not aware that their child has constipation unless specifically que ried as to the frequency and caliber of the stool. Simple treatment of constipation with stool softeners (e.g. min eral oil, Kondremul) or laxatives (e.g. Milk of Magnesia or Dulcolax) permit better overall toileting behavior. Voiding dysfunction may be treated by behavior modi fication or pharmacologic agents and does not require surgical intervention. A list of common pharmacothera peutic agents for neurovesical dysfunction is provided in Table 94.2.
Vaginal voiding Vaginal voiding is often confused with true urinary incontinence. Micturition into the vagina results in leak age when the child stands upright, allowing efflux of
a
b
table 94.2.
Pharmacotherapy for neurovesical dysfunction
Drug
Action
Dose/frequency
Bethanechol
Cholinergic
0.6 mg/kg/day 3–4 times daily
Dicyclomine
Anticholinergic
5–10 mg 3–4 times daily
Oxybutynin
Anticholinergic
0.2 mg/kg 2–4 times daily
Propantheline
Anticholinergic
1.5 mg/kg/day 3–4 times daily
urine from the vaginal vault. Simple maneuvers to direct the urinary stream more accurately by separating the legs further during voiding, and waiting a few minutes after micturition to allow efflux into the toilet, usually solve the problem (Fig. 94.2).
c
Figure 94.2. A 4-year-old girl with bilateral vesicoureteral reflux and daytime ‘dampness’ was treated with endoscopic implantation of Deflux. A voiding cystourethrogram 3 months later shows cure of reflux, but the presence of vaginal voiding. (a) Bladder filling; (b) voiding phase showing absence of reflux, the presence of filling defects in bladder base (Deflux implants, solid arrow), and beginning of vaginally voided contrast (dashed arrow); (c) postmicturition film shows the presence of dense contrast within the vagina (dashed arrow) and nearly empty bladder.
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congenItal abnormalItIes causIng IncontInence Congenital anomalies may cause incontinence by inter fering with the function of the sphincter mechanisms or the storage function of the bladder, or by anatomically bypassing normal sphincter mechanisms (Table 94.3). Imaging studies are essential to define the anatomic abnormalities causing the incontinence. The first studies obtained are usually renal and bladder ultrasonography and the voiding cystourethrogram (VCUG). The plain abdominal scout film of the VCUG assesses bony abnor malities and the presence or absence of fecal impaction. An intravenous pyelogram is useful to identify ectopic ureters, duplication anomalies, and ureteroceles, as well as providing useful information regarding renal function. Urodynamic studies are often useful in detecting sphinc teric, storage, and urinary flow abnormalities, and are essential in all patients with neurogenic incontinence. The goals of treatment for congenital abnormalities of the female urogenital tract are restoration of physical appearance and function, preservation of renal func tion, and achievement of manageable urine storage and continence.
abnormal storage Bladder exstrophy Bladder exstrophy (Fig. 94.3) has an incidence of 1/30,000 live births and is less common in females than in males. Debate continues about the development of the bladder wall and matrix proteins. Why some chil dren develop normal bladder capacities while others go on to develop small and poorly compliant bladders is incompletely understood. Treatment involves bladder closure within the first days of life. Bladder enhance ment or diversion are surgical options later on. Bladder neck reconstruction may be performed at the time of table 94.3.
Figure 94.3. A newborn girl with bladder exstrophy. Note separation of the labia and clitoris, and the normal vagina. bladder closure or afterward. Continence rates range from 43 to 87%.
Cloacal exstrophy Cloacal exstrophy (Fig. 94.4) has an incidence of 1:200,000 and is much less common in females. Cloacal exstrophy is much more complex than bladder exstro phy and requires extensive evaluation for associated abnormalities of the nervous system, upper urinary tract, and gastrointestinal tract. The treatment of storage abnormalities of the blad der usually involves bladder augmentation with intesti nal segments. Clean intermittent catheterization (CIC) may also be required to maintain urinary continence.
Myelomeningocele In the pediatric population, myelomeningocele (Fig. 94.5) is a common cause of neurogenic bladder leading to problems with urinary storage, sphincteric function, and elimination. In the United States, the prevalence
Mechanisms of incontinence in congenital genitourinary anomalies*
Abnormal storage
Abnormal sphincter
Bypass sphincter
Bladder exstrophy
Epispadias
Ectopic ureters
Cloacal exstrophy
Urogenital sinus
Vesicovaginal fistulae
Bladder agenesis
Ectopic ureteroceles
Bladder duplication
Neurogenic†
Neurogenic† * Multiple mechanisms for incontinence often coexist in a given patient. † Abnormalities of storage or sphincteric function may be seen with neurogenic bladders (e.g. spina bifida) and may be related to detrusor hypo- or hyperactivity, or from secondary changes within the detrusor muscle, resulting in stiff (non-compliant) or floppy (very compliant) bladders.
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with myelomeningocele. The use of CIC has been shown to promote continence, preserve renal function, and decrease the incidence of symptomatic pyelonephritis.4 McGuire and coworkers5 determined that a leakpoint pressure (LPP) greater than 40 cmH2O was predictive of renal deterioration over time. CIC serves to keep blad der pressure low, avoiding high LPP.
abnormal sphincter Anatomic abnormalities may impede normal develop ment of the bladder neck. Incompetence of the bladder neck may result in primary urinary incontinence and is seen in conditions such as female epispadias, urogenital sinus, bilateral ureteral ectopia, and ectopic ureteroceles. Conservative measures to improve sphincteric function are limited and a surgical approach is needed. The sur gical options focus on creation of an increase in bladder outlet resistance or of a new sphincter mechanism.
Female epispadias
Figure 94.4. Newborn with cloacal exstrophy illustrating separation of bladder halves, herniation of the hindgut and prolapse of the ileocecal segment.
Female epispadias (Fig. 94.6) may result in a variable pre sentation, depending on the severity of the urethral defect. In complete epispadias, incontinence results secondary to: 1) a foreshortened and widened urethra; 2) a par tially absent external urethral sphincter; and 3) a poorly developed bladder neck. Treatment is directed at recon struction of these deficient structures and ureteral reim plantation proximal to the reconstructed bladder neck region.6,7 Persistent incontinence may be treated with collagen injection at the bladder neck.
Urogenital sinus anomalies
Figure 94.5. A newborn with characteristic appearance of myelomeningocele protruding from the lower back.
The persistence of a urogenital sinus may result in the urethra emptying into the vaginal vault. This may not be readily apparent unless the urethra is not seen during attempts at catheterization. Infants may present with a dilated vagina, possibly resulting in an abdominal mass, if the posterior lip of the hymen causes partial obstruction at the orifice of the urogenital sinus (Fig. 94.7). Retained urine in the vagina (urocolpos) and uterine canal may increase to enormous volumes. Drainage of urine with vaginal catheterization followed by a vaginogram showing contrast within the cervical canal and uterus, and pos sibly into the peritoneal cavity, is diagnostic. Treatment involves endoscopic division of the posterior hymenal lip. Further reconstructive surgery will usually be required.
Duplicated ectopic ureters is approximately 1/1000 births. CIC in conjunction with anticholinergic medication has brought about a dramatic improvement in the management of patients
An ectopic upper pole ureter may join the lower end of the remnant mesonephric duct system comprising Gartner’s ducts. These ureters are associated with nonfunction of
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b
Figure 94.6. Appearance of a newborn girl with epispadias (a); note the open bladder neck with a catheter introduced superior to a normal catheterized vagina, and separation of the labia and clitoris (b).
b
a
Figure 94.7. (a) This contrast vaginogram in a newborn girl with an abdominal mass shows retained fluid and an obstructed vagina (urocolpos) secondary to a urogenital sinus abnormality. (b) A flush genitogram in another patient reveals a urogenital sinus with contrast seen within the bladder and vagina. (c) Line drawing showing the relationship between the urethra, narrow distal vagina, and urogenital sinus.
c
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the associated renal moiety and may result in cystic dila tion of Gartner’s duct with eventual rupture of the cyst and drainage into the vaginal opening. Drainage of fluid or pus into the vagina prompts further investigation. A renal and pelvic ultrasound scan may show a dilated or abnormal upper pole renal moiety, and a cystic structure may be seen in the pelvis or vaginal area. Computed tomography scanning or magnetic resonance imaging are helpful in further delineating the anatomy, while ret rograde fluoroscopic studies are diagnostic if the often elusive ectopic orifice can be identified (Fig. 94.8). The appropriate treatment of ectopic ureters depends on whether the ureter is ectopic or bilateral and whether it drains into the genital or urinary tracts. Ectopic ure ters to the genital tracts may be treated by simple upper pole nephrectomy; ectopia to the urinary tract usually involves ureterectomy in addition to heminephrectomy in order to prevent postoperative urinary reflux and infection (Fig. 94.9).
bypass of sphincter mechanism In instances where the bladder neck and sphincter mechanism have developed normally, urinary inconti
a
c
nence may develop as a result of ureteral ectopia distal to the continence mechanism. The most common cause of this abnormality is ectopic ureters. Incontinence may not be purely secondary to a bypass mechanism, as abnormal urethral development may contribute to poor urinary control.
Bilateral single ectopic ureters Ectopic ureters result when a ureteric bud develops more cranially than usual from the mesonephric duct. In females, ectopic ureters usually open into the ure thra, the vestibule or the vagina. Incontinence is a com mon complaint in girls with ectopic ureter(s). Bilateral ectopic ureters may enter the urethra just distal to the bladder neck. Because of the inadequacy of urethral length associated with this condition, incontinence may result. In single ectopic ureters, a cyclic VCUG may dem onstrate vesicoureteral reflux when the bladder neck relaxes upon micturition; reflux is often not demon strated during bladder filling when the bladder neck is in a contracted state. Treatment involves ureteral reim plantation and bladder neck reconstruction for bilateral single ectopic ureters, and upper pole partial nephrec tomy and lower pole reimplantation for duplicated
b
Figure 94.8. A young girl with continuously damp underpants was found to have ureteral ectopia to her vagina: (a) The vagina showing a ureteral stent placed within the ectopic ureter and a Foley catheter within the urethra; (b) retrograde pyelogram shows contrast within the ectopic ureter. (c) An intravenous urogram in another patient reveals an ectopic ureter of an upper pole moiety terminating beyond the bladder neck and into the vaginal introitus.
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(i)
(ii)
Figure 94.9. (a) Illustration of nephroureterectomy: (i) preoperatively and (ii) postoperatively; (b) nephroureterectomy specimen from the patient in Figure 94.7.
ectopic ureters. In unsuccessful cases, use of a continent catheterizable channel (e.g. appendicovesicostomy) or continent urinary diversion may be considered.
InterlabIal masses
b
thinwalled) partially arising within the urethral meatus but mostly external to it may resemble a bulging hymen associated with hydrometrocolpos, or a prolapsing ure terocele (fleshy, compressible, protruding through the urethra).
Masses within the vagina presenting in infants and young girls are generally referred to as interlabial masses. Although many of these lesions arise within the introi tus, those arising in the urethra or bladder must be rec ognized to afford proper management. Many patients with masses within the vaginal area complain of leakage of fluid (e.g. urine, pus, transudate). A thorough physi cal examination of the introitus is part of the complete evaluation of urinary incontinence.
skene’s glands (paraurethral glands) The tubular Skene’s glands (Fig. 94.10) arise from the urethral epithelium and are the counterparts to the male prostate gland. In females, these glands may end up in the urethral meatus and hymen. Cysts (tense, yellow,
Figure 94.10.
Skene’s glands in a newborn girl. 1337
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bartholin’s glands The major vestibular glands of Bartholin arise from the urogenital sinus and come to open into the vestibule on either side of the hymen. The main glands lie against the ischiopubic ramus deep to the bulbospongiosus muscle and cavernous tissue. Blockage of the main ducts of Bartholin’s glands may lead to cystic dilation at any age, but rarely become infected prior to puberty.1
Prolapsed ureterocele A ureterocele is a dilated distal ureter within the detru sor muscle which may extend beyond the bladder neck (ectopic ureterocele). These ureters are often associated with an upper pole renal moiety of a duplicated collect ing system.8 An interlabial mass may be identified if the ectopic ureterocele extends through the urethral meatus. Treatment is directed at ureterocele excision, bladder neck reconstruction, and ureteral reimplantation.
Hydro(metro)colpos Circulating maternal estrogen in the newborn girl may result in an increase in the production of cervical mucus. Hydrocolpos and hydrometrocolpos result when mucus collects in the vaginal vault and uterus, respec tively (Fig. 94.11). In these instances, the vaginal orifice may be blocked secondary to an imperforate hymen, within a urogenital sinus, anatretic rectocloacal canal, or vaginal/uterine atresia. Hydrometrocolpos, by virtue of its abdominal extension, may compress the urethra, rectum, and ureters.
a
Treatment of hydro(metro)colpos secondary to a normally located imperforate hymen may involve sim ple perforation of the hymen when the infant is in the newborn nursery. If the hymen appears thickened, inci sion under general anesthesia may be required. Higher obstruction involves a more formal approach to treat the associated urogenital abnormalities (e.g. urogenital sinus, atresia, rectocloacal canal).
urethral prolapse Eversion of the distal urethral mucosa through the ure thral meatus results in a circumferential interlabial lesion (Fig. 94.12). The lesion may be painful or may bleed or weep serosanguinous fluid, prompting medical atten tion; however, such lesions do not lead to urinary incon tinence. On examination, urethral prolapse appears edematous or necrotic, with the urethral meatus seen within its center. This lesion should be distinguished from neoplasms of the vagina or bladder (see below). A prolapsed urethra associated with mild edema without necrosis or significant pain may reasonably be treated conservatively with sitzbaths and estrogen cream over a 2 to 3week period. More significant lesions should be excised.9
rhabdomyosarcoma of the vagina Rhabdomyosarcoma of the vagina and bladder (Fig. 94.13) may present as a grapelike interlabial lesion asso ciated with vaginal bleeding.10 Because of the propensity of these lesions to spread, a complete endoscopic and radiographic evaluation is indicated to confirm the diag
b
Figure 94.11. A newborn girl with urinary obstruction: (a) external appearance of the prolapsing ectopic ureterocele; (b) illustration depicting the ectopic ureterocele with extension into the urethra. 1338
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Figure 94.13. A 5-year-old girl with rhabdomyosarcoma of the vagina (sarcoma botryoides) presented with blood spotting and dysuria. Figure 94.12. An 8-year-old African–American girl with urethral prolapse presented with ‘vaginal’ pain and blood spotting.
nosis and rule out local extension and distant lesions. Primary chemotherapy has resulted in better bladder salvage and can cure metastatic disease.11 Surgical exci sion, with or without radiation therapy, is reserved for postchemotherapy biopsyproven residual masses.
Introital hemangiomas Hemangiomas of the female genitalia are rare lesions. In most cases, hemangiomas are congenital and may involve any part of the genitalia. Cavernous hemangio mas (angioma cavernosum, cavernoma) are similar to strawberry hemangiomas but are more deeply situated. They may appear as a red–blue spongy mass of tissue filled with blood. Some of these lesions disappear on their own, usually as a child approaches school age. In some cases, the hemangiomas can be quite large and may be confused with tumors, or – if involving the cli
toris – may appear as clitoromegaly similar to that seen in cases of congenital adrenal hyperplasia (Fig. 94.14). Treatment may be by steroid injection, potassiumtit anylphosphate (KTP) laser ablation and/or excision, depending on the size and location.
urethral polyps Urethral polyps are rare anomalies, characterized as benign urotheliallined masses attached to a fibrovascu lar stalk, and may lead to symptoms by obstructing the ureter or bladder neck by a ball–valve mechanism. Some of these polyps, diagnosed later in life, may represent acquired lesions. Polyps may occur anywhere along the urinary tract. Primarily they are composed of connective tissue covered by epithelium. Additionally, smooth mus cles and islands of glandular cells and even nerve tissue have been found. Treatment is by endoscopic ablation or excision, depending on the origin. Fibroepithelial polyps may present as interlabial masses and may lead to bleeding or dysuria when located in the urethral meatus (Fig. 94.15). 1339
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a
Figure 94.14. the clitoris.
b
(a, b) A 1-year-old girl presenting with an enlarging introital mass revealing a large cavernous hemangioma of
Female pseudohermaphroditism
Figure 95.15. A 6-year-old girl presenting with blood spotting in underwear and dysuria. Arrow shows urethral polyp.
dIsorders oF tHe Female genItalIa Intersex disorders A complete description of the array of intersex dis orders is beyond the scope of this chapter. However, urologists and gynecologists must be familar with the more common intersex disorders whereby gender assignment and rearing is along female lines. These conditions include girls of normal appearance who are genetically male (male pseudohermaphrodites) and genetic females appearing as males (female pseudohermaphrodites).
Female pseudohermaphrodites are genetic females (XX karyotype) but may appear as males without testes (Fig. 94.16). The most common cause of female pseudoher maphroditism is congenital adrenal hyperplasia (21 hydroxylase deficiency in >90%). In this disorder, the absence of 21hydroxylase results in the overproduction of androgens and results in a wide spectrum of genital abnormalities, ranging from mild masculinization of the clitoris (clitoromegaly) to complete masculiniza tion. The labioscrotal folds are rugated and hyper pigmented, giving the physical appearance of severe hypospadias with cryptorchidism. In all cases, however, the internal female anatomy is normal. After the diagno sis is established, surgical treatment involves feminizing genitoplasty (reduction clitoroplasty, vaginoplasty, and labioplasty).
Male pseudohermaphroditism Male pseudohermaphrodites are genetic males (XY karyotype) but may appear as normal females. Testicular feminization is the most common cause of male pseudo hermaphroditism and results from the lack of androgen receptors at the cell surface of all tissues. The diagnosis should be suspected in all girls with inguinal hernias – the hernia sacs may be found to contain testes. The diagnosis should always be suspected in adolescent girls with normal development and primary amenorrhea. Development and sexual identity is female. Treatment involves bilateral orchidectomy. Testes left in place will produce testosterone, which is converted to estra diol, allowing spontaneous breast development. Testes should be removed because of the risk of gonadoblas toma. Estrogen must be replaced at puberty in girls who
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a
c
have undergone prepubertal orchidectomy, which is the standard treatment when the diagnosis is made.
Vaginal agenesis and the mayer–rokitansky syndrome Agenesis of the vagina in genetic females (Fig. 94.17) may be accompanied by various other defects in the genitourinary tract. Most patients present in adoles
b
Figure 94.16. This newborn with ambiguous genitalia, elevated 17-hydro-oxyprogesterone and XX chromosomes was diagnosed with congenital adrenal hyperplasia (21hydroxylase deficiency): (a) preoperative appearance showing phallic structure and non-palpable gonads; (b) prominent scrotal folds and clitoromegaly; (c) appearance 6 months after reduction clitoroplasty and scrotoplasty. cence with amenorrhea or pain, but this condition may also present in young girls with urinary tract infection or hydrocolpos. Genital defects range from vaginal agen esis alone to agenesis of the uterus and fallopian tubes. These genital defects are associated with (ipsilateral) renal agenesis.12 Some patients present after having urethral intercourse and stress urinary incontinence. Treatment of the Mayer–Rokitansky syndrome includes vaginoplasty or neovaginal reconstruction with bowel. 1341
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a
b
Figure 94.17. (a) Vaginal agenesis in a 16-year-old with Mayer–Rokitansky syndrome. The sexually active patient engaged in urethral coitus. (b) The sigmoid colon (8–10 cm) is isolated on its mesentery and will be mobilized to the vaginal introitus to create a neovagina. The colonic mucus allows for natural lubrication during coitus.
urInary tract reconstructIon
patients require bladder neck reconstruction19 to achieve continence and most will require CIC.20 Continent reconstruction of the lower urinary tract is often desired in the face of congenital or acquired anomalies of both the outlet and the bladder. Much of the principles and background of continent reconstruc tion is derived from experience with undiversion. The early work of Hendren, Mitrofanoff and others has led to surgical approaches that produce both better reser voir function and a continent outlet.21 Continent urinary diversion encompasses three inter related but independently functioning components. These include a channel by which urine is conducted to the skin, a reservoir or pouch, and a mechanism by which continence is achieved.22 A host of tissues are available to the reconstructive surgeon (Table 94.4). The flap valve principle for continence dictates that a portion of the continence channel be fixed on the inner wall of the reservoir. This is the same principle by which ureteral tunneling in the bladder muscle prevents reflux during voiding. In general, a 5:1 lengthtodiameter ratio of the continence structure is required. This is the case whether the structure is ureter, ileum or appendix. The Mitrofanoff principle of continent reconstruc tion describes a supple catheterizable structure (ureter, appendix, etc.) implanted into the inner wall of the reservoir to create a flap valve continence mechanism.23 The most popular form of flap valve construction for urinary continence is the use of appendix implanted into the bladder or reservoir (appendicovesicostomy). The small stoma may be concealed within the umbilicus table 94.4.
Tissues available for lower urinary tract reconstruction*
External conduit Urinary reservoir Continence mechanism Appendix
Bladder
Anal sphincter
lower urinary tract reconstruction
Fallopian tube
Cecum
Artificial urinary sphincter
Since 1950, bowel segments have been used to replace entirely a diseased or dysfunctional bladder. The cur rent success in reconstruction of the lower urinary tract reflects our improved understanding of the physiologic principles involved in bladder and urethral function.13–18 Spontaneous voiding can occasionally be achieved with a quite abnormal lower urinary tract. This, of course, is provided that the pressure gradient between the blad der and distal urethra is low. It follows, then, that even in cases where the bladder is replaced in part (intesti nal cystoplasty) or entirely (neobladder), patients may still be able to empty their bladders satisfactorily. Many
Ileum
Colon
Benchekroun (hydraulic valve)
Ileal tube
Ileum
Ileocecal valve
Skin tube
Rectum
Koch (nipple valve)
Stomach
Stomach
Mitrofanoff (flap valve)
Urethra
Urethral sphincter
Ureter In general, three components are required for continent diversion: 1) conduit from the reservoir to the skin; 2) a pouch or reservoir; and 3) a mechanism by which continence is attained.
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(Fig. 94.18). Assurance of complete bladder emptying is essential, as this type of continence channel is very effective in its ability to withstand very high intraluminal pressure. In the noncompliant patient, pouch rupture or upper tract injury may result from failure to empty the reservoir regularly.
urinary tract reconstruction and pregnancy Future pregnancy must be kept in mind when recon structing the genitourinary tract. Pregnancy may be complicated and requires care by both the obstetrician and urologist. Renal obstruction and incontinence may result as the uterus enlarges. Neobladder reconstruction has a good outcome, but chronic bacteriuria is frequent and occasionally requires an indwelling catheter in the third trimester.24 Similarly, when suprapubic catheteriz
able continent stomas have been constructed, indwell ing catheterization through the stoma during the third trimester may be needed to avoid serious urinary tract infections.25 Successful pregnancies and deliveries have been reported after both continent and loop urinary diver sions.26–28 The mode of delivery should be guided by obstetric indications,27 although vaginal delivery has been successful in the majority of cases. Alternatively, if the bladder neck has been reconstructed it is usually advisable for delivery to be by cesarean section to avoid damage to the bladder neck reconstruction. The urolo gist should be available to the obstetric team for consul tation if cesarean section is deemed necessary, especially if a bladder augmentation with bowel has been carried out, in order to avoid injury to the vascular pedicle to the bowel segment.
a
c
b
Figure 94.18. In the Mitrofanoff procedure, the appendix is mobilized with its blood supply as illustrated in (a) and reimplanted into the bladder in a tunneled non-refluxing fashion. The proximal appendix may be brought out to the umbilicus for clean intermittent catheterization (b). Same patient 2 years after appendicovesicostomy performing self-catheterization (c). 1343
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reFerences 1. Marshall FF. Embryology of the lower genitourinary tract. Urol Clin North Am 1978;5:3–15.
15. Koff SA. Guidelines to determine the size and shape of intestinal segments used for reconstruction. J Urol 1988;140:1150–1.
2. Stephens FD, Smith ED, Hutson JM. Congenital Abnor malities of the Urinary and Genital Tracts. Oxford: Isis Medical Media, 1996.
16. Hinman F Jr. Selection of intestinal segments for bladder substitution: physical and physiological characteristics. J Urol 1988;139:519–23.
3. Miller FJW. Children who wet the bed. In: Kolvin I, MacK eith RC, Meadow SR (eds) Bladder Control and Enuresis. London: Heinemann Medical Books, 1973; 47–52.
17. McDougal WS. Metabolic complications of urinary intesti nal diversion. J Urol 1992;147:1199–1208.
4. Scott JE, Deegan S. Management of neuropathic urinary incontinence in children by intermittent catheterization. Arch Dis Child 1982;57:253–8. 5. McGuire EJ, Woodside JR, Borden TA et al. Prognostic value of urodynamic testing in myelodysplastic patients. J Urol 1981;126:205–9. 6. Geahart JP, Peppas DS, Jeffs RD. Complete genitourinary reconstruction in female epispadias. J Urol 1993;149: 1110–3.
18. Hall MC, Koch MO, McDougal WS. Metabolic conse quences of urinary diversion through intestinal segment. Urol Clin North Am 1991;18:725–35. 19. Kropp KA, Angwafo FF. Urethral lengthening and reim plantation for neurogenic incontinence in children. J Urol 1986;135:533–6. 20. Lapides J, Dionko AC, Silber SJ et al. Clean intermittent catheterization in the treatment of urinary tract disease. J Urol 1972;107:458–61.
7. Mollard P, Basset T, Mure PY. Female epispadias. J Urol 1997;158:1543–6.
21. Hendren WH. Urinary tract refunctionalization after longterm diversion. Ann Surg 1990;212:478–95.
8. Mandell J, Colodny AH, Lebowitz R et al. Ureteroceles in infants and children. J Urol 1980;123:921–6.
22. Kirsch AJ, Snyder HM. Trends in continent reconstruction of the lower urinary tract. Contemp Urol 1997;9:61–9.
9. Jerkins GR, Verheeck K, Noe HN. Treatment of girls with urethral prolapse. J Urol 1984;132:732–3.
23. Duckett JW, Snyder HM. Use of the Mitrofanoff principle in urinary reconstruction. World J Urol 1985;3:191–3.
10. Hays DM. Pelvic rhabdomyosarcomas in childhood: diag nosis and concepts of management reviewed. Cancer 1980;45:1810–4.
24. Creagh TA, McInerney PD, Thomas PJ, Mundy AR. Preg nancy after lower urinary tract reconstruction in women. J Urol 1995,154:1323–4.
11. Hays DM, Raney RB, Crist W et al. Improved survival and bladder preservation among patients with bladder – prostate rhabdomyosarcoma primary tumors in Inter group Rhabdomyosarcoma Study III. Proc Am Soc Clin Oncol 1991;10:318 (abstract 1119). 12. Tarry WF, Duckett JW, Stephens FD. The Mayer–Rokitan sky syndrome: pathogenesis, classification and manage ment. J Urol 1986,136:648–57. 13. Kass EJ, Koff SA. Bladder augmentation in the pediatric neuropathic bladder. J Urol 1983;129:552–5. 14. Koch NG, Norlen L, Phillipson BM et al. The continent ileal reservoir (Koch pouch) for urinary diversion. World J Urol 1985;3:146–51.
25. Hatch TR, Steinberg RW, Davis LE. Successful term deliv ery by Cesarean section in a patient with a continent ileo cecal urinary reservoir. J Urol 1991:146:1111–2. 26. Greenberg M, Vaughan ED Jr, Pitts WR Jr. Normal preg nancy and delivery after ileal conduit urinary diversion. J Urol 1981;125:172–3. 27. Barrett RJ, Peters WA. Pregnancy following urinary diver sion. Obstet Gynecol 1983;62:582–6. 28. Akerlund S, Bokstrom H, Jonson O et al. Pregnancy and delivery in patients with urinary diversion through the continent ileal reservoir. Surg Gynecol Obstet 1991;173: 350–2.
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95 Complications of surgery for stress incontinence Walter Artibani, Maria Angela Cerruto, Giacomo Novara
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IntroductIon There are two main types of treatment available for women with stress urinary incontinence (SUI): conservative (lifestyle interventions, treatments aimed at improving pelvic floor muscle outcomes, and drugs) and surgical. When conservative therapy fails, or in cases of severe SUI, surgery might be effective in improving this condition. Several surgical procedures have been described in the literature – indicating that none is entirely satisfactory. The main surgical interventions currently available with increasing invasiveness, efficacy, and complications are:
• periurethral or transurethral bulking injections; • anterior colporrhaphy; • needle suspensions (Pereyra, Stamey, and Raz procedures);
• sling procedures (classic sling and tension-free • •
vaginal tape procedures); open and laparoscopic colposuspensions; artificial urinary sphincter (AMS 800).
The choice of surgical procedure should depend on the cause of SUI – bladder neck/urethral hypermobility (UH) and/or intrinsic sphincter deficiency (ISD) – and the assessment of postoperative outcomes should be based on the patient’s clinical symptoms and signs, urodynamic evaluation, and short- and longterm results as well as immediate and delayed complications.
complIcatIons of suI surgery Chaliha and Stanton1 comprehensively reviewed the literature on the complications of surgery for genuine stress incontinence. They identified studies assessing outcome by means of both an electronic and a hand search of the Medline Database from 1966 to 1997 of all English language articles, including randomized controlled trials, non-randomized trials, prospective and retrospective cohort studies, and case-control studies. A recently published French paper gave an exhaustive literature review up to 2003.2 SUI surgery consequences and complications may be conveniently classified as follows:
• • • •
immediate complications (within 24 hours); short-term complications (24 hours to 6 weeks); long-term complications (6 weeks onwards); impact on quality of life (QoL).
Immediate complications Significant bleeding A severe hemorrhage needing a transfusion may occur after a direct lesion of the perivesical venous plexus during different surgical procedures accessing the space of Retzius. The mean bleeding volume during colporrhaphy is 200 ml,3 and 260 ml during Burch colposuspension.4–6 No significant difference has been found between primary and secondary Burch colposuspension in terms of bleeding.4 Only one case of massive hemorrhage in a series of 180 Burch colposuspensions has been reported.5 The amount of perioperative bleeding after laparoscopic colposuspension is usually very low.4,7,8 After a Marshall–Marchetti–Kranz (MMK) procedure the mean bleeding volume is 142 ml (range 20– 500 ml)9–11 and after needle suspension is 53 ml (range 10–150 ml).12–14 After a polytetrafluoroethylene (Teflon) suburethral sling procedure the mean bleeding volume is 153 ml.15 A severe hemorrhage needing surgical drainage has been reported in up to 2.1% of cases after pubovaginal sling procedures.16–20 Bleeding after a tension-free vaginal tape (TVT) procedure usually originates from veins of the pelvic floor or epigastric vessels. A perioperative hemorrhage after TVT may occur in 0.5–17% of cases,21–27 and lesions of the iliac vessels, although very uncommon, have been reported.24,28–30 A retrospective study26 on 241 women having a previous TVT at six Canadian institutions detected a blood loss >500 ml in six patients (2.5%), none requiring transfusion. These data are consistent with those in the literature.23,31–33 Operative complications following transobturator suburethral tape (TOT) procedures are very few, and significant bleeding is rare.34 Hematomas in the space of Retzius range from 0.2 to 2% after direct colposuspension,9,12 and from 5 to 7% after needle colposuspension.9,13,14 This complication has been reported in less than 2% of cases after TVT,35,36 and very few cases needed surgical drainage.23,26,29 Abouassaly et al. reported pelvic hematomas in four patients (1.9%), often diagnosed when retention was accompanied by prolonged suprapubic or pelvic pain.26 Table 95.1 shows an overview of significant bleeding rates following SUI surgery. Case: Two weeks after a TVT procedure performed for stress urinary incontinence in a different hospital, a 58year-patient arrived at our outpatient clinic complaining of lower abdominal pain, which had started 3 days after surgery. The severity of the symptom required the use of an oral non-steroidal anti-inflammatory drug. At physical examination, the lower abdomen was tender and
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table 95.1. Complication Significant bleeding
Significant bleeding following stress urinary incontinence surgery Authors 3
Van Geelen et al. Alcalay et al.4 Stanton & Cardozo5 Wee et al.6 Green et al.9 Riggs10 Mainprize & Drutz11 Peattie & Stanton13 Varner14 Morgan et al.16 Amundsen et al.17 Young et al.18 Carbone et al.19 Crivellaro et al.20 Wang & Lo22 Meschia et al.23 Ward & Hilton24 Levin et al.25 Abouassaly et al.26 27 Rafii et al. Krauth et al.34
Operation
No. of patients treated
No. of complications (%)
Anterior colporrhaphy Burch Burch Burch MMK MMK MMK Needle suspension Needle suspension Sling Sling Sling Sling + bone anchor Sling + bone anchor TVT TVT TVT TVT TVT TVT ± other procedures TOT
56 109 180 99 21 490 2712 44 20 281 104 200 70 253 70 404 170 313 241 186 604
2 (3.6) 8 (7.3) 1 (0.6) 3 (3) 2 (10) 10 (2) 7 (0.3) 3 (6.8) 2 (10) 6 (2.1) 1 (0.9) 3 (1.5) 1 (1.4) 3 (1.3) 11 (16) 2 (0.5) 3 (1.7) 4 (1.3) 6 (2.5) 2 (1) 7 (1.1)
MMK, Marshall–Marchetti–Kranz; TOT, transobturator suburethral tape; TVT, tension-free vaginal tape.
painful. Mild lower urinary tract symptoms of the filling phase were elicited. No other symptoms were present. On general practitioner request, the patient had undergone an abdominal ultrasound scan 7 days previously, which showed a 6 cm round liquid lesion in the Retzius space. A further ultrasound scan was immediately performed, which demonstrated the enlargement of the pelvic lesion up to 12 cm in diameter. Hemoglobin was 9.5 g/dl but the patient was hemodynamically stable. A contrast CT scan was immediately carried out, which confirmed the presence of a large pelvic hematoma in the space of Retzius, dislodging the bladder posteriorly, without any contrast leakage, even in the late scans (Fig. 95.1). Once the available therapeutic options were explained, surgical drainage of the hematoma was performed. Through a midline infraumbilical prepubic incision, a large hematoma of the space of Retzius was drained, evacuating more than 800 ml of clots and blood. No source of active bleeding was found. The postoperative course was uneventful and the patient was discharged on the fourth postoperative day. The 2-month follow-up ultrasound scan was normal, and the patient remained continent and free of symptoms.
Urinary tract injuries A bladder lesion may occur during colposuspension, sling, and TVT procedures5,6,9,11,13,20,22–27,31,37–40 (Table 95.2). Lower urinary tract (LUT) injuries have been reported in 1–7% of cases after needle colposuspensions,9,13,41,42 and in 6.3% of cases after slings.38 Bladder perforation by TVT trocars is a common intraoperative complication reported in 0.8–21% of cases.22,35,36,39,43–46 To avoid
Figure 95.1. CT scan of a large pelvic hematoma in the space of Retzius. 1347
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intravesical misplacement of the tape, a careful cystoscopic examination must be performed to exclude any violation of the bladder mucosa. If any sign of bladder perforation is evident, correcting trocar placement is mandatory, prolonging catheter drainage for at least 3 days.45 When a primary bladder lesion has been missed, resulting in transvesical or submucosal tape placement with a secondary erosion, there is no possibility of correcting the position of the tape and it must be removed surgically. A synthetic suture or tape running through the bladder may promote bladder stone formation, recurrent urinary tract infections (UTIs), and severe voiding LUT symptoms.47–50 Abouassaly et al. reported 14/241 (5.8%) cases of bladder perforation during TVT.26 Bladder and urethral lesions after Burch colposuspension have been reported in up to 6% of cases;3,5,37 misdiagnosis of such lesions may lead to a urethrovaginal fistula.51 In about 1% of cases it is possible to detect an underestimated ureteral lesion after this procedure.9 Laparoscopy implies a higher risk of LUT injury, occurring in up to 10% of cases.7,52,53 After AMS 800
table 95.2.
implant, urethral as well as anterior and posterior cervical lesions may be found in 3.7%, 11%, and 3.7% of cases, respectively.54
Visceral injuries Before the advent of TVT, intestinal perforations were exceptional and usually occurred after suprapubic catheterization used during SUI surgery.55–57 To date, approximately 15 cases of bowel perforation after TVT have been reported to the manufacturer, and only a few cases have been reported in the literature31,58–62 (see Table 95.2). Potential predisposing risk factors for intestinal injury include previous intraperitoneal and retroperitoneal surgery, and abnormal bowel adhesion to the bladder and pelvic peritoneum. A case of small intestine erosion by AMS 800 reservoir tubing has been recently reported.63
Complications due to intraoperative patient position A prolonged gynecologic position (>3 hours) may be responsible for a compartment syndrome. Protracted
Urinary tract and visceral injury during stress urinary incontinence surgery
Complications
Authors
Operation
No. of patients treated
No. of complications (%)
Urinary tract injury
Green et al.9 Peattie & Stanton13 Stanton & Cardozo5 Pow-Sang et al.37 Van Geelen et al.3 Wee et al.6 Ward et al.24 Mainprize & Drutz11 Summitt et al.38 Crivellaro et al.20 Wang & Lo22 Soulie et al.39 Nilsson & Kuuva31 Meschia et al.23 Ward & Hilton24 Tsivian et al.40 Abouassaly et al.26 Levin et al.25 Rafii et al.27 Krauth et al.34
Needle suspension Needle suspension Burch Burch Burch Burch Colposuspension MMK Sling Sling + bone anchor TVT TVT TVT TVT TVT TVT TVT TVT TVT ± other procedures TOT
29 44 180 38 34 99 146 2712 48 253 70 52 161 404 170 55 241 313 186 604
1 (3.4) 1 (2) 2 (1.1) 2 (5.3) 1 (2.9) 1 (1) 3 (2) 34 (1.3) 3 (6.3) 5 (2.1) 3 (4.3) 6 (11.5) 6 (3.7) 24 (6) 20 (11.7) 4 (7.3) 14 (5.8) 313 18 (9.6) 15 (2.5)
Visceral injury
Peyrat et al.58 Meschia et al.59 Leboeuf et al.60 Amna et al.61 Castillo et al.62 Yuan et al.63 Crivellaro et al.20
TVT TVT TVT TVT TVT Artificial sphincter Sling + bone anchor
N/A N/A N/A N/A N/A N/A 253
1 1 1 1 1 1 2 (0.9)
MMK, Marshall–Marchetti–Kranz; N/A, not applicable; TOT, transobturator suburethral tape; TVT, tension-free vaginal tape.
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extrinsic lower limb compression could be responsible for impaired microcirculation with consequent edema compressing the nerves and affecting lower limb function. The involved nerves include the femoral, sciatic, and external sciatic–popliteus. Whenever a compartment syndrome is suspected, immediate treatment with long-lasting physiotherapy is mandatory.64,65
short-term complications Infections Overall infections have been reported in up to 13% of cases after anterior colporrhaphy,66 in up to 7% of infections after periurethral injection therapy,67 and in 1–10% after retropubic colposuspension5,6,12,24,66–68 (Table 95.3). Synthetic tapes increase the risk of infection, with sling erosion rates of up to 21% being reported.69–74 Osteomyelitis is the most feared complication of bone anchor procedures.75 This complication requires removal of the anchor and prolonged antibiotics. Leach76 reported five cases of infected anchor removal after implantation of 7000 anchors. Schulttheiss et al.77 described the removal of two anchors after a Vesica procedure: one for infection and one for a painful granuloma. From 1994 to 1998 there were eight confirmed table 95.3.
cases of osteomyelitis in over 30,000 Boston Scientific anchors placed via the suprapubic route.78 Infections arising after periurethral and/or transurethral injection therapy may result in abscesses and granuloma formation.79 Infections after AMS 800 implant may occur in up to 9.5% of cases.80,81 The risk of postoperative UTIs after TVT ranges from 3.9 to 22%.24,82 The incidence of postoperative UTIs is directly related with modality and duration of bladder drainage used to resolve bladder emptying problems.83 A prolonged indwelling catheter is associated with a high risk of bacteriuria,84 which increases by 6–7.5% per day with time.85 Hence, to drain the bladder postoperatively, intermittent (self)-catheterization [I(S)C] appears to be more suitable, having less morbidity.84
Osteitis pubis Osteitis pubis is a non-infectious, painful, inflammatory condition affecting periosteum, cartilage, and ligaments of the symphysis pubis, which may worsen in osteomyelitis. Its symptoms include severe pelvic pain, a tender suprapubic area, and a waddling gait. Its incidence is difficult to ascertain because of a lack of consensus about its definition. Its treatments range from conservative to aggressive, including anti-inflammatory agents, body-cast immobili-
Short-term complications of surgery for stress urinary incontinence (excluding transient voiding dysfunction)
Complications
Authors
Operation
Infections
Peters & Thornton66 Muznai et al.67 Lotenfoe et al.68 Stanton & Cardozo5 Wee et al.6 Ward & Hilton24 Peters & Thornton66 Bryans69 Beck et al.70 Young et al.18 Crivellaro et al.20 Ward & Hilton24 Abouassaly et al.26
Anterior colporrhaphy Periurethral injections Needle suspension Burch Burch Colposuspension MMK Sling Sling Sling Sling + bone anchor TVT TVT
Osteitis pubis
Green et al.9 Mainprize & Drutz11 Goldberg et al.87
Urogenital fistulae
Nerve injury
No. of patients treated
No. of complications (%)
294 98 27 180 99 146 102 69 170 200 253 241 170
38 (12.9) 7 (7.1) 1 (3.7) 1 (0.6) 2 (2) 10 (6.8) 10 (9.8) 4 (5.8) 8 (4.7) 5 (2.5) 1 (0.8) 1 (0.4) 4 (2.3)
Needle suspension MMK Anchor suspension
29 2712 225
1 (3.4) 68 (2.5) 3 (1.3)
Beck et al.89 Guam et al.90 Mainprize & Drutz11 Kersey91
Anterior colporrhaphy Needle suspension MMK Sling
519 60 2712 105
2 (0.4) 1 (1.7) 7 (0.3) 1 (0.9)
Miyazaki & Shook93 Young et al.18 Meschia et al.23
Needle suspension Sling TVT
402 200 404
7 (1.7) 1 (0.5) 1 (0.2)
MMK, Marshall–Marchetti–Kranz; TVT, tension-free vaginal tape.
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zation, surgical debridement, and pubectomy.86 Its natural course usually leads to spontaneous recovery, with operative procedures needed in only 5–10% of cases. Osteitis pubis represents the fourth major complication following MMK colposuspension and 2.5% of all complications after such a procedure.11 It has been reported in 3.4% of cases after needle suspension,9 and in up to 1.3% after bladder neck suspension using bone anchors, culminating in osteomyelitis.87 Only one case of pubic osteitis after periurethral collagen injection has been reported in the literature.88 A possible explanation for this complication is nicking of the pubic periosteum during blind periurethral injection, followed by subperiosteal collagen migration initiating an acute inflammatory reaction and venous obstruction of the pubic bone.
Urogenital fistulae A urogenital fistula is an uncommon complication of SUI surgery, usually occurring within the first 10 days after the operation. It may arise primarily as a result of infection or secondary to the erosion of synthetic material placed on a mistaken or poorly repaired lesion. It has been reported in 0.4% of cases after anterior colporrhaphy,89 in 0.3% after MMK procedure,11 and in 2% after needle suspension.90 A case of vesicovaginal fistula (1%) has been reported by Kersey in a series of 105 patients who previously underwent sling procedures.91 Figure 95.2 shows a case of urethrovaginal fistula after removal of an infected heterologous sling.
guinal.92 Seven cases of ilioinguinal nerve entrapment following 402 needle suspension procedures have been described,93 two of which were treated successfully with suture removal. Theoretically, the incidence of nerve entrapment should be minimal with anchor placement, as the anchor allows for more stable fixation medially on the pubic bone. To date, transvaginal placement of the anchors has not been associated with nerve entrapment.75 Few cases of nerve injury have been described after TVT23 or sling procedures.18
Transient voiding dysfunction A potential complication of all anti-incontinence procedures is iatrogenic outlet obstruction leading to voiding dysfunction. This may result in voiding symptoms with partial or total urinary retention, recurrent UTIs, or in severe storage symptoms such as frequency, urgency, and urge incontinence. In the early postoperative course, transient urinary retention occurred in up to 19.7% of patients after a TVT procedure,26 and in up to 100% after colposuspension.24 After resolution of postoperative edema and pain, temporary bladder drainage with I(S)C allows normal voiding to be regained. In patients who do not improve, conservative modalities such as prolonged I(S)C and pharmacologic therapy may be tried. If symptoms persist, surgical intervention may be required. Table 95.4 shows a literature overview of transient voiding dysfunction rates after SUI surgery.6,11,19,20,24,26,27,34,39,71,89,92,94–96
long-term complications
Nerve injuries Femoral nerve injury may occur indirectly due to the abduction and flexion of the thigh in the lithotomy position during SUI surgery. After needle suspension the following nerves may be involved: common peroneal, sciatic, obturator, femoral, saphenous, and ilioin-
a Figure 95.2. removal.
Persistent voiding dysfunction The incidence of permanent obstruction, urinary retention and/or voiding dysfunction after anti-incontinence procedures varies from 2.3 to 25%.4,17–20,23–28,31,40,96–102 This variability depends on the different definitions of urinary
b (a) Urethral erosion due to an infected heterologous sling; (b) appearance of urethrovaginal fistula after sling
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table 95.4.
Transient voiding dysfunction after stress urinary incontinence surgery
Complication
Authors
Transient voiding dysfunction
89
Beck et al. Karram et al.92 Galloway et al.94 Lose et al.95 Wee et al.6 Ward & Hilton24 Mainprize & Drutz11 Chin & Stanton71 Crivellaro et al.20 Carbone et al.19 Soulie et al.39 Ward & Hilton24 Abouassaly et al.26 Rafii et al.27 Delorme et al.96 Krauth et al.34
Operation
No. of patients treated
No. of complications (%)
Anterior colporrhaphy Needle suspension Burch Burch Burch Colposuspension MMK Sling Sling + bone anchor Sling + bone anchor TVT TVT TVT TVT ± other procedures TOT TOT
519 93 50 80 99 146 2712 88 253 70 52 170 241 186 32 604
3 (0.6) 14 (15) 8 (16) 20 (25) 13 (13.1) 146 (100) 98 (3.6) 2 (2.3) 20 (8.5) 10 (14) 9 (17) 64 (38) 47 (19.7) 30 (16) 6 (18.7) 17 (2.8)
MMK, Marshall–Marchetti–Kranz; TOT, transobturator suburethral tape; TVT, tension-free vaginal tape.
retention. There is a lack of consensus in the literature regarding the appropriate evaluation and management of this distressing problem.103 Specific diagnosis is often difficult, and its management represents a challenge for specialists. Persistent urinary retention is uncommon after injectable therapy. Voiding dysfunction rates vary from
table 95.5.
5 to 7% after needle suspension,12 4–10% after pubovaginal slings,104 2–4% after TVT,101 5–20% following a MMK procedure,105,106 and 4–22% following Burch colposuspension.107 The incidence of voiding dysfunction after bone anchor procedures is minimal, and almost all series showed a low incidence of prolonged urinary retention19,75,77 (Table 95.5).
Long-term complications of surgery for stress urinary incontinence (persistent voiding dysfunction and recurrent urinary tract infections)
Complications Persistent voiding dysfunction
Recurrent urinary tract infections
Authors
Operation
No. of patients treated
No. of complications (%)
Ward & Hilton Amundsen et al.17 Young et al.18 Arunkalaivanan & Barrington97 Carbone et al.19 Crivellaro et al.20 Meschia et al.23 Nilsson & Kuuva31 Ward & Hilton24 Arunkalaivanan & Barrington97 Tsivian et al.40 Abouassaly et al.26 Levin et al.25 Rafii et al.27 Delorme et al.96
Colposuspension Sling Sling Sling
146 91 200 74
11 (8) 1 (1) 7 (3.5) 11 (1.4)
Sling + bone anchor Sling + bone anchor TVT TVT TVT TVT
70 253 404 161 146 68
9 (12.8) 5 (2.1) 16 (4) 7 (4.3) 5 (3) 23 (3.4)
TVT TVT TVT TVT ± other procedures TOT
55 241 313 186 32
2 (3.6) 10 (4.1) 20 (8.3) 7 (3.7) 5 (15.6)
Nilsson & Kuuva31 Ward & Hilton24 Ward & Hilton24 Levin et al.25
Colposuspension TVT TVT TVT
161 170 146 313
10 (6.1) 38 (22.3) 46 (31.5) 2 (0.6)
24
TOT, transobturator suburethral tape; TVT, tension-free vaginal tape.
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Surgical relief of voiding dysfunction may be accomplished by two main surgical approaches: transvaginal and transabdominal. There is no universal consensus as to which technique is better, but most surgeons prefer the transvaginal approach because of its lower morbidity. Foster and McGuire108 reported that success rates following traditional urethrolysis varied according to the prior anti-incontinence procedure. Prior retropubic urethropexy had the highest success rate (71%), followed by needle suspension (63%), and pubovaginal sling (50%). The lowest success rates in the sling group can be attributed to the traditional urethrolysis technique, leaving the sling intact. More recently, surgeons preferred cutting or lyzing slings in the midline to improve the urethrolysis success rate.109 Klutke et al.102 stated that 17/600 patients (2.8%) who developed urinary retention after TVT required tape release; simple TVT release under local anesthesia resulted in normal voiding function in all 17. In 2000, a survey regarding urethrolysis was mailed or e-mailed to the members of the American Urogynecology Society. Of the 262 respondents, 84% stated that they performed urethrolysis.103 To evaluate postoperative voiding dysfunction they strongly recommended the following studies: pressure-voiding study (84%), cystoscopy (82%), and urodynamics (79%). Most surgeons chose a table 95.6.
vaginal approach to urethrolysis (74%) and a significant number of physicians did not routinely re-suspend the bladder neck following urethrolysis (82%). Although physical examination, urodynamics, and cystoscopy are crucial in the evaluation of postoperative voiding dysfunction, it may still be difficult to diagnose. The only absolute selection criterion for offering urethrolysis might be a clear temporal relationship of voiding dysfunction following anti-incontinence surgery. Overall, urethrolysis success rates are good, with both transvaginal and transabdominal approaches. Success rates are comparable following transvaginal urethrolysis with (77%) or without (68%) re-suspension of the bladder neck. Moreover, the incidence of postoperative SUI is acceptably low with (4%) or without (5.6%) re-suspension of the urethra following transvaginal urethrolysis.103
De novo overactive bladder Women with SUI show an overactive bladder (OAB) in 30–50% of cases.110 Treating SUI often means a resolution of OAB.111,112 Unfortunately, in up to 40% of cases, there is a persistence of OAB after SUI surgery.113,114 Persistent OAB complicates 8–25% of all sling procedures performed,73 7.6–12% of TVT and 1.4–16.6% of retropubic urethropexy.4,115,116 Moreover, in 7–21% of
Long-term complications of surgery for stress urinary incontinence (de novo overactive bladder)
Complication De novo overactive bladder
Authors 89
Beck et al. Hilton119 Raz et al.120 Cardozo et al.118 Alcalay et al.4 Ward & Hilton24 McGuire et al.121 Chin, 199571 Amundsen et al.17 Kuo122 Young et al.18 Barnes et al.123 Arunkalaivanan & Barrington97 Crivellaro et al.20 Carbone et al.19 Nilsson & Kuuva31 Ward & Hilton24 Arunkalaivanan & Barrington97 Abouassaly et al.26 Rafii et al.27 Delorme et al.96 Krauth et al.34
Operation
No. of patients treated
No. of complications (%)
Anterior colporrhaphy Needle suspension Needle suspension Burch Burch Colposuspension Sling Sling Sling Sling Sling Sling Sling
436 10 206 92 109 146 82 80 91 50 200 38 74
28 (6.4) 1 (10) 11 (5.3) 17 (18.4) 16 (14.7) 11 (7.5) 5 (6.1) 22 (27.5) 14 (15) 7 (14) 12 (8.8) 2 (5.2) 4 (6)
Sling + bone anchor Sling + bone anchor TVT TVT TVT
253 70 161 170 68
13 (5.5) 3 (4.2) 5 (3.1) 10 (5.8) 4 (9)
TVT TVT ± other procedures TOT TOT
241 186 32 131
36 (15) 54 (29) 2 (6.2) 2 (1.5)
TOT, transobturator suburethral tape; TVT, tension-free vaginal tape.
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cases a de novo OAB may occur95,113,117,118 (see also complication rates in Table 95.6). Possible risk factors include misdiagnosed preoperative OAB, bladder wall thickness, bladder neck dissection, patient age, and postoperative cervicourethral obstruction.117 Voiding dysfunction (2– 27%) and de novo OAB (8–27%) are the most frequent complications after both open and laparoscopic colposuspension.8,24,124,125 Abouassaly et al.26 reported de novo OAB in 15% of cases after TVT. At 1-year follow-up after TVT, de novo AOB decreased up to 5.9%.31,99,126
De novo pelvic organ prolapse After colposuspension, de novo pelvic organ prolapse (POP) may occur in up to 30% of cases.4 At a mean follow-up of 9 years, Burch127 detected enterocele in 8% of cases and cystocele in 3% after colposuspension. At a 5-year follow-up, Wiskind et al.128 described POP secondary to Burch colposuspension needing reintervention in 26.7% of cases. At a mean follow-up of 17 months after needle suspension, Nitti et al. detected enterocele in 6.5%, rectocele in 3%, and uterine prolapse in 2% of cases.129 Recently, Neuman130 found de novo POP after TVT in 0.3% of cases (Table 95.7). A rare case of urethral prolapse has been reported after periurethral Teflon injection.131
Sexual dysfunction Transvaginal SUI surgery may be responsible for sexual activity impairment132–134 (Table 95.8). Information about this complication is difficult to obtain because 8–13% of women complain of dyspareunia with aging.139,140 POP seems to negatively affect sexual activity and total sexual function more than SUI. Nevertheless, table 95.7.
overall sexual satisfaction depends on both these conditions.141 A combination of Burch colposuspension and posterior colporrhaphy may be associated with a more frequent occurrence of dyspareunia,136 but overall sexual function and satisfaction seem to improve or do not change in most women after surgery for either prolapse or urinary incontinence, or both. Although Maaita et al.142 did not find any significant modification of sexual function and activity after TVT, more recently sexual impairment of 20% (14.5% de novo dyspareunia and 5.4% of libido loss) has been reported following this procedure.134
Chronic pain The incidence of dyspareunia and chronic pain after SUI surgery is difficult to detect because it is rarely reported in the literature (see Table 95.8). Dyspareunia has been reported in 0.4% of cases after a MMK procedure11 and in up to 4% of cases after Burch colposuspension.94 The so-called ‘postcolposuspension syndrome’ is characterized by more than 1-year suprapubic or ilioinguinal chronic pain. It has been reported in up to 12% of cases after colposuspension.94 Only few isolated cases of ‘postcolposuspension syndrome’ after a TVT procedure have been reported in the literature.143 Recently, persistent suprapubic discomfort after TVT has been reported in up to 7.5% of cases.26 Chronic pain after needle suspension may be due to direct nerve binding or to a peri-nervous inflammation secondary to a suture placed too closely to the nerves.12 Up to 5% of patients who underwent this procedure needed suture ablation to soothe their persistent pain.144
Long-term complications of surgery for stress urinary incontinence (de novo pelvic organ prolapse)
Complications
Authors 94
Operation
No. of patients treated
No. of complications (%)
De novo pelvic organ prolapse
Galloway et al. Amundsen et al.17 Neuman130
Burch Sling TVT
50 91 314
4 (8) 1 (1) 1 (0.3)
Vault/uterine prolapse
Raz et al.120 Neuman130
Needle suspension TVT
206 314
2 (1) 1 (0.3)
Cystocele
Raz et al.120 Neuman130
Needle suspension TVT
206 314
4 (2) 1 (0.3)
Rectocele
Wiskind et al.128 Alcalay et al.4 Neuman130
Burch Burch TVT
131 109 314
29 (22.1) 28 (25.7) 1 (0.3)
Enterocele
Raz et al.120 Wiskind et al.128 Alcalay et al.4
Needle suspension Burch Burch
206 131 109
7 (3) 29 (22.1) 5 (4.6)
Urethral prolapse
Kiilholma et al.131
Teflon injection
22
1 (4.5)
TVT, tension-free vaginal tape.
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table 95.8.
Long-term complications of surgery for stress urinary incontinence (sexual dysfunction, dyspareunia, and chronic pain)
Complications Sexual dysfunction
Authors
Operation 134
Mazouni et al. 135
No. of patients treated
TVT
71
No. of complications (%) 4 (5.4)
Dyspareunia
Kursh et al. Raz et al.120 Galloway et al.94 Van Geelen et al.3 Weber et al.136 Mainprize & Drutz11 Carbone et al.19 Crivellaro et al.20 Mazouni et al.134
Needle suspension Needle suspension Burch Burch Burch + posterior colporrhaphy MMK Sling + bone anchor Sling + bone anchor TVT
142 206 50 34 21 2712 70 253 7
1 (0.7) 3 (1.5) 2 (4) 1 (0.3) 8 (38) 10 (0.4) 4 (5.7) 20 (7.9) 10 (14.5)
Chronic pain
Galloway et al.94 Wheelahan137 Griffith-Jones & Abrams137 Raz et al.120 Abouassaly et al.26 Crivellaro et al.20
Burch Burch Needle suspension Needle suspension TVT Sling + bone anchor
50 102 17 206 241 253
6 (12) 27 (26) 1 (5.9) 7 (3.4) 18 (7.5) 11 (4.7)
TVT, tension-free vaginal tape.
Recurrent urinary tract infections Pelvic surgery represents one of the main risk factors for recurrent UTIs together with age, menopause, genital and LUT dysfunction and abnormalities, and sexual activity145 (see Table 95.5). Predisposing conditions include preoperative recurrent UTIs, postoperative chronic retention, voiding dysfunction, and synthetic material erosion. Recurrent UTIs (see rate details in Table 95.4) may also hide other bladder diseases such as stones or tumors that should be investigated.
Complications due to biomaterials Intraurethral injection therapy is the least invasive surgical procedure for SUI, showing a continuous success rate decline over time. Repeat injections are often required to maintain efficacy, and the surgeon is unable to determine material quantity needed for each patient and the occurrence of side effects when using injection materials (migration, foreign body reaction, immunologic effects).146,147 Overall, urgency, UTIs, and urinary retention occur to a minimal extent after injectables. Many different bulking agents are available, including autologous fat, glutaraldehyde cross-linked bovine (GAX) collagen, silicone, carbon beads, microballoons, hyaluronic acid, and dextranomer microspheres. Teflon periurethral injection may elicit a foreign body local reaction, resulting in periurethral abscess or granuloma formation131,148 (Table 95.9). Moreover, there is a potential risk of particle migration with lymphatic and visceral
embolism.131 For all these reasons Teflon has not achieved universal acceptance and has never been approved by the United States Food and Drug Administration (FDA) for periurethral injections in female patients. Periurethral injections of autologous fat149 may cause hematomas and ecchymosis at the fat collecting site. Less than 1% of the patients reported pain or hematoma formation at the injection site.150 Glutaraldehyde cross-linked collagen is a sterile nonpyrogenic material dispersed in a phosphate-buffered physiologic saline. This cross-linking process increases the time before degradation takes place and reduces its immunogenic potential.150 This material should not elicit any foreign body local inflammation, and only one case of distal migration of collagen along the urethra has been reported, creating a periurethral pseudocyst.151 Adverse reactions and complications from this procedure are rare. The most important immediate complication of collagen is the risk of allergic reaction due to pre-existing hypersensitivity to collagen, seen in 1–4% of patients.150 To select suitable patients, it is advisable to perform an intradermic injection of collagen 1 month before the anti-incontinence procedure. Urinary retention develops in less than 8% of cases and most episodes are transient, requiring I(S)C for 24–36 hours.150 UTIs have been seen in up to 6% of patients, hematuria in 3%, and hematoma at the injection site in 2%.150 A prospective study152 comparing fat and collagen injection reported immediate postopera-
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table 95.9.
Common and uncommon complications due to biomaterials employed
Complications
Authors 18
Operation
No. of patients treated
No. of complications (%)
Tape erosion
Young et al. Kuo122 Ward & Hilton24 Levin et al.25 Tsivian et al.40 Abouassaly et al.26
Mersilene sling Polypropylene sling TVT TVT TVT TVT
200 50 170 313 55 241
8 (4) 1 (2) 1 (0.6) 4 (1.3) 3 (5.4) 1 (0.4)
Vaginal stenosis
Young et al.18
Mersilene sling
200
5 (2.5)
Periurethral abscess
131
Kiilholma et al.
Teflon injection
22
1 (4.5)
Urethral diverticulum
Kiilholma et al.131
Teflon injection
22
1 (4.5)
Periurethral granuloma
Kiilholma et al.131
Teflon injection
22
1 (4.5)
TVT, tension-free vaginal tape.
tive retention in up to 60% of patients with no significant difference between the two groups. Four patients (two in each group) required I(S)C for 2 weeks postoperatively. Other complications included postoperative UTIs in eight patients, transient voiding symptoms in seven and a subcutaneous abdominal wall hematoma in one patient from the fat group, without any local complications at the injection site. No patient had de novo OAB. Desirable qualities of sling materials are availability, durability, affordability, lack of immune response, resistance to infection, and no potential risk of disease transmission. Autologous materials offer biocompatibility and durability, and appear to be associated with higher cure rates and fewer complications than synthetic materials.153 Nevertheless, a second operative field is necessary with an attendant increase in postoperative pain and infection risk. Various cadaveric fascia allografts avoid this kind of morbidity but have questionable success rates (up to >20% failure)154 and secondary vaginal erosion (up to 25%).155 Usually, sling failure occurs within the first 6 months because of degeneration of fascia or failure of anchoring sutures. Repliform acellular human dermal allograft consists of human cryopreserved allogenic dermis from which the epidermal and dermal cellular components have been removed, leaving the basement membrane complex, which is rapidly revascularized following placement. It is biologically inert and less likely to induce an immune response, without any disease transmission to recipient patients to date. This material offers the possibility of using a single piece of graft for concomitant pubovaginal sling placement and anterior POP repair.20,156 The use of Repliform processed human cadaveric allograft skin
for the transvaginal sling procedure for SUI appears to be effective and safe at a mean follow-up of 18 months. A prospective study20 on a series of 253 patients with SUI treated with a transvaginal sling using a Repliform cadaveric human dermal allograft and bone anchor fixation reported the following immediate and early operative complications: bladder injury (2.1%), bowel injury (0.9%), significant bleeding (1.3%), transient urinary retention (8.5%), and perirectal abscess (0.8%). The perirectal abscess was due to spontaneous defecation during surgery and developed in a patient who underwent a transvaginal sling, anterior and posterior repair, vaginal hysterectomy, and sacrospinous suspension. Late complications included transient dyspareunia in 8.5% of cases, pain in 4.7%, constipation in 0.9%, voiding symptoms in 2.1%, de novo OAB in 5.5%, and slow vaginal wall healing associated with vaginal infection in 1.7%. Predisposing factors to the last complication include obesity, diabetes, and immunodeficiency. Since chronic inflammation of the tape is the main cause of altered wound healing, vaginal resection of the periurethral parts of the tape is mandatory. The advantages of synthetic materials over autologous grafts for the surgical treatment of SUI are the avoidance of an additional incision to harvest fascia lata or rectus muscle fascia, a decrease in operating time, consistent material strength, high cure rates, and decreased postoperative pain.157 While cure rates and durability seem promising, several serious complications are of concern. The most frequent complications are voiding dysfunction with retention (1–4%), de novo OAB (6–14%), and synthetic sling rejection or erosion in the bladder, urethra, and vagina.18,97,122,124 1355
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The average reported erosion rate of synthetic grafts used for urethral slings is 7.3% (range 3–34%).158 Teflon slings have erosion and infection rates as high as 23%.159 The ProteGen sling was associated with infection or erosion and was voluntarily recalled.160 More recently, polypropylene material has been used in tension-free sling procedures, such as TVT and TOT. While short-term follow-up studies show high success with a low complication rate, several complications not fully reported in the literature have been identified. A search through the FDA Adverse Event Reporting Program at www.fda.gov/ medwatch revealed notable TVT complications, including erosion, retention, bladder perforation, and major complications of vascular and bowel injuries, sepsis and, rarely, death. While these complications are probably not material related, caution is necessary in the use of TVT. It is important to bear in mind that the reported low morbidity of TVT as performed by experienced urologists and gynecologists does not reflect the real morbidity of this technique when performed by all practitioners. Bladder perforation is the most frequent intraoperative complication, occurring in around 1/25 procedures.24,31,161 Voiding dysfunction (3–5%), UTIs (6–22%), and de novo OAB (3–9%) can occur postoperatively.24,31,97,162,163 In up to 5% of cases, a retropubic hematoma can occur.162 Complications related to the tape (e.g. erosion into vagina or urinary tract) may rarely occur.161 Tsivian et al.40 reported 14 cases of tape-related complications, 12 of them occurring among the 200 women who previously underwent the TVT procedure at their department for SUI. One woman had intravesical tape erosion with encrustation and stone formation on the tape, four had vaginal tape erosion, eight had an obstructed urethra and one had concomitant vaginal erosion and an obstructed urethra. A total of 12 patients required partial tape removal or tape incision, which was done transvaginally in 11. The remaining patient underwent cystotomy and excision of the intravesical part of the eroded tape. One patient was awaiting corrective surgery and one with asymptomatic vaginal erosion was only being observed. There have been several recent reports in the literature on tape erosion into the urethra164–166 and vagina.146,148,149 The recommended treatment is foreign body removal.167–169 Aimed at reducing TVT complication rates, a tensionfree transobturator modality (TOT outside-in) to place the polypropylene tape was proposed.170,171 The TOT outside-in promoters stated that there might be no risk to bladder, urethra or bowel, and no vascular or nerve damage. Despite that, LUT injury has been reported in
six patients, three of whom subsequently developed a urethral fistula.172 A recent retrospective study,34 assessing the morbidity related to TOT outside-in, reported a number of operative complications: 0.5% bladder perforations, 0.3% vaginal perforations, no urethral wounds, 0.8% 200–300 ml hemorrhage, and two perineal hematomas (0.33%). Short-term complications included 1.5% transient retention, 2.3% transient pain, 2.5% UTIs, and 1.3% transient voiding dysfunction, with a 1.5% rate of de novo voiding symptoms and urgency after 1-year follow-up. To further reduce TOT complication rates, de Leval proposed a TOT inside-out procedure,173 which was performed in 107 consecutive patients. No bladder or urethral injuries, or vascular or neurologic complications were encountered. Minor vaginal erosion was noted in one patient, and three women (2.8%) complained of complete retention, successfully treated by releasing the tape. Twenty-seven patients (15.9%) complained of transient moderate pain or discomfort in the thigh folds. The authors did not provide de novo OAB rates owing to the short follow-up time. Mechanism failure after artificial urinary sphincter implant is common, even with today’s sophisticated and very expensive devices. There is a mean expected revision rate due to mechanical and non-mechanical failure of 7.6% and 9%, respectively, with an average rate of both infection and erosion of 3.4%.174 A recent metaanalysis carried out on 2606 patients showed an overall revision rate of 32% with mechanical and non-mechanical failure rates of 14% and 17%, respectively. Urethral erosion occurred in up to 11.7% of cases and infections in up to 4.5%.81 Uncommon reservoir-related complications include small intestine erosion,63 migration into the bladder,175 and infection causing peritonitis.176
Impact on quality of life Urinary incontinence negatively affects quality of life (QoL) of suffering women. Hence, any means to relieve this condition should theoretically improve patients’ physical, social, and psychological well-being. Black et al.177 found that 7% of 442 patients surgically treated for SUI reported a deterioration of their general health status 1 year after the intervention. Moreover, 25% of them reported worse mental health, reflecting the disappointing cure rate of only 28%. In that series, postoperative recovery was longer than anticipated, with 24% of women still on sick leave or left unpaid. The main instruments to measure patients’ QoL after SUI surgery are the Incontinence Impact Questionnaire (IIQ-7) and the Urogenital Distress Inventory (UDI-6).
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Scores for both systems appear to improve after SUI surgery in patients showing a subjective cure; on the other hand, only UDI-6 scores appear to improve in patients with an objective cure.178 Vassallo et al.,179 using the abovementioned QoL measurement tools, demonstrated an objective and significant improvement in quality of life in patients who previously underwent TVT alone or with associated POP surgery, reporting an improvement of 81% and 85% in IIQ and UDI scores, respectively. This improvement was constant and independent of preoperative SUI severity. Morgan et al.112 analyzing the measurements of QoL scores of patients previously treated with pubovaginal sling, detected a satisfaction rate of 92% at a 4-year follow-up. These patients showed a very low UDI score, an expression of the good clinical results achieved. On the other hand, those patients with postoperative storage symptoms were the most dissatisfied with surgery.
conclusIons In the last century, more than 150 different surgical procedures have been reported for the treatment of SUI, indicating that there is no operation showing satisfactory results for all patients or reference standard treatment. Knowledge of the functional consequences and complications of these procedures may play a role in the choice of a particular operation, together with other factors that influence this choice, such as anatomic defects and both the surgeon’s and patient’s preferences. It is crucial to monitor all new techniques. The complications outlined in the case reports highlight the need to consistently reassess why a patient does not do well after a supposedly less morbid procedure. Hence, the surgeon’s mastery of all techniques and complications is mandatory for comprehensive patient information, and the choice of treatment must be determined case by case.
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131. Kiilholma PJ, Chancellor MB, Makinen J et al. Complications of Teflon injection for stress urinary incontinence. Neurourol Urodyn 1993;12:131–7.
117. Bombieri L, Reeman RM, Perkins EP et al. Why do women have voiding dysfunction and de novo detrusor instability after colposuspension? BJOG 2002;109(4):402–12.
132. Creighton SM, Stanton SL. The surgical management of vaginal vault prolapse. Br J Obstet Gynaecol 1991;98(11):1150–4.
118. Cardozo LD, Stanton SL, Williams JE. Detrusor instability following surgery for genuine stress incontinence. Br J Urol 1979;51:204–7.
133. Drutz HP, Cha LS. Massive genital and vaginal vault prolapse treated by abdominal–vaginal sacropexy with use of Marlex mesh: review of the literature. Am J Obstet Gynecol 1984;149(6):685–6.
119. Hilton P. A clinical and urodynamic study comparing the Stamey bladder neck suspension and suburethral sling procedures in the treatment of genuine stress incontinence. Br J Obstet Gynaecol 1989;96:213–20. 120. Raz S, Sussman EM, Eriksen DB et al. The Raz bladder neck suspension: results in 206 patients. J Urol 1992;148:845–50. 121. McGuire EJ, Bennett CJ, Konnak JA et al. Experience with pubovaginal slings for urinary incontinence at the University of Michigan. J Urol 1987;138:525–6. 122. Kuo HC. Anatomical and functional results of pubovaginal sling procedure using polypropylene mesh for the treatment of stress urinary incontinence. J Urol 2001;166:152–7.
134. Mazouni C, Karsenty G, Bretelle F et al. Urinary complications and sexual function after the tension-free vaginal tape procedure. Acta Obstet Gynecol Scand 2004;83(10):955–61. 135. Kursh ED, Angell AH, Resnick MI. Evolution of endoscopic urethropexy: seven year experience with various techniques. Urology 1991;37:428–31. 136. Weber AM, Walters MD, Piedmonte MR. Sexual function and vaginal anatomy in women before and after surgery for pelvic organ prolapse and urinary incontinence. Am J Obstet Gynecol 2000;182:1601–5. 137. Wheelahan JB. Long-term results of colposuspension. Br J Urol 1990;65:329–32.
123. Barnes NM, Dmochowski RR, Park R et al. Pubovaginal sling and pelvic prolapse repair in women with occult stress urinary incontinence: effect on postoperative emptying and voiding symptoms. Urology 2002;59(6):856– 60.
138. Griffith-Jones MD, Abrams PH. The Stamey endoscopic bladder neck suspension in the elderly. Br J Urol 1990;65:170–2.
124. Smith T, Daneshgari F, Dmochowski RR et al. Surgical treatment of incontinence in women. In: Abrams P, Cardozo L, Khoury S, Wein A (eds) Incontinence, 2nd ed. Plymouth: Health Publication, 2002; 823–63.
140. Osborn MK, Hawton K, Gath D. Sexual dysfunction among middle aged women in the community. Br Med J 1988;296:959–62.
125. Bidmead J, Cardozo L, McLellan A et al. A comparison of the objective and subjective outcomes of colposuspension for stress incontinence in women. BJOG 2001;108: 408–13. 126. Wang AC. An assessment of the early surgical outcome and urodynamic effects of the tension-free vaginal tape (TVT). Int Urogynecol J Pelvic Floor Dysfunct 2000;11:282–4. 127. Burch JC. Cooper’s ligament urethrovesical suspension for stress incontinence. Nine years’ experience – results, complications, technique. Am J Obstet Gynecol 1968;100(6):764–74. 128. Wiskind AK, Creighton SM, Stanton SL. The incidence of genital prolapse after Burch colposuspension. Am J Obstet Gynecol 1992;167:399–404. 129. Nitti VW, Bregg KJ, Sussman EM et al. The Raz bladder neck suspension in patients 65 years old and older. J Urol 1993;149:802–7. 130. Neuman M. Low incidence of post-TVT genital prolapse. Int Urogynecol J Pelvic Floor Dysfunct 2003;14(3): 191–2.
139. Diokno AC, Brown MB, Herzog AR. Sexual function in the elderly. Arch Intern Med 1990;150(1):197–200.
141. Barber AG, Visco JF, Wyman JA et al. Sexual function in women with urinary incontinence and pelvic organ prolapse. Obstet Gynecol 2002;99(2):281–9. 142. Maaita M, Bhaumik J, Davies AE. Sexual function after using tension-free vaginal tape for the surgical treatment of genuine stress incontinence. BJU Int 2002;90:540–3. 143. Barrington JW, Arunkalaivanan AS, Swart M. Post-colposuspension syndrome following a tension-free vaginal tape procedure. Int Urogynecol J Pelvic Floor Dysfunct 2002;13(3):187–8. 144. Jarvis GJ. Surgery for genuine stress incontinence. BJOG 1994;101:371–4. 145. Dwyer PL, O’Reilly M. Recurrent urinary tract infection in the female. Curr Opin Obstet Gynecol 2002;14(5):537– 43. 146. Appell RA. Intra-urethral injection therapy. In: Cardozo L, Staskin D (eds) Textbook of Female Urology and Urogynaecology. London: Martin Dunitz, 2001; 479–91. 147. Pickard R, Reaper J, Wyness L et al. Periurethral injection therapy for urinary incontinence in women (Cochrane Review). In: The Cochrane Library. Chichester: Wiley, 2003; 4.
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148. Politano VA, Small MP, Harper JM et al. Periurethral Teflon injection for urinary incontinence. J Urol 1974;111:180–3.
163. Petri E. Retropubic cystourethropexies. In: Cardozo L, Staskin D (eds) Textbook of Female Urology and Urogynaecology. London: Martin Dunitz, 2001; 513–24.
149. Gonzales Garibay S, Jimeno C, York M et al. [Endoscopic autotransplantation of fat tissues in the treatment of urinary incontinence in the female.] J Urol (Paris) 1989;95:363–6.
164. Sweat SD, Itano NB, Clemens JQ et al. Polypropylene mesh tape for stress urinary incontinence: complications of urethral erosion and outlet obstruction. J Urol 2002;168:144–6.
150. Winters JC, Appell RA. Periurethral injection of collagen in the treatment of intrinsic sphincter deficiency in the female patient. Urol Clin North Am 1995;22:673–7.
165. Madjar S, Tchetgen MB, Van Antwerp A et al. Urethral erosion of tension-free vaginal tape. Urology 2002;59:601.
151. Wainstein MA, Klutke CG. Periurethral pseudocyst following cystoscopic collagen injection. Urology 1998;51(5):835–6. 152. Haab F, Zimmern PE, Leach GE. Urinary stress incontinence due to intrinsic sphincter deficiency: experience with fat and collagen periurethral injections. J Urol 1997;157:1283–6. 153. Bidmead J, Cardozo L. Sling techniques in the treatment of genuine stress incontinence. Br J Obstet Gynaecol 2000;107:147–56. 154. Fitzgerald MP, Mollenhauer J, Brubaker L. Failure of allograft suburethral slings. BJU Int 1999;84:785–8. 155. Kammerer-Doak DN, Rogers RG, Bellar B. Vaginal erosion of cadaveric fascia lata following abdominal sacrocolpopexy and suburethral sling urethropexy. Int Urogynecol J Pelvic Floor Dysfunct 2002;13:106–9; discussion 109. 156. Chung SY, Franks M, Smith CP et al. Technique of combined pubovaginal sling and cystocele repair using a single piece of cadaveric dermal graft. Urology 2002;59:538–41. 157. Kaplan SA, Santarosa RP, Te AE. Comparison of fascial and vaginal wall slings in the management of intrinsic sphincter deficiency. Urology 1996;47:885–9. 158. Iglesia CB, Fenner DE, Brubaker L. The use of mesh in gynecologic surgery. Int Urogynecol J Pelvic Floor Dysfunct 1997;8:105–15. 159. Bent AE, Ostergard DR, Zwick-Zaffuto M. Tissue reaction to expanded polytetrafluoroethylene suburethral sling for urinary incontinence: clinical and histologic study. Am J Obstet Gynecol 1993;169:1198–204. 160. Kobashi KC, Dmochowski R, Mee SL et al. Erosion of woven polyester pubovaginal sling. J Urol 1999;162:2070– 2. 161. Cody J, Wyness L, Wallace S et al. Systematic review of the clinical effectiveness and cost-effectiveness of tension-free vaginal tape for treatment of urinary stress incontinence. Health Technol Assess 2003;7:1–189. 162. Karram MM, Segal JL, Vassallo BJ et al. Complications and untoward effects of the tension-free vaginal tape procedure. Obstet Gynecol 2003;101:929–32.
166. Pit MJ. Rare complications of tension-free vaginal tape procedure: late intraurethral displacement and early misplacement of tape. J Urol 2002;167(2 Pt 1):647. 167. Volkmer BG, Nesslauer T, Rinnab L et al. Surgical intervention for complications of tension-free vaginal tape procedure. J Urol 2003;169(2):570–4. 168. Boublil V, Ciofu C, Traxer O et al. Complications of urethral sling procedures. Curr Opin Obstet Gynecol 2002;14:515–20. 169. Clemens JQ, DeLancey JO, Faerber GJ et al. Urinary tract erosions after synthetic pubovaginal slings: diagnosis and management strategy. Urology 2000;56:589–94. 170. Delorme E. La bandelette transobturatrice: un procédé mini-invasif pour traiter l’incontinence urinaire de la femme. Prog Urol 2001;11:1306–13. 171. de Tayrac R, Droupy S, Delorme E. Transobturator urethral support for female GSI: a new surgical procedure with one-year outcome. Int Urogynecol J Pelvic Floor Dysfunct 2002(Suppl 1);13:20. 172. Hermieu JF, Mesas A, Delmas V et al. Plaie vévicale après bandelette trans-obturatrice. Prog Urol 2003;13:115–7. 173. de Leval J. Novel surgical technique for the treatment of female stress urinary incontinence: transobturator vaginal tape inside-out. Eur Urol 2003;44:724–30. 174. Petrou SP, Elliott DS, Barrett DM. Artificial urethral sphincter for incontinence. Urology 2000;56(3):353–9. 175. Bartoletti R, Gacci M, Travaglini F et al. Intravesical migration of AMS 800 artificial urinary sphincter and stone formation in a patient who underwent radical prostatectomy. Urol Int 2000;64(3):167–8. 176. De Stefani S, Liguori G, Ciampalini S et al. AMS 800 artificial sphincter: an unusual case of circumscribed peritonitis due to prosthetic reservoir infection. Arch Esp Urol 1999;52(4):412–5. 177. Black NA, Bowling A, Griffiths LM et al. Impact of surgery for stress incontinence on the social lives of women. Br J Obstet Gynaecol 1998;105(6):605–12. 178. Fitzgerald MP, Kenton K, Shott S et al. Responsiveness of quality of life measurements to change after reconstructive pelvic surgery. Am J Obstet Gynecol 2001;185:20–4. 179. Vassallo BJ, Kleeman SD, Segal JL et al. Tension-free vaginal tape: a quality-of-life assessment. Obstet Gynecol 2002;100:518–24.
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96 The effect of hysterectomy (simple and radical) on the lower urinary tract Heinz Koelbl
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IntroductIon Altered bladder function is a commonly recognized feature of pelvic surgery. This includes difficulty in voiding, high residual volumes (including distension of the upper urinary tract), recurrent urinary tract infections, loss of bladder sensation, stress urinary incontinence, and the development of urinary fistulae. The extent of postoperative complications is related to the degree of tissue disruption.
SymptomS Voiding disorders are often encountered in patients postoperatively. There is increasing evidence that even simple hysterectomy may cause vesicourethral dysfunction which appears neuropathic in origin. However, the risk of persistent damage is only slight because the bulk of the pelvic plexus lies below the cardinal ligaments. There is a growing body of evidence that hysterectomy is not associated with an increased risk of urge or stress urinary incontinence at long-term follow-up.1 Clinical studies of bladder function after a radical pelvic operation are conflicting. At least a portion of the confusion involves the timing of evaluation postoperatively. Causes of bladder dysfunction after pelvic surgery include nerve injury (either direct or by traction), direct vesical trauma, traumatic aseptic pericystitis, loss of bladder base support and/or tumor invasion of nerves. Other factors contributing to dysfunction postoperatively are stretch injuries (urinary retention), irradiation, and infection. Radical pelvic surgery may alter bladder function through many processes, not least because the sympathetic pathways are highly susceptible to injury. On the one hand, parasympathetic decentralization results in adrenergic hyperinnervation of the detrusor; on the other, clinical studies suggest that bladder compliance changes may be seen frequently, but only temporarily, after a radical pelvic operation, and that detrusor motor denervation occurs in only a small number of patients. Rectal or extensive parametrial resection or traction during mobilization may cause direct injury to the parasympathetic nerves and part of the pelvic plexus, resulting in bladder areflexia in up to 7.7%.2 Sympathetic in addition to parasympathetic nerve injury may occur in patients with higher stage disease after dissection in the vicinity of the cardinal ligaments and in those who require extensive vaginal cuff removal.3 Techniques such as nerve-sparing radical hysterectomy have been introduced into radical surgical gynecologic oncology to avoid bladder function disorders. However, comparative trials are lacking.4,5
Various patterns of bladder dysfunction may occur after radical hysterectomy:6 1. decreased bladder capacity (low compliance) and incompetent bladder neck due to sympathetic denervation; 2. bladder areflexia with decreased proprioception sensation and increased bladder capacity due to parasympathetic denervation; 3. a combination of 1 and 2. Voiding difficulty has been defined as a condition of abnormally slow or incomplete micturition. When severe, increasing amounts of urine are retained (chronic retention) which can cause urinary tract infection or upper urinary tract damage. In the extreme condition, a complete inability to void occurs (acute retention). Voiding difficulty and retention present a spectrum of progressive inefficiency of bladder emptying. The postoperative development of stress incontinence de novo is related to a reduction in the urethral closure pressure. This is due to radical dissection of the paraurethral tissue, irritation or destruction of the sympathetic nerves of the urethral branch of the pudendal nerve. Radical hysterectomy and extensive anterior vaginal repair, pelvic exenteration, and urethral resection at vulvectomy are the procedures that typically have a detrimental impact on urethral closure function.
preventIon Women with a diagnosis of voiding difficulty prior to planned pelvic surgery should be carefully counseled regarding the possibility of exacerbating the problem of retention postoperatively. Discussion must include the options of intermittent self-catheterization after surgery.
ASSeSSment An accurate assessment of residual urine volume is essential, either by catheterization or ultrasound. Repeated measurements are recommended when volumes of more than 50 ml occur.7 Urodynamic evaluation in patients undergoing radical pelvic surgery is important to exclude preoperative bladder outlet obstruction, infiltration of the tumor into the pelvic neuroplexus, and to assess the pattern of voiding dysfunction, which may change markedly postoperatively or even resolve.
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therApy Catheterization will be a part of therapy for all forms of urinary retention. Where the cause of urinary retention is detrusor failure, bladder drainage will often allow detrusor function to recover. If the cause is outflow obstruction, catheterization will provide temporary relief until spontaneous or surgical cure is obtained. Catheterization can be continuous or intermittent. After radical pelvic surgery, the bladder should be drained immediately, either with a suprapubic catheter or with clean intermittent catheterization. This period of drainage should continue for 2–4 weeks. If the patient suffers bladder dysfunction, urodynamic studies should be performed. In patients with impaired urethral closure function, a thorough assessment – including urodynamics and imaging to rule out complex disorders – is mandatory.
follow-up after vaginal hysterectomy. Am J Obstet Gynecol 2004;191:90–4. 2. Gerstenberg TC, Nielsen ML, Clausen S. Bladder function after abdomino-perineal resection. Ann Surg 1980;191:81– 6. 3. Ralph G, Winter R, Michelitsch L et al. Radicality of parametrial resection and dysfunction of the lower urinary tract after radical hysterectomy. Eur J Gynaecol Oncol 1991;12:27–30. 4. Hockel M, Horn LC, Hentschel B et al. Total mesometrial resection: high resolution nerve-sparing radical hysterectomy based on developmentally defined surgical anatomy. Int J Gynecol Cancer 2003;13:791–803. 5. Trimbos JB, Maas CP, Deruiter MC et al. A nerve-sparing radical hysterectomy: guidelines and feasibility in Western patients. Int J Gynecol Cancer 2001;11:180–6.
reFerenceS
6. Benedetti-Panici P, Zullo MA, Plotti F et al. Long-term bladder function in patients with locally advanced cervical carcinoma treated with neoadjuvant chemotherapy and type 3-4 radical hysterectomy. Cancer 2004;100:2110–7.
1. de Tayrac R, Chevalier N, Chauveaud-Lambling A et al. Risk of urge and stress urinary incontinence at long-term
7. Fischer W, Koelbl H. Urogynäkologie in Klinik und Praxis. Berlin: DeGruyter, 1995; 159–74.
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97 Recognition and management of urologic complications of gynecologic surgery Kevin R Loughlin
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IntroductIon The management of urologic injuries during gynecologic surgery represents a challenging problem to the surgeon. In this chapter, the methods of operative repair that are necessary to manage these injuries are reviewed. First, the female pelvic anatomy is described; the techniques necessary to manage these iatrogenic injuries (whether they are recognized intraoperatively or postoperatively) are then discussed.
enters the bladder in the deep pelvis. The ureterovesical junction is the third common site of ureteral injury during female pelvic surgery. An outline of female pelvic anatomy and its relationship to the urinary tract appears in Figure 97.1. Laparoscopic surgery and repeat pelvic surgery are associated with a higher risk of ureteral injury. In such circumstances, placement of ureteral stents prior to surgery is an option.
Female PelvIc anatomy and Its relatIonshIP to the urInary tract
ureteral InjurIes – IntraoPeratIve recognItIon and rePaIr
Ureteral injuries are less likely to occur if the operating surgeon has a thorough knowledge of the female pelvic anatomy and its relationship to the urinary tract. To that end, some of the female pelvic anatomy as it relates to ureteral injuries is reviewed briefly here. The ureters cross over the pelvic brim and enter the pelvis in close proximity to the ovarian vessels. This is one of the three most common sites of urologic injury during gynecologic surgery.1 The ureter then courses medially into the lower and medial portions of the broad ligament. At this juncture, the ureter is crossed by the uterine artery and this is the second area of the ureter that is commonly injured during gynecologic operations.2 The ureter then continues its medial course and
Ureteral injuries occur in 0.5–2.5% of routine pelvic operations and in as many as 30% of radical pelvic procedures performed for malignancy.3 However, less than one-third of these injuries are identified intraoperatively.4 Ideally, the ureters should be identified and isolated prior to any extensive pelvic dissection. A useful maneuver is to identify the ureters as they cross the iliac vessels and then place Vascu-ties (vesiloop) around each ureter for later reference as the operation proceeds. Most ureteral injuries occur when there is extensive bleeding, or when the anatomy is distorted from previous surgery or radiation treatment. If the surgeon encounters extensive bleeding or there is a question of ureteral injury, the gynecologist or urologic consultant
Aorta Superior mesenteric artery
Ureter
Ovarian vessels Ureter Inferior mesenteric artery Point of common injury to ureter
Promontory Rectum Ovary Round ligament Uterus
Fallopian tube Internal iliac artery External iliac artery Point of common injury to ureter Uterine artery Point of common injury to ureter Bladder
Figure 97.1. An overview of the course of the ureters in the pelvis. The three most common sites of injury are at the pelvic brim near the ovarian vessels, at the point where the uterine artery crosses the ureter, and at the ureterovesical junction.
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should identify the ureter from above and trace out its course to the bladder.
the role oF the urologIc consultant When the urologist is called to the operating room for consultation on a possible urologic injury, he should do several things before scrubbing up. First, he should read the chart for any relevant history that may affect the patient’s urologic status. Second, he should ask if any preoperative radiologic studies, such as an intravenous pyelogram (IVP), are available for review. It is my practice to take a ‘urology bag’ with me when called for an intraoperative consultation. This bag contains ureteral stents, infant feeding tubes, Malecot catheters, and three-way urethral catheters, which are often unfamiliar to non-urologic nurses. After scrubbing up, the urologist should assess the situation. If exposure is poor, there should be no reluctance about repositioning retractors or extending the surgical incision, if necessary. In addition, if hemostasis is inadequate, the urologist should ensure a relatively dry surgical field before proceeding. The ureter should be identified and traced out above and below the area of concern. The urologist should be aware that, if a ureter has been injured, the contralateral ureter or bladder might also have been injured; depending on the circumstances, these structures should also be examined intraoperatively. Indigo carmine or methylene blue may be given intravenously to aid in checking the integrity of the ureters; these dyes may be instilled via a urethral catheter to help identify or confirm bladder injuries.
wall. Such injuries are difficult to close because the exposure is awkward and these injuries carry an increased risk of postoperative vesicovaginal fistula formation. It is often prudent, when faced with a posterior bladder wall repair, to interpose omentum between the bladder repair and vaginal wall to decrease the likelihood of postoperative fistula formation. All bladder injuries should be drained with an indwelling bladder catheter and either a closed or an open drainage system from the space of Retzius. The customary postoperative regime is to remove the drain from the space of Retzius on postoperative day 2 or 3 and to perform a cystogram about a week postoperatively to confirm satisfactory bladder repair before discontinuing the urethral catheter.
IntraoPeratIve rePaIr – lower ureter Injuries to the distal 4 cm of the ureter can be handled in one of three ways, outlined below.
ureteroureterostomy If the ureteral injury is within 3–4 cm above the ureterovesical junction it can often be repaired by a primary ureteral anastomosis. It is important to resect a small portion of both the proximal and distal ureteral segments to ensure that viable tissue is being anastomosed. It is preferable to spatulate either end of the ureter that is being repaired and to use interrupted, absorbable sutures (Fig. 97.2). Whether to stent the anastomosis is best left to the discretion of the surgeon, but all anas-
IntraoPeratIve rePaIr – Bladder InjurIes Most bladder injuries are relatively straightforward to repair. They usually occur during a hysterectomy and usually involve the anterior bladder wall. Most bladder injuries are satisfactorily repaired with two layers of absorbable suture. Occasionally, the bladder wall will need to be debrided before closure. If a Foley catheter is not in place, one should be inserted and either indigo carmine or methylene blue can be injected to verify the adequacy of the closure. The urologist should remember the caveat of associated ureteral injuries. If there is uncertainty about a ureteral injury at the time of a bladder injury, 5 Fr or 8 Fr infant feeding tubes can be inserted into the ureteral orifices prior to closure of the bladder. This often makes identification of the ureters easier. Bladder injuries associated with cesarean section are more difficult to manage. These bladder injuries are often more posterior and frequently are near the vaginal
a
b
Figure 97.2. A primary ureteroureterostomy is best performed after each ureteral segment has been resected back to viable tissue and with each end spatulated. 1369
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tomoses should be drained. Non-transecting injuries of the ureter, such as ureteral tears or inadvertent ureteral clamping, are also best left to the judgment of the individual surgeon; however, in most cases, such injuries are best excised and a ureteral anastomosis performed to complete the repair.
ureteral implant When the ureteral injury is quite low – in the distal 2 cm – primary ureteral repair is usually difficult. In these situations, a ureteral reimplant is usually preferable. I prefer to utilize the Leadbetter–Politano technique of ureteral reimplantation (Fig. 97.3), but any method of reimplantation with which the surgeon feels comfortable is acceptable. A non-refluxing reimplantation is preferable in women who are in the age group where sexual activity is likely. Whether to stent the reimplanted ureter is, again, best left to the individual surgeon’s judgment; however, all ureteral reimplants should be drained.
a
c
If the primary ureteroureterostomy or ureteral implant cannot be performed with a tension-free anastomosis, then a psoas hitch is a very good solution for lower ureteral injuries.5–7 The techniques used for performing the psoas hitch have been described previously; below, I describe the technique that I have used over the years.8,9 Bladder mobilization is important in order to provide a tension-free ureteral reimplantation. It is usually necessary to mobilize the bladder bilaterally, not just on the side of the ureteral injury. The cystostomy should be made on the anterior wall of the bladder, away from the dome. This enables the surgeon’s fingers to be placed in the bladder dome, thus aiding mobilization of the bladder as well as placement of the anchoring stitches in the psoas muscle (Fig. 97.4). My own preference is to use non-absorbable stitches to anchor the bladder to the psoas muscle. During this maneuver, care should be taken to avoid injury to the genitofemoral nerve or inad-
Buried ties
b
d
Psoas hitch
e
Figure 97.3. The Leadbetter– Politano ureteral reimplantation technique.
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Cystostomy on lower portion of anterior bladder wall
Fingers in bladder help push bladder toward psoas muscle when anchoring sutures are placed
Figure 97.4. The cystostomy should be made on the interior portion of the anterior bladder wall to permit the surgeon’s finger to aid in bladder mobilization and guide in the anchoring stitches to the psoas muscle. vertent incorporation of the nerve within the sutures. In most cases I use the Leadbetter–Politano technique for ureteral reimplantation and, in these cases, I find it preferable to leave an indwelling ureteral stent (Fig. 97.5). The cystostomy is closed in the usual manner. A urethral catheter is left in place and a suprapubic tube is usually not necessary. An external drain is left near the reimplantation site.
IntraoPeratIve rePaIr – mIdureter Midureteral injuries that are not extensive can be repaired with a ureteroureterostomy, as described above. However, when a primary repair is not possible, other operative techniques are useful.
transureteroureterostomy The technique of transureteroureterostomy was first described in 1934 by Higgins to manage persistent unilateral ureteral reflux.10 Since that time it has been used to treat unilateral ureteral injuries.6,9,10 However, the concern has been that, if a complication occurs following a transureteroureterostomy, then both ureters are jeopardized.11,12 A history of stone disease is a contraindication to this procedure. The technique of transureteroureterostomy is straightforward. Both the donor and recipient ureters should
Figure 97.5.
Completed psoas hitch and ureteral implant.
be mobilized to prepare for a tension-free anastomosis. Under no circumstances should the recipient ureter be angulated in order to reach the donor ureter. My own preference is to spatulate the donor ureter and then to place stay sutures in the recipient ureter and perform the ureteroureterostomy between the stay sutures (Fig. 97.6a). I prefer to use 4-0 chromic sutures for the anastomosis: I perform a running suture line, with the knots on the outside on the posterior wall, and use interrupted sutures on the anterior wall (Fig. 97.6b). Because stenting a transureteroureterostomy is usually an awkward procedure, in most cases the anastomosis is left unstented; however, an external drain is always used.
Boari flap The Boari flap is an attractive solution for repair of extensive midureteral injuries. Boari first described his operative technique for ureteral replacement in a canine model in 1894.13 Subsequently, the Boari flap has been incorporated into clinical practice and is par1371
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a
b (i)
(ii)
ticularly adaptable to the management of injuries to the midureter.14–17 As with preparation for a psoas hitch, the bladder must be thoroughly mobilized. Before the flap is created, the bladder should be distended with saline and the flap carefully planned with a sterile marker. The most critical maneuver is to make sure that the base of the flap is wide enough to prevent distal ischemia in the flap: the flap should have its blood supply based on the superior vesicle artery; usually, the base of the flap should be at least 4 cm wide, depending on the length of the flap required (Fig. 97.7a). After the flap is created, it is tubularized with running absorbable sutures. The distal ureter is then anastomosed to the flap (Fig. 97.7b) in the standard fashion. These anastomoses are preferably stented and all are drained. A urethral catheter is left indwelling to drain the bladder and a suprapubic tube is used at the surgeon’s discretion.
a
b
Figure 97.6. (a) Stay sutures mark the area of planned ureterotomy; (b) the transureteroureterostomy anastomosis: anastomosis of the posterior (i) and anterior (ii) walls of the ureter.
IntraoPeratIve rePaIr – uPPer ureter Injuries to the upper ureter that cannot be repaired with a straightforward ureteroureterostomy can be problematic. In most cases, a Boari flap will not reach an upper ureteral injury; therefore, the choices usually include autotransplantation, ileal ureter or nephrectomy.
autotransplantation Autotransplantation of the kidney is a formidable procedure and should not be undertaken if other options exist.16,18,19 It is usually considered when the contralateral kidney is absent or poorly functioning. The kidney is harvested with maximal vessel length and the vascular anastomoses to the iliac vessels are performed in the standard fashion. The upper ureter or renal pelvis can then be anastomosed directly to the bladder.
Figure 97.7. (a) The Boari flap is planned out on the distended bladder wall; (b) the proximal ureter is anastomosed to the tubularized Boari flap.
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Ileal ureter
that can be seen with other techniques used to manage upper ureteral injuries.
The use of ileal interposition for extensive upper ureteral injuries has also been reported.6,16,20 As with autotransplantation, ileal interposition should be considered only when simpler alternatives are not practical. It is preferable to create an ileal ureter in patients who have had thorough preoperative bowel preparation; in emergency situations, however, an ileal segment can be isolated without such preparation. The techniques used for creation of an ileal ureter are similar to those used in an ileal conduit. The proximal and distal ureteral segments should be fully mobilized and the ureteral–ileal anastomoses are performed with absorbable sutures (Fig. 97.8). No stents are utilized and an external drain is necessary.
nephrectomy When a normal contralateral kidney is present, a simple nephrectomy should be considered as an expeditious solution to extensive upper ureteral injury.6,21 A nephrectomy is often attractive because it obviates the postoperative complications, such as urinary leak or infection,
Figure 97.8.
Completed ileal ureter.
PostoPeratIve Procedures Postoperative recognition of bladder injuries Postoperative symptoms associated with delayed recognition of bladder injuries include fever, abdominal pain, abdominal distension, infection, decreased urine output, and rising serum creatinine. The management of these cases should be individualized, since the patient’s overall condition is an important consideration. In general, however, extraperitoneal injuries can be managed with a trial of catheter drainage, whereas intraperitoneal injuries merit surgical exploration and repair. The most direct way to diagnose the presence and location of a bladder injury is a cystogram.
Postoperative recognition of ureteral injuries Postoperative symptoms of ureteral injuries may include flank pain, fever, sepsis, decreased urine output, abdominal mass, elevated creatinine or urinary fistula. However, ureteral injuries can also be asymptomatic. If a ureteral injury is suspected, an IVP is the diagnostic study of choice,21,22 although an abdominal ultrasound or computed tomography scan may also be helpful. Once a diagnosis of ureteral injury is suspected or confirmed, a retrograde pyelogram can give more information regarding the precise location of the injury. There is genuine debate as to whether stent placement should be attempted at the time of a retrograde pyelogram. Dowling and associates21 found that, in 19 of 20 patients, a retrograde stent could not be placed beyond the site of the urologic injury. However, others feel that, if a stent can be negotiated through the area of injury, in some cases this will promote satisfactory ureteral healing and avoid the need for open surgery.23 When ureteral stent placement is not possible, nephrostomy tube placement is an option.21,24 Nephrostomy tube placement has two potential benefits. First, if the patient is septic or in other ways not ideally suitable for surgical re-exploration, the nephrostomy tube can temporize until the patient’s condition improves to the point where surgery is a more realistic alternative. Second, some cases of ureteral obstruction secondary to suture entrapment have been reported to resolve successfully with nephrostomy tube drainage alone.25 Again, which cases can be adequately managed with nephrostomy tube drainage can best be judged by the individual surgeon. 1373
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Conservative management of ureteral injuries recognized in the postoperative period can, in some cases, be successful. Ku et al. reported successful management in 11 of 17 patients treated with nephrostomy tube, stent, or both, following ureteral injury. However, the management of such cases must be individualized.26 If conservative measures are unsuccessful, and surgical re-exploration is required, the options available are identical to those mentioned previously for the management of injuries recognized intraoperatively.
Postoperative management
5. Gross M, Peng B, Waterhouse K. Use of the mobilized bladder to replace the pelvic ureter. J Urol 1969;101:40. 6. Zinman LM, Libertino JA, Ruth RA. Management of operative ureteral injury. Urology 1978;12:290–303. 7. Ehrlich RM, Melman A, Skinner DG. The use of vesicopsoas hitch in urologic surgery. J Urol 1978;119:322–5. 8. Matthews R, Marshall FF. Versatility of the adult psoas hitch ureteral reimplantation. J Urol 1997;158:2078–82. 9. Hodges CV, Moore RJ, Lehman TH, Benham AM. Clinical experiences with transuretero-ureterostomy. J Urol 1963;90:552–62. 10. Smith IB, Smith JC. Transuretero-ureterostomy: British experience. Br J Urol 1975;47:519–23.
The urologic consultant should always dictate a separate operative note. Following the operation, the urologist should meet the family members and explain the urologic part of the surgery. The urologist should also make postoperative visits to the patient and be the only physician to order urologic radiographic studies or the removal of tubes. In general, suprapubic tubes are removed on postoperative day 2 or 3, or when the urine is clear. Urethral catheters are removed after a cystogram shows no leak – this is usually on about postoperative day 7. Internal stents and nephrostomy tubes are ordinarily removed later, about 2–3 weeks postoperatively, and after either an IVP or a nephrostogram has confirmed good healing of the surgical repair.
11. Ehrlich RM, Skinner DG. Complications of transureteroureterostomy. J Urol 1975;113:467–73.
conclusIons
17. Bright TC III, Peters PC. Ureteral injuries secondary to operative procedures. Urology 1977;9:22–6.
Bladder and ureteral injuries during gynecologic surgery present a difficult challenge to both the gynecologist and urologist. If the guidelines reviewed above – together with good judgment and good technique – are employed, most of these injuries can be resolved successfully.
reFerences 1. Tarkington MA, Detjer SW, Bresette JF. Early surgical management of extensive gynecologic ureteral injuries. Surg Gynecol Obstet 1991;173:17–21. 2. Gangi MP, Agee RE, Spence CR. Surgical injury to ureter. Urology 1976;8:22–7. 3. Neuman M, Eidelman A, Langer R et al. Iatrogenic injuries to the ureter during gynecologic and obstetric operations. Surg Gynecol Obstet 1991;173:268–72. 4. Turner-Warwick R, Worth PHL. The psoas bladder hitch procedure for the replacement of the lower third of the ureter. Br J Urol 1969;41:701–9.
12. Sandoz IL, Paull DP, MacFarlane CA. Complications with transuretero-ureterostomy. J Urol 1977;117:39–42. 13. Boari A. Chirurgia dell uretere, con pretazience de Dott: I. Albarran, 1,900 contribute sperementale alla plastica delle uretere. Atti Accad Med Ferrara 1894;14:444. 14. Konigsberg H, Blunt KJ, Muecke EC. Use of Boari flap in lower ureteral injuries. Urology 1975;5:751–5. 15. Colimbu M, Block N, Morales P. Ureterovesical flap operation for middle and upper ureteral repair. Invest Urol 1973;10:313–7. 16. Benson MC, Ring KS, Olsson CA. Ureteral reconstruction and bypass: experience with ileal interposition, the Boari flap–psoas hitch and renal autotransplantation. J Urol 1990;143:20–3.
18. Hardy JD. High ureteral injuries: management by autotransplantation of the kidney. J Am Med Assoc 1963;184:97–101. 19. Novick AC, Stewart BH. Experience with extracorporeal renal operations and autotransplantation in the management of complicated urologic disorders. Surg Gynecol Obstet 1981;153:10–8. 20. McCullough DL, McLaughlin AP, Gittes RF, Kerr WS. Replacement of the damaged or neoplastic ureter by ileum. J Urol 1977;118:375–8. 21. Dowling RA, Corriere JN, Sandler CM. Iatrogenic ureteral injury. J Urol 1986;135:912–15. 22. Mann WJ. Intentional and unintentional ureteral surgical treatment in gynecologic procedures. Surg Gynecol Obstet 1991;172:453–6. 23. Mitty HA, Train JS, Dan SJ. Antegrade ureteral stenting in the management of fistulas, strictures and calculi. Radiology 1983;149:433–8. 24. Persky L, Hampel N, Kedia K. Percutaneous nephrostomy and ureteral injury. J Urol 1981;125:298–300.
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25. Harshman MW, Pollack HM, Banner MP, Wein AJ. Conservative management of ureteral obstruction secondary to suture entrapment. J Urol 1982;127:121–3.
26. Ku JH, Kim ME, Jeon YS, Lee NK, Park YH. Minimally invasive management of ureteral injuries recognized late after obstetric and gynecologic surgery. Injury 2003;34(7):480–3.
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98 Cosmetic vaginal surgery James Balmforth, Linda Cardozo
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IntroductIon In recent years there has been growing interest in the subject of cosmetic vaginal surgery, which parallels the ever-increasing public awareness of cosmetic surgery generally. Despite the large number of articles in the popular press on the subject of ‘designer vaginas’, there is very little evidence in the peer-reviewed medical literature to guide clinicians on possible surgical procedures and their indications, risks, and benefits. Reconstructive pelvic surgery for congenital developmental abnormalities of the female genital tract such as the Mayer–Rokitansky–Kuster–Hauser syndrome (congenital absence of the vagina)1–4 or ambiguous genitalia in childhood5 is a well-established area of adolescent gynecology. However, the largely patient-driven demand for purely esthetic vaginal surgery in adulthood is a more recent phenomenon. The principal driving forces behind the rise in the number of requests for such procedures are the increasing consumerism of medical practice, greater willingness to undergo esthetic surgery generally and more widespread discussion of this subject in the popular media (Table 98.1). The last 3 years have seen articles published on cosmetic vaginal surgery in over 75 different women’s magazine titles in Europe and North America as the number of women undergoing all forms of cosmetic surgery increases year on year. The gulf between reporting in the lay and professional literature is starkly made by the contrasting results of electronically searching for evidence on cosmetic gynecologic surgery. An internet search using the Google search engine yields several thousand matches for enquiries on topics such as ‘cosmetic vaginal surgery’, ‘designer vagina’, ‘esthetic vaginal surgery’ or ‘laser labiaplasty’, whereas Pub-med and Medline yield fewer than 50 relevant papers. There table 98.1.
Reasons behind the rise of consumer demand in gynecologic practice
1. Increased access to information • Popular media • Internet 2. Society becoming more egalitarian 3. Delivery of healthcare becoming a partnership between the patient–consumer’s ‘wishes’ and the doctor’s ‘professional opinion’ 4. Most gynecologic disorders are not lethal and therefore qualitative outcome is increasingly important 5. Emergence of ‘quality of life’ as an important treatment outcome 6. ‘Bothersomeness’ of a condition is perceived by the patient within their own psychosocial context. This may be different from the ‘doctor-centered’ view of the condition
is therefore very scant medical evidence to guide the clinician confronted by a women seeking cosmetic vaginal surgery. Even the evidence that exists is mostly derived from the more ‘mainstream’ management of vaginal laxity and pelvic organ prolapse. This is mostly observational, non-randomized and employs ‘doctor-orientated’ outcome measures rather than ‘patient-centred’ quality of life measures. However, as public interest in this type of gynecologic surgery is increasing it is important that doctors keep abreast of current trends and developments. A wide variety of surgical procedures can be included under the term ‘cosmetic vaginal surgery’ ranging from purely esthetic operations like labiaplasty, hymenoplasty and ‘vaginal rejuvenation’ to the more conventional gynecologic reconstructive procedures like vaginal pelvic floor repair, which aim to restore function as well as enhance appearance (Table 98.2). The labia minora of the vulva are two cutaneous– mucosal refolds located between the labia majora, the internal aspect of which is separated by the interlabial cleft. Relatively enlarged labia minora may be attributable to several factors. They are most commonly congenital but may also rarely be due to chronic irritation, exogenous androgenic hormones, or stretching with weights. Although some women require surgical reduction for functional reasons, most seek reduction of their labia minora because of psychological concerns relating to body image. Reduction labiaplasty is the most commonly performed esthetic surgical procedure and is usually undertaken on a day case basis. This is frequently suggested for so-called ‘hypertrophic’ labia minora. In fact, as any practicing gynecologist knows, there is a wide range of naturally occurring sizes and shapes of perfectly normal labia minora. The effect of body image on psychological well-being and sexual behavior is comprehensively described in the literature. Ackard et al.6 reported on the relationship between body image, self-worth, and sexual behaviors in 3627 women. They found that women who were more ‘satisfied’ with their body image reported more sexual activity, orgasms, and initiating sex, together with greater comfort undressing in front of their partner, having sex with the lights on or trying new sexual behaviors, than those who were ‘dissatisfied’. Positive body image was inversely related to self-consciousness and importance of physical attractiveness, and positively related to relationships with others and overall satisfaction. As we move further towards a ‘culture of physical perfection’, many social commentators have suggested that increased dissatisfaction with physical aspects of our appearance is likely to lead to increased demand for esthetic surgery.
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table 98.2.
Range of cosmetic vaginal procedures
Procedure
Description
Reduction labiaplasty
There is a wide variety of different techniques to alter the size and contour of external female genitalia7–9
Augmentation labiaplasty
Esthetically enhances labia majora to give a supposedly ‘more youthful’ appearance
Vulvar lipoplasty
Removal of unwanted fat from mons pubis and labia to alter cosmetic appearance
Reversal of female genital mutilation (FGM)
Exact technique is dependent upon the original extent of the FGM
Hymenoplasty
Partial or complete reconstruction of the hymen
G-spot amplification
Injectable bulking agent into Grafenberg spot on anterior vaginal wall
Perineal reconstruction
To restore perineal length following childbirth trauma or previous surgery
Pelvic floor repair
To restore normal vaginal contour and repair prolapse
Z-plasty or incision of constriction ring10 11
Use of myocutaneous flaps
To resolve iatrogenic narrowing of vagina In cases where more extensive reconstruction needs to be undertaken in order to restore function
Esthetically, asymmetric or enlarged labia minora cause self-consciousness sexually and when wearing tight underwear or clothing. They can also occasionally interfere with micturition, leading to voiding difficulties, ‘anatomic entrapment’ of urine, and poor hygiene. Most commonly, reduction labiaplasty is performed either by amputation of the protuberant segment and oversewing the edge or by a wedge excision and reapproximation of labial tissue. Choi and Kim7 suggest that these techniques remove the natural contour and color of the edge of the labia, and offer an alternative method to preserve the contour and anatomy of the labia minora by simply reducing its central width through bilateral de-epithelialization and reapproximation of the central portion with preservation of the neurovascular supply to the edge. In the largest reported series of reduction labiaplasty operations reported, 163 women who underwent surgical reduction of the labia minora were followed up over a 9-year period to determine whether they were satisfied with the procedure.9 The women’s age ranged from 12 to 67 years (median = 26 years) and the principal motives for requesting surgery were esthetic concerns (87%), discomfort in clothing (64%), discomfort with exercise (26%), and entry dyspareunia (43%). No significant surgery-related complications were reported. Anatomic results were satisfactory from the doctor’s perspective in 93% of cases. Eighty-nine percent of the women found the results of surgery to be satisfactory from an esthetic standpoint and 93% were happy with the functional outcome; 4% of women said they would not undergo the same procedure again. An exciting new technology that was originally developed for use in correcting major congenital vaginal anomalies and cloacal malformations that require
extensive surgical reconstruction is in vivo tissue engineering of vaginal epithelial and smooth muscle cells.12 In time, as these tissue engineering techniques become more widespread, they are likely to be used in the field of cosmetic surgery. Vaginal epithelial and smooth muscle cells can be grown, expanded in culture, and characterized immunocytochemically before being seeded on polymer scaffolds to form vascularized vaginal tissue that has phenotypic and functional properties similar to those of normal vaginal tissues. The contractile properties of the tissue-engineered vagina constructs respond to electrical field stimulation in a similar way to normal, host vaginal tissue. This technology is being actively pursued to achieve the engineering of large sheets of immunologically comparable vaginal tissue in vivo for use in clinical applications.
can Surgery Improve Female Sexual FunctIon? As well as purporting to restore normal anatomic relationships following the effects of childbirth and aging, some surgeons offer the promise of enhanced sexual gratification as a result of these procedures. Many of the claims made in the advertising literature of clinics that offer this type of surgery are unsubstantiated by clinical trial evidence, or indeed anything other than client testimonials. There is currently no objective evidence to support the idea that esthetic genital surgery leads to subjective or objective improvement in sexual function (Table 98.3). Indeed, most of the published literature on reconstructive pelvic surgery suggests that repeated vaginal surgery risks causing scarring, loss of sensation, and 1379
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table 98.3.
Claims made for cosmetic vaginal surgery
Claim
Evidence
Enhanced esthetic appearance
Possibly
Increased sexual gratification
No evidence to support this
decreased sexual function.13,14 If sexual dysfunction is the primary reason for seeking surgical intervention, then it is often more appropriate to consider other avenues of treatment first, including psychosexual counseling and pelvic floor muscle training. In 1966, Masters and Johnson15 described four classic phases in female sexual response: excitement, plateau, orgasm, and resolution. More recent theories stress the role of psychological components such as ‘desire’, together with physical sexual stimulus, leading to arousal, and modified by situational variables. Most studies looking at vaginal surgery and sexual function report a deterioration of frequency and increased discomfort associated with reconstructive vaginal surgery. This is particularly so for trials reporting the use of prosthetic mesh to augment intrinsically weak tissues. Milani et al.16 reported a fall in sexual activity of 12% and an increase in dyspareunia of 63% in women undergoing anterior or posterior vaginal prolapse repair with Prolene mesh augmentation, despite an impressive ‘anatomic’ success rate of 94%. This and other similar studies involving the use of prosthetic materials underline the difference between functionally and anatomically successful surgical reconstruction. ‘Traditional’ levator plication posterior vaginal repairs are also associated with very high rates of sexual dysfunction. A retrospective review13 of 231 women undergoing posterior repair found an increase in sexual dysfunction (18–27%), increased constipation (22–33%), and increased fecal incontinence (4–11%) despite a good rate of anatomic defect correction. Helstrom and Nilsson17 studied the effect of vaginal surgery for urinary incontinence and prolapse on sexual function and quality of life. In a questionnaire study of 118 women they found that sexual function deteriorated postoperatively and the mean frequency of sexual intercourse was reduced. Although pelvic floor disorders are known to impair sexual function, there was no improvement in sexuality after surgery to correct them. On the contrary, sexual function deteriorated and dyspareunia worsened after vaginal surgery. The explanation offered for this was vulnerability to disturbance of the nerve and blood supply of the vaginal wall resulting in impaired sexual arousal and lubrication. Tunuguntla and Gousse18 recently reviewed the mechanisms by which vaginal surgery affects female
sexual function and related pathophysiology to potential causes. Altered anatomy, neurovascular supply of the clitoris and introitus, and pelvic innervation are all important factors. The vast majority of the literature on this subject supports the idea that, at best, surgery does not always harm sexual function, but rarely improves it.
ethIcal conSIderatIonS Female genital mutilation affects over 130 million women worldwide, mostly from just 28 African countries. However, it is increasingly encountered by healthcare workers in the developed world because of the influx of political and economic refugees. Female genital mutilation is mostly performed on young girls and the World Health Organization estimates that 2 million girls are at risk each year. As consent is usually not given, it constitutes assault. Therefore, in the UK and in most of the developed world, female genital mutilation is unlawful – not only when performed on minors, but also when performed on adult women. It is interesting to contrast the banning of female genital mutilation – even for competent, consenting women – with cosmetic surgery, towards which the law takes a very permissive stance. There are those that argue that this legal dichotomy is ethically unsustainable:19 that either the ban on female genital mutilation or the law’s permissive attitude towards cosmetic surgery is unjustified as no woman could ‘validly’ consent to either practice as they involve the intentional infliction of injury. This argument contends that people in countries where female genital mutilation is practiced resent references to ‘barbaric practices imposed on women by male-dominated primitive societies’, especially when they look at the developed world and see women undergoing their own potentially hazardous ‘feminization rites’ intended to increase sexual desirability. Other authors20 have also juxtaposed the trend in cosmetic vaginal surgery in the West with the implications of the laws governing female genital mutilation, and highlighted the double morality of the situation. It is important to maintain the legal principle of equality before the law with respect to ‘alterations’ of the female genitalia. In essence the argument comes down to the principal of informed consent: that an adult woman can decide to request that a surgical procedure be undertaken, and as long as she can find a doctor who is willing to perform that procedure, then it is legal. If consent is not given, then it constitutes assault. The other area of practice that arouses ethical debate is surgical hymen repair (hymenorrhaphy). This is predominantly requested by women from some African
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and Mediterranean cultures, where the suggestion of premarital sex places women from these cultures at risk of violence or being ostracized. The question then arises as to whether this makes hymenorrhaphy morally more justified than purely cosmetic surgery or whether, by performing such surgery, it is perpetuating a belief system that is degrading to women. In considering how best to restore normal pelvic anatomy and function, it is important to consider all three pelvic organ systems – urinary, genital, and gastrointestinal. Appropriate preoperative assessment of function and the degree to which normal pelvic floor support has been lost is important in planning the most suitable type of surgical procedure. As well as the traditional methods of ‘doctor-centered’ assessment, there is currently an increased awareness of the need to formally evaluate the mental and physical impact of any condition on the patient’s quality of life (QoL). Condition-specific sexual dysfunction QoL questionnaires have been designed and validated for this purpose.21 In order to provide women with realistic expectations, a thorough preoperative discussion about the aims and likely outcomes of any planned surgery is invaluable (Table 98.4). This may sometimes need to include a table 98.4.
Outline of a pragmatic approach to requests for cosmetic vaginal surgery: how should it be managed?
1. Find out what is really troubling the woman 2. Evaluate symptoms from the patient’s perspective • Concerns about esthetic appearance • Functional disorders • Specific postpartum problems – physical and psychological • Symptomatic prolapse 3. Consider other aspects of the woman’s life • Overall quality of life and social function • Hormonal status • Family complete? 4. Consider function of all three pelvic compartments 5. Consider underlying psychosexual problems (female sexual dysfunction) ? ‘hidden agenda’ • Explore body image and sexuality • Expectations of future sexual function 6. Examination with prolapse grading • Quality of tissues/? atrophic 7. Counseling – to include • Discussion about body image and what is ‘normal’ • Reassurance that sexual dysfunction commonly increases with age22 and after childbirth23,24 and may be better treated by more conservative measures initially 8. Initial conservative measures 9. Later surgery if appropriate and after realistic preoperative discussion between doctor and patient about likely outcomes
careful psychological assessment of their motivations in requesting surgery over more conservative treatments. Women should be made aware that while cosmetic vaginal surgery is not specifically directed towards correction of bladder or bowel function, it can adversely affect it. Postoperative urinary retention, voiding difficulties, urinary incontinence and altered sexual sensation are possible sequelae of all vaginal operations. Urinary retention is often a temporary effect of anterior vaginal surgery caused by edema, pain, and mild obstruction. It will generally be alleviated by time, but may need a shortterm indwelling transurethral or suprapubic catheter or clean intermittent bladder drainage. Urinary incontinence can be unmasked when there is occult stress incontinence due to kinking of the urethra with a major anterior vaginal wall prolapse. Objective urodynamic assessment is therefore advisable as an aid to preoperative decision making and counseling in anyone undergoing any significant degree of vaginal reconstruction, as opposed to more local vulval surgery. An additional procedure to rectify occult lower urinary tract symptoms may be offered, or at least the patient be made aware of the possible sequelae.
vagInal laxIty The sensation of vaginal laxity is a commonly reported concern in parous women (Table 98.5)24 and one of the commonest reasons cited by patients requesting cosmetic vaginal surgery. It is more commonly reported in women who have sustained perineal trauma23 as a result of a vaginal delivery, than in those who are delivered by cesarean section or with an intact perineum. It is not uncommon for sexual function to alter after the upheaval of childbirth and caring for an infant. Barrett et al.24 studied 796 women delivered of a live birth in a 6-month period. Sexual problems (e.g. vaginal dryness, painful penetration, pain during sexual intercourse, pain on orgasm, vaginal tightness, vaginal looseness, bleeding/irritation after sex, and loss of sexual desire) increased significantly after the birth. In the first 3 months after delivery 83% of women experienced such problems, declining to table 98.5.
• • • • • •
Common complaints associated with vaginal laxity
Discomfort and symptoms of prolapse Tampons fall out Lack of friction during intercourse Penis falls out during intercourse Vaginal wind25 Bathwater entrapment
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64% at 6 months; 89% had resumed some sexual activity within 6 months of the birth. By 6 months there was no association with type of delivery; only the experience of dyspareunia before pregnancy and current breastfeeding were significant risk factors. Requests for consideration of cosmetic surgery from women who have recently delivered should therefore be treated with particular caution. It commonly takes at least 6 months for the effects of pregnancy-induced progesterone, which relaxes the smooth muscle of the lower genital tract, to resolve. Restoration of normal vaginal health may be delayed further as a result of the hypoestrogenic state caused by breastfeeding. Women are best advised to wait until they have finished breastfeeding and if necessary use topical estrogens before considering any surgical treatment in the postpartum period. Psychological factors are also extremely important to consider in recently delivered women requesting an opinion on possible surgical correction of perceived ‘birth-related’ problems. A questionnaire-based study examining the influence of psychological factors26 (role quality, relationship satisfaction, fatigue, and depression) on women’s sexuality after childbirth found that depression was an important predictor of reduced sexual desire and sexual satisfaction during pregnancy, and of reduced frequency of intercourse at 12 weeks postpartum. At 6 months postpartum, the quality of the ‘mother role’ strongly related to measures of sexuality. Throughout the perinatal period, fatigue impacted strongly on measures of sexuality. Initial conservative measures for the treatment of vaginal laxity include referral to a specialist physiotherapist for a course of pelvic floor muscle training (PFMT), the use of vaginal cones, correction of any urogenital atrophy present, and lifestyle advice to bring about a reduction in straining and high-impact exertion. Women should be advised that although moderate cardiovascular exercise promotes general health and weight loss, not all exercise is beneficial for improving pelvic floor function.
concluSIonS All doctors, from whichever specialty, working in the field of reconstructive pelvic surgery should be aware of the likely increase in the numbers of women requesting cosmetic vaginal surgery. Although this reflects a wider public demand for cosmetic surgery generally, there are issues relating to sexual function that are of particular relevance to surgeons operating on the genital tract. It may be necessary to disabuse potential patients of some of the wilder and unsubstantiated claims made for this
type of surgery in order that they have realistic and informed expectations. It is vital to take a thorough history on anyone requesting such surgery and to explore in some depth the underlying desire for cosmetic vaginal surgery and what the patient hopes to achieve as a result of the operation. The request may be quite reasonable, but often it is worth trying conservative measures first. It is also important to pick up any underlying sexual problems, as surgery may only make these worse. A multicompartment approach to investigating and treating pelvic floor disorders should always be encouraged. The almost total lack of good quality evidence in the medical literature on this subject makes advising women accurately on the possible risks and benefits more difficult. Despite these problems, the demand for this type of gynecologic surgery is likely to increase as medicine in the developed world becomes ever more consumerdriven. More research is therefore needed into all aspects of pelvic reconstructive surgery and its association with sexual function.
reFerenceS 1. McIndoe AH. Discussion on treatment of congenital absence of the vagina. Proc R Soc Med 1959;52:952–7. 2. Cali RW, Pratt JH. Congenital absence of the vagina. Long-term results of vaginal reconstruction in 175 cases. Am J Obstet Gynecol 1968;100:752–63. 3. Ashworth MF, Morton KE, Dewhurst J et al. Vaginoplasty using amnion. Obstet Gynecol 1986;67:443–6. 4. Williams AE. Uterovaginal agenesis. Ann R Coll Surg Engl 1976;58:266–72. 5. Creighton SM, Minto CL, Steele SJ. Objective cosmetic and anatomical outcomes at adolescence of feminising surgery for ambiguous genitalia done in childhood. Lancet 2001;358:124–5. 6. Ackard DM, Kearney-Cooke A, Peterson CB. Effect of body image and self-image on women’s sexual behaviors. Int J Eat Disord 2000;28(4):422–9. 7. Choi HY, Kim KT. A new method for aesthetic reduction of labia minora (the de-epithelialized reduction of labioplasty). Plast Reconstr Surg 2000;105(1):419–22. 8. Giraldo F, Gonzalez C, de Haro F. Central wedge nymphectomy with a 90-degree Z-plasty for aesthetic reduction of the labia minora. Plast Reconstr Surg 2004;113(6):1820–5. 9. Rouzier R, Louis-Sylvestre C, Paniel BJ, Haddad B. Hypertrophy of labia minora: experience with 163 reductions. Am J Obstet Gynecol 2000;182:35–40. 10. Vassallo BJ, Karram MM. Management of iatrogenic vaginal constriction. Obstet Gynecol 2003;102(3):512–20. 11. Cordeiro PG, Pusic AL, Disa JJ. A classification system and
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reconstructive algorithm for acquired vaginal defects. Plast Reconstr Surg 2002;110(4):1058–65. 12. De Filippo RE, Yoo JJ, Atala A. Engineering of vaginal tissue in vivo. Tissue Eng 2003;9(2):301–6. 13. Kahn MA, Stanton SL. Posterior colporrhaphy: its effects on bowel and sexual function. BJOG 1997;104(1):82–6. 14. Weber AM, Walters MD, Piedmonte MR. Sexual function and vaginal anatomy in women before and after surgery for pelvic organ prolapse and urinary incontinence. Am J Obstet Gynecol 2000;182(6):1610–15. 15. Masters WH, Johnson VE Human Sexual Response. Boston: Little, Brown, 1966. 16. Milani R, Salvatore S, Soligo M, Pifarotti P, Meschia M, Cortese M. Functional and anatomical outcome of anterior and posterior vaginal prolapse repair with prolene mesh. BJOG 2005;112(1):107–11. 17. Helstrom L, Nilsson B. Impact of vaginal surgery on sexuality and quality of life in women with urinary incontinence or genital descensus. Acta Obstet Gynecol Scand 2005;84(1):79–84. 18. Tunuguntla HS, Gousse AE. Female sexual dysfunction following vaginal surgery: myth or reality? Curr Urol Rep 2004;5(5):403–11. 19. Sheldon S, Wilkinson S. Female genital mutilation and cosmetic surgery: regulating non-therapeutic body modification. Bioethics 1998;12(4):263–85.
20. Essen B, Johnsdotter S. Female genital mutilation in the West: traditional circumcision versus genital cosmetic surgery. Acta Obstet Gynecol Scand 2004;83(7):611–13. 21. Rogers RG, Kammerer-Doak D, Villarreal A, Coates K, Qualls C. A new instrument to measure sexual function in women with urinary incontinence or pelvic organ prolapse. Am J Obstet Gynecol 2001;184(4):552–8. 22. Hisasue S, Kumamoto Y, Sato Y et al. Prevalence of female sexual dysfunction symptoms and its relationship to quality of life: a Japanese female cohort study. Urology 2005;65(1):143–8. 23. Signorello LB, Harlow BL, Chekos AK, Repke JT. Postpartum sexual functioning and its relationship to perineal trauma: a retrospective cohort study of primiparous women. Am J Obstet Gynecol 2001;184(5):881–8. 24. Barrett G, Pendry E, Peacock J, Victor C, Thakar R, Manyonda I. Women’s sexual health after childbirth. BJOG 2000;107(2):186–95. 25. Krissi H, Medina C, Stanton SL. Vaginal wind – a new pelvic symptom. Int Urogynecol J Pelvic Floor Dysfunct 2003;14(6):399–402. 26. DeJudicibus MA, McCabe MP. Psychological factors and the sexuality of pregnant and postpartum women. J Sex Res 2002;39(2):94–103.
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Index Page numbers in italics indicate figures or tables. abdominal examination 750 abdominal (or Valsalva) leak point pressure (VLPP) 259 definition 754–5, 766 measurement 267–8 as outcome measure 455 pad tests and 208 stress urinary incontinence 306–7, 308, 309, 310 urethral pressure profile and 268 videourodynamics 305 abdominal pressure (pabd) ambulatory urodynamics 317 definition 752, 763 flow rates and 152 leak point 267, 268 measurement 229, 792, 793 quality control 227, 227 rectal contractions and 232–3, 233 urethral continence mechanism 125, 125 videourodynamics 303, 305 abdominal straining see straining abdominal surgery previous 192 suprapubic catheterization after 546 abdominal trauma, ureteric injuries 1291 abdominal wall anterior see anterior abdominal wall muscles 1154, 1155 abdominoperineal resection 575–6 ACET trial 500–1 acetylcholine 151, 158, 159 -like drugs 488–9 Acinetobacter 619 acontractile detrusor 756, 767 see also detrusor areflexia; detrusor underactivity; underactive bladder acquired immune deficiency syndrome (AIDS) 574 activities ambulatory urodynamics 316, 319 fitness see sports/fitness activities measures of overactive bladder impact 439 see also physical activity acupuncture 420 Ad-afferent fibers 147 bladder sensation 148, 159 loss of sensation via 149 micturition reflex 160 pharmacological targeting 165–6 urine storage reflexes 159 adenocarcinoma, urethral diverticulum 1253 adenosine triphosphate see ATP adenoviruses 619, 620 adherence, bacterial 617 adhesions conscious pain mapping 1175 fistula risk and 1224, 1226 laparoscopic treatment (adhesiolysis) 1173–5 laparoscopy safety and 1212 pelvic pain 1166–7, 1173–4 adolescents 46 adrenal hyperplasia, congenital 1324, 1324, 1340, 1341 adrenergic receptors 146, 163–4
advanced practice nurses (APNs) 92, 93–4, 94 education/training 93–4, 95 adverse drug reactions (ADRs) 440–3 objective tests 440–3, 441 spontaneous vs elicited reports 440–1, 441 aerobics, high impact 658, 659 afferent neurons see sensory neurons age frequency and 187, 188, 201, 202 nocturia and 187–8, 188 overactive bladder and 59, 61 pelvic organ prolapse and 1004 quality of life impairment and 66 urinary incontinence and 395–6, 698, 698, 699 Asia 54, 55, 57 Australia 42, 43 Europe 32, 32, 33, 35 United States 14, 14 urinary tract infection risk and 617–18 uroflowmetry and 218 voiding parameters and 201, 201, 202 volume voided and 201, 202 Agency for Health Care Policy and Research (AHCPR) (US) 95, 96 aging effects on continence mechanism 699–700 see also elderly AIDS 574 aids and appliances 555, 555–8 alarms, enuresis 558, 558 albuterol (salbutamol) 488 alcohol consumption 192, 410 Aldridge procedure 7, 836, 882 alfuzosin 488, 493 allantois 129, 129 Allen–Masters syndrome 1168 allergic vulvovaginitis 649, 651 allograft sling materials 846, 847–53, 885, 914 complications 850–1, 852 results 850, 851, 888 a-adrenergic agonists 515–17 a-adrenergic antagonists 488 a1-specific 493 facilitating bladder contractility 490 voiding difficulty 491–3, 589 a-adrenergic receptors (a-ARs) 144, 162, 163–4 distribution 146, 491 initiation of normal voiding 151 subtype distribution 163–4 Altemeier procedure (perineal rectosigmoidectomy) 732, 1140, 1141, 1143 ambulatory urodynamics 260, 314–24 analysis 317–18 asymptomatic volunteers 320 clinical report 318 definition 316, 751, 763 diary 318, 319, 319 equipment 314, 314–16, 315 ICS standardarization 316–20, 787–8 indications 316, 320–2 methodology 316–17
patient instructions 317, 318 patient preparation 318 pressure–flow studies 322 procedure 318–20 systems available 322, 322–3, 323 terminology 316 variables recorded 320 amenorrhea hypothalamic 659 obstetric fistula 1243 American College of Obstetricians and Gynecologists, chronic pelvic pain definition 606 American Urological Association (AUA) stress incontinence outcomes assessment 450, 804, 810, 811–20 symptom score 437 amitriptyline, painful bladder syndrome 599–600 amoxicillin 622, 623, 624 anal canal childbirth-related nerve damage 687 somatosensory evoked potentials 293–4 anal endosonography see endoanal ultrasonography anal incontinence see fecal incontinence anal neosphincters 717–18, 1127–9 anal plugs 715–16 anal reflex, neurophysiologic conduction studies 294–5 anal sphincter anatomy 1100–1, 1101 electromyography 279–81, 1125 concentric needle 283 single fiber 283, 283–4 neurophysiologic conduction studies 291, 292, 292, 294–5 obstetric injury see obstetric anal sphincter injury pregnancy-related changes 686 replacement procedures 717–18, 1127–9 surgical repair 716–17, 1125–6 factors predicting outcome 716 failure 716 primary, obstetric injury 1113–18 results 717, 1125–6, 1126 techniques 716, 1125, 1126 ultrasonography 714, 715 see also external anal sphincter; internal anal sphincter anal triangle 1100–1 anatomy 116–26 functional terms 119 laparoscopic 1154–64 lower urinary tract 116, 116–19 MRI 340–2, 341, 342, 343 pelvic floor 119–22, 120 underlying urinary continence 123–5 androgen insensitivity syndrome 1324, 1340–1 androgens receptors 697, 700 sexual differentiation 129–30 anemia, preoperative correction 828 anesthesia complications, laparoscopic surgery 1218
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
I-1
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anesthesia – continued midurethral slings 892 preoperative assessment 829 SPARC sling 926 tension-free vaginal tape 918–19 anismus 1138 electromyography 280 obstructed defecation 724–5, 726 rectocele and 1037, 1039 ankylosing spondylitis 573 anococcygeal ligament 1162 anococcygeal nerves 1163 anorectal malformation 1325 anorectal manometry constipation 727–8 fecal incontinence 714, 714, 1122 rectal prolapse 1138 rectocele 1041 anterior abdominal wall 1154, 1155 laparoscopic vaginal suspension 1207 trocar placement sites 1213 vasculature 1213, 1214–15 anterior colporrhaphy 1013–16 AUA outcomes assessment 811–12, 813, 814, 818 complications 1020 history 7 operative technique 1013–16, 1014, 1015 prevention of failure 401 prosthetic augmentation 1014–15, 1015, 1016, 1019 results 1019 sacrospinous vault suspension with 1058 vs colpourethropexy 871 anterior sacral root stimulation, muscleevoked potentials 291–2, 292 anterior urethrovesical angle 331, 334 anterior vaginal wall cyst 1255, 1256 making/recording measurements 775, 775–6 masses, differential diagnosis 1255, 1256 measurement points 773, 774 anterior vaginal wall prolapse (cystocele) 1010–21 3D ultrasound 369, 369 after anti-incontinence surgery 1353 leak point pressure testing 271, 271, 274–5 after hysterectomy, prevention 399 anatomy and pathology 121, 1010, 1010–12, 1011 dynamic nature 461 evaluation 1012–13 ICS definition 751 leak point pressures and 305 making/recording measurements 775, 775–6 midline (central) defects 1010, 1010, 1012 paravaginal (lateral) defects see paravaginal defects reduction pressure–flow studies and 237–8, 239 urodynamic testing after 1013 stress incontinence with 1012, 1013 surgical repair 1013–20 abdominal repair 1018 anterior colporrhaphy see anterior colporrhaphy prevention of failure 401 rectal prolapse surgery with 1145 results 1018–20
vaginal paravaginal repair 1016–18, 1017–18 symptoms and signs 1012 terminology 773, 1003, 1010 transverse defects 1010, 1010 ultrasonography 359, 359, 361 uroflowmetry 221 videourodynamics 307, 309 antibiotics bactericidal vs bacteriostatic 622 prophylactic 625 perioperative 831 postcoital 669 urogenital fistulae 1230 resistance patterns 623 sensitivities 623, 624 trichomoniasis 650 urinary tract infections 622, 622–3 children 626 duration of therapy 623 elderly 626 pregnancy 625 anticholinergic drugs 192–3, 497–502 as cause of voiding difficulty 584 neurogenic voiding dysfunction 566–7 urinary retention 589 see also antimuscarinic agents antidepressants 488, 510–12 antidiuretic hormone (ADH) 186 -like agents 488, 520–1 antifungal agents 648, 649 anti-incontinence surgery alternative therapies 826–7 artificial urinary sphincter 962–70 biologic graft materials 846–54 colpourethropexy see colpourethropexy complications 831–3, 1346–62 immediate 1346–9 long-term 1350–6 short-term 1349–50 failed definition 809–10 leak point pressure testing 269–71, 270, 271, 272–5 preoperative risk factors 867, 868 prevention 400–1 tension-free vaginal tape for 920, 920 urethrocystoscopy 378–9 future prospects 9 history 6–8 indications 866 nulliparous women 678 obstruction complicating see under obstruction, bladder outflow outcomes 8–9, 20, 811–20 outcomes assessment 802–23 AUA guidelines 803 future considerations 808–9 ICI recommendations 805–8 questionnaires 803 Urodynamic Society recommendations 803–5 see also stress urinary incontinence (SUI), outcome measures patient selection 826 perioperative care 826–34 postoperative care 831–3 postoperative urodynamics 221, 245–6 preoperative assessment anesthetist 829 investigations 221, 246, 321–2, 828–9 preoperative considerations 826–31
previous artificial urinary sphincter 962 history taking 192 success of subsequent surgery 867, 868 prolapse surgery with see prolapse surgery, incontinence surgery with quality of life impact 1356–7 rates 20 selection of procedure 826, 866–7 sexual function after 667–8, 1353, 1354 sling procedures see sling procedures synthetic graft materials 836, 840–1 ultrasonography after 362, 362–3 voiding difficulty after see under voiding difficulty vs pelvic floor muscle training 413 antimicrobial agents see antibiotics antimuscarinic agents 488, 497–502 efficacy–tolerability ratios 443–4 overactive bladder 635–8, 638 safety 444 side effects 499 tolerability 440–3 see also anticholinergic drugs antiproliferative factor (APF) 594 apomorphine 162 appendicovesicostomy 1342–3, 1343 appliances 555, 555–8 arcus tendineus fasciae pelvis (ATFP) 121, 121, 124, 124 arcus tendineus levator ani (ATLA) 122, 122, 124, 124 Aris™ TOT 948, 949, 951 artificial bowel sphincter (ABS) 717–18, 1127–9, 1129 indications 1129 results 1129, 1130 artificial urinary sphincter (AUS) 962–70 complications 967–8, 969, 1356 device 962, 962 myelodysplasia 266 patient evaluation 962–3 patient selection 963 results 968, 969 transabdominal implantation 966, 966–7, 967 transvaginal implantation 963–6, 964, 965 ASE model, patient education 109, 109 aseptic intermittent catheterization 757 Asia, epidemiology 52–62 athletes, female elite 657, 658–9, 660 see also sports/fitness activities ATP 158, 165, 166 atropine 488, 497–8, 499 resistance 498 attitudes, public (to incontinence) 76–7 changing see continence promotion factors affecting 76, 76 AUA see American Urological Association augmentation cystoplasty fistula repair 1306 irreparable obstetric fistula 1248 overactive bladder 639–40, 1307–8 Australia epidemiology 40–50 National Continence Management Strategy (NCMS) 78–80 nurse continence advisor 93 autoaugmentation, bladder 1308–9 autologous graft materials 846–7, 883–5 periurethral injections 972–3 see also interposition grafts; pubovaginal slings (PVS), autologous
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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autonomic dysreflexia 567, 572 autonomic nervous system lower urinary tract 158, 158–9, 573 neurophysiologic conduction studies 295–6 pelvis and pelvic floor 608, 1163–4 average flow rate see flow rate, average awareness, promoting continence see continence promotion azithromycin 623 back pain 192 baclofen 488 to decrease outlet resistance 494–6 detrusor overactivity 162, 513 intrathecal 495–6 bacteria biofilms, catheter systems 544, 546–7 uropathogenic 616–17, 619 urothelial adherence 617 bacterial vaginosis (BV) 647 diagnosis 646, 646 management 647 bacteriuria 614–15 asymptomatic (ASB) 614, 615, 620 pregnancy 625 significant 614 Baden–Walker system (vaginal profile) 462, 462, 1000, 1000–1 balloon expulsion test, rectal 729 barium enema 714, 726 Barrington, FJF 142 Bartholin’s glands 1100, 1100 pediatric patients 1338 bed protection products 553, 554, 558 bedwetting see nocturnal enuresis behavioral risk factors, urinary tract infections 618 behavioral therapies 468–73 continence nurse specialist 86–7 definition 757 encouraging patient participation 472 future developments 9 lifestyle changes and 471–2 overactive bladder 634–5 physical therapist 107 techniques used 468–71 benign prostatic enlargement 757 benign prostatic hyperplasia (BPH) 493, 757 benign prostatic obstruction 757 benzodiazepines 192, 494 b-adrenergic agonists 488 stress incontinence 517–18 urge incontinence 510 voiding dysfunction 493, 496 b-adrenergic antagonists 517–18 b-adrenergic receptors (b-ARs) 146, 164 distribution 491 type 3 (b3) 159, 164 b-lactamases, extended-spectrum (ESBLs) 623 bethanechol chloride 488–9, 589 pediatric patients 1332 BioArc™ sling system 940, 940–1, 941 BioArc™ TO 948, 949, 951 biofeedback constipation 730–1 definition 757 detrusor overactivity 107 electromyography 85, 104, 481, 482 equipment 104, 480, 481 evidence for effectiveness 412 fecal incontinence 715, 1122
manometry 481 pelvic floor educator 480–1, 481 pelvic floor ultrasound 481 pelvic organ prolapse 421 stress urinary incontinence 85, 104, 469, 479–81 vaginal palpation 480 see also vaginal cones/balls biofilms, catheter systems 544, 546–7 biologic prosthetic materials 846–57 allografts 847–53 autologous 846–7 complications 1354–6, 1355 cystocele repair 1015, 1019 midurethral slings 940, 940–1, 941 rectocele repair 1045–6, 1048, 1048–9 sacral colpopexy 1199 xenografts 853–4 biomechanics, lower urinary tract 236–7 BION® device 1285, 1285 biopsy, bladder see bladder biopsy bipolar electrochemical energy, laparoscopic colposuspension 1181 bladder anatomy 116, 147 augmentation see augmentation cystoplasty autoaugmentation 1308–9 biomechanics 236–7 defense mechanisms 616 distension test, interstitial cystitis 597 diverticula 385 embryological development 130–1, 134 endometriosis 191, 1168 epithelium bacterial adherence 617 defense mechanisms 616 deficiency, interstitial cystitis 594 exstrophy 1333, 1333 foreign bodies 385 hypertonic 150 innervation 158, 158–9 early studies 142, 145 malakoplakia 384 mucosal grafts, fistula repair 1303 muscle see detrusor neuronal changes, interstitial cystitis 595 overdistension injury 586 physiology 142–55 contemporary studies 146–7 early experimental studies 142–5 early urodynamic studies 145–6 structural features relevant to 147 see also micturition, clinical physiology polyps/fronds 383 somatosensory evoked potentials 293–4 squamous metaplasia 383, 384 storage function see storage, urine submucosal hemorrhages (glomerulations) 597 substitution, interstitial cystitis 601 trabeculations, endoscopy 384, 384–5 trigone see trigone bladder biopsy painful bladder syndrome 597–8 recurrent urinary tract infections 621 bladder calculi endoscopy 385, 385 obstetric fistula 1242 bladder cancer see bladder tumors bladder capacity 150 absolute 150 cystometric 18, 754, 765 drugs increasing 513–15
during filling cystometry 233, 754, 765 functional 150, 750 maximum anesthetic 754, 765 maximum cystometric (MCC) 239, 754, 765 pregnancy 683 voiding diary assessment 199 bladder compliance 149–50 calculation 753–4, 764 filling cystometry 230–1, 305, 753–4, 764 leak point pressures and 268, 271, 275, 305–6 low ambulatory urodynamics 320, 321 pathogenesis 147, 150 bladder cycle 142, 147–52 ambulatory urodynamics and 318 I (diastole; filling phase) 148–50 II (systole; emptying phase) 150–2 bladder diary see voiding diary bladder emptying 486 completeness 152 drugs facilitating 193, 488–97 impaired, urethral pressure measurements 260 incomplete, feeling of 190–1, 748 nervous control 160 physiology 150–2 see also voiding bladder erosion artificial urinary sphincter 968 midurethral slings 897–8 synthetic grafts 1356 transobturator tape 958 bladder expression 757 bladder filling 486 ambulatory urodynamics 318 artificial 751 cystometry 226, 230–1 first sensation 432, 752, 763 medium, urodynamics 227–8, 238 natural 316, 751 nervous control 159–60 physiology 148–50 rates 228 non-physiologic 752, 763 physiologic 752, 763 videourodynamics 304 see also storage, urine Bladder Health Questionnaire (BHQ) 65–6 bladder hypersensitivity 230 see also bladder sensation, increased bladder injuries anti-incontinence surgery 1347–8, 1348 colpourethropexy 871–2, 872 cystocele repair 1020 intraoperative recognition/repair 1369 laparoscopic surgery 1187, 1217 midurethral slings 895 postoperative recognition/management 1373 sacrospinous vault fixation 1060 tension-free vaginal tape 921, 921 transobturator midurethral slings 949–51 bladder leak point pressure see detrusor leak point pressure bladder neck 116, 119 childbirth-related damage 345 descent, pelvic floor ultrasound 357, 358 dysfunction, ureterocele 138, 139 embryological development 131 incision 589 intrinsic sphincter see intrinsic urethral sphincter
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
I-3
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bladder neck – continued mobility 123, 124, 124 perineal ultrasound 357, 357–9 postpartum 686 Q-tip test 194 see also urethral hypermobility; urethral mobility MRI 343–4, 344 open, cystourethrography 334–5 opening, bladder emptying 150–1 position perineal ultrasound 357, 357–9 postpartum changes 686 urethrocystoscopy 379 pseudopolyps 383 reflex responses to stimulation 294 see also urethrovesical junction bladder neck plication anterior colporrhaphy with 1013–14, 1015, 1019 Neugebauer–Le Fort colpocleisis 1082 see also Kelly plication bladder neck slings see pubovaginal slings bladder neck suspension see colpourethropexy bladder outflow obstruction see obstruction, bladder outflow bladder outlet 177 classification of dysfunction 174, 177–80, 178 overactive 178, 179–80 sensory disorders 179, 180 underactive 177–9, 178 see also intrinsic urethral sphincter bladder outlet resistance drugs decreasing 491–7 drugs increasing 515–20 urine flow rate and 219, 786, 789, 791 bladder output relation (BOR) 236 bladder pain 191, 748 altered bladder sensation and 175 during filling cystometry 432, 752, 764 see also painful bladder syndrome bladder perforation after augmentation cystoplasty 1308 after bladder autoaugmentation 1309 see also bladder injuries bladder reflex triggering 757 bladder retraining see bladder training bladder sensation 148–9, 159 absent 432, 747, 752, 764 altered, and pain 175 disorders 148–9, 179, 180 drugs decreasing 165–6, 513–15 filling cystometry 230, 432, 752, 763–4 ICS definitions 432, 747, 752, 761 increased 432, 747, 752, 763–4 ambulatory urodynamics 322 filling cystometry 230 non-specific 432, 747, 752, 764 normal 747, 752, 763 reduced 747, 752, 764 voiding diary assessment 199 bladder spasm 191, 748, 761 bladder suspension defects classification 332 cystourethrography 329–32, 333, 334 bladder training 417, 418–20, 468 continence nurse specialist 86, 86–7 evidence for effectiveness 412, 418–19 factors affecting outcome 419–20 guidelines 468 overactive bladder 634–5
painful bladder syndrome/interstitial cystitis 598 physical therapist 107 prevention of urinary incontinence 397 protocols 418, 420 bladder tumors cystoscopy 379, 386, 386–7, 387 translabial ultrasound 363, 364 bladder ulcers, interstitial cystitis cystoscopic diagnosis 597 treatment 601, 601 bladder volume urine flow rate and 219, 786 see also bladder capacity bladder wall thickness increased see detrusor hypertrophy ultrasound measurement 359–60, 360 bladder washouts, catheterized patients 545, 545 bleeding see hemorrhage/bleeding blood transfusion, after colpourethropexy 871, 872 Boari flap 1294, 1295–6, 1371–2, 1372 body image 1378 body mass index (BMI) anti-incontinence surgery outcome and 867, 868 midurethral slings and 898 reduction see weight loss urinary incontinence and 19, 45, 45, 408, 471 body-worn female continence devices 558 Bolam principle 829 bone anchors 936–8 historical perspective 936 osteomyelitis complicating 938, 1349 transvaginal slings 936–8 complications 938 operative technique 936–7, 937 results 937–8 vaginal wall slings 939 bone morphogenetic protein type 4 (BMP4) 129, 133 Bonney, Victor 7 Bonney test 194 borreliosis, Lyme 574 bothersomeness overactive bladder 60, 437–8 quality of life assessment and 66–7 symptoms in nulliparous women 675 urinary incontinence epidemiologic studies 20, 53, 54 help-seeking and 56, 57 see also quality of life botulinum toxin (BTX) 166, 488 detrusor overactivity 512, 639, 1307 to facilitate bladder emptying 496–7 bovine collagen see collagen, bovine bovine pericardium, slings 854, 888 bowel frequency, normal 722 bowel injuries anti-incontinence surgery 895, 1348, 1348 laparoscopic 1215–17 underwater test 1217 see also rectal injury bowel management 87, 472 bowel preparation 828 laparoscopic surgery 1199, 1217 bowel problems after augmentation cystoplasty 1308 prolapse 780, 1139, 1140 urinary incontinence and 19 bowel retraining 730–1
brain lesions 566, 567–70 brainstem, voiding center 143 brain tumors 567, 569 branching morphogenesis, renal 132, 132 Bristol Female Lower Urinary Tract Symptoms (BFLUTS) 69, 437, 438 broad ligament 1158 Brown–Sequard syndrome 572 Brubaker, Linda 5 bulbocavernosus reflex 193 neurophysiologic conduction studies 293, 294–5 bulbospongiosus muscle 1100, 1100 bumetanide 521 buprenorphine 161 Burch, John 8 Burch colposuspension AUA outcomes assessment 814, 815 enterocele after 875, 1025, 1027 prevention 1029 failed, leak point pressures 273 intraoperative complications 871–2, 872, 1346, 1347 laparoscopic 870, 1180, 1181–4 postoperative complications 872–5, 873, 874 preoperative pressure–flow studies 246 risk factors for failure 867, 868 technique/modifications 868–9 ultrasound findings after 362, 362 urodynamic changes after 871, 872 vs other procedures 895 see also colpourethropexy cadaveric prolapse repair and sling (CAPS) procedure 853, 936 results 938 cadaveric sling materials see allograft sling materials caffeine intake 409, 471, 730 C-afferent fibers 147 pathophysiology of urgency 149 pharmacological targeting 165–6 sensory function 159 vesicospinovesical micturition reflex 160 calcium, intracellular 164 calcium antagonists 164–5, 507–8 calcium channels 163, 164–5 calcium hydroxylapatite, injectable spheres 861–2, 972, 972 Camper’s fascia 1154 Candida, urinary tract infections 619, 619 candidiasis recurrent 648 vulvovaginal 647–8, 648, 649 capsaicin 488, 513–15 mechanism of action 160, 165–6 overactive bladder 638 carbachol 163 carbon-coated zirconium oxide beads (Durasphere™) 860, 861 carbon dioxide, gas cystometry 228 carcinoma in situ, bladder 386, 387 cardiac failure 192 cardinal ligaments 120 Cardozo, Linda 6 care pathways, continence 96 caruncle, urethral 1255, 1256 categorical responses 803 catheterization 542–50 ICS definitions 757 indications 542 indwelling 757, 1309
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
I-4
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intermittent 757 intermittent self- see intermittent self-catheterization nurse’s role 88–9 obstetric fistulae 1244 postoperative 549–50, 588 colpourethropexy 872–3 fistula repair 1236, 1301 hysterectomy 1365 incontinence surgery 832 pubovaginal slings 910–11 sexual health and 546, 668 suprapubic 545, 545–6, 618 urethral see urethral catheterization urinary tract infections 544, 615, 618, 626–7 uroflowmetry and 219 catheters 542–50 drainage bags 546–7, 547, 548 materials 542 suprapubic 545, 545–6 urethral see urethral catheters urodynamic see urodynamic catheters valves 548, 548 cauda equina lesions electromyography 282, 284 sacral reflex responses 295 stimulation, muscle-evoked potentials 291–2, 292 syndrome 573 celiac plexus 607 cell–cell interactions, smooth muscle development 130–1 central motor pathways, neurophysiologic assessment 292–3 central nerve conduction times 292 Centrasorb™ T-Sling system 941 cephalosporins preoperative prophylactic 831 urinary tract infections 622, 624 cerebral cortex, control of micturition 143, 160 cerebral disease 566, 567–70 cerebral palsy 567 cerebral somatosensory evoked potentials (SEPs) 293, 293–4 cerebrovascular accident (CVA) 567, 568 cervical cancer, uroflowmetry 221 cervix congenital absence 1322 development 1318, 1318 cesarean section after anti-incontinence surgery 867 after uterine prolapse repair 1080 bladder injuries 1369 fecal incontinence and 686, 688 pelvic organ prolapse and 1004–5 prevention of perineal trauma 1106 prevention of urinary incontinence/ prolapse 397, 679 urinary incontinence risk and 19, 24–5, 25, 55 CGP55845 162 Chagas disease 724 chair protection products 553, 554 chaperones 476 Chassar Moir fistula repair procedure 1233 childbirth 682–93 3D ultrasound after 367, 367–8 after anti-incontinence surgery 867 artificial urinary sphincter deactivation 963
fecal incontinence related to see fecal incontinence, childbirth-related mechanisms of pelvic floor injury 682–3 MRI-based simulation 349–50, 350 pelvic floor MRI after 344–5 pelvic floor ultrasound after 358, 358 pelvic organ prolapse and 689, 1004–5 perineal trauma see perineal trauma pudendal nerve terminal motor latency after 291 rectocele formation and 1036–7 urethral diverticulum and 1252 urinary incontinence after 684–5 etiologic mechanisms 394, 394, 685–6 prevention 396–8 urodynamic changes before/after 685, 685–6 vaginal laxity after 1381–2 see also pregnancy children see pediatric patients Chlamydia trachomatis 619, 620, 621, 624 chondrocytes, autologous, periurethral injection 972–3 chronic obstructive pulmonary disease (COPD) 1005 chronic pelvic pain 606–12, 1166 after anti-incontinence surgery 1353, 1354 after colpourethropexy 874, 875 causes 1166 clinical implications 610 definitions 606 diagnostic laparoscopy 1166–7 epidemiology 606 laparoscopic treatment 1167–76 neuropathology 609–10 pelvic denervation procedures 1172–3 pharmacologic aspects 610 cimetidine, painful bladder syndrome 600 cisapride 489 clam cystoplasty 1307 clean intermittent catheterization (CIC) 757 myelomeningocele 1334 clean intermittent self-catheterization (CISC) 549, 549–50 catheter types 550 indications 549–50 neurogenic voiding dysfunction 566–7 postoperative voiding dysfunction/ obstruction 832, 986 urinary tract infections 626–7 voiding difficulty/retention 589 clenbuterol 488 detrusor overactivity 164 stress incontinence 517–18 urge incontinence 510 climacteric 696 clinical effectiveness 443–4 clinical nurse specialists 93, 94 Clinical Research Assessment Groups, ICS 741–2 clinical trials outcome measures see outcome measures quality of life assessment 65, 68–9 clitoral nerve stimulation sacral reflex responses 293, 294–5 somatosensory evoked potentials 293, 293 cloaca 128–30 division 128–30, 129 formation 128–9 molecular control of differentiation 129, 130, 130 persistent common 134, 1319, 1325 cloacal exstrophy 1333, 1334
cloacal membrane 128, 128 clonidine 491, 497 closing pressure 755, 767 clothing 556, 556 clotrimazole 648, 649 clue cells 646, 646 co-amoxiclav 622, 624 Coaptite® 862 coccygeal ganglion 1163 coccygeal plexus 1163 cognitive impairment anti-muscarinic agent-induced 440 objective measures 441, 441–2 see also dementia coital incontinence 633, 664–5 history taking 189–90, 664 pathophysiology 665 prevalence 664, 664–5 treatment 667–8 colectomy, with ileorectal anastomosis 731–2 collagen bovine, periurethral injection 861, 972, 972, 1354 deposition in bladder interstitium 147 Novasys micro-remodeling system 977, 978 pelvic floor dysfunction and 10 urinary incontinence and 677, 686 collagen vascular diseases 1005 colonic scintigraphy 727 colonic sphincter-cystoplasty 1310–11 colonic transit time normal 722–3 testing constipation 726–7, 728 rectal prolapse 1139 rectocele 1041 colonoscopy 714, 726 color Doppler ultrasound, pelvic floor 359, 359, 360 colostomy, fecal incontinence 718 colovaginoplasty 1323 colpocleisis, Neugebauer–Le Fort 1082–4, 1083 colporrhaphy see anterior colporrhaphy; posterior colporrhaphy colpourethropexy (CU) (colposuspension) 866–78 complications intraoperative 871–2, 872 postoperative 832, 872–5, 873, 874, 984 history 7–8, 866 indications 866–7 laparoscopic 866, 868, 1180–8 complications 1187, 1217 cost 1188 disadvantages 1188 methods 1180–1, 1181 non-suture methods 1187 operative technique 1181–4, 1182, 1183, 1184 success rates 869–70, 1185, 1185 ultrasound findings after 362 uterosacral plication with 1183, 1184 variations in technique 1183–4 vs open colposuspension 1186, 1186–7 vs tension-free vaginal tape 1188 minimally invasive 866, 868 results 869–70 prevention of failure 399, 868–9 prolapse repair with 1015–16 retropubic AUA outcomes assessment 811–12, 813, 814, 815
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
I-5
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retropubic – continued results 9, 869–71, 870 technique 867–9, 873 see also Burch colposuspension; Marshall–Marchetti–Krantz procedure risk factors for failure 867, 868 sacrocolpopexy with 875–6 transvaginal see needle bladder neck suspension ultrasound findings after 362, 362 urodynamic changes after 245, 871, 872 vs other procedures 870–1, 871 vs tension-free vaginal tape 870, 871, 894–5, 920–1, 921 commodes 557, 557 compartment syndrome, postoperative 1348–9 complementary therapies 420, 422 complex reconstructive surgery 1290–315 compliance, bladder see bladder compliance compliance, patient behavioral therapies 472 physical therapy interventions 415 voiding diary completion 198–9 compound muscle action potential (‘M’ response) 290, 291 compound nerve action potential 290 compressor urethrae 117, 118, 118 computed tomography (CT) central nervous system 336 pelvic organ prolapse 778 upper urinary tract 327 urogenital fistulae 1229 computer software 3DSlicer 348, 350, 351 urodynamic 797 conditions, ICS definition 746, 756–7, 768 congenital adrenal hyperplasia 1324, 1324, 1340, 1341 congenital malformations see developmental abnormalities connective tissues embryological development 130–1 nulliparous women 677 pelvic floor dysfunction and 10, 686 pelvic support function 121, 123 conscious pain mapping 1175–6 consent, informed anti-incontinence surgery 829–30 capacity 829–30 knowledge 830 physiotherapy 476–7 volition 829 conservative treatment fecal incontinence 715–16, 1122 iatrogenic bladder outflow obstruction 986 painful bladder syndrome/interstitial cystitis 598, 599 pelvic organ prolapse 420–2, 422, 1029, 1041 ureteric injuries 1293–4, 1373–4 urinary incontinence 826–7 complementary therapies 420 continence nurse specialist 84, 84–9 lifestyle interventions 408–11 nulliparous women 678 outcomes 407–27 scheduled voiding regimes 417–20 summary of evidence 422 urinary vaginal fistulae 1298
see also devices, incontinence; drug treatment; pessaries; physical therapy consistency, internal 802–3 constipation 722–34 after rectocele repair 1046, 1047, 1047 causes 722 children 1332 clinical examination 726 clinical history 725–6 investigations 726–9, 727 management 87, 410, 472 pathophysiology 723–5 pelvic organ prolapse risk 395, 1005 posthysterectomy 725 postrectopexy 1141, 1142, 1143 rectocele and 1037 Rome II criteria 722 slow-transit (STC) 722, 723–4 diagnosis 725, 726–7 obstructed defecation combination syndrome 724 treatment 729, 730, 731–2 treatment 729–33 urinary incontinence and 45, 192 voiding difficulty/retention 585 continence, urinary see urinary continence continence care pathways 96 Continence Foundation (UK) 78, 555 Continence Foundation of Australia (CFA) 78–80 Continence Guard device 538 continence nurse advisor (CNA) 92–3 continence nurse practitioner (CNP) 92, 93 continence nurse specialist 82–90 assessment role 83, 83, 84 education 94–6, 95 functions 82–3 global perspective 92–4 management role 84–9 USA perspective 92–8 Continence Product Evaluation (CPE) network 550, 552–3, 557–8 continence products 550–8 assessment guidelines 551 information sources 78 see also aids and appliances; pads; pants continence promotion 77–8 International Continence Society 80 national organizations 78–80 recommendations 80 survey of national organizations 77–8, 78 Continence Worldwide 80 contraception, urinary tract infections and 618, 669 contrast media, videourodynamics 304 contrast radiography, pelvic organ prolapse 778, 1028, 1038–9, 1039, 1040 Contrelle Activguard 87, 87 coping strategies, urinary incontinence 20 corticosteroids interstitial cystitis 600 intravesical 600 urinary vaginal fistulae 1298 cosmetic vaginal surgery 1378–81 ethical considerations 1380–1 preoperative approach 1381, 1381 procedures available 1379 reasons for increased demand 1378, 1378 sexual function and 1379–80, 1380 vaginal laxity 1381–2 cost-effectiveness analysis overactive bladder 439 quality of life assessment 65
costs, economic laparoscopic colposuspension 1188 urinary incontinence 20, 35–6, 49, 82 cost–utility analysis overactive bladder 439 quality of life assessment 65 tension-free vaginal tape 922 co-trimoxazole 622 cough chronic 25, 192, 677, 1005 cystometry 227, 227, 231, 232, 233 leak point pressure 259, 268, 455 pressure–flow studies 239, 240 urethral pressure measurements 257–9 cough profile 258 pressure transmission ratio (PTR) 258–9 time separation during 259, 259 urodynamic stress incontinence 231, 232 videourodynamics 304 cough stress test (CST) epidemiologic study 18–19 as outcome measure 455 prolapse surgery 400, 1092, 1093 counseling, preoperative anti-incontinence surgery 827, 867 cosmetic vaginal surgery 1381, 1381 fistula surgery 1230 cranberry juice 622, 669 Crede maneuver 151, 304, 761 Creutzfeldt-Jakob disease (CJD) 847, 850, 885 cromakalim 165, 509 Cronbach’s coefficient alpha 803 cube pessaries 535, 538 cul-de-sac see pouch of Douglas culdoplasty, McCall see McCall culdoplasty cure overactive bladder 430 stress incontinence 450, 451, 809 cyclosporine 600 cystectomy, partial 589 cystic fibrosis 46 cystitis acute (infectious) 614, 619 eosinophilic 384 ‘honeymoon’ 668 interstitial see interstitial cystitis cystitis cystica 384 cystitis glandularis 384 cystocele see anterior vaginal wall prolapse cystodefecoperitoneography (CDP) 463 cystometry 226–34, 237 aims 226 definition 226 equipment 228, 228–9, 229 calibration 226, 794–5 minimum requirements 793–4 filling 226, 230–1 definition 752, 763 ICS good practice guidelines 787–97 ICS-recommended terminology 752–5, 763–6 normal 233 filling medium 227–8, 238 filling rates 228, 752 historical aspects 8 indications 226 measurements 229–30 method 230–1 normal 233 patient position 227, 228 pitfalls 231–3
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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preparation for 226–9 problem solving 795–6 quality control 226–7, 227, 233, 795 retrospective artifact correction 796–7 videourodynamics 305 voiding 226, 231 voiding difficulty/retention 587–8 cystoplasty augmentation see augmentation cystoplasty pediatric patients 1342, 1342–3 sphincter- 1310–11, 1311 stoma- 1310, 1311, 1311 terminology 1310 urinary reservoir reconstructions 1309–11, 1311 cystoproctography, dynamic 1028, 1038–9, 1039, 1040 cystoscopes bridges 380 flexible 381, 381 history 6 rigid 379–80, 380 sheaths 380 vs urethroscopes 380–1 cystoscopy abnormal findings 384–7 diagnostic 382 infection risk 618 normal findings 383, 383 painful bladder syndrome 597 perioperative cystocele repair 1018 midurethral slings 892, 893 pubovaginal slings 882–3, 909 SPARC sling procedure 930 tension-free vaginal tape 919 see also endoscopy, urinary tract cystotomy, inadvertent see bladder injuries cystourethrography 328–36, 330–2 continent vs incontinent elderly women 18 evaluation of bladder support 329–32, 333 limitations of static 8 obstruction 985, 986 open bladder neck/proximal urethra 334–5 residual urine measurement 333 videourodynamics 328, 329, 329 voiding (VCUG) 328, 330, 331, 332 bladder outlet obstruction 241, 242 urethral diverticulum 335, 335–6, 1256–8, 1257, 1258 urethrovaginal fistula 1266 urogenital fistulae 1228–9, 1298, 1298 cystourethroscope, flexible 381, 381 cystourethroscopy see endoscopy, urinary tract dance activities 658 Danish Prostate Symptom Score Schedule (DAN-PSS-1) 437 dantrolene 494, 496 darifenacin 488, 501–2 cognitive effects 442 overactive bladder 636, 638 da Vinci robotic surgical system 1180 DDAVP see desmopressin deep circumflex iliac artery 1213, 1215 deep transverse perineal muscle 1100 deep venous thrombosis (DVT), after colposuspension 873 defecation digital assistance 1037, 1039 disorders, rectocele and 1037–8
obstructed 724–5 diagnosis 725 functional causes 724–5 slow transit constipation combination syndrome 722, 724 structural anorectal disorders 724 treatment 729, 730–1, 732 physiology 722–3, 723 proctography see defecography defecography constipation 728–9, 729 MRI 1040–1, 1139 rectal prolapse 1139 rectocele 1038–9, 1039, 1040 DeLancey hammock theory 125, 125, 881, 946 delivery mode perineal trauma and 1106 urinary incontinence and 19, 24, 25, 54, 55 position 1106 techniques 1106 see also cesarean section; forceps delivery; vaginal delivery; ventouse/vacuum delivery Delorme procedure 732, 1140, 1141 results 1143 surgical technique 1141, 1142 dementia 192, 570 see also cognitive impairment denervation, muscle electromyography 281, 282, 284–5 neurophysiologic conduction studies 291 see also pelvic floor muscles, denervation/ nerve damage Denny-Brown, D 143–4 deodorants 558 dermal allografts, cadaveric pubovaginal slings 851–3, 885 complications 852, 852, 1355 results 851, 852–3 rectocele repair 1044, 1045–6, 1048 dermatitis, urine 1242, 1243 dermis, porcine 853, 854, 885–7 descending perineum syndrome 724, 731 enterocele formation 1026, 1026 rectocele formation 1037 desipramine 511 desmopressin 488, 520–1, 638 desquamative inflammatory vaginitis (DIV) 652 detrusor 116 acontractile 756, 767 mechanical properties 236–7 physiology see bladder, physiology wall thickness see bladder wall thickness detrusor areflexia (DA) 566, 567–8 after hysterectomy 1364 multiple sclerosis 570 spinal cord disease 571, 573–4, 575 see also detrusor underactivity; underactive bladder detrusor contractility assessment 236 drugs decreasing 497–513 drugs facilitating 488–90 impact of obstruction 236–7 postoperative voiding dysfunction and 983 urine flow rate and 218, 786, 790 detrusor contractions
after voiding (after-contraction) 231 bladder emptying 151 involuntary (IVCs) drugs decreasing 497–513 epidemiologic study 18 ICS definition 753, 764 detrusor function/activity asymptomatic volunteers 320 during filling cystometry 230, 753, 764 during voiding 755–6, 767 ICS definitions 305, 432, 753 index 320 normal during filling cystometry 233, 432, 753, 764 during voiding 755–6, 767 reflexes inducing 143 sex hormones and 700–1 spontaneous 142–3, 144, 149 stability 149 structural features relevant to 147 detrusor hyperreflexia see detrusor overactivity (DO), neurogenic detrusor hypertrophy causes 150 ultrasound 360, 360 detrusor inhibition reflex (DIR) 107 detrusor instability (DI) see detrusor overactivity detrusor leak point pressure (DLPP) 266–7 definition 755, 766 myelodysplasia 266–7 urethral pressure profiles and 267 videourodynamics 305–6 detrusor loop 116 detrusor myopathy 585–6 detrusor overactivity (DO) after urethral diverticulectomy 1265, 1265–6 ambulatory urodynamics 321, 322 asymptomatic volunteers 320 clinical presentation 633 conservative treatment 414, 416, 418 continence nurse specialist 84 continence nurse’s role 86 definition 432, 753, 764 de novo, after incontinence surgery see overactive bladder, de novo, after anti-incontinence surgery drug treatment 497–515, 635–8, 638 idiopathic 632, 753, 764 filling cystometry 230, 305 pathophysiology 632–3 incontinence 305, 632, 753, 764 neurogenic (detrusor hyperreflexia) 566– 7, 632, 753, 764 cerebral conditions 567, 568, 569, 570 with detrusor–sphincter dyssynergia 566–7 filling cystometry 230, 305 spinal cord disease 571, 574, 575 surgical treatment 1306–9 with synergistic external sphincteric function 566 see also neurogenic voiding dysfunction nulliparous women 676 pathophysiology 143 phasic 149, 230, 632, 753, 764 physical therapy 101, 107–8, 109 prevention 401 provocative maneuvers 432, 753 quality of life impairment 66 surgery 1306–9
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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detrusor overactivity (DO) – continued terminal 230, 632, 753, 764 urethral relaxation and 259 urgency and 144, 149 urodynamic diagnosis 149, 230, 231, 232, 633, 634 videourodynamics 305 see also overactive bladder detrusor pressure (pdet) ambulatory urodynamics 320 area under the curve (AUCdet) 242–3, 243, 244 definition 752, 763 filling phase 229, 305 isometric (piso) 587 isovolumetric (pdet.iso) 236 leak point see detrusor leak point pressure at maximum flow (pdetQmax) 231 bladder outlet obstruction 241, 241 maximum voiding 233 bladder outlet obstruction 242 normal values 233, 233 urinary flow relations 236–7 voiding phase 231, 306, 306 vs intravesical pressure 303 detrusor–sphincter dyssynergia (DSD) 151, 566–7 definition 756, 768 drug treatment 491, 495, 496–7 electromyography 280, 281 historical aspects 8 multiple sclerosis 570 spinal cord disease 571 videourodynamics 308, 310 detrusor underactivity 756, 767 urodynamic diagnosis 231, 232 see also detrusor areflexia; underactive bladder development, embryological see embryology developmental abnormalities 1318–28 associated with other anomalies/syndromic 1325 causing urinary incontinence 1333, 1333–7 clinical examples 133–9 complex 1322–4 imaging 1318–19, 1319 simple/isolated 1319–22 devices, incontinence 87, 534–40, 537 adverse effects 538–9 body-worn female 558 during exercise 659 effectiveness 537–8 nurse’s role 87 use before surgery 826–7 see also pessaries dextranomer macrospheres (Zuidex™) 862, 973, 973–4 diabetes insipidus 192, 520–1 diabetes mellitus 192 constipation 726 neurogenic voiding dysfunction 567, 576, 585 pelvic organ prolapse 1005 urinary incontinence 19, 25 diabetic cystopathy 576 diagnosis accuracy of clinical 186 future developments 10 historical aspects 8 DIAPPERS mnemonic 395 diary ambulatory urodynamics 318, 319, 319
voiding see voiding diary diazepam 494, 589 dicyclomine 488, 505–6 pediatric patients 1332 dietary management constipation 730 painful bladder syndrome/interstitial cystitis 598, 599 urinary incontinence 409–10 diethylenetriaminepentaacetic acid (DTPA) indium-labeled 727 technetium-labeled 621 diltiazem 507–8 dimercaptosuccinic acid (DMSA) scans 621 dimethyl sulfoxide (DMSO) ethylene vinyl alcohol suspended in (Uryx®) 861, 973, 973 intravesical 512–13, 600 dipstick tests, urinary tract infections 619–20 disability definition 102 incontinence outcome assessment 808, 821 distal urethral electrical conductance test (DUEC) 206, 316, 317 distigmine bromide 589 diuretics 192, 521 Doderlein crossbar colporrhaphy 1083 dopamine 162, 640 dopamine receptors 162 dorsal clitoral nerve stimulation see clitoral nerve stimulation dorsal root ganglia 159 doxazosin 162, 164, 488, 493 doxepin 511 doxycycline 651 drainage bags, catheter 546–7, 547, 548 dribbling postmicturition 191, 217, 748 terminal 217, 748, 761 urethral diverticulum 1253 drug history 192–3, 193 drugs affecting bladder function 635 causing voiding difficulty 584 drug treatment chronic pelvic pain 610 constipation 730, 731 fecal incontinence 715 overactive bladder 497–515, 635–8, 638 monitoring 322 painful bladder syndrome/interstitial cystitis 598–600 pediatric neurovesical dysfunction 1332 stress urinary incontinence 515–20, 977–9, 979 voiding dysfunction 486–532 bladder training with 419 circumventing the problem 520–1 CNS targets 160–2 continence nurse’s role 87 facilitating bladder emptying 193, 488–97 facilitating urine storage 193, 497–520 functional classification 487 ICI assessment 486, 488 nulliparous women 678 peripheral targets 163–6 principles 160–6, 486–8 vs bladder training 419 vs electrical stimulation 414 vs pelvic floor muscle training 412–13 Drutz, Harold 6
dry eyes, antimuscarinic-induced 441, 443 dry mouth, antimuscarinic-induced 636, 637 objective measures 441, 442–3, 443 placebo-controled trials 440 spontaneous vs elicited reports 441, 441 duloxetine 146 fecal incontinence 715 molecular structure 979 prior to surgery 826 stress urinary incontinence 518, 977–9, 979 dura mater, lyophilized, for slings 847, 885 Durasphere™ 860, 861 Durasphere EXP™ 860, 861 Dwyer, Peter 6 dye studies fistula detection 1228, 1243, 1298 ureteric injuries 1292, 1293, 1369 dynamic graciloplasty (DGP) 717, 1127, 1127 indications 1129 results 1127, 1128, 1129 dyschezia see defecation, obstructed dysmenorrhea endometriosis 1171 pelvic denervation procedures 1172, 1172–3 dyspareunia endometriosis 1171 postoperative anti-incontinence surgery 667–8, 1353, 1354 colpourethropexy 874, 875 rectocele repair 1046, 1047, 1048 sacrospinous vault fixation 1060 synthetic meshes 667–8, 841 transvaginal bone-anchor slings 938 vaginal surgery 1380 postpartum 682 urethral diverticulum 1253 dysuria 191, 748, 761 postcoital 668 urethral diverticulum 1253 eating disorders 659 economic burden measures 439, 456 urinary incontinence 20, 35–6, 49, 82 economic evaluations, quality of life assessment 65 ectoderm 128 education 9 continence nurse specialist 94–6, 95 patient see patient education public see continence promotion educational attainment overactive bladder and 59 urinary incontinence and 57 efficacy measures, overactive bladder treatments 431–9 efficacy–tolerability ratios, overactive bladder treatments 443–4 Egypt, ancient 4 Ehlers-Danlos syndrome 1005, 1056 ejaculation, female 665 elderly drug treatment 635 midurethral slings 898 Neugebauer–Le Fort colpocleisis 1082–4 tricyclic antidepressants 511, 512 urinary incontinence outcome assessment 808, 821 pathogenesis 699–700, 700 prevention 395–6
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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urinary tract infections 618, 619, 626, 704, 704 see also postmenopausal women electrical conductance test, urinary loss 206, 316, 317 electrical stimulation (ES) clitoral nerve cerebral somatosensory evoked potentials 293, 293 sacral reflexes 294–5 ICS definition 757 lower urinary tract 1276–87 BION® device 1285, 1285 history 1276 peripheral nerve stimulator 1283, 1283–4 motor cortex 292–3 pelvic floor 478–9, 479 detrusor overactivity 107–8, 108, 109 evidence for effectiveness 412, 413–14, 416–17 stress urinary incontinence 85, 104–5, 105, 479 urge urinary incontinence 479 sacral nerve roots see sacral nerve stimulation urethra, bladder and anal canal 293–4 electrocardiogram (ECG), preoperative 829 electroencephalography (EEG), quantitative 441–2 electromyography (EMG) 278–88 biofeedback 85, 104, 481, 482 concentric needle electrode (CNE) 278, 281 denervation and reinnervation 281, 282, 284–5 diagnostic usefulness 286 genuine stress incontinence 282, 285 motor-evoked potentials 292 normal findings 281–3 primary muscle disease 286 urinary retention/obstructed voiding 285–6 during voiding 239, 240 fecal incontinence 1122, 1125 kinesiologic 278, 279–81 diagnostic usefulness 281 method 279–80 normal and abnormal findings 280, 280–1 motor unit 278, 281–6 rectocele 1041 single fiber (SFEMG) 283–4 diagnostic usefulness 286 electrode 278, 283 genuine stress incontinence 285 method and normal findings 283–4 videourodynamics 306 voiding difficulty/retention 285–6, 588 electronic pelvic floor symptoms assessment questionnaire (e-PAQ) 71 electronic voiding diaries 200, 435 electrosurgical therapy bowel injuries 1216 endometriosis 1168 embryology 128–40, 697 division of cloaca 128–30 early embryogenesis 128, 128 female genital tract 1318, 1318, 1330, 1330, 1331 Müllerian differentiation 130, 131 smooth muscle differentiation 130–1 sphincters 131
trigone and upper urinary tract 131–3 see also developmental abnormalities EMG see electromyography emphysema, subcutaneous 1217–18 emptying see bladder emptying endoanal ultrasonography (EAUS) anal incontinence 714, 715 obstetric anal sphincter injury 398, 687, 687–8, 688 rectal prolapse 1138 endocervical swabs 646 endocrine disorders, urinary retention 585 endoderm 128, 130 endometriomas, ovarian 1170–1, 1171 endometriosis bladder 191, 1168 chronic pelvic pain 1166–7 conscious pain mapping 1175–6 laparoscopic diagnosis 1167, 1167, 1168 laparoscopic treatment 1167–71, 1169, 1170 peritoneal disease 1167–70 rectovaginal septum 1171, 1171 vs painful bladder syndrome 596 endopelvic fascia 120, 120–1, 121 defects, enterocele 1026, 1027, 1027, 1028 endoscopes, flexible 381, 381 endoscopy, urinary tract (urethrocystoscopy) 378–89 bladder abnormalities 384–7 iatrogenic obstruction 985 indications 378–9 instrumentation 379–81 intraoperative midurethral slings 892, 893 pubovaginal slings 882–3, 909 tension-free vaginal tape 919 normal findings 382–3 pelvic organ prolapse 777 techniques 381–2 ureteral anomalies 387–8 ureteric injuries 1293–4 urethral diverticulum diagnosis 378, 384, 384, 1254–5, 1257 urethral diverticulum therapy 1260, 1260 urethral evaluation 383–4, 388 urethrolysis 990 urethrovaginal fistula 1266 urinary incontinence evaluation 378–9 urinary tract infections 621 urogenital fistulae 378, 382, 385, 386, 1229 voiding difficulty/retention 588 see also cystoscopy Endo Stitch, sacrospinous vault suspension 1059 enemas 730, 731 Enhorning theory, stress incontinence 8, 880–1 enteric nervous system (ENS) 723 Enterobacter 619, 619, 624 Enterobacteriaceae 617, 619, 623 enterocele 1024–34 after anti-incontinence surgery 832–3, 1353 after Burch colposuspension 875, 1025, 1027 prevention 1029 after hysterectomy 399, 725, 1056 prevention 399, 1028–9 surgical repair 1057, 1058 anatomy 1024 anterior 1012, 1024, 1028
prevention after hysterectomy 1029 apical 1028 clinical assessment 1028, 1028 congenital 1027 conservative treatment 1029 definition and scope 1024 epidemiology 1027 etiology and pathophysiology 1024–7, 1136–7 iatrogenic 1027 investigations 1028, 1029, 1039, 1040 obstructed defecation 724 perineal ultrasound 361, 362 prevention 1028–9 pulsion 777, 1027 rectal prolapse with 1139, 1146 surgical treatment 1029–31, 1058 laparoscopic 1209 symptoms 1027–8 terminology 773, 774, 1003 traction 777, 1027 enterococci 624 enterovesical fistulae, cystoscopic assessment 385 enuresis definition 747, 761 nocturnal see nocturnal enuresis ephedrine 515 Ephrin B 130 epidemiology Asia 52–62 Australia 40–50 Europe 32–7 South America 24–9 USA 14–22 Epidemiology of Prolapse and Incontinence Questionnaire (EPIQ) 461 epidural anesthesia/analgesia perineal trauma and 1106 stress incontinence risk after 685 voiding difficulty after 584, 684 episiotomy 1101–3 anal sphincter damage and 398, 682, 687, 688–9, 1113 ideal rate 1103 incidence 1102, 1102 indications 1102–3 mediolateral 1101–2 midline 1101, 1102 prevention 1106–7 stress urinary incontinence and 397 structures involved 1101 see also perineal trauma epispadias, female 1335, 1336 erosion artificial urinary sphincter 968, 969 pessaries 536 synthetic meshes see under synthetic meshes Escherichia coli antibiotic resistance 623 antibiotic susceptibilities 624 microbiologic culture 620, 620 urinary tract infections 614, 616, 619, 619 Estring 625, 706 estrogen 518–20 continence mechanism and 700, 701 deficiency female athletes 659 recurrent urinary tract infections and 704, 704 urinary symptoms 696, 697–8 vaginal changes 644, 649–50 see also postmenopausal women
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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estrogen – continued lower urinary tract effects 518, 696–7 receptors 696, 697, 700 replacement therapy recurrent urinary tract infections 623– 5, 704, 705 urinary incontinence prophylaxis 702–3 urinary incontinence risk 19, 703 urinary incontinence treatment 518– 20, 701, 701–2 urogenital atrophy 705–6 see also hormone replacement therapy vaginal administration 519, 520 atrophic vaginitis 650 pessary wearers 536 postcoital urinary tract infections 669 recurrent urinary tract infections 623, 625, 704, 705 urogenital atrophy 706 vs pelvic floor muscle training 413 ethical issues, cosmetic vaginal surgery 1380–1 ethnic differences see racial differences ethylene vinyl alcohol co-polymer suspended in dimethyl sulfoxide (Uryx®) 861, 973, 973 Europe, epidemiology 32–7 European Agency for the Evaluation of Medicinal Products, Committee for Human Medicinal Products (CHMP) 450 European Association of Urology, chronic pelvic pain definition 606 evacuatory failure see defecation, obstructed event recording, ambulatory urodynamics 318–19 Everett, Houston 6 examination, physical 193–4 continence nurse specialist 84, 85 gynecologic 193–4 ICS definitions 750–1, 762 physical therapist/physiotherapist 102, 476 examination under anesthesia, urogenital fistulae 1229, 1298 exercise as cause of urinary incontinence 409, 658–9, 676, 676–7 pad tests 206, 209 pelvic floor muscles see pelvic floor muscle training preoperative 827–8 see also physical activity; sports/fitness activities explantation artificial urinary sphincter 967, 969 see also erosion exstrophy bladder 1333, 1333 cloacal 1333, 1334 external anal sphincter (EAS) 3D MRI reconstruction 348 anatomy 122, 1100–1, 1101 childbirth-related nerve damage 687 electromyography 283, 285 MRI 340, 341 obstetric damage see obstetric anal sphincter injury primary repair after obstetric injury 1114– 15, 1115, 1116–17, 1117 see also anal sphincter
external genitalia ambiguous 1324, 1324, 1340, 1341 development 129–30, 1318 hemangiomas 1339, 1340 inspection 750–1 pediatric disorders 1340–1 externally readjustable sling 975, 976 external urethral sphincter (striated urogenital sphincter; rhabdosphincter) 177 anatomy 116, 117, 117–18, 118 drugs relaxing 491, 494–7 electromyography see urethral sphincter, electromyography embryological development 131 function in neurologic disease 566, 567 mechanism of continence 119, 147, 880 MRI 344, 345 neural reflexes 160 relaxation coordination 151–2 normal voiding 151 sensory nerves 159 extraurethral incontinence 751, 762 fallopian tubes anatomy 1159, 1159–60, 1160 development 1318, 1318 family history overactive bladder 61 pelvic organ prolapse 1006 urinary incontinence 19, 54, 55, 56–7, 396 faradism, evidence for effectiveness 414 fascia autologous slings see pubovaginal slings (PVS), autologous deep, anterior abdominal wall 1154, 1155 pelvic 1158 fascia lata autologous, pubovaginal slings 883 complications 819–20, 847 harvesting 846 results 814, 883–5, 884 cadaveric (CFL) pubovaginal slings 847, 850–1, 885 complications 889 results 850, 851, 888 sacrocolpopexy 1199 fat, autologous, periurethral injections 1354–5 fecal impaction 472 fecal incontinence 712–20, 1122–33 after rectocele repair 1047, 1047 after rectopexy 1141, 1142 biofeedback 715, 1122 childbirth-related 686–9 pathogenesis 687–9, 712–13 prevention 397–8 see also obstetric anal sphincter injury etiology 712 functional rehabilitation 1122–5 history taking 192, 713 investigations 714, 714, 1122 management 714–18 pads and pants 552 pathogenesis 687–9, 712–13 patient assessment 713–14, 1122 pudendal nerve terminal motor latencies 291, 714 St. Mark’s scoring system 713, 713 surgery 716–18, 1125–9, 1130 urinary incontinence and 19 female genital mutilation (FGM) 585, 1240
ethical issues 1380 reversal 1379 Female Sexual Function Index (FSFI) 26 FemAssist® device 536 femoral nerve injury 1350 FemSoft® device 536–7, 538, 539 ferrous sulfate 828 fetal weight, pelvic organ prolapse and 1005 fiber, dietary 730 fiber density (FD) 283, 283–4 fibroblasts, autologous, periurethral injection 973 fibroids, uterine, uroflowmetry and 221 filling, bladder see bladder filling filum terminale, short 575 fimbriae, uropathogenic bacteria 617 first desire to void (FDV) 230, 233, 432, 752, 763 first sensation of bladder filling 432, 752, 763 fistulae, urogenital 1224–38, 1297–306 abdominal repair 1232, 1234, 1301–3 combined transperitoneal/ transvesical 1301–3, 1304–5 transperitoneal 1234 transvesical 1234 after anti-incontinence surgery 1349, 1350, 1350 classification 1224–7, 1297 complex 1297 vaginal repair 1301, 1302–3 conservative management 1298 endoscopic assessment 378, 382, 385, 386, 1229 etiology 1224, 1225, 1226–7, 1297 investigations 1228–9, 1297–8 obstetric see obstetric fistulae pessary-related 536 postoperative management 1235–7 preoperative care 1230 presentation 188, 1227–8 prevalence 1224 prognosis 1237 risk factors 1224, 1226 simple 1297 surgical treatment 1230–5 choice of route 1231, 1299–300 dissection principles 1231, 1232–3 instruments 1231 interposition grafting 1234–5, 1303–6, 1304–5 suture materials 1231 techniques 1231–5, 1300–6 timing 1230–1, 1298–9 vaginal repair 1231–4 dissection and repair in layers 1231–2, 1232–6 saucerization technique 1232 in specific circumstances 1232–4 testing 1235 see also specific types fitness activities see sports/fitness activities training, preoperative 827–8 ‘flat tire’ test, urinary vaginal fistulae 382 flatus incontinence, after childbirth 686 flavoxate 488, 506 vs bladder training 419 flow see urine flow flow delay 755, 767 flow rate 152, 217 accelerated (AFR), before antiincontinence surgery 246 ambulatory urodynamics 320
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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average (Qaverage) 217, 755, 766 epidemiologic study 17 healthy volunteers 220, 220 catheter effects 237 curves see uroflow curves definition 755, 766 maximum (Qmax) 217, 217, 755, 766 bladder outlet obstruction 241, 241, 242 epidemiologic study 17 healthy volunteers 220, 220 interpretation 220, 786–7 normal 233 pressure–flow studies 791–2 recording 220, 787 measurement see uroflowmetry pressure–flow studies 790–2 videourodynamics 304–5 voiding difficulty/retention 587 flow rate controlling zone (FRCZ) 784–5, 790–1 flow time 217, 217, 755, 766 healthy volunteers 220 flow/volume nomograms 219, 220 fluconazole 648, 649 fluid management after fistula repair 1235 catheterized patients 545 constipation 730 urinary incontinence 87, 409–10, 471 fluoroquinolones 622–3, 624 fluoroscopy sacral neuromodulation surgery 1278, 1278, 1279, 1279–80 videourodynamics 303–4, 328, 329, 329 flurbiprofen 509–10 follow-up losses to 808 outcomes assessment 807 forceps delivery fecal incontinence and 398, 688 pelvic organ prolapse and 1005 perineal trauma and 1106 urinary incontinence and 397 foreign bodies, bladder 385 Fowler’s syndrome, electromyography 285, 286 FOXc1 133, 135 French gauge 543–4 frequency 187, 187, 188 24-hour 750, 762 bladder training to decrease see bladder training causes of abnormal 188 classification 175 continence nurse specialist 86 daytime 750, 762 detrusor overactivity and 144 drug treatment 502, 504 epidemiologic studies 16–17, 53, 54 increased daytime 633, 747, 760 increasing, as management intervention 468–9 normal values 201, 202 overactive bladder syndrome 633 patient-centred measures 436 pregnancy 397, 683–4 frequency–volume (FV) chart 198, 198–200 definition 749, 762 see also voiding diary functional ability, measures of impact on 439 functional profile length 754, 765 functional urinary incontinence 175 fungal infections, vulvovaginal 647–8, 648
funicular meso 1158 funneling, proximal urethra, pelvic floor ultrasound 359, 359 furniture protection 558 GABA 161–2 detrusor overactivity and 640 drugs acting on 494, 495 GABAA receptors 162, 495 GABAB receptors 162, 495 gabapentin 162, 600 Gaeltec NanoLogger™ ambulatory urodynamic system 322, 322 g-aminobutyric acid see GABA ganglion impar 1163 Gartner’s duct cysts 1255, 1256 embryologic basis 130, 136 translabial ultrasound 363, 364 gas embolism 1218 Gellhorn pessary 535, 535–6 gender differences childhood enuresis 47 urinary incontinence 33, 34, 40, 40, 42, 43 general practitioners (GPs), diagnostic role 100–1 genital hiatus see urogenital hiatus of levator ani genitalia, external see external genitalia genital ligament 1158 genital mutilation, female see female genital mutilation genital tract, female see reproductive tract, female genitogram, persistent urogenital sinus 134, 136, 1336 genitoplasty, feminizing 1324, 1340 genitourinary pain syndromes 748–9, 761 genuine stress incontinence (GSI) 754, 765 see also urodynamic stress incontinence germ cell layers 128 Gibson, James 5–6 giggle incontinence 190, 675 Gillick competence 830 Gittes procedure, outcome 814, 817 glial derived neurotrophic factor (GDNF) 133 global assessment scales 71–2, 72 stress urinary incontinence 453–4 gluteus transposition, anal sphincter 717 glyceryl trinitrate 513 glycine 494 glycopyrrolate 499 glycosaminoglycans, intravesical 600 gonadectomy, androgen insensitivity syndrome 1324, 1340–1 gonadotropin-releasing hormone (GnRH) analogs 828 Good Urodynamics Practices guidelines (ICS) 784–98 filling cystometry/pressure–flow studies 226–7, 787–97 calibration of equipment 794–5 computer software 797 equipment: minimum requirements 793–4 measurement of intravesical/abdominal pressures 792 measurement of urine flow rate 790–2 pressure signal quality control 795 pressure transducers 792–3 problem solving 795–6 retrospective artifact correction 796–7 urodynamic catheters 793
recording micturitions and symptoms 784 strategy for repetition of tests 797 uroflowmetry 216, 218, 784–7 Gore-Tex mesh 889, 1084 gracilis muscle interposition, fistula repair 1235 graciloplasty dynamic see dynamic graciloplasty fecal incontinence 717 graft rejection allograft slings 850 synthetic midurethral slings 897–8 xenograft slings 853 Gram-negative bacteria 614, 619 antibiotic resistance 623 Gram stain 620, 646 grande fosse pelvienne 1024–5, 1025 Green types 1 and 2 urethral descent 8, 332, 334 G-spot amplification 1379 guarding reflex 148, 159–60 sacral nerve stimulation actions 1276, 1277 stroke patients 568 Guillain–Barré syndrome 573 gynecologic developmental abnormalities see developmental abnormalities gynecologic examination 193–4 gynecologic surgery prevention of incontinence/prolapse after 398–400 urologic complications 1290, 1368–75 see also hysterectomy; pelvic surgery gynecologic symptoms 192 habit training 86–7, 417 Haemophilus influenzae 619, 620 Halban-type pouch of Douglas obliteration 1030, 1030 laparoscopic 1209 hamartoma, urethral/vaginal wall 1256 Hamlin and Nicholson fistula repair procedure 1233 hammock theory, DeLancey 125, 125, 881, 946 handicap, definition 102 health, WHO definition 24, 438 health systems, overactive bladder impact 439 Heart and Estrogen/Progestin Replacement Study (HERS) 19, 702 help-seeking overactive bladder 60 urinary incontinence 20, 41–2, 56 factors influencing 56, 57, 58 types of practitioners consulted 56, 56, 58 hemangiomas, introital 1339, 1340 hematocolpos 585, 1320 hematologic investigations, preoperative 829 hematomas, postoperative anti-incontinence surgery 1346–7, 1347 translabial ultrasound 363, 364 hematometra 1319, 1320 hematuria 192, 1292 hemorrhage/bleeding anti-incontinence surgery 831–2, 1346–7, 1347 colpourethropexy 871, 872 laparoscopic surgery 1215, 1216 midurethral sling procedures 895 sacrospinous vault suspension 1059–60 tension-free vaginal tape 921, 922
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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heparin intravesical 600 thromboprophylaxis 830–1 hernia trocar site 1214 true, enterocele 1026–7 see also incisional hernias herpes simplex, anogenital 584 herpes zoster 574–5 hesitancy 190 definition 217, 748, 761 pregnancy 684 hiatus, genital see urogenital hiatus of levator ani Hill equation 236 Hinman syndrome 151 Hirschsprung’s disease 724 anorectal manometry 728, 728 treatment 732 history, clinical 186–93 drug 192–3, 193 neurologic 192 obstetric see obstetric history past medical 192 physical therapist/physiotherapist 102, 476 urinary symptoms 186–92 history of urogynecology 4–12 home delivery, perineal trauma and 1107 pad tests 210–11 uroflowmetry 219 hormone replacement therapy (HRT) pelvic organ prolapse and 1006 prior to surgery 831 risk–benefit balance 520 Turner’s syndrome 1325 urinary incontinence prophylaxis 396, 702–3 urinary incontinence risk 19, 25, 703 urinary incontinence therapy 518–20, 702–3 see also estrogen Hormones and Urogenital Therapy (HUT) Committee 701, 704, 706 hospital-acquired infections 619, 619 hospitals, prevalence of urinary incontinence 48–9 host defense mechanisms 616 HRT see hormone replacement therapy human immunodeficiency virus (HIV), transmission via allografts 850–1, 885 Hunner’s ulcers 6, 386 hyaluronic acid (HA) dextranomer macrospheres (Zuidex™) 862, 973, 973–4 intravesical 600 hydrogel-coated catheters 542, 543 hydrometrocolpos 1338, 1338 hydronephrosis ectopic ureter 137, 138 imaging 326, 326 hydroxychloroquine 600 21-hydroxylase deficiency 1324, 1324, 1340, 1341 hydroxyzine 599 hymen imperforate 1319–20 measurements to/from 773, 774–5 hymenoplasty/hymenorrhaphy 1379, 1380–1 hyoscyamine 488, 499 hyperalgesia, referred pain with 609–10 hypermobile stress incontinence (HSI) 866–7
see also urethral hypermobility hypersensitive female urethra 584–5 hypertension autonomic dysreflexia 572 pelvic organ prolapse and 1005 hypertonic bladder 150 hypnosis 420 hypocalcemia 726 hypogastric nerves 159, 573 early stimulation studies 142, 144 laparoscopic sacrocolpopexy and 1195 hypogastric plexus 607, 1163–4 hypothalamus, control of micturition 160 hypothyroidism 585, 726 hysterectomy abdominal sacrocolpopexy with 1070 bladder injuries 1369 constipation after 725 cystocele repair with 1018 fistulae complicating 1224, 1225, 1227 laparoscopic, complications 1217 lower urinary tract problems after 1364–5 assessment 1364 prevention 1364 symptoms 1364 treatment 1365 pelvic organ prolapse and 399, 1006 prevention of enterocele after 399, 1028–9 radical lower urinary tract problems after 576, 1364–5 uroflowmetry before/after 221 rectocele after 1042 sexual dysfunction and 666–7 urinary incontinence after 398–9, 1364 epidemiology 34, 35, 42, 45 prevention 399 uterine prolapse 1078, 1078–9 vaginal apex fixation 1054 vaginal supports/attachments after 121, 121, 1054–5, 1055, 1194 vaginal vault prolapse after see vaginal vault prolapse hysterosalpingography (HSG), developmental anomalies 1319 hysteroscopy metroplasty 1321 uterine anomalies 1319 ICI see International Consultation on Incontinence ICS see International Continence Society IgA, secretory 616 IIQ see Incontinence Impact Questionnaire ileal conduit urinary reservoir 1310 ileal segment augmentation cystoplasty 1307 ileal sphincter-cystoplasty 1310–11 ileal ureter, ureteric injuries 1294–5, 1373, 1373 ileal vaginoplasty 1323 ileorectal anastomosis, colectomy with 731–2 iliococcygeal fixation, vaginal vault 1061 iliococcygeal muscle anatomy 122, 122, 1156 MRI 340, 341, 342 imaging 326–38 future developments 10 iatrogenic obstruction 985, 986 lower urinary tract 328–36 nervous system 336 pelvic organ prolapse 463–4, 778 preoperative 829 rectocele 1038–41
upper urinary tract 326–8 urogenital fistulae 1228–9 voiding difficulty/retention 588 see also specific modalities and techniques imipramine 488, 510–11 overactive bladder 638 side-effects 511–12 stress incontinence 517 vs bladder training 419 immunosuppressive drugs, interstitial cystitis 600 impairment, definition 102 improvement overactive bladder 430 patient-centered measures 438 stress incontinence 450–1, 810 incisional hernias after colposuspension 873 after laparoscopic surgery 1214 incomplete emptying, feeling of 190–1, 748 Incontinence Impact Questionnaire (IIQ) 69, 438, 438 ICI recommendations 805 nulliparous women 675 Incontinence on the Sexual Response/RJ (IIURS-RJ) 26 Incontinence Quality of Life Questionnaire 438 Incontinence Screening Questionnaire (ISQ) 49, 49 Incontinence severity index 69 Indevus Urgency Severity Scale (IUSS) 435, 435–6 indigo carmine, fistula detection 1228 infections complicating anti-incontinence surgery 1349, 1349 surgical mesh implants 838, 840 transmission via allografts 847, 850–1, 885 vaginal 644, 645, 647–8 see also urinary tract infections; wound infections inferior epigastric artery 1213, 1214–15 laparoscopic localization 1215, 1215 management of bleeding 1215, 1216 inferior fascia of levator ani 121–2 inferior gluteal artery 1055, 1055–6 surgical injury 1056, 1060 inferior gluteal nerve 1055, 1163 inferior hypogastric plexus see pelvic plexus inferior mesenteric artery 1162 inferior mesenteric ganglia (IMF) 158 inflammation interstitial cystitis 595 vulvovaginal, voiding difficulty 584 information leaflets, patient 82, 827 information provision, preoperative 827, 830 infundibulopelvic ligament 1157, 1158 Ingelman-Sundberg, Axel 4–5, 6 inguinal hernia, androgen insensitivity and 1324 injections, urethral 860–3 see also urethral bulking agents, injectable institutional settings, urinary incontinence 48, 48–9, 82 integral (midurethra) theory (Petros & Ulmsten) 881, 890–1, 918, 926 intention to treat analysis (ITT) 431 interferential therapy 414 interlabial masses, pediatric patients 1337–9 intermittent catheterization 757 intermittent self-catheterization (ISC) 588–9 after augmentation cystoplasty 1307–8
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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clean see clean intermittent self-catheterization continence nurse’s role 88, 88 definition 757 intermittent stream 217, 748, 761 internal anal sphincter (IAS) 1101, 1101 primary repair after obstetric injury 1114–15, 1115, 1116 internal iliac artery 1162 internal pudendal artery/vein 1055, 1160, 1162 internal urinary meatus 116–17 International Association for the Study of Pain (IASP) 606 International Classification of Diseases (ICD10) 746 International Classification of Functioning, Disability and Health (ICIDH-2) 101, 102, 746 International Consultation on Incontinence (ICI) continence nursing 92 Continence Promotion, Prevention, Education and Organization (CPPEO) committee 77–8, 80 Imaging and Other Investigations committee 209, 210 outcomes assessment standards 450, 805–8 baseline data/demographics 805 clinician observations 805–6 follow-up 807 patient observations 805 quality of life measures 69, 69, 72, 807–8 specific patient groups 808, 821–2 tests 806–7 pharmacotherapy recommendations 486, 488 International Consultation on Incontinence Questionnaire (ICIQ) 64, 69–71, 72 International Consultation on Incontinence Questionnaire Short Form (ICIQ-SF) 69–71 overactive bladder 437 pad tests and 211–12 stress incontinence 451–2 International Continence Society (ICS) 1-hour pad test 206, 206, 208–9 ambulatory urodynamics standardization 316–20, 787–8 Clinical Research Assessment groups 741–2 Continence Promotion Committee (CPC) 80 Good Urodynamics Practices guidelines see Good Urodynamics Practices guidelines outcome measures 450, 460 quality of life assessment 64, 68–9 questionnaire for males (ICSmale) 437 standardization of terminology and methods see standardization of terminology and methods Standardization of Terminology Committee 757–8, 772 International Federation of Gynecology and Obstetrics (FIGO) 4 International Urogynecology Association (IUGA) history 4–6 training standards 9 International Urogynecology Journal 5
interposition grafts fistula repair 1234–5, 1246, 1303–6, 1304–5 see also Martius fat-pad grafts intersex disorders 1340–1, 1341 InterStim® system 1284 interstitial cells of Cajal 723 interstitial cystitis (IC) 594–604 capsaicin therapy 515 clinical evaluation 595–8 cystoscopic assessment 385–6, 386, 597 diagnostic criteria/definition 594 ICS recommendation 749, 761 possible etiologies 594–5 treatment 598–601 see also painful bladder syndrome Interstitial Cystitis Association 598 interureteric ridge 117 endoscopic appearance 383, 383 intervertebral disk disease 567, 572–3 intervoid interval 436, 436 intestine embryological development 128 laparoscopic anatomy 1161–2 see also bowel injuries; enterocele; rectum; sigmoidocele intra-abdominal pressure see abdominal pressure intraurethral devices (inserts) urinary incontinence 87, 536–7, 537, 538 urinary retention 589 intravaginal (resistance) devices (IVRD) 87, 87, 537 effectiveness 537–8 pelvic floor muscle training with 412 intravaginal slingplasty (IVS) 1062 3D ultrasound imaging 369–70 pelvic floor ultrasound after 363, 363 surgical technique 1062, 1062 intravenous pyelography/urography (IVP/ IVU) 326, 326–7, 327 ureteric injuries 1292 urethral diverticulum 1259, 1259 urinary tract infections 621 urogenital fistulae 1228, 1229, 1298 intravesical pressure (pves) ambulatory urodynamics 317 changes during filling phase 149 definition 752, 763 drugs increasing 488–90 early studies 143–4 flow rates and 152 measurement 228–30, 792 quality control recordings 227, 227 videourodynamics 305 vs detrusor pressure 303 intrinsic sphincter deficiency (ISD) 147 artificial urinary sphincter 962, 963, 968 classification 177–9, 178 ICS view 754, 765 pubovaginal slings 846 surgical failure rates 400 surgical options 866–7 tension-free vaginal tape 920, 920 urethral pressure measurements 257, 257 urethrocystoscopy 379, 383, 384 Valsalva leak point pressure 305 videourodynamics 307 intrinsic urethral sphincter 177, 880 continence mechanism 119, 147 drugs decreasing outlet resistance at 491–3 see also bladder outlet
introital hemangiomas 1339, 1340 Introl prosthesis 535, 536, 537–8 involuntary detrusor contractions see detrusor contractions, involuntary ion channels 164–5 iron replacement therapy 828 irritable bowel syndrome (IBS), constipationpredominant 724, 725 ischial spines, as anatomic landmarks 773 I STOP® 948, 949, 951 JO1870 513 John Paul II, Pope 6 juxtacervical fistulae 1224, 1232–3 Karram, Mickey M. 5 Kegel, Arnold 9, 469, 481 Kelly, Howard A. 6, 7 Kelly plication 7 anterior colporrhaphy 1013–14, 1015, 1019 current consensus 931, 1092 outcomes 814, 818, 1094 kidneys autotransplantation, ureteric injuries 1372 duplex 136 embryological development 131, 132, 132–3, 134, 135 pregnancy/postpartum period 683 King’s Health Questionnaire (KHQ) 69, 70, 438 minimal important difference (MID) assessment 71 pad tests and 211 Klebsiella 619, 619, 624 ‘knack,’ the 470, 478 Kralj, Bozo 5 Kretz Voluson system 365, 365 Labhardt partial colpocleisis 1083 labia minora, enlarged 1378–9 labiaplasty augmentation 1379 reduction 1378, 1379, 1379 labor management see obstetric management obstructed 1240 lactobacilli 644 effects of estrogen 704 increased levels, vaginal disease 650–1 lactulose 730 laparoscopic surgery 1152 advantages 1152 colposuspension see colpourethropexy, laparoscopic complications 1152, 1212–20 access-related 1212 anesthesia 1218 bladder injuries 1217 bowel injuries 1215–17 pneumoperitoneum-related 1217–18 trocar-associated 1212–15 ureteric injuries 1217 disadvantages/problems 1152 endometriosis 1167–71 enterocele/rectocele 1209 paravaginal repair 1180, 1188–9, 1189 rectopexy/resection rectopexy 1143, 1143–4 robotic assistance 1180, 1180, 1199 sacral colpopexy 1194–203 support procedures 1206–10 surgeon’s experience 1217
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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laparoscopic surgery – continued ureteric injuries 1217, 1290 uterine-preserving, for uterine prolapse 1086, 1207–9 vaginal agenesis 1323, 1323 laparoscopic uterine nerve ablation (LUNA) endometriosis 1170 pelvic pain 1172, 1172–3 laparoscopy, diagnostic developmental anomalies 1319 endometriosis 1167, 1167, 1168 pelvic pain 1166–7 Lapides procedure 814, 815 laser treatment bladder ulcers 601, 601 endometriosis 1168, 1168–71, 1169, 1170 pelvic adhesions 1174 lateral inguinal fossae 1157 lateral umbilical fold 1157, 1157 latex catheters 542, 543 laxatives 730, 731 Leadbetter–Politano ureteral reimplantation technique 1370, 1370 leakage, urine see urine loss leak point pressures 259, 266–76 abdominal see abdominal (or Valsalva) leak point pressure cough 259, 268, 455 detrusor see detrusor leak point pressure ICS definitions 754–5, 766 measurement technique 267–8 as outcome measures 455 stress incontinence 267–71 videourodynamics 305–6 Learmonth, J.R. 144 Le Fort colpocleisis 1082–4, 1083 leg catheter drainage bags 547, 547 leg pain, postoperative sacrospinous vault fixation 1060 transobturator tape 952–3, 958 leiomyoma, urethral/vaginal wall 1256 levator ani muscles 121–2, 122, 1155–6 3D ultrasound 366–8, 367 activity (contractions) 3D/4D ultrasound 366, 367 perineal ultrasound 360–1, 361 childbirth-related damage 3D ultrasound 367, 367–8 MRI 343, 345 MRI-based simulation 349–50, 350 connective tissue interaction 123 electromyography kinesiologic 280–1 needle electrodes 281 inferior fascia 121–2 MRI 340, 341, 342, 343–4 color thickness mapping 348, 349 racial differences 345–6 superior fascia 121–2, 124 urethral/vesical neck support 124, 124 urogenital hiatus see urogenital hiatus of levator ani see also pelvic floor muscles levator ani syndrome 724 levatorplasty, posterior colporrhaphy with 1036, 1046 levator–symphysis gap (LSG) 344 levcromakalim 509 lidocaine, intravesical 600 lifestyle factors, modifiable constipation 730 pelvic organ prolapse 421, 1005 urinary incontinence 408–11, 471–2
lifting, heavy 409, 421, 1005 Likert scales 437, 803 limb contractures, obstetric fistula 1242 linea alba 1154, 1155 local anesthesia conscious pain mapping 1175–6 midurethral slings 892 SPARC sling 926 tension-free vaginal tape 918–19 loin pain 191, 191 long-term care, overactive bladder 439 loop diuretics 521 lower motor neuron lesions 145, 566 sacral reflex responses 295 lower urinary tract (LUT) anatomy 116, 116–19 functional 123–5 biomechanics 236–7 electrical stimulation 1276–87 embryology 128–40, 697 functional terms 119 hormonal influences 696–7, 697 imaging 328–36 instrumentation, infection risk 618 nervous control 158, 158–60, 571, 573 pregnancy 683–5 reconstruction 1309–11, 1311 pediatric patients 1342, 1342–3 rehabilitation 757 lower urinary tract exercises (LUTE) 107, 109 see also pelvic floor muscle training lower urinary tract symptoms (LUTS) 186– 92, 746 after fistula repair 1237 associated with sexual intercourse 748 classification into groups 187, 187 cystometry and 226 flow-related 217 hormonal influences 697 ICS definitions 746–9, 760–2 measuring frequency, severity and impact 749–50, 762–3 overactive bladder syndrome 633 pad tests and 211–12 pathophysiology 149 poor correlation with urodynamics 321 postmenopausal 696, 697–8, 698 postmicturition 748, 761 pregnancy/postpartum 683 prolapse-related 780 quality of life impact 66–7 questionnaires 186, 186, 187, 803 recording, during urodynamics 784 severity analysis of treatment outcomes and 431 assessment 186–7, 749–50 storage 747, 760–1 urinary incontinence and 19 voiding 747–8, 761 see also symptoms lumbar intervertebral disk herniation 572–3 lumbosacral spine X-rays 336 lung disease, chronic 46 LUT see lower urinary tract LUTS see lower urinary tract symptoms Lyme disease 574 lymphatic system, pelvic 1163 Macroplastique® see silicone macroparticles magnetic resonance imaging (MRI) 10 anterior vaginal wall prolapse 1011, 1011 chemical shift artifact 347
defecography rectal prolapse 1139 rectocele 1040–1 developmental anomalies 1319, 1319 endoanal 714, 714 enterocele 1028, 1029 pelvic floor 340–53 3D reconstruction 348, 349 basic anatomy 340–2, 341, 342, 345 childbirth-related changes 344–5 childbirth simulation 349–50, 350 color thickness mapping 348, 349 data processing/evaluation tools 350, 351 imaging protocols 347–8 pitfalls 346–7 racial differences 345–6 symptomatic findings 342–4, 343, 344 pelvic organ prolapse 342, 343, 344, 463–4, 778 rectocele 1039–41, 1040 sigmoidocele 1136 slice acquisition angle 346, 346–7, 347 upper urinary tract 326, 327 urethral diverticulum 336, 336, 1259, 1259–60 urogenital fistulae 1229 voiding difficulty/retention 588 vs 3D ultrasound 365, 366 magnetic stimulation anterior sacral roots 291–2, 292 clitoris 294 motor cortex 292, 292–3 therapy 414–15, 417, 479 Mainz 2 ureterosigmoid pouch 1312 malakoplakia, bladder 384 malignant disease fistula formation 1224, 1225, 1229 fistula repair 1306 urethral diverticulum 1253, 1253 urethral/vaginal 1256 see also bladder tumors malnutrition, obstetric fistulae and 1242 Manchester procedure 1079–80, 1080, 1087 manometry anorectal see anorectal manometry biofeedback 481 Marfan syndrome 1005, 1056 Marlex mesh 836, 839 Marshall–Marchetti–Krantz (MMK) procedure 7–8, 866 complications 1346, 1347, 1350, 1351, 1353 osteitis pubis after 875, 1350 pressure–flow parameters after 245 results 814, 815 vs Burch colposuspension 868 marsupialization, transvaginal, urethral diverticulum 1260, 1261 Martius fat-pad grafts 7 fistula repair 1234–5, 1246, 1301, 1302–3 transvaginal urethrolysis 990 urethral diverticulectomy 1263, 1266 urethrovaginal fistula repair 1268, 1269, 1301 mast cells, activation in interstitial cystitis 594–5 mattress covers 558 maximum cystometric capacity (MCC) 239, 754, 765 maximum flow rate see flow rate, maximum maximum pressure 755, 767
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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maximum urethral closure pressure (MUCP) see urethral closure pressure, maximum maximum urethral pressure (MUP) see urethral pressure, maximum maximum voided volume 750, 763 Mayer–Rokitansky–Küster–Hauser syndrome 134–5, 1323, 1341, 1342 McCall culdoplasty surgical technique 1030, 1030–1 at time of hysterectomy 1028–9 vaginal vault prolapse 1061–2 McGuire technique, augmentation cystoplasty 1307 means (statistical) 430–1 meatal masses 1255 mechanical properties, synthetic meshes 839 mechanical stimulation, sacral reflexes 294–5 mechanoafferent signaling, urothelial 165 media, mass 77 medial inguinal fossae 1157 medial umbilical fold 1157, 1157 medians 430–1 median sacral artery 1162 median umbilical fold 1157 Medical, Epidemiologic and Social Aspects of Aging (MESA) study 14–15, 16–19 medical history, past 192 medical illness, pelvic organ prolapse and 1005 medicolegal issues, incontinence surgery 827, 829–30 medroxyprogesterone acetate (MPA) 520 melanoma, bladder metastases 386–7, 387 men diagnosis of incontinence type 101 ICI-recommended outcomes assessment 808, 821 physical therapy 108 prevalence of urinary incontinence 33, 34, 40, 40 severity of urinary incontinence 48, 48 Menfis Blu Runner ambulatory urodynamic system 323, 323 menopause 696–710 continence mechanism and 699–701 sexual dysfunction and 666 symptoms, prevalence 26, 27 urinary incontinence and 33–4, 34 see also perimenopausal women; postmenopausal women menstrual cycle urinary symptoms and 697 uroflowmetry and 221 menstrual flow, obstructed 1319, 1319, 1320 mental health, obstetric fistulae and 1242 mercaptoacetyl triglycine (MAG3) scans 621 Mersilene mesh/tape 836, 838, 841, 890 pectineal ligament uterine suspension 1085–6 sacrohysteropexy 1084 mesenchyme 128, 130–1 mesenteries, pelvic 1157–8 meshes, synthetic see synthetic meshes mesoderm 128 mesonephros 131 meso-ovarium 1158 mesosalpinx 1158 meta-analyses 431 metanephros 131 metastatic tumors, bladder 386–7, 387 methantheline 499 methotrexate 600 metoclopramide 489
metronidazole 650 metroplasty, hysteroscopic 1321 Meyer Weigert law 136 MIchaelis–Gutmann bodies 384 microbiologic culture urinary tract infections 620, 620 vaginitis 646, 649 microorganisms, vaginal flora 644, 644 microscopy urine 620 vaginal 646, 646, 649 micturition 486 clinical physiology 142–55 bladder cycle 142, 147–52 contemporary studies 146–7 early experimental studies 142–5 early urodynamic studies 145 structural aspects 147 development of voluntary control 147–8 habits 676 hormonal effects on control 700 pontine center see pontine micturition center preventative 676 recording, during urodynamics 784 reflexes 160 sacral nerve stimulation inhibiting 1276, 1277 sacral cord center 145, 571 time chart 749, 762, 784 urethral mobility 123, 124 middle rectal artery 1162 middle sacral artery/vein 1195, 1195 midodrine 517 midpubic line, pelvic organ prolapse 464 midurethral slings 870, 880, 890–9 after obstetric fistula repair 1248 complications 895–8 elderly patients 898 history 890 hybrid procedures 940, 940–1, 941 materials available 891 mechanism of effect 881, 881, 890–1, 918, 946 obese patients 898 obstruction complicating sling loosening/incision 988 timing of intervention 984 transvaginal sling incision 988–9, 990 operative techniques 891–3 pressure–flow parameters and 245–6 prevention of urge incontinence after 399–400 prolapse surgery with 898–9, 1016, 1019 results 894, 894–5 transpubic technique 893 transvaginal technique 892–3 see also SPARC sling; tension-free vaginal tape; transobturator midurethral slings midurethra (integral) theory (Petros & Ulmsten) 881, 890–1, 918, 926 midwifery training 1107–8 minimal important difference (MID) assessment, quality of life scores 64, 71, 453 minimum voiding pressure 755, 767 Mitrofanoff procedure, continent reconstruction 1342–3, 1343 mixed urinary incontinence 84, 100 conservative treatment 418 definition 747, 760 history taking 189
pathophysiology 143 physical therapy 108 prevalence 15, 33, 34, 53, 54, 56 tension-free vaginal tape 920, 920, 921–2 urodynamic diagnosis 232 Miya hook 1058, 1058, 1081 MMS Luna ambulatory urodynamic system 322, 322–3 mobility problems association with incontinence 19 cystometry 227 mobilization, postoperative, fistula repair 1236–7, 1247 Monarc™ 948, 949, 951 montelukast 600 morphine 160, 161 Moschcowitz procedure 1029, 1030 laparoscopic 1209 motor conduction velocity 290, 290 motor cortex stimulation, motor-evoked potentials 292, 292–3 motor-evoked potentials (MEPs) anterior sacral root stimulation 291–2, 292 motor cortex stimulation 292, 292–3 perineal/perianal stimulation 290 motor pathways, central, neurophysiologic assessment 292–3 motor unit 278, 279 motor unit potentials (MUPs) concentric needle EMG 281–3, 282 denervation and reinnervation 282, 283, 284 kinesiologic EMG 280, 280 ‘M’ response 290, 291 MRI see magnetic resonance imaging Müllerian ducts development 1318, 1318 differentiation 130, 131 Müllerian remnant cyst 1256 multichannel urodynamic recorder 302–3, 303 Multinational Interstitial Cystitis Association 598 multipara, pelvic floor MRI 340–2 multiple sclerosis (MS) 570 drug treatment 503 neurophysiologic conduction studies 292, 293 sexual dysfunction 666 voiding dysfunction 566, 567, 570 multiple system atrophy (MSA) 569 electromyography 283, 284–5 muscarinic receptors 146, 158, 163, 498 muscimol 162 muscle damage, nulliparous women 677 denervation see denervation, muscle disease, primary, electromyography 286 reinnervation, electromyography 284–5 muscle-evoked potentials see motor-evoked potentials muscle fibers classification 278 density (FD) 283, 283–4 innervation ratio 278 muscle transposition anal sphincter 717 stimulated (dynamic) 717, 1127, 1127 musculotropic relaxants 502–7 Mycobacterium tuberculosis 620 Mycoplasma hominis 620–1 mycoplasmas 619, 620, 624
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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myelodysplasia 147, 567 cystourethrography 335 detrusor leak point pressures 266–7 myelomeningocele 1333–4, 1334 drug treatment 503 electromyography 284 myoblasts, autologous, periurethral injection 973 myocutaneous flaps, vaginal reconstruction 1379 myopathy detrusor 585–6 electromyography 286 nalbuphine 161 nalidixic acid 623 naloxone 160, 161, 490 National Continence Management Strategy (NCMS) (Australia) 78–80 national continence organizations 77–80, 79 continence promotion role 78–80 results of survey 77–8, 78 National Foundation for Continence (US) 78 National Institute of Child Health and Human Development (NICHD), outcomes of treatment standards 450, 455, 456 National Institute of Diabetes, Digestive and Kidney Diseases (NIDDK), interstitial cystitis criteria 594, 597 National Institutes of Health (NIH) definition of pelvic organ prolapse 1003 Terminology Workshop for Researchers in Female Pelvic Floor Disorders 804, 809–10 needle bladder neck suspension (NBNS) (transvaginal colpourethropexy) 866, 870 complications 1346, 1347 laparoscopic 1181 postoperative voiding dysfunction 832, 984 results 9, 811–12, 813, 814, 816, 817 urethral diverticulectomy with 1260, 1261 vs retropubic colpourethropexy 871 see also Pereyra procedure; Raz procedure; Stamey procedure neobladder construction, pediatric patients 1342, 1342–3 neodymium:YAG laser, bladder ulcers 601, 601 Neomedics Acquilog ambulatory urodynamic system 323, 323 neosphincters, anal 717–18, 1127–9 neovagina formation 1323, 1323, 1342 nephrectomy, ureteric injuries 1373 nephrogenic adenoma, urethral diverticulum 1253 nephrostomy tube, ureteric injury 1293–4, 1373–4 nephroureterectomy, duplicated ectopic ureter 1336, 1337 nerve growth factor 147, 149 nerve injury anti-incontinence surgery 1349, 1350 laparoscopic surgery 1164 midurethral slings 895 obstetric fistulae 1242 sacrospinous vault suspension 1060 nerve supply female pelvis 607, 607–9, 1163–4 lower urinary tract 158, 158–60, 571, 573 nervous system, imaging 336
Neugebauer–Le Fort procedure 1082–4, 1083 neural plasticity, interstitial cystitis 595 neurogenic voiding dysfunction 566–81 ambulatory urodynamics 321 cerebral lesions 567, 568–70 classification 174, 177 clean intermittent self-catheterization 549 current issues 742 cystourethrography 334–5 drug treatment 492, 495–6, 497, 503, 506, 514 ICI-recommended outcomes assessment 808, 821–2 peripheral nervous system disease 567, 575–6 spinal cord disease 566, 567, 570–5 surgical treatment 1306–9 urodynamic diagnosis 232 videourodynamics 307–9, 310, 311 see also detrusor areflexia; detrusor overactivity (DO), neurogenic; detrusor–sphincter dyssynergia neurologic disorders 566–81, 567 urinary incontinence in childhood 1331 voiding dysfunction see neurogenic voiding dysfunction neurologic examination 193 neurologic history 192 neuromodulation, sacral see sacral nerve stimulation neuropathic bladder see neurogenic voiding dysfunction neurophysiologic conduction studies 290–9 autonomic nervous system 295–6 parameters measured 290, 290 rectocele 1041 sacral motor system 290–3 sacral reflexes 294–5 sacral sensory system 293–4 neurophysiologic tests see electromyography; neurophysiologic conduction studies neurosyphilis 573–4 NFO Worldgroup survey 20 nicotonic cholinergic receptors 158, 159, 160 nifedipine 507–8, 600 nitric oxide (NO) 147, 159 host defense role 616 initiation of voiding 151 therapies targeting 493, 513 nitric oxide synthetase inhibitors 493, 513 neuronal (nNOS) 131 nitrofurantoin 623, 624 pregnancy 625 nociception bladder 148 pelvic visceral 608–9 nociceptors mechano-insensitive (silent) 609 visceral 609 nocturia 187–8 drug-mediated control 521 ICS definitions 747, 750, 760, 762 overactive bladder syndrome 633 patient-based measurement 436–7 postmenopausal women 699–700 pregnancy 397, 683–4 prevalence 17, 54 nocturnal enuresis 190 alarms 558 childhood 1331 drug treatment 511, 520–1
urinary incontinence risk in adult life 46, 46–7 definition 747, 761 drug treatment 520–1 overactive bladder syndrome 633 prevalence 41, 42 primary 190, 1331 secondary 190 nocturnal polyuria 190, 750, 762 nocturnal urine volume 190, 750, 762 nomograms bladder outlet obstruction 236, 242 flow/volume 219, 220 non-adrenergic, non-cholinergic (NANC) neurotransmitters 147, 158, 498 non-inferiority study design 431 non-neurogenic neuropathic bladder 151 non-neurogenic voiding difficulty/retention see voiding difficulty, non-neurogenic non-relaxing urethral sphincter obstruction 756, 768 non-steroidal anti-inflammatory drugs (NSAIDs) 509–10 noradrenaline (norepinephrine) 159, 162, 640 norephedrine chloride 515 norfenefrine 515–16 normality, standardization and 740 Nottingham Health Profile 67, 68 Novasys micro-remodeling system 977, 978 nulliparous women 674–80 giggle incontinence 675 pelvic floor dysfunction etiologic factors 675–7 management 678 prevalence 674–5 prevention 678–9 significance of symptoms 675 pelvic floor MRI 340, 342 pelvic floor ultrasound 358 pelvic organ prolapse 674–5, 676 urinary tract infections 675 nurse continence advisor (NCA) 92, 93 nurse practitioners 93, 94 nurses advanced practice see advanced practice nurses continence see continence nurse specialist preoperative counseling 827 registered (RN) 94 Nurses’ Health Study 702–3 nursing assessment 83, 83, 84 nursing home residents urinary incontinence 48, 48 urinary tract infections 626 nystatin 649 OABq 437 OASI; OASIS see obstetric anal sphincter injury obesity anti-incontinence surgery and 867, 868 midurethral slings 898 pelvic organ prolapse and 1005 preoperative preparation 828 urinary incontinence and 19, 45, 408 urinary tract infections and 618, 675 weight loss 396, 408–9, 471–2 OBJECT trial 500 obstetric anal sphincter injury (OASI; OASIS) 1112–20 classification 1112, 1112 early recognition 714–15
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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fecal incontinence 686–9, 687, 688 incidence 1113, 1114 patient assessment 713 surgical repair 716–18 incidence 1113 prevention 397–8 primary repair 1113–18 definition 1112 end-to-end technique 1113, 1115 end-to-end vs overlap techniques 1115 outcome 1113, 1114 overlap technique 1113–15, 1115 principles and technique 1116–18 techniques 1113–14 secondary repair 1112 obstetric fistulae 1224, 1240–50, 1297 circumferential 1247, 1247 classification 1243–4, 1244 epidemiology 1240 etiology 1225, 1240 future 1249 immediate management 1244 investigations 1243 irreparable 1248 prevalence 1240–1 surgical repair 1244–8 absent urethra 1246, 1246–7 complications 1248 failed 1248 flap splitting technique 1245, 1245 interposition grafts 1246 postoperative care 1247–8 results 1248 route 1244–5 specific problems 1246–7 timing 1230, 1244 symptoms and signs 1241–3 obstetric history 192 urinary incontinence and 19, 24–5, 25, 28 obstetric management fecal incontinence prevention 398 perineal trauma prevention 1106–7 urinary incontinence prevention 397 obstetric trauma rectocele formation and 1036–7 see also perineal trauma obstructed defecation see defecation, obstructed obstructed labor 1240 obstruction, bladder outflow (BOO) after incontinence surgery 982–95 diagnostic evaluation 983–6 etiology 982–3 identifying risks 983 incidence 982 management 986–93, 987 presentation 983 see also voiding difficulty, after antiincontinence surgery a-adrenergic receptor subtypes and 164 before anti-incontinence surgery 246 causes 585 clean intermittent self-catheterization 549 current issues 741–2 detrusor function and 236–7 detrusor overactivity 632–3 electromyography 285–6, 588 ICS definition 756, 768 non-relaxing urethral sphincter 756, 768 prolapse reduction and 237–8, 239 symptom syndrome suggesting 749, 761–2 treatment 589 urethrolysis see urethrolysis
urodynamic definition/diagnosis 236 after incontinence surgery 984–5 pressure–flow studies 239–45, 241, 242, 243, 244 voiding cystometry 231, 232 videourodynamics 241, 244, 306, 306, 309–10, 985 see also urinary retention; voiding difficulty ObTape® 946 complications 951–2 mesh characteristics 949, 951 operative technique 948 ObTryx™ 948, 949, 951 obturator artery 1162 obturator nerve 1163 occupation overactive bladder and 59, 61 pelvic organ prolapse and 1005 urinary incontinence and 54, 55 odor control 558 omental pedicle grafts, fistula repair 1235, 1303, 1304–5, 1306 omental urethra-cystoplasty 1310–11 Onuf’s (Onufrowicz’s) nucleus 159–60, 608 degeneration, electromyography 284 pharmacological targets 160, 161 opening pressure 755, 767 opening time 755, 767 OPERA trial 500 opioid agonists 513, 730 opioid antagonists 490 opioid receptors 160–1 oral contraceptive pill 831 orchidectomy, androgen insensitivity syndrome 1324, 1340–1 oropharyngeal membrane 128, 128 Ortiz, Oscar Contreras 5 osteitis pubis 875, 1349, 1349–50 osteomyelitis, postoperative 938, 1349 Ostergard, Donald 5 outcome 740 outcome measures 740 clinician (investigator)-based 432, 454–6, 461–4 incontinence interventions 802–23 AUA guidelines 803, 810, 811–20 future considerations 808–9 ICI recommendations 805–8 NIH Terminology Workshop recommendations 809–10 Urodynamic Society recommendations 803–5, 810–21 overactive bladder 430–48 patient-centred 432, 435–9, 451–4, 460–1 pelvic organ prolapse 460–5 physiologic 432–5 primary 803 questionnaires 803 secondary 803 stress incontinence 450, 450–8 subjective vs objective 451 surrogate 456 validity and reliability 430, 460, 802–3 outcome research 740 ovarian artery/vein 1160, 1162 ovarian endometriomas 1170–1, 1171 ovarian failure, Turner’s syndrome 1325 ovarian fossa 1158 ovarian ligament 1158, 1160 ovarian plexus 1164 ovaries 1160, 1160 overactive bladder (syndrome) (OAB) 632–42
classification 174, 176, 178, 180 clinical presentation 633 de novo, after anti-incontinence surgery 833, 1352, 1352–3 colpourethropexy 873–4, 874 midurethral slings 896, 897 prevention 399–400 pubovaginal slings 886–7, 889 urethrocystoscopy 378–9 drug treatment 497–513, 635–8, 638 dry 632 estrogen therapy 702 future developments 640 history 632 outcome measures 430–48 efficacy 431–9 efficacy–tolerability ratios 443–4 placebo response 440 principles of evaluation 430 safety 444 statistical evaluation 430–1 tolerability 440–3 pathophysiology 161, 632–3 peripheral nerve stimulation 1283–4 pregnancy 397 prevalence 633–4 Asia 58–60, 59, 60, 61 Europe 34, 35 quality of life assessment 64 sacral nerve stimulation 639, 1276 spinal cord injury 145 surgical treatment 1306–9 terminology 632, 749, 761 treatment 634–40 urgency and 144, 149 urodynamic diagnosis 149, 232, 633, 634 videourodynamics 308, 310 wet 632 see also detrusor overactivity overactive bladder outlet 178, 179–80 Overactive Bladder Questionnaire 438 overactive bladder symptoms and healthrelated quality of life questionnaire (OABq) 437 overdistension injury, bladder 586 overflow incontinence 84 classification 175 ICS recommendation 756, 768 Oxford grading system, pelvic floor muscles 85, 85, 477, 477 oxybutynin 488, 503–5 cost-effectiveness analysis 439 evidence for effectiveness 500–1, 503–4 extended release (ER) 504, 636, 638 intravesical administration 504–5 overactive bladder 635–6, 638 pediatric patients 1332 placebo-controled trials 440 side effects 504, 636 tolerability measures 441, 441, 442–3, 443 transdermal (OXY-TDS) 505, 636, 638 vs bladder training 419 vs pelvic floor muscle training 412–13 pad-and-pants systems, disposable 553 pads 88, 550–5, 552 all-in-one 553, 553 bed 553, 554 disposable 552–3, 555 during exercise 659 guidelines for assessing 551 nursing management 87–8 pouch 553, 554
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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pads – continued reusable 553, 555 skin care 555 urogenital fistulae 1230 pad tests 206–14 1-hour 206, 208–9, 433 ICS standard 206, 206, 208–9 modified 209 ambulatory urodynamics 315 historical aspects 206 indications 206 long 210–11 detection limit 210 reliability and validity 210–11 overactive bladder evaluation 433, 433 paper towel test 212 Pyridium test 209–10 recommendations 751, 763, 806 reliability and validity 207 short 207–10 detection limit 207–8 reliability and validity 208–9 vs long 211 stress incontinence evaluation 455–6 symptoms/quality of life correlation 211–12 pain 191 bladder see bladder pain chronic pelvic see chronic pelvic pain conscious laparoscopic mapping 1175–6 ICS definitions 748 loin 191 pelvic see pelvic pain pelvic pathways 608 postoperative laparoscopic surgery 1152 transobturator tape 952–3, 958, 959 somatic vs visceral 609–10 syndromes, genitourinary 748–9, 761 urethral 191 visceral see visceral pain painful bladder syndrome (PBS) 594–604 clinical evaluation 594–8 ICS definition 594, 749, 761 treatment 598–601 see also interstitial cystitis pants 550 designs 554, 554 selection guidelines 552 skin care 555 paper towel test 212 paracervical ganglia 608 paracervix 1158 parachute jumping 659 paracolpium 120, 120, 121, 1054–5, 1068, 1194 see also pelvic organ support paradoxical puborectalis syndrome 1138 see also anismus parametrium 120, 120, 1054, 1158, 1194 pararectal fascia 1036 pararectal fossa (space) 1055, 1158, 1162 parasympathetic nerves bladder cycle control 148, 151 early physiologic studies 142 lower urinary tract 158, 158–9, 573 neurophysiologic studies 295 pelvis 608 parasympathomimetic agents 488–9 paraurethral glands (Skene’s glands) 119 blockage by catheters 544, 544 cyst/abscess 1255, 1256 infection 1252
pediatric patients 1337, 1337 paraurethral structures 116 paravaginal (lateral vaginal) defects 1010, 1010–11 3D ultrasound 368 causes of failed repair 401 laparoscopic repair 1180, 1188–9, 1189 MRI 1011, 1011 physical examination 1012 retropubic repair 1016 AUA outcomes assessment 814, 815 vaginal repair 1016–18, 1017–18 results 1019 vs laparoscopic repair 1189 paravaginal supports/attachments 124, 1010 3D ultrasound 367, 368 MRI 1011, 1011 paravesical fossa 1158 parity overactive bladder and 59, 61 urinary incontinence risk and Asia 54, 55 Australia 42, 44, 45, 45 Europe 34, 35 South America 24, 25, 28 Parkinson’s disease 162, 568–9 electromyography 280 voiding dysfunction 567, 568–9, 569 patient-centered outcome measures 432 overactive bladder 435–9 pelvic organ prolapse 460–1 stress urinary incontinence 451–4 patient derived outcome measures (PDO) 64 patient education constipation 730–1 physical therapy 103, 107, 108–9, 476–7 Patient Global Impression of Improvement (PGI-I) scale 72, 72, 438, 454 Patient Global Impression of Severity (PGI-S) scale 72, 72, 437, 454 patient perception of bladder condition questionnaire 71, 72, 437 peak flow rate see flow rate, maximum pectineal ligament uterine suspension 1085–6 pediatric patients 1330–44 capacity to give consent 829–30 interlabial masses 1337–9 urinary incontinence 1331–7 congenital abnormalities causing 1333–7 enuresis alarms 558 etiology 1331 functional causes 1331–2 outcomes assessment 808, 821 prevalence 47 urethral injections 862 urinary incontinence in adult life and 46, 46–7 see also nocturnal enuresis, childhood urinary symptoms, management 396, 401 urinary tract infections 617, 626 urinary tract reconstruction 1342–3 see also developmental abnormalities pelvic brim 1154–5, 1155 pelvic denervation procedures, chronic pelvic pain 1172–3 pelvic diaphragm 119–20, 121–2, 1155–6 pelvic fascia 1158 parietal 1158 visceral 1158 pelvic floor 3D reconstruction 348, 349
anatomy 119–22, 120 functional 123–5 MRI 340–2, 341 connective tissue/muscle interaction 123 mechanisms of injury 682–3 MRI see under magnetic resonance imaging repair 1379 ultrasound 356–77 viscerofascial layer 120, 120–1, 121 Pelvic Floor Distress Inventory (PFDI) 460–1 pelvic floor dysfunction (PFD) classification 177–80, 178–9 description of functional symptoms 780–1 diagnostic tools 1138–9 ICS standardization of terminology 772–81 MRI 340, 342–4, 343, 344 nulliparous women 674–80 obstructed defecation 724–5, 726, 732 pathophysiology and etiology 1138 prevention 395–401, 678–9 pelvic floor dyssynergia 724, 1138 see also anismus pelvic floor educator device 480–1, 481 pelvic floor exercises see pelvic floor muscle training Pelvic Floor Impact Questionnaire (PFIQ) 460–1 pelvic floor muscles (PFM) anatomy 121–2, 122 assessment of function 477 continence nurse specialist 85, 85 ICS recommendations 751, 778–80 Oxford grading system 85, 85, 477, 477 childbirth-related trauma 683 rectocele formation and 1036–7 connective tissue interaction 123 contraction, urethral pressure measurements 259 denervation/nerve damage childbirth-related 683, 686, 687 electromyography 285 neurophysiologic conduction studies 291 nulliparous women 677 rectocele formation and 1037 electrical stimulation see electrical stimulation, pelvic floor electromyography 280, 280–1 during voiding 239, 240 ICS recommendations 779 female athletes 658–9 inspection 779 obstetric fistulae and 1242 palpation 779 pressure recordings 779–80 see also levator ani muscles pelvic floor muscle training (PFMT) 9, 469–70, 477–8 biofeedback 104, 469, 479–81 electromyography 85, 104, 107 equipment 104, 480, 481 evidence for effectiveness 412, 421 perineal ultrasound 360 daily regimes 469–70 definition 757 detrusor overactivity 107, 108, 109 electrical stimulation with 414 evidence for effectiveness 411–13, 416, 476 female athletes 660 guidelines 106, 106 intravaginal resistance devices with 412
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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measures of efficacy 455 in men 108 overactive bladder 635 pelvic organ prolapse 421 prevention of fecal incontinence 398 prevention of urinary incontinence 397 prior to surgery 826 programs 411, 478 stress strategies (the ‘knack’) 470, 478 stress urinary incontinence 84–5, 103–4 teaching 469 urge incontinence 470, 470 vaginal cones and 86, 105–6, 480 pelvic inflammatory disease 191 pelvic (splanchnic) nerves bladder innervation 158, 159, 573 pelvis innervation 607, 608, 1164 sensory function 148, 159 stimulation studies 142 surgical injury 575–6 pelvic organ prolapse (POP) 1000–8 anatomical basis 121 classification 463, 1000, 1000–1 conservative treatment 420–2, 422, 1029 definition 1003–4 de novo, after anti-incontinence surgery 875, 1353, 1353 epidemiology 20, 395, 1003, 1004–6 estrogen deficiency and 705 hysterectomy and 399, 1006 ICS definitions 751 ICS description system 772–8 ancillary techniques 777–8 conditions for examination 772–3 imaging procedures 778 ordinal staging 776–7, 777, 1002, 1002–3 quantitative see Pelvic Organ Prolapse Quantification System surgical assessment 778 ICS standardization of terminology 772–81 leak point pressure testing 268 MRI 342, 343, 344, 463–4, 778 natural history 395 nulliparous women 674–5, 676–7 outcome measures 460–5 objective 461–4 subjective 460–1 pathogenesis 394, 394, 689 pessaries and devices 534–40, 535 physical examination 193–4, 751, 772–7 conditions for 772–3 supplementary techniques 777 prevention 395–400 reduction pressure–flow studies and 237–8, 239 to reveal stress incontinence 400, 1090, 1091 risk factors/etiology 395–7, 1003–6, 1136 nulliparous women 676–7 sexual function and 666, 780, 1028 surgery see prolapse surgery symptoms associated with 192, 748 ICS-recommended description 780–1 ultrasonography 778 3D 367, 368–9, 369 4D 366 translabial/perineal 361, 361–2, 362, 371 upper urinary tract imaging 326, 326 urodynamic diagnosis 232 uroflowmetry 221
voiding difficulty 191, 585, 586 see also anterior vaginal wall prolapse; enterocele; rectocele; sigmoidocele; uterine prolapse; vaginal vault prolapse Pelvic Organ Prolapse Quantification System (POP-Q) 773–6, 1001–3 clinical use 463, 1001 definition of anatomic landmarks 773–4, 774, 1001 making/recording measurements 774–6, 775, 1002 normal ranges 463 ordinal staging system 776–7, 777, 1002, 1002–3 as outcome measure 462, 462–3 population studies using 1003, 1003 rectocele assessment 1038 specific site defects 463 technique of use 1001–3 vs other grading systems 1000, 1000 Pelvic Organ Prolapse/Urinary Incontinence Sexual Questionnaire (PISQ) 461 pelvic organ support 120–3, 1024, 1036, 1068–9 ‘boat in a dry dock’ analogy 123, 1068 classification 1000, 1000–1 endopelvic fascia 120, 120–1, 121 level I (suspension) 121, 1054, 1055, 1068, 1068 level II (attachment) 121, 1054, 1068, 1068 level III (fusion) 121, 1054–5, 1068, 1068 muscle/connective tissue interaction 123 pelvic diaphragm 121–2, 122 pelvic pain 748, 1164–78 acute, causes 1166 chronic see chronic pelvic pain conscious pain mapping 1175–6 laparoscopic management 1164–78 pelvic denervation procedures 1172–3 syndrome 606, 749 pelvic plexus (inferior hypogastric plexus) 142, 607, 608, 1163–4 injury 575 pelvic surgery previous pelvic organ prolapse and 1006 urinary incontinence and 45, 192 radical, voiding dysfunction after 567, 575–6 urogenital fistulae complicating 1224, 1225, 1226 urologic complications 1368–75 see also gynecologic surgery pelvic-to-pudendal reflex see guarding reflex pelvic wall 1154–6, 1155, 1156 pelvis bony 1155 obstetric fistulae 1242 pelvic floor dysfunction 343 cellular tissues 1158 greater (false) 1154–5, 1155 laparoscopic anatomy 1154–64 laparoscopic visualization 1152 lesser (true) 1155, 1155 lymphatic system 1163 masses 194 nervous system 607, 607–9, 1163–4 peritoneum, fascia, fossae and ligaments 1156–9, 1157 ureteral anatomy 1368, 1368 vascular system 1160, 1162–3
penicillin, preoperative prophylactic 831 pentosan polysulfate (PPS) 598–9 percutaneous nerve evaluation (PNE) 1123, 1278–9 acute stage 1123 subchronic stage 1123 percutaneous vaginal tape (PVT) 941–2 Pereyra (and Pereyra modified) procedure 866 outcome 814, 816 sacrospinous fixation with 1093 periaqueductal gray (PAG) 159, 160 pericardium, bovine 854, 888 perimeatal masses 1255 perimenopausal women stress incontinence 26–7 urinary incontinence 32, 33, 698, 698 see also menopause; postmenopausal women perineal body 122, 1101 measurement point 774, 774, 1001 recording measurements 775, 775 perineal descent assessment 726 excessive see descending perineum syndrome perineal membrane see urogenital diaphragm perineal pain 748 syndrome 749 perineal rectosigmoidectomy see Altemeier procedure perineal stimulation motor conduction responses 290–1 reflex responses 294 perineal trauma 682, 1100 assessment 1104–5 classification 1112, 1112 definition 1101 first degree 1101, 1112 fourth degree 1112 management 1103–6 non-suture management 1103–4 prevention 1106–7 repair continuous suturing method 1104, 1105, 1105 interrupted suturing method 1104, 1105, 1105–6 procedure 1104–6 rectocele repair with 1042–3 skin closure 1104 suture material 1104 training 1107–8 second degree 1101, 1112 structures involved 1101 third degree 1112 see also episiotomy perineometer 469 perineorrhaphy, rectocele surgery 1043–4 perineum anatomy 1100, 1100–1 congenital absence 1037 embryology 128–30 inspection 750–1 manual support, during delivery 1106 massage, pregnancy and labor 1106–7 reconstruction 1379 perioperative care anti-incontinence surgery 826–34 laparoscopic sacral colpopexy 1199 see also postoperative care peripheral nerve evaluation see percutaneous nerve evaluation
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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peripheral nerve stimulation 1283, 1283–4 peripheral nervous system disease 567, 575–6 peritoneal flap grafts, fistula repair 1235, 1303 peritoneal fossae 1157–8 peritoneum endometriosis 1167–70 parietal/visceral layers 1156 pelvic 1156–8 rectal 1162 periurethral glands see paraurethral glands periurethral injection therapy 860–3 see also urethral bulking agents, injectable pernicious anemia 567 peroneal neuropathy, obstetric fistula with 1242 per protocol analysis (PPA) 431 perspiration, measurement 441, 443 pessaries 534–40, 1029 adverse effects 538–9 care programs 536 choosing 534–6 effectiveness 537 incontinence 534–5, 535 rectocele 1041 space-occupying 534, 535, 535 supportive 534, 534 use before surgery 827 pessary test post-void residual volume 238 before prolapse surgery 400, 1090, 1091 Petri, Eckhard 5 Petros & Ulmsten integral theory 881, 890–1, 918, 926 PFS see pressure–flow studies pH, vaginal 644, 646 pharmacology bladder 146, 158–71 clinical concepts 486–8 pharmacotherapy see drug treatment phenazopyridine (Pyridium) fistula detection 1228 test, urinary incontinence 209–10 phenoxybenzamine (POB) 491, 492 phentolamine 491, 492 phenylephrine 164 phenylpropanolamine (PPA) 516–17, 519 photography, pelvic organ prolapse 777–8 physical activity 409 assessment of incontinence during 656, 656–7 as cause of urinary incontinence 409, 658–9, 676, 676–7 pad tests 206, 209 see also exercise; sports/fitness activities physical examination see examination, physical physical therapy (physiotherapy) 100–12, 476–84 assessment 101–2, 103, 476–7 detrusor overactivity 107–8, 109 evaluation of effectiveness 110 evidence for effectiveness 411–17, 476 factors affecting outcome 415 interventions 103–8, 476, 477–82 men 108 mixed incontinence 108 painful bladder syndrome/interstitial cystitis 598 patient education 108–9, 476–7 pelvic organ prolapse 421 process 103 referral diagnosis 100–1, 103
stress incontinence 103–6, 106, 477–82 physiologic outcome measures, overactive bladder 432–5 physiotherapy see physical therapy pili, uropathogenic bacteria 617 pinacidil 165, 509 pirenzepine 498 placebo response, overactive bladder 439 plastic catheters 542, 543, 550 plastics, technology 837–8 pneumoperitoneum, complications 1217–18 poliomyelitis 575 pollakisuria 633, 747, 760 see also frequency polydipsia 188 polymer technology 837–8 polyomaviruses 619, 620 polypropylene mesh 836, 838, 839, 840 cystocele repair 1019 SPARC sling system 927 tension-free vaginal tape 918 transobturator midurethral slings 949, 951 polypropylene sling, distal urethral 941–2 polyps bladder 383 urethral 1339, 1340 polysynaptic inhibitors 513 polytetrafluoroethylene (PTFE) see Teflon polyuria ICS definition 750, 762 nocturnal 190, 750, 762 pontine micturition center (PMC) 160, 571 discovery 143 pharmacological targets 160, 162 sex hormone influences 700 POP see pelvic organ prolapse POP-Q see Pelvic Organ Prolapse Quantification System porcine dermis 853, 854, 885–7 porcine small intestinal submucosa (SIS) 854, 887–8 position, patient childbirth 1106 cystometry 227, 228 intraoperative, complications due to 1348–9 leak point pressure testing 268 pelvic floor ultrasound 356, 357–8 pressure-flow studies 238 SPARC sling procedure 926 videourodynamics 302, 304 see also posture positive pressure urethrography (PPUG), urethral diverticulum 335–6, 1258, 1260, 1260 postanal repair (PAR) 717 postcolposuspension syndrome 874, 875, 1353 posterior colporrhaphy 732, 1036 levatorplasty with 1036, 1046 operative technique 1044–5 results and complications 1046 vs transanal rectocele repair 1047–8 posterior intravaginal slingplasty see intravaginal slingplasty posterior urethrovesical angle (PUV) (retrovesical angle) 8 cystourethrography 329–32, 331, 334 epidemiologic study 18 obliteration during micturition 123 pelvic floor ultrasound 357, 358 posterior vaginal wall
ICS-defined points for measurement 774, 774 making/recording measurements 775, 776 posterior vaginal wall prolapse ICS definition 751 making/recording measurements 775, 776 terminology 774 see also enterocele; rectocele postmenopausal women estrogen therapy see estrogen, replacement therapy pelvic organ prolapse risk 1006 recurrent urinary tract infections 704, 704, 705 statistics 696, 696 urinary incontinence 698, 698, 699 urinary symptoms 696, 697–8, 698 urogenital atrophy 705–6 see also elderly; hormone replacement therapy; menopause postmicturition dribble 191, 217, 748 postmicturition symptoms 748 postoperative care abdominal sacrocolpopexy 1071–2 fistula repair 1235–7, 1247–8, 1301 incontinence surgery 831–3 midurethral slings 893 pubovaginal slings 883, 910–11 SPARC sling 931–2, 932 ureteric injuries 1295–7 urethral diverticulectomy 1264 urinary catheterization 588 postpartum period anal sphincter morphology 686 early voiding difficulty 585 lower urinary tract changes 683 pudendal nerve terminal motor latencies 291, 686 urinary retention 684 urodynamic values 685, 685–6 uroflowmetry 221 post-polio syndrome 575 posture preventing urinary incontinence 410 uroflowmetry and 219 see also position, patient post-void residual (volume) (PVR) 756, 767 after urethral reconstruction surgery 1264, 1271 cystourethrography 333 epidemiologic study 17–18 prolapse reduction and 238 uroflowmetry 220, 787 potassium-channel openers 165, 509 potassium channels 165 ATP-sensitive (KATP) 163, 165 large conductance calcium-activated (BKCa) 165 potassium sensitivity testing (PST) 597 pouch of Douglas (rectouterine pouch) 1157, 1157, 1162 anatomy 1024 depth, enterocele formation and 1024–5, 1025, 1027 endometriosis 1171 obliteration 1029–31 prophylactic 1028–9 surgical techniques 1030, 1030–1 Poussan urethral advancement technique 6–7 PRAFAB-score 102
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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Index
prazosin 193, 491, 492–3 pregnancy 682–93 after obstetric fistula repair 1243 after urinary tract reconstruction 1343, 1343 after uterine prolapse repair 1080, 1082, 1085 anal sphincter morphology 686 artificial urinary sphincter deactivation 963 cervical atresia 1322 fecal incontinence after see fecal incontinence, childbirth-related irritative symptoms 397 lower urinary tract changes 683 mechanisms of pelvic floor injury 682–3 non-communicating rudimentary uterine horn 1322 pelvic organ prolapse and 1004–5 pessaries 534 prevention of pelvic floor dysfunction after 679 Turner’s syndrome 1325 urinary incontinence during/after 42–4, 684–5 etiologic mechanisms 394, 394, 685–6 risk factors 19, 24–5, 25, 28, 396–7 urinary tract infections 615, 625 urodynamic values 685, 685–6 uroflowmetry 221 see also childbirth; postpartum period premicturition pressure 755, 767 prenatal diagnosis, congenital anomalies 134–5, 137, 138 preoperative assessment 828–9 anesthetist 829 investigations 221, 246, 321–2, 828–9 preoperative considerations anti-incontinence surgery 826–31 midurethral slings 891–2 pubovaginal slings 882 preoperative management, urogenital fistulae 1230 preoperative preparation incontinence surgery 826–8 alternative therapies 826–7 psychological 827 informed consent 829–30 thromboprophylaxis 830–1 pre-ovarian fossa 1158 presacral nerve (superior hypogastric plexus) 607, 608, 1163–4 presacral neurectomy 1173 presacral space 1195, 1195 laparoscopic approach 1197, 1198 pressure at maximum flow rate 755, 767 pressure–flow studies (PFS) 152, 226, 236–49 after anti-continence surgery 245–6 ambulatory urodynamics 322 biomechanical aspects 236–7 defining bladder outflow obstruction 239– 45, 241, 242, 243, 244 equipment, minimum requirements 793–4 factors affecting 237–8 ICS definitions 755–6, 766–8, 767 ICS good practice guidelines 787–97 interpretation 239, 240 normal volunteers 243 predictive value 246 pressure measurements 755 quality control 239, 795 recording 237
retrospective artifact correction 796–7 troubleshooting 238, 795–6 urethrolysis and 246–7 videourodynamics 306, 306 pressure sores 555 pressure transducers abdominal pressure measurements ambulatory urodynamics 314, 314–15, 318 cystometry 229, 229 ICS recommendations 792–3 videourodynamics 304 calibration 226, 317, 794–5 fixation 229, 317, 318 intravesical pressure measurements (urethral) ambulatory urodynamics 314, 314–15, 318 cystometry 228–9, 229 ICS recommendations 792–3 videourodynamics 304 reference levels (heights) 227, 317, 792–3 urethral pressure measurements 252–5 balloon catheters 254, 255 catheter-tip transducer catheters 254, 254–5 perfused catheters with side holes 252, 254 zeroing to atmospheric pressure 226, 317, 792 see also urodynamic catheters pressure transmission ratio (PTR) 258–9, 754, 765 preterm labor 625 proctalgia fugax 724 proctography, defecation see defecography proctologic examination 1138 progesterone continence mechanism effects 700–1 lower urinary tract effects 696–7 receptors 696–7 voiding difficulty and 493 progestogens 520, 700–1, 703 prokinetic agents 730 prolapse, pelvic organ see pelvic organ prolapse prolapse surgery 1194 anterior vaginal wall prolapse 1013–20 bone anchors 936 enterocele 1029–31, 1058 incontinence surgery with 1015, 1092–6 indications 1092 as prophylactic measure 400 results 1019, 1094–5, 1096 selection of continence procedure 1092 vaginal vault prolapse 1199–200 laparoscopic 1194–203, 1206–10 midurethral slings with 898–9 prevention of failure 401 rectocele 1042–9 sexual function after 667–8, 1020 SPARC sling procedure with 931 synthetic mesh 836, 840–1 urinary incontinence after 1090–8 definitions 1090 diagnosis 400, 1091–2 management 1092–6, 1093 pathophysiology 1090–1 prevention 400 summary of study results 1094–5 uterine prolapse 1078–87 see also specific procedures
Prolene mesh 836, 838, 890 promotion, continence see continence promotion prompted voiding 417 pronephros 131 propantheline bromide 488, 498–9, 503 pediatric patients 1332 propiverine 488, 506–7, 637–8 propranolol 517 proprioception, bladder 148 prostaglandins (PGs) inhibitors 509–10 intravesical administration 489–90, 589 prostatectomy, incontinence after 101, 108 prostatic enlargement, benign 757 prostatic hyperplasia, benign (BPH) 493, 757 prostatic obstruction benign 757 bladder instability 149 prostatodynia 749 prosthetic materials categories 836–7, 837 see also biologic prosthetic materials; synthetic prosthetic materials Proteus (mirabilis) 619, 624 provocative maneuvers ambulatory urodynamics 319 cystometry 231, 232 cystourethrography 328–9 detrusor overactivity 432, 753 videourodynamics 304 see also cough; Valsalva maneuver pseudoephedrine 515 pseudohermaphroditism female 1340, 1341 male 1340–1 Pseudomonas aeruginosa 619, 619, 623, 624 psoas hitch 1294, 1370–1, 1371 psychogenic retention of urine 285, 286, 585 psychological factors, cosmetic vaginal surgery 1378, 1382 Psychosocial Adjustment to Illness Scale 67 puboanal muscle 122, 122 pubocervical fascia 121 pubococcygeal line 1038, 1039–40, 1040 pubococcygeus muscle 122, 1156, 1156 electromyography 280, 280 puboperineal muscle 122, 122 puborectalis muscle 122, 122, 1156, 1162 childbirth-related disruption 344–5 MRI 341, 342, 344 neurophysiologic conduction studies 293 pubourethral ligaments 123, 124, 125, 918 pubovaginal muscle 122, 122 pubovaginal slings (PVS) 880, 881–90, 908–15 allografts 846, 847–53, 885, 914 complications 850–1, 852 results 850, 851, 888 autologous 846–7, 883–5 complications 847, 849–50, 885, 886–7 current and future role 914 harvesting 846, 882 operative technique 881–2, 908–10 results 847, 848, 883–5, 884 biologic materials 846–54 bone anchors 936–8 complications 913, 1346, 1347 history 881–2 myelodysplasia 266–7 obstruction complicating timing of intervention 984 transvaginal sling incision 988–9, 989
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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pubovaginal slings (PVS) – continued operative technique 881–2, 908–10, 909–12 postoperative management 883, 910–11 pressure–flow studies 245, 246 results 882–90, 911–13, 913 synthetic materials 888–9, 914 with urethrovaginal fistula repair 1267 xenografts 846, 853, 853–4, 885–8, 914 pubovesical ligaments 124–5, 1157, 1159, 1161 pubovesical muscles 116, 124, 124–5 pubovisceral muscle 122, 341 pudendal nerve anatomy 607, 608, 1163 childbirth-related damage 683 anal incontinence and 687, 712–13 rectocele formation and 1037 urinary incontinence and 686 electrical stimulation (BION® device) 1285, 1285 reflex responses to stimulation 294 sensory function 148, 159, 180 somatic function 159, 573 somatosensory evoked potentials 293 terminal motor latencies (PNMTL) 290–1 after childbirth 686, 687, 712–13 constipation 729 fecal incontinence 291, 714 pudendal neuropathy 291 pudendal neurovascular complex 1055, 1055 surgical injury 1056, 1060 puerperium see postpartum period PVT (percutaneous vaginal tape) 941–2 pyelography intravenous see intravenous pyelography/urography retrograde, urogenital fistulae 1228 pyelonephritis 625 Pyridium see phenazopyridine Qmax see flow rate, maximum QT (QTc) interval drug-induced prolongation 508 measurement 440, 441, 442 Q-tip test 194 qualitative data 430 quality adjusted life years (QALYs) 64, 65, 439 quality assessment, ambulatory urodynamics 317–18 quality assurance, role of standards 738 quality control ambulatory urodynamics 317 cystometry 226–7, 227, 233, 795 invasive urodynamics 787–90 pressure–flow studies 239, 795 pressure signals 795 quality of life (QoL) 10, 64–74 after anti-incontinence surgery 1356–7 assessment 64, 67–73 applications 65–6, 66, 67–8 clinical measures and 66–7 ICI recommendations 69, 69, 72, 807–8 methods 65 overactive bladder 438, 438–9 pelvic organ prolapse 460–1 stress incontinence 453 definition 64, 438 dimensions 65 pad tests and 211–12 predictors of impairment 66 questionnaires 64, 65, 67–72
computerization 71 disease-specific 68–71, 69 generic 67–8 minimal important difference (MID) assessment 64, 71, 453 simple global scoring systems 71–2, 72, 453–4 urinary incontinence impact 17, 25–6, 45 vs bothersomeness 437 Quality of life in persons with urinary incontinence (I-QoL) 69 quantitative data 430 quantitative electroencephalography (qEEG) 441–2 questionnaires outcomes assessment 803–4 quality of life see quality of life (QoL), questionnaires racial differences attitudes to incontinence 674 connective tissue 677 pelvic floor MRI 345–6 pelvic organ prolapse 1005–6, 1037 urethral diverticulum 1252 urinary incontinence 14, 27 radiation fistulae 1224, 1225 prognosis 1237 surgical repair 1306 timing of surgery 1230 radiation injury, ureters 1291 radiofrequency therapy, stress urinary incontinence 976–7, 977, 978 radiologic imaging see imaging radiopaque markers, colonic transit testing 727, 728 raphe nuclei 161 Raz procedure (vaginal wall sling) 938–40 complications 817, 940 operative technique 938–9, 939 results 814, 940 receiver operator characteristics (ROC), bladder outlet obstruction 241, 241, 244 reconstructive surgery biologic prosthetic materials 846–57 complex 1290–315 fecal incontinence 1125–9 pediatric patients 1342, 1342–3 synthetic prosthetic materials 836–43 recovery, laparoscopic surgery 1152 rectal balloon catheters abdominal pressure measurements 229, 229, 793 see also pressure transducers rectal balloon expulsion test 729 rectal contractions, during cystometry 232–3, 233 rectal examination 194, 726, 751 rectal injury isolated obstetric 1112, 1113, 1116 surgical 1060 rectal intussusception 1137 rectal ligament 1158 rectal mucosal intussusception 724, 725 rectal mucosal prolapse 1137 rectal prolapse 1136–48, 1137 classification 1137–8 complete (procidentia) 1137, 1137 diagnostic tools 1138–9 genital prolapse with 1136 diagnostic evaluation 1139, 1140 pathophysiology and etiology 1136–8
surgical techniques 1145–6 history and examination 725, 726 pathophysiology and etiology 724, 1025, 1027, 1137–8 surgical techniques 732, 1139–45 abdominal 1140, 1141–4 perianal 732, 1140, 1141 rectal resection pelvic nerve injury 575–6 rectopexy with see rectopexy, resection rectoanal inhibitory reflex (RAIR) 723, 728, 728 rectocele 1036–51 3D ultrasound 369, 369, 370 after anti-incontinence surgery 832–3, 1353 anatomical basis 121, 1036 etiology 1036–7 investigations 1038–41 management 1041–2 obstructed defecation 724 physical examination 1038 surgical repair 1042–9 defect-specific 1042–4, 1043, 1044 results and complications 1046, 1046 indications 1041 laparoscopic 1209 mesh or graft augmentation 1045, 1045–6 results and complications 1048, 1048–9 rectopexy with 1145 results and complications 1046–9 selection of procedure 1042 transanal (transrectal) approach 732, 1045 results and complications 1047, 1047–8 transvaginal approach see posterior colporrhaphy symptoms 1037, 1037–8 terminology 774, 1003 ultrasonography 361, 362 rectopexy 732, 1141–4 anterior sling 1142 choice of procedure 1144–5 genital prolapse surgery with 1145–6, 1146 Ivalon sponge 1141–2 laparoscopic methods 1143, 1143–4 posterior mesh 1142, 1143 resection 732, 1142–3, 1144 laparoscopic 1143, 1143–4 suture 1141, 1142, 1143 rectosigmoidectomy, perineal see Altemeier procedure rectosigmoid junction 1162 rectouterine fold 1157 rectouterine pouch see pouch of Douglas rectovaginal fascia (septum) 121, 1024, 1036 defects, rectocele 1038, 1042, 1043 surgical repair 1042–3, 1043, 1044 endometriosis 1171, 1171 enterocele formation and 1026 laparoscopic anatomy 1157 rectovaginal fistula, obstetric 1241, 1247, 1248 rectovaginal space see pouch of Douglas rectum contrast medium, cystourethrography 328, 332 development 129, 129–30 laparoscopic anatomy 1161–2 rectus fascia slings 883
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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complications 819–20, 847 harvesting 846, 882, 908, 908 results 814, 883–5, 884 see also pubovaginal slings, autologous rectus sheath 1154, 1155 reference height, urodynamics 227, 317, 792 referred visceral pain, mechanisms 609–10 reflex incontinence 753 registered nurse (RN) 94 rehabilitation functional, fecal incontinence 1122–5 lower urinary tract 757 see also physical therapy reinnervation, muscle, electromyography 284–5 rejection, graft see graft rejection reliability 430, 460, 802–3 alternate form 802 interobserver and intraobserver 802 pad tests 207, 208, 210–11 test–retest 802 urethral pressure measurements 255, 256 voiding diary 199 Remeex system 975, 976 renal failure 192 renal function, diabetic cystopathy 576 reproductive tract, female 1159, 1159–60 development 1318, 1318, 1330, 1330, 1331 developmental abnormalities 1318–28 obstetric injury 1241–2 research outcome 740 outcome measures see outcome measures residual urine 152 clean intermittent self-catheterization 549–50 measurement 333 normal 233 see also post-void residual resiniferatoxin (RTX) 166, 488, 513–15, 638 responder analyses 431 responsiveness, test 460 restriction in participation (handicap), definition 102 retention of urine see urinary retention retrograde pyelography, urogenital fistulae 1228 retropubic colpourethropexy see colpourethropexy, retropubic retropubic space see space of Retzius retropubic suspension, uterovaginal prolapse (Nesbit) 1086 retrorectal space 1157 retrovesical angle see posterior urethrovesical (PUV) angle Retzius, space of see space of Retzius rhabdomyosarcoma, vaginal 1338–9, 1339 rhabdosphincter see external urethral sphincter Rho-kinase 163 ring pessaries 534, 535, 535–6 Roberts catheter 543, 543 Robertson, E.G. 143–4 Robertson, Jack Rodney 4, 5, 6 robotic-assisted laparoscopic surgery 1180, 1180 sacral colpopexy 1199 round ligament 1157 laparoscopic uterine suspension with 1208–9 mesentery 1158 sling operation for stress incontinence 7
Royal Dutch Foundation for Physiotherapy (KNGF) 106 rural–urban differences see urban–rural differences Sabre™ sling system 941 sacral colpohysteropexy, laparoscopic 1207, 1207–8 sacral colpopexy see sacrocolpopexy sacral dysgenesis, videourodynamics 311 sacral micturition center 145, 571 sacral nerve roots 608 sacral nerve stimulation (SNS) constipation 732–3 fecal incontinence 718, 1122–5 acute test stimulation 1123 implant placement 1123–4, 1124, 1125 results and complications 1124–5, 1125 subchronic test stimulation 1123 history 1276 lower urinary tract 1276–87 anatomic landmarks 1278, 1278 clinical results 1281–3, 1283 complications 1284–5, 1285 future directions 1285–6 indications 1282 mechanisms of action 1276, 1276, 1277 patient selection 1276–8 surgical techniques 1278–81, 1279–81 muscle-evoked potentials 291–2, 292 overactive bladder 639, 1276 painful bladder syndrome/interstitial cystitis 601 voiding difficulty/retention 589, 1276, 1282–3, 1283 sacral parasympathetic nucleus (SPN) 158, 160, 608 sacral plexus 607, 1163 sacral promontory anatomy 1195, 1195 laparoscopic appearance 1197, 1197 prosthesis fixation methods 1199 sacral reflexes 193, 294–5 sacral sympathetic trunks 1163 sacrocolpopexy (abdominal) 1068–74 anatomic considerations 1194–5 colpourethropexy with 875–6 enterocele repair with 1031 laparoscopic (LSC) 1073, 1194–203, 1206 complications 1201, 1217 concomitant anti-incontinence surgery 1199–200 contraindications 1196 patient assessment/selection 1195–6 perioperative care 1199 prosthesis types 1198–9 results 1200, 1200–1 robotic assistance 1199 surgical technique 1196–9, 1197, 1198 vs vaginal sacrospinous colpopexy 1061 patient selection and evaluation 1069, 1069–70 results and complications 1072–3, 1073 surgical principles 1201–2 surgical technique 1070–2, 1071, 1072 vs sacrospinous colpopexy 1061, 1072–3, 1194 sacrohysteropexy/sacrocervicopexy 1084, 1084–5 laparoscopic (LSH) 1200, 1201, 1207–8 sacrospinous ligament 1055, 1055
sacrospinous uterosacral fixation (sacrospinous hysteropexy) 1080–2, 1081, 1082 sacrospinous vault suspension (sacrospinous colpopexy) 1057–61 complications 1059–60 contraindications 1057 failures 1060–1 indications 1057 laparoscopic extraperitoneal 1207 Pereyra suspension and 1093 results 1059 surgical techniques 1057–9 vascular structures at risk 1056 vs abdominal sacrocolpopexy 1061, 1072–3, 1194 safety overactive bladder treatments 444 stress incontinence treatments 456 salbutamol 488 saline, cystometry filling medium 227–8 saliva production, measurement 442–3, 443 sarcoma botyroides 1338–9, 1340 saucerization technique fistula repair 1232 urethral diverticulum 1260 Scarpa’s fascia 1154 scheduled voiding regimes 417–20 schizophrenia 192 sciatic nerve 1055, 1163 surgical injury 1060 scopolamine 499 scrotal pain 748 syndrome 749 selective serotonin reuptake inhibitors (SSRIs) 161 sensation bladder see bladder sensation pelvic visceral 608–9 sensitization, visceral nociceptors 609 sensory action potential 290 sensory disorders 179, 180 sensory neurons (primary afferents) 148, 159, 573, 608 capsaicin-sensitive (CSPAs) 514–15 childbirth-related damage 687 drugs targeting 165–6, 513–15 serotonergic pathways 161, 640 serotonin (5-HT) receptors 161 sex steroid hormones continence mechanism and 700–1 lower urinary tract effects 696–7, 697 see also androgens; estrogen; progesterone sexual abuse, previous 1166 sexual differentiation, external 129–30 sexual dysfunction 665–8 after anti-incontinence surgery 667–8, 1353, 1354 after prolapse surgery 1020, 1046, 1047 after rectocele repair 732 after vaginal surgery 1380 prevalence 25–6, 26, 27, 665 treatment 667–8 urinary incontinence and 665–7, 666 see also dyspareunia sexual function 664–72 assessment 460, 461 catheterization and 546, 668 cosmetic vaginal surgery and 1379–80, 1380 epidemiologic studies 25–6 pelvic organ prolapse and 666, 780, 1028 sexual intercourse
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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sexual intercourse – continued symptoms associated with 748 urinary incontinence during see coital incontinence urinary tract infections and 618, 668–9 sexually transmitted diseases (STDs) 645 shapes test, colonic transit 727, 728 Sharp technique, sacrospinous vault suspension 1059 Sherrington, C.S. 142–3 Short Form 36 (SF36) health status questionnaire 67, 68, 72 Shy–Drager syndrome 567, 569 Sickness Impact Profile (SIP) 67–8 Sidaway v Board of Governors of Bethlem Royal Hospital [1985] 830 sigmoidocele 1039, 1136, 1136–7 after hysterectomy 725 classification 1136 sigmoidoscopy 714, 726 sigmoid segment augmentation cystoplasty 1307 signs, lower urinary tract dysfunction clinical assessment (ICS) 749–51, 762–3 definition 746 see also examination, physical silicone catheters 542, 543 silicone macroparticles (Macroplastique®) 862–3 3D ultrasound 370, 371 perineal ultrasound 363, 364 siliconized catheters 542, 543 simplified urinary outcome score (SUIOS) 911, 913 Sims, Marion 6 single photon emission computed tomography (SPECT) 336 Skene’s glands see paraurethral glands skin care urinary incontinence 555 urogenital fistulae 1230 sling procedures 880–906 3D ultrasound imaging 369–70, 370 AUA outcomes assessment 811–12, 813, 814, 819–20 biologic materials 846–54 bone anchor 936–8 externally readjustable 975, 976 failed, leak point pressures 269–71, 270, 271, 273 history 7–8 minimally invasive 9 myelodysplasia 266–7 perineal ultrasound after 363, 363 postoperative voiding problems 832 prolapse repair with 1015–16 synthetic materials 836, 840 vaginal wall 938–40, 939 variants 936–43 vs colpourethropexy 871 see also midurethral slings; pubovaginal slings; specific procedures slow stream 191, 217, 748, 761 small intestinal submucosa (SIS), porcine 854, 887–8 smoking cessation advice 87, 678, 679, 828 pelvic organ prolapse and 1005 urinary incontinence and 25, 45–6, 409, 677, 677 smooth muscle bladder see detrusor embryological development 130–1
social consequences, obstetric fistulae 1242 Society for Urodynamics and Female Urology see Urodynamic Society Society of Urologic Nurses and Associates (SUNA) 94, 96–7 socioeconomic impact 35–6 measures 456 socioeconomic status overactive bladder and 59, 61 urinary incontinence and 40, 54–6, 57, 57 sodium bicarbonate cytolytic vaginosis 651 intravesical 600 solifenacin 488, 501–2 overactive bladder 636, 637, 638 side effects 636, 637 vs tolterodine 636, 637 solitary rectal ulcer syndrome 724, 725 somatic nerves, pelvic 158, 159, 573, 608 somatosensory evoked potentials (SEPs), cerebral 293, 293–4 somatosensory perception, bladder 148, 159 sonic hedgehog (Shh) 129, 130, 130 South America, epidemiology 24–9 space of Retzius 124, 1156–7, 1161 hematomas, postoperative 1346–7, 1347 MRI 344 SPARC sling 926–33 3D ultrasound imaging 369–70 BioArc version 940, 940–1, 941 concomitant procedures 931 device design 927 mechanism of action 926 pelvic floor ultrasound after 363, 363 postoperative care 931–2, 932 postoperative extrusion 932 pressure–flow studies after 246 surgical technique 926–31, 928, 929, 930, 931 Spence technique, urethral diverticulum 1260, 1261 sphincter-cystoplasty 1310–11, 1311 sphincter electromyography 279, 279–86, 284 videourodynamics 306 sphincters see anal sphincter; urethral sphincter spina bifida see myelomeningocele spinal cord disease neurophysiologic conduction studies 292, 293 voiding dysfunction 566, 567, 570–5 spinal cord injury (SCI) 571 autonomic dysreflexia 572 bladder instability 149 cystourethrography 334–5 drug therapy 489, 492, 495, 497, 514 electromyography 284 physiologic studies 144, 145, 146 somatosensory evoked potentials 293, 293 videourodynamics 308, 310 voiding dysfunction 566, 567, 571, 572 spinal shock 571 spinal surgery, previous 192 spiroperidol 162 splitting, urine stream 217, 748, 761 sponge, intravaginal 87 sports/fitness activities 656–62 as cause of urinary incontinence 658–9, 676, 676–7 stress incontinence during assessment 656–7, 657 consequences 658
prevalence 657 prevention 659 treatment 660 spraying, urine stream 217, 748, 761 squamous cell carcinoma bladder, cystoscopic evaluation 386 urethral diverticulum 1253 squamous metaplasia, bladder 383, 384 St. Mark’s fecal incontinence scoring system 713, 713 St. Mark’s stimulator 291, 294 Stamey procedure outcome 814, 816 postoperative voiding problems 832 standardization of terminology and methods (ICS) ambulatory urodynamic monitoring 316–18 lower urinary tract dysfunction 760–70 current issues 741–2 future needs 742, 742–3 purpose 738–44 Standardisation Subcommittee report (2002) 746–58 units of measurement/symbols 768, 768, 769 pelvic organ prolapse/pelvic floor dysfunction 772–81 see also Good Urodynamics Practices guidelines standards 738–40 application and acceptance 738–9 creation and institution 739 methods, measurements and terms 739–40 normality and 740 updating and revising 739 staphylococci 619, 619, 624 Staphylococcus aureus 619, 624 Staphylococcus saprophyticus 619, 624 statistical analysis, treatment outcomes 430–1 stenting, ureteric 1293–4, 1373, 1374 steps model, patient education 109, 109 stigma, of incontinence 76–80 basis 76–7 definition 76 survey of national organizations 77–8 tackling 77–80 see also continence promotion Stoller afferent nerve stimulator (SANS) 1283, 1283–4 stoma-cystoplasty 1310, 1311, 1311 stomas, fecal incontinence 718, 1129 stop test 236 storage, urine 148–50, 486 congenital abnormalities affecting 1333, 1333–4 drugs facilitating 193, 497–520 symptoms related to 747, 760–1 see also bladder filling Storz, Karl 5 straining defecation pelvic floor changes 723, 723 rectocele formation and 1037 urinary incontinence and 410 to void 190, 217 iatrogenic obstruction 984 ICS definition 748, 761 urinary incontinence and 676 uroflowmetry 219 see also Valsalva maneuver strangury 191, 748, 761
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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Stratasis TF™ sling system 941, 941 streptococci 624 Streptococcus pneumoniae 619, 620 Stress Incontinence Surgical Treatment Efficacy Randomized (SISTER) trial 245 stress tests, provocative see provocative maneuvers stress urinary incontinence (SUI) 83–4, 100 after fistula repair 1237, 1246–7, 1248 after hysterectomy 1364 after prolapse surgery 400, 1090–6 after sacrospinous vault fixation 1060 ambulatory urodynamics 321 anterior vaginal wall prolapse with 1012, 1013 classification 307 conservative treatment see under conservative treatment cure 450, 451, 809 cystourethrography 332–3 definition 656, 747, 760 drug treatment 515–20, 977–9, 979 electromyography 280, 282, 285 estrogen therapy 518–20, 701, 701–2 etiology/pathogenesis 880–1, 890–1, 918 hammock theory 125, 125, 881, 946 hypothesis 394, 394 integral theory see midurethra theory failure of treatment 809–10 function/activity-based classification 175, 176 historical aspects 7–8 history taking 186, 189 improvement 450–1, 810 injection therapy 860–3 leak point pressures 267–71 surgical failures 269–71, 270, 271, 272–5 worst cases 268–9, 269, 270 masked 1090 diagnosis 1090, 1091 management 1092, 1093 surgical procedures 1094–5 medical correlates 19 natural history 394–5 new technologies in treatment 972–80 evolutionary 972–5 novel approaches 976–9 nursing assessment 84–5, 85 nursing management 84, 84–9 outcome measures 450, 450–8 AUA guidelines 804 economic 456 investigator observations 454–6 NIH Terminology Workshop for Researchers in Female Pelvic Floor Disorders recommendations 804, 809–10 patient observations 451–4 standards 450, 450 pelvic floor MRI 342–3, 344, 344, 345 pelvic floor ultrasound 358–9, 359, 360 pessaries and devices 534–40, 535 physical examination 194, 750–1, 762 physical therapy 103–6, 477–82 potential 1090–1 diagnosis 1090, 1091 prevention 400, 1092–3 surgical procedures 1094 vaginal vault prolapse 1200 pregnancy/childbirth-related 684–5 etiologic mechanisms 685–6
pressure–flow studies 243 prevalence Asia 53, 54, 56 Australia 42 during sports/fitness activities 657 Europe 33, 34 postmenopausal women 698, 699 South America 26–7, 27 United States 15, 15 prevention 395–400 quality of life impact 17, 66 recurrence after interventions for obstruction 987, 987, 991 urethrocystoscopy 379 sports/fitness activities see under sports/ fitness activities surgical treatment see anti-incontinence surgery type I 177, 307 videourodynamics 306, 308 type II 177 type IIa 307 videourodynamics 306–7, 308, 309 type IIb 307 videourodynamics 307, 309 type III 177–9, 307 artificial urinary sphincter 962 cystourethrography 335 leak point pressure testing 271, 271, 272 videourodynamics 307, 310 see also intrinsic sphincter deficiency ureterocele 138, 139 urethral pressure measurements 257, 257–9, 258, 258, 259 urgency/urge incontinence with see mixed urinary incontinence urodynamic diagnosis see urodynamic stress incontinence uroflowmetry 221 vaginal vault prolapse and 1057, 1069, 1199–200 videourodynamics 306–7, 307, 308–10, 310–11 stroke (cerebrovascular accident) 567, 568 strong desire to void (SDV) 230, 432, 752, 763 subsymphysial fistulae 1224 vaginal repair 1233 sugar substitutes 471 superficial circumflex iliac artery 1213 superficial epigastric artery 1213, 1215 superior fascia of levator ani 121–2, 124 superior gluteal nerve 1163 superior hypogastric plexus 607, 608, 1163–4 superior rectal artery 1162 superior vesical artery 1162 suprapubic arc sling see SPARC sling suprapubic catheterization 545, 545–6 infection rates 618 supravesical fossa 1157 surgical assessment, pelvic organ prolapse 778 surgical treatment constipation 731–3 fecal incontinence 716–18 overactive bladder 639–40 painful bladder syndrome/interstitial cystitis 601 postoperative obstruction 986–93, 987 prolapse see prolapse surgery stress urinary incontinence see antiincontinence surgery
voiding difficulty/retention 589 see also specific procedures Surgipro mesh 838 SURx transvaginal system 976–7, 977 suture materials fistula repair 1231 perineal repair 1104 repair of obstetric anal sphincter injury 1116 sweating, measurement 441, 443 Sweden population studies 32–4, 33, 34 socioeconomic costs 35–6 symbols, ICS recommendations 768, 769 sympathetic chain ganglia 159, 607, 608 sympathetic nerves early physiologic studies 142, 144 lower urinary tract 158, 159, 573 pelvis 608 urine storage reflex 159 sympathetic skin responses 295–6, 296 sympathomimetic drugs 193, 515–17 symphysis orifice distance 332, 334 symphysis pubis bladder neck distance, perineal ultrasound 357, 358 pelvic organ descent, perineal ultrasound 361, 361 reference height (urodynamics) 227, 317, 792 symptoms 746 diaries 452, 452–3 gynecologic 192 history taking 186–92 lower urinary tract see lower urinary tract symptoms pelvic organ prolapse 748 prolapse-related, ICS guidelines 780–1 scales/assessment 435–7, 451–2 ICI recommendations 805, 806 Symptom Severity Index (SSI) 69, 211 symptom syndromes, suggesting lower urinary tract dysfunction 748–9, 761–2 synthetic meshes 3D ultrasound 370, 371 absorbable 837, 837 bonded 839, 839, 840 classification 839–40, 840, 841 combined genital and rectal prolapse surgery 1145 current surgical practice 840–1 dyspareunia caused by 667–8, 841 erosion/extrusion 836, 840–1 abdominal sacrocolpopexy 1073 anti-incontinence surgery 1355, 1356 cystocele repair 1019 laparoscopic sacral colpopexy 1201 midurethral slings 897–8 rectocele repair 1049 SPARC procedure 932 transobturator approach 951–2, 958, 959 filament types 838 incontinence surgery laparoscopic colposuspension 1180–1, 1187 pubovaginal slings 889 SPARC sling 927 tension-free vaginal tape 836, 838, 840, 840, 891, 918 transobturator midurethral slings 949, 951 infections 838, 840
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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synthetic meshes – continued mechanical properties 839 non-absorbable 837–40 pore size 838, 838–9 prolapse surgery 836, 840–1 cystocele repair 1015, 1015, 1016, 1019, 1058 laparoscopic sacral colpopexy 1197–8, 1198 other laparoscopic techniques 1207–8 rectocele repair 1044, 1045–6, 1048, 1048–9 rectopexy 1142, 1143 sacrocolpopexy 1070–1, 1072 sacrohysteropexy 1084, 1084 technology 838–40 weave 839 weight 839 synthetic prosthetic materials 836–43 3D ultrasound 369–70, 370, 371 categories 836–7, 837 complications 1354–6, 1355 history of use 836 perineal ultrasound 363, 363 periurethral bulking agents 862–3 polymer technology 837–8 pubovaginal slings 888–9, 914 systematic reviews 431 tabes dorsalis 567, 573–4 Tamm–Horsfall protein 616 tampons anal 715–16 vaginal 87, 537, 537, 538 tamsulosin 488, 493 tear production, measurement 443 Teflon (PTFE) mesh 836, 838, 839 sacrohysteropexy 1084 particles, injectable 861 complications 1354, 1355 tegaserod 730 telemetry, ambulatory urodynamics 314 teleoscopy, laparoscopic colposuspension 1181 temperature, perineal, urine leakage detection 206, 315–16 tension-free vaginal tape (TVT) 9, 918–23 3D ultrasound imaging 369–70, 370 bleeding complications 921, 922, 1346–7, 1347 complications 895–8, 921, 921–2, 1356 development 918–19 elderly patients 898 obese patients 898 obstruction complicating tape loosening or cutting 988 timing of intervention 984 transvaginal tape incision 988–9, 990 operative technique 919 pelvic floor ultrasound after 363, 363 postoperative leak point pressures 270, 271, 272 postoperative pressure–flow studies 245–6 postoperative uroflowmetry 221 preoperative pressure–flow studies 246 prepubic 974, 974–5 prevention of urge incontinence after 399–400 prolapse surgery with 898–9, 1019, 1200 rationale 918 results 894–5, 919–21, 920, 921 sexual function after 668
synthetic materials 836, 838, 840, 840, 891, 918 vs colposuspension 870, 871, 894–5, 920–1, 921 vs laparoscopic colposuspension 1188 vs transobturator tape 949, 952 tension-free vaginal tape-obturator (TVT-O) 947 mesh characteristics 949, 951 operative technique 948 terazosin 488, 492, 493 terbutaline 488, 493, 496, 510 terminal dribble 217, 748, 761 terminology, standardization of see standardization of terminology and methods terodiline 440, 508 testicular feminization (androgen insensitivity) 1324, 1340–1 tethered cord syndrome 575 tetracycline 622, 624 therapeutic index 443–4, 444 thiphenamil hydrochloride 513 3DSlicer software 348, 350, 351 three-dimensional (3D) reconstruction, pelvic floor 348, 349 three swab test, fistula detection 1228, 1243, 1298, 1299 thromboembolism prophylaxis 830–1, 1236–7 risk assessment 830 thymoxamine 491 Tiemann catheter 543, 543 timed voiding 86–7, 417, 420 time to maximum flow 217, 755, 766 healthy volunteers 220 tissue engineering, vaginal reconstruction 1379 toilet aids 556, 556 ‘mapping’ 79 type 55, 61 toileting aided 556, 556 scheduled 417–20 toilet training 107 early childhood 147–8 tolerability definition 440 overactive bladder treatments 439–43 tolterodine 488, 500–1 bladder training with 419 cost-effectiveness analysis 439 evidence for effectiveness 500–1 extended release (ER) 635–6 overactive bladder 635–6, 638 placebo-controled trials 440 side effects 500, 636, 637 tolerability measures 442–3, 443 vs bladder training 419 vs solifenacin 636, 637 tomoxetine 511 TOT see transobturator midurethral slings total pelvic floor repair (TPFR) 717 traditional medical practitioners 56, 58 training 9 continence nurse specialists 94–6, 95 laparoscopic surgery 1152 perineal repair 1107–8 tramadol 161 tranexamic acid 832 transducers 3D ultrasound 365
pressure see pressure transducers transitional cell carcinoma (TCC), bladder 386, 386, 387 transobturator midurethral slings (transobturator tape; TOT) 946–54, 956–60 complications 949–53, 951, 958, 959, 1346, 1356 inside-out technique 893, 948 mechanism of action 946, 956, 956 operative technique 893, 948, 956–8, 957, 958 outside-in technique 948 pressure–flow studies after 245–6 prolapse surgery with 1019 results 895, 949, 950, 958, 958 surgical anatomy 946–8, 947 transureteroureterostomy 1371, 1372 transverse myelitis 574 transverse vaginal septum 1320 transverse vesical fold 1157 transversus abdominis muscle training 659, 659 trauma perineal see perineal trauma ureteric injuries 1291, 1292 treatment functional classification 487 ICS definitions 746, 757 outcome measures see outcome measures trichomoniasis 648, 648–9, 650 tricyclic antidepressants 488, 510–12 trigone anatomy 116–17, 117 during bladder emptying 150–1 embryological development 131–3, 134 endoscopic appearance 383 trimethoprim 622, 623, 624 pregnancy 625 trocars, laparoscopic placement sites 1213 primary 1212–14, 1214 secondary 1214–15 tropical spastic paraparesis 574 trospium chloride 488, 506–7 overactive bladder 636–7, 638 TRPV1 receptors 609 T-Sling 941 tubo-ovarian recess 1158 turbine valve, intraurethral 589 Turner’s syndrome 1325 TVT see tension-free vaginal tape UDI see Urogenital Distress Inventory ultrasonography 10 3D 10, 364–70, 365, 371 display modes 365, 365–6 practical applications 366–70 4D 365 developmental anomalies 1319 endoanal see endoanal ultrasonography enterocele 1028 intraurethral 10 introital 356 pelvic floor 356–77 pelvic organ prolapse see under pelvic organ prolapse rectocele 1041 translabial/transperineal 356, 356–63, 370–1 biofeedback 481 vs urethrocystoscopy 379 transvaginal 356
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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urethral diverticulum 362, 362, 1258, 1258 urogenital fistulae 1229 voiding difficulty/retention 588 umbilical artery 1162 umbilical peritoneal folds 1157 umbilicus 1154, 1155 uncategorized incontinence 751, 762 underactive bladder 174 classification 178–9, 180 clean intermittent self-catheterization 549 see also detrusor areflexia; detrusor underactivity underactive bladder outlet 177–9, 178 underwater test, bowel injury 1217 United Kingdom (UK), continence nurse specialists 82–90, 92–3 United States continence nurse specialist 92–8 epidemiology 14–22 units of measurements 768, 768 upper motor neuron lesions 145, 566 upper urinary tract (UUT) damage, obstetric fistulae 1242 embryological development 131–3, 132 imaging 326–8 investigations, urinary tract infections 621 urachus 129 UraTape® 948 complications 951–2 mesh characteristics 949, 951 urban–rural differences overactive bladder 59, 61 urinary incontinence 55, 57 Ureaplasma urolyticum 619, 621 ureter(s) cystoscopic evaluation 387–8 descending 1160 dilation, pregnancy 683 ectopic 136–7, 138 cystoscopic evaluation 387 duplicated 136, 1334–6, 1336, 1337 embryological basis 134 imaging 326, 327 urinary incontinence 1336–7 vaginal 136 embryological development 131, 133, 134, 135 intraligamentary 1160 laparoscopic anatomy 1160–1, 1161 lumbar 1160 orifices 116–17 cystoscopy 383, 383 pelvic anatomy 1368, 1368 polyps/fronds 383 reimplantation techniques 1370, 1370–1, 1371 retroligamentary 1160 retrovesical 1160 stenting 1293–4, 1373, 1374 stricture formation 1291 uterine artery relations 1160–1, 1161, 1293 ureterectomy, duplicated ectopic ureter 1336, 1337 ureteric buds abnormal development 136, 137 branching morphogenesis 132, 132 formation 131, 132, 133 Mackie & Stephens hypothesis 132, 134, 136 ureteric fistulae 1291, 1292 conservative management 1293 see also ureterovaginal fistulae
ureteric injuries 1290–7 colpourethropexy 872 diagnosis 1292 gynecologic surgery 1368–74 iatrogenic 1290–1 prevention 1292–3 risk factors 1290 types 1291 intraoperative recognition and repair 1292, 1293, 1368–73 lower ureter procedures 1369–71 midureter procedures 1371–2 role of urologic consultant 1369 upper ureter procedures 1372–3 laparoscopic surgery 1217, 1290 non-iatrogenic 1291 obstetric 1241 postoperative management 1293–7, 1373–4 conservative methods 1293–4, 1373–4 diagnosis 1291–2, 1373–4 open surgical repair 1294–5, 1294–6 postoperative care/follow-up 1295–7, 1374 timing of surgery 1293 ureterocele 138–9 cystoscopic evaluation 387–8 ectopic 1256 prolapsed 1255, 1256, 1338, 1338 ureteroneocystostomy, ureteric injuries 1294 ureteroscopy, ureteric injuries 1291, 1293 ureterosigmoidoscopy 1310, 1312 ureteroureterostomy 1294, 1294, 1369, 1369–70 ureterovaginal fistulae conservative treatment 1298 diagnosis 1298, 1299 endoscopic ‘flat tire’ test 382 iatrogenic 1292 imaging 327 Uretex® TO 948, 949, 951 urethra 3D ultrasound 366 absent, fistula surgery 1233, 1246, 1246–7 anatomy 116, 117–19 biomechanics 237 caruncle 1255, 1256 compression, in prolapse 1090 connective tissue 118–19 duplication, endoscopic evaluation 383, 383, 388, 388 electrical conductance, urinary loss 206, 316, 317 embryological development 129, 129–31, 131 endoscopic evaluation 382, 382–4, 388 fibrosed drainpipe 188 glands see paraurethral glands hypersensitive female 584–5 innervation 158, 158–9 kinking, in prolapse 1090 knee angle 946 laparoscopic anatomy 1161 malignant neoplasms 1256 masses, differential diagnosis 1255, 1256 MRI anatomy 344, 345 mucosa 118 mucosal prolapse 1255, 1256 pain 191 polyps 1339, 1340 position 123–5, 124 pregnancy-related changes 683, 685 proximal
funneling, pelvic floor ultrasound 359, 359 open, cystourethrography 334–5 pseudopolyps 383 reflex responses to stimulation 294 sensory nerves 159 smooth muscle 118, 119 somatosensory evoked potentials 293–4 stress relaxation 257, 258 submucosal vasculature 118, 124 supporting tissues 123–5, 124 surgical injuries 1348 unstable 754, 765 urethra-cystoplasty 1310–11 urethral bulking agents, injectable 860–3 3D ultrasound 370, 371 complications 1354–5, 1355 history of use 7 materials available 861 materials in development 861–3 new materials 972–4 optimal attributes 860–1 perineal ultrasound 363, 364 recurrent stress incontinence 991 urethral catheterization 542–5 complications 544–5 indwelling 1309 intermittent self- see intermittent self-catheterization urinary tract infections 544, 618 urethral catheters 88, 542–5 care 545 clean intermittent self-catheterization 550 design 543, 543 drainage bags 546–7, 547, 548 effects on flow rates 237 infection-inhibiting 544 leakage, bypassing and blockage 544–5 materials 542, 543 nursing management 88–9 pressure measurements see under pressure transducers selection 543–4 size and length 543–4, 544 urinary loss measurement 316 urodynamics 228, 229, 793 valves 548, 548 urethral closure mechanism incompetent 754, 765 normal 754, 765 urethral closure pressure (UCP) filling cystometry 231 low see intrinsic sphincter deficiency maximum (MUCP) 255, 255–6, 754, 765 colpourethropexy success and 867, 868 drugs increasing 515, 516, 517 intrinsic sphincter deficiency 257, 257 MRI-detected puborectalis disruption and 345 normative and comparative data 256 reliability 256 measurement 252, 253 as outcome measure 455 pregnancy/postpartum 685 profile 754, 765 urethral crest 382, 382–3 urethral dilation 589 postoperative obstruction 986 urethral diverticulectomy 1260–6 postoperative care 1264 preoperative preparation 1260 results and complications 1264–6, 1265
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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urethral diverticulectomy – continued surgical technique 1261, 1261–4, 1262, 1263, 1264 urethral diverticulum (UD) 1252–66, 1271 associated complications 1252–3 carcinoma 1253, 1253 classification 1254, 1257 diagnosis 596, 1254–60 differential diagnosis 1254, 1255, 1256 etiology and pathophysiology 119, 1252 history 1252 incidence/patient profile 1252 presentation 1253, 1253–4, 1254 radiologic imaging 335, 335–6, 336, 1255–60 recurrent 1265, 1266 stones 1252 treatment 1258–66 endoscopic 1258 history 1258 observation 1258 results and complications 1264–6, 1265 vaginal flap technique 1258–64 ultrasonography 362, 362, 1258, 1258 urethral pressure measurements 260 urethroscopic diagnosis 378, 384, 384, 1254–5, 1257 urethral erosions artificial urinary sphincter 968 midurethral slings 897–8 synthetic grafts 1356 urethral fistulae see urethrovaginal fistulae urethral function abnormal 768 bladder emptying 150–1 continence and 266–7 during filling cystometry 231, 754–5, 765–6 during voiding 756, 768 endoscopic evaluation 379, 382 normal 756, 768 quantitative measures 455 sex hormones and 701 urethral hypermobility 754, 765 colpourethropexy 867–8, 868 midurethral slings and 891 radiofrequency thermal therapy 976–7 surgical options 866–7 urethral inclination 334 urethral injection therapy 860–3 see also urethral bulking agents, injectable urethral mobility 123–5, 124 leak point pressure test 269, 270, 271, 273–4 Q-tip test 194 see also urethral hypermobility urethral occlusive devices 536–7, 537, 538 urethral pain 748 syndrome 749, 761 urethral pressure cross-sectional area (CA) relationship 256–7, 257 definition 252 fluctuations 754, 765 functional profile length 754 ICS definition 754, 765 maximum (MUP) 255, 256, 754, 765 drugs increasing 515 transmission ratio (PTR) 258–9, 754, 765 urethral pressure measurements 252–63 ambulatory urodynamics 260, 317 circumstances/types 252
clinical measurements and parameters 255–60 continuous recording 252, 252 during coughing/pelvic floor contraction 257–9 dynamic, in resting urethra 257, 258 ICS recommendations 754–5, 765 new catheter-free methods 260 reliability 255, 256 research tool 260 static, in resting urethra 255–7, 257 techniques 252–5 urethral pressure profile (UPP) 252, 253 abdominal leak point pressure and 268 cough 258 detrusor leak point pressure and 267 functional length 754, 765 ICS definition 754, 765, 765 stress 252, 253, 257–9 urethral pressure profilometry (UPP) 252, 253 epidemiologic study 18 ICS definitions of terms 255, 754, 765, 765 reliability 255 urethral prolapse after anti-incontinence surgery 1353 mucosal 1255, 1256 pediatric patients 1338, 1339 urethral reflectometry 260 urethral relaxation incontinence 259, 754, 765 urethral resistance 237 bladder outlet obstruction 241 drugs decreasing 491–7 measurement 266, 267 as outcome measure 455 urethral retroresistance pressure (URP) 260 urethral sphincter congenital abnormalities 1334–6 congenital abnormalities bypassing 1336–7 continence mechanism 880 electromyography kinesiologic 279–81 needle (‘motor unit’) 281, 282 stress urinary incontinence 285 urinary retention/obstructed voiding 285–6 videourodynamics 306 hypertrophy 586 mechanism of continence 119, 147 neurophysiologic conduction studies 292, 292, 293 obstruction, non-relaxing 756, 768 see also external urethral sphincter; intrinsic urethral sphincter urethral strictures/stenosis after urethral diverticulectomy 1265, 1266 treatment 589 urethral pressure measurements 260 urethrocystography see cystourethrography urethro-cystoplasty 1311 urethrocystoscopy see endoscopy, urinary tract urethrography, positive pressure (PPUG), urethral diverticulum 335–6, 1258, 1260, 1260 urethrolysis 989–93, 1352 after SPARC sling 932 failed 993 predictors of success 985, 986–7 pressure–flow studies and 246–7 results 986–7, 987 retropubic 992, 992–3
timing aspects 984 transvaginal 989–92, 991 urethropelvic angle (UP) 332, 334 urethropelvic ligaments, MRI 343, 344 urethropexy see colpourethropexy urethroscopes 380–1, 381 history 5 urethroscopy dynamic 381–2 urethral diverticulum 378, 384, 384, 1254–5, 1257 see also endoscopy, urinary tract urethrovaginal fistulae (UVF) 1266–71 after urethral diverticulectomy 1265, 1266 complications of surgery 1270–1 diagnosis 1266 presentation 1228, 1266 results of surgery 1270 secondary to urethral diverticulum 1252 surgical repair 1266–70, 1267–9, 1270, 1301 urethrovaginal sphincter 117, 118, 118 urethrovesical angle anterior 331, 334 posterior see posterior urethrovesical angle urethrovesical junction (UVJ) 1161 endoscopic evaluation 379, 382, 383 poor support, surgical options 866–7 see also bladder neck urge 633 suppression strategies 470 Urge Impact Scale 438 Urge Incontinence Impact Questionnaire (Urge – IIQ) 69, 438 urgency classification 175 continence nurse specialist 86 definition 747, 760 de novo, after anti-incontinence surgery 982 detrusor overactivity and 144, 149 filling cystometry 230, 752, 764 history taking 189, 190 motor 752, 764 overactive bladder syndrome 633 pathophysiology 143, 144, 148–9 patient-centred measurement 435–6 prevention 396 sensory 752, 764 drug treatment 513–15 see also bladder sensation, increased symptom syndromes 749 urodynamic definition 432 urgency–frequency syndrome 632, 749 sacral nerve stimulation 1282, 1283 see also overactive bladder Urgency Perception Scale (UPS) 435–6, 436 urge syndrome 632, 749 see also overactive bladder Urge – UDI 69 urge urinary incontinence (UUI) 84, 100, 632 behavioral training 470, 470 classification 175, 176 conservative treatment 415, 418 continence nurse’s role 86 definition 747, 760 de novo, after anti-incontinence surgery 982 midurethral slings 896, 897 prevention 399–400 pubovaginal slings 886–7, 889, 913 tension-free vaginal tape 921, 922
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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transvaginal bone-anchor slings 938 drug treatment 504, 507, 510 history taking 189 medical correlates 19 motor and sensory 741 overactive bladder syndrome 633 pathophysiology 143, 149 physical therapy 479 postmenopausal women 698, 699, 702 pregnancy 397 prevalence Asia 53, 54, 59 Europe 33, 34 United States 15, 15 prevention 396 sacral nerve stimulation 1282, 1283 stress incontinence with see mixed urinary incontinence Urilos monitor 8, 206 ambulatory urodynamics 315, 315 urinals, female 557, 557–8 urinalysis, preoperative 829 urinary continence DeLancey hammock theory 125, 125, 881, 946 effects of aging 699–700 extrinsic 119, 147 intrinsic 119, 147 mechanism 147, 880–1, 881, 1161 menopause and 699–701 midurethra theory see midurethra theory sex hormones and 700–1 urethral supports 123–5, 125 urinary diversion 1309–11 continent 1309, 1310–11, 1311, 1312 pediatric patients 1342, 1342 free-draining 1309 interstitial cystitis 601 irreparable obstetric fistula 1248 options available 1309–10 overactive bladder 640 pregnancy after 1343 sexual function after 668 terminology 1309, 1310–11 voiding difficulty/retention 589 urinary incontinence (UI) after fistula repair 1237, 1248 after prolapse surgery 400, 1090–6 after urethral diverticulectomy 1265, 1265–6 aids and appliances 555, 555–8 behavioral therapies see behavioral therapies catheterization see catheterization, urinary causes 24–5, 25, 42–4, 189 conservative treatment 407–20, 422, 826–7 continuous 188, 747, 761, 1227 coping strategies 20 definition 14, 24, 32, 632, 747, 760 current issues 741 devices see devices, incontinence duration, quality of life impairment and 66 economic burden 20, 35–6, 49, 82 ectopic ureter 136–7 endoscopic evaluation 378–9 extraurethral 751, 762 fistula related 1227–8 functional 175 help-seeking see help-seeking, urinary incontinence history of management 6–8 history taking 188–90
incidence 14–15, 16 medical correlates 19, 25 natural history 394–5 nocturnal see nocturnal enuresis overactive bladder 436, 437 pediatric patients see under pediatric patients physical examination 193–4, 750–1, 762 physical therapy see physical therapy prevalence 24, 82 Asia 53, 54, 56 Australia 40, 49, 49–50 Europe 32, 32–5, 33, 34 institutional settings 48, 48–9, 82 men vs women 33, 34, 40, 40 nulliparous women 674–5 postmenopausal women 698, 698, 699 by severity 16, 40, 41, 47, 47–8, 48 by type 15, 15, 24, 33, 34, 41, 53, 54 United States 14, 14 prevention 395–401, 678–9, 702–3 quality of life impact 17, 25–6, 45 radiologic imaging 330–1, 332–3, 336 remission 14–15 risk factors 395–7 Asia 54–6, 55 Australia 44, 44–6, 45 Europe 34–5, 35 nulliparous women 675–7 South America 24–5, 25 United States 19 severe intermittent 188 severity assessment 189 epidemiologic studies 16, 16, 47, 47–8 help-seeking and 56 pad test-based staging 206, 207, 433, 433 pad test correlations 211 quality of life impairment and 66 situational 747, 761 stigma see stigma, of incontinence surgery see anti-incontinence surgery treatment experience 41–2 uncategorized 751, 762 ureterocele 138 urethral diverticulum 1252 videourodynamics 306–7, 307 see also specific types Urinary Incontinence Quality of Life Instrument 438 Urinary Incontinence Severity Score, pad tests and 211 urinary retention 584–91 acute 756, 768 causes 584–6, 585 cerebrovascular accident 568 chronic 756, 768 drug treatment 489–90, 496–7, 589 electromyography 285–6, 588 investigations 587–8 non-neurogenic see voiding difficulty, non-neurogenic peripheral nerve injury 575–6 postoperative 832 anti-incontinence surgery 983, 1350–2, 1351 hysterectomy 1364–5 see also voiding difficulty, after antiincontinence surgery postpartum 684 pregnancy 684 presenting symptoms 586–7
prolapse reduction and 238 prophylactic treatment 588 psychogenic 285, 286, 585 sacral nerve stimulation 589, 1276, 1277, 1282–3, 1283 signs 587 spinal cord injury 571 treatment 588–9 see also obstruction, bladder outflow; voiding difficulty urinary symptoms see lower urinary tract symptoms urinary tract anatomy 1160–1, 1161 embryology 128–33 see also lower urinary tract; upper urinary tract urinary tract infections (UTI) 614–30 after ambulatory urodynamics 319–20 after augmentation cystoplasty 1308 AIDS 574 catheter-associated 544, 615, 618, 626–7 causative organisms 619 clinical symptoms 619 complicated 615, 615, 625–7 congenital anomalies 137, 139 definitions 614–15 history taking 192 hospital- vs community-acquired 619, 619 host defenses 616 interstitial cystitis and 595 intraurethral devices and 538–9 investigations 619–21, 620, 621 nulliparous women 675 nursing advice 87 pathogenesis 615–17 postcoital 618, 668–9 postoperative colpourethropexy 873, 873 tension-free vaginal tape 921, 921 prevalence 614 prophylaxis 621, 625 recurrent 615 after anti-incontinence surgery 1351, 1352, 1354 estrogen deficiency and 704, 704, 705 investigations 621 risk factors 615 treatment/prophylaxis 623–5 urethral diverticulum 1252 urinary incontinence risk 24, 25, 42, 44, 45, 45 relapse 615 risk factors 617, 617–18 treatment 621–5 urinary tract injuries anti-incontinence surgery 1347–8, 1348 gynecologic surgery 1368–75 see also bladder injuries; ureteric injuries urine 24-hour production 750, 762 extravasation, ureteric injuries 1292 residual see residual urine storage see storage, urine urine dermatitis, fistula-associated 1242, 1243 urine flow continuous 218, 218, 755, 766 curves see uroflow curves detrusor pressure relations 236–7 ICS definitions 755, 766 intermittent 218, 218, 755, 766, 766 measurement see uroflowmetry rate see flow rate
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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urine flow – continued symptoms related to 217, 747–8 time see flow time see also urine stream urine loss (leakage) color Doppler ultrasound 359, 360 pad tests 206–12, 433, 433 paper towel test 212 pelvic floor ultrasound 359 quantification methods 206 ambulatory urodynamics 315–16, 317 voiding diary 199 see also leak point pressures urine stream hesitancy see hesitancy intermittent 217, 748, 761 slow 191, 217, 748, 761 splitting or spraying 217, 748, 761 see also urine flow urine volume nocturnal 190, 750, 762 post-void residual see post-void residual voided see voided volume urocolpos 1335, 1336 urodynamic catheters ambulatory urodynamics 314, 314–15, 318 cystometry 229, 229 effects on flow rates 237 ICS recommendations 793 urethral pressure measurements 252–5 videourodynamics 304 urodynamic observations ICS definition 746, 763 ICS recommendations 751–6, 763–8 urodynamics (UDS) 142 ambulatory see ambulatory urodynamics bladder cycle components measured 148–52 computer software 797 conventional 751, 763 cystometry see cystometry development 145 early studies 145–6 epidemiologic study 17–19 flow measurements see uroflowmetry iatrogenic obstruction 984–5 ICS good practice guidelines see Good Urodynamics Practices guidelines inconclusive 320–1 indications 226 leak point pressures see leak point pressures limitations of standard 314 outcomes assessment ICI recommendations 806–7 overactive bladder 432, 432–3 stress incontinence 454–5 painful bladder syndrome 596–7 poor correlation with symptoms 321 pregnancy/postpartum 685, 685–6 pressure-flow studies see pressure–flow studies prolapse surgery candidates 1091 repetition 797 units of measurements and symbols 768, 768, 769 urethral diverticulum 1255–6, 1257 urethral pressure measurements see urethral pressure measurements video- see videourodynamics voiding difficulty/retention 587–8 vs endoscopy 378 vs pad tests 207, 208–9, 211
Urodynamic Society (UDS), outcomes assessment standards 450, 804–5, 810–21 urodynamic stress incontinence (USI) classification 176, 177–9 diagnosis/definition 231, 232, 754, 765 pad tests 208 treatment outcome evaluation 454–5 urethrocystoscopy 383, 384 see also stress urinary incontinence uroflow curves 152, 218, 218 definitions 755, 766, 766 normal patterns 218, 784–5 smoothing recommendations 219–20, 786–7 uroflowmeters 216–17 accuracy 216–17, 785–6 calibration 794 electronic dip-stick 216 gravimetric 216 rotating disk 216 technical problems 219, 786 videourodynamics 303, 304 uroflowmetry 216–23, 237 in clinical practice 221 data from healthy volunteers 220 epidemiologic study 17 history 8, 216 ICS good practice guidelines 216, 218, 784–7 ICS terminology 755, 766, 766 parameters 217, 217–18 pressure–flow studies 790–2 problems 218–19, 786 recommendations 219–20, 786–7, 788–91 videourodynamics 304–5 voiding difficulty/retention 220, 221, 587 see also pressure–flow studies urogenital atrophy, postmenopausal 705–6 urogenital diaphragm (perineal membrane) 123, 1100, 1100 MRI 344 Urogenital Distress Inventory (UDI) 69, 437, 805 urogenital hiatus of levator ani (genital hiatus) 122 3D imaging 366, 367, 368 making/recording measurements 775, 775 measurement point 774, 774, 1001 pathophysiology of prolapse 1056 surgical repair, rectocele 1043 urogenital sinus 130, 131, 1318 persistent 133–4, 136, 1335, 1336 urogenital triangle 1100 urography, intravenous see intravenous pyelography/urography urogynecologist, definition 10 urogynecology, history 4–12 uropharmacology 9 urorectal septum 129, 129, 130 urothelium bacterial adherence 617 embryological development 130–1 host defenses 616 mechanoafferent signaling 165 Uryx® solution 861, 973, 973 uterine anomalies 1320–2 American Fertility Society classification 1320, 1321 diagnosis 1319, 1319 uterine artery 1160, 1162 relations to ureter 1160–1, 1161, 1293
uterine horn, non-communicating rudimentary 1322, 1322 uterine nerve ablation, laparoscopic (LUNA) endometriosis 1170 pelvic pain 1172, 1172–3 uterine prolapse 1078–88 after anti-incontinence surgery 1353 anatomical basis 121 and enterocele, surgical repair 1031 history 1078 hysterectomy 1078, 1078–9 with laparoscopic sacrocolpopexy 1196 vaginal apex fixation see vaginal apex, fixation perineal ultrasound 361, 361 treatment options 1078, 1078 uterus-preserving procedures 1078, 1078–87 abdominal 1084–6 combined vaginal/abdominal 1086 indications 1078–9 laparoscopic 1086, 1207–9 vaginal 1079–84 uterosacral ligaments 120, 1158–9 uterosacral ligament-vault suspension, laparoscopic 1206, 1206–7 uterosacral suspension/plication enterocele 1030, 1030, 1031 uterine prolapse 1080 laparoscopic 1183, 1184, 1208, 1208 uterovaginal anastomosis 1322 uterus anatomy 1159, 1159, 1160 bicornuate 1321 development 130, 1318, 1318 didelphic 1322 septate 1321 support by pelvic floor 123 unicornuate 1321–2 UTI see urinary tract infections vacuum delivery see ventouse/vacuum delivery vagina abdominal pressure measurements 793 anatomy 1159, 1159, 1160 congenital absence 1323, 1341, 1342 congenital anomalies 134–5, 137, 1320 cosmetic surgery 1378–81 ecosystem 644 embryological development 130, 131, 1318, 1318 laxity 1381, 1381–2 malignant neoplasms 1256 masses, pediatric patients 1337–9 normal flora 644, 644 effects of estrogen 704 pelvic supports/attachments 121, 121, 1054–5, 1055, 1068, 1068 connective tissue/muscle interaction 123, 1068 posthysterectomy 121, 1194 see also pelvic organ support rhabdomyosarcoma 1338–9, 1339 tissue engineering 1379 vaginal apex anatomic supports 121, 1054–5, 1055 fixation abdominal approach 1068–75, 1194 laparoscopic techniques 1194–203, 1206–7 rectopexy with 1145, 1146 vaginal approach 1054–66
Pages 1–798 are in Volume 1; pages 799–1384 are in Volume 2.
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vaginal vs abdominal routes 1061, 1072–3, 1194 measurement point 773–4, 774 prolapse ICS definition 751 see also vaginal vault prolapse vaginal artery/vein 1160, 1162 vaginal atresia 130, 134–5, 137 vaginal axis enterocele formation and 1025–6 rectocele formation and 1036–7 vaginal cones/balls 480, 480 continence nurse specialist 86, 86 evidence for effectiveness 412, 413, 416 physical therapist 105, 105–6 vaginal delivery 682 after anti-incontinence surgery 867 mechanisms of pelvic floor injury 682–3 pelvic floor muscle EMG changes 285 pelvic organ prolapse and 1004–5 pudendal nerve terminal motor latency after 291 urinary incontinence risk 19, 24, 25, 54, 55, 396–7 see also childbirth vaginal dilators 1323, 1323 vaginal discharge 644 vaginal erosion artificial urinary sphincter 968 midurethral slings 897 pessaries 536, 538 synthetic grafts 1356 synthetic mesh slings 840–1 transobturator midurethral slings 951–2 vaginal examination 194, 751 vaginal fistulae, urinary 1297–306 see also ureterovaginal fistulae; urethrovaginal fistulae; vesicovaginal fistulae vaginal length, total measurement 774, 774, 1001 recording measurements 775, 775 vaginal pain 748 syndrome 749 vaginal profile (Baden–Walker) 462, 462, 1000, 1000–1 vaginal prolapse history taking 192 leak point pressure testing 271, 271, 274–5 see also anterior vaginal wall prolapse; enterocele; posterior vaginal wall prolapse; rectocele; sigmoidocele vaginal septum longitudinal 1320 transverse 1320 vaginal speculum, notched 1058, 1058 vaginal vault fistulae 1224 abdominal repair 1234 vaginal repair 1232–6, 1233–4 vaginal vault prolapse 399 after anti-incontinence surgery 1353 anatomy 1194–5 cystourethrography 328–9, 333 and enterocele, surgical repair 1031, 1058 etiology and pathophysiology 1056, 1068–9 making/recording measurements 775, 775 prevalence 1194 prevention 399 and rectocele, surgical repair 1045–6 stress incontinence with 1057, 1069, 1199–200
surgical repair abdominal approach 1068–74, 1194 laparoscopic sacral colpopexy 1194–203 other laparoscopic techniques 1206, 1206–7 recurrent stress incontinence after 400 vaginal approach 1054–66 vaginal vs abdominal routes 1061, 1072–3, 1194 symptoms, presentation and evaluation 1056–7, 1069, 1069–70 vaginal voiding 1332, 1332 vaginal wall anterior see anterior vaginal wall cyst 1255, 1256 flap, urethrovaginal fistula repair 1269, 1270 posterior see posterior vaginal wall slings see Raz procedure vaginitis 644–53 atrophic 649–50, 651 causes 645, 647–52 chronic 652 desquamative inflammatory (DIV) 652 epidemiology 644 history and examination 645, 645–6 investigations 646, 646–7 vaginoplasty androgen insensitivity syndrome 1324 esthetic 1379 obstetric fistula repair with 1247 vaginal agenesis 1323, 1323, 1342 vaginosis bacterial see bacterial vaginosis cytolytic 651 lactobacillus 651 validity 430, 460, 803 concurrent 803 concurrent criterion 803 construct 803 content 803 external 430 internal 430 pad tests 207, 208, 210–11 predictive criterion 803 voiding diaries 199, 434–5 Valsalva leak point pressure see abdominal leak point pressure Valsalva maneuver 190 3D/4D ultrasound 365, 367, 367 bladder emptying 151 pelvic floor MRI 348 transperineal/translabial ultrasound 357, 358, 358, 359, 359, 360 urethrocystoscopy 383 videourodynamics 304 see also straining van Geelen, Hans 6 vanilloid agents 513–15 vanilloid receptors 165–6 vascular injuries, laparoscopic surgery 1212, 1213–15 management 1215, 1216 prevention 1212–15, 1215 vasculature anterior abdominal wall 1213, 1214–15 pelvic 1160, 1162–3 urethral submucosal 118, 124 vasopressin analogs 488, 520–1 VATER syndrome 134 VBN micturition model 243 Vecchietti procedure, laparoscopic 1323, 1323
ventouse/vacuum delivery fecal incontinence and 398, 688 perineal trauma and 1106 urinary incontinence and 397 verapamil 507–8 vesical ligament 1158 vesical neck see bladder neck vesical/urethral sensory threshold 752, 764 Vesica™ procedure 936 vesicoanal reflexes 294 vesicobulbovesical micturition reflex 160 vesicocervical fistulae presentation 1227–8 vaginal repair procedures 1232–3 vesicospinovesical micturition reflex 160 vesicospinovesical storage reflex 159 vesicoureteral reflux children 626 cystoscopic evaluation 387 infection risk 618 videourodynamics 307, 309, 310, 311 vesicourethral reflexes 294 vesicouterine fistula, presentation 1227–8 vesicouterine ligaments 1159 vesicouterine pouch 1157, 1157 vesicovaginal fistulae 1297 abdominal repair 1301–6 complex 1301, 1302–3, 1306 conservative treatment 1298 diagnosis 382, 1297–8 endoscopic assessment 385, 386, 1229 etiology 1240 history of treatment 6 imaging 1228–9 interposition grafting 1303–6, 1304–5 obstetric 1240, 1241, 1241 surgical repair 1245, 1245 see also obstetric fistulae vaginal repair 1231–3, 1300, 1300–1 dissection and repair in layers 1231–3, 1232–6, 1300–1 postoperative care 1301 vestibular bulb 1100, 1100 videourodynamics (v-UDS) 302–12, 329 development 8 equipment 302, 302–4, 303, 304 fluoroscopy 303–4, 328, 329, 329 future developments 311–12 indications 306–10 obstruction 241, 244, 306, 306, 309–10, 985 pitfalls 310–11 technique 304 tests performed 304–6 voiding difficulty/retention 588, 588 vs pad tests 207, 208–9, 211 vs ultrasound 356–7, 357 vs urethrocystoscopy 379 viral infections, lower urinary tract 619 virilization, female genitalia 1324, 1324 visceral injuries anti-incontinence surgery 1348, 1348 see also bowel injuries; rectal injury visceral nociceptors 609 visceral pain pelvic, neurobiology 607, 607–9 referred, mechanisms 609–10 vs somatic pain 609–10 visual accommodation, antimuscarinic effects 441, 442 visual analog scale (VAS) 803 bothersomeness 437 dry mouth 442–3, 443 frequency 436
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Index
voided volume 755, 766 ambulatory urodynamics 320 maximum 750, 763 uroflowmetry 217, 217 healthy volunteers 220 recording 220, 787 voiding diary values 201, 202 voiding ambulatory urodynamics 318 center, brainstem see pontine micturition center dysfunctional 756, 768 infrequent 587 interval between 436, 436 neural control 160, 571 obstructed see obstruction, bladder outflow phase, bladder cycle 148, 150–2 physiology see micturition, clinical physiology pressure–flow studies see pressure–flow studies prompted 417 reflexes 160 scheduled 417–20 see also bladder training symptoms related to 747–8, 761 timed 86–7, 417, 420 vaginal 1332, 1332 videourodynamics 304 see also bladder emptying voiding cystometry 226, 231 voiding cystourethrography (VCUG) see cystourethrography, voiding voiding diary (bladder diary) 198–203 duration 199–200 electronic 200, 435 ICI recommendations 806 ICS definition 750, 762 instructions 198–9 intelligent character recognition 200, 200 normative values 201, 201, 202 overactive bladder evaluation 433–5, 434, 436 painful bladder syndrome 596 paper 101, 198, 198, 200 physiotherapy assessment 476 stress incontinence evaluation 452, 452–3 therapeutic use 471 validity and reliability 199, 434–5 voiding difficulty/retention 587 voiding difficulty after anti-incontinence surgery 245–6, 832, 982–95
allograft slings 852, 889 autologous slings 847, 849–50, 885, 886–7 colpourethropexy 872–3, 873, 874, 875 combined with prolapse surgery 899 diagnostic evaluation 983–6 etiology 982–3 identifying risks 983 incidence 982 management 986–93 midurethral slings 895–7, 896 persistent 1350–2, 1351 presentation 983 SPARC sling 931–2 tension-free vaginal tape 921, 921, 952 transient 1350, 1351 transobturator tape 952, 952, 958, 959, 959 after hysterectomy 1364–5 after prolapse surgery 1020 after sacrospinous vault fixation 1060 children 1331–2 drug treatment 488–97, 589 non-neurogenic 584–91 causes 584–6, 585 investigations 587–8 presenting symptoms 586–7 signs 587 postpartum 585 pregnancy 684 prophylactic treatment 588 psychogenic 585 sacral nerve stimulation 589, 1276, 1277 symptoms 190–1 treatment 588–9 uroflowmetry 220, 221, 587 see also urinary retention voiding dysfunction classification 174–81 expanded to include pelvic floor activity 177–80, 178–9 by function/activity 174–6, 175, 176 by symptoms 174 complex, videourodynamics 310, 311 drug treatment 486–532 infection risk 618 neurogenic see neurogenic voiding dysfunction voiding time 217, 755, 766 healthy volunteers 220, 220 vulval pain 748 syndrome 749 vulvar lipoplasty 1379
vulvodynia 749 vulvovaginal candidiasis 647–8, 648, 649 vulvovaginitis allergic 649, 651 voiding difficulty 584 ‘warning time’ effects of darifenacin 501–2 measurement 433–4 water, cystometry filling medium 227–8 water births 1107 Watson, B.P. 7 Watts factor 236 websites, national continence organizations 78 weight loss 408–9, 471–2 nulliparous women 678 preoperative 828 prevention of incontinence 396 whiff test 646 whistle-tipped catheter 543, 543 willingness-to-pay assessment 65, 68, 439 wolffian ducts 131, 132, 133, 134 müllerian duct interactions 130, 131 Women’s Health Australia 40, 42, 44–6 Women’s Health Initiative 20, 395, 461, 520, 703 work heavy lifting 409, 421, 1005 measures of overactive bladder impact 439 pelvic organ prolapse and 1005 World Health Organization (WHO) definition of health 24, 438 definition of quality of life 438 episiotomy recommendation 1103 Wound, Ostomy and Continence Nurses Society (WOCN) 94, 96 wound infections anti-incontinence surgery 1349, 1349 colpourethropexy 873, 873 laparoscopic surgery 1214 prophylaxis 831 tension-free vaginal tape 921 transvaginal bone-anchor slings 938 xenografts, for slings 846, 853, 853–4, 885–8, 914 X-rays, lumbosacral spine 336 yolk sac 128, 128 zero pressure 226, 317, 792 Zuidex™ system 862, 973, 973–4
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