Urogynecology and Reconstructive Pelvic Surgery Third edition
1600 John F. Kennedy Blvd. Suite 1800 Philadelphia, PA 19103-2899 UROGYNECOLOGY AND RECONSTRUCTIVE PELVIC SURGERY Copyright © 2007, 1999, 1993 by Mosby Inc., an affiliate of Elsevier Inc.
ISBN-13: 978-0-323-02902-5 ISBN-10: 0-323-02902-7
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Notice Knowledge and best practice in this field are constantly changing. As new research and experience broaden our knowledge, changes in practice, treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on their own experience and knowledge of the patient, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the Editors assumes any liability for any injury and/or damage to persons or property arising out or related to any use of the material contained in this book. The Publisher
Library of Congress Cataloging-in-Publication Data Urogynecology and reconstructive pelvic surgery/[edited by] Mark D. Walters, Mickey M. Karram. – 3rd ed. p.; cm. Includes bibliographical references and index. ISBN 0-323-02902-7 1. Urogynecology. 2. Pelvis–Surgery. 3. Generative organs, Female–Surgery. I. Walters, Mark D. II. Karram, Mickey M. [DNLM: 1. Genital Diseases, Female. 2. Fecal Incontinence. 3. Urinary Incontinence. 4. Urodynamics. 5. Urogenital Surgical Procedures. 6. Uterine Prolapse. WJ 190 U775 2007] RG484.W35 2007 616.6–dc22 2006044898 Acquisitions Editor: Rebecca S. Gaertner Developmental Editor: Martha Limbach Project Manager: Bryan Hayward
Printed in The United States of America. Last digit is the print number: 9 8 7 6 5 4 3 2 1
To Ginny, for over 20 years of love and friendship, and to my children, Samantha, Max, and Zoe, who continue to make me proud. Mark D. Walters In memory of my mother, Mary Karram, for her love, kindness and unselfish support. To my father, Mike Karram, Sr., for instilling in me the values of education, discipline, and hard work. Mickey M. Karram
Acknowledgments We would like to acknowledge the indispensable and exemplary work of Beth Dobish and Rose Sirks for the huge volume of administrative support and transcribing work involved in this book, and Joe Chovin from Cincinnati and
Ross Papalardo from Cleveland Clinic for their creation of particularly clear surgical, anatomic, and urodynamic drawings. We also wish to again thank Dr. Anne M. Weber for her invaluable medical editing of our manuscripts.
List of Authors Matthew D. Barber, MD
Kathryn L. Burgio, PhD
Director of Clinical Research Section of Urogynecology and Reconstructive Pelvic Surgery Department of Obstetrics and Gynecology Cleveland Clinic Cleveland, Ohio Neurophysiologic Testing for Pelvic Floor Disorders; Outcome and Quality-of-Life Measures in Pelvic Floor Research
Associate Director for Research Birmingham VA Medical Center Birmingham, Alabama Stress Urinary Incontinence and Pelvic Organ Prolapse: Nonsurgical Management
J. Thomas Benson, MD Clinical Professor, Department of Obstetrics and Gynecology Indiana University Medical Center Director of Obstetrics and Gynecology Education Methodist Hospital of Indiana Indianapolis, Indiana Neurophysiology and Pharmacology of the Lower Urinary Tract
Alfred E. Bent, MD, FRCSC Professor and Head, Division of Gynaecology Dalhousie University Department of Obstetrics and Gynaecology Halifax, Nova Scotia, Canada Endoscopic Evaluation of the Lower Urinary Tract; Urethral Injection of Bulking Agents for Intrinsic Sphincter Deficiency
Jerry Blaivas, MD Clinical Professor of Urology Weill Medical College of Cornell University New York Presbyterian Hospital and Lenox Hill Hospital New York, New York Urodynamics: Cystometry and Urethral Function Tests
Raymond A. Bologna, MD Assistant Professor of Urology Northeastern Ohio University College of Medicine Akron, Ohio Painful Bladder Syndromes
Geoffrey W. Cundiff, MD Professor Department of Obstetrics and Gynecology University of British Columbia Vancouver, B.C., Canada Endoscopic Evaluation of the Lower Urinary Tract
Nicole Fleischmann, MD Assistant Professor Department of Urology Mount Sinai School of Medicine New York, New York Voiding Dysfunction and Urinary Retention
Tara L. Frenkl, MD, MPH Fellow, Female Pelvic Medicine and Reconstructive Surgery Glickman Urologic Institute Cleveland Clinic Cleveland, Ohio Sacral Neuromodulation Therapy
W. Thomas Gregory, MD Assistant Professor Division of Urogynecology and Reconstructive Pelvic Surgery Department of Obstetrics and Gynecology Oregon Health and Science University Portland, Oregon Obstetrics and Pelvic Floor Disorders vii
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List of Authors
Alexander G. Heriot, MD, MA, FRCS
Steven D. Kleeman, MD
Advanced Colorectal Fellow The Department of Colorectal Surgery Cleveland Clinic Cleveland, Ohio Rectal Prolapse
Assistant Professor Department of Obstetrics and Gynecology University of Cincinnati Cincinnati, Ohio Overactive Bladder Syndrome and Nocturia; Urinary Tract Infection
Wen-Chen Huang, MD Division of Urogynecology Department of Obstetrics and Gynecology Cathay General Hospital Taipei, Taiwan, Republic of China Radiologic Studies of the Lower Urinary Tract and Pelvic Floor
Tracy L. Hull, MD Head, Section of Anal Physiology Department of Colorectal Surgery Cleveland Clinic Cleveland, Ohio Fecal Incontinence
W. Glenn Hurt, MD Professor Department of Obstetrics and Gynecology Medical College of Virginia Richmond, Virginia Gynecologic Injury to the Ureters, Bladder and Urethra: Prevention, Recognition and Management
J. Eric Jelovsek, MD Section of Urogynecology and Reconstructive Pelvic Surgery Department of Obstetrics and Gynecology Cleveland Clinic Cleveland, Ohio Constipation
Mickey M. Karram, MD Director, Division of Urogynecology and Reconstructive Pelvic Surgery Good Samaritan Hospital Professor of Obstetrics and Gynecology University of Cincinnati School of Medicine Cincinnati, Ohio Urodynamics: Cystometry and Urethral Function Tests; Urodynamics: Voiding Studies; Sling Procedures for Stress Urinary Incontinence; Surgical Treatment of Vaginal Vault Prolapse and Enterocele; Obliterative Procedures for Vaginal Prolapse; Rectovaginal Fistula and Perineal Breakdown; Overactive Bladder Syndrome and Nocturia; Urinary Tract Infection; Lower Urinary Tract Fistulas
Tristi W. Muir, MD Assistant Professor Section of Female Pelvic Medicine and Reconstructive Surgery Department of Obstetrics and Gynecology Scott & White Clinic Temple, Texas Surgical Treatment of Rectocele and Perineal Defects
Edward R. Newton, MD Professor and Chairman Department of Obstetrics and Gynecology East Carolina University Greenville, North Carolina The Urinary Tract in Pregnancy
Victor W. Nitti, MD Associate Professor and Vice Chairman Director of Residency Training Department of Urology New York University School of Medicine New York, New York Voiding Dysfunction and Urinary Retention
Ingrid Nygaard, MD, MS Professor Department of Obstetrics and Gynecology University of Utah Salt Lake City, Utah Obstetrics and Pelvic Floor Disorders
Marie Fidela R. Paraiso, MD Section of Urogynecology and Reconstructive Pelvic Surgery Department of Obstetrics and Gynecology Cleveland Clinic Cleveland, Ohio Laparoscopic Surgery for Stress Urinary Incontinence and Pelvic Organ Prolapse; The Use of Biologic Tissue and Synthetic Mesh in Urogynecology and Reconstructive Pelvic Surgery
List of Authors
ix
Raymond R. Rackley, MD
Anthony P. Tizzano, MD
Co-Head, Section of Female Urology and Voiding Dysfunction Glickman Urological Institute Cleveland Clinic Cleveland, Ohio Sacral Neuromodulation Therapy
Wooster Clinic Wooster, Ohio Historical Milestones in Female Pelvic Surgery, Gynecology, and Female Urology
Feza H. Remzi, MD
Co-Head, Section of Female Urology and Voiding Dysfunction Glickman Urological Institute Cleveland Clinic Cleveland, Ohio Urethral Diverticula
Colorectal Surgeon Department of Colorectal Surgery Cleveland Clinic Cleveland, Ohio Rectal Prolapse
Holly E. Richter, PhD, MD Associate Professor Department of Medical and Surgical Gynecology University of Alabama–Birmingham Medical Center Birmingham, Alabama Stress Urinary Incontinence and Pelvic Organ Prolapse: Nonsurgical Management
Baha M. Sibai, MD Professor Department of Obstetrics and Gynecology University of Cincinnati Cincinnati, Ohio The Urinary Tract in Pregnancy
William Andre Silva, MD Pacific Northwest Gynecology Federal Way, Washington Obliterative Procedures for Vaginal Prolapse
Andrew M. Steele, MD Department of Obstetrics, Gynecology and Women's Health Saint Louis University School of Medicine St. Louis, Missouri Case Presentations with Expert Discussions
Kevin J. Stepp, MD Urogynecology and Reconstructive Pelvic Surgery MetroHealth Medical Center Cleveland, Ohio Anatomy of the Lower Urinary Tract, Rectum, and Pelvic Floor
Carmen J. Sultana, MD Assistant Professor Thomas Jefferson Medical College Philadelphia, Pennsylvania Bladder Drainage and Urinary Protective Methods
Sandip P. Vasavada, MD
Mark D. Walters, MD Head, Section of General Gynecology, Urogynecology and Reconstructive Pelvic Surgery Department of Obstetrics and Gynecology Cleveland Clinic Cleveland, Ohio Anatomy of the Lower Urinary Tract, Rectum, and Pelvic Floor; Neurophysiology and Pharmacology of the Lower Urinary Tract; Description and Classification of Lower Urinary Tract Dysfunction and Pelvic Organ Prolapse; Evaluation of Urinary Incontinence and Prolapse: History, Physical Examination, and Office Tests; Radiologic Studies of the Lower Urinary Tract and Pelvic Floor; Pathophysiology of Urinary Incontinence; Retropubic Operations for Stress Urinary Incontinence; Sling Procedures for Stress Urinary Incontinence; Surgical Correction of Anterior Vaginal Wall Prolapse; Surgical Treatment of Vaginal Vault Prolapse and Enterocele; Case Presentations with Expert Discussions
Anne M. Weber, MD Pelvic Floor Disorders Program National Institutes of Health Bethesda, Maryland Epidemiology and Psychosocial Impact of Pelvic Floor Disorders
James L. Whiteside, MD Assistant Professor Dartmouth-Hitchcock Medical Center Dartmouth Medical School Lebanon, New Hampshire Pathophysiology of Urinary Incontinence; The Effects of Gynecologic Cancer on Lower Urinary Tract Function
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List of Authors
Kristene E. Whitmore, MD Clinical Associate Professor Department of Urology Drexel University Director, Pelvic and Sexual Health Institute Graduate Hospital Philadelphia, Pennsylvania Painful Bladder Syndromes
Massarat Zutshi, MD Clinical Associate Department of Colorectal Surgery Cleveland Clinic Cleveland, Ohio Fecal Incontinence We wish to specially acknowledge the following physicians who we believe represent some of the true experts in the fields of urogynecology/reconstructive pelvic surgery, urology, and colorectal surgery, and who reviewed the case presentations in Chapter 40 and provided their opinions.
Michael P. Aronson, MD, Worcester, Massachusetts
John B. Gebhart, MD, Rochester, Minnesota Howard B. Goldman, MD, Cleveland, Ohio Cheryl B. Iglesia, MD, Washington, DC Lisa C. Labin, MD, Worcester, Massachusetts Fah Che Leong, MD, St. Louis, Missouri Christopher F. Maher, MD, Brisbane, Australia Mary T. McLennan, St. Louis, Missouri G. Rodney Meeks, MD, Jackson, Mississippi John R. Miklos, MD, Atlanta, Georgia Ingrid Nygaard, MD, Salt Lake City, Utah Rachel Pauls, MD, Cincinnati, Ohio Rebecca G. Rogers, MD, Albuquerque, New Mexico
Matthew D. Barber, MD, Cleveland, Ohio
Carlos J. Sarsotti, MD, Buenos Aires, Argentina
Alfred E. Bent, MD, Halifax, Canada
Bobby Shull, MD, Temple, Texas
Linda Brubaker, MD, Chicago, Illinois
Andrew C. Steele, MD, St. Louis, Missouri
Richard C. Bump, MD, Indianapolis, Indiana
James P. Theofrastous, MD, Asheville, North Carolina
Susan M. Congilosi, MD, Minneapolis, Minnesota Jeffrey L. Cornella, MD, Scottsdale, Arizona Patrick J. Culligan, MD, Morristown, New Jersey Geoffrey W. Cundiff, MD, Vancouver, B.C., Canada Peter L. Dwyer, MD, Melbourne, Australia Stephen P. Emery, MD, Pittsburgh, Pennsylvania
Paul K. Tulikangas, MD, Hartford, Connecticut Sandip P. Vasavada, MD, Cleveland, Ohio Brett J. Vassallo, MD, Park Ridge, Illinois Anthony G. Visco, MD, Chapel Hill, North Carolina
Andrew J. Walter, MD, Sacramento, California
Foreword During the past 30 years the management of disorders of the pelvic floor has assumed an increasingly important role for gynecologists, urologists, and colon and rectal surgeons. Organizations such as the American Urogynecologic Society and the Society of Gynecologic Surgeons were formed to provide a more structured environment for physicians, nurses, and other medical providers to share their experiences in the care of women with disorders of the pelvic floor. Internationally, organizations such as the International Continence Society and the International Urogynecologic Association have provided a similar forum for physicians worldwide. Drs. Mark Walters and Mickey Karram are leaders who have been recognized nationally and internationally for their contributions to patient care, education, and research. Their book, Urogynecology and Reconstructive Pelvic Surgery, has been an invaluable reference for doctors around the world. In their Third Edition, Drs. Walters and Karram have assembled a multidisciplinary group of authors who represent the perspective of all surgical specialists involved in the care of women with disorders of the pelvic floor. All of the authors are individually committed to excellence in patient care, education, and research. Many of the current and future leaders in our discipline have been educated under the tutelage of these men and women. The current edition has been updated to include discussions on the use
of materials and mesh in reconstructive surgery, the place of neuromodulation in disorders of the pelvic floor, and a chapter on outcomes analysis and the evaluation of qualityof-life measures and research. I personally have found their text to be valuable not only in the care of my own patients, but in the education of residents, fellows, and practitioners. The section on case presentations with expert discussion in particularly valuable because of its clinical relevance. Drs. Walters and Steele have assembled a group of well-respected experts to give their opinions on the management of problems that many of us face on a regular basis. I find the format of the text to be very satisfying, beginning with an overview of the history of the subject matter followed by a discussion of the pathophysiology, the clinical evaluation, and the clinical treatment options available to our patients. The inclusion of discussion of research methods is timely and appropriate. My hope is that, in the future, investigators will have learned enough about the pathophysiology of disorders of the pelvic floor that we can have a chapter on prevention strategies. As Drs. Walters and Karram and their contributing authors continue to educate future clinicians and scientists, prevention is a realistic goal. Bob L. Shull, M.D. Professor of Obstetrics and Gynecology Scott & White Clinic and Hospital
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Preface As the population lives longer and has improved health, the prevalence of various pelvic floor disorders is increasing. The term pelvic floor disorders incorporates a broad array of inter-related clinical conditions that includes urinary incontinence, pelvic organ prolapse, fecal incontinence, sensory and emptying abnormalities of the lower urinary tract, defecatory dysfunction, and sexual dysfunction. More than half of women experience one or more of these disorders for some period in their lives, and one in nine will undergo surgery for pelvic floor abnormalities by age 80. Economic analyses estimate that the total annual cost of urinary incontinence in the United States alone is up to $19.5 billion. Beyond the economic costs and general health care burden, pelvic floor disorders result in significant psychosocial costs and can have a profound impact on an individual's quality of life. Women desire and are able to remain active longer and are less interested in tolerating the lower quality of life that accompanies these conditions. This leads to a greater number of otherwise healthy women presenting to their physicians with various pelvic floor disorders. It is estimated that the growth and demand for services to care for women with pelvic floor disorders will increase at twice the rate of growth of the population over the next 30 years. International interest in diseases of women and older persons in general has helped to increase awareness of the high prevalence of urinary and fecal incontinence in women. Clinical care guidelines were developed by the National Institute on Aging and the Office of Medical Application of Research within the National Institutes of Health in conjunction with other agencies. This was followed by expanded national research funding; the resulting research data and manuscripts are now gradually being reported. The demographics of incontinence also have stimulated corporate interest, and many new drugs, products, and surgical devices for the evaluation and treatment of pelvic floor disorders have been or are being developed. Recent popularity and increased circulation of journals such as International Urogynecology Journal (Springer Publishing) and Neurourology and Urodynamics (Wiley Publishing) underscore the heightened level of interest among clinicians and researchers. Furthermore, the expanding membership and attendance at annual meetings of the American Urogynecology Society (AUGS), the International Continence Society (ICS), and
the International Urogynecology Association (IUGA) are evidence to this specialty's popularity. The First International Consultation on Incontinence held in 1998 in Monaco further highlighted the plight of some 200 million sufferers from urinary incontinence worldwide. The Third Consultation on Incontinence was held in June 2004 and was represented by an international faculty of almost 200 individuals from a wide range of professions and specialties. The spectrum of subcommittees spanned all of the basic and clinical problems of pelvic floor disorders and led to a recent comprehensive publication from this group. There continues to be a widespread need for education and training in urogynecology and reconstructive pelvic surgery for practicing generalists and residents in obstetrics and gynecology. More physicians with special expertise in urogynecology and vaginal and laparoscopic surgery are needed to meet the increasing patient volume and the additional training needs within this specialty. Over the last 10 years, the specialty of Urogynecology—since renamed Female Pelvic Medicine and Reconstructive Surgery—has expanded to a fourth subspecialty approved by the American Board of Obstetrics and Gynecology. Formal 3-year fellowships conform with the other subspecialties and allow for advanced training and research. This updated textbook is an effort to address the educational needs of physicians and advanced care practitioners interested in female pelvic floor disorders and to serve as a core reference text in urogynecology and reconstructive pelvic surgery. The third edition of Urogynecology and Reconstructive Pelvic Surgery is a clinically oriented yet comprehensive textbook addressing our subspecialty. We believe that this subject fundamentally encompasses three main topics: female urinary incontinence and voiding dysfunction, pelvic organ prolapse, and disorders of defecation. This book is separated into nine sections. Chapter 1 is a new chapter reviewing historical milestones in pelvic surgery and female urology. Chapters 2 through 5 describe in detail basic principles and subjects needed to understand and treat disorders of the lower urinary tract and pelvic floor. Chapters 6 through 11 outline basic and advanced concepts in the evaluation of lower urinary tract and pelvic floor disorders in woman. Chapters 12 through 23 present management guidelines for women with stress urinary incontinence and pelvic organ prolapse. Chapters xiii
xiv
Preface
24 through 27 address disorders of defecation. Chapters 28 through 31 address the subjects of overactive bladder and painful and irritative voiding disorders, as well as their expanding list of innovative treatments. Chapters 32 through 38 discuss specific conditions and special subjects that are occasionally encountered by physicians treating patients with pelvic floor disorders. In a new section, Chapter 39 reviews important research methods regarding outcome analysis and quality-of-life measures in pelvic floor research. Finally, using an innovative and popular format, Chapter 40 presents a series of 19 interesting and difficult cases, with opinions from international experts in urogynecology, urology, colorectal surgery, and obstetrics. The Third Edition has been expanded to include historical highlights, neurophysiologic testing and more complete information on neuromodulation therapy, the latest information on the use of biologic and synthetic prosthesis
in urogynecologic and reconstructive pelvic surgery, and important concepts on research methods in pelvic floor research. Because female incontinence is best managed in a multidisciplinary fashion, recognized authorities in urology, maternal fetal medicine, and colorectal surgery have contributed chapters related to their particular areas of expertise. Some of the original drawings from the First and Second Editions are retained, but a large number of new anatomic and surgical drawings were added. We hope that this book will meet the training needs of residents in obstetrics and gynecology, urology, and other specialties and can be used by fellows in Female Pelvic Medicine and Reconstructive Surgery and Female Urology as an important reference text. We also hope that generalists and urogynecologists alike will find it interesting and useful as they strive to take better care of their patients.
Historical Milestones in Female Pelvic Surgery, Gynecology, and Female Urology
1
Anthony P. Tizzano
ON THE SHOULDERS OF GIANTS: AN INTRODUCTION 1 GYNECOLOGY IN ANTIQUITY: THE EBERS PAPYRUS TO THE 5TH CENTURY 1 MEDIEVAL MEDICINE: THE AGE OF FAITH (AD 476 TO 1453) 1 THE RENAISSANCE: 1453 TO 1600 4 THE SEVENTEENTH CENTURY: THE CLARIFICATION OF ANATOMY, EMBRYOLOGY, AND PHYSIOLOGY 4 THE EIGHTEENTH CENTURY: THE OLD VERSUS THE NEW 4 THE NINETEENTH CENTURY BEFORE THE ASEPTIC AGE: THE RISE OF GYNECOLOGY 7 THE MID-NINETEENTH CENTURY: THE DAWN OF ASEPTIC SURGERY 8 THE TWENTIETH CENTURY: A SUBSPECIALTY EVOLVES 11
GYNECOLOGY IN ANTIQUITY Gynecology in antiquity finds its roots in the Ebers papyrus (1500 bc) that portrayed the uterus as a wandering animal— usually a tortoise, newt, or crocodile—capable of movement within its host. Hippocrates perpetuated this animalistic concept, stating that the uterus often went wild when deprived of male semen. He provided the earliest description of a pessary, using a pomegranate to reduce uterine prolapse and using catheters fashioned from tin and lead to irrigate and drain the uterus. The seven cells doctrine of the Common Era replaced the animalistic concept, depicting the uterine cavity as being divided into seven compartments whereby male
ON THE SHOULDERS OF GIANTS From the earliest days of recorded medical history, physicians struggled with the problems of pelvic organ prolapse (Fig. 1-1), urinary incontinence, and vesicovaginal fistula. An inadequate understanding of pelvic anatomy plagued practitioners before the nineteenth century. Ignorance of asepsis, the absence of anesthesia, faulty suture materials, inadequate instrumentation, and suboptimal exposure delayed any consistent success until the mid-nineteenth century. The evolution of pelvic surgery from the Hippocratic age to the antiseptic period is a fascinating one, where original theories occasionally fell from favor only to be resurrected and popularized by subsequent generations. Equally intriguing is the development of a wide array of innovative instrumentation and materials that often paralleled many surgical advances. This chapter is an attempt to touch upon the milestones that occurred along the way and to pay homage to the pioneers who helped shape a specialty and upon whose shoulders we stand. The author's selection of important milestones in our specialty up to 1961 is shown in Table 1-1. Note that this chapter emphasizes American contributions and milestones that influenced contemporary thought, patient care, and surgical practices. I am grateful for the works of Dr. Thomas Baskett, Dr. James V. Ricci, and, particularly, Dr. Harold Speert, whose extensive research on the subject made this chapter possible.
Figure 1-1 ■ Sixteenth-century woodcut showing examination of women with uterine prolapse. (From Stromayr C. Die Handschrift des Schnitt-und Augenarzles Caspar Stromayr, Lindau Munscript, 1559.)
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Part 1
Table 1–1
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History
Timeline of Milestones Related to Pelvic Surgery and Female Urology
Second half of first century AD Soranus’s (De Morbis Mulierum) first good description of the human uterus. 1561 First accurate description of the human oviduct. Observationes Anatomicae by Gabriele Falloppio. 1672 First accurate account of the female reproductive organs and ovarian follicles (“Graafian Follicles”) De Mulierum Organis Generationi Inservientibus by Regnier de Graaf. 1677 Description of the vulvovaginal glands,”Bartholin Glands.” De Ovariis Mulierum by Caspar Bartholin. 1691 Description of the female inguinal canal. Adenographia by Anton Nuck. 1705 François Poupart describes the inguinal ligament and its function. 1727 Jacques Garengeot modifies a trivalve speculum to better differentiate ”vaginal hernias” during pelvic examination. 1737 Description of the peritoneum and posterior cul-de-sac. A Description of the Peritoneum by James Douglas. 1759 Description of the embryonic mesonephros or ”Wolffian Body and Duct.” Theoria Generationis by Caspar Fredrich Wolff. 1774 William Hunter completes his monumental work, Anatomy of the Gravid Uterus, which remains the finest work on uterine anatomy to date. 1801 Joseph Claude Récamier popularizes the use of a tubular vaginal speculum to treat ulcers and infections of the vagina and cervix. 1803 Pieter Camper describes the superficial layer of abdominal fascia. 1804 Astley Paston Cooper describes the ligamentous covering of the pubis and its condensation above the linea ileo-pectinea as it extends from the pubis outward. 1805 Philipp Bozzini introduces his lichtleiter (light conductor), the earliest endoscope. 1809 Ovariotomy is performed by Ephraim McDowell. 1813 Conrad Johann Martin Langenbeck carries out the first planned and successful vaginal hysterectomy. 1825 Marie Anne Victorie Boivin devises the bivalve vaginal speculum. 1836 Charles Pierre Denonvilliers describes the rectovesical fascia. 1838 John Peter Mettauer uses lead sutures to perform the first surgical correction of vesicovaginal fistula in the United States. 1849 Anders Adolf Retzius describes prevesical space. 1852 James Marion Sims describes his knee-chest positioning of patients for vesicovaginal fistula repair. 1860 Hugh Lenox Hodge details the use of his pessary to correct for uterine displacement. 1877 Léon Le Fort describes his method of partial colpocleisis as a simple and safe means for treatment of uterine prolapse. 1877 Max Nitze introduces an electrically illuminated cystoscope. 1878 T.W. Graves designs a speculum that combines features of both bivalve and Sims’s specula. 1879 Alfred Hegar introduces his metal cervical dilator to replace laminaria. 1890 Friedrich Trendelenburg describes his technique for positioning patients to facilitate a transvesical approach in the repair of vesicovaginal fistula. 1893 Howard Atwood Kelly devises the air cystoscope for inspection of the bladder and identification and catheterization of the ureters. 1895 Alwin Mackenrodt provides a comprehensive and accurate description of the pelvic connective tissue and correlation with pelvic prolapse. 1898 Ernst Wertheim performs radical hysterectomy for cervical cancer. 1899 Thomas James Watkins performs an ”interposition” operation for treatment of uterine prolapse associated with cystocele. Thus, the uterus is brought forth through an anterior colpotomy incision and sutured under the anterior vaginal wall, with the cervix secured posteriorly. The markedly anteverted uterus essentially pivots on twisted broad ligaments, thus producing antagonistic forces, because any dropping of the bladder increases the anterior displacement of the uterus, and any prolapse of the uterus elevates the cystocele. 1900 David Todd Gilliam describes his method of uterine ventrosuspension, whereby he ligated the proximal round ligament and attached it to the anterior rectus sheath lateral to the rectus muscle. 1900 Hermann Johannes Pfannenstiel introduces a transverse incision for laparotomy. 1901 Alfred Ernest Maylard advocates the oblique transection of the rectus muscles to improve exposure. 1901 John Clarence Webster and John Baldy introduce their suspension technique for correction of uterine retroversion, whereby the proximal round ligament is brought under an opening made under the utero-ovarian ligament and, ultimately, secured at just above the uterosacral ligament. 1909 George Reeves White noted that certain cases of cystocele were due to lateral paravaginal defects and thus could be repaired by reconnecting the vagina to the ”white line” of the pelvic fascia. 1910 Max Montgomery Madlener introduces a popular female sterilization technique using ligation of the tube alone. 1911 Max Brödel becomes head of the world’s first Department of Medical Illustration at Johns Hopkins University. 1912 Alexis Victor Moschcowitz describes the passage of silk sutures around the cul-de-sac of Douglas to prevent prolapse of the rectum. 1913 Howard Atwood Kelly describes the Kelly plication stitch, a horizontal mattress stitch placed at the urethrovesical junction to plicate the pubocervical fascia and ”reunite the sphincter muscle.” 1914 Wilhelm Latzko describes a technique for vaginal closure of vesicovaginal fistula following hysterectomy. 1915 Arnold Sturmdorf introduces his tracheloplasty technique. 1917 W. Stoeckel is the first to successfully combine a fascial sling and sphincter plication for treatment of stress urinary incontinence. 1929 Ralph Hayward Pomeroy devises a method of female sterilization involving ligation and resection of the tube. 1940 Noble Sproat Heaney describes his technique for vaginal hysterectomy using a clamp, needle holder, and retractor of his own design. His method for closing the vaginal cuff that incorporates peritoneum, vessels, and ligaments is known as the ”Heaney stitch.” 1941 Leonid Sergius Cherney suggests a modified low transverse abdominal incision, whereby the rectus muscle is cut at its very insertion into the pubis to provide better access to the space of Retzius. 1941 Raoul Palmer popularizes the use of the laparoscope in gynecology. 1942 Albert H. Aldridge reports on rectus fascia transplantation as a sling for relief of stress urinary incontinence. 1946 Richard W. TeLinde continues the Johns Hopkins legacy in gynecology with the introduction of his text, Operative Gynecology. 1948 Arnold Henry Kegel describes his progressive resistance exercise to promote functional restoration of the pelvic floor and perineal muscles. 1949 Victor Marshall, with Marchetti and Krantz, describe retropubic vesicourethral suspension for stress urinary incontinence. 1957 Milton L. McCall describes his posterior culdoplasty to prevent or treat enterocele formation at vaginal hysterectomy. 1961 John Christopher Burch introduces his method of urethrovaginal fixation for treatment of stress urinary incontinence.
Chapter 1
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Historical Milestones in Female Pelvic Surgery, Gynecology, and Female Urology
embryos developed on the right, females on the left, and hermaphrodites in the center. Similar notions remained popular until the Middle Ages. Soranus of Ephesus (ad 98 to 138) is commonly considered the foremost gynecologic authority of antiquity. He described the uterus based on human dissection and performed a hysterectomy for uterine prolapse. His writings provided the foundation for gynecologic texts up to the seventeenth century. The ancients used instruments fashioned from tin, iron, steel, lead, copper, bronze, wood, and horn. Those made of iron and steel were likely quite popular, but very few survived the oxidation of more than two millennia. Gynecologic instruments from the first century bc were unearthed at Pompeii, including forceps, catheters, scalpels, as well as massive bivalve, trivalve, and quadrivalve vaginal specula.
MEDIEVAL MEDICINE The medieval period (Middle Ages) (ad 476 to 1453), from the Fall of Rome to the Goths to the Fall of Constantinople to the Turks, are often referred to as the Age of Faith or Era of Monastatic Medicine, when confidence in any one individual was replaced by divine trust. As such, St. Benedict, founder of the Benedictine Order, encouraged his monks to tend to the sick but forbade any formal study of medicine. The struggle against leprosy, plagues, and prostitution was the focus of the day, and little was added to the fund of medical knowledge. Surgery rarely took place during the period, and the majority of physicians were itinerant practitioners, many of whom were quacks and charlatans.
THE RENAISSANCE The Renaissance period was marked by the rebirth of individualism and the release from the ban of authority. The rise of universities, the printing press, and the subsequent emergence of self-education elevated medicine to the next level and provided for a clearer understanding of female anatomy. Leonardo da Vinci (1452–1519), founder of iconographic and physiologic anatomy, provided the basis for modern anatomic illustration. His illustrations of female pelvic anatomy provide the earliest accurate descriptions of the fetus in utero. Unfortunately, his sketches were seen by only a few of his contemporaries and were not published until the end of the nineteenth century. The first authenticated report of vaginal hysterectomy was given by Giacomo Berengario Da Capri (1470–1550) in 1521. He described two cases: one performed by him in 1507 and the other by his father. Ambrose Paré (1510–1590), a renowned military surgeon of the period, was the first to introduce vascular ligatures for hemostasis in place of cautery. However, the use of ligatures was not popularized until Baron Joseph Lister (1827–1912), a British surgeon, introduced a longer lasting aseptic suture in the mid-nineteenth century. Andreas Vesalius (1514–1564) commissioned Jan Stefan van Kalkar to produce the most famous anatomic illustrations of all time, revolutionizing the science of anatomy and
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the manner in which it was taught. He was among the first to successfully challenge the teachings of Galen (ancient Greek physician) and asserted that the physician must perform cadaver dissection firsthand to learn the art. Hence, Vesalius made human dissection a viable and respectable profession. His illustrations provided an accurate description of the entire female urogenital tract and its vasculature, depicting the left ovarian vein entering the left renal vein for the first time. Distinguished pupils of Vesalius include Gabriele Falloppio (1523–1562), who provided the earliest accurate description of the human oviduct and who described the clitoris as a vasomuscular structure. Another pupil was Matthaeus Columbus (1484–1559), who is credited with the earliest use of the term labia, which he considered essential in protecting the uterus from dust, cold, and air. Last, his student Bartolomeo Eustachio (1520–1574) furnished the earliest accurate delineation of the uterine cavity and cervical canal. Among the more comprehensive accounts of sixteenth century gynecologic surgery is Caspar Stromayr's Practica Copiosa, which contains beautifully executed watercolors depicting diseases of women. Included are illustrations of the examination of uterine prolapse and placement of a pessary comprised of sponge bound by twine, sealed with wax, and dipped in butter (Figs. 1-2 and 1-3). Despite the many advances regarding pelvic anatomy during the Renaissance, the approach to most gynecologic problems changed very little from that which was popular during the classical period.
THE SEVENTEENTH CENTURY Throughout the seventeenth century, theories regarding physiology, generation, and anatomy were clarified. Regnier de Graaf (1641–1673) described ovarian follicles and uterine fibroids and provided the first accurate account of the ovary's gross morphology, anatomic relations, and function. Pelvic surgery and instruments of the period are nicely portrayed by the engravings of Johannes Scultetus (1595–1645) in his Armamentarium Chirurgicum. He was the first to use a series of illustrations to provide a stepwise account of surgical procedures (Fig. 1-4). Included are examples of treatment of imperforate hymen, hematocolpos, clitoral hypertrophy, and the use of a T-binder following vaginal surgery.
THE EIGHTEENTH CENTURY The eighteenth century might be best characterized by the constant conflict that occurred between old and new ideas. As such, relatively few advances occurred in medicine while numerous notable contributions were made in the fields of natural philosophy, including microscopy, physics, and biology. Surgery during the century began to rise above the skills of an individual surgeon with the founding of surgical societies and the publishing of various medical journals. Physicians, however, remained under close public scrutiny at the hands of popular medical caricaturists, such as Thomas Rowlandson. Many outstanding contributions were made toward the
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Figure 1-4 ■ Seventeenth-century woodcut illustrating incision and drainage of a hematocolpos. (From Schultes J. Armamentarium Chirurgicum. Ulmae Suevorum, Balthasari, 1655.)
Figure 1-2 ■ Sixteenth-century woodcut depicting placement of a pessary to treat uterine prolapse. (From Stromayr C. Die Handschrift des Schnitt-und Augenarzles Caspar Stromayr, Lindau Munscript, 1559.)
Figure 1-3 ■ Sixteenth-century woodcut showing a pessary fashioned from a sponge, bound by twine, covered in wax, and dipped in butter before placement. (From Stromayr C. Die Handschrift des Schnitt-und Augenarzles Caspar Stromayr, Lindau Munscript, 1559.)
understanding of pelvic anatomy. In 1730, James Douglas gave the first adequate description of the peritoneum that helped to pave the way for retroperitoneal surgery and the concomitant decrease in peritonitis that typically plagued abdominal procedures during that time. Later, in 1774, William Hunter (1718–1783) completed his monumental work, Anatomy of the Gravid Uterus. Thanks to the artistic talent of Jan van Rymsdyk, many regard this work as the finest anatomical atlas ever produced, including Choulant (1791–1861), who described it as “anatomically exact and artistically perfect.” Vaginal specula continued to evolve with a modification in 1727 by RenéJacques-Croissant de Garengeot (1688–1759), who devised blades with a distinctly concave surface. Garengeot used the speculum for vaginal examinations and to differentiate the various “vaginal hernias” (presumably cystocele and rectocele) (Fig. 1-5) (Ricci, 1948–1949).
Figure 1-5 ■ Eighteenth-century vaginal speculum used to differentiate the various “vaginal hernias.”
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THE NINETEENTH CENTURY BEFORE THE ASEPTIC AGE Before the nineteenth century, surgical attempts at managing uterine prolapse and cervical disease were, for the most part, limited to amputation of the cervix. In 1813, Conrad Langenbeck (1776–1851) performed the first planned and successful vaginal hysterectomy. Moreover, he did so alone and without the benefit of anesthesia. “At one point Langenbeck was left clutching the bleeding area in one hand and holding one end of the ligature in his teeth while tying the other end with his right hand” (Baskett, 1996). The following occurred in America during the first half of the nineteenth century, before the aseptic age: Ephraim McDowell performed an ovariotomy in 1809; William Dewees published the first American textbook on gynecology in 1826; and James Marion Sims (Fig. 1-6) described the treatment of vesicovaginal fistula in 1838. The first successful operation for vesicovaginal fistula used lead suture and is believed to have been performed in August 1838 by John Peter Mettauer (1787–1875), a Virginia gynecologist. However, the first published report of an acceptable result did not appear until a year later when George Hayward, unaware of Mettauer's success and using silk for his repair, performed eight operations that resulted in only two cures, at the Massachusetts General Hospital. Mettauer is also credited with the introduction of metallic suture and a retention catheter.
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Surgical instruments manufactured during the preseptic era, which finally came to a close around 1890, were nothing short of extraordinary in terms of variety and beauty. “Surgical instruments made before 1890 exhibited standards of workmanship, fit, finish and overall artistry that were later sacrificed in the production of aseptic instruments. Moreover, instruments of the earlier period frequently incorporated rare and beautiful materials in their design, including ebony, tortoise shell, ivory, agate, gold and silver” (Edmonson, 1997). Among the most notable examples was the vaginal speculum that, as described by Ricci (1948–1949), continued to evolve with literally hundreds of modifications by inventors in an attempt to enhance exposure. Charriere introduced a novel form designed for use as a bivalve, threeblade, or four-blade speculum (Fig. 1-7) in 1838. The more familiar “duckbill” design used by clinicians today was initially put forth by Edward Gabriel Cusco in 1870. However, the most popular speculum currently in use was designed by T.W. Graves, a general practitioner from Massachusetts, and introduced more than a century ago in 1878. In 1845, Sims began a series of surgical experiments on his now legendary slaves, Anarcha, Betsy, and Lucy, who suffered from vesicovaginal fistulas. After nearly 40 fruitless attempts at fistula repair, over the course of 6 years, Sims finally succeeded. His triumph was due, in part, to his use of silver sutures and the exposure afforded him by a speculum of his own design and used with the patient in knee-chest position. Sims originally reported on his technique in January 1852 and then more formally in Silver Sutures in Surgery, his 1857 discourse before the New York Academy of Medicine. An immodest man, Sims declared, “Silver as a suture is the greatest surgical achievement of the century.” In a subsequent narrative Sims described the events surrounding his conception of the “Sims knee-chest position” (Fig. 1-8): “Full of thought I hurried home and the patient (with the vesicovaginal fistula) was placed in the position described, with an assistant on each side to elevate and retract the nates. I cannot, nor is it needful to describe my emotions, when the air rushed in and dilated the vagina to its greatest capacity, whereby its whole surface was seen at one view, for the first time by any mortal man. With this sudden flash of light, with the fistulous opening seen in its proper relations, all the principles of the operation were presented to my mind. And thus, in a moment, in the twinkling of an eye, new hopes and aspirations filled my soul, for a flood of dazzling light had suddenly burst upon my enraptured vision, and I saw in the distance the great and
Figure 1-6 ■ James Marion Sims (1813–1883). (From Clinical Notes on Uterine Surgery. London, 1866.)
Figure 1-7 ■ Four-valve vaginal speculum with detachable blades by Charriere, circa 1850, private collection.
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Figure 1-8 ■ Sims knee-chest position. (From Bourgery JM. Traitem Complet de L'Anatomie de L' Homme Comprenant la Medicine Operatorie. Guerin, Paris, 1866–1868.)
glories triumph that awaited determined and persevering effort. I thought only of relieving the loveliest of all God's creations of one of the most loathsome maladies that can possibly befall poor human nature…. Full of sympathy and enthusiasm, I found myself running headlong after the very class of sufferers that I had all of my professional life most studiously avoided.”
sized lithographs, nearly all of which are in the very realistic style of Nicolas Jacob” (Roberts and Tomlinson). Figure 1-9, A–C shows an example of Bourgery's work illustrating Sims's operation for vesicovaginal fistula. (Also see Color Plate 1.) The latter half of the century is marked by many noteworthy contributions to pelvic surgery and an improved understanding of pelvic anatomy. Anders Adolf Retzius defined the boundaries of the prevesical space in 1849. In 1877, Léon Clément Le Fort (1829–1893) described his procedure for partial colpocleisis, which continues to provide a simple and safe way to manage uterine prolapse in the highrisk patient. Alwin Mackenrodt (1859–1925) (Fig. 1-10) elegantly described the cause and cure of uterine prolapse in 1895 and put forth an accurate description of the pelvic connective tissue, including the transverse cervical or cardinal ligaments (Mackenrodt's ligaments) (Fig. 1-11). Soon thereafter, Archibald Donald (1908) and William Fothergill (1915) developed the Manchester operation, uniting parametrial and paravaginal tissues to one another anterior to the cervix to effectively counter uterine prolapse. Thomas Watkins proposed a novel approach to uterine prolapse and cystocele reduction by using the uterus as a prosthesis. He introduced his interposition operation in 1898, contending that it was ill-advised to remove the uterus in any case of
Although one may argue that Sims was not the first to use silver sutures in surgical repairs, most will concede that he was the first to combine the essentials for cure and thus popularize one of the first major innovations in pelvic surgery. Within the same decade, Washington Atlee performed a myomectomy in 1844, and Walter Burnham conducted the first successful abdominal hysterectomy in 1853.
THE MID-NINETEENTH CENTURY During the later half of the nineteenth century, the requisites for advancement of surgery began to fall into place. These included adequate anesthesia, antisepsis, and acceptable suture materials. Throughout the latter half of the century, the evolution of pelvic surgery gained momentum because advances in gynecologic therapy were unparalleled in the entire realm of medicine. For more than two millennia, therapy was primarily medical and, in less than half a century, it became surgical and spectacular. The rapidly increasing frequency of successful surgery was made possible by the advent of adequate anesthesia in 1846, Joseph Lister's treatise on asepsis in 1867, and his introduction of aseptic suture (silk soaked in carbolic) in 1869. The extraordinary range of pelvic surgical techniques performed before the last quarter of the nineteenth century is beautifully illustrated in Jean-Baptiste Marc Bourgery's and Nicolas Henri Jacob's magnificent Traite complet de l' anatomie comprenant la medicine operatorie (1831–1854). “In the entire literature of medicine during the nineteenth century there is nothing that compares with the 749 hand-colored folio-
Figure 1-9 ■ A series of watercolor lithographs depicting Sims's operation for vesicovaginal fistula. (From Bourgery JM. Traitem Complet de L'Anatomie de L' Homme Comprenant la Medicine Operatorie. Guerin, Paris, 1866–1868.) A. Trimming the edge of vesicovaginal fistula. (Note silver catheter in place.)
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cont’d B. Placement of silver sutures. C. Completed closure of fistula. (See Color Plate 1.)
prolapse unless it was diseased. Thus, through an anterior colpotomy incision, Watkins brought the uterus forward such that the bladder rests on the posterior wall of uterus, thereby elevating the lower uterine segment and creating antagonistic forces between the prolapsing bladder and uterus. During the same year, Ernst Wertheim (1864–1920) introduced and, ultimately, popularized radical hysterectomy to the extent that the procedure became known as the Wertheim operation (1900). The popularity of pessaries flourished throughout the latter half of the century because practitioners were apparently concerned with uterine malposition (Fig. 1-12; Color Plate 2). In 1860 Hugh Lenox Hodge (1796–1873) spoke for many gynecologists of the era, when he stated: “The mechanical treatment of uterine displacements by intravaginal supports is essential, a ‘sine qua non,’ for their perfect relief; that by pessaries, of suitable material, size and form, the uterus may very generally be replaced and be maintained in situ; that the local symptoms of weight, pain, etc., the leukorrhea, the menorrhagia, the dysmenorrhea, and all the innumerable direct and indirect symptoms of spinal and cerebral irritation, including neuralgia, nervous headache, nervous affections of the larynx, lungs, heart, stomach, bowels, etc., and also spasms, cramps, and convulsions, may often thus be dissipated; that the intellectual and spiritual being may be elevated from the lowest states of depression, bordering on melancholy,
or delivered from the highest degree of maniacal excitement. Patients often are amazed at their own altered sensations; they can hardly realize their identity—feeling as if they were either renovated, or that they had been transported to a ‘new world.’” Among the most important diagnostic and operative innovations of the century occurred in 1877, when Max Nitze (1848– 1906) introduced an electrically illuminated cystoscope. This made possible great improvements in surgery, including excision of bladder tumors in situ and endoscopic photography. Shortly afterward, in 1893, Howard Atwood Kelly (1858–1943) (Fig. 1-13) introduced his air cystoscope and published a bulletin on aeroscopic examination of the female bladder and the catheterization of the ureters under direct inspection (Figs. 1-14 and 1-15). His innovation occurred, in part, by accident while using a water cystoscope in the kneechest position. The instrument apparently fell to the floor, breaking the glass diaphragm. Kelly reintroduced the cystoscope into the bladder without its glass diaphragm, and the bladder immediately distended with air permitting visualization of its interior and ureteric orifices. Kelly's two-volume Operative Gynecology (1898), Medical Gynecology (1908), and Diseases of the Kidneys, Ureters, and Bladder (with Burnam, 1914)—the latter distinguished by the great illustrations by the German artist Max Brödel (1870–1941)—defined the specialty and laid the foundation for progress well into the
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F.2.
Fig.3.
F.6.
F.7.
F.5.
F.10.
F.8.
F.15.
Figure 1-12 ■ Various nineteenth-century pessaries. (From Bourgery JM. Traitem Complet de L'Anatomie de L' Homme Comprenant la Medicine Operatorie. Guerin, Paris, 1866–1868.) (See Color Plate 2.)
Figure 1-10 ■ Alwin Karl Mackenrodt (1859–1925). (From Baskett TF. Eponyms and Names in Obstetrics and Gynaecology. RCOG Press, London, UK, 1996, with permission.)
Figure 1-11 ■ An illustration of the cardinal ligaments in a fetus of 8 months. (From Mackenrodt A. Uber die Ursachen der normalen und pathologischen Lagen des Uterus. Arch Gynakol 1895;48:394, with permission.) U.Rd.d lig. truasp.coll
lig.sa.-ut
Fasr pelv ni. lig.transadert coll.
Hafd.d.lig. lat.corp.
Corp.ut.
Symph.
Uebg.d.sept.-i Fasc.pl. Sept.rerl.
Sept.ves.vag. Vag.wd.
Vag.wd.
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Figure 1-15 ■ Beginning catheterization of the left ureter in knee-chest posture through an open-air cystoscope. (From Kelly HA, Burnam CS. Diseases of the Kidneys, Ureters, and Bladder, vol. 1. D. Appleton & Co., New York, 1914, p. 269, fig. 141, with permission.)
Figure 1-13
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Howard Atwood Kelly (1858–1943).
sibly higher standard of ethics—there is no measure which can compare with the decrease in physical suffering in man, woman, and child when stricken by disease or accident…. This is the Promethean gift of the century to man.”
Retro pubic (5) Vertex (4) Right cornu (3) Sacral area (2)
Base (1)
Figure 1-14 ■ Various positions that air cystoscope may take to illuminate all parts of the bladder. (From Kelly HA, Burnam CS. Diseases of the Kidneys, Ureters, and Bladder, vol. 1. D. Appleton & Co., New York, 1914, p. 262, fig. 135, with permission.)
next century. With a thorough study of anatomy, gynecology, and surgery, Brödel revolutionized the appearance of medical literature and went on to become head of the world’s first “Department of Art as Applied to Medicine” at Johns Hopkins University in 1911. William Osler, addressing the Johns Hopkins Historical Club in January 1901, reflected on the accomplishments of medicine in the nineteenth century, stating: “In the fullness of time, long expected, long delayed, at last Science emptied upon him from the horn of Amalthea blessings which cannot be enumerated, blessings which have made the century forever memorable; and which have followed each other with a rapidity so bewildering that we know not what to expect next…. Measure as we may the progress of the world—materially, in the advantages of steam, electricity, and other mechanical appliances; sociologically, in the great improvements in the conditions of life; intellectually, in the diffusion of education; morally, in a pos-
THE TWENTIETH CENTURY The rapid evolution of technology and procedures related to gynecology and female urology continued into the twentieth century. In 1900, David Gillman introduced round-ligament ventrosuspension of the uterus for treatment of uterine prolapse, whereby he carried the proximal round ligament through the peritoneum just lateral to the rectus muscle and sutured it to the posterior rectus sheath. Shortly thereafter, in 1902, John Montgomery Baldy (1860–1934) and John Clarence Webster (1863–1950) independently devised a virtually identical operation for uterine retrodisplacement. The Baldy-Webster uterine ventrosuspension involved plication of redundant uterosacral ligaments to the posterior aspect of the uterus at a point just above the insertion of the uterosacral ligaments. In 1900 Herman Pfannenstiel (1862–1909) proposed his low transverse incision to help reduce postoperative hernias. Frederick Foley introduced a new plastic operation for stricture at the ureteropelvic junction for treatment of hydronephrosis. The pathogenesis of rectal prolapse as a form of sliding hernia was put forth by Alexis Moschcowitz (1865– 1933) in 1912. He devised an operation whereby silk sutures were passed circumferentially about the cul-de-sac of Douglas. Subsequently, gynecologists appropriated the operation to prevent and treat enterocele at the time of hysterectomy. Throughout the twentieth century, the evolution of urinary incontinence procedures took place. In 1913 Kelly first described his anterior plication stitch, a horizontal mattress stitch placed at the urethrovesical junction and thereby effectively plicating the pubocervical fascia. The Kelly plication stitch, as shown in Fig. 1-16, resulted in the narrowing of a patulous urethra and elevation of the urethrovesical junction and was the essential component of anterior colporrhaphy for stress urinary incontinence.
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Figure 1-16 ■ The Kelly plication stitch for stress urinary incontinence. (From Kelly HA. Incontinence of urine in women. Urol Cutaneous Rev 1913;17:291, with permission.)
Although the Kelly plication was somewhat effective and popular, stress incontinence frequently recurred. Various muscular and fascial suburethral sling operations were thus devised to treat this distressing and persistent problem. The slings used adjacent anatomic structures with the purpose of providing proper support for the urethra and developing a substitute muscular sphincter-like action to replace the one that had been damaged or lost. Muscle transposition procedures to create a sling under the urethra using rectus muscle, pyramidalis muscle, and levator ani were used in the early twentieth century. In 1917, Stoeckel, building on previous work by Goebell (1910) and Frangenheim, was the first to combine sphincter plication and the use of a fascial sling with complete success. In 1942 Aldridge described a technique of making a transverse suprapubic incision and developing bilateral strips of fascia attached at the midline: “In such circumstances or when the sphincter muscles have undergone too much destruction, complete restoration of function by the usual vaginal procedures can hardly be expected.” The fascial strips were brought down through the rectus muscle, behind the symphysis, and united as a sling beneath the urethra. Aldridge was one of the first to emphasize that much of stress incontinence might be due to disruption from birth trauma. The Aldridge rectus fascia sling became the model for similar fascial sling procedures used for recurrent stress incontinence and sphincter deficiency for the next 50 years. In 1949 a New York urologist, Victor Marshall (b. 1913), began to develop an operation for urinary incontinence in men during the mid-1940s. He used a suprapubic approach to suspend the bladder and bladder neck by placement of interrupted chromic catgut sutures to the periosteum of the symphysis and posterior rectus sheath. Thereafter, he collaborated with two gynecologists, Andrew Anthony Marchetti (1901–1970) and Kermit Edward Krantz (b. 1923), to refine and modify the procedure to treat incontinence in women.
During the half century since its introduction, the MarshallMarchetti-Krantz procedure remained a standard approach to female incontinence. Necessity being the mother of invention gave rise to a modification of the procedure in 1961, when John Christopher Burch (1900–1970) was unable to secure sutures into the retropubic periosteum and, ultimately, found the support he required in Cooper's ligaments. His publication on the procedure remains one of the simplest, most widely accepted, and most studied methods of elevating the urethrovesical junction in cases of stress urinary incontinence (Fig. 1-17A, B). In 1934 Nobel Sproat Heaney (1880–1955) reported on 565 vaginal hysterectomies performed for benign disease. Henceforth, he became one of the most influential proponents of the procedure praising its lower morbidity and mortality compared to an abdominal approach. While developing the technique, he designed a needle holder, retractor, and pedicle clamp to facilitate the procedure, and incorporated peritoneum, vessels, and ligaments in a maneuver known as the Heaney stitch. The development of an enterocele subsequent to vaginal hysterectomy was addressed in 1957 by Milton McCall's posterior culdoplasty. The operation was performed from below with obliteration of redundant posterior cul-de-sac by a series of continuous sutures along the length of the uterosacral ligaments. Operative laparoscopy was first used in gynecologic procedures by Raoul Palmer (1905-1985) in 1943. At a time when laparoscopy was largely the domain of surgeons, he established its role for evaluating infertility and visualizing pelvic organs by placing the patient in the Trendelenburg position and elevating the uterus by means of a transcervical manipulator. However, credit for devising the earliest endoscope goes to Philipp Bozzini (1773–1809) who described his “lichtleiter” in 1806. He advocated the inspection of all “interior cavities …by looking through natural openings or at least small wounds.” Expounding on the use of his device, Bozzini wrote: “To give an idea how distinctly the light transmitter reflects the rays, I would like to site just one example: if, observing proper cleanliness, one places a piece of writing in the fundus of the uterus of a woman who died during delivery, it can be read through the vagina with the help of the light transmitter containing an ordinary wax candle as clearly as by light of a candle standing at the same distance on a table.” Furthermore, he correctly predicted the development of operative endoscopy, writing: “Surgery will not only develop new and previously impossible procedures, but all uncertain operations which rely on luck and approximation will become safe under the influence of direct vision, since the surgeon's hand will now be guided by his eyes.” Amazingly, Bozzini was formally reprimanded for his “undue curiosity” after visualizing the interior of the urethra of a living patient, a reaction that repeats itself on many occasions throughout history as innovations or new ideas are initially put forth. In 1914 Wilhelm Latzko (1863–1945) introduced a partial colpocleisis technique for closure of vesicovaginal
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Urethra and neck of bladder
Cooper's lig.
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Symphysis Cooper’s lig.
Symph
Arcus tendineus
Perivaginal fascia Foley catheter
Perivaginal fascia elevated by finger in vagina
Bladder Peritoneum
A B Figure 1-17 ■ Burch urethrovaginal fixation procedure. A. The suture has been passed through the perivaginal fascia and the wall of the vagina but not through the mucous membrane. The sutured point is now matched to that point on Cooper's ligament to which it is most easily approximated, and the suture is passed through this point and tied. B. The lateral edges of the vagina have been approximated to Cooper's ligament by three interrupted sutures. (From Burch JC. Urethrovaginal fixation to Cooper's ligament for correction of stress incontinence, cystocele, and prolapse. Am J Obstet Gynecol 1961;81:281, with permission.)
fistula following hysterectomy. By dissecting and removing the vaginal mucosa surrounding the fistula and inverting the denuded area with multiple layers, he effectively obliterated the fistulous opening. From the end of the nineteenth century and well into the twentieth century, the faculty from the Departments of Obstetrics and Gynecology at Johns Hopkins Hospital became a guiding force for the specialty. Among the leaders was Howard Atwood Kelly, often regarded as the father of American gynecology due to his important role in establishing gynecology as a surgical specialty in America (see Fig. 1-13). For three decades he was the chairman of gynecology at the Johns Hopkins Hospital, where he established the first residency program in gynecology, an innovation in surgical training and an important contribution to the development of the specialty. He was, by all measures, a prolific author with a bibliography of 485 book titles, journal articles, and pamphlets by 1919. In 1899 Kelly consented to the department's division and delegated responsibility for obstetrics to John Whitridge Williams (1866–1931). Williams and Kelly introduced a new standard of scholarship into America's obstetric and gynecologic literature and teaching. For three decades Williams exercised a near monopoly in filling the “chairs” of the Departments of Obstetrics and Gynecology at the country's major universities. His widely popular textbook continues to bear his name under new editorship. Later, Richard Wesley TeLinde was appointed chairman in 1939, a post that he held for 21 years. During his tenure, he played a role in the development of fascial slings for stress incontinence and performed much of the preliminary work in delineating the diagnosis of and appropriate treatment for cervical
carcinoma-in-situ. Perhaps TeLinde is best known for his text Operative Gynecology, which was published in 1946 and was destined to be and remains the standard American work on the subject under successive authors. Thus, we owe a great debt of gratitude to these and many others who established the foundation for successful pelvic surgery and, ultimately, for our specialty. Perhaps Kelly, an avid historian and bibliophile, summarized it best by stating, “No group should ever neglect to honor the forebears upon whom their contributions are based. Great is the loss to anyone who neglects to study the lives of those he follows.”
Bibliography Aldridge AH. Transplantation of fascia for relief of urinary stress incontinence. Am J Obstet Gynecol 1942;44:398. American Armamentarium Chirurgicum (intro by Edmonson JM, Hambrecht FT), Centennial ed. George Tiemann & Company, San Francisco/ Boston, 1989. Baldy JM. A new operation for retrodisplacement. Am J Obstet 1902;45:650. Baskett TF. Eponyms and Names in Obstetrics and Gynaecology. RCOG Press, London, UK, 1996. Bourgery JM. Traitem Complet de L'Anatomie de L' Homme Comprenant la Medicine Operatorie. Guerin, Paris, 1866–1868. Bush RB, Leonhardt H, Bush IM, Landes RR. Dr. Bozzini's lichtleiter: a translation of his original article (1806). Urology 1974;3:119. Burch JC. Urethrovaginal fixation to Cooper's ligament for correction of stress incontinence, cystocele, and prolapse. Am J Obstet Gynecol 1961;81:281. Choulant L. History and bibliography of anatomic illustration (reprint; originally published in 1852). Hafner Publishing, New York, 1962. De Graaf R. De Mulierum Organis Generationi Inservientbus. Hackiana, Leyden, 1672. Donald, A. Operation in cases of complete prolapse. J Obstet Gynaecol Br Emp 1908;13:195.
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Douglas J. A Description of the Peritoneum and of that Part of the Membrana Cellularis Which Lies on Its Outside. J. Roberts, London, 1730. Edmonson JM. American Surgical Instruments: An Illustrated History of Their Manufacture and a Directory of Instrument Makers to 1900. Norman Publishing, San Francisco, 1997. Fallopius G. Observationes Anatomicae. Marco Antonio Ulmun, Venice, 1561, p. 221. Fothergill WE. Anterior colporrhaphy and its combination with amputation of the cervix as a single operation. J Obstet Gynaecol Br Emp 1915;27:146. Goebell R. Zur operativen beesitigung der angelborenen incontinez vesicae. Z Gynaek Urol 1910;2:187. Graves TW. A new vaginal speculum. NY Med J 1878;28:506. Heaney NS. A report of 565 vaginal hysterectomies performed for benign pelvic disease. Am J Obstet Gynecol 1934;28:751. Hodge HL. On Diseases Peculiar to Women, Including Displacements of the Uterus. Blanchard and Lea, Philadelphia, 1860. Hunter W. The Anatomy of the Human Gravid Uterus. John Baskerville, Birmingham, England, 1774. Kelly HA. The examination of the female bladder and the catheterization of the ureters under direct inspection. Bull Johns Hopkins Hosp 1893;4:101. Kelly HA. Medical Gynecology. D. Appleton and Co., New York, 1908. Kelly HA. Operative Gynecology, 2 vols. D. Appleton and Co., New York, 1898. Kelly HA. Incontinence of urine in women. Urol Cutaneous Rev 1913;17:291. Kelly HA, Burnam CS. Diseases of the Kidneys, Ureters and Bladder, 2 vols. D. Appleton & Co., New York, 1914. Langenbeck CJ. Geschichte einer von mir glucklich verichteten extirpation der ganger gebarmutter. Bibliotheck Chir Ophthalmol Hanover 1817;1:557. Latzko W. Behandlung hochsitzender blasen und mastdarmscheidenfisteln nach uterusextipation mit hohem schedienverschluss. Zentralbl Gynakol 1914;38:906. Latzko W. Postoperative vesicovaginal fistulas: genesis and therapy. Am J Surg 1942;58:211. Le Fort L. Nouveau procede pour la guersison du prolapsus uterin. Bull Gen Therapie 1877;92:337. Mackenrodt A. Uber die Ursachen der normalen und pathologischen Lagen des Uterus. Arch Gynakol 1895;48:394. Marshall VF, Marchetti AA, Krantz KE. The correction of stress incontinence by simple vesicourethral suspension. Surg Gynecol Obstet 1949;88:509. McCall ML. Posterior culdeplasty: surgical correction of enterocele during vaginal hysterectomy: a preliminary report. Obstet Gynecol 1957;10:595. McDowell E. Three cases of extirpation of diseased ovaria. Elect Repertory Analyst Re Phila 1817;7:242. Mettauer JP. Vesico-vaginal fistula. Boston Med Surg J 1840;22:154.
Moschcowitz AV. The pathogenesis, anatomy and cure of prolapse of the rectum. Surg Gynecol Obstet 1912;15:7. Osler W. Medicine in the Nineteenth Century. In Aeguanimitas with Other Addresses. McGraw-Hill, New York, 1932. Palmer R. La coelioscopie gynecocgique. Acad Chir 1946;72:363. Pare A. The Works of Ambroise Parey, Johnson TH, transl. Clark Publishing, London, 1678. Pfannenstiel J. Uber die vortheile des wuprasymphysaren Fascienquerschnitts fur die Gynakologischen Koliotomein zugleich ein Beitrag zu der Indikationsstellung der Operationswerge. Samml Klin Vortr Leipzig 1900;268:1753. Retzius AA. Uber das ligamentum Pelvoprostaticum oder den apparat, durch welchen die Harnblasee, die Prostata und die Harnrohre an den untern Beckenoffnung befestigt sind. Muller's Arch Anat Physiol Wiss Med 1849;11:182. Ricci JV. The Genealogy of Gynecology: History of the Development of Gynecology Throughout the Ages, 2000 bc–ad 1800. The Blakiston Company, Philadelphia, 1972. Ricci JV. The Vaginal Speculum and Its Modifications Throughout the Ages. New York Medical College, New York, 1948–1949. Scultetus J. L'Arsenal de Chirurgie. Antoine Celleier, Lyon, 1653. Schultheiss D, Udo J. Max Brödel (1870–1941) and Howard A. Kelly (1858– 1943)—Urogynecology and the birth of modern medical illustration. Eur J Obstet Gynecol 1999;86:113. Sims JM. Silver Sutures in Surgery. The Anniversary Discourse before the New York Academy of Medicine. Samuel S. and William Wood, New York, 1858. Sims JM. Clinical Notes on Uterine Surgery. Robert Hardwicke, London, 1866. Speert H. Obstetric and Gynecologic Milestones: Essays in Eponymy. Macmillan, New York, 1958. Speert H. Obstetrics and Gynecology in America: A History. ACOG, Chicago, 1980. Stoeckel W. The use of the pyramidal muscle in the surgical treatment of urinary incontinence. Zentralbl Gynakol 1917;41:11. Stromayr C. Die Handschrift des Schnitt-und Augenarzles Caspar Stromayr, Lindau Munscript. 1559. TeLinde RW. Operative Gynecology, 1st ed. Lippincott, Philadelphia, 1946. TeLinde RW. The modified Goebell-Stoeckel operation for urinary incontinence. South Med J 1934;27:193. Temkin O, transl. Soranus' Gynecology. Johns Hopkins University Press, Baltimore, 1956. Watkins TJ. The treatment of cystocele and uterine prolapse after the menopause. Am J Obstet Dis Wom 1899;15:420. Webster JC. A satisfactory operation for certain cases of retroversion of the uterus. JAMA 1901;37:913. Wertheim E. Zur frage der radical operation beim uteruskrebs. Arch Gynakol 1900;61:627.
Anatomy of the Lower Urinary Tract, Rectum, and Pelvic Floor
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Kevin J. Stepp and Mark D. Walters
EMBRYOLOGY 17 Lower Urinary Tract 17 Rectum and Anal Sphincters 20 ANATOMY 20 Bones of the Pelvis 20 Bladder 20 Trigone 21 Pelvic Ureter 21 Urethra 21 Vagina 22 Pelvic Floor and Sidewalls 23 Perineum 25 Transobturator Anatomy 25 PELVIC ORGAN SUPPORT 26 Support of Uterus and Vagina 26 Urethral Support 28 RECTUM AND ANAL SPHINCTERS 28
EMBRYOLOGY Lower Urinary Tract FORMATION OF INTRAEMBRYONIC MESODERM At approximately 15 days after fertilization, invagination and lateral migration of mesodermal cells occur between the ectodermal and endodermal layers of the presomite embryo. These migrating cells form the intraembryonic mesoderm or mesodermal germ layer. By the seventeenth day of development, the endoderm and ectoderm layers are separated entirely by the mesoderm layer, with the exception of the prochordal plate cephalically and the cloacal plate caudally. The cloacal plate consists of tightly adherent endodermal and ectodermal layers. FORMATION OF ALLANTOIS AND CLOACA Concomitantly, at about the 16th day of development, the posterior wall of the yolk sac forms a small diverticulum, the allantois, which extends into the connecting stalk. With ventral bending of the embryo cranially and caudally dur-
ing somite development, the connecting stalk and contained allantois, as well as the cloacal membrane, are displaced onto the ventral aspect of the embryo. The hindgut undergoes slight dilation to form the cloaca; it receives the allantois ventrally and the two mesonephric ducts laterally. Ventral mesodermal elevations occur, forming the urethral folds (primordia of the labia minora) and genital tubercle (primordium of the clitoris). PARTITIONING OF CLOACA INTO UROGENITAL SINUS AND RECTUM A spur of mesodermal tissue migrates from the base of the allantois toward the cloacal membrane around 28 days after fertilization, forming the urorectal septum (Fig. 2-1). This structure partitions the cloaca into a ventral urogenital sinus and a dorsal rectum. The urogenital opening (future vestibule) is formed by the independent involution of the urogenital membrane. The point at which the urorectal septum intersects with the cloacal membrane will become the perineal body. FORMATION OF URETERIC BUD AND INDUCTION OF FUTURE KIDNEY By 28 days of development, the mesonephric ducts have reached and fused with the urogenital sinus. At this time, the ureteric bud appears as a diverticulum from the posteromedial aspect of the mesonephric duct, at the point where the terminus of the duct bends to enter the cloaca. The free cranial end of the ureter grows dorsally, then cranially, and induces the formation of the metanephrogenic blastema (future kidney; see Fig. 2-1). The presence of the developing ureter is essential for this differentiation; absence of the ureteric bud is invariably associated with renal agenesis. The ureteric bud branches and dilates to create the renal pelvis, major and minor calyces, and collecting ducts. The remaining parts of each are derived from the mesoderm of the metanephrogenic blastema. At this time in the woman, the mesonephric system is undergoing degeneration. The renal blastema originates at the level of the upper sacral segments. The final position of the kidney at the level of the upper lumbar vertebrae is attributed to ascent of the renal blastema. According to Maizels (1986), the four mechanisms that lead to normal renal ascent are caudal growth of
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Figure 2-1 ■ Embryo approximately 32 days (8-mm crown-rump length) after fertilization. The urorectal septum is shown dividing the cloaca into a ventral urogenital sinus and dorsal rectum. Definitive ureter and mesonephric duct share a common opening into partially divided cloaca. Note that the ureter has induced formation of a kidney from metanephrogenic blastema. (From Gosling JA, Dixon J, Humpherson JR. Functional Anatomy of the Urinary Tract. Gower Publishing, London, 1982, with permission.)
Figure 2-2 ■ By day 37 (14-mm crown-rump length), kidney has continued to ascend and undergo medial rotation, and the mesonephric duct and future ureter have separated. Also, cloaca has been divided into ventral urogenital and dorsal alimentary parts. (From Gosling JA, Dixon J, Humpherson JR. Functional Anatomy of the Urinary Tract. Gower Publishing, London, 1982, with permission.)
the spine, active elongation of the ureter into the metanephrogenic blastema, intrinsic growth and molding of the renal parenchyma, and axial growth of the spine after fixing of the kidney to the retroperitoneum. FORMATION OF BLADDER, TRIGONE, AND URETHRA At the point of its connection with the mesonephric ducts, the urogenital sinus is divided into the vesicourethral canal cranially and the definitive urogenital sinus caudally. Dilation of the cranial portion of the vesicourethral canal forms the definitive bladder, which is of endodermal origin. The vesicourethral canal communicates at its cranial end with the allantois, which becomes obliterated at about 12 weeks of fetal life, forming the urachus. This structure runs from the bladder dome to the umbilicus and is called the median umbilical ligament in the adult. The ureteric bud begins as an outgrowth of the mesonephric duct, but with positional changes of the embryo during growth, the mesonephric duct and the ureteric bud shift positions so that the ureter comes to lay posterolaterally to the duct (Fig. 2-2). The segment of the mesonephric duct distal to the site of origin of the ureteric bud dilates and is absorbed into the urogenital sinus, forming the bladder trigone. The bladder trigone effectively gives the endodermal wall of the vesicourethral canal a mesodermal contribution. At about 42 days after fertilization, the trigone may be defined as the region of the vesicourethral canal lying between the ureteric orifices and the termination of the mesonephric ducts (Fig. 2-3). The caudal portion of the vesicourethral canal remains narrow and forms the entire urethra. A small
Figure 2-3 ■ Urogenital sinus and associated ducts approximately 40 days (17-mm crown-rump length) after fertilization. Trigone lies between separated ureteric and mesonephric ducts. (From Gosling JA, Dixon J, Humpherson JR. Functional Anatomy of the Urinary Tract. Gower Publishing, London, 1982, with permission.)
portion of the posterior proximal urethra may be derived, like the trigone, from the mesoderm of the mesonephric duct, although this theory is controversial. A timetable and schematic representation of the embryologic contributions of the various structures of the urogenital system are shown in Table 2-1 and Figure 2-4, respectively.
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Table 2-1
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Timetable of Events in the Development of the Lower Urinary Tract
Time After Fertilization
Event
15 days 16–17 days 17 days 28–38 days 28 days 30–37 days 41 days 42–44 days
Ingrowth of intraembryonic mesoderm Allantois appears Cloacal plate forms Partitioning of cloaca by urorectal septum Mesonephric duct reaches cloaca; ureteric bud appears Ureteric bud initiates formation of metanephros (permanent kidney) Lumen of urethra is discrete; genital tubercles prominent Urogenital sinus separates from rectum; mesonephric ducts and ureters drain separately into urogenital sinus, defining boundaries of trigone Kidneys in lumbar region; glomeruli appear in kidney First likelihood of renal function External genitalia become distinctive for sex Bladder becomes muscularized Further growth and development complete the urogenital organs
51–52 days 9 weeks 12 weeks 13 weeks 20–40 weeks
Trigone
Mesonephric ducts
Ureters, renal pelvis, calyces, and collecting tubules
Urethra (posterior proximal part only)
Bladder Urogenital sinus
Urethra (main part)
Urethra
Rectum
Distal 1/5 - 1/3 of vagina Hymen Vestibule of vagina
Vagina
Cloaca
Proximal 2/3 - 4/5 of vagina Paramesonephric ducts Uterus and tubes Figure 2-4
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Schematic representation of the embryologic contributions of various structures of the female urogenital system.
The separate development of the trigone and bladder may explain why the muscle laminas of the trigone are contiguous with the muscle of the ureter and not with the detrusor muscle of the bladder. This separate development may also account for pharmacologic responses of the musculature of the bladder neck and trigone, which differ partially from those of the detrusor.
CONGENITAL ANOMALIES OF THE URINARY TRACT Knowledge of the embryology of the genitourinary system is necessary for understanding the causes of the multiple congenital anomalies of the upper and lower urinary tracts. Selected congenital anomalies of the urinary tract and their embryologic causes are shown in Table 2-2.
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Table 2-2
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Selected Congenital Anomalies of the Urinary Tract and Their Embryologic Causes
Condition
Embryologic Cause
Renal agenesis Pelvic kidney Horseshoe kidney
Early degeneration of the ureteric bud Failure of kidney to ascend to the lumbar region Fusion of lower poles of both kidneys; ascent to lumbar region prevented by root of inferior mesenteric artery Variable persistence of the intraembryonic portion of allantois, from bladder to umbilicus Early splitting of the ureteric bud Two ureteric buds develop from one mesonephric duct. One bud is in normal position; the abnormal bud moves downward with the mesonephric duct to enter into the urethra, vagina, vestibule, or uterus Failure of the ventral wall of the urogenital sinus to increase to accommodate positional changes, followed by breakdown of the urogenital membrane
Urachal fistula, cyst, sinus Double ureter Ectopic ureter Bladder exstrophy
Rectum and Anal Sphincters NORMAL DEVELOPMENT OF THE HINDGUT The hindgut, which in the embryo extends from the posterior intestinal portal to the cloacal membrane, gives rise to the distal third of the transverse colon, the descending colon, the sigmoid, the rectum, and the upper part of the anal canal. The terminal portion of the hindgut enters into the cloaca, an endoderm-lined cavity that is in direct contact with the surface ectoderm. In the contact area between the endoderm and ectoderm, the cloacal membrane is formed. During further development, a transverse ridge, the urorectal septum, arises in the angle between the allantois and the hindgut. This septum gradually grows caudad, thereby dividing the cloaca into an anterior portion, the primitive urogenital sinus, and a posterior portion, the anorectal canal. The primitive perineum is formed when the urorectal septum reaches the cloacal membrane when the embryo is 7 weeks old. The cloacal membrane is thus divided into the posterior anal membrane and the anterior urogenital membrane. The anal membrane is then surrounded by mesenchymal swellings, and in the ninth week it is found at the bottom of an ectodermal depression, known as the anal pit. The surrounding swellings are the anal folds. Soon thereafter, the anal membrane ruptures and an open pathway is formed between the rectum and the outside, which is the amniotic cavity. The upper part of the anal canal is thus endodermal in origin; the lower third of the anal canal is ectodermal. The external anal sphincter appears in human embryos at approximately 8 weeks or perhaps 7 weeks. The sphincter, together with the levator ani, is believed to originate from hypaxial myotomes. Although the anal sphincter and levator ani may arise from distinct primordia, their relationship is very close. CONGENITAL MALFORMATIONS OF THE HINDGUT Imperforate anus is one of the more common abnormalities of the hindgut. In simple cases, the anal canal ends blindly at the anal membrane, which then forms a diaphragm between the endodermal and ectodermal portions of the anal canal. In more severe cases, a thick layer of connective tissue may be found between the terminal end of the rectum and the surface because of either a failure of the anal pit to develop or atresia of the ampullar part of the rectum (rectal atresia).
A slight deviation of the urorectal septum in the dorsal direction probably causes many rectal and anal abnormalities. Rectal fistulas are often observed in association with an imperforate anus and may be found between the rectum and vagina, urinary bladder, or urethra. Fistulas may also open to the surface of the perineal region.
ANATOMY Bones of the Pelvis The bones of the pelvis provide the foundation to which all of the pelvic structures are ultimately anchored. In the standing position, forces are dispersed to minimize the pressures on the pelvic viscera and musculature and to distribute forces to the bones that are better suited to the long-term, cumulative stress of daily life. In the upright position, the iliopubic rami are oriented in an almost vertical plane. Similar to the supports of an archway or bridge, the weight of the woman is transmitted along these bony supports to her femurs. This directs the pressure of the intra-abdominal and pelvic contents toward the bones of the pelvis instead of the muscles and endopelvic fascia attachments of the pelvic floor. The pubic rami are nearly horizontal where they articulate in the midline. The weights of the abdominal viscera and some of the pelvic viscera are supported inferiorly by the bony articulation.
Bladder The bladder is a hollow, muscular organ that is the reservoir for the urinary system. The bladder is flat when empty and globular when distended. The superior surface and upper 1 or 2 cm of the posterior aspect of the bladder are covered by peritoneum, which sweeps off the bladder into the vesicouterine pouch. The anterior bladder is extraperitoneal and adjacent to the retropubic space (space of Retzius). Between the bladder and pubic bones lie adipose tissue, pubovesical ligaments and muscle, and a prominent venous plexus. The bladder rests inferiorly on the anterior vagina and lower uterine segment, separated by an envelope of adventitia (endopelvic fascia). The epithelium lining the bladder lumen is loosely attached to the underlying musculature, except at the trigone, where it is firmly adherent. The bladder lining consists of transitional epithelium (urothelium) supported by a layer
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of loose connective tissue, the lamina propria. The internal surface of the bladder has a rugose appearance formed by mucosal folds in the contracted state. In the distended state, a variably prominent mesh-like appearance is formed by mucosa-covered detrusor musculature. The bladder wall musculature is often described as having three layers: inner longitudinal, middle circular, and outer longitudinal. However, this layering occurs only at the bladder neck; the remainder of the bladder musculature is composed of fibers that run in many directions, both within and between layers. This plexiform arrangement of detrusor muscle bundles is ideally suited to reduce all dimensions of the bladder lumen on contraction. The inner longitudinal layer has widely separated muscle fibers that course multidirectionally. Near the bladder neck, the muscle fibers assume a longitudinal pattern that is contiguous through the trigone and, according to Tanagho (1986), into the inner longitudinal muscular layer of the urethra. The middle circular layer is prominent at the bladder neck, where it fuses with the deep trigonal muscle, forming a muscular ring. This layer does not continue into the urethra. The outer longitudinal layer forms a sheet of muscle bundles around the bladder wall, above the level of the bladder neck. These fibers continue anteriorly past the vesical neck as the pubovesical muscles and insert into tissues on the posterior surface of the pubic symphysis. The pubovesical muscles may facilitate bladder neck opening during voiding. The longitudinal fibers fuse posteriorly with the deep surface of the trigonal apex and communicate with several detrusor muscle loops at the bladder base; the loops probably aid in bladder neck closure.
Trigone In the bladder base is a triangular area: the trigone. The trigone has a flattened appearance with a smooth epithelial covering. The corners of the trigone are formed by three orifices: the paired ureteral orifices and the internal urethral orifice. The superior boundary of the trigone is a slightly raised area between the two ureteric orifices, called the interureteric ridge. The two ureteral openings are slit-like and, in an undistended organ, lie about 3 cm apart. The trigone has two muscular layers: superficial and deep. The superficial layer is directly continuous with longitudinal fibers of the distal ureter and is also continuous posteriorly with smooth muscle of the proximal urethra. The deep muscular layer of the trigone forms a dense, compact layer that fuses somewhat with detrusor muscle fibers. The deep layer is in direct communication with a fibromuscular sheath, Waldeyer’s sheath, in the intravesical portion of the ureter (Fig. 2-5). The deep trigonal muscle has autonomic innervation identical to that of the detrusor, being rich in cholinergic (parasympathetic) nerves and sparse in noradrenergic (sympathetic) nerves. In contrast, the superficial trigonal muscle has few cholinergic nerves and a greater number of noradrenergic nerves.
Pelvic Ureter As the ureter courses retroperitoneally from the renal pelvis to the bladder, it is divided anatomically into abdominal and pelvic segments, which are approximately equal in
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length of 12 to 15 cm each. The ureter enters the pelvis by crossing over the iliac vessels where the common iliac artery divides into the external iliac and hypogastric vessels. The ureter travels lateral to the hypogastric artery and, eventually, crosses to lie medial to the branches of the anterior division of the hypogastric artery and lateral to the peritoneum of the cul-de-sac. The ureter is attached to the peritoneum of the lateral pelvic wall. As the ureter proceeds more distally, it courses along the lateral side of the uterosacral ligament and enters the endopelvic fascia of the parametrium (cardinal ligament). The ureter courses medially as the uterosacral ligament is traced from the sacrum toward the vagina. At the level of the ischial spine, the ureter is approximately 2.3 cm lateral to the uterosacral ligament (Buller et al., 2001). The ureter is closest to the uterosacral ligament at its distal end, approximately 1 cm. The ureter passes beneath the uterine artery approximately 1.5 cm lateral to the cervix. The distal ureter then moves medially over the lateral vaginal fornix and travels through the wall of the bladder until reaching the trigone. The ureter has only one muscular coat that forms an irregular, helical pattern of muscle bundles, with fibers oriented in almost every direction. As the ureter approaches and enters the bladder wall, its helical fibers elongate and become parallel to its lumen. The intravesical ureter is about 1.5 cm long and is divided into an intramural segment (totally surrounded by the bladder wall) and a submucosal segment directly under the urothelium. The longitudinal muscle fibers of the distal ureter proceed uninterrupted into the superficial trigonal muscle. The distal and intramural segments of the ureter are surrounded by Waldeyer’s sheath, which fuses proximally with the intrinsic musculature of the ureter and distally acts as an added fixation, linking the ureter proper to the detrusor muscle (see Fig. 2-5). Waldeyer’s sheath has been described thoroughly by Tanagho (1986) and Woodburne (1968).
Urethra The female urethra is about 4 cm long and averages 6 mm in diameter. Its lumen is slightly curved as it passes from the retropubic space, perforates the perineal membrane, and ends with its external orifice in the vestibule directly above the vaginal opening. Throughout its length, the urethra is embedded in the adventitia of the anterior vagina. The urethral epithelium has longitudinal folds and many small glands that open into the urethra throughout its entire length. The epithelium is continuous externally with that of the vulva and internally with that of the bladder. It is primarily stratified squamous epithelium that becomes transitional near the bladder. The epithelium is supported by a layer of loose fibroelastic connective tissue, called lamina propria. The lamina propria contains many bundles of collagen fibrils and fibrocytes, as well as an abundance of elastic fibers oriented both longitudinally and circularly around the urethra. Numerous thin-walled veins are another characteristic feature. This rich vascular supply contributes to urethral resistance. The urethral smooth muscle is composed primarily of oblique and longitudinal muscle fibers, with a few circularly
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Figure 2-5 ■ Normal ureterovesico-trigonal complex. A. Side view with Waldeyer’s muscular sheath surrounding vestige of the intravesical ureter and continuing downward as the deep trigone, which extends to the bladder neck. The ureteral musculature becomes the superficial trigone, which extends to just short of the external meatus in the woman. B. Waldeyer’s sheath connected by a few fibers to the detrusor muscle in the ureteral hiatus. This muscular sheath, inferior to the ureteral orifice, becomes the deep trigone. The musculature of the ureters continues downward as the superficial trigone. (From Tanagho EA. Anatomy of the lower urinary tract. In Walsh PC, Gittes RF, Perlmutter AD, Stamey TA, eds. Campbell’s Urology, 5th ed. WB Saunders, Philadelphia, 1986, with permission.)
oriented outer fibers. This muscle and the detrusor muscle in the bladder base form what is called the intrinsic urethral sphincter mechanism. This smooth muscle is usually noted to be under both α-adrenergic and cholinergic control, although Gosling et al. (1981) found an extensive cholinergic nerve supply with few noradrenergic nerves. The longitudinally directed muscles probably shorten and widen the urethral lumen during micturition, whereas the circular smooth muscle (along with the striated urogenital sphincter muscle) contributes to urethral resistance to outflow at rest. The striated urethral and periurethral muscles form the extrinsic urethral sphincter mechanism, which has two components: an inner portion, which lies within and adjacent to the urethral wall, and an outer portion, composed of skeletal muscle fibers of the pelvic diaphragm. The inner portion is made up of the sphincter urethrae (a striated band of muscle that surrounds the proximal two thirds of the urethra) and the compressor urethrae and urethrovaginal sphincter (formerly known together as the deep transverse perineus muscle), which consist of two strap-like bands of striated muscle that arch over the ventral surface of the distal one third of the urethra (Fig. 2-6, inset). These three muscles, which function as a single unit, have been called the striated urogenital sphincter (Oelrich, 1983). It is composed primarily of small-diameter, slow-twitch muscle, making it
ideally suited to exert tone on the urethral lumen over prolonged time periods. The muscles may also contribute (along with the levator ani) to voluntary interruption of the urine stream and to urethral closure with stress, via reflex muscle contraction.
Vagina The vagina is a hollow, fibromuscular tube with rugal folds that extends from the vestibule to the uterine cervix. In the standing woman, the upper two thirds of the vagina is almost horizontal, whereas the lower one third is nearly vertical. Histologically, the vaginal wall is composed of three layers. It is lined by nonkeratinizing stratified squamous epithelium that lies over a thin, loose layer of connective tissue, called the lamina propria. The lamina propria contains no glands. Coursing through the lamina propria are small blood vessels. Vaginal lubrication is via a transudate from the vessels, cervix, and from the Bartholin’s and Skene’s glands. Beneath this is the vaginal muscularis, a well-developed fibromuscular layer consisting primarily of smooth muscle with smaller amounts of collagen and elastin. The muscularis is surrounded by an adventitial layer, which is a variably discrete layer of collagen, elastin, and adipose tissue containing blood vessels, lymphatics,
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Figure 2-6 ■ Diagrammatic representation showing the component parts of the urethral support and sphincteric mechanisms. Note that the proximal urethra and bladder neck are supported by the anterior vaginal wall and its musculofascial attachments to the pelvic diaphragm. (Inset) Contraction of the levator ani muscles elevates the anterior vagina and overlying bladder neck and proximal urethra, contributing to bladder neck closure. The sphincter urethrae, urethrovaginal sphincter, and compressor urethrae are all parts of the striated urogenital sphincter.
and nerves. The adventitia represents an extension of the visceral endopelvic fascia that surrounds the vagina and adjacent pelvic organs and allows for their independent expansion and contraction. The walls of the vagina are in contact except where its lumen is held open by the cervix. The vagina has an H-shaped lumen, with the principal dimension being transverse. In addition, the upper vagina is supported by connective tissue attachments to the sacrum, coccyx, and lateral pelvic sidewalls; these are identified at surgery as the cardinal and uterosacral ligament complex. The presence of a true fascia between the vagina and adjacent organs has been debated. Surgical terms, such as pubocervical and rectovaginal fascia, refer to layers that are developed as a result of separating the vaginal epithelium from the muscularis, or by splitting the vaginal muscularis layer. The vagina lies anteriorly adjacent to and supports the bladder base, from which it is separated by the vesicovaginal adventitia (endopelvic fascia). The urethra is fused with the anterior vagina, with no distinct adventitial layer separating them. The terminal portions of the ureters cross the lateral fornices of the vagina on their way to the bladder base. The vagina is related posteriorly to the cul-de-sac and rectal ampulla and related inferiorly to the perineal body. Embryologically an extension and fusion of peritoneum from the cul-de-sac, and attached to the posterior surface of the vaginal muscularis, forms the rectovaginal septum. A layer of adventitia separates the muscular layer of the rectum from the rectovaginal septum, except at the level of the perineal body, where there is fusion of the vaginal muscularis and connective tissue of the perineal body. The connective tissue of the perineal body extends 2 to 3 cm cephalad from the hymenal ring along the posterior vaginal wall and forms what is sometimes called the rectovaginal fascia. Although, at the time of surgery, an identifiable fascial plane is apparent, Weber and Walters (1997) and DeLancey (1999) have concluded that between the adjacent organs is primarily vaginal muscularis, and no fascia is present histologically.
Pelvic Floor and Sidewalls With the change from plantigrade to erect posture, the pelvis and vertebral column of humans underwent various evolutionary changes that restored balance between intra-abdominal pressure and visceral support. The lumbosacral curve, a specific human characteristic, directs abdominal pressure forward onto the abdominal wall and nearly horizontal, flattened pubic bones. Downward pressure is directed backward onto the sacrum and the rearranged pelvic muscles, which now fill in the pelvic cavity to form the pelvic floor and sidewalls. The pelvic floor and sidewalls are made up of muscular and fascial structures that enclose the abdominal-pelvic cavity, the external vaginal opening (for intercourse and parturition), and the urethra and rectum (for elimination). The fascial components consist of two types of fascia: parietal and visceral (endopelvic). Parietal fascia covers the pelvic skeletal muscles and provides attachment of muscles to the bony pelvis; it is characterized histologically by regular arrangements of collagen. Visceral endopelvic fascia is less discrete and exists throughout the pelvis as a meshwork of loosely arranged collagen, elastin, and adipose tissue through which the blood vessels, lymphatics, and nerves travel to reach the pelvic organs. By surgical convention, condensations of visceral endopelvic fascia of the pelvis have been described as discrete “ligaments,” such as the cardinal or uterosacral ligaments. The role of the endopelvic fascia in pelvic organ support will be discussed in detail later in the chapter. The obturator internus and piriformis are the muscles of the pelvic sidewalls. The obturator membrane is a fibrous membrane that covers the obturator foramen. Lying on the superior (intrapelvic) side of the obturator membrane, the obturator internus originates on the inferior margin of the superior pubic ramus and passes through the lesser sciatic foramen to insert onto the greater trochanter of the femur to laterally rotate the thigh. The piriformis is dorsal and lateral to the coccygeus. It extends from the anterolateral
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sacrum to pass through the greater sciatic foramen and to insert on the greater trochanter. The skeletal muscles of the pelvic floor include the levator ani muscles, the coccygeus muscle, the external anal sphincter, the striated urethral sphincter, and the superficial perineal muscles (bulbocavernosus, ischiocavernosus, and superficial transverse perinei). The pelvic diaphragm consists of the levator ani muscles and the coccygeus muscle. The levator ani muscles are the puborectalis, pubococcygeus, and iliococcygeus muscles. The pelvic diaphragm is stretched hammock-like between the pubis in front and the coccyx behind, and is attached along the lateral pelvic walls to a thickened linear band in the obturator fascia, called the arcus tendineus levator ani (Fig. 2-7). This thickened fascia forms an identifiable line from the ischial spine to the posterior surface of the ipsilateral superior pubic ramus. The levator ani muscles originate from this musculofascial attachment. The puborectalis muscle originates on the posterior inferior pubic rami and arcus tendineus levator ani. Its fibers pass posteriorly, forming a sling around the vagina, rectum, and perineal body to form the anorectal angle and to contribute to fecal continence. Some muscle fibers may blend with the muscularis of the vagina and rectum. The pubococcygeus has a similar origin but inserts in the midline onto the anococcygeal raphe and the anterolateral borders of the coccyx. The levator crura are formed by the pubococcygeus and puborectalis muscles. The iliococcygeus originates along the arcus tendineus levator ani from the pubis to the ischial spine and inserts on the anococcygeal raphe to form the leva-
Obturator internus muscle and fascia
Cooper's ligament
Pubococcygeus muscle
tor plate. The space between the levator crura through which the rectum, vagina, and urethra pass is called the genital hiatus. The coccygeus muscle, although not part of the levator ani, does make up the posterior part of the pelvic floor and plays a role in support. It originates on the ischial spine and sacrospinous ligament, overlies the sacrospinous ligament, and inserts on the lateral lower sacrum and coccyx. The coccygeus becomes thin and fibrous with age and often blends with the sacrospinous ligament, which can be difficult to distinguish from the coccygeus because both have the same origin and insertion. The levator ani muscles exhibit constant baseline tone and can also be voluntarily contracted. The muscles contain both type I (slow-twitch) fibers to maintain constant tone, and type II (fast-twitch) fibers to provide reflex and voluntary contractions. Constant tone of the pelvic floor, except during voiding, defecation, and during a Valsalva maneuver, provides constant support for the pelvic viscera. The levator ani muscles and the skeletal components of the urethral and anal sphincters all have the ability to contract quickly at the time of an acute stress, such as a cough or sneeze, to maintain continence. Although the muscles of the pelvic floor were initially thought to have innervation from direct branches of the sacral nerves on the pelvic surface and via the pudendal nerve on the perineal surface, recent anatomic, neurophysiologic, and experimental evidence indicates that these standard descriptions are inaccurate and that the levator ani muscles are innervated predominantly by a nerve traveling on the superior (intrapelvic) surface of the muscles without
Urethra
Vagina
Arcus tendineus fasciae pelvis
Obturator canal and neurovascular bundle
Arcus tendineus levator ani
IIiococcygeus muscle
Rectum Coccygeus muscle Ischial spine
Piriformis muscle
Levator plate
Figure 2-7 ■ The relationships of the muscles of the pelvic floor and sidewalls and their attachments from an abdominal view. The arcus tendineus fasciae pelvis has been removed on the left, showing the origins of the levator ani muscles. On the right, the arcus tendineus fasciae pelvis remains intact showing the attachment of the lateral vagina via the endopelvic fascia (cut away). (Reprinted with the permission of The Cleveland Clinic Foundation.)
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contribution of the pudendal nerve. Small branches penetrate the body of each muscle as the nerve traverses them.
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then travels along the medial surface of the obturator internus, through the ischiorectal fossa in a thickening of fascia called Alcock’s canal. It emerges posteriorly and medially to the ischial tuberosity and divides into three branches to supply the perineum: clitoral, perineal, and inferior rectal (also called inferior hemorrhoidal). The blood supply to the perineum is from the pudendal artery, which travels with the pudendal nerve to exit the pelvis.
Perineum The perineum is divided into two compartments: superficial and deep. These are separated by a fibrous connective tissue layer called the perineal membrane. The perineal membrane is a triangular sheet of dense fibromuscular tissue that spans the anterior half of the pelvic outlet. It had been called the urogenital diaphragm previously; this change in name reflects the appreciation that it is not a two-layered structure with muscle in between, as had been thought in the past. The perineal membrane provides support to the vagina and urethra as they pass through it. Cephalad to the perineal membrane lies the striated urogenital sphincter muscle, which, as already mentioned, compresses the mid- and distal urethra. The borders of the perineum are the ischiopubic rami, ischial tuberosities, sacrotuberous ligaments, and coccyx. The perineal body marks the point of convergence of the bulbospongiosus muscles, superficial and deep transverse perinei, perineal membrane, external anal sphincter, posterior vaginal muscularis, and the insertion of the puborectalis and pubococcygeus muscles. The deep perineal compartment is composed of the deep transverse perineus muscle, portions of the external urethral sphincter muscles (compressor urethrae and urethrovaginal sphincter), portions of the anal sphincter, and the vaginal musculofascial attachments. The neurovascular anatomy of the perineum is illustrated in Figure 2-8. The motor and sensory innervation of the perineum is via the pudendal nerve. The pudendal nerve originates from S2–S4 and exits the pelvis through the greater sciatic foramen, hooks around the ischial spine,
Transobturator Anatomy The obturator membrane is a fibrous sheath that spans the obturator foramen, through which the obturator neurovascular bundle penetrates via the obturator canal. The obturator artery and vein originate as branches of the internal iliac vessels. As they emerge from the inferior side of the obturator membrane and enter the obturator space, they divide into many small branches supplying the muscles of the adductor compartment of the thigh. Recent cadaver work by Whiteside and Walters (2004) has contradicted previous reports of the obturator vessels bifurcating into medial and lateral branches. Rather, the vessels are predominately small (<5 mm in diameter) and splinter into variable courses. The muscles of the medial thigh and adductor compartment are from superficial to deep: the gracilis, adductor longus, adductor brevis, adductor magnus, and obturator externus muscles (Fig. 2-9). In contrast to the vessels, the obturator nerve emerges from the obturator membrane and bifurcates into anterior and posterior divisions traveling distally down the thigh to supply the muscles of the adductor compartment. With the patient in the dorsal lithotomy position, the nerves and vessels follow the thigh and course laterally away from the ischiopubic ramus.
Bulbospongiosus muscle Ischiocavernosus muscle
Inferior pubic ramus
Innervation of the ilioinguinal nerve
Perineal membrane
Innervation of the pudendal nerve
Ischial spine
Superficial transverse perineus muscle Sacrotuberous ligament
Perineal body
External anal Levator ani sphincter
Gluteus maximus muscle
Pudendal nerve and branches -Clitoral -Perineal -Interior rectal
Figure 2-8 ■ Neurovascular anatomy of the perineum. Muscles and nerves of the perineum, including the distribution of the pudendal and ilioinguinal innervation (shaded on left). (Reprinted with the permission of The Cleveland Clinic Foundation.)
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Adductor longus Adductor brevis
Adductor magnus
Figure 2-9 ■ Transobturator anatomy. Diagrammatic representation showing the muscles of the obturator compartment. The superficial muscles are illustrated on the left. On the right, the superficial muscles have been made transparent to illustrate the deeper muscles. (Reprinted with the permission of The Cleveland Clinic Foundation.)
Obturator externus
Obturator internus
PELVIC ORGAN SUPPORT Support of Uterus and Vagina Normal pelvic support is provided by interaction between the pelvic floor muscles and connective tissue attachments. Under most conditions, the pelvic muscles are the primary support for the pelvic organs, providing a firm yet elastic base on which they rest. The connective tissue (endopelvic fascia) attachments stabilize the pelvic organs in the correct position to receive optimal support from the pelvic muscles. When the pelvic muscles are relaxed, as during micturition or defecation, the connective tissue attachments temporarily hold up the pelvic organs. The endopelvic fascia is a loose connective tissue network that envelops all of the pelvic organs and connects them loosely to the supportive musculature and pelvic bones. The term endopelvic fascia is used here to describe the tissues located between the surfaces of the peritoneum, muscles, and pelvic organs. Histologically, it is composed of collagen, elastin, adipose tissue, nerves, vessels, lymph channels, and smooth muscle. Its properties provide stabilization and support yet allow for mobility, expansion, and contraction of the viscera to permit storage of urine and stool, coitus, parturition, and defecation. Other than the cervix, the uterus does not have fixed supports, as indicated by its ability to enlarge without restriction during pregnancy. The upper two thirds of the vagina is in a nearly horizontal orientation in a standing woman. Connective tissue attachments stabilize the vagina at different levels, as described by DeLancey (1992) and others (Fig. 2-10). Level I refers to the uterosacral/cardinal ligament complex and are the most cephalad-supporting structures. Level II support is provided by the paravaginal attachments along
the length of the vagina to the arcus tendineus fasciae pelvis. Level III support describes the most inferior or distal portions of the vagina, including the perineum. Each area plays a significant role in maintaining pelvic organ support and will be discussed individually. However, it is important to remember that levels I, II, and III are all connected through continuation of the endopelvic fascia. Comprising level I support, the cardinal and uterosacral ligaments attach to the cervix from the lateral and posterior sides, respectively, with fibers intermingling. The cardinal ligaments blend with the uterosacral ligaments, and they are difficult, if not impossible, to precisely delineate from one another. Fibers traveling predominately laterally make up the cardinal ligaments, whereas fibers going to the sacrum make up the uterosacral ligaments. These fibers form a three-dimensional complex attaching the upper vagina, cervix, and lower uterine segment to the sacrum and lateral pelvic sidewalls at the piriformis, coccygeus, levator ani, and perhaps the obturator internus fascia overlying the ischial spine. Together, the uterosacral/cardinal ligament complex supports the cervix and upper vagina to maintain vaginal length and to keep the vaginal axis nearly horizontal so that it rests on the rectum and can be supported by the levator plate. This keeps the cervix just superior to the level of the ischial spine. Contiguous with the cardinal/uterosacral ligament complex at the location of the ischial spine is level II support—the paravaginal attachments. These are the connections of the lateral vagina and endopelvic fascia, anteriorly to the arcus tendineus fasciae pelvis and posteriorly to the arcus tendineus rectovaginalis (level II support functions to keep the vagina midline, directly over the rectum). The arcus tendineus fasciae pelvis, or “white line,” is a thickened condensation of the parietal fascia, into which
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Cervix Level I Uterosacral/cardinal ligament complex
To arcus tendineus fasciae pelvis Level II
To arcus tendineus rectovaginalis Level III
Obturator foramen
External anal sphincter Arcus tendineus rectovaginalis
Arcus tendineus levator ani
Arcus Perineal Vagina Urethra tendineus fasciae pelvis membrane
Perineal membrane Superficial transverse Perineal External perineus muscle anal sphincter body
Figure 2-10 ■ Integrated levels of support. The three levels of support of the vagina and uterus showing the continuity of supportive structures throughout the entire length of the genital tract. In level I, endopelvic fascia suspends upper vagina and cervix from lateral pelvic walls. Fibers of level I extend both vertically and posteriorly toward sacrum. In level II, the vagina is attached to the arcus tendineus fasciae pelvis and superior fascia of levator ani muscles. In level III, the distal vagina is supported by the perineal membrane and muscles. (Reprinted with the permission of The Cleveland Clinic Foundation.)
the paravaginal endopelvic fascia connects supporting the vagina and creating the anterior lateral vaginal sulci. Like the arcus tendineus levator ani, the arcus tendineus fasciae pelvis originates on the ischial spine. However, as it approaches the pubic symphysis, it travels medially and inferiorly to the arcus tendineus levator ani, inserting on the inferior aspect of the superior pubic rami over the origin of the puborectalis muscle. The axes of both the arcus tendineus levator ani and the arcus tendineus fasciae pelvis are nearly horizontal in the standing woman, which establishes the normal axis of the upper vagina. Similar to the anterior paravaginal supports, posterior lateral supports are also present. The endopelvic fascia extends posteriorly from the posterior lateral vaginal sulci around the rectum to attach the vagina to the pelvic floor. These fibers blend anteriorly with the vaginal muscularis, posteriorly with the rectal muscularis, and inferiorly with the perineal body. The lateral endopelvic fascia attachments of the posterior vaginal wall do not have significant connections across the midline. Rather, they anchor the posterior lateral vaginal sulci to the ipsilateral levator ani. The pos-
terior vaginal muscularis is attached laterally through this endopelvic fascia to the fascia of the levator ani at the arcus tendineus rectovaginalis. The arcus tendineus rectovaginalis represents a condensation of the parietal fascia of the levator ani coursing inferiorly from the perineal body and laterally along the levator ani, where it intersects the midpoint of the arcus tendineus fasciae pelvis (see Fig. 2-10). The arcus tendineus rectovaginalis is approximately 4 cm in length. The connection to the arcus tendineus rectovaginalis creates the vertical axis of the distal vagina. Level III support is provided by the perineal body, perineal membrane, superficial and deep perineal muscles, and endopelvic fascia. These structures support and maintain the normal position of the distal one third of the vagina and introitus. The endopelvic fascia blends anteriorly with the vaginal muscularis and is continuous with the supportive structures of the urethra. The perineal body is critical for support of the lower part of the vagina and proper function of the anal canal. The perineal membrane anchors laterally to the perineal body and distal vagina and anteriorly to the ischiopubic rami. Separation of the perineal body from the
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perineal membrane results in perineal descent and can contribute to defecation dysfunction. The three levels of support are connected and interdependent. Level III structures are connected to the endopelvic fascia that surrounds the vagina and rectum and are therefore continuous with level II support. Level II support is connected to level I support through the confluence of the lateral endopelvic fascia attachments and the uterosacral/cardinal ligament complex. Adequate support at all levels maintains the pelvic organs in their normal anatomic positions. When the vagina, bladder, and rectum are kept in the horizontal plane over the levator plate and pelvic floor muscles, intra-abdominal and gravitational forces are applied perpendicularly to the vagina and pelvic floor while the pelvic floor musculature counters those forces with its constant tone. This horizontal position and support by the levator ani maintain pelvic organ support. With proper tone of the pelvic floor muscles (levator ani), stress on the lateral paravaginal attachments is minimized. Furthermore, in times of acute stress, such as a cough or sneeze, a reflex contraction of the pelvic floor musculature counters and further stabilizes the viscera. The genital hiatus also responds by narrowing to maintain level III support. With pelvic floor weakness, such as with neuropathic injury or mechanical muscular damage, the endopelvic fascia becomes the primary mechanism of support. Over time, this stress can overcome the endopelvic fascial attachments and result in loss of the normal anatomic position through breaks, stretching, or attenuation of endopelvic fascia supports. This can result in changes in the vector forces applied to the viscera and may lead to pelvic organ prolapse and/or visceral dysfunction. Re-creation of these supportive connections and proper position of the organs, while maintaining adequate vaginal length to keep the vaginal apex in a natural position, should be the goal of reconstructive pelvic surgery.
Urethral Support Normally, the vagina provides support to the bladder and urethra. Traditionally, support of the urethra and bladder neck was thought to be provided by the interaction of the pubourethral ligaments, the perineal membrane, and the muscles of the pelvic floor. Numerous investigators have described the so-called pubourethral ligaments as extending from the inferior surface of the pubic bones to the urethra. Milley and Nichols (1971) found bilaterally symmetric anterior, posterior, and intermediate pubourethral ligaments and stated that the anterior and posterior ligaments were formed, respectively, by inferior and superior fascial layers of the perineal membrane. An anatomic defect of the pubourethral ligaments has been cited as a contributing factor to stress urinary incontinence in women. Studies by DeLancey (1986, 1988, 1989) provide a more complete view of urethral support. Rather than being suspended ventrally by ligamentous structures, the proximal urethra and bladder base are supported in a sling-like fashion by the anterior vaginal wall, which is attached bilaterally to the muscles of the pelvic diaphragm (levator ani muscles) at the arcus tendineus fasciae pelvis. Similar anatomic connections between the pelvic diaphragm and vagina have been described by Olesen and Grau (1976) and others. These
attachments extend caudally and blend with the superior fibers of the perineal membrane. The tissues, described as pubourethral ligaments, are made up of the perineal membrane and the most caudal portion of the arcus tendineus fasciae pelvis, which fix the distal urethra beneath the pubic bone. Figure 2-6 illustrates the anatomic structures that contribute to urethral support and closure. Anterior vaginal attachment at the arcus tendineus fasciae pelvis may contribute to urethral closure by providing a stable base onto which the bladder neck and proximal urethra are compressed with increases in intra-abdominal pressure. These attachments are also responsible for the posterior movement of the vesical neck seen at the onset of micturition (when the pelvic floor relaxes) and for the elevation noted when a patient is instructed to arrest her urinary stream (see Fig. 2-6, inset). Defects in these attachments probably result in proximal urethral support defects (urethral hypermobility) and anterior vaginal prolapse (cystocele), conditions associated with stress urinary incontinence. These defects also correspond to the paravaginal fascial defects, with detachment of the vagina from its lateral connective tissue supports, described by Richardson et al. (1976).
RECTUM AND ANAL SPHINCTERS The rectum extends from its junction with the sigmoid colon to the anal orifice. The distribution of smooth muscle is typical for the intestinal tract, with inner circular and outer longitudinal layers of muscle. At the perineal flexure of the rectum, the inner circular layer increases in thickness to form the internal anal sphincter. The internal anal sphincter is under autonomic control (sympathetic and parasympathetic) and is responsible for 85% of the resting anal pressure. The outer longitudinal layer of smooth muscle becomes concentrated on the anterior and posterior walls of the rectum, with connections to the perineal body and coccyx, and then passes inferiorly on both sides of the external anal sphincter. The external anal sphincter is composed of striated muscle that is tonically contracted most of the time and can also be voluntarily contracted. Various divisions of the external anal sphincter have been described, and, although there is no consensus, recent descriptions favor superficial (combining the previous superficial and subcutaneous components) and deep compartments. The external anal sphincter functions as a unit with the puborectalis portion of the levator ani muscle group. The anal sphincter mechanism comprises the internal anal sphincter, the external anal sphincter, and the puborectalis muscle (Fig. 2-11). As with the bladder neck and urethra, a spinal reflex causes the striated sphincter to contract during sudden increases in intra-abdominal pressure, such as coughing. The anal-rectal angle is produced by the anterior pull of the puborectalis muscles. These muscles posteriorly form a sling around the anorectal junction. The anal-rectal angle was previously thought to be important in maintaining fecal continence, but its importance has been questioned. More recent studies suggest that fecal incontinence in women
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Figure 2-11 ■ Diagram of the rectum, anal canal, and surrounding muscles. The puborectalis muscle forms a sling posteriorly around the anorectal junction. The external anal sphincter (skeletal muscle) surrounds the anal canal and is closely associated with the puborectalis muscle. The internal anal sphincter muscle (smooth muscle) lies within the ring of the external sphincter muscle and is a continuation of the inner circular layer of the smooth muscle of the rectal wall. (From Madoff RD, Williams JG, Caushaj
is often related to denervation of the muscles of the pelvic diaphragm and to disruption and denervation of the external anal sphincter.
Bibliography EMBRYOLOGY Gosling JA. Anatomy. In Stanton SL, ed. Clinical Gynecologic Urology. Mosby, St. Louis, MO, 1984. Gosling JA, Dixon J, Humpherson JR. Functional Anatomy of the Urinary Tract. Gower Publishing, London, 1982. Langman J. Medical Embryology. Williams & Wilkins, Baltimore, 1976. Maizels M. Normal development of the urinary tract. In Walsh PC, Gittes RF, Perlmutter AD, Stamey TA, eds. Campbell’s Urology, 5th ed. WB Saunders, Philadelphia, 1986. Muckle CW. Developmental abnormalities of the female reproductive organs. In Sciarra JJ, ed. Gynecology and Obstetrics, vol 1. Harper & Row, Hagerstown, MD, 1981. Shapiro E, Huang H, Wu XR. New concepts on the development of the vagina. Adv Exp Med Biol 2004;545:173. Snyder HM. Anomalies of the ureter. In Gillenwater JY, Grayhack JT, Howards SS, Duckett JW, eds. Adult and Pediatric Urology, vol 2. Mosby, Chicago, 1987.
ANATOMY Aronson MP, Lee RA, Berquist TH. Anatomy of anal sphincters and related structures in continent women studied with magnetic resonance imaging. Obstet Gynecol 1990;76:846. Barber MD, Bremer RE, Thor KB, et al. Innervation of the female levator ani muscles. Am J Obstet Gynecol 2002;187:64. Buller JL, Thompson JR, Cundiff GW, et al. Uterosacral ligament: description of anatomic relationships to optimize surgical safety. Obstet Gynecol 2001;97:873.
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Curtis AH, Anson BJ, Ashley FL. Further studies in gynecological anatomy and related clinical problems. Surg Gynecol Obstet 1942;74:709. Curtis AH, Anson BJ, McVay CB. The anatomy of the pelvic and urogenital diaphragms, in relation to urethrocele and cystocele. Surg Gynecol Obstet 1939;68:161. Dalley AF. The riddle of the sphincters: the morphophysiology of the anorectal mechanism reviewed. Am Surg 1987;53:298. DeLancey JO. Correlative study of paraurethral anatomy. Obstet Gynecol 1986;68:91. DeLancey JO. Structural aspects of the extrinsic continence mechanism. Obstet Gynecol 1988;72:296. DeLancey JO. Pubovesical ligament: a separate structure from the urethral supports (“pubo-urethral ligaments”). Neurourol Urodyn 1989;8:53. DeLancey JO. Anatomy of the female bladder and urethra. In Ostergard DR, Bent AE, eds. Urogynecology and Urodynamics, 3rd ed. Williams & Wilkins, Baltimore, 1991. DeLancey JO. Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 1992;166:1717. DeLancey JO. Structural anatomy of the posterior pelvic compartment as it relates to rectocele. Am J Obstet Gynecol 1999;180:815. DeLancey JO, Starr RA. Histology of the connection between the vagina and levator ani muscles. J Reprod Med 1990;35:765. Dickinson RL. Studies of the levator ani muscle. Am J Obstet Dis Women Child 1889;22:897. Elbadawi A. Neuromorphologic basis of vesicourethral function: I. Histochemistry, ultrastructure and function of the intrinsic nerves of the bladder and urethra. Neurourol Urodyn 1982;1:3. Funt MI, Thompson JD, Birch H. Normal vaginal axis. South Med J 1978;71:1534. Gosling JA. The structure of the female lower urinary tract and pelvic floor. Urol Clin North Am 1985;12:207. Gosling JA, Dixon JS, Critchley HO, et al. A comparative study of the human external sphincter and periurethral levator ani muscles. Br J Urol 1981;53:35. Gosling JA, Dixon JS, Humpherson JR. Functional Anatomy of the Urinary Tract: an Integrated Text and Color Atlas. University Park Press, Baltimore, 1982. Halban J, Tandler J. Anatomie und Atiologie der Genital-prolapse (translated by Porges RF, Porges JC. The anatomy and etiology of genital prolapse in women). Obstet Gynecol 1960;15:790. Krantz KE. The anatomy of the urethra and anterior vaginal wall. Am J Obstet Gynecol 1951;62:374. Lawson JO. Pelvic anatomy. I. Pelvic floor muscles. Ann R Coll Surg Engl 1974;52:244. Leffler KS, Thompson JR, Cundiff GW, et al. Attachment of the rectovaginal septum to the pelvic sidewall. Am J Obstet Gynecol 2001;185:41. Lund CJ, Fullerton RE, Tristan TA. Cinefluorographic studies of the bladder and urethra in women. Am J Obstet Gynecol 1959;78:706. Madoff RD, Williams JG, Caushaj PF. Fecal incontinence. N Engl J Med 1992;326:1003. McGuire EJ. The innervation and function of the lower urinary tract. J Neurosurg 1986;65:278. Mengert WF. Mechanics of uterine support and position. Am J Obstet Gynecol 1936;31:775. Milley PS, Nichols DH. The relationship between the pubo-urethral ligaments and the urogenital diaphragm in the human female. Anat Rec 1971;170:281. Muellner SR. The physiology of micturition. J Urol 1951;65:805. Nichols DH, Randall CL. Vaginal Surgery, 3rd ed. Williams & Wilkins, Baltimore, 1989. Oelrich TM. The striated urogenital sphincter muscle in the female. Anat Rec 1983;205:223. Olesen KP, Grau V. The suspensory apparatus of the female bladder neck. Urol Int 1976;31:33. Redman JF. Anatomy of the genitourinary system. In Gillenwater JY, Grayhack JT, Howards SS, Duckett JW, eds. Adult and Pediatric Urology, vol 1. Mosby, Chicago, 1987. Richardson AC, Lyon JB, Williams NL. A new look at pelvic relaxation. Am J Obstet Gynecol 1976;126:568. Tanagho EA. Anatomy of the lower urinary tract. In Walsh PC, Gittes RF, Perlmutter AD, Stamey TA, eds. Campbell’s Urology, 5th ed. WB Saunders, Philadelphia, 1986. Weber AM, Walters MD. Anterior vaginal prolapse: review of anatomy and techniques of surgical repair. Obstet Gynecol 1997;89:331.
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Whiteside JL, Walters MD. Anatomy of the obturator region: relations to a transobturator sling. Int Urogynecol J 2004;15:223. Wood BA, Kelly AJ. Anatomy of the anal sphincters and pelvic floor. In Henry MM, Swash M, eds. Coloproctology and the Pelvic Floor, 5th ed. Butterworth-Heinemann, Oxford, UK, 1992. Woodburne RT. Anatomy of the bladder and bladder outlet. J Urol 1968;100:474.
Woodburne RT. Essentials of Human Anatomy, 5th ed. Oxford University Press, New York, 1976. Zacharin RF. The suspensory mechanism of the female urethra. J Anat 1963;97:423. Zacharin RF. Pelvic Floor Anatomy and the Surgery of Pulsion Enterocoele. Springer-Verlag, New York, 1985.
Neurophysiology and Pharmacology of the Lower Urinary Tract
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J. Thomas Benson and Mark D. Walters
GENERAL NERVOUS SYSTEM ARRANGEMENTS 31 NEURAL CONTROL OF THE LOWER URINARY TRACT 32 Autonomic Nervous System 32 Sensory Innervation 35 Central Nervous System Modulation 35 MECHANISMS OF NORMAL BLADDER FILLING, STORAGE, AND VOIDING 36 Filling and Storage 36 Voiding 36 CLINICAL EFFECTS OF NEUROLOGIC DISEASE ON LOWER URINARY TRACT FUNCTION 38 Brainstem lesions 38 Spinal cord disease 38 Cauda equina 39 Peripheral innervation and bladder dysfunction 39 Pelvic nerve injury 39 CLINICAL PHARMACOLOGY OF THE LOWER URINARY TRACT 40 Therapy to facilitate bladder emptying 40 Therapy to facilitate urine storage 41
The two functions of the lower urinary tract are the storage of urine within the bladder and the timely expulsion of urine from the urethra. The precise neurologic pathways and neurophysiologic mechanisms that control these functions of storage and micturition are complex and not completely understood. However, an extremely important concept that is now appreciated for its application to treatment of lower urinary tract dysfunction is the principle of neuroplasticity, as it applies to the pathways and mechanisms. The nervous system is composed of varying sizes and types of nerves. They are classified generally by size. The largest, myelinated, fast-conducting A alpha nerves are sensory (afferent) nerves conveying touch, or motor (efferent) nerves activating large muscles. The smallest, nonmyelinated C nerve fibers are slowconducting nerves that convey pain and temperature on the sensory side or act as postganglionic autonomic nerves on the motor side. The bladder afferent nerves are largely C fibers at birth, until maturation changes the afferents to A delta (lightly myelinated, small) fibers. Many now appreciate that bladder insults, such as obstruction, bladder inflamma-
tion, or spinal cord disease, affecting pathways involved in lower urinary tract function lead to neuroplastic changes in which the afferents again become C fibers as the bladder’s response to the insults. Understanding the anatomy and physiology of the basic reflex pathways and central voluntary control involved in lower urinary tract function is necessary, but appreciating the dynamic ability of the neurons to modify these pathways is essential to application of modern therapies. This chapter reviews normal and abnormal function and neurologic control, as well as clinical pharmacology, of the lower urinary tract in women.
GENERAL NERVOUS SYSTEM ARRANGEMENTS The nervous system is composed of neurons (nerve cells) with characteristic functions of propagation and transmission of signals. A neuron propagates a signal, the “action potential,” along an axon and then transmits the signal to another neuron or an end organ to elicit a response (e.g., a muscle contraction). The neural propagation depends on electrical events, with channels allowing ions to move through the cell membrane that depolarizes the membrane and establishes electrical current that conveys action potentials to the junctions of the nerve with another nerve or with end organs. At this site, chemical events that depend on neurotransmitters and receptors effect action potentials in the second nerve or end organ to elicit the response. Neurotransmitters are chemicals, selectively released from a nerve terminal by an action potential, which interact with a specific receptor on an adjacent structure and elicit a specific physiologic response. Most neurotransmitters come from amino acids. Some neurons modify the amino acid to form “amine” transmitters; for example, norepinephrine, serotonin, acetylcholine, and others combine to form peptides. The chemical event at the junction gives origin to further electrical events in the secondary neurons or in the end organs. These chemical synapses can be excitatory (Na+ channels open, and Na+ influx depolarizes and creates action potentials) or inhibitory (Cl− and K+ channels allow influx and egress, and hyperpolarization develops, preventing action potential development).
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The nervous system is arranged into the central and the peripheral systems. The central nervous system (CNS) includes the brain and spinal cord. Within the brain and cord, nerve cell bodies are arranged in groups of various sizes and shapes called nuclei. Fibers with a common origin and destination are called a tract; some are so anatomically distinct that they may be called fasciculus, brachium, peduncle, column, or lemniscus. Synaptic relationships in the central nervous system are very complex, with contacts occurring between axons and cell bodies, axons and dendrites, cell body and cell body, or dendrite and dendrite. Twelve pairs of cranial and 31 pairs of spinal nerves with their ganglia compose the peripheral nervous system. Synaptic relationships in the peripheral nervous system involve only neuron-neuron or neuron-effector interactions. The somatic component of the peripheral system innervates skeletal muscle and receives somatic sensory input. The autonomic division innervates cardiac muscle, smooth muscle, and glands, is involved with ganglionic activities, and is indirectly involved in conveying visceral afferent input. The autonomic nervous system consists, in part, of general visceral efferent fibers, supplying the smooth muscle of viscera. General visceral afferent fibers are closely associated with the autonomic efferents, and both the motor and sensory visceral neural activities ordinarily function at a subconscious level. Unlike the somatic motor system, the peripheral efferent autonomic fibers reach the effector organ by, at least, a two-neuron chain, constituting a preganglionic and a postganglionic neuron. The preganglionic neuron arises in the intermediolateral cell column of the brainstem or spinal cord and terminates at an outlying ganglion, where the postganglionic neuron continues the impulse transmission to the end organ. Fibers arising from the intermediolateral cell column of the 12 thoracic and first 2 lumbar segments of the spinal cord constitute the sympathetic division of the autonomic nervous system. The parasympathetic division consists of fibers arising from the second through the fourth intermediolateral cell column sacral segments and from cranial outflows. Sympathetic nerves to the pelvic cavity originate in cord levels T5 to L2. Some preganglionic axons pass via white rami communicantes to the paravertebral sympathetic chain, synapse, and pass by gray rami communicantes to the skeletal nerves. These constitute the paravertebral sympathetics. Other preganglionic sympathetic axons pass to ganglia located at roots of arteries, for which they are named (e.g., lumbar splanchnic nerves terminate in inferior mesenteric and hypogastric ganglia). Postganglionic fibers from these ganglia follow the visceral arteries to the organs of the lower abdomen and pelvis. These constitute the prevertebral sympathetics. Pelvic parasympathetic system preganglionic fibers originate in spinal segments S2 through S4 and extend to ganglia located within or very near the organs that they supply, thus having very short postganglionic fibers.
NEURAL CONTROL OF THE LOWER URINARY TRACT Local innervation is chiefly by parasympathetic and sympathetic autonomic and peripheral somatic motor and sen-
sory systems. A summary of the neural pathways involved in bladder filling and voiding is shown in Figures 3-1 and 3-2.
Autonomic Nervous System The autonomic nervous system controls the lower urinary tract by its actions on the ganglia, detrusor muscle, and smooth muscle of the trigone and urethra. SYMPATHETIC ACTIONS ON DETRUSOR MUSCLE AND GANGLIA During physiologic bladder filling, little or no increase in intravesical pressure is observed, despite large increases in urine volume. This process, called accommodation, is caused primarily by passive elastic and viscoelastic properties of the smooth muscle and connective tissue of the bladder wall. During filling, muscle bundles in the bladder wall undergo reorganization, and the muscle cells are elongated up to four times their length. As bladder filling progresses and at a certain bladder wall tension, a desire to void is felt, although it has not been determined where this sensation is processed in the brain. Mechanoreceptors in the bladder wall are activated, and action potentials run with afferents following parasympathetic pelvic nerves to the spinal cord at the S2 to S4 and with afferents following sympathetic nerves to the thoracolumbar cord. As filling increases to a critical intravesical pressure, or with rapid bladder filling, detrusor muscle contractility is inhibited by activation of a spinal sympathetic reflex. The sympathetic neural pathways are as follows: Sympathetic preganglionic fibers from thoracolumbar spinal segments form white rami communicantes to synapse in the paravertebral or prevertebral sympathetic pathways, the latter predominating. Postganglionic neurons reach inferior mesenteric ganglia by the lumbar splanchnic nerves and continue through the hypogastric plexus to the presacral fascia, across the upper posterior lateral pelvic wall, 1 to 2 cm behind and below the ureter. After these neurons join the pelvic nerves, the pelvic plexus is formed, running below and medial to the internal iliac vessels overlying the anterior lateral lower rectum near the anorectal junction. The plexus spreads in the lateral wall of the upper one third of the vagina beneath the uterine artery, medial to the ureter and 2 cm inferolateral to the cervix. Within the vesicovaginal space, the plexus supplies the upper vagina, bladder, proximal urethra, and lower ureter. Sympathetic preganglionic neurons generally use acetylcholine neurotransmitter acting on nicotinic receptors. The sympathetic postganglionic fibers are primarily noradrenergic, with norepinephrine being the chief neurotransmitter. Norepinephrine stimulation of β adrenergic receptors located in the bladder body causes relaxation of the smooth muscle, as the β receptors are stimulated by lower norepinephrine doses. Stimulation of α1 receptors in bladder base and urethral smooth muscle by higher doses of norepinephrine causes muscle contraction. Norepinephrine also acts as a neurotransmitter at the parasympathetic ganglia, and α-adrenergic receptors, when stimulated, depress parasympathetic pelvic ganglion transmission by suppression of presynaptic cholinergic neurotransmitter release. Thus, sympathetic relaxation of detrusor body smooth muscle, contraction of bladder base and urethral smooth muscle, and depression of parasympathetic ganglionic transmission,
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Peripheral innervation of the female lower urinary tract.
Actions of the autonomic and somatic nervous systems during bladder filling/storage and voiding.
all act to promote urine storage. Other sympathetic modulators of neurotransmission include purinergic, peptidergic, and nitrergic factors. PARASYMPATHETIC ACTIONS: DETRUSOR The parasympathetic preganglionic fibers arise from nerve roots S3 and S4 and, occasionally, S2, the cell bodies being in the sacral cord, the conus medullaris. These fibers emerge from the piriformis muscle overlying the sacral foramina and enter the presacral fascia near the ischial spine at the posterior layer of the hypogastric sheath, where they contribute to the already described pelvic plexus. The pelvic plexus has freely interconnected nerves in the pelvic fascia that supply the rec-
tum, genitalia, and lower urinary tract. The parasympathetic fibers to the urinary tract terminate in pelvic ganglia located within the wall of the bladder, a location quite vulnerable to end-organ disease, such as overstretch, infection, or fibrosis. At the ganglia, excitatory transmission occurs from activation of nicotinic acetylcholine receptors, with some ganglionic cells having secondary muscarinic receptors. Multiple neuropeptide agents also function at ganglia. Transmission regulation is complex, and precise knowledge is not available at present. At the detrusor muscle, postganglionic, parasympathetic detrusor nerve fibers diverge and store neurotransmitter agents in axonal varicosities called synaptic vesicles. The agent is diffused to neuromuscular bundles of 12 to 15
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smooth muscle fibers enclosed in a collagen capsule that acts similarly to the tendon insertion of a muscle. Stimulating electrical pulses produce two episodes of depolarization, suggesting the release of two neurotransmitters. The chief neurotransmitter is cholinergic, with muscarinic receptors, and the second neurotransmitter is noncholinergic and nonadrenergic. This observation accounts for detrusor atropine resistance. The studies of Burnstock et al. in 1972 demonstrated that adenosine triphosphate (ATP) was the mediator of these noncholinergic, nonadrenergic contractions. Variability is present between species, and some studies suggest that the purine (ATP) pathway responses lead to more rapid bladder contractions, perhaps being useful in animals that use short, quick squirts of urine for property marking. Muscarinic receptors have received much attention by pharmaceutical companies. The receptors are present in the CNS, eye lacrimal glands, salivary glands, heart, gallbladder, stomach, and colon. Five types (M1–5) have been identified. In detrusor muscle, M2 and M3 predominate, with M3 used more for detrusor contractions. Dry mouth, slowed gastrointestinal motility, blurred vision, increased heart rate, heat intolerance, sedation with reductions in memory and attention, delirium, drowsiness, fatigue, and other cognitive functions are side effects related to the various receptors. Anticholinergic medications using M2 and M3 receptors, without affecting the other muscarinic receptor pathways, should have more therapeutic effects against bladder overactivity with fewer side effects. Cholinergic receptors are more present in the body than in the base of the bladder, whereas adrenergic and neuropeptide receptors are more prevalent in the base. Neuropeptide modulators include vasoactive intestinal polypeptide and substance P. Histaminic and purinergic receptors may also be present in detrusor smooth muscle. SMOOTH MUSCLE OF TRIGONE AND URETHRA The trigone is a separate anatomic and embryologic region where smooth muscle fibers have an almost exclusively adrenergic innervation with chiefly α1 receptors. Cholinergic development in the bladder is present at birth, whereas adrenergic development occurs later. Prostaglandins act as intracellular messengers to relax trigonal muscles. The proximal urethral smooth muscle is rich in αadrenergic receptors responsive to norepinephrine neurotransmitter. Acetylcholine, substance P, vasoactive intestinal polypeptide, and histamine are all additional potential transmitters in the urethra. Nitric oxide (NO) is prominent in the parasympathetic postganglionic innervation of the urethra, and exogenous NO or parasympathetic nerve stimulation relaxes urethral smooth muscle. Parasympathetic stimulation has been thought by Khanna (1981) to cause contraction of urethral smooth muscle, using acetylcholine neurotransmission and muscarinic receptors. However, McGuire (1978) thought this increase in urethral “resistance” was due to simple transmission of intravesical pressure. He demonstrated, by diverting the urinary stream, that pelvic nerve stimulation caused urethral smooth muscle relaxation. The relaxation effect was blocked by propranolol, indicating a β-adrenergic response.
SKELETAL MUSCLE OF LOWER URINARY TRACT: SOMATIC INNERVATION In the lower urinary tract, the somatic system involves skeletal muscle in the lower urinary tract outlet. The neuronal cell bodies for the urethral sphincter and for the distal periurethral striated muscles and pelvic floor muscles are located in Onuf ’s somatic nucleus in the lateral aspect of the anterior horn of the gray matter of the sacral spinal cord from S2 to S4. This nucleus gives rise to the pudendal nerve, which is classically thought to provide the efferent innervation of the striated sphincter. Thor (2004) has shown that serotonin and norepinephrine enhance the effects of glutamate, the primary excitatory neurotransmitter for pudendal motor neurons. The pudendal nerve, using acetylcholine, activates nicotinic cholinergic receptors to contract the rhabdosphincter. The exact neuropathways supplying the urethral sphincter skeletal muscle are controversial. The proximal intramural component of the striated urogenital sphincter muscle (urethral sphincter, rhabdosphincter) is variably innervated by somatic efferent branches of the pelvic nerves, a component of the pelvic plexus. Elbadawi (1983) believed this intramural component to have somatic and autonomic (both cholinergic and adrenergic) innervation. However, the more distal periurethral striated muscles (compressor urethra and urethrovaginal sphincter) are innervated by the pudendal nerve, as is the skeletal muscle of the external anal sphincter and perineal muscles. Typically, somatic motor activity regulates skeletal muscle contraction by spinal reflexes, with the afferent arm of the reflex originating in muscle spindles, synapses taking place in the spinal cord, and the efferent arm originating in anterior horn cells with the axon going to the muscle. Unlike typical somatic reflex pathways that are regulated by sensory nerves from muscle spindles, the afferent regulation of the urethral sphincter somatic reflex is different because urethral skeletal muscle has no spindles. Embryologic speculation is that pelvic caudal muscles (tail waggers), which compose the levator group in humans, are supplied from the pelvic plexus on the pelvic surface side, whereas the sphincter cloacal derivatives are supplied from the perineal aspect by the pudendal nerve. The pudendal nerve passes between the coccygeus and piriformis muscles, leaves the pelvis through the greater sciatic foramen, crosses the ischial spine, and reenters the pelvis through the lesser sciatic foramen. Here the nerve accompanies the pudendal vessels along the lateral wall of the ischiorectal fossa in a tunnel formed by a splitting of the obturator fascia, called Alcock’s canal. At the perineal membrane, the nerve divides into the inferior rectal nerve, supplying the external anal sphincter, the perineal nerve, and the dorsal nerve to the clitoris (see Fig. 2-8). The perineal nerve splits into a superficial branch to the labia and a deep branch to the periurethral striated muscles. The branching of the pudendal nerve shows considerable variation. The urethral sphincter muscle is an integral part of the urethral wall and is made up of all slow-twitch (type 1) fibers. The periurethral muscles (compressor urethra and urethrovaginal sphincter) are composed of mostly slowtwitch fibers with a variable concentration of fast-twitch (type 2) fibers. These fibers combine to provide constant
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tonus, with emergency reflex activity mainly in the distal half of the urethra. The response of segmental spinal reflex leading to pudendal nerve function involves several spinal cord segments. Afferent fibers involved in the reflex have both segmental and supraspinal routing. This dual routing explains the bimodal response of pudendal motor neurons when pudendal sensory nerves are stimulated, and it differs from stimulation of pelvic detrusor afferents. The neurotransmitter at the periurethral skeletal neuromuscular junction is acetylcholine and the receptors are nicotinic type. The intimate adherence of the neuromuscular junction to the striated muscle fibers conveys a resistance to blockade by neuromuscular blocking agents.
Sensory Innervation Detrusor proprioceptive endings exist as nerve endings in collagen bundles. They are stimulated by stretch or contraction and are responsible for the feeling of bladder fullness. Pain and temperature nerve endings are free in bladder mucosa and submucosa. The sensory endings in the detrusor probably contain acetylcholine and substance P. Two types of bladder sensors have been postulated: the first sensor perhaps being at the trigone, the second being stretch receptors in the bladder body. Loss of the first sensor may lead to urge incontinence because the bladder is ready to contract before sensation is noted. Sensory innervation can follow both the sympathetic and parasympathetic nerves. Urgency is transmitted along parasympathetic pathways. Urethral sensation is carried principally by the pudendal nerve, although the pelvic nerve also contributes (Fig. 3-3). Urethral smooth muscle sensory innervation, like that of the detrusor, has both a contralateral and an ipsilateral supply.
Central Nervous System Modulation CNS neurons affecting bladder function may be spinal or supraspinal, with extensive dendritic communications. The chief excitatory neurotransmitter in the CNS is glutamate, frequently acting on N-methyl-d-aspartate (NMDA) receptors, which creates areas of possible therapeutic pharmaceuticals. The chief inhibitory CNS neurotransmitters are γ-aminobutyric acid (GABA) and glycine. The detrusor and the periurethral striated muscle mechanisms have separate cortical and other higher-center regulation. The effects of such regulation are chiefly on the brainstem for the detrusor and on the sacral cord for the periurethral mechanisms. The brain pathways known to be associated with bladder and pelvic floor activity include cortical pathways originating in the precentral gyrus, lateral prefrontal cortex, and anterior cingulate gyrus. Subcortical pathways originate in basal ganglia, brainstem raphe nuclei, locus ceruleus, hypothalamus, and the midbrain periaqueductal gray, and affect the brainstem, specifically the medial and lateral pons. These pathways use substances that modulate the chief CNS neurotransmitters, glutamate and GABA.
Figure 3-3 ■ Longitudinal sensory innervation of urethra. Column on left shows responses evoked in the pelvic nerve. Column on right shows responses evoked in the pudendal nerve. (From Bradley WE. Physiology of urinary bladder. In Walsh PC, Perlmutter AD, Gittes RF, et al. [eds]. Campbell’s Urology, 5th ed. WB Saunders, Philadelphia, 1986, with permission.)
CORTICAL AND SUBCORTICAL PATHWAYS The brainstem’s importance in the lower urinary tract function has been known since 1921, when Barrington ablated this area in cats and produced permanent urinary retention. He demonstrated that the middle pons was the level in the brain at which the motor tone of the bladder arises. This region in the pons has been called the pontine micturition center or the M region by Holstege et al. (1979). Stimulation results in the decrease in urethral pressure and silence of pelvic floor electromyographic (EMG) signal, followed by a rise in detrusor pressure. Tracing studies reveal direct projections from the M region to the intermediolateral cell column of the sacral cord and the parasympathetic preganglionic bladder motor neurons. Other projections are to sacral cord interneurons that activate GABA inhibition of Onuf ’s nucleus neurons. These detrusor motor nuclei in the pons receive suppressive afferents from basal ganglia, coordinating afferents from the cerebellum, and sensory cord afferents from tension receptors in the detrusor muscle, which synapse here to constitute the “long routing” detrusor reflex. Some speculate that because the detrusor reflex is a brainstem function rather than a spinal function, temporal amplification can occur, allowing for complete bladder emptying. Brainstem neurotransmitters include substance P, GABA, and serotonin, which is produced from tryptophan. Stimulation of the same level of the pons at a more lateral position, the L region, results in contraction of the urethral sphincter, by fibers in Onuf’s nucleus. Direct cortical relay to the L region gives voluntary micturition control. These brainstem activities, which are important for continence (L region) and micturition (M region) in adults, are replaced by reemerging pathologic primitive reflexes in disease states. Most important in this respect is the C-fiber–mediated reflex that emerges following disconnection from pontine regulatory influences as
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a consequence of spinal cord disease. These effects are mediated by sensory neurotransmitters that are prompted to appear by nerve growth factors, as shown by Steers et al. (1996), and that are alleviated by intravesical capsaicinoids. Similar development of C-fiber–afferentation is seen with bladder outlet obstruction and with bladder inflammatory states. The basal ganglia are associated with the production of dopamine, one of the catecholamine neurotransmitters that is largely inhibitory to bladder activity. Seventy-five percent of patients with decreased dopamine resulting from Parkinson’s disease have slowness of movement, gait disturbance, and tremor; 45% to 75% have bladder overactivity. The vast majority of cell bodies of origin for serotonin are in the raphe nuclei. Serotonin acts to inhibit reflex bladder and pelvic nerve activity by suppressing afferent bladder information. The sympathetic autonomic nuclei and the sphincter motor nuclei also receive a serotonergic input from the raphe nucleus. Fibers from the raphe nuclei of the reticular formation may moderate responsiveness to different phases of the sleep-wake cycle or emotional states. The locus ceruleus is the brainstem’s CNS container of norepinephrine cell bodies. Norepinephrine acts to tonically facilitate continence-related reflexes. The hypothalamus and midbrain periaqueductal gray (PAG) are activated during micturition. The paraventricular nucleus of the hypothalamus has connections to the sacral parasympathetic nucleus and the sphincter motor neurons. The anterior hypothalamus projects to the pons M region and can induce bladder contraction via pontine parasympathetic pathways. The posterior hypothalamus has sympathetic inhibitory pathways. The hypothalamus function, although poorly delineated, is known to involve β-endorphin neurotransmitters, the opioid peptides constituting an entire class of brain neurotransmitters. Interneurons in the lumbosacral cord project strongly to the PAG, which in turn projects to the pons M region, thus making the PAG an important component in bladder reflex activities. Pudendal cortical pathways affect periurethral striated muscle innervation by direct descending paths originating in the central vertex of the pudendal cerebral cortical area and going to pudendal nuclei in the ventromedial portion of the ventral gray matter of the S1 to S3 cord segments. At this level, the pudendal motor nuclei act as described to affect lower urinary tract skeletal muscle activity. Ascending axons from periurethral striated muscle go to the pudendal cortical area, possibly synapsing in the nucleus ventralis posterolateralis of the thalamus, the brain’s chief relay station. Sensory afferents from both pudendal and detrusor pelvic nerves send input to the anterior vermis of the cerebellum, which then originates an axon relay to the cortex in the dentate nucleus. Fibers for both detrusor and pudendal proprioception and exteroception (pain, temperature, and touch) ascend in posterior columns and spinothalamic tracts, respectively. Neurotransmitters involved in these pathways include acetylcholine and peptides, especially substance P and enkephalin. Neurotransmitter agents are stored in astrocytes, which may also regulate extracellular concentrations. The limbic system in the temporal lobes exerts controls affecting all autonomic functions and is a favored site for
epileptiform activity. Enkephalin is a notable neurotransmitter here as well as in the reticular formation. The cerebellum, where GABA is prominent along with standard neurotransmitters, regulates muscle tone and coordinates movement. Disease in this area produces spontaneous, high-amplitude detrusor overactivity.
SPINAL CORD By adolescence, disparity in growth of the spinal cord and the vertebral column leads to the cord’s terminating around the first lumbar vertebra. The adult conus medullaris is quite short and contains the entire S1 to S5 segment. Although the thoracolumbar levels are important in sympathetic autonomic influence of the lower urinary tract, the conus medullaris has greater significance because autonomic detrusor nuclei and pudendal somatic nuclei are housed in the intermediolateral and ventromedial anterior gray matter, respectively. The conus medullaris also houses neurons involved with defecation and sexual function, with relays for cortical separation of these visceral functions (encephalization) developing after birth.
MECHANISMS OF NORMAL BLADDER FILLING, STORAGE, AND VOIDING Filling and Storage Storage depends on sympathetic neural activity. As noted by McGuire (1986), three sympathetic neural responses to afferent pelvic nerve firing associated with increasing bladder volume have been demonstrated experimentally: βreceptor–mediated relaxation of the detrusor musculature, α-receptor–mediated increase in urethral smooth muscle activity and urethral pressure, and inhibition of ganglionic transmission in the pelvic (vesical) ganglia, which, in effect, inhibits sacral parasympathetic outflow to the bladder. These actions are illustrated in Figure 3-2. Somatic activation of lower urinary tract outlet is regulated by afferent pelvic nerve spinal reflexes that keep tonic resistance to the urethra so that urethral pressure is greater than detrusor pressure. Cortical tracts to the urethra and tracts involving the L region of the pons also take part in the voluntary assistance to storage.
Voiding The mechanisms responsible for switching reflexes from storage to voiding, that is, from chiefly sympathetic to parasympathetic, or adrenergic to cholinergic, or spinal to supraspinal reflex pathways, rely on axodendritic contacts between parasympathetic, sympathetic, and somatic pathways in the spinal cord. Voiding is largely a parasympathetic event. Our understanding of the neurophysiology of micturition developed from a large body of literature based primarily on animal models. Precise neural pathways involved in voiding remain
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controversial. The concepts presented here are based primarily on those by Bradley et al. (1974) and by de Groat et al. (1979), as synthesized by Blaivas (1982) and McGuire (1986). Figure 3-4 is a summary of the major neurologic pathways involved in bladder filling and voiding. Normal voiding is a voluntary act involving reflexcoordinated relaxation of the urethra and sustained contraction of the bladder until emptying is complete. In healthy women, the micturition reflex is probably not a simple segmental sacral reflex but is modulated supraspinally in the pontine micturition center. Voluntary control of the micturition reflex is mediated by connections between the frontal cerebral cortex and the pons. Voluntary control of the external urethral sphincter is via the corticospinal pathway connecting the frontal cortex with the pudendal nucleus in the ventral horn of the sacral spinal cord. Bradley et al. (1974) believe that connections between the sensorimotor cortex and the pudendal nucleus control voluntary sphincter activity and that voiding is controlled voluntarily by complex
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interactions among cortical areas (frontal cortex), subcortical areas (thalamus, hypothalamus, basal ganglia, and limbic system), and brainstem (mesencephalic-pontine-medullary reticular formation). With filling to bladder capacity, stimuli from the bladder cause afferent discharges in the pelvic nerve, which traverse pathways in the spinal cord to synapse in a supraspinal micturition center in the pontine mesencephalic reticular formation. Voiding is initiated voluntarily or when the bladder volume is so large that it is no longer possible to suppress micturition. To initiate voiding, the external urethral sphincter relaxes voluntarily via inhibition of somatic motor neurons from the ventral horn. Efferent impulses from the pontine micturition center run in the reticulospinal tracts to inhibit pudendal firing (relaxing the external sphincter) and to stimulate parasympathetic neurons situated in the intermediolateral cell column at levels S2 through S4, causing detrusor contraction. During voiding, sympathetic efferents are inhibited, which opens the bladder neck and permits
Figure 3-4 ■ Summary of major neurologic pathways involved in bladder function. Storage: Bladder distention results in afferent pelvic nerve discharge. After synapse in pudendal nucleus, efferent pudendal nerve impulses result in contraction of external urethral sphincter. At the same time, afferent sympathetic discharges traverse hypogastric nerve. After synapse in sympathetic nuclei, efferent firing causes (1) inhibition of transmission of postganglionic parasympathetic neuron, which inhibits detrusor contraction, and (2) increased tone at bladder neck. Net effect is that urethral pressure remains greater than detrusor pressure, facilitating urine storage. Voiding: Afferent pelvic nerve discharges ascend in spinal cord and synapse in pontine micturition center. Descending efferent pathways cause (1) inhibition of pudendal firing, which relaxes external sphincter, (2) inhibition of sympathetic firing, which opens bladder neck and permits postganglionic parasympathetic transmission, and (3) pelvic parasympathetic firing, which causes detrusor contraction. Net result is that relaxation of external sphincter causes decrease in urethral pressure, followed almost immediately by detrusor contraction, and voiding ensues. Stop: Voluntary interruption of urinary stream. Descending corticospinal pathways emanating from motor complex synapse in pudendal nucleus, resulting in contraction of external sphincter. Urethral pressure increases above detrusor pressure, interrupting stream. (Modified with permission from Blaivas JG. The neurophysiology of micturition: a clinical study of 550 patients. J Urol 1982;127:958.)
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postganglionic parasympathetic transmission. The micturition reflex depends upon glutamate activation of AMPA and NMDA receptors and is modulated by serotonergic and noradrenergic systems of brainstem that tend to support storage reflexes. Fight-or-flight situations affect micturition via 5-hydroxytryptamine (5-HT) and NE modulation. The highest densities of 5-HT and NE in lower urinary tract reflex pathways are in the lateral pathway (LP), primary afferents in sacral dorsal horn, sacral parasympathetic nucleus (SPN) and Onuf ’s nucleus, and lumbar sympathetic intermediolateral nucleus. 5-HT neurons in medullary neurons (raphe magnus) and NE neurons are medullary and pontine nuclei, for example, locus coeruleus (pons), and Kolliker-Fuse nucleus (pontomedullary junction). A delta afferents, activated by stretch, travel via Lissauer’s tract, to the PAG and to the M region to constitute a spinobulbospinal reflex. The efferent arm activates sacral parasympathetic neurons that travel to the pelvic nerve, with acetylcholine neurotransmitters acting on M2 and M3 receptors, and via interneuron GABA activity inhibiting Onuf ’s nucleus. Urodynamically, the micturition reflex begins with sudden and complete relaxation of the striated muscles of the urethra and pelvic floor and a decrease in urethral pressure. Several seconds later, intravesical pressure is increased by a highly controlled coordinated contraction of the bulk of the detrusor muscle. Descent and funneling of the bladder neck and proximal urethra occur and urine flow begins (Fig. 3-5). Brainstem modulation of the micturition reflex allows for a detrusor contraction long enough to completely evacuate intravesical contents. With voluntary termination of voiding or with the stop test, the striated muscles of the urethra and pelvic floor contract to elevate the bladder base, increase
intraurethral pressure, and empty the urethra of urine. The detrusor muscle is reflexly inhibited, and intravesical pressure returns to normal.
CLINICAL EFFECTS OF NEUROLOGIC DISEASE ON LOWER URINARY TRACT FUNCTION Clinical studies of patients with brain lesions demonstrate urgency and frequency with urodynamic studies revealing “neurogenic detrusor overactivity” (new terminology of the standardization subcommittee of the International Continence Society; see Appendix B) with coordinated detrusor and sphincter function if the lesion is above the pons (Fig. 3-6, B). Lesions below the pons interfere with detrusor and sphincter coordination, so the neurogenic detrusor overactivity is not associated with coordinated outlet activity (Fig. 3-6, C). If the brain lesion is limited to small frontal lobe areas, the patients are generally socially aware, understandingly embarrassed, and without dementia. In patients with parkinsonism, a diagnosis of multiple system atrophy (MSA) should be considered if urinary symptoms are severe. MSA involves processes of atrophy of neurons. The neurons involved are frequently those involved in bladder control. Thus, neurogenic detrusor overactivity may be due to cell loss in the brainstem region, and incomplete bladder emptying may be due to loss of parasympathetic drive with atrophy of intermediolateral cell columns. Weakening of the sphincter may be due to loss of cells in Onuf ’s nucleus; anal sphincter needle EMG may be helpful in diagnosis.
Brainstem Lesions Nearly half of all patients with brainstem lesions have urinary symptoms, especially voiding difficulty, as shown by Betts et al. (1992). Eye movement disorders may accompany bladder dysfunction resulting from pons lesions because of the proximity of the medial longitudinal fasciculus to the pontine micturition center. The bladder dysfunctions associated with brainstem lesions include emptying disorders, nocturnal urinary frequency, and urgency with neurogenic detrusor overactivity.
Spinal Cord Disease
Figure 3-5 ■ Urodynamic representation of normal female micturition. A. Voluntary initiation of voiding with relaxation of external urethral sphincter and pelvic floor muscles and associated decrease in urethral pressure. B. Detrusor contraction occurs with increase in intravesical pressure; intraurethral pressure equals intravesical pressure, and urine flow is initiated. C. Voluntary termination of voiding. (From Walters MD. Mechanisms of continence and voiding, with International Continence Society classification of dysfunction. Obstet Gynecol Clin North Am 1989;16:773, with permission.)
Urinary storage and micturition are dependent upon spinal cord reflexes. Storage reflexes include direct spinal activation of Onuf ’s nucleus to activate tonic, somatic, skeletal periurethral muscle. Sympathetic reflexes involve low-level bladder afferent firing, which traverses the spinal cord, activating lumbar sympathetic preganglionic neurons. Secondary sympathetic neurons, chiefly via the prevertebral hypogastric postganglionic nerves, cause bladder outlet contraction and parasympathetic ganglionic inhibition by α-receptor activity and detrusor relaxation by β-receptor activity. Micturition reflexes involve GABA inhibition of urethral sphincter EMG activity. This activity is initiated in the pontine micturition center and involves the spinal cord for transmission. The pontine micturition center is also associated with stimulating sacral preganglionic parasympathetic
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as with multiple sclerosis. The detrusor-sphincter dyssynergia causes poor bladder emptying. Hence, both storage and emptying phases of bladder function are altered, although the resulting symptoms are chiefly problems of storage. The overactive, small capacity bladder with relative outlet obstruction leads to the development of urgency/frequency and urge incontinence as the chief symptoms. An important clinical note presented by Fowler (1999) is that unless completely restricted to the conus medullaris, spinal cord disease, which is responsible for the development of a neurogenic bladder, will produce clinical signs in the lower limbs because the innervation of the bladder arises more caudally than the innervation of the lower limbs. Because spinal cord injury is a nonprogressive neurologic disease, and, because the neurogenic detrusor overactivity and detrusor-sphincter dyssynergia and loss of bladder compliance can cause ureteric reflux and resultant upper renal tract damage, therapy must be directed to prevention of upper tract disease. An example of such therapy is the avoidance of sustained bladder drainage, which may add to compliance loss. In contrast, progressive spinal cord disease (e.g., multiple sclerosis) very rarely causes upper tract involvement. The therapies, therefore, may be more symptomatic. Transverse myelitis has a consistent, surprising finding in that, although there may be excellent clinical recovery from tetraparesis, bladder dysfunction remains as a sole residual neurologic complaint.
Cauda Equina
Figure 3-6 ■ Interruption of nervous system at various levels and subsequent voiding dysfunction. A. Lesions in higher cortical centers have various effects, including inability to voluntarily postpone voiding, urge incontinence, enuresis, urethral spasm, and loss of social concern about incontinence. B. Suprapontine lesions result in involuntary detrusor contractions with coordinated urethral relaxation. C. High spinal cord (upper motor neuron) lesions lead to neurogenic detrusor overactivity without coordinated urethral relaxation (detrusor-sphincter dyssynergia). D. Lower motor neuron lesions cause detrusor areflexia.
bladder contraction via glutamic acid neurotransmission and NMDA and non-NMDA glutaminergic receptors. Thus, trans-spinal pathways to connect the pontine micturition center and the sacral cord are necessary to effect coordinated bladder and outlet activities so detrusor contraction and sphincter relaxation may be synchronous with voiding, and detrusor relaxation and sphincter contraction may act in harmony for urinary storage. Following disconnection from the pons, this synergistic activity is altered, and the detrusor and the sphincter tend to contract simultaneously, a condition known as detrusor-sphincter dyssynergia. During “spinal shock,” immediately following spinal cord trauma, the bladder is acontractile. In a few weeks, the bladder develops new reflexes leading to detrusor hyperreflexia, with C fibers becoming the major afferents of these poorly effective reflexes. The bladder capacity is diminished. Detrusorsphincter dyssynergia commonly develops in patients with spinal cord disease, whether acute as with trauma, or chronic
Damage in cauda equina syndromes involves both anterior and posterior sacral roots and hence have somatic and parasympathetic motor effects and somatic and visceral sensory effects. The clinical picture involves sensory loss, in a patchy “saddle hypesthesia” pattern and variable loss of anal and urethral and sexual response functions.
Peripheral Innervation and Bladder Dysfunction Bladder disturbances are seen in peripheral neuropathies that involve small fibers, for example, diabetes, amyloidosis, and pan-autonomic neuropathy. The most common in developed countries is diabetes, which typically involves small sensory and postganglionic parasympathetic fibers, leading to excessive accommodation, reduced bladder sensation, increased residual urine, decreased urine flow, and markedly increased capacity. Other signs of neurologic disturbance are common, and bladder dysfunction in isolation is not seen.
Pelvic Nerve Injury Pelvic nerve injury, resulting in bladder dysfunctions, can be produced by resection surgery (e.g., radical hysterectomy or rectal carcinoma or prostate excision surgery). The chief damages are to the parasympathetic innervation. Nerve injury may also be seen with vaginal deliveries. A particularly common type is bladder overdistention injury, which is seen in conjunction with epidural anesthesia and labor and where bladder volumes are not consistently known. Varying degrees of urinary retention are seen with overdistention injuries.
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Urinary retention in young girls without evidence of neurologic disease may be seen in conjunction with pseudomyotonia, a distinct auditory and waveform pattern seen on needle examination of the urethral sphincter. This type of EMG activity is not specific and may also be seen in other types of bladder dysfunction or in patients with normal lower urinary tract function. Many patients with urinary retention and EMG abnormality have polycystic ovaries, suggesting the possibility of a linkage of disturbances to a hormonal abnormality, the overall condition referred to as Fowler’s syndrome. The syndrome appears to be responsive to sacral neuromodulation therapy.
CLINICAL PHARMACOLOGY OF THE LOWER URINARY TRACT Thorough understanding of the neurologic control of the urinary bladder and its outlet allows one to intelligently use pharmacologic agents to manage many types of lower urinary tract dysfunction. Basic concepts of pharmacologic treatment are summarized within a functional scheme of therapy for micturition disorders, as developed by Wein et al. (1991) (see Box 5-2). More specific guidelines for pharmacologic treatments of various lower urinary tract complaints and reviews of the clinical studies using these agents are found in the chapters describing individual urogynecologic disorders. Most pharmacologic agents produce their effects by combining with cell receptors. The drug-receptor interaction initiates a series of biochemical and physiologic changes that characterize the effects produced by the agent. In general, drugs alter lower urinary tract function by affecting synthesis, transport, storage, and release of the neurotransmitter; the combination of the neurotransmitter with postjunctional receptors; or the inactivation, degradation, or reuptake of the neurotransmitter. Most drugs used to treat lower urinary tract disorders were developed originally for their actions on other organ systems whose functions are also controlled by innervation or drug-receptor interaction. The pharmacologic effects on other organ systems are responsible for many of the unwanted side effects of these agents. Improving specificity and selectivity of the therapeutic agents is an important area of future development in uropharmacology. Clinically, pharmacologic agents can be grouped into those that facilitate bladder emptying and those that facilitate urine storage (Box 3-1). Patients with disorders of bladder emptying usually have voiding dysfunction; drugs that improve bladder emptying do so by increasing bladder contractility or by decreasing outlet resistance. Patients with disorders of urine storage often present with urinary frequency, urgency, or urinary incontinence (stress and/or urge), which is usually caused by either an overactive detrusor or an incompetent urethral sphincter mechanism. Agents that facilitate urine storage act by inhibiting bladder contractility—thereby increasing bladder capacity—by increasing outlet resistance, or by reducing sensation or afferent input necessary to trigger voiding. The most effective and
BOX 3-1
DRUG EFFECTS ON LOWER URINARY TRACT FUNCTION
Therapy to Facilitate Bladder Emptying1
Therapy to Facilitate Urine Storage
Increasing intravesical pressure/bladder contractility
Inhibiting bladder contractility/increasing bladder capacity
Parasympathomimetic agents Prostaglandins Blockers of inhibition α-Adrenergic antagonists Opioid antagonists
Antimuscarinic agents Anticholinergic agents β-Adrenergic agonists Prostaglandin inhibitors Tricyclic antidepressants Botulinum toxin Potassium channel openers
Decreasing outlet resistance at the level of the smooth sphincter β-Adrenergic agonists α-Adrenergic agonists
At the level of the striated sphincter Skeletal muscle relaxants Centrally acting relaxants Botulinum toxin Dantrolene Baclofen α-Adrenergic antagonists
Increasing outlet resistance α-Adrenergic antagonists Tricyclic antidepressants SNRI β-Adrenergic antagonists Estrogen β-Adrenergic agonists
Afferent nerve inhibitors/ decreasing sensory input Vanilloid receptor agonists Local anesthetics Dimethyl sulfoxide
SNRI, Serotonin (5-HT)–norepinephrine reuptake inhibitor.
commonly used agents act on either the parasympathetic or sympathetic systems.
Therapy to Facilitate Bladder Emptying INCREASING INTRAVESICAL PRESSURE A major portion of the final common pathway in a physiologic bladder contraction is stimulation of the muscarinic cholinergic receptor sites at the postganglionic, parasympathetic neuromuscular junction. Parasympathetic nerve stimulation causes the release of acetylcholine at postsynaptic, parasympathetic receptor sites. Acetylcholine release produces muscarinic and nicotinic effects; one of the muscarinic effects is contraction of the detrusor muscle and relaxation of the trigone. Acetylcholine itself cannot be used for therapeutic purposes because of actions at central and ganglionic levels and because of its rapid hydrolysis by acetylcholinesterase and nonspecific cholinesterase. Bethanechol chloride exhibits a selective acetylcholine-like action on the urinary bladder and gut, with little or no action at therapeutic dosages on ganglia or the cardiovascular system. Bethanechol chloride is cholinesterase resistant and causes a contraction of smooth muscle from the bladder, bladder neck, and urethra, thus preventing coordinated and complete bladder emptying. Although bethanechol chloride has been used extensively for treatment of postoperative and postpartum urinary retention, it is no longer considered to be effective to facilitate voiding. Other pharmacologic methods of achieving a cholinergic effect include the use of cholinesterase agents, dopamine
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antagonists (metoclopramide), and α-adrenergic blocking agents (to block the inhibitory effect of sympathetics on pelvic parasympathetic ganglionic transmission). In addition, prostaglandins may facilitate bladder emptying by inducing detrusor contraction and maintaining smooth muscle tone. Unfortunately, drug therapy is generally ineffective in causing detrusor contraction and improving voiding, especially in the presence of neurogenic disease. The best treatments remain intermittent self-catheterization and sacral neuromodulation (see Chapters 31 and 38). DECREASING OUTLET RESISTANCE The lower urinary tract has α- and β-adrenergic receptor sites, the functions of which have been discussed. Facilitation of bladder emptying could be achieved by the use of α-adrenergic antagonists, which decrease outlet resistance by smooth muscle relaxation of the bladder neck and proximal urethra. Some investigators have suggested that these agents may also affect striated sphincter tone. Alpha-sympathetic blocking agents have thus been used to treat both smooth sphincter dyssynergia and detrusor-striated sphincter dyssynergia. Wein et al. (1991) published a review of the effectiveness of these agents. Botulinum toxin, a substance that inhibits acetylcholine release from cholinergic nerve terminals, is a presynaptic neuromuscular blocking agent inducing selective and reversible muscle weakness for up to several months when injected intramuscularly in minute quantities. In urology, indications for botulinum-A toxin have been neurogenic detrusor overactivity, detrusor-sphincter dyssynergia, motor and sensory urge, and certain pain disorders. Botulinum toxin appears to be effective to treat detrusor-sphincter dyssynergia when injected either transurethrally or transperineally into the external urethral sphincter. Best indications seem to be multiple sclerosis and incomplete spinal cord injury patients suffering from neurogenic detrusor overactivity and detrusor-sphincter dyssynergia.
Therapy to Facilitate Urine Storage DECREASING BLADDER CONTRACTILITY Overactivity of the bladder during filling may present as involuntary detrusor contractions, decreased bladder compliance, and/or urgency with or without incontinence. The pathophysiology and treatments of detrusor overactivity are discussed thoroughly in Chapter 28. Pharmacologic agents used to treat detrusor overactivity are directed toward inhibiting bladder contractility or decreasing sensory input during filling. Atropine and atropine-like agents depress detrusor overactivity of any cause by inhibiting muscarinic cholinergic receptor sites. Propantheline bromide is an oral agent with this mechanism of action; however, side effects limit its use. Currently available anticholinergic agents include oxybutynin, tolterodine, propiverine, trospium chloride, solifenacin, and darifenacin. Efficacy for the treatment of overactive bladder is probably similar among these agents, although their side effect profiles may differ somewhat. This is probably due, at least in part, to their differing selectivity for muscarinic receptor subtypes, and thus they have different effects on the body in addition to their actions on the
41
bladder. Oxybutynin has moderate selectivity for M3 over M2, M4, and M5 receptors but greater affinity for M3 and M1 receptors. Tolterodine, propiverine, and trospium chloride have only modest selectivity for one type of muscarinic receptor compared to another. Solifenacin, like oxybutynin, is more selective for M1 and M3 receptors over other types, and darifenacin shows the highest selectivity for M3 receptors. The impact of these differences in receptor selectivity is probably responsible for some of the differences between drugs in rates of dry mouth, slowed gastrointestinal motility, blurred vision, heart rate changes, and sedation. Patients can also have reductions in memory, attention, delirium, drowsiness, and fatigue, and these changes are partially due to the drug’s relative ability to cross the blood-brain barrier. Blood-brain barrier permeability increases with age, stress, and certain diseases. All five receptor subtypes are expressed in the brain. M1 is predominant in forebrain and hippocampus (working memory and inhibition), M2 affects flexibility and memory, and M3 and M5 affects learning. Darifenacin is more selective for M3 and least likely to block M1. Oxybutynin has small molecular weight, high lipophilicity, and neutral polarity, making it more likely to cross the barrier than larger, less lipophilic, polarized drugs, such as darifenacin, tolterodine, and trospium. Tricyclic antidepressants, particularly imipramine hydrochloride, have prominent systemic anticholinergic effects, weak antimuscarinic effects on bladder smooth muscle, antihistaminic effects, and local anesthetic properties. Imipramine also appears to increase bladder outlet resistance by a peripheral blockade of noradrenaline uptake. Thus, it may be effective for the treatment of urine storage disorders by both decreasing bladder contractility and increasing outlet resistance. Injections of botulinum-A toxin into the detrusor muscle was first tested to treat neurogenic detrusor activity in spinal cord injured patients and in myelomeningocele children. Excellent results of this therapy into the detrusor in neurogenic detrusor overactivity led to an expansion of this treatment to incontinence due to idiopathic detrusor overactivity. Although preliminary results are promising, adequate dosage of the toxin required for this indication, as well as long-term outcomes, are not yet known. Several new intravesical treatment options to treat neurogenic detrusor overactivity appear promising. Currently available intravesical treatments either act on the afferent arc of the reflex, such as local anesthetics or vanilloid, or on the efferent cholinergic transmission to the detrusor muscle, such as intravesical oxybutynin or botulinum toxin. Vanilloid receptor agonists reduce sensation or afferent input that is necessary to trigger micturition. These drugs include capsaicin and resiniferatoxin. Resiniferatoxin is a pungent substance from a cactus that is 1000 times more potent than capsaicin in interacting with vanilloid receptors to excite and then desensitize afferent nerves, particularly C fiber or bladder afferents, while being much less painful than capsaicin for bladder injection. These drugs might raise volume threshold for micturition and are potentially useful for pain disorders and overactive bladder, with or without urge incontinence. Other drugs that have been used to decrease bladder contractility include β-adrenergic agonists, prostaglandin inhibitors, and dimethyl sulfoxide. The overall clinical response has generally been small with these agents.
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INCREASING OUTLET RESISTANCE Because of the preponderance of α-adrenergic receptor sites in the bladder neck and proximal urethra, α-adrenergic agonists have been used to produce urethral smooth muscle contraction, thereby increasing resting urethral pressure and resistance to outflow. Beta-adrenergic blocking agents may be expected to increase urethral resistance as well, potentiating an α-adrenergic effect. However, few studies have tested this hypothesis and the clinical effects of either drug type are relatively small. Duloxetine is a potent and balanced dual serotonin (5-HT)-norepinephrine reuptake inhibitor (SNRI) that potentiates the physiologic actions of endogenous serotonin and NE (by inhibiting the reuptake of these neurotransmitters in the presynaptic element) and thereby enhancing the CNS continence control mechanisms. Duloxetine is believed to stimulate pudendal nerve motor output resulting from increased levels of 5-HT and norepinephrine in the pudendal motor nucleus. This appears to improve urethral closure pressure and urethral resistance. Studies have shown an improvement in stress incontinence symptoms in over 60% of women and a decrease in incontinence episodes by over 50%, with variable side effects. FDA approval of duloxetine for the indication of urinary incontinence is pending. Estrogens affect adrenergic nerves by influencing excitability, neuronal influences on the muscle, receptor density and sensitivity, and transmitter metabolism. The clinical use of estrogen to augment lower urinary tract function is discussed in Chapter 14.
Bibliography Barrington FJ. The nervous mechanism of micturition. Q J Exp Physiol 1914;8:33. Barrington FJ. The relation of the hind-brain to micturition. Brain 1921;44:23. Beck RP. Neuropharmacology of the lower urinary tract in women. Obstet Gynecol Clin North Am 1989;16:753. Bennett BC, Kruse MN, Roppolo JR, et al. Neural control of urethral outlet activity in vivo: role of nitric oxide. J Urol 1995;153:2004. Betts CD, Kapoor R, Fowler CJ. Pontine pathology and voiding dysfunction. Br J Urol 1992;70:100. Blaivas JG. The neurophysiology of micturition: a clinical study of 550 patients. J Urol 1982;127:958. Blaivas JG. Pathophysiology of lower urinary tract dysfunction. Urol Clin North Am 1985;12:216. Bradley WE. Cerebro-cortical innervation of the urinary bladder. Tohoku J Exp Med 1980;131:7. Bradley WE. Physiology of urinary bladder. In Walsh PC, Perlmutter AD, Gittes RF, et al. (eds). Campbell’s Urology, 5th ed. WB Saunders, Philadelphia, 1986. Bradley WE, Timm GW, Scott FB. Innervation of the detrusor muscle and urethra. Urol Clin North Am 1974;1:3. Burnstock G, Dumsday B, Smythe A. Atropine resistant excitation of the urinary bladder: the possibility of transmission via nerves releasing a purine nucleotide. Br J Pharmacol 1972;44:451. Cardozo L, Drutz HP, Baygani SK, Bump RC. Pharmacological treatment of women awaiting surgery for stress urinary incontinence. Obstet Gynecol 2004;104:511. Chancellor MB, de Groat WC. Intravesical capsaicin and resiniferatoxin therapy: spicing up ways to treat the overactive bladder. J Urol 1999;162:3. Cruz F. Mechanisms involved in new therapies for overactive bladder. Urology 2004;63:65. de Groat WC. Nervous control of the urinary bladder in the cat. Brain Res 1975;87:201.
de Groat WC, Booth AM, Krier J, et al. Neural control of the urinary bladder and large intestine. In Brooks CM, Koizumi K, Sato A, eds. Integrative Functions of the Autonomic Nervous System. Elsevier/North Holland, Biomedical Press, Amsterdam, 1979. de Groat WC, Ryall RW. Recurrent inhibition in sacral parasympathetic pathways to the bladder. J Physiol 1968;196:579. de Groat WC, Yoshimura N. Pharmacology of the lower urinary tract. Ann Rev Pharmacol Toxicol 2001;41:691. Downie JW, Armour JA. Relation of afferent nerve activity in the pelvic plexus with pressure, length, and wall strain in the urinary bladder of the cat. Soc Neurosci Abstr 1982;8:858. Edvardsen P. Changes in urinary-bladder motility following lesions in the nervous system in cats. Acta Neurol Scand 1966;42:25. Elbadawi A. Neuromorphologic basis of vesicourethral function. I. Histochemistry, ultrastructure, and function of intrinsic nerves of the bladder and urethra. Neurourol Urodyn 1982;1:3. Elbadawi A. Autonomic muscular innervation of the vesical outlet and its role in micturition. In Hinman F Jr, ed. Benign Prostatic Hypertrophy. Springer-Verlag, New York, 1983, pp. 330–348. Finkbeiner A, Welch L, Bissada N. Uropharmacology. IX. Direct acting smooth muscle stimulants and depressants. Urology 1978;12:128. Fletcher TF, Bradley WE. Neuroanatomy of the bladder-urethra. J Urol 1978;119:153. 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;297:1436. Fowler CJ. Neurological disorders of micturition and their treatment. Brain 1999;122:1213. Gibson A. The influence of endocrine hormones on the autonomic nervous system. J Auton Pharmacol 1981;1:331. Gosling JA, Dixon JS. The structure and innervation of smooth muscle in the wall of the bladder neck and proximal urethra. Br J Urol 1975;47:549. Gosling JA, Dixon JS, Critchley HO. A comparative study of the human external sphincter and periurethral levator ani muscles. Br J Urol 1981;53:35. Holstege G, Kuypers HG, Boer RC. Anatomical evidence for direct brain stem projections to the somatic motoneuronal cell groups and autonomic preganglionic cell groups in cat spinal cord. Brain Res 1979;171:329. Ioanid CP, Noica N, Pop T. Incidence and diagnostic aspects of the bladder disorders in diabetics. Eur Urol 1981;7:211. Jünemann K, Thüroff J. Innervation. In Brubaker LT, Saclarides TJ, eds. The Female Pelvic Floor: Disorders of Function and Support. FA Davis, Philadelphia, 1996. Kelin LA. Urge incontinence can be a disease of bladder sensors. J Urol 1988;139:1010. Khanna OP. Vesicourethral smooth muscle: function and relation to structure. Urology 1981;18:211. Leippold T, Reitz A, Schurch B. Botulinum toxin as a new therapy options for voiding disorders: current state of the art. Eur Urol 2003;44:165. Mahoney DT, Laberte RO, Blais DJ. Integral storage and voiding reflexes: neurophysiologic concept of continence and micturition. Urology 1977;10:95. McGuire EJ. Experimental observations on the integration of bladder and urethral function. Invest Urol 1978;15:303. McGuire EJ. The innervation and function of the lower urinary tract. J Neurosurg 1986;65:278. Morrison J, Steers WD, Brading A, et al. Neurophysiology and neuropharmacology. In The 3rd International Consultation on Incontinence. Health Publication Ltd, Paris, 2005. Mundy AP. Clinical physiology of the bladder, urethra and pelvic floor. In Mundy AP, Stephenson TP, Wein AJ, eds. Urodynamics: Principles, Practice and Application. Churchill Livingstone, New York, 1984. Pernow B. Substance P. Pharmacol Rev 1983;35:85. Raezer D, Wein AJ, Jacobowitz D, et al. Autonomic innervation of canine urinary bladder: cholinergic and adrenergic contributions and interaction of sympathetic and parasympathetic systems in bladder function. Urology 1973;2:211. Reitz A, Schurch B. Intravesical therapy options for neurogenic detrusor overactivity. Spinal Cord 2004;42:267. 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;45:510. Sakakibara R, Hattori T, Yasuda K, Yamanishi T. Micturition disturbance in acute transverse myelitis. Spinal Cord 1996;34:481.
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Sillen U: Central neurotransmitter mechanisms involved in the control of urinary bladder function. Scand J Urol Nephrol 1980;58:1. 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. Steers WD, Creedon D, Tuttle JB. Immunity to NGF prevents afferent plasticity following hypertrophy of the urinary bladder. J Urol 1996;155:378. Steers WD. Physiology and pharmacology of the bladder and urethra. In Walsh PC, Retik AB, Vaughan ED, et al., eds. Campbell’s Urology, 7th ed. WB Saunders, Philadelphia, 1998. Stohrer M, Schurch B, Kramer G, Schmid D. Botulinum A toxin detrusor injections in the treatment of detrusor hyperreflexia. J Urol 2000;163:244A. Swash M. Innervation of the bladder, urethra and pelvic floor. In Drive JO, Hilton P, Stanton SL, eds. Micturition. Springer-Verlag, London, 1990. Tanagho EA, Miller ER. Initiation of voiding. Br J Urol 1970;42:175. Thor KB. Targeting serotonin and norepinephrine receptors in stress urinary incontinence. Int J Gynaecol Obstet 2004;86(Suppl):S38. 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.
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Tulloch AG. Sympathetic activity of internal urethral sphincter in empty and partially filled bladder. Urology 1975;5:353. Uvelius B, Gabella G. Relation between cell length and force production in urinary bladder smooth muscle. Acta Physiol Scand 1980;110:357. 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. Walters MD. Mechanisms of continence and voiding, with International Continence Society classification of dysfunction. Obstet Gynecol Clin North Am 1989;16:773. Wang P, Luthin GR, Ruggieri MR. Muscarinic acetylcholine receptor subtypes mediating urinary bladder contractility and coupling to GTP binding proteins. J Pharmacol Exp Ther 1995;273:959. Wein AJ. Pharmacology of incontinence. Urol Clin North Am 1995;22:557. Wein AJ, Arsdalen KV, Levin RM. Pharmacologic therapy. In Krane RJ, Siroky MB, eds. Clinical Neurourology, 2nd ed. Little Brown & Co., Boston, 1991. Wein AJ, Barrett DM. Voiding Function and Dysfunction. Mosby, Chicago, 1988. Winter DL. Receptor characteristics and conduction velocities in bladder efferents. J Psychiatr Res 1971;8:225.
Epidemiology and Psychosocial Impact of Pelvic Floor Disorders
4
Anne M. Weber
PREVALENCE, INCIDENCE, AND REMISSION 44 Urinary Incontinence 44 Fecal Incontinence 45 Pelvic Organ Prolapse 45 Concomitant Pelvic Floor Disorders 45 RISK FACTORS FOR PELVIC FLOOR DISORDERS 45 Sex 45 Age 46 Race 47 Childbirth 47 Menopause and Estrogen 48 Obesity 48 Smoking 49 PSYCHOSOCIAL IMPACT OF PELVIC FLOOR DISORDERS Social Changes 49 Psychological Changes 51 Quality of Life 51 Sexual Changes 51 ECONOMIC ISSUES 52
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Because the prevalence of pelvic floor disorders increases with age, the changing demographics of the U.S. population will result in even more affected women. Based on projections from the Census Bureau, the number of women age 60 and over will almost double between 2000 and 2030. For example, the number of women ages 60 to 69 will increase from 10 to 20 million. Even absolute population numbers do not fully reflect the real and growing burden of pelvic floor disorders on women as they age. Luber et al. (2001) estimated that the demand for health care services related to pelvic floor disorders will increase at twice the rate of the population.
PREVALENCE, INCIDENCE, AND REMISSION When interpreting information from the medical literature, a clear understanding of key epidemiologic terms is important; unfortunately, these terms are commonly misused. Prevalence refers to the proportion of individuals who have the condition of interest (numerator) divided by the popu-
lation at risk (denominator) at a particular point in time. Prevalence data can be obtained from cross-sectional studies or from baseline information at the beginning of a cohort study. Incidence is the number of individuals who develop the condition of interest (numerator) divided by the population at risk (those without the condition at baseline; denominator) over a certain period. Incidence is a rate with a unit of time in the denominator. Incidence data can be obtained only from longitudinal cohort studies that identify individuals without the condition of interest at entry and follow them through time to determine how many develop the condition. Remission is the opposite of incidence, that is, the number of individuals (numerator) in whom the condition resolves with time, divided by the population with the condition at baseline (denominator). As with incidence, remission is a rate with a unit of time in the denominator. Similarly, remission data can be obtained only from longitudinal studies that follow individuals over time.
Urinary Incontinence Urinary incontinence is defined by the International Continence Society (ICS) as “the complaint of any involuntary leakage of urine.” As broad as this definition is, it is easy to see why the reported prevalence of urinary incontinence in women varies widely with differences in populations studied, methods of data collection, and specific definitions of disease. Incorrect estimates may result from biases in sample surveys, such as selection and respondent bias. Studies have shown moderately strong agreement between patient selfreport and clinicians’ assessments of urinary incontinence. For these reasons, estimates from the literature should be considered as close approximations only. Considerable variation exists in the estimated prevalence of any urinary incontinence, that is, any urine loss during a 12-month period in women in the community. When the continence mechanism is subjected to extreme forces, a significant prevalence is present even in women not traditionally thought to be at risk for urinary incontinence, such as nulliparous elite athletes (e.g., trampolinists) or female paratroopers. Among adult women in the community, the prevalence of any urinary incontinence ranges from 9% to 69%.
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Epidemiology and Psychosocial Impact of Pelvic Floor Disorders
Severity of incontinence can be characterized by the frequency of incontinent episodes, quantity of urine lost, or both. When the severity of urine loss is defined as “daily,” “weekly,” or “most of the time,” the reported prevalence ranges from 3% to 17% for women in the community. This estimate corresponds more closely to the clinical estimate of disease because it probably identifies women at the more severe end of the spectrum who present for clinical care. The prevalence of urinary incontinence in women in nursing homes is much higher than in women in the community, with most studies reporting prevalence greater than 50%, especially in facilities where residents have more severe functional impairments. Much less information is available on incidence, progression, or remission, compared with prevalence, for urinary incontinence (and even less for all other pelvic floor disorders). Young and middle-aged women develop urinary incontinence at a lower rate, 3% to 8% per year, than older women. Herzog et al. (1990) reported a 20% incidence of incontinence per year in women age 60 and over. However, Grodstein et al. (2004) reported a much lower incidence per year of 3.2% occasional and 1.6% frequent incontinence in women ages 50 to 75. As noted earlier, this emphasizes the difficulty of directly comparing findings across the literature due to the use of different definitions of disease. Traditionally, urinary incontinence has been viewed as a chronic progressive disease. However, recent findings challenge this. In a 3-year study of raloxifene for osteoporosis, most women (60%) with incontinence at baseline did not experience a significant change in their symptoms; 27% improved, and only 13% worsened. Remission occurs in 6% to 38% of young and middle-aged women versus 10% in older women. These estimates include both chronic and acute causes of urinary incontinence. Incontinence due to transient causes, such as infection, drug use, and delirium, often regresses after treatment. Thus, a yearly fluctuation occurs in the development and regression of incontinence among individuals.
Fecal Incontinence As with urinary incontinence, the reported prevalence of fecal incontinence varies by the definition used and the population surveyed. Unlike urinary incontinence, however, even the term itself is problematic. Some clinicians refer to fecal incontinence only for loss of stool (liquid or solid) and prefer anal incontinence to collectively describe loss of stool or gas; however, many others do not make that distinction and use fecal incontinence to refer to loss of any bowel contents, whether gas or stool. For the purposes of this chapter, the term fecal incontinence will refer to the involuntary loss of gas and stool (either or both). No consensus is known as to what constitutes severe or clinically important fecal incontinence. Severity can be expressed by the type of loss (gas, liquid stool, or solid stool) or the frequency of incontinent episodes. Several scales combine these two components and express the level of symptoms as a numeric score. Many studies use frequency of incontinent episodes of once a week or more, or loss that requires sanitary protection, to define fecal incontinence. The prevalence of fecal incontinence in the general population ranges from 1.5% to 2.3%. In the elderly, the prevalence is higher, ranging from 3.7% to 18.4%. Women in nursing homes experience fecal incontinence at an even
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higher rate of at least 30% and up to 63%. Information on the incidence of fecal incontinence is unavailable, as is information on progression from mild or infrequent fecal incontinence to more severe forms.
Pelvic Organ Prolapse Epidemiologic characteristics of prolapse are even more difficult to determine than those of urinary and fecal incontinence. Symptoms associated with prolapse are nonspecific, and the presence of mild to moderate prolapse cannot be determined reliably by questionnaire assessment without confirmation by physical examination. Although a standardized staging system for prolapse has been accepted by the ICS, no consensus exists as to what level of physical findings defines clinically significant prolapse. Reports of prevalence in the medical literature must be viewed with these limitations in mind. In studies of women who were not seeking care for prolapse, mild to moderate prolapse (at or above the hymen, stages I–II prolapse by ICS standards) has been found in up to 48% of women. More advanced prolapse (beyond the hymen, stage III or IV) occurs in about 2% of women. In 412 women enrolled in the Women’s Health Initiative, Handa et al. (2004) reported an annual average incidence of 9.3 cases of anterior vaginal prolapse, 5.7 cases of posterior vaginal prolapse, and 1.5 cases of uterine prolapse per 100 women per year. In women with at least grade 1 prolapse at baseline, progression occurred in 10.7 cases of anterior vaginal prolapse, 14.8 of posterior, and 2.0 of uterine prolapse per 100 women per year. Interestingly, regression occurred more commonly than incidence or progression, especially from grade 1 to grade 0. Anterior vaginal prolapse regressed from grade 1 to 0 in 23.5 cases per 100 women per year, and from grades 2 to 3 to 0 in 9.3 cases per 100 women per year. Posterior vaginal prolapse regressed in 25.3 cases, as did uterine prolapse in 48 cases per 100 women per year. This serves to emphasize that prolapse is a dynamic condition, and factors related to progression and remission need further study.
Concomitant Pelvic Floor Disorders Clinicians are well aware that pelvic floor disorders commonly occur together, although evidence in the literature has only recently confirmed this. Urinary and fecal incontinence (“double incontinence”) coexists in up to 69% of women. Different populations and differing definitions for both types of incontinence are responsible for some of the variation in reported results. Because symptoms of all pelvic floor disorders tend to be underreported by patients, clinicians are required to inquire routinely as to the spectrum of disorders whenever a patient presents with one symptom.
RISK FACTORS FOR PELVIC FLOOR DISORDERS Sex Urinary incontinence is two to three times more common in women than in men. The gender difference is most
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of incontinence may differ by age, with many studies suggesting a higher prevalence of stress incontinence in younger women, compared with more urge incontinence in older women; however, not all studies confirm this, and the prevalence of mixed (stress and urge) incontinence varies widely in different studies. Urinary symptoms are found in over half of institutionalized elderly women. In addition to lower urinary tract dysfunction contributing to incontinence, nonurologic causes of incontinence, such as cognitive impairment, immobility, medications, and metabolic causes of excess urine output (e.g., diabetes) are often present. Jirovec and Wells (1990) observed that when multiple variables were examined together, mobility emerged as the best predictor of urinary control, followed by cognitive impairment. Therapy should always include a combination of urologic treatments with nonurologic treatments in dealing with urinary incontinence in the elderly, particularly in nursing home residents. Most studies of fecal incontinence show increased prevalence with age. In a study of over 10,000 men and women in the United Kingdom, Perry et al. (2002) reported fecal incontinence in 0.9% of adults ages 40 to 64 and in 2.3% age 65 and over. Also from the United Kingdom, Crome et al. (2001) reported that the rate of fecal incontinence roughly doubled by decade of age, from 4.7% in women ages 70 to 79, to 10.1% in women ages 80 to 89, to 20.3% in women ages 90 to 99. As with urinary function, the effect of age on anorectal function is multifactorial, and the presence of comorbid conditions contributes to worsening symptoms. Incontinence, both urinary and fecal, is strongly associated with cognitive impairment and physical limitations.
pronounced among adults under age 60 because of the very low prevalence of urinary incontinence in younger men. These sex differences are consistent, whether the measure is any incontinence, severe incontinence, or irritative bladder symptoms. The symptom of stress incontinence is uncommon in men who have not had surgery, but voiding problems are more common, especially in elderly men, in part due to prostate conditions. The comparison of fecal incontinence between men and women depends on the population studied. Many studies show a higher prevalence of fecal incontinence in women than in men, although some studies report similar rates, and, in a few studies, men had higher rates than women. Women are uniquely susceptible to damage to fecal continence mechanisms at vaginal childbirth, but its influence toward the prevalence and causes of fecal incontinence in women compared with men is unknown. Studies of anorectal function show that, compared with men, women have lower anal squeeze pressures, greater perineal descent, and more evidence of nerve damage to the pelvic muscles and anal sphincters. Although only women are at risk for pelvic organ prolapse, rectal prolapse affects men and women in approximately equal proportions, which requires an explanation that does not rely on damage incurred at childbirth.
Age The prevalence of urinary incontinence increases with age, although it is not a linear relationship. Recent studies show a broad peak in prevalence from ages 40 to 60, with a steady increase occurring after ages 65 to 70 (Fig. 4–1). The type 40 Unknown Slight
35
Moderate
Prevalence (%)
30
Severe
25 20 15 10 5 0
Unknown Slight
20−24 25−29 30−34 35−39 40−44 45−49 50−54 55−59 60−64 65−69 70−74 75−79 80−84 4.2 1.6 3.1 3 3.6 4.8 4 0.6 1 1.1 5.2 0.3 2.4 7.8 5.9 6.3 8 12.3 5.7 11.5 9.3 5.6 7 10.7 13.7 11.6
Moderate
2.5
Severe
1.3
4.5 1.2
4.9
6
1.6
2.6
7.5 3.3
8.3 4.1
8.8 6.1
8.4 6.8
7.6 7.2
85+ 5.7 2.6
8.3
8.1
8.1
8.1
8.2
8.7
12.1
14.6
16.1
19.3
Age Figure 4-1 ■ Prevalence of urinary incontinence by age group and severity. (From Hannestad YS, Rortveit G, Sandvik H, Hunskaar S. A community-based epidemiological survey of female urinary incontinence: the Norwegian EPINCONT Study. J Clin Epidemiol 2000;53:1150, with permission.)
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Although available data are limited, virtually all studies show that the prevalence of pelvic organ prolapse increases steadily with age. This has been shown in case-control studies, prospective studies, and studies of surgery for prolapse. In the Women’s Health Initiative, at baseline, uterine prolapse was observed in 14.2% of 16,616 women. Anterior vaginal prolapse was observed in about one-third of the study population, regardless of hysterectomy status (32.9% with and 34.3% without hysterectomy); posterior vaginal prolapse was present in about one-fifth, similarly unrelated to hysterectomy (18.3% and 18.6%, respectively). For uterine prolapse, regression analyses showed a 16% to 20% increase in the odds ratio (OR) for having prolapse by decade of life. Studies of surgery for prolapse, which are likely to reflect the more severe end of the clinical spectrum of prolapse, consistently show increased rates of surgery by age (until age 80 and above). Olsen et al. (1997) reported prolapse surgery rates (per 1000 women per year) of 1.24 for women ages 50 to 59, 2.28 for those ages 60 to 69, and 3.43 for those ages 70 to 79.
Race Racial differences have been reported for some pelvic floor disorders, although it is not yet clear whether the differences are biologic or sociocultural (related to health care access or likelihood of seeking health care), both, or other factors. Different levels of risk may be based on genetic or anatomic attributes; lifestyle factors, such as diet, exercise, and work habits; or cultural expectations and tolerance of symptoms. Populations traditionally thought to enjoy relative protection from pelvic symptoms have been shown, under closer study, to have a significant prevalence of urinary incontinence and other urinary symptoms, including black, Hispanic, and Asian (Japanese, Chinese) women. Differences may be present in the distribution of presenting symptoms or confirmed diagnoses, with some reports suggesting a lower risk for stress incontinence and a higher risk for detrusor overactivity in black or Hispanic women than in white women. However, these reports are not population based, which would provide the best estimate of true racial differences. No reports related to race or ethnicity are available for fecal incontinence. In many studies of prolapse, the populations are predominantly white, thereby limiting analyses related to race and ethnicity. In studies that do have significant minority representation, differences seem to appear in the occurrence of prolapse by race. In the Women’s Health Initiative, black women had a lower risk of prolapse (odds ratio of 0.65 or less), compared with white women. Hispanic women had a higher risk of uterine and anterior vaginal prolapse, with odds ratios of 1.24 and 1.20, respectively; the risk of posterior vaginal prolapse was not significantly different compared with white women. In a case-control study of 447 women, Swift et al. (2001) reported a statistically significant lower risk for prolapse in women of nonwhite race (although the magnitude of the lowered risk was not reported). Racial differences in the bony pelvis may play a role in determining a woman’s risk of prolapse, possibly by influencing the likelihood or extent of injury to pelvic support at childbirth.
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Childbirth Parity is a well-established risk factor for urinary incontinence in young and middle-aged women (up to age 50); however, the effect of childbirth diminishes with age and even disappears in older women. Large randomized trials (Heart and Estrogen/Progestin Replacement Study [HERS]) and observational studies (the Nurses’ Health Study) have shown no or weak effects of parity in older women. The prevalence of incontinence was 50% in a study of 149 nulliparous nuns, with two thirds of incontinent women having stress or mixed symptoms. Early after delivery, the type of delivery has the strongest effect. In one of the few randomized trials of delivery type to address this (although not as a primary aim), the Term Breech Trial (Hannah et al., 2002) found less urinary incontinence in the planned cesarean delivery group (4.5%, relative risk 0.62) compared with the planned vaginal delivery group (7.3%) at 3 months postpartum. Because 43% of women in the planned vaginal delivery group actually had cesarean delivery, the results of this study probably underestimate the magnitude of the early difference between cesarean and vaginal delivery. In a large community-based observational study in Norway of women less than age 65 (the Epidemiology of Incontinence in the County of Nord-Trondelag [EPINCONT] study), the prevalence of any incontinence was 10.1% in nulliparous women, compared with 15.9% in women delivered by cesarean, and 21.0% in women who delivered vaginally. The effect of delivery type diminished with age, such that the prevalence of incontinence was similar regardless of the type of delivery in the oldest age group of women studied (ages 50 to 64). Viktrup (2002) showed that incontinence 5 years after the first delivery was not influenced by the type of delivery. A study by Wilson et al. (1996) showed that the risk of incontinence accumulated with the number of cesarean deliveries; after three or more cesarean deliveries, the prevalence of incontinence was similar (38.9%), compared with women who delivered vaginally (37.7%). In the few studies that have directly evaluated anorectal function in pregnancy, no changes have been consistently identified. Few women develop new symptoms of fecal incontinence during pregnancy (in contrast to urinary incontinence), although this has not been well studied. However, fecal incontinence or other symptoms of disordered defecation, especially fecal urgency, develop commonly after vaginal delivery. The risk of fecal incontinence for women delivering vaginally is highest in those who sustain direct anal sphincter damage (third- or fourth-degree perineal laceration). Symptoms of fecal urgency and incontinence to gas occur in up to 50% of women in the early postpartum period; loss to liquid or solid stool is less common but still significant, at 2% to 10%. Subsequent vaginal delivery, particularly if another anal sphincter laceration occurs, is associated with a higher risk of persistent fecal incontinence symptoms. The increased risk of fecal incontinence with anal sphincter damage persists and worsens with time. Most studies show midline episiotomy as one of the strongest risk factors for anal sphincter damage and, therefore, fecal incontinence. Especially because current methods of surgical repair leave persistent anal sphincter defects in
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up to 85% of women and are associated with high rates of postpartum symptoms, it is critically important to prevent the initial damage at vaginal delivery. Even cesarean delivery does not protect women completely from the possibility of postpartum anorectal dysfunction. Recent studies have identified new fecal incontinence symptoms even after elective cesarean delivery without labor. At this point, it is unknown whether this reflects changes due to pregnancy, the surgical delivery, or possibly both. Most (but not all) studies show that parity is linked to the prevalence of prolapse, although the magnitude of the effect varies in different studies. Mant et al. (1997) reported a strong cumulative effect of parity on the risk of inpatient admission for prolapse. The effect was greatest for the first and second births and less so for three or more births (Fig. 4–2). In cross-sectional data from the Women’s Health Initiative, Hendrix et al. (2002) found that the first birth approximately doubled the risk of uterine prolapse and anterior and posterior vaginal prolapse; each additional birth increased the risk by 10% to 21%. In longitudinal data from a subset of women enrolled in the Women’s Health Initiative, Handa et al. (2003) showed that the incidence of anterior vaginal prolapse increased by 31% for each additional pregnancy; similar associations were seen for uterine and posterior vaginal prolapse, although specific data were not reported. Beyond parity, the type of delivery (i.e., spontaneous versus operative vaginal delivery; vaginal versus abdominal delivery; abdominal delivery with or without labor) and its association with subsequent prolapse has not been well studied. Two case-control studies have identified operative vaginal delivery (either vacuum or forceps) as a risk factor in women who undergo surgery for prolapse or urinary incontinence. However, conclusions regarding the relative effect of different modes of delivery cannot be made at this time, due to limited data.
Menopause and Estrogen The vagina and urethra have similar epithelial linings because of their common embryologic origin. Urinary cytologic changes are similar to those of vaginal cytology during the menstrual cycle, during pregnancy, and after menopause. The classic estrogen receptor (ER-α) has been identified through12 Relative risk
10
out the pelvis; the second estrogen receptor (ER-β), discovered in 1996, has not yet been well characterized. Urogenital atrophy due to estrogen deficiency is at least partly responsible for sensory urinary symptoms and decreased resistance to infection often found after menopause. Estrogen treatment administered vaginally reduces bladder infections in postmenopausal women with recurrent infections and may improve sensory lower urinary tract symptoms. Despite some evidence that endogenous estrogen plays a role in maintaining normal urinary function, the effect of exogenous estrogen is less certain. Trials of pharmacologic use of estrogen for the prevention or treatment of incontinence have not shown strong benefits, and studies of estrogen for other uses (e.g., cardiovascular outcomes) suggest that estrogen worsens or even causes incontinence in some women. In women with incontinence at baseline in the HERS, incontinence worsened in more women randomly assigned to estrogen and progestin (39%) compared with placebo (27%). The difference was evident by 4 months of treatment and was observed for both stress and urge incontinence. Certain selective estrogen receptor modulators (SERMs) carry important risks for pelvic floor disorders. An osteoporosis trial of levormeloxifene reported by Goldstein and Nanavati (2002) was halted before completion due to significant adverse effects on pelvic symptoms. Compared with placebo, there was a fourfold increased incidence of urinary incontinence (17% vs 4%) and a twofold increased incidence or progression of prolapse (9% vs 4%). In contrast, raloxifene had no effect on urinary incontinence over a 3-year period, and women on raloxifene were half as likely to have prolapse surgery compared with women on placebo. Little is known about the potential independent effects of menopause or estrogen status on fecal incontinence. Estrogen receptors have been demonstrated in the external anal sphincter and pelvic muscles. Donnelly et al. (1997) reported a benefit for postmenopausal women with fecal incontinence treated with estrogen, but overall the effect of hormonal status and estrogen on fecal incontinence has not been well studied. Except for the studies of SERMs and prolapse, information is very limited on the effect of menopause (independent of age) and estrogen status on the risk of prolapse. In a casecontrol study of women who underwent surgery for prolapse or incontinence, Moalli et al. (2003) reported a decreased risk associated with postmenopausal hormone use, although this achieved statistical significance only when the duration of hormone use exceeded 5 years (adjusted odds ratio, 0.1).
8 6
Obesity
4 2 0
0
1
2 Parity
3
4+
Figure 4-2 ■ Adjusted effects of parity on inpatient admission rates for genital prolapse. Relative risks adjusted for age, parity, or calendar period, as appropriate. (From 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, with permission.)
Obesity has been consistently identified as a strong independent risk factor for urinary incontinence of all types. Incontinence is also associated with an increased waist-hip ratio, which supports the theory that obese women generate higher intra-abdominal pressures that overcome the continence mechanism. Weight loss may result in resolution of incontinence without further specific therapy. Less is known about the relationship between obesity and fecal incontinence. Fornell et al. (2004) showed elevated
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relative risks by univariate analysis in obese women (body mass index [BMI] = 30 kg/m2) compared with normal women (BMI 25) for incontinence to gas (relative risk, 1.8), liquid stool (2.5), and solid stool (1.3), although only the risk with liquid stool attained statistical significance. Multivariate analyses were not performed. Many, but not all, studies of prolapse show a higher risk in overweight and obese women. In cross-sectional data from the Women’s Health Initiative, the effect of increased weight was consistent and showed the greatest magnitude in obese women with posterior vaginal prolapse (adjusted odds ratio, 1.75) compared with normal women. In addition, women with “apple” body shapes (waist greater than hip circumference) had a 17% higher risk of anterior and posterior vaginal prolapse, supporting the theory that increased intraabdominal pressure may play a role in prolapse occurrence. Mant et al. (1997) reported a stronger effect of weight alone (adjusted relative risk, 1.50) compared with BMI (weight and height). Longitudinal data from the Women’s Health Initiative showed a strong association between increasing BMI and the development of posterior vaginal prolapse but not uterine or anterior vaginal prolapse.
Smoking Smoking has been identified as an independent risk factor for urinary incontinence in several studies, with the strongest effect seen for stress and mixed incontinence in heavy smokers. The pathophysiologic mechanism may include direct effects on the urethra and indirect effects, where smokers generate greater increases in bladder pressure with coughing, thus overwhelming the urethra’s ability to maintain a watertight seal. No information is available on the effect of smoking on fecal incontinence. Data on smoking and prolapse are contradictory. One study showed no effect of smoking in menopausal women Table 4-1
■
with and without prolapse. In a case-control study of women who underwent surgery for prolapse or incontinence, smoking was associated with a doubled risk. However, in large epidemiologic studies, smoking shows a paradoxical protective effect. In the Women’s Health Initiative, the adjusted odds ratio for prolapse in women with current tobacco use ranged from 0.81 to 0.85; the upper limit of the 95% confidence interval approached but did not cross 1.0, thereby achieving statistical significance. Mant et al. (1997) reported an adjusted relative risk of 0.78 in women with inpatient admissions for prolapse (although this was not statistically significant, 95% confidence interval of 0.57–1.07). At this point, it is unknown whether these data represent a potential biologic effect, changes in management due to smoking status (i.e., recommending surgery less often), or other effect.
PSYCHOSOCIAL IMPACT OF PELVIC FLOOR DISORDERS Prolapse and loss of control of urine, gas, and stool can have a significant impact on the social well-being of affected people. Although the ICS has changed its definition of urinary incontinence (the complaint of any involuntary leakage of urine), such that it no longer requires that incontinence be a social or hygienic problem, this does not diminish the importance of the psychosocial impact of incontinence and other pelvic floor disorders. A summary of potential psychosocial consequences of pelvic floor disorders is shown in Table 4–1. In contrast to urinary and fecal incontinence, little specific information is available on social and psychological changes related to prolapse.
Social Changes Many techniques have been used to measure the psychosocial impact of pelvic floor disorders, and condition-specific
Summary of Psychosocial Consequences of Pelvic Floor Disorders
Individual Psychological symptoms Insecurity Anger Apathy Dependence Guilt Indignity Feeling of abandonment Shame Embarrassment Depression Denial Sense of self Loss of self-confidence Loss of self-esteem Sexual difficulties Lack of attention to personal hygiene Social interaction Reduction in social activities Socially disengaged Socially isolated
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Psychological and functional decline Potential for institutionalization
Family Caregiver burden and emotional stress Impaired interpersonal relationships Economic worries Health deterioration of primary caregiver Potential for abuse or neglect Decision to institutionalize Delayed discharge from institutional care
Health Care Professional Negative feelings and behaviors toward patients with pelvic floor disorders Reaction formation Overindulgence Excessive permissiveness Excessive caring Extra care responsibilities Staff frustration, depression, and guilt Reduction in staff morale “Burn-out” syndrome
Modified with permission from Ory MG, Wyman JF, Yu L. Psychosocial factors in urinary incontinence. Clin Geriatr Med 1986;2:657.
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quality-of-life instruments have been developed and validated for use in research and clinical settings (Table 4–2). In a review on the impact of lower urinary tract symptoms in older patients, Naughton and Wyman (1997) found a considerable impact of urinary incontinence on overall quality of life and well-being. Social relationships and activities were reduced as a result of involuntary leakage, related, at least in part, to fear of odor and embarrassment. Areas affected include social, domestic, physical, occupational, and recreational activities. Fear of or occurrence of incontinent episodes may lead patients to give up or restrict household activities, church attendance, shopping, traveling, vacations, sports and recreation, entertainment outside the home, and hobbies. Some patients make detailed plans to conceal or prepare for incontinent episodes. Some incontinent individuals become increasingly isolated as they limit social activities and contacts. Even incontinent homebound women, compared to continent homebound women, have significantly fewer social interactions, particularly with family members. Spousal relationships appear to be most impaired, perhaps because of an additional adverse effect on sexual relationships. Urinary incontinence among the elderly can lead to such disability and dependency that family or home caregivers have difficulty coping and responding to increased demands. Incontinence, especially the occurrence of both fecal and urinary incontinence, may be the last straw in a family’s attempts to care for an elderly person at home. Incontinence is a major factor leading to institutionalization of the elderly, particularly in patients with dementia. In one study, 5% of incontinent nursing home residents indicated that inconti-
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nence was the main reason for nursing home admission, and it was a secondary reason for many more. Studies of the perceived social impact of incontinence are not entirely consistent in their results. Some, but not all, studies have shown greater distress and emotional disturbances associated with urinary urgency and urge incontinence, compared with stress incontinence. Symptoms in younger women tend to produce more distress than in older women. Many studies report a modest relationship between the severity of symptoms and the psychosocial consequences. However, it is likely that other, still undefined factors play a role in determining each individual’s threshold for tolerance of symptoms and the associated disability or distress. Widely accepted is that pelvic floor disorders are underrecognized and undertreated. For example, fewer than half of people with urinary incontinence in the community consult their health care providers about the problem. The reasons include embarrassment, easy availability of absorbent products, low expectations of benefit from treatment, fear of surgical treatment, and lack of information regarding options for treatment. Even with widespread direct-to-consumer advertising for pharmaceuticals to treat urinary incontinence, underreporting and undertreatment remain serious impediments to optimizing care for women with urinary incontinence. The few studies on the prevalence of fecal incontinence also describe underreporting by patients and lack of appropriate evaluation by health care providers, even when the patient volunteers symptoms. No documentation is found related to reporting of prolapse.
Generic and Condition-Specific Quality-of-Life Questionnaires
Reference
Title
Number of Items
Nottingham Health Profile (NHP) Sickness Impact Profile (SIP) Medical Outcomes Study SF-36 SF-12 (physical and mental health domains)
38 136 36 12
Pelvic Floor Distress Inventory (PFDI) Pelvic Floor Impact Questionnaire (PFIQ)
61 93
Incontinence Impact Questionnaire (IIQ); Urogenital Distress Inventory (UDI) IIQ-7; UDI-6
30 19 7; 6
Fecal Incontinence Severity Index Fecal Incontinence Quality of Life Scale Gastrointestinal Quality of Life Index
4 29 36
Prolapse Quality of Life (P-QOL)
20
Pelvic Organ Prolapse/Urinary Incontinence Sexual Questionnaire (PISQ) PISQ-12 Sexual Function Questionnaire
31
Generic Health-Related Quality-of-Life Questionnaires Hunt et al., 1985; Grimby et al., 1993 Bergner et al., 1981; Hunskaar and Vinsnes, 1991 Ware, 1989; Ho-Yin et al., 2003 Ware et al., 1995; Fialkow et al., 2003
Comprehensive Pelvic Floor Disorders Questionnaires Barber et al., 2001
Urinary Incontinence Shumaker et al., 1994; van der Vaart et al., 2003 Uebersax et al., 1995
Fecal Incontinence Rockwood et al., 1999; Cavanaugh et al., 2002 Rockwood et al., 2000 Eypasch et al., 1995; Rothbarth et al., 2001
Pelvic Organ Prolapse Digesu et al., 2003
Sexual Function Rogers et al., 2001 Rogers et al., 2003 Barber et al., 2002
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Psychological Changes Urinary incontinence leads to heightened psychological distress, which contributes to emotional disturbances, anxiety, and depression. Because most objective studies report similar results with various diagnoses of incontinence, psychological changes are more likely related to the symptom of urine loss and related disability and distress, rather than to specific urogynecologic conditions. Similar adverse effects have been described for fecal incontinence, which are compounded when both urinary and fecal incontinence are present. Specific psychological effects of prolapse have not been described. With improved tools for measuring psychosocial aspects of incontinence, significant changes have been described when incontinence has been successfully treated. Several studies of nonsurgical incontinence treatment have reported improvements in subjective quality of life measures, such as depression, isolation, embarrassment, and fear of odor. The magnitude of improvement in psychosocial factors has been related to decreased frequency of incontinent episodes and improved overall health status.
Quality of Life Pelvic floor disorders and their associated psychosocial distress constitute a spectrum related to the actual severity of the symptoms and to the woman’s perception of her disability. Health-related quality of life is an important concept in clinical research and clinical practice. Many instruments have been developed, primarily for use in clinical research, to measure the influence of symptoms on quality of life, either on health in general (generic questionnaires) or specifically related to the condition of interest (condition-specific questionnaires). Symptom-based questionnaires measure symptoms in terms of occurrence, frequency, and severity. Quality-of-life instruments measure the impact of disease or treatment on an individual’s perception of physical, psychological, and social well-being. The most effective tools are simple, short (can be completed rapidly by the patient), and psychometrically sound. The psychometric characteristics of a questionnaire refer to its reliability, validity, and responsiveness; these properties of currently available instruments are well summarized in a review by the Symptom and Quality of Life Assessment Committee of the First International Consultation on Incontinence (Corcos et al., 2002). Measuring quality of life, both generic and conditionspecific, has become an important part of outcomes assessment for clinical research, which is especially true for pelvic floor disorders that do not typically cause mortality but can result in severe impairments in psychosocial functioning. Scores or scales that focus on frequency of symptoms do not adequately capture the tremendous negative impact that pelvic floor disorders can have on day-to-day functioning. For example, some women are severely affected, despite infrequent episodes of incontinence (urinary or fecal). This may occur if they experience overwhelming anxiety that incontinence may occur, or if they have curtailed previously enjoyable activities for fear of incontinence. This has important implications for the evaluation of treatment benefits. Quality-of-life information can be critically important when clinicians and patients are making choices between treat-
51
ments that might otherwise appear similar on purely symptom-based comparisons. Patient expectations of treatment, particularly surgery, is a relatively new area of focus in outcomes research. Patient goals, ranging from specific symptom relief to general lifestyle improvement, may be quite different than what the clinician hopes or expects to be able to achieve with treatment. Understanding patient expectations may be especially important for pelvic floor disorders, when treatment is recommended to improve quality of life, rather than treat or prevent life-threatening disease. Unmet expectations are closely associated with patient dissatisfaction after surgery. Providing a comprehensive review of all quality-oflife instruments related to pelvic floor disorders is beyond the scope of this chapter. A sample of validated generic and condition-specific questionnaires is listed in Table 4–2; the interested reader is referred to the bibliography for further reading on this important topic and to Chapter 39 for a comprehensive review of quality-of-life instruments related to pelvic floor disorders.
Sexual Changes Considering the close anatomic proximity of the vagina to the bladder, urethra, and rectum, it seems obvious that pelvic floor disorders are likely to be associated with possible sexual dysfunction. In addition, one of the primary goals of pelvic reconstructive surgery is the restoration or maintenance of normal sexual capacity. Despite this, rigorous scientific study of sexual function related to pelvic floor disorders is relatively limited. Recent years have seen improved study designs (including comparisons before and after treatment) and the development of specific instruments to assess sexual function in women with pelvic floor disorders. Nevertheless, this critically important area remains understudied. Examples of conditions in which sexual activity affects the lower urinary tract are the increase in urinary tract infections with intercourse, especially in women who use diaphragms, and dyspareunia experienced by some women with urethral diverticula. Women may experience urgency to void during or after sexual intercourse. Urine loss during vaginal intercourse occurs in 2% of women in population-based samples and in 10% to 56% of clinical populations of incontinent women. Because sexual incontinence is rarely volunteered, clinicians should routinely ask patients with all pelvic floor disorders. Urine loss may occur with penetration, during clitoral stimulation or with orgasm. Early reports suggested a relationship between stress incontinence and urine loss with penetration, versus detrusor overactivity and urine loss with orgasm; however, subsequent studies have not confirmed this and no consistent relationship is apparent between the type of incontinence and typical sexual symptoms. Many factors affect the quality of sexual function. Age and attendant life events, especially the availability and health status of sexual partners, are important factors. In studies of women with and without urinary incontinence and pelvic organ prolapse, age is an important predictor of sexual function, more so than the presence or absence of incontinence or prolapse. Satisfaction with sexual function remains high for most women, even when pelvic floor symptoms adversely affect their sexual activity.
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Sexual function may be positively or negatively affected by pelvic reconstructive surgery. When pelvic symptoms improve, such as relief from urinary incontinence, sexual function may also improve. However, surgery may introduce new symptoms. Posterior colporrhaphy has been associated with dyspareunia in many studies, even recent studies when the surgical technique did not compromise introital caliber; one study reported a particularly strong association between dyspareunia and posterior repair when Burch colposuspension was concomitantly performed. Although information on the sexual impact of fecal incontinence is limited, its effect seems likely similar or even worse than in women with urinary incontinence. Vaginal intercourse may produce rectal urgency and the fear or occurrence of flatulent or fecal incontinence in affected women. Fear of this nature may severely impair sexual function even when actual incontinent episodes are rare.
ECONOMIC ISSUES Despite the high prevalence of pelvic floor disorders, estimates of economic impact are incomplete. Estimated costs should include direct and indirect medical costs, including costs of treating complications, and nonmedical costs. Direct costs are the resources from the economy used to diagnose, treat, care for, and rehabilitate patients with pelvic floor disorders. Indirect costs include lost productivity, consequences ranging from skin ulcers to mortality, and the cost of time spent by unpaid caregivers. One study estimated a national annual cost of more than $6 billion for incontinence-related informal care. Indirect costs are not consistently captured in overall cost estimates for pelvic floor disorders. The annual direct cost of urinary incontinence in the United States has been estimated at $16.3 billion; women account for 76% of the costs, or $12.4 billion per year. The largest cost category was routine care (70%) followed by nursing home admissions (14%). Incontinence is strongly associated with nursing home admission; incontinent elderly women are 2.5 times more likely to be admitted to a nursing home than continent elderly women. Appropriate diagnosis and treatment of urinary incontinence in the community may decrease overall costs. However, in current estimates, treatment accounted for only 9% of the total direct costs, only slightly higher than the 6% of costs attributed to care of complications. This likely represents the effect of underdiagnosis and undertreatment. The specific cost attributable to overactive bladder has been estimated at $12 billion per year. For women in the community, direct costs were estimated at about $7 billion and indirect costs (lost productivity) at $400 million. Institutional costs for men and women were estimated at $2.8 billion. The largest single cost for women was for additional nursing home admissions ($1.5 billion) followed by routine care costs ($1.3 billion), with pharmacologic costs a close third at $1.1 billion. Once nursing home admission has occurred, costs for care of women with urinary incontinence are increased; one study estimated increased costs of about $5000 per year per incontinent individual. Despite the large economic burden of urinary incontinence in nursing homes, whether inter-
ventions decrease or increase overall costs remain unknown. Although interventions clearly decrease the occurrence of fecal and urinary incontinence, costs do not necessarily decrease. Quality of life and other second-order benefits must be considered if continence rehabilitation is to be costeffective. In the community, behavioral therapy would not incur labor costs and so may be more cost-effective, although this comparison has not been studied. Few cost estimates are related solely to prolapse. One study estimated the annual direct cost of prolapse surgery in the United States at just over $1 billion, representing procedures performed on approximately 226,000 women per year. Hysterectomy accounted for about half the costs (almost $500 million). Twenty-one percent of the prolapse operations included procedures for urinary incontinence, at an estimated yearly cost of $218 million. Few studies report costs of fecal incontinence, and no cost estimates are known on a nationwide or populationwide basis. The few studies published focus on surgical treatments of fecal incontinence. Reproductive-aged women with fecal incontinence due to obstetric injury are likely to incur the highest lifetime costs because the limited effectiveness and durability of currently available surgeries consign them to a high risk of multiple procedures. Dynamic graciloplasty was more cost-effective in one study, compared to conventional treatment (protective undergarments and supportive care) or colostomy. However, cost estimates for colostomy reflect clinical practice in the Netherlands, which involves more costly hospital-based care and less patientcontrolled care. The authors speculated that colostomy costs in the United States would be lower, where patients are more directly involved in their colostomy care.
Bibliography PREVALENCE, INCIDENCE, AND REMISSION
Urinary Incontinence Abrams P, Cardozo L, Fall M, et al. The standardization of terminology of lower urinary tract function: report from the Standardisation Subcommittee of the International Continence Society. Neurourol Urodyn 2002;21:167. Aggazzotti G, Pesce F, Grassi D, et al. Prevalence of urinary incontinence among institutionalized patients: a cross-sectional epidemiologic study in a midsized city in northern Italy. Urology 2000;56:245. Eliasson K, Larsson T, Mattson E. Prevalence of stress incontinence in nulliparous elite trampolinists. Scand J Med Sci Sports 2002;12:106. Grodstein F, Lifford K, Resnick NM, Curhan GC. Postmenopausal hormone therapy and risk of developing urinary incontinence. Obstet Gynecol 2004;103:254. Hanley J, Capewell A, Hagen S. Validity study of the severity index, a simple measure of urinary incontinence in women. Br Med J 2001;322:1096. Hannestad YS, Rortveit G, Sandvik H, Hunskaar S. A community-based epidemiological survey of female urinary incontinence: the Norwegian EPINCONT Study. J Clin Epidemiol 2000;53:1150. Herzog AR, Diokno AC, Brown MB, et al. Two-year incidence, remission, and change patterns of urinary incontinence in noninstitutionalized older adults. J Gerontol 1990;45:M67. Herzog AR, Fultz NH. Prevalence and incidence of urinary incontinence in community-dwelling populations. J Am Geriatr Soc 1990;38:273. Hunskaar S, Burgio K, Diokno A, et al. Epidemiology and natural history of urinary incontinence in women. Urology 2003;62(Suppl 4A):16. Luber KM, Boero S, Choe JY. The demographics of pelvic floor disorders: current observations and future projections. Am J Obstet Gynecol 2001;184:1496.
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Epidemiology and Psychosocial Impact of Pelvic Floor Disorders
Melville JL, Miller EA, Fialkow MF, et al. Relationship between patient report and physician assessment of urinary incontinence severity. Am J Obstet Gynecol 2003;189:76. Nygaard IE, Lemke JH. Urinary incontinence in rural older women: prevalence, incidence, and remission. J Am Geriatr Soc 1996;44:1049. Samuelsson EC, Victor FT, Svardsudd KF. 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. Waetjen LE, Brown JS, Modelska K, et al. for the MORE Study Group. Effect of raloxifene on urinary incontinence: a randomized controlled trial. Obstet Gynecol 2004;103:261.
Fecal Incontinence Baxter NN, Rothenberger DA, Lowry AC. Measuring fecal incontinence. Dis Colon Rectum 2003;46:1591. Delvaux M. Digestive health in the elderly: faecal incontinence in adults. Aliment Pharmacol Ther 2003;18:84. Jorge JM, Wexner SD. Etiology and management of fecal incontinence. Dis Colon Rectum 1993;36:77. Nelson R, Norton N, Cautley E, et al. Community-based prevalence of anal incontinence. JAMA 1995;274:559. Vaizey CJ, Carapeti E, Cahill JA, Kamm MA. Prospective comparison of faecal incontinence grading systems. Gut 1999;44:77.
Pelvic Organ Prolapse 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. Bump RC, Mattiasson A, Bo K, et al. The standardization of terminology of female pelvic floor dysfunction. Am J Obstet Gynecol 1996;175:10. Ellerkmann 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. 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. Handa VL, Jones M. Do pessaries prevent the progression of pelvic organ prolapse? Int Urogynecol J 2002;13:349. Samuelsson EU, Victor FT, 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. Swift SE. The distribution of pelvic organ support in a population of women presenting for routine gynecologic healthcare. Am J Obstet Gynecol 2000;183:277.
Concomitant Pelvic Floor Disorders 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. Lacima G, Pera M. Combined fecal and urinary incontinence: an update. Curr Opin Obstet Gynecol 2003;15:405. Soligo M, Salvatore S, Milani R, et al. Double incontinence in urogynecologic practice: a new insight. Am J Obstet Gynecol 2003;189:438.
RISK FACTORS FOR PELVIC FLOOR DISORDERS Alling Moller L, Lose G, Jorgensen T. Risk factors for lower urinary tract symptoms in women 40 to 60 years of age. Obstet Gynecol 2000;96:446. Brown JS, Grady D, Ouslander JG, et al. Prevalence of urinary incontinence and associated risk factors in postmenopausal women. Obstet Gynecol 1999;94:66. 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. Crome P, Smith A, Withnall A, Lyons R. Urinary and faecal incontinence: prevalence and health status. Rev Clin Gerontol 2001;11:109. Donnelly V, O’Connell PR, O’Herlihy C. The influence of oestrogen replacement on faecal incontinence in postmenopausal women. Br J Obstet Gynaecol 1997;104:311.
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Erata YE, Kilic B, Guclu S, et al. Risk factors for pelvic surgery. Arch Gynecol Obstet 2002;267:14. Eva UF, Gun W, Preben K. Prevalence of urinary and fecal incontinence and symptoms of genital prolapse in women. Acta Obstet Gynecol Scand 2003;82:280. Fitzpatrick M, Behan M, O’Connell PR, O’Herlihy C. A randomized clinical trial comparing primary overlap with approximation repair of thirddegree obstetric tears. Am J Obstet Gynecol 2000;183:1220. 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. Fynes M, Donnelly V, Behan M, et al. Effect of second vaginal delivery on anorectal physiology and fecal continence: a prospective study. Lancet 1999;354:983. Goldstein SR, Nanavati N. Adverse events that are associated with the selective estrogen receptor modulator levormeloxifene in an aborted phase III osteoporosis treatment study. Am J Obstet Gynecol 2002;187:521. Goldstein SR, Neven P, Zhou L, et al. Raloxifene effect on frequency of surgery for pelvic floor relaxation. Obstet Gynecol 2001;98:91. Grady D, Brown JS, Vittinghoff E, et al. for the HERS Research Group. Postmenopausal hormones and incontinence: the Heart and Estrogen/Progestin Replacement Study. Obstet Gynecol 2001;97:116. 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;189:428. Handa VL, Pannu HK, Siddique S, et al. Architectural differences in the bony pelvis of women with and without pelvic floor disorders. Obstet Gynecol 2003;102:1283. Hannah ME, Hannah WJ, Hodnett ED, et al. for the Term Breech Trial 3-Month Follow-up Collaborative Group. Outcomes at 3 months after planned cesarean vs planned vaginal delivery for breech presentation at term: the International Randomized Term Breech Trial. JAMA 2002;287:1822. Hannestad YS, Rortveit G, Daltveit AK, Hunskaar S. Are smoking and other lifestyle factors associated with female urinary incontinence? The Norwegian EPINCONT Study. Br J Obstet Gynaecol 2003;110:247. 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. 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. Hunskaar S, Arnold EP, Burgio K, et al. Epidemiology and natural history of urinary incontinence. Int Urogynecol J 2000;11:301. Jameson JS, Chia YW, Kamm MA, et al. Effect of age, sex and parity on anorectal function. Br J Surg 1994;81:1689. Jirovec MM, Wells TJ. Urinary incontinence in nursing home residents with dementia: the mobility-cognition paradigm. Appl Nurs Res 1990;3:112. Lal M, Mann CH, Callender R, Radley S. Does cesarean delivery prevent anal incontinence? Obstet Gynecol 2003;101:305. 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. Moalli PA, Ivy SJ, Meyn LA, Zyczynski HM. Risk factors associated with pelvic floor disorders in women undergoing surgical repair. Obstet Gynecol 2003;101:869. Olsen AL, Smith VJ, Bergstrom JO, et al. Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 1997;89:501. Perry S, Shaw C, McGrother C, et al. Prevalence of faecal incontinence in adults aged 40 years or more living in the community. Gut 2002;50:480. Resnick NM, Yalla SV. Geriatric incontinence and voiding dysfunction. In Walsh, PC, Retik AB, Vaughan ED Jr, Wein AJ, eds. Campbell’s Urology, 8th ed. WB Saunders, Philadelphia, 2002. Robinson D, Cardozo LD. The role of estrogens in female lower urinary tract dysfunction. Urology 2003;62(4 Suppl 1):45. Rortveit G, Daltveit AK, Hannestad YS, Hunskaar S. Urinary incontinence after vaginal delivery or cesarean section. N Engl J Med 2003;348:900. Rother P, Loffler S, Dorschner W, et al. Anatomic basis of micturition and urinary continence. Muscle systems in urinary bladder neck during ageing. Surg Radiol Anat 1996;18:173. Ryhammer AM, Laurberg S, Bek KM. Age and anorectal sensibility in normal women. Scand J Gastroenterol 1997;32:278. Samuelsson E, Victor A, Svardsudd K. Determinants of urinary incontinence in a population of young and middle-aged women. Acta Obstet Gynecol Scand 2000;79:208.
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Sultan AH, Kamm MA, Hudson CN, Bartram CI. Effect of pregnancy on anal sphincter morphology and function. Int J Colorectal Dis 1993;8:206. Swift S, Pound T, Dias J. Case-control study of the etiology of severe pelvic organ prolapse. Int Urogynecol J 2001;12:176. Thom DH, Haan MN, van den Eden S. Medically recognized urinary incontinence and risks of hospitalization, nursing home admission and mortality. Age Ageing 1997;26:367. Versi E, Harvey M, Cardozo L, et al. Urogenital prolapse and atrophy at menopause: a prevalence study. Int Urogynecol J 2001;12:107. Viktrup L. The risk of lower urinary tract symptoms five years after the first delivery. Neurourol Urodyn 2002;21:2. Waetjen LE, Brown JS, Modelska K, et al. for the MORE Study Group. Effect of raloxifene on urinary incontinence: a randomized controlled trial. Obstet Gynecol 2004;103:261. Wagenius J, Laurin J. Clinical symptoms after sphincter rupture: a retrospective study. Acta Obstet Gynecol Scand 2003;82:246. 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. Yip S-K, Chung TK-H. Treatment-seeking behavior in Hong Kong Chinese women with urinary symptoms. Int Urogynecol J 2003;14:27. Zetterstrom J, Lopez A, Anzen B, et al. Anal sphincter tears at vaginal delivery: risk factors and clinical outcome of primary repair. Obstet Gynecol 1999;94:21.
PSYCHOSOCIAL IMPACT OF PELVIC FLOOR DISORDERS 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;185:1388. Barber MD, Visco AG, Wyman JF, et al. Sexual function in women with urinary incontinence and pelvic organ prolapse. Obstet Gynecol 2002;99:281. Bergner M, Bobbit RA, Carter WB, Gilson BS. The Sickness Impact Profile: development and final revision of a health status measure. Med Care 1981;19:787. Cavanaugh M, Hyman N, Osler T. Fecal Incontinence Severity Index after fistulotomy: a predictor of quality of life. Dis Colon Rectum 2002;45:349. Corcos J, Beaulieu S, Donovan J, et al. for members of the Symptom, Quality of Life Assessment Committee of the First International Consultation on Incontinence. Quality of life assessment in men and women with urinary incontinence. J Urol 2002;168:896. Digesu GA, Santamato S, Khullar V, et al. Validation of an Italian version of the prolapse quality of life questionnaire. Eur J Obstet Gynecol Reprod Biol 2003;106:184. Elkadry EA, Kenton KS, FitzGerald MP, et al. Patient-selected goals: a new perspective on surgical outcome. Am J Obstet Gynecol 2003;189:1551. Eypasch E, Williams JI, Wood-Dauphinee S, et al. Gastrointestinal Quality of Life Index: development, validation, and application of a new instrument. Br J Surg 1995;82:216. Fialkow MF, Melville JL, Lentz GM, et al. The functional and psychosocial impact of fecal incontinence on women with urinary incontinence. Am J Obstet Gynecol 2003;189:127. Grimby A, Milsom I, Molander U, et al. The influence of urinary incontinence on the quality of life of elderly women. Age Ageing 1993;22:82. Ho-Yin PL, Man-Wah P, Shing-Kai Y. Effects of aging on generic SF-36 quality of life measurements in Hong Kong Chinese women with urinary incontinence. Acta Obstet Gynecol Scand 2003;82:275. Hullfish KL, Bovbjerg VE, Gibson J, Steers WD. Patient-centered goals for pelvic floor dysfunction surgery: what is success, and is it achieved? Am J Obstet Gynecol 2002;187:88. 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. Hunt SM, McEwen J, McKenna SP. Measuring health status: a new tool for clinicians and epidemiologists. J R Coll Gen Pract 1985;35:185. Kelly CE. Which questionnaires should be used in female urology practice? Curr Urol Rep 2003;4:375. Naughton MJ, Wyman JF. Quality of life in geriatric patients with lower urinary tract dysfunction. Am J Med Sci 1997;314:219. Ory MG, Wyman JF, Yu L. Psychosocial factors in urinary incontinence. Clin Geriatr Med 1986;2:657. 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.
Rockwood TH, Church JM, Fleshman JW, et al. Patient and surgeon ranking of the severity of symptoms associated with fecal incontinence: the Fecal Incontinence Severity Index. Dis Colon Rectum 1999;42:1525. Rogers RG, Coates KW, Kammerer-Doak D, et al. A short form of the Pelvic Organ Prolapse/Urinary Incontinence Sexual Questionnaire (PISQ-12). Int Urogynecol J 2003;14:164. Rogers RG, Kammerer-Doak D, Villarreal A, et al. A new instrument to measure sexual function in women with urinary incontinence or pelvic organ prolapse. Am J Obstet Gynecol 2001;184:552. Rothbarth J, Bemelman WA, Meijerink WJ, et al. What is the impact of fecal incontinence on quality of life? Dis Colon Rectum 2001;44:67. Shaw C. A review of the psychosocial predictors of help-seeking behaviour and impact on quality of life in people with urinary incontinence. J Clin Nurs 2001;10:15–24. 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. Shumaker S, Wyman J, Uebersax J, 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. Uebersax J, Wyman J, Shumaker S, et 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. Van der Vaart CH, de Leeuw JR, Roovers J-PW, Heintz AP. Measuring health-related quality of life in women with urogenital dysfunction: the Urogenital Distress Inventory and Incontinence Impact Questionnaire revisited. Neurourol Urodyn 2003;22:97. Ware J, Kosinski M, Keller S. SF-12: how to score the SF-12 physical and mental health summary scales. Health Institute, New England Medical Center, Boston, 1995. Ware JE. SF-36: Health status questionnaire. Quality Quest Inc., Boston, 1989. Weber AM, Walters MD, Schover LR, Mitchinson A. Sexual function in women with uterovaginal prolapse and urinary incontinence. Obstet Gynecol 1995;85:483. 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;182:1610. Yip S-K, Chan A, Pang S, et al. The impact of urodynamic stress incontinence and detrusor overactivity on marital relationship and sexual function. Am J Obstet Gynecol 2003;188:1244.
ECONOMIC ISSUES Adang EM, Engel GL, Rutten FF, et al. Cost-effectiveness of dynamic graciloplasty in patients with faecal incontinence. Dis Colon Rectum 1998;41:725. Azam U, Castleden M, Turner D. Economics of lower urinary tract symptoms (LUTS) in older people. Drugs Aging 2001;18:213. Buttafuoco A, Keighley MR. Cost of pelvic floor repair for faecal incontinence. Dig Surg 2000;17:623. Hu T-W, Wagner TH, Bentkover JD, et al. Estimated economic costs of overactive bladder in the United States. Urology 2003;16:1123. Langa KM, Fultz NH, Saint S, et al. Informal caregiving time and costs for urinary incontinence in older individuals in the United States. J Am Geriatr Soc 2002;50:733. Malouf AJ, Chambers MG, Kamm MA. Clinical and economic evaluation of surgical treatments for faecal incontinence. Br J Surg 2001;88:1029. Mellgren A, Jensen LL, Zetterstrom JP, et al. Long-term cost of fecal incontinence secondary to obstetric injuries. Dis Colon Rectum 1999;42:857. 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. Shih Y-CT, Hartzema AG, Tolleson-Rinehart S. Labor costs associated with incontinence in long-term care facilities. Urology 2003;62:442. Subak LL, Waetjen LE, van den Eden S, et al. Cost of pelvic organ prolapse surgery in the United States. Obstet Gynecol 2001;98:646. Wilson L, Brown JS, Shin GP, et al. Annual direct cost of urinary incontinence. Obstet Gynecol 2001;98:398.
Description and Classification of Lower Urinary Tract Dysfunction and Pelvic Organ Prolapse
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Mark D. Walters
CLASSIFICATION SYSTEMS OF LOWER URINARY TRACT DYSFUNCTION 55 International Continence Society Classification 55 Functional Classification 56 DIFFERENTIAL DIAGNOSIS OF URINARY INCONTINENCE 56 DESCRIPTION AND STAGING OF PELVIC ORGAN PROLAPSE 58
CLASSIFICATION SYSTEMS OF LOWER URINARY TRACT DYSFUNCTION The purpose of any classification system is to facilitate understanding of the etiology and pathophysiology of disease, to help establish and standardize treatment and research guidelines, and to avoid confusion among those who are concerned with the problem. Several classification systems for voiding disorders and urinary incontinence have been developed. These classifications have been based on various anatomic, radiographic, and urodynamic findings. The advantages, disadvantages, and applicability of the various classification systems of voiding dysfunction were described by Wein and Barrett (1988). This chapter reviews two practical systems for the classification of voiding dysfunction in women. Also, the differential diagnosis of urinary incontinence in women is discussed using updated terminology from the International Continence Society (ICS). Hopefully, the nomenclature used in these classification systems will become more widely understood and used and further research will be aimed at defining their clinical applicability.
International Continence Society Classification In 1973 the ICS established a committee for the standardization of terminology of lower urinary tract function. Five of the first six reports from this committee were published. These reports were revised, extended, and collated in a monograph published in 1990 (see Appendix A). The definitions were updated and revised by the Standardization Subcommittee of the ICS in 2002 (see Appendix B). The following is a summary of its findings. The lower urinary tract is composed of the bladder and urethra, which work together as a functional unit to promote
storage and emptying of urine. Symptoms, signs, urodynamic observations, and conditions are separate categories with unique but overlapping terminologies. Although a complete urodynamic investigation is not necessary for all symptomatic patients, some clinical or urodynamic assessment of the filling and voiding phases is essential for each patient. Examining bladder and urethral activity separately is useful in each phase. If urodynamic studies are performed, results should clearly reflect the patient’s symptoms and signs. FILLING AND STORAGE PHASE The ICS classification of abnormalities of the storage and voiding phases is outlined in Box 5-1. Cystometry is used to examine the bladder during filling and storage. Function should be described in terms of bladder sensation, detrusor activity, bladder capacity, and bladder compliance. Detrusor activity may be normal or overactive. Overactive detrusor function is characterized by involuntary detrusor contractions during filling. They may be spontaneous or provoked and cannot be suppressed completely. Overactive detrusor function in the absence of a known neurologic abnormality is called idiopathic detrusor overactivity; overactivity caused by disturbance of the nervous control mechanisms is called neurogenic detrusor overactivity. These conditions are often associated with the symptom of urinary urgency. Urgency, with or without urge incontinence, usually with frequency and nocturia, is described as the overactive bladder syndrome, urge syndrome, or urgency-frequency syndrome. Urethral function during storage can be assessed clinically (direct observation of urine loss with cough or Valsalva maneuver), urodynamically (urethral closure pressure profilometry and leak point pressure measurements), or radiographically (cystourethrography with or without video). The urethral closure mechanism may be competent or incompetent. An incompetent urethral closure mechanism is one that allows leakage of urine in the absence of a detrusor contraction. Leakage may occur during increased abdominal pressure, in the absence of a detrusor contraction (urodynamic stress incontinence) or due to urethral relaxation in the presence of raised abdominal pressure or detrusor overactivity (urethral relaxation incontinence). The definition and significance of the latter condition await additional data.
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BOX 5-1
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THE INTERNATIONAL CONTINENCE SOCIETY CLASSIFICATION OF LOWER URINARY TRACT DYSFUNCTION
I. Storage Phase A. Bladder Function During Storage 1. Detrusor activity a. Normal b. Overactive 2. Bladder sensation a. Normal b. Increased (hypersensitivity) c. Reduced d. Absent e. Nonspecific bladder sensations f. Bladder pain g. Urgency 3. Bladder capacity 4. Bladder compliance B. Urethral Function During Storage 1. Normal 2. Incompetent 3. Urethral relaxation II. Voiding Phase A. Detrusor Function During Voiding 1. Normal 2. Abnormal a. Underactive b. Acontractile B. Urethral Function During Voiding 1. Normal 2. Abnormal a. Bladder outlet obstruction b. Dysfunctional voiding c. Detrusor sphincter dyssynergia d. Nonrelaxing urethral sphincter obstruction
Urinary incontinence is the complaint of any involuntary (urethral or extraurethral) leakage of urine. Urinary incontinence is a symptom, a sign, and a condition. Urinary incontinence as a symptom means that the patient states that she has involuntary urine loss. Types of incontinence symptoms include stress incontinence, urge incontinence, mixed incontinence, nocturnal enuresis, situational incontinence, and continuous incontinence. 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 leakage, and whether or not the individual seeks or desires help because of urinary incontinence. The sign of stress incontinence denotes the observation of urine loss from the external urethral meatus synchronously with physical exertion, such as a cough or Valsalva maneuver. Because symptoms and signs of urinary incontinence are sometimes misleading, accurate diagnosis often requires urodynamic investigation in addition to careful history and physical examination. VOIDING PHASE During the voiding phase, the detrusor muscle may be normal, underactive, or acontractile. Normal voiding is usually 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. An underactive detrusor during micturition implies that the detrusor contraction is of inadequate magnitude or duration to effect bladder emptying within a normal time span. Acontractile detrusor is one that cannot be demonstrated to contract during urodynamic studies. During voiding, urethral function may be normal or abnormal. Abnormal urethral function may be due to either obstruction or urethral overactivity, or to a urethra that cannot open due to anatomic abnormality, such as severe pelvic organ prolapse or urethral stricture. Simultaneous measurement of intravesical or detrusor pressure and urine flow is necessary to determine whether the patient’s voiding is obstructive. In general, high detrusor pressures with low flow rates suggest an obstructive problem, whereas low detrusor pressures with low flow rates imply that the problem is one of detrusor underactivity or acontractility. Simultaneous external urethral sphincter electromyography is necessary to determine whether an obstructive voiding pattern is a result of urethral overactivity or mechanical obstruction.
Functional Classification Wein (1981) classified voiding dysfunction on a functional basis, describing the dysfunction simply in terms of whether the deficit is primarily one of the filling/storage phase or the voiding phase. Each section is subcategorized into whether the deficit is one of the bladder or the outlet. The expanded functional classification, with relevant conditions as suggested by Wein (1998), is shown in Box 5-2. A reasonably accurate urodynamic description is required for proper use of this system for a given voiding problem, but an exact diagnosis is not required for treatment. Several deficits can be present in the same patient, and all of them must be recognized to properly use this classification system.
DIFFERENTIAL DIAGNOSIS OF URINARY INCONTINENCE Among women complaining of urinary incontinence, the differential diagnosis includes genitourinary and nongenitourinary conditions (Box 5-3). As previously mentioned, genitourinary disorders include problems of bladder filling and storage and extraurethral disorders, such as fistula and congenital abnormalities. Nongenitourinary conditions that cause urinary incontinence are generally functional conditions that occur simultaneously with normal or abnormal urethral and bladder function. These conditions are most common in elderly women. The most common urine storage disorder in women is urodynamic stress incontinence. Bladder filling disorders caused by overactive detrusor function are the second most common cause of urinary incontinence. Underactive or acontractile detrusor function may result in voiding dysfunction or urinary incontinence. The ICS no longer recommends the term overflow incontinence, but if it is used, a
Chapter 5
BOX 5-2
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Description and Classification of Lower Urinary Tract Dysfunction and Pelvic Organ Prolapse
EXPANDED FUNCTIONAL CLASSIFICATION
Failure to Store Because of the bladder Detrusor overactivity Involuntary contractions Neurologic disease, injury, or degeneration Bladder outlet obstruction Inflammation Idiopathic cause Decreased compliance Neurologic disease Fibrosis Idiopathic cause Detrusor hypersensitivity Inflammation Infection Neurologic disease Psychological cause Idiopathic cause
Because of the outlet Stress incontinence (hypermobility related) Nonfunctional bladder neck-proximal urethra (intrinsic sphincter dysfunction)
Failure to Empty Because of the bladder Neurologic disease Myogenic cause Psychological cause Idiopathic cause
Because of the outlet Anatomic abnormality Urethral compression: extramural (e.g., vaginal mass, prolapse, hematocolpos) Urethral mass (intramural or intraluminal) Urethral stricture Bladder neck contracture Functional cause Smooth sphincter dyssynergia Striated sphincter dyssynergia Modified from Wein AJ. Pathophysiology and categorization of voiding dysfunction. In Walsh PC, Retik AB, Vaughan ED, et al., eds. Campbell’s Urology, 7th ed. WB Saunders, Philadelphia, 1998.
precise definition and any associated pathophysiology, such as reduced urethral function or detrusor overactivity/low bladder compliance, should be stated. Voiding disorders with incontinence in women are usually associated with diabetes, neurologic diseases, severe genital prolapse, or postsurgical obstruction. Functional incontinence is associated with cognitive, psychological, or physical impairments that make it difficult to reach the toilet or interfere with appropriate toileting. With these conditions, continent women may not have enough time to avoid an accident. Functional causes may also act synergistically with other urinary problems. For example, women with manageable detrusor overactivity may become incontinent if another disease or physical problem keeps them from reaching the toilet. Physical conditions that may cause functional incontinence include joint abnormalities, arthritic pain, or muscular weakness. An unfamiliar
BOX 5-3
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DIFFERENTIAL DIAGNOSIS OF URINARY INCONTINENCE IN WOMEN
Genitourinary Etiology Filling/storage disorders Urodynamic stress incontinence Detrusor overactivity (idiopathic) Detrusor overactivity (neurogenic) Mixed types
Fistula Vesical Ureteral Urethral
Congenital Ectopic ureter Epispadias
Nongenitourinary Etiology Functional Neurologic Cognitive Psychological Physical impairment Environmental Pharmacologic Metabolic
setting, lack of convenient toilet facilities, or other environmental factors can aggravate this condition. Psychological difficulties and repressed or hostile behavior may be related to incontinence, especially in the institutionalized elderly. Finally, iatrogenic factors, such as drugs, can cause or aggravate incontinence (see Chapter 6). The relative likelihood of each condition that causes incontinence varies with the age and health of the individual (Fig. 5-1). Among ambulatory incontinent women, the most common condition is urodynamic stress incontinence, which represents 50% to 70% of cases. Detrusor abnormalities and mixed forms (usually stress incontinence and detrusor overactivity) account for 20% to 40% of incontinence cases. Among the elderly, noninstitutionalized incontinent women who are evaluated in referral centers, urodynamic stress incontinence is found less often (30%–46%), and detrusor abnormalities and mixed disorders are more common,
Figure 5-1 ■ Estimated likelihood of conditions causing incontinence in women in various age categories.
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occurring in 30% to 60% of cases, than in younger ambulatory women. However, in a urodynamic study of elderly community-dwelling women with incontinence, Diokno et al. (1988) reported a prevalence of detrusor abnormalities of only 12%, probably reflecting a healthier group of women. Institutionalized elderly women who are incontinent have detrusor overactivity (with or without impaired bladder contractility) in 38% to 60% of cases and urodynamic stress incontinence in only 16% to 21% of cases.
DESCRIPTION AND STAGING OF PELVIC ORGAN PROLAPSE As with voiding dysfunction, a systematic description and classification of pelvic organ prolapse are useful to help document and communicate the severity of the problem, to establish treatment guidelines, and to improve the quality of research by standardizing definitions. Two general classification systems are in use, although the recommendation is that ICS terminology be used by clinicians and researchers in the future. For many years, the severity of pelvic organ prolapse has been described using criteria modified from Beecham (1980) and Baden et al. (1968). This grading system is simple to use, is widely understood among gynecologic surgeons, and has been found to have reasonable interobserver variability for all segments of the vagina and for uterine support. The most dependent position of the pelvic organs during maximum straining or standing is used and graded as normal or first, second, and third degree. First-degree prolapse is used for vaginal segments that descend halfway (but not to) the hymen; second-degree for descent to the hymen; and third-degree for prolapse beyond the hymen. Classification of rectoceles can be aided by performing a rectovaginal examination. In 1996, Bump et al. described the ICS standardization of terminology of female pelvic organ prolapse. In the Pelvic Organ Prolapse Quantitation (POPQ) system, the pelvic organ anatomy is described during physical examination of the external genitalia and vaginal canal. Segments of the lower reproductive tract replace the terms cystocele, enterocele, rectocele, and urethrovesical junction because these terms imply an unrealistic certainty as to the structures on the other side of the vaginal bulge, particularly in women who have had previous prolapse surgery. The examiner sees and describes the maximum protrusion noted by the patient during her daily activities. The details of the examination, including criteria for the end point of the examination and full development of the prolapse, should be specified. Suggested criteria for demonstration of maximum prolapse include one or all of the following: Any protrusion of the vaginal wall has become tight during straining by the patient; traction on the prolapse causes no further descent; the subject confirms that the size of the prolapse and the extent of the protrusion seen by the examiner are as extensive as the most severe protrusion she has had (a small handheld mirror to visualize the protrusion may be helpful); and a standing/straining examination confirms that the full extent of the prolapse was observed in the other positions used. Details about the patient position, types of vaginal specula or retractors, the type and intensity of straining used to develop the prolapse maximally, and the fullness of the bladder should be stated.
This descriptive system contains a series of site-specific measurements of the woman’s pelvic organ support. It can be learned easily and taught by means of a video tutorial. Prolapse in each segment is evaluated and measured relative to the hymen (not introitus), which is a fixed anatomic landmark that can be identified consistently and precisely. The anatomic position of the six defined points for measurement 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. For example, a cervix that protrudes 3 cm distal to the hymen should be described as +3 cm. Six points (two on the anterior vaginal wall, two in the superior vagina, and two on the posterior vaginal wall) are located with reference to the plane of the hymen (Fig. 5-2). In describing the anterior vaginal wall, the term anterior vaginal wall prolapse is preferable to cystocele or anterior enterocele, unless the organs involved are identified by ancillary tests. Two anterior sites are known and described: Point Aa: A point located in the midline of the anterior vaginal wall 3 cm proximal to the external urethral meatus, corresponding to the proximal location of the urethrovesical crease. By definition, the range of position of point Aa relative to the hymen is −3 to +3 cm. Point Ba: A point that represents the most distal (i.e., most dependent) position of any part of the upper 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. Two points are on the superior vagina. These points represent the most proximal locations of the normally positioned lower reproductive tract: Point C: A point that represents either the most distal (i.e., most dependent) edge of the cervix or the leading edge of the vaginal cuff (hysterectomy scar) after total hysterectomy.
Figure 5-2 ■ Six sites (points Aa, Ba, C, D, Bp, and Ap), genital hiatus (gh), perineal body (pb), and total vaginal length (tvl) used for pelvic organ support quantitation. (From 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.)
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Point D: A point that represents a location of the posterior fornix in a woman who still has a cervix. It represents a level of uterosacral ligament attachment to the proximal posterior cervix and is included as a point of measurement to differentiate suspensory failure of the uterosacral cardinal ligament complex from cervical elongation. Point D is omitted in the absence of the cervix. Two points are located on the posterior vaginal wall. Analogous to anterior prolapse, posterior prolapse should be discussed in terms of segments of the vaginal wall rather than the organs that 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 the small bowel is present in the rectovaginal space, the examiner should comment on this fact and clearly describe the basis for this clinical impression (e.g., by observation of peristaltic activity in the distended posterior vagina or palpation of loops of small bowel between one examining finger in the rectum and one in the vagina). In such cases, a “pulsion” addendum to the point Bp position may be noted (e.g., Bp equals +5 [pulsion]; see following text for further discussion). Point Bp: A point that represents the most distal (i.e., most dependent) position of any part of the upper 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 point Ap relative to the hymen is −3 to +3 cm. Other landmarks include the genital hiatus, which is measured from the middle of the external urethral meatus to the posterior midline hymen. The perineal body is measured from the posterior margin of the genital hiatus to the midanal opening. The total vaginal length is the greatest depth of the vagina in centimeters when point C or D is reduced to its
Figure 5-4 ■ A. Grid and line diagram of complete eversion of vagina. Most distal point of anterior wall (point Ba), vaginal cuff scar (point C), and most distal point of the posterior wall (point Bp) are all at same position (+8), and points Aa and Ap are maximally distal (both at +3). Because total vaginal length equals maximum protrusion, this is stage IV prolapse. B. Normal support. Points Aa and Ba and points Ap and Bp are all −3 because there is no anterior or posterior wall descent. Lowest point of the cervix is 8 cm above hymen (−8) and posterior fornix is 2 cm above this (−10). Vaginal length is 10 cm, and genital hiatus and perineal body measure 2 and 3 cm, respectively. This represents stage 0 support. (From 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.)
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full normal position. The points and measurements are presented in Figure 5–2. The positions of points Aa, Ba, Ap, Bp, C, and D (if applicable), with reference to the hymen, are measured and recorded. Positions are expressed as centimeters above or proximally to the hymen (negative number) or centimeters below or distally to the hymen (positive number), with the plane of the hymen defined as zero. 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). Alternatively, a 3 × 3 grid can be used to concisely organize the measurements, as shown in Figure 5-3, or a line diagram of a configuration can be drawn, as shown in Figures 5-4 and 5-5. Figure 5-4 is a grid and line diagram contrasting measurements indicating normal support to those of
Figure 5-3 ■ Three-by-three grid for recording quantitative description of pelvic organ support. (From 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.)
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Figure 5-5 ■ A. Grid and line diagram of predominant anterior support defect. Leading point of prolapse is upper anterior vaginal wall, point Ba (+6). There is significant elongation of bulging anterior wall. Point Aa is maximally distal (+3), and vaginal cuff scar is 2 cm above hymen (C = −2). Cuff scar has undergone 4 cm of descent because it would be at −6 (total vaginal length) if it were perfectly supported. In this example, total vaginal length is not maximum depth of vagina with elongated anterior vaginal wall maximally reduced but rather depth of vagina at cuff with point C reduced to its normal full extent, as specified in text. This represents stage III Ba prolapse. B. Predominant posterior support defect. Leading point of prolapse is upper posterior vaginal wall, point Bp (+5). Point Ap is 2 cm distal to hymen (+2), and vaginal cuff scar is 6 cm above hymen (−6). Cuff has undergone only 2 cm of descent because it would be at −8 (total vaginal length) if it were perfectly supported. This represents stage III Bp prolapse. (From 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.)
posthysterectomy vaginal eversion. Figure 5-5 is a grid and line diagram representing predominant anterior and posterior vaginal wall prolapse with partial vault descent. The profile for quantifying prolapse provides a precise description of anatomy for individual patients. An ordinal staging system of pelvic organ prolapse is suggested using these measurements and can be useful for the description of populations and for research comparisons. Stages are assigned according to the most severe portion of the prolapse when the full extent of the protrusion has been demonstrated. For a stage to be assigned to an individual subject, her quantitative description should essentially be completed first. The five stages of pelvic organ support (0–IV) are described in Box 5-4. Ancillary techniques for describing pelvic organ prolapse include (1) performance of a digital rectal examination while the patient is straining; (2) digital assessment of the contents of the rectovaginal septum during examination to differentiate between a “traction” enterocele (the posterior cul-desac is pulled down by the prolapsing cervix or vaginal cuff but is not distended by intestines) and a “pulsion” enterocele (the intestinal contents of the enterocele distend the rectalvaginal septum and produce a protruding mass); (3) cotton swab testing for the measurement of urethral axis mobility (Q-tip test); (4) measurement of perineal descent; (5) measurement of the transverse diameter of the genital hiatus or of the protruding prolapse; (6) measurement of vaginal volume; (7) description and measurement of rectal prolapse; and (8) examination techniques differentiating between various types of defects (e.g., central versus paravaginal defects of the anterior vaginal wall). Cystoscopy and photography can be useful in describing pelvic organ prolapse. Imaging procedures include ultrasonography, contrast radiography,
BOX 5-4
STAGES OF PELVIC ORGAN PROLAPSE
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 −TVL (total vaginal length) cm and −(TVL–2) cm (i.e., the quantitation value for point C or D is ≤−[TVL–2] cm). Fig. 5-4, B represents stage 0.
Stage I The criteria for stage 0 are not met, but the most distal portion of the prolapse is >1 cm above the level of the hymen (i.e., its quantitation value is <−1 cm).
Stage II The most distal portion of the prolapse is ≤1 cm proximal to or distal to the plane of the hymen (i.e., its quantitation value is ≥−1 cm but ≤+1 cm).
Stage III The most distal portion of the prolapse is >1 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 >+1 cm but <+[TVL–2] cm). Fig. 5-5, A represents stage III Ba, and Fig. 5-5, B 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 (TVL–2) cm (i.e., its quantitation value is ≥+[TVL–2] cm). In most instances, the leading edge of stage IV prolapse is the cervix or vaginal cuff scar. Fig. 5-4, A represents stage IV C prolapse. From 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.
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computed tomography, and magnetic resonance imaging. Intraoperative evaluation of pelvic support defects is intuitively attractive but of unproven value. The effects of anesthesia, diminished muscle tone, and loss of consciousness probably result in minor worsening of the prolapse, but the clinical significance of this is unknown. Limitations because of the position of the patient must be evaluated. Precise characterization of pelvic floor muscle strength and the description of functional symptoms are important. The reader is referred to the ICS committee document for further details (Bump et al., 1996).
Bibliography CLASSIFICATION OF URINARY INCONTINENCE Abrams P, Blaivas JG, Stanton SL, et al. Sixth report on the standardization 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; Scand J Urol Nephrol 1986;20:161. Abrams P, Blaivas JG, Stanton SL, et al. The standardization of terminology of lower tract function. Scand J Urol Nephrol 1988;114(Suppl):5. 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. Am J Obstet Gynecol 2002;187:116. Bates P, Bradley WE, Glen E, et al. First report on the standardization of terminology of lower urinary tract function. Urinary incontinence. Procedures related to the evaluation of urine storage: cystometry, urethral closure pressure profile, units of measurement. Br J Urol 1976;48:39; Eur Urol 1976;2:274; Scand J Urol Nephrol 1976;11:193; Urol Int 1976;32:81. Bates P, Bradley WE, Glen E, et al. Second report on the standardization 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; Br J Urol 1977;49:207; Scand J Urol Nephrol 1977;11:197. Bates P, Bradley WE, Glen E, et al. Third report on the standardization 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; Eur Urol 1980;6:170; Acta Urol Jpn 1980;27:1566; Scand J Urol Nephrol 1980;12:191. Bates P, Bradley WE, Glen E, et al. Fourth report on the standardization of terminology of lower urinary tract function. Terminology related to neuromuscular dysfunction of lower urinary tract. Br J Urol 1981;52:333; Urology 1981;17:618; Scand J Urol Nephrol 1981;15:169; Acta Urol Jpn 1981;27:1568. Bent AE, Richardson DA, Ostergard DR. Diagnosis of lower urinary tract disorders in postmenopausal patients. Am J Obstet Gynecol 1983;145:218. Blaivas JG. Classification of stress urinary incontinence. Neurourol Urodyn 1983;2:103.
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Blaivas JG, Olsson CA. Stress incontinence: classification and surgical approach. J Urol 1988;139:727. Castleton CM, Duffin HM, Asher MJ. Clinical and urodynamic studies in 100 elderly incontinent patients. Br Med J 1981;282:1103. Diokno AC, Brown MB, Brock BM, et al. Clinical and cystometric characteristics of continent and incontinent non-institutionalized elderly. J Urol 1988;140:567. Enhorning G. Simultaneous recording of intravesical and intraurethral pressure. Acta Chir Scand 1961;276(Suppl):1. McGuire EJ, Lytton B, Pepe V, et al. Stress urinary incontinence. Am J Obstet Gynecol 1976;47:255. Ouslander J, Staskin D, Raz S, et al. Clinical versus urodynamic diagnosis in an incontinent female geriatric population. J Urol 1987;37:68. Resnick NM, Yalla SV, Laurino E. The pathophysiology of urinary incontinence among institutionalized elderly persons. N Engl J Med 1989;320:1. Wein AJ. Classification of neurogenic voiding dysfunction. J Urol 1981;125:605. Wein AJ. Pathophysiology and categorization of voiding dysfunction. In Walsh PC, Retik AB, Vaughan ED, et al., eds. Campbell’s Urology, 7th ed. WB Saunders, Philadelphia, 1998. Wein AJ, Barrett DM. Voiding Function and Dysfunction. Mosby, Chicago, 1988. Williams ME, Pannill FC. Urinary incontinence in the elderly. Ann Intern Med 1982;97:895.
CLASSIFICATION OF PELVIC ORGAN PROLAPSE Baden WF, Walker T. Fundamental, symptoms, and classification. In Baden WF, Walker T, eds. Surgical Repair of Vaginal Defects. JB Lippincott, Philadelphia, 1992. Baden WF, Walker T, Lindsey JH. The vaginal profile. Tex Med 1968;64:56. Beecham CT. Classification of vaginal relaxation. Am J Obstet Gynecol 1980;136:957. 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. Hall AF, Theofrastous JP, Cundiff GW, et al. Interobserver and intraobserver reliability of the proposed International Continence Society, Society of Gynecologic Surgeons, and American Urogynecology Society pelvic organ prolapse classification system. Am J Obstet Gynecol 1996;175:467. Kobak WH, Rosenberger K, Walters MD. Interobserver variation in the assessment of pelvic organ prolapse. Int Urogynecol J 1996;7:121. Porges RF. A practical system of diagnosis and classification of pelvic relaxations. Surg Gynecol Obstet 1963;117:769. Steele A, Mallipeddi P, Welgoss J, et al. Teaching the pelvic organ prolapse quantitation system. Am J Obstet Gynecol 1998;179:1458. Vierhout ME, Stoutjesdijk J, Spruijt J. A comparison of preoperative and intraoperative evaluation of patients undergoing pelvic reconstructive surgery for pelvic organ prolapse using the Pelvic Organ Prolapse Quantification system. Int Urogynecol J 2005;17:46.
Evaluation of Urinary Incontinence and Pelvic Organ Prolapse
6
History, Physical Examination, and Office Tests Mark D. Walters
HISTORY AND PHYSICAL EXAMINATION 66 History of Urinary Incontinence 66 Urinary Diary 66 History of Pelvic Organ Prolapse 66 Gynecologic Examination 68 Neurologic Examination 69 Techniques for Measuring Urethral Mobility 70 PERINEAL PAD TESTS 71 DIAGNOSTIC TESTS 71 Laboratory 71 Radiologic 72 Evaluation of Bladder Filling and Voiding 72 MAKING THE INCONTINENCE DIAGNOSIS 73 DIAGNOSTIC ACCURACY OF OFFICE EVALUATIONS 73 INDICATIONS FOR URODYNAMIC TESTS AND CYSTOSCOPY
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Urinary incontinence can be a symptom of which patients complain, a sign demonstrated on examination, or a condition (i.e., diagnosis) that can be confirmed by definitive studies. When a woman complains of urinary incontinence, appropriate evaluation includes exploring the nature of her symptoms and looking for physical findings. The history and physical examination are the first and most important steps in the evaluation. A preliminary diagnosis can be made with simple office and laboratory tests, with initial therapy based on these findings. If complex conditions are present, if the patient does not improve after initial therapy, or if surgery is being considered, definitive, specialized studies are usually necessary. Pelvic organ prolapse is a heterogeneous condition in which weaknesses of the pelvic floor musculature and connective tissue result in herniation of pelvic organs into the vaginal lumen. In more severe cases, prolapse can protrude through the vaginal introitus and beyond the hymenal ring. Organs that may potentially herniate into the vaginal canal include the bladder, with or without involvement of the urethra, resulting in cystoceles and cystourethroceles, respectively.
Patients may have uterine prolapse or, after hysterectomy, the vaginal cuff may herniate, resulting in apical vaginal prolapse. The rectum, small bowel, and sigmoid colon may also herniate, resulting in rectoceles, enteroceles, and sigmoidoceles, respectively. Many of the accepted definitions of pelvic organ prolapse are based on expert opinions and consensus rather than epidemiologic or clinical data. The American College of Obstetrics and Gynecology defines pelvic organ prolapse as the protrusion of pelvic organs into the vaginal canal (1995, bull no. 214). More specifically, in a terminology workshop convened by the National Institutes of Health (NIH) for researchers in female pelvic floor disorders, pelvic organ prolapse is defined as the descent of vaginal segments to within 1 cm of the hymen or lower (Weber et al., 2001). Terminologies such as cystocele and rectocele were intentionally not used by Weber et al. because they implied an unrealistic certainty as to the specific organs behind the vaginal wall at the time of physical examination. Importantly, although most clinicians can recognize the extremes of normal support versus severe prolapse, most cannot objectively state at what point vaginal laxity becomes pathologic and requires intervention. Limited data are available concerning the normal distribution of pelvic organ prolapse in the population and the correlations between symptoms and physical findings. In a study of 497 women, Swift (2000) demonstrated that the distribution of prolapse in a population exhibited a bell curve, with the majority of women having stage I or II prolapse by the Pelvic Organ Prolapse Quantification (POPQ) classification system (see Chapter 5) and only 3% having stage III prolapse. This signifies that, at baseline, a majority of women, especially those who have borne children, have some degree of pelvic relaxation. However, these women are generally asymptomatic and will develop symptoms only as their prolapse increases in severity (Swift et al., 2005). Therefore, even if prolapse is found on physical examination by the earlier definition, it may not be clinically relevant and may not require intervention if the patient is asymptomatic.
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HISTORY AND PHYSICAL EXAMINATION History of Urinary Incontinence Early in the interview, one should elicit a description of the patient’s main complaint, including duration and frequency. A clear understanding of the severity of the problem or disability and its effect on quality of life should be sought. Assessment of mobility and living environment is especially important in certain patients. Questions should be asked about access to toilets or toilet substitutes and about social factors, such as living arrangements, social contacts, and caregiver involvement. Box 6-1 lists questions that are helpful in evaluating incontinence in women. The first question is designed to elicit the symptom of stress incontinence (i.e., urine loss with events that increase intra-abdominal pressure). The symptom of stress incontinence is usually (but not always) associated with the diagnosis of urodynamic stress incontinence. Questions 2 through 8 help elicit the symptoms associated with detrusor overactivity. The symptom of urge incontinence is present if the patient answers question 3 affirmatively. Frequency (questions 4 and 5), bed-wetting (question 6), leaking with intercourse (question 8), and a sense of urgency (questions 2 and 7) are all associated with detrusor overactivity. Questions 9 and 10 help define the severity of the problem. Questions 11 through 13 screen for urinary tract infection and neoplasia, and questions 14 through 16 are designed to elicit symptoms of voiding dysfunction. After the urologic history, thorough medical, surgical, gynecologic, neurologic, and obstetric histories should be obtained. Certain medical and neurologic conditions, such as diabetes, stroke, and lumbar disk disease, may cause uri-
BOX 6-1
HELPFUL QUESTIONS IN THE EVALUATION OF FEMALE URINARY INCONTINENCE
1. Do you leak urine when you cough, sneeze, or laugh? 2. Do you ever have such an uncomfortable strong need to urinate that if you don’t reach the toilet you will leak? 3. If you answered “yes” to question 2, do you ever leak before you reach the toilet? 4. How many times do you urinate during the day? 5. How many times do you void during the night after going to bed? 6. Have you wet the bed in the past year? 7. Do you develop an urgent need to urinate when you are nervous, under stress, or in a hurry? 8. Do you ever leak during or after sexual intercourse? 9. How often do you leak? 10. Do you find it necessary to wear a pad because of your leaking? 11. Have you had bladder, urine, or kidney infections? 12. Are you troubled by pain or discomfort when you urinate? 13. Have you had blood in your urine? 14. Do you find it hard to begin urinating? 15. Do you have a slow urinary stream or have to strain to pass your urine? 16. After you urinate, do you have dribbling or a feeling that your bladder is still full?
nary incontinence. Furthermore, strong coughing associated with chronic pulmonary disease can markedly worsen symptoms of stress incontinence. A bowel history should be noted because chronic severe constipation has been associated with voiding difficulties, urgency, stress incontinence, and increased bladder capacity. A history of hysterectomy, vaginal repair, pelvic cancer and/or radiotherapy, or surgery for incontinence should alert the physician to the possibility of prior surgical trauma to the lower urinary tract. A complete list of the patient’s medications (including nonprescription medications) should be sought to determine whether individual drugs might influence the function of the bladder or urethra, leading to urinary incontinence or voiding difficulties. A list of drugs that commonly affect lower urinary tract function is shown in Table 6-1. In these cases, altering drug dosage or changing to a drug with similar therapeutic effectiveness, but with fewer lower urinary tract side effects, will often improve or cure the offending urinary tract symptom.
Urinary Diary Patient histories regarding frequency and severity of urinary symptoms are often inaccurate and misleading. Urinary diaries are more reliable and require the patient to record volume and frequency of fluid intake and of voiding, usually for a 1- to 7-day period. A 3-day diary seems to be as accurate as a 7-day diary to document symptoms, and compliance is improved. Episodes of urinary incontinence and associated events or symptoms, such as coughing, urgency, and pad use, are noted. The number of times voided each night and any episodes of bed-wetting are recorded the next morning. The maximum voided volume also provides a relatively accurate estimate of bladder capacity. The physician should review the frequency/volume charts with the patient and corroborate or modify the initial diagnostic impression. If excessive frequency and volume of fluid intake are noted, restriction of excessive oral fluid intake (combined with scheduled voiding) may improve symptoms of stress and urge incontinence by keeping the bladder volume below the threshold at which urinary leaking results. Urinary diaries are a useful and accepted research method to measure the severity of incontinence and as an outcome measure after interventions. This is reviewed in detail in Chapter 39.
History of Pelvic Organ Prolapse Patients with pelvic organ prolapse may present with symptoms directly related to the prolapse, such as vaginal bulge, pressure, and discomfort, as well as a plethora of associated symptoms relating to voiding, defecatory, and sexual dysfunctions. The severity of the prolapse is not necessarily associated with increased visceral symptomatology. Vaginal prolapse in any compartment—anterior, apical, or posterior—can manifest as vaginal fullness, pain, and/or protruding mass. In a recent study by Tan et al. (2005), the feeling of “a bulge or that something is falling outside the vagina” had a positive predictive value of 81% for pelvic organ prolapse, and the lack of this symptom had a negative
Chapter 6
Table 6-1
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Medications That Can Affect Lower Urinary Tract Function
Type of Medication
Lower Urinary Tract Effects
Diuretics Caffeine Alcohol Narcotic analgesics Anticholinergic agents Antihistamines Psychotropic agents Antidepressants Antipsychotics Sedatives/hypnotics α-Adrenergic blockers α-Adrenergic agonists Calcium-channel blockers
Polyuria, frequency, urgency Frequency, urgency Sedation, impaired mobility, diuresis Urinary retention, fecal impaction, sedation, delirium Urinary retention, voiding difficulty Anticholinergic actions, sedation Anticholinergic actions, sedation Anticholinergic actions, sedation Sedation, muscle relaxation, confusion Stress incontinence Urinary retention, voiding difficulty Urinary retention, voiding difficulty
predictive value of 76% for predicting prolapse at or past the hymen. Not surprisingly, increased degree of prolapse, especially beyond the hymen, is associated with increased pelvic discomfort and visualization of a protrusion. The association of POPQ measures on examination with three commonly related symptoms—urinary splinting, digital assistance with defecation, and vaginal bulge—is shown in Figure 6-1. Stress urinary incontinence and voiding difficulties can occur in association with anterior and apical vaginal prolapse. However, women with advanced degrees of prolapse
may not have overt symptoms of stress incontinence because the prolapse may cause a mechanical obstruction of the urethra, thereby preventing urinary leakage. Instead, these women may require vaginal pressure or manual replacement of the prolapse to accomplish voiding. Therefore, they 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. Patients who require digital assistance to void, in general, have more advanced degrees of prolapse. In addition to
Figure 6-1 ■ Prevalence of prolapse symptoms per POPQ group. The percentage of patients who report urinary splinting, digital assistance, and vaginal bulge for each relevant POPQ measurements. (Modified from Tan JS, Lukacz ES, Menefee SA, et al. Predictive value of prolapse symptoms: a large database study. Int Urogynecol J 2005;16:203.)
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difficulty voiding, other urinary symptoms, such as urgency, frequency, and urge incontinence, are found in women with prolapse. However, it is not clear whether the severity of prolapse is directly associated with more irritative voiding symptoms or bladder pain. Pelvic organ prolapse, especially in the apical and posterior compartments, can be (but is not always) associated with defecatory dysfunction, such as pain with defecation, the need for manual assistance with defecation, and anal incontinence of flatus, liquid, or solid stool. These patients often have outlet-type constipation secondary to the trapping of stool within the rectal hernia, necessitating the need for splinting or applying manual pressure in the vagina, rectum, or perineum to reduce the prolapse aiding in defecation. Although defecatory dysfunction remains an area that is least understood in patients with prolapse, clinical and radiographic studies have shown that the severity of prolapse is not strongly correlated with increased symptomatology. Although the relationship between sexual function and pelvic organ prolapse is not clearly defined, questions regarding sexual dysfunction must be included in the evaluation of any patients with prolapse. Patients may report symptoms of dyspareunia, decreased libido and orgasm, and increased embarrassment with altered anatomy that affects body image. Some studies have reported that prolapse adversely affected sexual functioning, with subsequent improvement in sexual function after repair of prolapse (Barber et al., 2002; Rogers et al., 2001; Weber et al., 2000). However, Burrows et al. (2004) showed little correlation between the extent of prolapse and sexual dysfunction. Evaluating sexual function may be especially difficult in this patient population because the hindrances to sexual function may include factors other than prolapse, such as partner limitations and functional deficits. Symptoms of incontinence and prolapse and their impact on the woman can be measured or quantified using a number of easy-to-use and validated questionnaires measuring symptom severity, quality of life, and sexual function. These outcome measures can be useful in clinical practice and in research; they are reviewed in detail in Chapter 39.
Gynecologic Examination General, gynecologic, and lower neurologic examinations should be performed on every woman with incontinence and/or prolapse; the pelvic examination is of primary importance. A bimanual examination is performed to rule out coexistent gynecologic pathology, which can occur in up to two thirds of patients. The rectal examination further evaluates for pelvic pathology and fecal impaction, the latter of which may be associated with voiding difficulties and incontinence in elderly women. Urinary incontinence has been shown to improve or resolve after the removal of fecal impactions in institutionalized geriatric patients. The physical examination for incontinence and prolapse should be conducted with the patient in dorsal lithotomy position, as for a routine pelvic examination. If physical findings do not correspond to symptoms, or if the maximum extent of the prolapse cannot be confirmed, the woman can be reexamined in the standing position.
Initially, the external genitalia are inspected, and, if no displacement is apparent, the labia are gently spread to expose the vestibule and hymen. Vaginal discharge can mimic incontinence, so evidence of this problem should be sought and, if present, treated. Palpation of the anterior vaginal wall and urethra may elicit urethral discharge or tenderness that suggests a urethral diverticulum, carcinoma, or inflammatory condition of the urethra. The integrity of the perineal body is evaluated, and the extent of all prolapsed parts are assessed. A retractor, a Sims speculum, or the posterior blade of a bivalve speculum can be used to depress the posterior vagina to aid in visualizing the anterior vagina and vice versa for the posterior vagina. Because most patients with prolapse are postmenopausal, the vaginal mucosa should be examined for atrophy and thinning because it may impact upon management. Healthy, estrogenized tissue, without significant evidence of prolapse, will be well perfused, have rugation, and have physiologic moisture. Atrophic vaginal tissue consistent with hypoestrogenemia appears pale, thin, without rugation, and can be friable; this finding suggests that the urethral mucosa is also atrophic. After the resting vaginal examination, the patient is instructed to perform Valsalva maneuver 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 increased intra-abdominal pressure. The presence and severity of anterior vaginal relaxation, including cystocele and proximal urethral detachment and mobility, or anterior vaginal scarring, are estimated. Associated pelvic support abnormalities, such as rectocele, enterocele, and uterovaginal prolapse, are noted. The amount or severity of prolapse in each vaginal segment should be measured, staged, and recorded according to POPQ guidelines noted in Chapter 5. A rectovaginal examination is required to fully evaluate prolapse of the posterior vaginal wall and perineal body. Digital assessment of bowel contents in the rectovaginal septum during straining examination can help to diagnose an enterocele. Other clinical observations and tests that help delineate prolapse include (1) cotton swab testing for the measurement of urethral axis mobility (Q-tip test); (2) measurement of perineal descent; (3) measurement of the transverse diameter of the genital hiatus or of the protruding prolapse; (4) measurement of vaginal volume; (5) description and measurement of posterior prolapse; and (6) examination techniques differentiating between various types of defects (e.g., central versus paravaginal defects of the anterior vaginal wall). Inspection should also be made of the anal sphincter because fecal incontinence is often associated with posterior vaginal support defects. Grossly, women with a torn external sphincter may have scarring or a “dovetail” sign on the perineal body. Anterior vaginal wall descent usually represents bladder descent with or without concomitant urethral hypermobility. However, in 1.6% of women with anterior vaginal prolapse, an anterior enterocele can mimic a cystocele on physical examination. Furthermore, lateral paravaginal defects, identified as detachment of the lateral vaginal sulci, may be distinguished from central defects, seen as a midline protrusion with preservation of the lateral sulci, by using a curved forceps placed in the anterolateral vaginal sulci directed toward the ischial spine. Bulging of
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the anterior vaginal wall in the midline between the forceps blades implies a midline defect; blunting or descent of the vaginal fornices on either side with straining suggest lateral paravaginal defects. However, researchers have shown that the physical examination technique to detect paravaginal defects is not particularly reliable or accurate. In a study by Barber et al. (1999), of 117 women with prolapse, the sensitivity of clinical examination to detect paravaginal defects (92%) was good, yet the specificity (52%) was poor. Despite a high prevalence of paravaginal defects, the positive predictive value was only 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. (2004) 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. In regard to posterior prolapse, clinical examinations do not always accurately differentiate between rectoceles and enteroceles. Some investigators thus have advocated performing imaging studies to further delineate the exact nature of the posterior wall prolapse. Traditionally, most clinicians believe that they are able to detect the presence or absence of these defects without anatomically localizing them. However, little is known regarding the accuracy or use of clinical examinations in evaluating the anatomic locations of prolapsed small or large bowel or of specific defects in the rectovaginal space. Burrows et al. (2003) found that clinical examinations often did not accurately predict the specific location of defects in the rectovaginal septum that were subsequently found intraoperatively. Clinical findings corresponded with intraoperative observations in 59% of patients and differed in 41%; sensitivities and positive predicative values of clinical examinations were less than 40% for all posterior defects. However, the clinical consequence of not detecting preoperative defects remains unclear. As noted earlier, the POPQ classification should be done on all women with prolapse. This descriptive system contains a series of site-specific measurements of the woman’s pelvic organ support. The measurements can be obtained quickly in both experienced and nonexperienced hands and can be easily learned and taught by means of a brief video tutorial. Prolapse in each segment is evaluated and measured relative to the hymen (not introitus), which is a fixed anatomic landmark that can be identified consistently and precisely. The anatomic position of the six defined points for measurement 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. For example, a cervix that protrudes 3 cm distal (beyond) to the hymen should be described as +3 cm. Studies have demonstrated excellent interexaminer and intraexaminer reliability when using the POPQ system to quantify prolapse. The POPQ system does not take into account lateral defects and perineal descent, but these can be added in descriptive terms. Despite its limitations, POPQ system is currently the classification system used in most research studies and NIH trials and is gaining popularity in clinical practice.
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Neurologic Examination Urinary (and fecal) incontinence may be the presenting symptom(s) of neurologic disease. The screening neurologic examination should evaluate mental status, sensory and motor function of both lower extremities, and lumbosacral neurologic function. The screening lumbosacral examination should include assessments of (1) pelvic floor muscle strength, (2) anal sphincter resting tone, (3) voluntary anal contraction, and (4) perineal sensation. This simple screening examination can be performed quickly and easily as part of the gynecologic examination. When abnormalities are noted, or when an individual is suspected of having neurologic dysfunction, a comprehensive neurologic examination, with particular emphasis on the lumbosacral nerve roots, should be performed. This comprehensive evaluation should be performed before any neurophysiologic testing, because any such testing should be interpreted only in the context of the patient’s history and physical examination findings. Mental status is determined by noting the patient’s level of consciousness, orientation, memory, speech, and comprehension. Disorders associated with mental status aberrations that may result in changes in bowel or bladder function include senile and presenile dementia, brain tumors, stroke, Parkinson’s disease, and normal pressure hydrocephalus. Evaluation of the sensory and motor systems may identify an occult neurologic lesion or can help determine the level of a known lesion. Common diseases associated with sensory and motor abnormalities that can produce urologic disturbances include Parkinson’s disease, multiple sclerosis, cerebrovascular disease, infections, and tumors. Sacral segments 2 through 4, which contain the important neurons controlling micturition, are particularly important (Fig. 6-2). Sensory function is evaluated by testing the lumbosacral dermatomes for the ability to sense light-touch, pinprick, and temperature. The sensory dermatomes of interest include the perineum and perianal skin (pudendal nerve, S2–S4), mons pubis and upper aspect of labia majora (ilioinguinal nerve, L1–L2), front of the knees (L3–L4), and sole of the foot (S1). Dermatome maps are useful for characterizing sensory deficits, although it is important to remember that there can be considerable overlap between dermatomes. To test motor function, the patient extends and flexes the hip, knee, and ankle and inverts and everts the foot. The strength and tone of the levator ani muscle and external anal sphincter are estimated digitally. The strength of pelvic floor musculature is assessed by palpating the levator ani muscle complex in the posterior vaginal wall approximately 2 to 4 cm cephalad to the hymen. The patient is then asked to squeeze around the examiner’s fingers. Weakness in this muscle can be a result of neurologic deficits or direct trauma during childbirth. Skeletal muscle strength is graded on a scale from 0 to 5 (Box 6-2). Position sense and vibration should be assessed in the distal extremities. The patellar, ankle, and plantar reflex responses are tested. Visceral sensation of the bladder and rectum can be assessed with cystometry and anal manometry, respectively. Loss of perineal sensation in a patient with bowel or bladder dysfunction, particularly if acute, should always alert the examiner to a potentially serious neurologic problem.
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may have gross abnormalities of the perineal body with a “dovetail” sign in the area of the disrupted sphincter. A digital rectal examination should be performed, noting the resistance to entry of the examining finger. Between 50% and 85% of overall resting anal tone is generated by the internal anal sphincter. Loss of resting tone suggests disruption of the internal anal sphincter and/or an injury to its sympathetic innervation (i.e., pelvic plexus injury). The patient then should be asked to maximally squeeze her anal sphincter. The presence of a strong voluntary anal sphincter contraction indicates intact pudendal innervation and external anal sphincter. Unlike pelvic muscle strength, no widely accepted validated scale is known for quantifying anal squeeze strength. Kaushal and Goldner (1991) used a zero to 3+ scale and found that it had a high correlation with maximum squeeze pressure as measured by anal manometry. Weidner et al. (2000) used a modified version of the pelvic muscle rating scale to quantify anal squeeze strength. Absence or decrease of both anal sphincter tone and voluntary contraction suggests a possible sacral or peripheral nerve lesion. Preservation of resting tone in the absence of a voluntary contraction suggests a suprasacral lesion.
Techniques for Measuring Urethral Mobility
Figure 6-2 ■ Sensory dermatomes of the lower extremities and perineum. Shaded area represents sacral segments 2, 3, and 4. (Modified from Boileau Grant JC: Grant’s Atlas of Anatomy, 6th ed. Williams & Wilkins, Baltimore, 1972.)
Neurophysiologic testing and/or radiologic evaluation should be performed to assess for conus medullaris or cauda equina syndrome. Two reflexes may help in the examination of sacral reflex activity. In the anal reflex, stroking the skin adjacent to the anus causes reflex contraction of the external anal sphincter muscle. The bulbocavernosus reflex involves contraction of the bulbocavernosus and ischiocavernosus muscles in response to tapping or squeezing of the clitoris. Unfortunately, these reflexes can be difficult to evaluate clinically and are not always present, even in neurologically intact women. Both resting tone and voluntary contraction of the anal sphincter should be assessed. The examiner should first inspect the anus, looking for scarring or a gaping sphincter. Women with disruption of the external anal sphincter
BOX 6-2
SCORE 0/5 1/5 2/5 3/5 4/5 5/5
Examination of the anterior vaginal wall is inaccurate in predicting the amount of urethral mobility. Using the physical examination is difficult to differentiate between cystocele and rotational descent of the urethra, and the two often coexist. Measuring urethral mobility aids in the diagnosis of urodynamic stress incontinence and in planning treatment for this condition (bladder neck suspension versus periurethral injection of bulking agents). Several tests are available for estimating the amount of urethral mobility in women. RADIOLOGIC ASSESSMENT Lateral cystourethrography in the resting and straining view can identify mobility or fixation of the bladder neck, funneling of the bladder neck and proximal urethra, and degree of cystocele. The voiding component can identify a urethral diverticulum, fistula, obstruction, or vesicoureteral reflux. Videocystourethrography allows a dynamic assessment of the anatomy and function of the bladder base and urethra during retrograde filling with contrast material and during voiding. It is most helpful in sorting out causes of complex incontinence problems. However, it is invasive, expensive, and not widely available. For these reasons, other methods are usually used to measure urethral mobility in incontinent women.
GRADING SCALES FOR MUSCLE STRENGTH LIMB MUSCLES No movement Trace of contraction Active movement when gravity eliminated Active movement against gravity only Active movement against resistance, but not normal Normal strength
LEVATOR ANI No contraction Flicker, barely perceptible Loose hold, 1 to 2 seconds Firmer hold, 1 to 2 seconds Good squeeze, 3 to 4 seconds, pulls fingers in and up loosely Stronger squeeze, 3 to 4 seconds, pulls in and up snugly
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ULTRASONOGRAPHY Ultrasonography is an alternative method of evaluating urethrovesical anatomy and is described in detail in Chapter 10. When compared with bead-chain cystourethrography, fluoroscopy, and the Q-tip test, perineal and vaginal ultrasonography accurately displays descent of the urethrovesical junction, opening of the bladder neck, and detrusor contractions. This technique appears to hold promise as a noninvasive and accurate method of evaluating the position and mobility of the urethrovesical junction and proximal urethra in incontinent women. Q-TIP TEST Placement of a cotton swab in the urethra to the level of the vesical neck and measurement of the axis change with straining can be used to demonstrate urethral mobility. To perform the Q-tip test, a sterile, lubricated cotton-tipped applicator is inserted transurethrally into the bladder, then withdrawn slowly until definite resistance is felt, indicating that the cotton tip is at the bladder neck. The Q-tip test is best accomplished with the patient in the supine lithotomy position during a pelvic examination. The resting angle of the applicator stick in relation to the horizontal is measured with a goniometer or protractor. The patient is then asked to cough and perform a Valsalva maneuver, and the maximum straining angle from the horizontal is measured. Results are not affected by the amount of urine in the bladder. Care should be taken to ensure that the cotton tip is not in the bladder or at the mid-urethra because this results in a falsely low measurement of urethral mobility. Although maximum straining angle measurements greater than 30 degrees are generally considered to be abnormal, few data are available to differentiate normal from abnormal measurements. Urethral mobility in continent women is probably related to age, parity, and support defects of the anterior vaginal wall. Walters and Diaz (1987) noted that asymptomatic women with a mean parity of 2 and a mean age of 32 years had an average resting Q-tip angle of 18 degrees and an average maximum straining angle of 54 degrees. Women with urodynamic stress incontinence had a significantly higher maximum straining angle of 73 degrees, although a wide overlap occurred in measurements between the continent and incontinent women. The data indicate that arbitrary cutoff values around 30 degrees are too low to define “normal” urethral mobility for parous women. Although pelvic examination alone is generally considered to be unreliable in predicting urethral mobility, one recent study by Noblett et al. (2005) showed that, essentially, all of the women with stages II–IV prolapse by POPQ had a Q-tip angle greater than 30 degrees. Thus, perhaps measures of urethral mobility would be useful only in women with stage 0 or I prolapse or in those with prior surgical repairs or other interventions.
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evaluate as long of a period as possible, yet be practical. A 1hour period of testing is recommended and can be extended for additional 1-hour periods if the result of the first test is not considered representative of the symptoms by either the patient or the physician. Alternatively, the test can be performed after filling the bladder to a defined volume or at home over a 24-hour period. The total amount of urine lost during the test is determined by weighing a collecting device, such as an absorbent pad. The pad should be worn inside waterproof underpants or should have a waterproof backing. Care should be taken to use a collecting device of adequate capacity. Immediately before the test begins, the collecting device is weighed to the nearest gram. A typical test schedule is started without the patient voiding and with drinking approximately 500 mL of fluid. A period of walking, coughing, exercising, and handwashing is done. At the end of the 1-hour test, the collecting device is removed and weighed. If the test is regarded as representative, the patient voids and the volume is recorded; if not, the test is repeated for an additional hour. If the collecting device becomes saturated or filled during the test, it should be removed, weighed, and replaced. The total weight of urine lost during the test period is taken to be equal to the gain in weight of the collecting device(s). In interpreting the results of the test, one should remember that a weight gain of up to 1 g may be due to weighing errors, sweating, or vaginal discharge. Two critical variables determine the sensitivity of pad weighing: the amount of fluid in the bladder during exercise and the type of activity used to generate increased intra-abdominal pressure. Lose et al. (1986) found that pad weight correlated significantly with the fluid load on the bladder (i.e., the initial volume plus diuresis). Pad weighing has acceptable test-retest reliability and is easy to perform in a clinical setting. However, it has low sensitivity and poor correlation between pad gain and videographic assessment of incontinence severity. These shortcomings have limited acceptance of pad weighing as a routine part of the evaluation of incontinence. Phenazopyridine hydrochloride (Pyridium) is sometimes used to aid clinicians in differentiating urinary continence from incontinence in women with disturbing vaginal wetness. Patients are given Pyridium tablets and instructed to wear a sanitary pad for a given time. The pad is then removed and examined. Red-orange staining is taken as evidence that urine loss has occurred. Although this test may occasionally be useful, Wall et al. (1990) demonstrated that although all incontinent women had pad staining, 52% of healthy continent women also had staining, reflecting a high rate of falsepositive tests.
DIAGNOSTIC TESTS Laboratory
PERINEAL PAD TESTS Perineal pad weighing may be used when one wants to document objectively the presence and amount of urine loss. The test should approximate activities in daily life and should
Few laboratory tests are necessary for the evaluation of incontinence and prolapse. A clean midstream or catheterized urine sample should be obtained for dipstick urinalysis. Urine culture and sensitivity should be obtained when the dipstick test indicates infection. Acute cystitis can present
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with multiple irritative symptoms, such as dysuria, frequency, urgency, incontinence, and voiding difficulty. In these cases, treatment of the infection usually eradicates the symptoms. However, bacteriuria is often asymptomatic, especially in the elderly. Boscia et al. (1986) demonstrated that no differences in urinary symptoms were found when elderly bacteriuric subjects were compared with themselves when they were nonbacteriuric. In view of the conflicting data, it seems reasonable to examine the urine for infection in all incontinent patients and, if bacteriuria is found, to prescribe appropriate antibiotics and reevaluate the patient in several weeks. Blood testing (blood urea nitrogen [BUN], creatinine, glucose, and calcium) is recommended if compromised renal function is suspected or if polyuria (in the absence of diuretics) is present. Urine cytology is not recommended in the routine evaluation of the incontinent patient. However, patients with microscopic hematuria (two to five red blood cell count per high-power field [RBC/HPF]), those older than age 50 with persistent hematuria, or those with acute onset of irritative voiding symptoms in the absence of urinary tract infection require cystoscopy and cytology to exclude bladder neoplasm.
Radiologic After a careful history and physical examination, few diagnostic tests are needed to further evaluate patients with pelvic organ prolapse if there is no concomitant voiding or defecatory dysfunction. Although hydronephrosis does occur in a small proportion of women with prolapse, even if identified, it usually does not change management in the women for whom surgical repair is planned. Therefore, routine imaging of the kidneys and ureters is not necessary. As discussed in previous sections, preoperative clinical assessments of specific support defects involved in prolapse often do not correspond to subsequent intraoperative findings. Therefore, some investigators have advocated using imaging procedures, such as ultrasonography, contrast radiography, and magnetic resonance imaging (MRI), to further describe the exact nature of the support defects before attempting surgical repairs. For example, some practitioners have used contrast ultrasonography to evaluate for paravaginal defects by placing a water-filled condom in the vaginal canal to better delineate the paravaginal spaces (Ostrzenski et al., 1997). Others have used MRI to better characterize the soft tissue and viscera of the pelvis. However, currently, a lack of standardized radiologic criteria exists for diagnosing pelvic organ prolapse. Therefore, the clinical use of imaging studies remains unknown; they are currently mostly used for research purposes. Patients with prolapse who are without symptoms of defecatory dysfunction generally do not warrant ancillary bowel testing. For example, although defecating proctography can provide additional information regarding rectal emptying, Siproudhis et al. (1993) demonstrated that it is no more sensitive at detecting rectoceles compared with physical examination alone. However, patients with concomitant defecatory dysfunction or motility disorders do merit further evaluation. In patients with defecatory dysfunction, differentiating is necessary between those with colonic motility disorders versus those with pelvic outlet symptoms. Useful ancillary
tests include anoscopy and proctosigmoidoscopy to evaluate for prolapsing hemorrhoids and intrarectal prolapse. Motility disorders can be assessed with colonic transit studies. In patients with apical and posterior vaginal prolapse who also complain of difficult or incomplete bowel emptying, evaluating for pelvic floor dyssynergia is important. During the physical examination, patients with pelvic floor dyssynergia often have hypercontracted and tender puborectalis muscles that may not relax on command. Tests for diagnosing pelvic floor dyssynergia include electromyogram and balloon expulsion test demonstrating a paradoxical contraction of the puborectalis muscle during defecation. Defecating proctography, which involves dynamic and still images of patients at rest, during defecation, and while contracting the anal sphincter, can also be used for diagnosis. Defecography has the added advantage of providing radiographic evidence of the specific organ that is herniating into the posterior vaginal wall and is the gold standard for measuring perineal descent. Dynamic MRI defecography can also be used to provide information regarding defecation and anatomic soft tissue defects. It has the advantages of being noninvasive, does not require ionizing radiation, and is unrivaled in its depictions of pelvic soft tissue. However, the clinical use of this costly imaging modality is debatable because it has not yet been shown to alter clinical decision-making.
Evaluation of Bladder Filling and Voiding The office evaluation of incontinence should involve some assessment of voiding, detrusor function during filling, and competency of the urethral sphincteric mechanism. During the assessment, one should try to determine the specific circumstances leading to the involuntary loss of urine. If possible, such circumstances should be reproduced and directly observed during clinical evaluation. The examination is most easily initiated with the patient’s bladder comfortably full. The patient is allowed to void as normally as possible in private. The time to void and the amount of urine voided are recorded. The patient then returns to the examination room, and the volume of residual urine is noted by transurethral catheterization. If a sterile urine sample has not yet been obtained for analysis, it can be obtained at this time. A 50-mL syringe without its piston or bulb is attached to the catheter and held above the bladder. The patient is then asked to sit or stand and the bladder is filled by gravity by pouring 50-mL aliquots of sterile water into the syringe (Fig. 6-3). The patient’s first bladder sensation and maximum bladder capacity are noted. The water level in the syringe should be closely observed during filling, because any rise in the column of water can be secondary to a detrusor contraction. Unintended increases in intra-abdominal pressure by the patient should be avoided. The catheter is then removed and the patient is asked to cough in a standing position. Loss of small amounts of urine in spurts, simultaneous with the coughs, strongly suggests a diagnosis of urodynamic stress incontinence. Prolonged loss of urine, leaking 5 to 10 seconds after coughing, or no urine loss with provocation indicates that other causes of incontinence, especially detrusor overactivity, may be present. Interpretation of these office tests can be difficult because of artifact intro-
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Figure 6-3 ■ Office evaluation of bladder filling function. In sitting or standing position with a catheter in the bladder, the bladder is filled by gravity by pouring sterile water into the syringe.
duced by rises in intra-abdominal pressure caused by straining or patient movement. Borderline or negative tests should be repeated to maximize their diagnostic accuracy.
MAKING THE INCONTINENCE DIAGNOSIS Based on the clinical evaluation, the physician can formulate a presumptive diagnosis and initiate treatment, using the algorithm in Figure 6-4 as a guide. Similar guidelines for evaluation of incontinence were proposed by Fantl et al. (1996) and have been used with success in elderly patients. The initial goal should be to diligently seek out and treat all reversible causes of urinary incontinence and voiding difficulty (Box 6-3). Complex causes of incontinence are triaged for urodynamic testing or for consultation (Box 6-4). After the evaluation, patients can be categorized as having probable urodynamic stress incontinence or probable detrusor overactivity (with or without coexistent stress incontinence). For either diagnosis, appropriate behavioral or medical therapy can be given and a substantial percentage of patients expected to respond. Even patients with mixed disorders (coexistent stress incontinence and detrusor overactivity) respond to various forms of conservative therapy in about 60% of cases.
DIAGNOSTIC ACCURACY OF OFFICE EVALUATIONS The findings of a careful history and physical examination predict the actual incontinence diagnosis with reasonable accuracy. Women who have the symptom of stress incontinence as their only complaint have a 64% to 90% chance of
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having urodynamic stress incontinence confirmed on diagnostic urodynamic testing. Of these patients, 10% to 30% are found to have detrusor overactivity (alone or coexistent with urodynamic stress incontinence). Other rare conditions that can cause the symptom of stress incontinence are urethral diverticulum, genitourinary fistula, ectopic ureter, and urethral instability. Physical findings associated with urodynamic stress incontinence are anterior vaginal relaxation, urethral hypermobility, and observed transurethral loss of urine with coughing. Sensory urgency, urge incontinence, diurnal and nocturnal frequency, and bed-wetting all have been associated with overactive bladder. The more of these abnormal urinary symptoms the patient has, the greater the chance that she has detrusor overactivity. Cantor and Bates (1980) observed that 81% of patients with three or more of these symptoms had detrusor overactivity on cystometry. The physical findings of abnormal neurologic examination and absent urethral hypermobility in a woman with incontinence have been associated with overactive detrusor function. Is the determination of urethral mobility useful in diagnosing the cause of urinary incontinence? The angle of urethral inclination does not differ between continent and incontinent women with pelvic relaxation. Numerous authors have shown that, although the Q-tip test accurately reflects the amount of urethral mobility with stress, it is of little value in differentiating urodynamic stress incontinence from detrusor overactivity. Furthermore, serial addition of the measurement of urethral inclination with a Q-tip to the history and pelvic examination does not appreciably change the sensitivity or specificity for diagnosing urodynamic stress incontinence. However, because most women with primary urodynamic stress incontinence have urethral hypermobility, a negative test should cause one to question that diagnosis, perhaps indicating the need to perform urodynamic testing. Clearly, the measurement of urethral mobility should not be used to differentiate urethral sphincter incompetence from abnormalities of voiding or detrusor function because these diagnoses require the measurement of detrusor pressure during filling and emptying. Although the determination of urethral mobility is not useful in the diagnosis of urinary incontinence, it may provide some information about which surgical therapy is most appropriate. In patients with urodynamic stress incontinence, mid-urethral sling or a retropubic suspension procedure is used when urethral hypermobility is found to coexist with relatively normal intrinsic urethral sphincteric function. When urethral hypermobility is found in a patient with findings of intrinsic sphincter deficiency, a pubovaginal sling (or perhaps TVT) procedure is usually recommended. When the urethra is nonmobile or intrinsically functionless, periurethral injection of bulking agents or artificial urinary sphincter is likely to provide better results. Thus, measurement of urethral mobility can aid the surgeon in choosing one group of surgical procedures over another, but it cannot determine which procedures yield the best results in each clinical situation. Retrograde bladder filling provides an assessment of bladder sensation and an estimate of bladder capacity. Patients without urgency and frequency who note a sensation of bladder fullness and have an estimated bladder
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Urinary incontinence in women History, physical examination, and urinary diary Urinalysis Post-void catheterization for residual urine Reversible condition? (see Box 6-3)
Yes
Treat
No Patient cured or satisfied?
Yes
Follow-up
No
Complex condition? (see Box 6-4)
Yes
Consult with urogynecologist or urologist
No Symptom of stress incontinence?
Yes
No Urgency, frequency, enuresis?
Stress test? (sign of stress incontinence)
Urgency, frequency, enuresis?
Positive
Yes
Negative Yes
Presume DO
Presume mixed DO and USUI
No
Presume USUI
Prominent USUI symptom Pelvic exercising Bladder retraining Medical therapy Mechanical devices
Prominent DO symptoms Bladder retraining Medical therapy Continue treatment Patient cured or satisfied?
Yes
Continue treatment
No
Yes
Patient cured or satisfied? No
Consultation for urodynamic tests and consideration of surgery
Consultation for urodynamic tests Figure 6-4
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Algorithm for clinical assessment of urinary incontinence in women. USUI, Urodynamic stress urinary incontinence; DO, detrusor overactivity.
capacity that is within normal range probably have normal bladder filling function. There seems to be no clear consensus about the definition of normal bladder capacity. Values range from 300 to 750 mL. However, large bladder capacities are not always pathologic. Weir and Jaques (1974) showed that 33% of women with bladder capacities greater than 800 mL were urodynamically normal and only 13% had true bladder atony. In the absence of symptoms of voiding difficulty, patients usually have normal voiding function. The inci-
dence of asymptomatic voiding dysfunction among women with other urologic complaints is only about 3%. Normal values for postvoid residual urine measurements have not been established. Volumes less than 50 mL indicate adequate bladder emptying, and volumes greater than 200 mL can be considered inadequate emptying. Clinical judgment must be exercised in interpreting the significance of postvoid residual urine volumes, especially in the intermediate range of 50 to 200 mL. Because isolated instances of elevated residual urine volume may not be significant, the test should be repeated
Chapter 6
BOX 6-3
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Evaluation of Urinary Incontinence and Pelvic Organ Prolapse
REVERSIBLE CONDITIONS THAT CAUSE OR CONTRIBUTE TO URINARY INCONTINENCE
Conditions affecting the lower urinary tract Urinary tract infection Urethritis Atrophic vaginitis/urethritis Pregnancy Drug side effects (see Table 6-1) Increased urine production Metabolic (hyperglycemia, hypercalcemia) Excess fluid intake Volume overload Stool impaction Impaired ability or willingness to reach toilet Restricted mobility Delirium Chronic illness, injury, or restraint that interferes with mobility Psychological
BOX 6-4
SITUATIONS THAT WARRANT CONSULTATION FOR THE EVALUATION AND TREATMENT OF LOWER URINARY TRACT DYSFUNCTION
Uncertain diagnosis and inability to develop a reasonable treatment plan based on the basic diagnostic evaluation. Uncertainty in diagnosis may occur when there is lack of correlation between symptoms and clinical findings. Failure to respond to the patient’s satisfaction to an adequate therapeutic trial, and the patient is interested in pursuing further therapy. Consideration of surgical intervention, particularly if previous surgery failed or the patient has a high surgical risk. The presence of other comorbid conditions: Incontinence associated with recurrent symptomatic urinary tract infection Persistent symptoms of difficult bladder emptying History of previous anti-incontinence surgery, radical pelvic surgery, or pelvic radiation therapy Symptomatic pelvic prolapse, especially if beyond hymen Abnormal postvoid residual urine Neurologic condition, such as multiple sclerosis or spinal cord lesions or injury Fistula or suburethral diverticulum Hematuria without infection ●
● ●
● ● ●
when abnormally high values are obtained. Among women with symptoms of voiding difficulty and those who appear to void abnormally or have retention, more sophisticated testing is required to determine the causes and the mechanism of the voiding dysfunction. As patients with anterior, apical, or posterior prolapse may have voiding dysfunction due to obstruction of the urethra, the completeness of bladder emptying should be assessed with the prolapse reduced. Kinking of the urethra may obscure any indication that urinary incontinence may be present. Therefore, assessing for evidence of incontinence
75
after reduction of the prolapse is important. This can be done with a pessary, vaginal packing, or ring forceps at the time of the office bladder filling or urodynamic testing. If urinary leakage 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 can occur in up to half of women with stage III or IV prolapse. In this situation, the surgeon should choose a mid-urethral sling or Burch procedure in conjunction with the prolapse repair (Meschia et al., 2004; Brubaker et al., 2006). If sphincteric incompetence is not present even after reduction of the prolapse, an anti-incontinence procedure may not be indicated, although a recent study by Brubaker et al. (2006) showed that prophylactic Burch procedure at the time of abdominal sacrocolpopexy resulted in lower rates of postoperative urinary incontinence than when no Burch procedure was done.
INDICATIONS FOR URODYNAMIC TESTS AND CYSTOSCOPY The physician must recognize that even under the most typical clinical situations, the diagnosis of incontinence based only on clinical evaluation may be uncertain. This diagnostic uncertainty may be acceptable if medical or behavioral treatment (as opposed to surgery) is planned because of the low morbidity and cost of these treatments and because the ramifications of noncure (continued incontinence) are not severe. Limited data support the need for cystometric testing in the routine or basic evaluation of urinary incontinence; it is indicated as part of the evaluation of more complex disorders of bladder filling and voiding, such as the presence of neurologic disease and other comorbid conditions. When surgical treatment of stress incontinence is planned, urodynamic testing is recommended to confirm the diagnosis, unless the patient has an uncomplicated history and compatible physical findings of stress incontinence and has not had previous surgery for incontinence. Consultation should be considered for complex cases that may require urodynamic testing or surgical treatment. Whenever objective clinical findings do not correlate with or reproduce the patient’s symptoms, urodynamic testing is indicated for diagnosis. Finally, when trials of therapy are used, patients must be followed up periodically to evaluate response. If the patient fails to improve to her satisfaction, appropriate further testing is indicated. Cystoscopy is indicated for the evaluation of patients with incontinence who have (1) sterile hematuria or pyuria; (2) irritative voiding symptoms, such as frequency, urgency, and urge incontinence, in the absence of any reversible causes; (3) bladder pain; (4) recurrent cystitis; (5) suburethral mass; (6) suspected foreign body; and (7) when urodynamic testing fails to duplicate symptoms of urinary incontinence. Bladder lesions are found in less than 2% of patients with incontinence (Fantl et al., 1996); therefore, cystoscopy should not be performed routinely in patients with incontinence to exclude neoplasm.
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Part 3
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Evaluation
Bibliography HISTORY AND PHYSICAL EXAMINATION Abrams P, Klevmark B. Frequency-volume charts: an indispensable part of lower urinary tract assessment. Scand J Urol Nephrol 1996;179(Suppl):47. American College of Obstetricians and Gynecologists. Pelvic organ prolapse. Technical bulletin no. 214. The College, Washington, DC, 1995. American College of Obstetricians and Gynecologists. Urinary incontinence in women. ACOG Practice Bulletin No. 63. Obstet Gynecol 2005;105:1533. Assessment and treatment of urinary incontinence. Scientific Committee of the First International Consultation on Incontinence. Lancet 2000;355:2153. Bannister JJ, Laurence WT, Smith A, et al. Urological abnormalities in young women with severe constipation. Gut 1988;29:17. 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. Barber MD, Visco AG, Wyman JF, et al. Sexual function in women with urinary incontinence and pelvic organ prolapse. Continence Program for Women Research Group. Obstet Gynecol 2002;99:281. Barber MD. Symptoms and outcome measures of pelvic organ prolapse. Clin Obstet Gynecol 2005;48:724. Blaivas JG, Zayed AA, Kamal BL. The bulbocavernosus reflex in urology: a prospective study of 299 patients. J Urol 1981;126:197. Bradley CS, Nygaard IE. Vaginal wall descensus and pelvic floor symptoms in older women. Obstet Gynecol 2005;106:759. Brink CA, Wells TJ, Sampsell CM, et al. A digital test for pelvic muscle strength in women with urinary incontinence. Nurs Res 1994;43:352. 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. Burrows LJ, Meyn LA, Walters MD, Weber AM. Pelvic symptoms in women with pelvic organ prolapse. Am J Obstet Gynecol 2004;104:982. Burrows LJ, Sewell C, Leffler KS, Cundiff GW. The accuracy of clinical evaluation of posterior vaginal wall defects. Int Urogynecol J 2003;14:160. Diokno AC, Wells TJ, Brink CA. Comparison of self-reported voided volume with cystometric bladder capacity. J Urol 1987;137:698. Ellerkmann 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. Fantl JA, Wyman JF, Wilson MS, et al. Diuretics and urinary incontinence in community-dwelling women. Neurourol Urodyn 1990;9:25. Frenckner B, Ihre T. Influence of autonomic nerves on the internal anal sphincter in man. Gut 1976;17:306. Ghetti C, Gregory WT, Edwards SR, et al. Pelvic organ descent and symptoms of pelvic floor disorders. Am J Obstet Gynecol 2005;193:53. Gormley EA, Griffiths DJ, McCracken PN, et al. Polypharmacy and its effect on urinary incontinence in a geriatric population. Br J Urol 1993;71:265. Groutz A, Blaivas J, Chaikin D, et al. Noninvasive outcome measures of urinary incontinence and lower urinary tract symptoms: a multicenter study of micturition diary and pad test. J Urol 2000;164:698. Hilton P, Stanton SL. Algorithmic method for assessing urinary incontinence in elderly women. Br Med J 1981;282:940. Julian TM. Pseudoincontinence secondary to unopposed estrogen replacement in the surgically castrate premenopausal female. Obstet Gynecol 1987;70:382. Kaushal JN, Goldner F. Validation of the digital rectal examination as an estimate of anal sphincter squeeze pressure. Am J Gastroenterol 1991;86:886. Kelvin FM, Hale DS, Maglinte DD, et al. Female pelvic organ prolapse: diagnostic contribution of dynamic cystoproctography and comparison with physical examination. Am J Roentgenol 1999;173:31. Kelvin FM, Maglinte DD, Hornback JA. Dynamic cystoproctography of female pelvic floor defects and their interrelationships. Am J Radiol 1997;169:769. Kenton K, Shott S, Brubaker L. Vaginal topography does not correlate well with visceral position in women with pelvic organ prolapse. Int Urogynecol J 1997;8:336. Larson G, Victor A. The frequency-volume chart in genuine stress incontinent women. Neurourol Urodyn 1992;1:23.
Lestar B, Penninckx F, Kerremans R. The composition of anal basal pressure. An in vivo and in vitro study in man. Int J Colorectal Dis 1989;4:118. Melville JL, Miller EA, Fialkow MF, et al. Relationship between patient report and physician assessment of urinary incontinence severity. Am J Obstet Gynecol 2003;189:76. Nygaard I, Holcomb R. Reproducibility of the seven-day voiding diary in women with stress urinary incontinence. Int Urogynecol J 2000;11:15. Rogers RG, Villarreal A, Kammerer-Doak D, et al. Sexual function in women with and without urinary incontinence and/or pelvic organ prolapse. Int Urogynecol J 2001;12:361. Romanzi LJ, Chaiken DC, Blaivas JG. The effect of genital prolapse on voiding. J Urol 1999;161:581. Romanzi LJ, Polaneczky M, Glazer HI. Simple test of pelvic muscle contraction during pelvic examination: correlation to surface electromyography. Neurourol Urodyn 1999;18:603. Sampselle CM, Brink CA, Wells TJ. Digital measurement of pelvic muscle strength in childbearing women. Nurs Res 1989;38:134. Steele A, Mallipeddi P, Welgoss J, et al. Teaching the pelvic organ prolapse quantification system. Am J Obstet Gynecol 1998;179:1458. Swift SE. The distribution of pelvic organ support in a population of women presenting for routine gynecologic healthcare. Am J Obstet Gynecol 2000;183:277. 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;192:795. Tan JS, Lukacz ES, Menefee SA, et al. Predictive value of prolapse symptoms: a large database study. Int Urogynecol J 2005;16:203. Tulikangas PK, Lukban JC, Walters MD. Anterior enterocele: a report of three cases. Int Urogynecol J 2004;15:350. Walters MD, Realini JP. The evaluation and treatment of urinary incontinence in women: a primary care approach. J Am Board Fam Pract 1992;5:289. 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. 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;182:1610. Weidner AC, Barber MD, Visco AC, 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;183:1390. Whiteside JL, Barber MD, Paraiso MF, et al. Clinical evaluation of anterior vaginal wall support defects: interexaminer and intraexaminer reliability. Am J Obstet Gynecol 2004;191:100. Williams ME, Gaylord SA. Role of functional assessment in the evaluation of urinary incontinence, National Institutes of Health Consensus Development Conference on Urinary Incontinence in Adults, Bethesda, MD, October 3–5, 1988. J Am Geriatr Soc 1990;38:296. Wyman JF, Choi SC, Harkins SW, et al. The urinary diary in evaluation of incontinent women: a test-retest analysis. Obstet Gynecol 1988;71:812.
TECHNIQUES FOR MEASURING URETHRAL MOBILITY Crystle CD, Charme LS, Copeland WE. Q-tip test in stress urinary incontinence. Obstet Gynecol 1971;38:313. Fantl JA, Hurt WG, Bump RC, et al. Urethral axis and sphincteric function. Am J Obstet Gynecol 1986;155:554. Gordon D, Pearce M, Norton P. Comparison of ultrasound and lateral chain urethrocystography in the determination of bladder neck position and descent. Neurourol Urodyn 1987;5:181. Karram MM, Narender N, Bhatia MD. The Q-tip test: standardization of the technique and its interpretation in women with urinary incontinence. Obstet Gynecol 1988;71:807. Koelbl H, Hanzal E, Bernaschek G. Sonographic urethrocystography: methods and applications in patients with genuine stress incontinence. Int Urogynecol J 1991;2:25. Montella JM, Ewing S, Cater J. Visual assessment of urethrovesical junction mobility. Int Urogynecol J 1997;8:13. Mouritsen L, Strandberg C, Jensen AR, et al. Inter- and intra-observer variation of colpo-cysto-urethrography diagnoses. Acta Obstet Gynecol Scand 1993;72:2000.
Chapter 6
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Evaluation of Urinary Incontinence and Pelvic Organ Prolapse
Noblett K, Lane FL, Driskill CS. Does pelvic organ prolapse quantification exam predict urethral mobility in stages 0 and I prolapse? Int Urogynecol J 2005;16:268. Schaer GN, Koechli OR, Schuessler B, et al. Perineal ultrasound for evaluating the bladder neck in urinary stress incontinence. Obstet Gynecol 1995;85:220. Walters MD, Diaz K. Q-tip test: a study of continent and incontinent women. Obstet Gynecol 1987;70:208.
PERINEAL PAD TESTS Abrams P, Blaivas JG, Stanton SL, et al. The standardization of terminology of lower urinary tract function recommended by the International Continence Society. Int Urogynecol J 1990;1:45. Fantl JA, Harkins SW, Wyman JF, et al. Fluid loss quantitation test in women with urinary incontinence: a test-retest analysis. Obstet Gynecol 1987;70:739. Haylen BT, Frazer MI, Sutherst JR. Diuretic response to fluid load in women with urinary incontinence: optimum duration of pad test. Br J Urol 1988;62:331. Jakobsen H, Vedel P, Andersen JT. Which pad-weighing test to choose: ICS one hour test, the 48 hour home test or a 40 min test with known bladder volume? Neurourol Urodyn 1987;4:23. Jorgensen L, Lose G, Anderson JT. One hour pad-weighing test for objective assessment of female urinary incontinence. Obstet Gynecol 1987;69:39. Kinn A-C, Larsson B. Pad test with fixed bladder volume in urinary stress incontinence. Acta Obstet Gynecol Scand 1987;55:369. Lose G, Gammelgaard J, Jorgenson TJ. The one-hour pad-weighing test: reproducibility and the correlation between the test result, the start volume in the bladder, and the diuresis. Neurourol Urodyn 1986;5:17. Richmond DH, Sutherst JR, Brown MC. Quantification of urine loss by weighing perineal pads. Observation on the exercise regimen. Br J Urol 1987;59:224. Ryhammer AM, Djurhuus JC, Laurberg S. Pad testing in incontinent women: a review. Int Urogynecol J 1999;10:111. 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;58:273. Versi E, Orrego G, Hardy E, et al. Evaluation of the home pad test in the investigation of female urinary incontinence. Br J Obstet Gynaecol 1996;103:162. Wall LL, Wang K, Robson I, et al. The Pyridium pad test for diagnosing urinary incontinence. J Reprod Med 1990;35:682. Walters MD, Dombroski RA, Prihoda TJ. Perineal pad testing in the quantitation of urinary incontinence. Int Urogynecol J 1990;1:3.
DIAGNOSTIC TESTS Boscia JA, Kobasa WD, Abrutyn E, et al. Lack of association between bacteriuria and symptoms in the elderly. Am J Med 1986;81:979. Brocklehurst JC, Dillane JB, Griffiths L, et al. The prevalence and symptomatology of urinary infection in an aged population. Gerontol Clin 1968;10:242. Chahal R, Gogi NK, Sundaram SK. Is it necessary to perform urine cytology in screening patients with haematuria? Eur Urol 2001;39:283. Cohen RA, Brown RS. Clinical practice. Microscopic hematuria. N Engl J Med 2003;348:2330. Eastwood HD, Warrell R. Urinary incontinence in the elderly female: prediction in diagnosis and outcome of management. Age Ageing 1984;13:230. Fantl JA, Newman DK, Colling J, et al. Urinary Incontinence in Adults: Acute and Chronic Management. Clinical Practice Guideline No 2, 1996 Update, U.S. Department of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research, AHCPR Pub No 96–0682. Rockville, MD, March 1996. Kelvin FM, Maglinte DD. Dynamic evaluation of female pelvic organ prolapse by extended proctography. Radiol Clin North Am 2003;41:395. Matsuoka H, Wexner SD, Desai MB. A comparison between dynamic pelvic magnetic resonance imaging and videoproctography in patients with constipation. Dis Colon Rectum 2001;30:199. Mohr DN, Offord KP, Owen RA, Melton LJ III. Asymptomatic microhematuria and urologic disease. A population-based study. JAMA 1986;256:224. Ostrzenski A, Osborne NG, Ostrzenska K. Method for diagnosing paravaginal defects using contrast ultrasonographic technique. J Ultrasound Med 1997;16:673.
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Poston G, Joseph A, Riddle P. The accuracy of ultrasound and the measurement of changes in bladder volume. Br J Urol 1983;55:361. Siproudhis L, Robert A, Vilotte J, et al. How accurate is clinical examination in diagnosing and quantifying pelvirectal disorders? A prospective study in a group of 50 patients complaining of defecatory difficulties. Dis Colon Rectum 1993;36:430. Sourander LB. Urinary tract infection in the aged. An epidemiological study. Ann Med Intern Fenn 1966;55(Suppl 45):1. Stanton SL, Ozsoy C, Hilton P. Voiding difficulties in the female: prevalence, clinical and urodynamic review. Obstet Gynecol 1983;61:144. Utz DC, Zincke H. The masquerade of bladder cancer in situ as interstitial cystitis. J Urol 1974;111:160. Wein AJ, Barrett DM. Voiding Function and Dysfunction. Mosby, Chicago, 1988.
DIAGNOSTIC ACCURACY OF OFFICE EVALUATION AND INDICATIONS FOR URODYNAMIC TESTING Arnold EP, Webster JR, Loose H, et al. Urodynamics of female incontinence: factors influencing the results of surgery. Am J Obstet Gynecol 1973;117:805. Brubaker L, Cundiff GW, Fine P, et al. Abdominal sacrocolpopexy with Burch colposuspension to reduce urinary stress incontinence. N Engl J Med 2006;345:1557. Byrne DJ, Hamilton Stewart PA, Gray BK. The role of urodynamics in female urinary stress incontinence. Br J Urol 1987;59:228. Cantor TJ, Bates CP. Comparative study of symptoms and objective urodynamic findings in 214 incontinent women. Br J Obstet Gynaecol 1980;87:889. Cundiff GW, Fenner D. Evaluation and treatment of women with rectocele: focus on associated defecatory and sexual dysfunction. Obstet Gynecol 2004;104:1403. Drutz HP, Mandel F. Urodynamic analysis of urinary incontinence symptoms in women. Am J Obstet Gynecol 1979;134:789. Farrar DJ, Whiteside CG, Osborne JL, et al. A urodynamic analysis of micturition symptoms in the female. Surg Gynecol Obstet 1975;144:875. Fischer-Rasmussen W, Hansen RI, Stage P. Predictive values of diagnostic tests in the evaluation of female urinary stress incontinence. Acta Obstet Gynecol Scand 1986;65:291. Jensen JK, Nielsen FR, Ostergard DR. The role of patient history in the diagnosis of urinary incontinence. Obstet Gynecol 1994;83:904. Kadar N. The value of bladder filling in the clinical detection of urine loss and selection of patients for urodynamic testing. Br J Obstet Gynaecol 1988;95:698. Karram MM, Bhatia NN. Management of coexistent stress and urge urinary incontinence. Obstet Gynecol 1989;73:4. Korda A, Krieger M, Hunter P, et al. The value of clinical symptoms in the diagnosis of urinary incontinence in the female. Aust N Z J Obstet Gynecol 1987;27:149. 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. Moolgaoker AS, Ardran GM, Smith JC, et al. The diagnosis and management of urinary incontinence in the female. J Obstet Gynaecol Br Commonw 1972;79:481. Ouslander JG. Diagnostic evaluation of geriatric urinary incontinence. Clin Geriatr Med 1986;2:715. Ouslander J, Staskin D, Raz S, et al. Clinical versus urodynamic diagnosis in an incontinent female geriatric population. J Urol 1987;37:68. Quigley GJ, Harper AC. The epidemiology of urethral-vesical dysfunction in the female patient. Am J Obstet Gynecol 1985;151:220. Sand PK, Hill RC, Ostergard DR. Incontinence history as a predictor of detrusor stability. Obstet Gynecol 1988;71:257. Swift SE, Ostergard DR. Evaluation of current urodynamic testing methods in the diagnosis of genuine stress incontinence. Obstet Gynecol 1995;86:85. 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. Webster GD, Sihelnik SA, Stone AR. Female urinary incontinence: the incidence, identification, and characteristics of detrusor instability. Neurourol Urodyn 1984;3:235. Weir J, Jaques PF. Large capacity bladder. Urology 1974;4:544.
Urodynamics: Cystometry and Urethral Function Tests
7
Mickey M. Karram and Jerry Blaivas
PRINCIPLES OF CYSTOMETRY 78 STANDARDIZED TERMINOLOGY NORMAL CYSTOMETRIC PARAMETERS 79 EQUIPMENT 80 METHODOLOGY 80 Filling Media 80 Position of Patient and Provoking Maneuvers 82 Temperature of Fluid 82 Technique of Bladder Filling 82 Rate of Bladder Filling 82 Types of Catheters 82 Technique of Cystometry 82 INDICATIONS FOR CYSTOMETRY 84 VIDEO-URODYNAMIC TESTING 84 AMBULATORY URODYNAMICS (AUD) 85 CYSTOMETRY: ABNORMAL STUDIES 85 URETHRAL FUNCTION TESTS 88 URETHRAL PRESSURE PROFILOMETRY 88 Definitions 88 Methodology 89 Interpretations Variables 93 Clinical Applications 94 Urethral Function During Filling Cystometry 95 LEAK POINT PRESSURES 95 Definitions 95 Methodology 95 Interpretation Variables 97 Clinical Applications 97 CONTROVERSIES AND CORRELATIONS 98
The term urodynamics means observation of the changing function of the lower urinary tract over time. Two principal methods of urodynamic investigation are known. Conventional urodynamic studies take place in the urodynamic laboratory and involve filling the bladder via a catheter, usually at a specified rate. Ambulatory urodynamic (AUD) studies are defined as a functional test of the lower urinary tract, using natural filling and thus reproducing the subject’s everyday activities. Urodynamic tests have been
slow to achieve acceptance and are by no means universally used; however, in recent years there has been a resurgence of interest in the hydrodynamic and neurophysiologic aspects of the storage and evacuation of urine. An abundance of new diagnostic procedures, methodologies, and testing equipment has made it exceedingly difficult for the clinician to decide what tests are necessary to adequately evaluate lower urinary tract dysfunction in women. To understand the fundamental value of urodynamics, one should realize that the female bladder responds similarly to various pathologies. Symptoms do not always reflect accurately the physiologic state of the bladder. For example, a patient may feel that her bladder is full when it is nearly empty, or that her bladder is contracting when it is not. Nevertheless, the evaluation of a woman with lower urinary tract complaints should not exclude the basic history and physical examination. The validity of any urodynamic diagnosis is linked to the patient’s symptoms and the reproduction of these symptoms during the testing session. To obtain the most accurate, clinically relevant interpretation of urodynamic studies, the urodynamicist should clearly understand lower urinary tract function and correlate urodynamic data with other clinical information. Ideally, the urodynamicist should be the physician who takes the history, performs the physical examination, interprets other tests, explains the diagnosis, and develops a reasonable management plan. Results of urodynamic investigations should be recorded in a way that can be communicated among physicians and other health care personnel. For this reason, the recommendations detailed in the standardization reports of the International Continence Society (ICS) should be followed (see Appendices A and B). Chapters 7 and 8 discuss urodynamic modalities used in the evaluation of filling, storage, and evacuation of urine. The intent is to give the reader a clear understanding of the rationale, technique, use, and limitations of each test.
PRINCIPLES OF CYSTOMETRY The first cystometer dates back to 1872 when Schatz accidentally discovered a crude technique for measuring bladder pressure while trying to record intra-abdominal pressure.
Chapter 7
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Urodynamics: Cystometry and Urethral Function Tests
Shortly thereafter, in 1876, DuBois studied the effects of changes in body position on intravesical and intrarectal pressures and observed that the desire to void was associated with contraction of the detrusor muscle. The currently popular water cystometer was designed by Lewis in 1939. The later use of air and carbon dioxide as filling media further simplified the procedure. Cystometry is a urodynamic test that measures the pressure and volume relationship of the bladder and is used to assess detrusor activity, sensation, capacity, and compliance. Every factor has unique implications, and before any definitive conclusions can be reached, each parameter must be examined in association with symptoms and clinical findings. A normal bladder has the power of accommodation; it can maintain an almost constant low intravesical pressure throughout filling, regardless of volume. A normal woman should be able to suppress voiding even at maximum capacity. Then, in an acceptable environment, she should be able to initiate a voiding reflex that involves a detrusor contraction and a complete relaxation of the urethra and pelvic floor musculature. The basic principle of cystometry is the coupling of a manometer to the bladder lumen. A filling medium is instilled into the bladder and, as it fills, intravesical pressure is measured against volume. Testing apparatuses range from simple single-channel methods, which are performed manually or electronically, to complex methods combining electronic measurements of bladder, abdominal, and urethral pressure, together with electromyography (EMG) and fluoroscopy. A cystometrogram has two phases: a filling/storage phase and an emptying (voiding) phase (Fig. 7-1). The filling phase is subdivided into a brief initial rise in pressure to achieve resting bladder pressure, followed by a tonus limb that reflects viscoelastic properties of accommodation of the smooth muscle and collagen of the bladder wall. There may be a third increase in the pressure, which is attributed to the stretching of detrusor muscle and collagenous elements of the bladder wall beyond their limits at bladder capacity. During this third stage, the patient is still able to suppress
Figure 7-1 ■ Normal cystometrogram. Note filling phase is divided into an initial slight rise in bladder pressure (phase I), followed by a tonus limb reflecting bladder accommodation (phase II). At maximum capacity, the detrusor muscle and elastic bladder wall tissue are stretched to their limits, causing a rise in bladder pressure (phase III). A detrusor contraction is then initiated voluntarily and the patient voids (phase IV). (Modified with permission from Wein AJ, Barrett DM. Voiding Function and Dysfunction. Mosby, Chicago, 1988.)
79
voiding. A detrusor contraction is then initiated voluntarily in conjunction with a relaxation of the outlet, and the patient voids.
STANDARDIZED TERMINOLOGY AND NORMAL CYSTOMETRIC PARAMETERS The ICS has recently redefined certain terms that are used in the reporting of cystometric results. Intravesical pressure is the pressure within the bladder. Abdominal pressure is taken to be the pressure surrounding the bladder; it is generally estimated from rectal, vaginal, or, less commonly, extraperitoneal pressure or a bowel stoma. Detrusor pressure is the component of intravesical pressure that is created by both active and passive forces in the bladder wall; it is estimated by subtracting abdominal pressure from intravesical pressure. The filling phase starts when filling commences and ends when the patient and the urodynamicist decide that “permission to void” has been given. The rate at which the bladder is filled is divided into either a physiologic filling rate or a nonphysiologic filling rate. A physiologic filling rate is defined as a filling rate less than the predicted maximum filling rate—that is, the body weight in kilograms divided by 4 and expressed in milliliters per millimeter. Bladder storage function should be described according to bladder sensation, detrusor activity, bladder compliance, and bladder capacity. First sensation of bladder filling is when a patient becomes aware of the bladder filling. First desire to void is when a patient would pass urine at the next convenient moment. Strong desire to void is a persistent desire to void without the fear of leakage. Increased bladder sensation is defined as an early, first sensation or an early, strong desire to void, which occurs at low bladder volumes and which persists. Reduced bladder sensation is diminished sensation throughout bladder filling. Absent bladder sensation means that during filling cystometry, the individual has no bladder sensation. Nonspecific bladder sensations may make the individual aware of bladder filling, for example, abdominal fullness or vegetative symptoms. Bladder pain is a self-explanatory term and is an abnormal finding. Urgency 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. Compliance (C) is the change in volume for a change in pressure; it is calculated by dividing the volume change (ΔV) by the change in detrusor pressure (ΔPdet) during that change in bladder volume (C = ΔV/ΔPdet). Compliance is expressed in milliliters per centimeter. Cystometric capacity is the bladder volume at the end of the filling cystometrogram when permission to void is usually given. The cystometric capacity is the volume voided together with any residual urine. Maximum cystometric capacity is the volume at which the patient feels she can no longer delay micturition. Maximum anesthetic bladder capacity is the volume to which the bladder can be filled under deep general or spinal anesthesia. The speed of filling, filling time, filling pressure, and type of anesthesia should be specified.
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Part 3
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A female bladder normally experiences a first desire to void at a volume of approximately 150 to 250 mL, a normal desire to void at 300 to 400 mL, and a strong desire to void at 400 to 600 mL. During filling, an initial rise in true detrusor pressure between 2 and 8 cm H2O usually occurs. The average pressure rise is approximately 6 cm H2O and normally never exceeds 15 cm H2O. Provocation of a normal bladder by rapid filling, change of posture, coughing, or catheter movement should not incite any abnormal rises in detrusor pressure. 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 become overcome by detrusor overactivity. Incompetent urethral closure mechanism allows leakage of urine in the absence of a detrusor contraction. Urethral relaxation incontinence is leakage caused by urethral relaxation in the presence of raised abdominal pressure or detrusor overactivity. 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.
eter that produces an electronic signal, creating a graph on a recording device (Fig. 7-2). Multichannel cystometry relies on the measurement of both abdominal (Pabd) and intravesical pressures (Pves), thereby enabling one to distinguish changes in intra-abdominal pressure from changes in intravesical pressure (Fig. 7-3). Abdominal pressure can be measured via either transrectal or transvaginal catheters or less commonly from extraperitoneal pressure or a bowel stoma. We prefer vaginally placed catheters because they are more comfortable and easier to clean and maintain, and measurements are not cluttered by rectal peristalsis. Electronic subtraction of intra-abdominal from intravesical pressure allows for the calculation of true detrusor pressure (Pdet). Subtracted cystometry may be enhanced further by additional measurement of urethral pressure (Pure). This measurement allows for the calculation of urethral closure pressure (Pucp), which is the difference between urethral and bladder pressures. Certain machines also allow for the simultaneous measurement of EMG activity and the performance of flow studies (Fig. 7-4). These standard urodynamic techniques may be combined with videocystourethrography, which is termed video urodynamics.
METHODOLOGY EQUIPMENT A discussion of all commercially available cystometers is beyond the scope of this chapter, but reviews by Blaivas (1990) and Rowan et al. (1987) provide an overview of available urodynamic machines. The simplest cystometer is a water manometer connected by a Y tube to both a reservoir and a catheter. A variation of this technique is discussed in Chapter 5. Commercially available cystometers can be broadly classified into single-channel and multi-channel machines (subtracted cystometry). Single-channel cystometry involves the placement into the bladder of a pressure-measuring cath-
Figure 7-2
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Despite the widespread use of filling cystometry, the optimal technique for performing the test is unknown. The following section addresses the various technical aspects, controversies, and techniques for performing filling cystometry.
Filling Media The commonly used infusants for cystometry include water, carbon dioxide, and radiographic contrast material. In 1971, Merrill et al. introduced the use of carbon dioxide (CO2). Although once popular in North America, it is rarely, if ever, used for the following reasons: (1) It further decreases the
Single-channel cystometry. Pves, Bladder pressure.
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Figure 7-3 ■ Subtracted cystometry. Intravesical and intra-abdominal pressures are measured, and true detrusor pressure is electronically derived (Pves – Pabd). Pves, Bladder pressure; Pabd, abdominal pressure; Pdet, detrusor pressure.
Figure 7-4 ■ Multichannel urodynamics. Intravesical, intra-abdominal, and intraurethral pressures are measured. True detrusor pressure (Pdet) and urethral closure pressure (Pucp) are electronically derived. EMG and flow studies are also performed. Pves, Bladder pressure; Pabd, abdominal pressure; Pdet, detrusor pressure; Pure, urethral pressure; Pucp, urethral closure pressure; EMG, electromyography.
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physiologic nature of the test; (2) if gas is used, the bladder volume cannot be assessed because CO2 is compressible; (3) CO2 dissolves in urine to form carbonic acid, which irritates and reduces cystometric bladder capacity; (4) abdominal pressure is not usually measured during CO2 cystometry, making interpretation more difficult; and (5) when CO2 is used for filling cystometry, it is impossible to perform a stress test or voiding studies. Water or physiologic saline is the most commonly used filling medium unless radiologic screening is also being performed, in which case contrast medium is used. The cystometric findings are not affected by the choice of liquid medium.
Position of Patient and Provoking Maneuvers Cystometry should mimic everyday stresses on the bladder as much as possible. Thus, performing the test with the patient in the sitting or standing position is preferable. During cystometry, the bladder should be provoked by a series of tests that usually include coughing, heel bouncing, walking in place, and listening to running water. These maneuvers may provoke uninhibited detrusor contractions or induce stress incontinence. Physical factors may influence the positioning of patients during urodynamic tests; for example, in elderly patients or those with neurologic disease, it may be difficult to undertake cystometry in any position other than supine.
Temperature of Fluid Most laboratories use fluid at room temperature, although some investigators believe that the installation of warm or cold fluid may provoke abnormal bladder activity. The installation of ice water (Bor’s test) is occasionally used as a test for neurologic disorders.
Technique of Bladder Filling Theoretically, the most physiologic method of filling is by diuresis, combined with a suprapubically placed pressure line. The long time needed to investigate the patient prohibits natural filling as a practical method of performing cystometry in most centers. Therefore, cystometry is usually performed through a transurethrally placed catheter. Filling is accomplished using either simple gravity or a water pump. The bladder is filled through either a small catheter or, preferably, a separate channel on the pressure-measuring catheter.
Rate of Bladder Filling The ICS no longer divides filling rates into slow, medium, and fast. In practice almost all investigations are performed using medium filling rates that 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.
Types of Catheters Various catheters have been used for cystometry. Simple or manual cystometry can be performed with a transurethral Foley catheter. Electronically monitored studies require more
Figure 7-5 ■ Two microtransducer catheters. One catheter has a single microtransducer and is used for estimating abdominal pressure. The other catheter has two microtransducers approximately 6 cm apart used to measure intravesical and intraurethral pressure. This catheter also contains a fluid-filling port.
sophisticated balloon or microtransducer catheters. Water-filled balloon catheters or water perfusion catheters have been used with moderate success. These catheters are inexpensive, disposable, and easy to use. However, more sophisticated laboratories usually use sensitive microtransducer catheters (Fig. 7-5). These catheters are available with one to six microtransducers on the catheter. They have small diameters, are flexible, and can measure accurately rapid changes in pressure during repetitive coughing or other provoking maneuvers. Disadvantages include their expense, their need to be replaced after approximately 100 studies, and their tendency to produce rotational artifacts; pressure readings may vary depending on the orientation of the transducer to the bladder or urethral wall.
Technique of Cystometry The technique of subtracted urethrocystometry used in our laboratory is as follows: 1. The patient presents with a symptomatically full bladder. She voids spontaneously in a uroflow chair. A postvoid residual urine volume is obtained via a transurethral catheter. With the catheter in place, approximately 50 mL of sterile, room-temperature saline or water is placed into the bladder to facilitate placement of the microtransducer catheters and to decrease the amount of initial artifact secondary to the bladder wall collapsing around the microtip. 2. The microtransducer catheters are connected to the appropriate cables and to the tubing from the water pump. The machine is calibrated with the catheters in water, and all channels are set at zero. A small amount of water is flushed through the tubing to remove any air. 3. With the patient in the supine position on a birthing or urodynamic chair, the abdominal catheter is placed into the vagina and taped to the inside of the leg. If the patient has severe vaginal prolapse or has undergone previous vaginal surgery resulting in a narrowed vagina, the catheter is placed into the rectum. A dual microtransducer catheter with a filling port is then placed into the bladder. The patient is moved to a sitting position and the cath-
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eter secured to a mechanical puller (if urethral pressure studies are anticipated) or to the inside of the leg, so that the proximal transducer is near the mid-urethra (area of maximum urethral closure pressure). 4. After the catheters are appropriately placed, the subtraction is checked by asking the patient to cough. Coughinduced pressure spikes should be seen on the Pves, Pabd, and Pure channels, but not on the true detrusor pressure channel. If there is an inappropriate deflection on Pdet, it is usually a result of inaccurate placement of the vaginal (or rectal) catheter. If repositioning the catheter does not correct the problem, all connections and calibration techniques should be rechecked. 5. Bladder filling is begun. First sensation, first desire to void, and strong desire to void are recorded. Throughout the
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filling portion of the examination, the patient is asked to perform provocative activities, such as coughing and straining. The external urethral meatus is constantly observed for any involuntary urine loss. Leak point pressures can be obtained at various bladder volumes. Any abnormal rise in true detrusor pressure is noted. If the patient’s symptoms are reproduced during filling, the test can be completed in the sitting position. If they are not, the patient should be asked to stand and perform provocative maneuvers in an attempt to reproduce her symptoms. 6. At the completion of filling, urethral pressure and flow studies can be performed, if indicated. Figure 7-6 illustrates an example of filling and voiding urethrocystometry. No urodynamic abnormalities are noted in this study.
Figure 7-6 ■ Normal filling and voiding subtracted cystometry. Note that provocation in the form of coughing and straining does not provoke any abnormal rise in true detrusor pressure. At maximum capacity on command, a detrusor contraction is generated and voiding is initiated. USUI, Urodynamic stress urinary incontinence.
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INDICATIONS FOR CYSTOMETRY The indications for cystometry are somewhat controversial. Each patient must be evaluated individually. Based on clinical findings and planned treatments, the physician must decide whether cystometry is indicated and, if it is, whether it should be performed via a simple office test or with more sophisticated electronic testing. In our opinion, an electronic single-channel study does not offer any more information than does a carefully performed nonelectronic test. We believe that the only reason to perform electronic urodynamic testing is to measure pressures from several anatomic sites, thus obtaining subtracted pressures of importance. Indications for single-channel cystometry versus subtracted or multichannel cystometry have been debated extensively; however, few comparisons exist in the literature. One study by Ouslander et al. (1987) reported a sensitivity of 75% in geriatric patients undergoing simple supine cystometry when compared with multichannel testing. Sutherst and Brown (1984) compared single-channel and multichannel urodynamics in a blinded crossover study of 100 incontinent women. They noted single-channel studies to be 100% sensitive and 89% specific compared with multichannel studies. Multichannel cystometry may have a higher sensitivity for recognizing low-pressure detrusor contractions. Multichannel techniques also improve the specificity of cystometry by avoiding false-positive test results created by increases in abdominal pressure. Whether the cost of multichannel testing is justified for most patients remains to be proved. Box 7-1 lists suggested indications for subtracted cystometry.
BOX 7-1
INDICATIONS FOR MULTICHANNEL SUBTRACTED CYSTOMETRY
Complicated history Inconclusive single-channel studies Stress incontinence before surgical correction Urge incontinence not responsive to therapy Recurrent urinary loss after previous surgery for stress incontinence Frequency, urgency, and pain syndromes not responsive to therapy Nocturnal enuresis not responsive to therapy Lower urinary tract dysfunction after pelvic radiation or radical pelvic surgery Neurologic disorders Continuous leakage Suspected voiding difficulties
VIDEO–URODYNAMIC TESTING Video-urodynamic studies of the lower urinary tract represent a combination of video-cystourethrography and standard urodynamic techniques. Video-urodynamics requires equipment for cystometry, plus an image intensifier and a videotape recorder. In addition, various interface modules are necessary, depending on the exact design of the system. A television camera positioned above the recorder with a mixing device projects the recording channels on a television monitor alongside the radiographic image of the bladder (Fig. 7-7). Radiopaquefilling medium is used for video-urodynamic studies. As with all other urodynamic studies, every effort must be made to
Figure 7-7 ■ Video-urodynamic testing. Multichannel urodynamic tests are performed under fluoroscopy, thus allowing simultaneous visualization of the lower urinary tract during recording of pressures. Pves, Bladder pressure; Pabd, abdominal pressure; Pdet, detrusor pressure; Pucp, urethral closure pressure.
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limit the inhibitory effect of the additional machinery and personnel imposed on the patient. Potential advantages of video-urodynamic studies include the consolidation of multiple evaluation modalities into one examination, thereby providing information about lower urinary tract anatomy and function under various provocative environments. Descent of the bladder neck, milkback of urine from the urethra to the bladder, and bladder neck funneling all may be visualized during simultaneous recording and imaging of bladder, urethral, and abdominal pressures. Anatomic abnormalities, such as urethral or bladder diverticula, may also be noted. The major disadvantages of video-urodynamic testing are the radiation exposure, cost, and technical expertise and support necessary for its use. The indications for video-urodynamic studies are controversial. Some authorities believe that no additional information is obtained when these studies are compared with more conventional nonimaged multichannel studies; however, others believe that valuable additional information can be obtained from simultaneous imaging, especially in recurrent cases of incontinence or complicated neurologic conditions. Visualizing bladder neck opening at rest and during straining may help differentiate stress incontinence secondary to bladder neck hypermobility from intrinsic sphincter deficiency.
AMBULATORY URODYNAMICS (AUD) The largest deficiency of currently available urodynamic techniques is that laboratory observations may not always represent accurately physiologic behavior of the bladder and urethra. At times, the urodynamicist cannot reproduce the patient’s symptoms in the laboratory setting. Several companies have recently developed commercially available AUD systems (AUDS). This equipment uses indwelling cathetermounted transducers that are connected to a microcomputer worn over the patient’s shoulder. This allows freedom of movement to the extent that the patient can reproduce the activities that incite lower urinary tract dysfunction. In principle, these systems are the same as those used for conventional urodynamics, and the same basic methodology applies. AUDS should be considered when conventional urodynamics fail to provide a pathophysiologic explanation for the patient’s symptoms. The most common example of this is in a patient who complains of incontinence that cannot be objectively demonstrated and has failed nonsurgical modes of therapy. Before a more invasive intervention, such as surgery, is considered, AUDS could be used to objectively demonstrate the incontinence. AUDS are also helpful in determining whether detrusor overactivity or urethral incompetence is the main cause of incontinence in women for whom surgery is being contemplated. The technique for performing AUDS, as described by Abrams (1997), involves the recording of three micturition cycles: a resting cycle, when the patient sits in a chair; an ambulant cycle, when the patient moves around the hospital; and an exercising cycle, which should include any specific incontinence-provoking measures. Once the three cycles are recorded, the information is downloaded to a computer for
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analysis. This analysis is time-consuming and requires considerable expertise. Ideally, the data acquired should include information on voiding and urine leakage. The recent development of an electronic urine-loss detector has markedly improved AUDS. This device fits into a commercially available female pad. The advantage of electronic urine-loss detection is that it is noted instantaneously and therefore does not depend on the patient filling in her diary. This device is also very useful in patients who cannot sense urine loss. The AUDS unit should allow the connection of a flowmeter so that the urine flow rate can be recorded synchronously with intravesical and intra-abdominal pressure, which is particularly important if bladder outlet obstruction is suspected. The equipment should have an event marker, which the patient uses in conjunction with a diary to signal sensations, such as first desire to void, urgency, or leakage. Besides providing objective evidence and the cause of the patient’s lower urinary tract symptoms, additional interesting information is being generated by AUDS. Present ideas on bladder compliance, detrusor overactivity, and voiding function are being questioned. AUDS studies performed on asymptomatic, neurologically intact volunteers have shown a 30% incidence of detrusor overactivity. It has been previously suspected that bladder compliance is related to the speed of bladder-filling, and AUDS has confirmed this fact (Kulseng-Hanssen and Klevmark, 1996). Finally, voiding pressures during AUDS in women have been shown to be significantly higher than those obtained during conventional urodynamics. AUDS testing has some drawbacks. During the investigation, there is no control on the validity of the measured signals. Therefore, before the patient is sent away with the monitor, the catheter position must be checked, and the patient must be adequately instructed. Ambulatory monitoring of the upper and lower urinary tract is still developing and is currently performed in specialized urodynamic centers only. A real breakthrough in the technique will be the development of automated analysis and quantitative interpretation.
CYSTOMETRY: ABNORMAL STUDIES Abnormalities of bladder-filling are categorized into abnormal detrusor activity, compliance, sensation, and capacity. If urethral pressure is being measured simultaneously, the urethral response to filling and provocation can be elicited. For descriptive purposes, these abnormalities tend to be compartmentalized; however, no single urodynamic finding should be taken in isolation. Many patients have more than one cystometric abnormality (Fig. 7-8). Any significant rise in true detrusor pressure during filling or provocation should be interpreted as abnormal detrusor activity or compliance. A pressure increase of 15 cm H2O has been used previously by the ICS to differentiate between normal and abnormal. It has recently become apparent that this cutoff is too arbitrary, and any pressure rise must be assessed in terms of the patient’s symptoms. The most recent ICS recommendations have redefined detrusor overactivity as a urodynamic observation characterized by involuntary detrusor
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Figure 7-8 ■ Multichannel urethrocystometry in a patient with combined detrusor overactivity and urodynamic stress incontinence. USUI, Urodynamic stress urinary incontinence.
contractions during the filling phase, which may be spontaneous or provoked. No lower limit is present for the amplitude of an involuntary detrusor contraction but a confident interpretation of low-pressure waves (amplitude smaller than 5 cm H2O depends on “high quality” urodynamic technique). Although it is useful to categorize pressure changes during cystometry, the different patterns that occur are not mutually exclusive. Examples of the various cystometric findings in detrusor overactivity are shown in Figure 7-9. Detrusor overactivity may present as phasic contractions that return to baseline after each contraction or as phasic contractions in which there is a gradual rise in pressure that could be seen,
for example, in spinal cord injury patients when attempted voiding occurs against a dyssynergic sphincter. A steady rise in true detrusor pressure may indicate an organic reason for the poor bladder compliance, such as end-stage interstitial cystitis or radiation cystitis. The clinical relevance of these various patterns is not fully understood. The management of detrusor overactivity is discussed in Chapter 28. Sensory abnormalities, as previously mentioned, have recently been redefined as normal, increased, reduced, absent, nonspecific, and bladder pain. Increased bladder sensation is similar whether there is a definable cause, such as interstitial cystitis, or whether the cause is unknown. In these patients,
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Figure 7-9 ■ Various detrusor responses to filling: A. Normal filling cystometry. B. Phasic contractions that return to baseline. C. Phasic contractions with gradual rise in true detrusor pressure. D. Steady rise in true detrusor pressure (low-compliance bladder). Figure 7-10 ■ A. Urodynamic diagnosis of sensory urgency. Patient experiences severe urgency at abnormally low bladder capacity in the absence of any significant rise in true detrusor pressure. B. Urodynamic diagnosis of hyposensitive bladder. Patient experiences no sensation of fullness at abnormally high bladder volume.
catheterization is often painful. Volumes at first sensation of bladder filling, first desire to void, and maximum capacity are reduced. Increased bladder sensation is present when the patient experiences a strong desire to void at abnormally low bladder volumes in the absence of any rise in true detrusor pressure (Fig. 7-10, A). Bladder overactivity may be associated with hypersensitivity from causes such as radiation therapy and interstitial cystitis. Therapy may result in bladder stability; however, the symptoms of frequency and urgency may persist if the bladder sensation remains increased. Urodynamically, reduced bladder sensation behaves similarly, whatever the cause. The bladder has a large capacity and a flat cystometrogram (Fig. 7-10, B). At maximum
capacity, there may rarely be a rise in pressure as the limits of compliance are reached. This rise does not represent a detrusor contraction, and there may be little or no sensation to filling up to this point. Weir and Jaques (1974) noted that 30% of patients with bladder capacities over 800 mL were able to generate a normal detrusor contraction and void to completion on command. Reduced bladder sensation resulting in an overdistended bladder, in itself, is not necessarily an indication of pathology. During cystometry, functional and cystometric bladder capacity should be differentiated. Maximum cystometric capacity, in patients with normal sensation, is the volume at which the patient feels she can no longer delay micturition.
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Functional bladder capacity is the amount of urine that the bladder can hold under natural conditions. This amount can be checked easily by asking the patient to drink a large amount of water and hold it until she feels a maximum sensation to void. She then urinates, and a postvoid residual urine volume is measured. The sum of the volumes of urine voided plus the residual urine provides the maximal functional bladder capacity. The artifacts of catheter insertion, the environment of cystometric examination, and the presence of medical personnel may change the patient’s bladder capacity. Thus, it is important to interpret bladder capacity data as derived from cystometry on a comparative basis with the patient’s functional capacity, as determined on frequency volume charts. Both local and systemic conditions can result in abnormal bladder capacity. Box 7-2 reviews the differential diagnosis of low-volume and high-volume bladder capacity. When urethral pressure is measured simultaneously during filling, cystometry urethral responses, as previously mentioned, should be termed normal or incompetent urethral closure mechanism, urethral relaxation incontinence, or urodynamic stress incontinence (Fig. 7-11). Cystometry is the most important and most commonly performed urodynamic test. It assesses bladder filling and storage and is also important in evaluating bladder emptying, when used in conjunction with the other urodynamic and radiologic tests. Although it is clinically useful, its limitations should be recognized. Gynecologists should become familiar with cystometry so that they can perform and interpret basic office tests and work with urogynecologic or urologic consultants when more sophisticated tests are indicated. Figure 7-12 demonstrates numerous examples of various functional and anatomic abnormalities diagnosed on video-urodynamic studies. BOX 7-2
DIFFERENTIAL DIAGNOSIS OF LOW-VOLUME AND HIGH-VOLUME BLADDER
Low Volume Detrusor overactivity (idiopathic) Neurogenic detrusor overactivity Urodynamic stress incontinence Increased bladder sensation Interstitial cystitis Radiation cystitis or fibrosis Bladder tumor Urinary tract infection Emotional factors
High Volume Chronic outlet obstruction Uterovaginal prolapse Urethral stricture Urethral tumor Neuropathy Diabetes mellitus Hypothyroidism Tabes dorsalis Pernicious anemia Lumbosacral disk disease Previous radical pelvic surgery Multiple sclerosis Habitual infrequent voiding
URETHRAL FUNCTION TESTS No general consensus exists on how to best evaluate urethral function in women with lower urinary tract dysfunction. Ideally, urethral function is assessed quantitatively in the hope of providing objective parameters that can be used to make important clinical decisions. Urinary continence depends on the pressure in the urethra exceeding the pressure in the bladder at all times, even with increases in abdominal pressure. Contributing to normal urethral compliance and pressure are smooth and striated urethral muscles; fibroelastic tissue of the urethral wall; vascular tension caused by the rich, spongy network around the urethra; and extrinsic compression from surrounding pelvic floor musculature. The urethra lies on the supportive layer composed of the endopelvic fascia and the anterior vaginal wall. This layer is structurally stable because of its bilateral attachment (as a hammock) to the arcus tendineus fasciae pelvis and the levator ani. Intraabdominal pressures compress the urethra to close its lumen; that is, urethral closure pressure during stress rises because the urethra is compressed. Attempts to evaluate and quantify the urethra’s role in storage and voiding disorders have led to the development and use of urethral pressure profilometry and leak point pressure studies.
URETHRAL PRESSURE PROFILOMETRY The first attempt to measure urethral pressure was published in 1923 by Bonney, who used the technique of retrograde sphincterometry. This method was replaced by a balloon catheter in 1936. Karlson (1953) introduced the technique of simultaneous measurement of intraurethral and intravesical pressure (urethrocystometry), and, in 1969, the fluid profusion method was described by Brown and Wickham. More recent technology has introduced the use of microtransducer catheters.
Definitions The ICS has standardized terminology relating to urethral pressure profilometry. A urethral pressure profile (UPP) indicates the intraluminal pressure along the length of the urethra with the bladder at rest. When describing this method, one should specify the catheter type and size, the measurement technique, the rate of infusion (if a perfusion system is used), the rate of catheter withdrawal, the bladder volume, and the position of the patient. The maximum urethral pressure is the maximum pressure of the measured profile. The maximum urethral closure pressure is the difference between the maximum urethral pressure and the intravesical pressure. The functional urethral length is the length of the urethra along which the urethral pressure exceeds the intravesical pressure, and the anatomic urethral length is the total length of the urethra (Fig. 7-13). The pressure transmission ratio (PTR) is the increment in urethral pressure on stress as a percentage of the simultaneously reported increment in vesical pressure. For stress profiles obtained during coughing, PTRs can be obtained at any
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Figure 7-11 ■ Urodynamic diagnosis of the condition of urodynamic stress incontinence. Visual loss of urine occurs in the absence of any rise in true detrusor pressure with complete pressure equalization. USUI, Urodynamic stress urinary incontinence.
point along the urethra. If single values are given, the position of the urethra should be stated. If several PTRs are defined at different points along the urethra, a pressure transmission profile is obtained. The term transmission is commonly used, but transmission implies a completely passive process. Such an assumption is not yet justified by scientific evidence because a role for muscular activity cannot be excluded.
Methodology Urethral pressure profilometry involves the withdrawal of a catheter through the urethra at a constant rate of speed. Pressure is measured along the entire urethral length as well as in the bladder. Urethral pressure profilometry can be per-
formed using open or balloon catheters perfused with liquid or gas, catheter-mounted (microtip) transducers, or fiberoptic catheters. The perfusion systems measure the pressure required to push the gas or liquid through the catheter holes against the urethral wall. Technical difficulties with fluid perfusion systems included delay in response time, clamping due to air bubbles and leak of fluid in connections, the effect of variation in infusion rate and catheter withdrawal rate, and inaccuracies in transducer position and calibration. These problems lead to the development of microtip transducers that measure the pressure of the urethral wall against the transducer’s membrane. Although microtip transducers are sensitive and produce high-quality pressure recordings, they are expensive and fragile and can be
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Figure 7-12 ■ Examples of functional and anatomic abnormalities seen on video-urodynamic studies (A–F). A. Stress incontinence with high leak point pressure and little urethral mobility. Forty-two-year-old woman with stress incontinence with physical activity; no prior surgery; Q-tip straining angle 10. Point 1. X-ray obtained during Valsalva (ALPP = 90 cm H2O) Point 2. X-ray obtained during voiding (Pdetmax = 33 cm H2O; Qmax = 20 mL/sec) B. Seventy-five-year-old woman who complains of urinary frequency, urgency, and urge incontinence of 3 years duration. At point 1 there is an involuntary detrusor contraction. The patient is aware of it and tries to abort it by contracting her pelvic floor, and she is successful at temporarily preventing incontinence. The X-ray obtained at this time shows contrast in the proximal urethra and a bladder diverticula, but no incontinence. After about 20 seconds the sphincter fatigues and she voids involuntarily (point 2). X-ray at point 2 shows an unobstructed urethra and the bladder diverticula is a bit larger.
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Figure 7-12 ■ Cont’d C . Primary bladder neck obstruction and bilateral bladder diverticula. Fifty-one-year-old woman who sees a plastic surgeon because of a “pot belly.” She denies any urinary symptoms but is found to have a palpable bladder and is catheterized for 2500 mL. An X-ray obtained at point 1 (125 mL) shows bilateral bladder diverticula and a closed bladder neck. During a voluntary detrusor contraction to 187 cm H2O (point 2), there is no contrast seen in the urethra confirming the vesical neck as the point of obstruction. (Pdetmax = 187 cm H2O; Qmax = 0 mL/sec.) D. Urethral obstruction due to a urethral diverticulum. Sixty-seven-year-old white woman with a 20-year history of severe disabling pain during and after micturition. She underwent multiple urethral dilations and various empiric therapies but never had urodynamics evaluation or lower urinary tract imaging. During a voluntary detrusor contraction the urethra is obstructed by a multilocular urethral diverticulum (arrow); Pdetmax = 70 cm H2O; Qmax = 6 mL/sec. (Continued)
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Figure 7-12 ■ Cont’d E. Detrusor overactivity due to previously undiagnosed bladder cancer. Seventy-year-old woman who complains of urinary frequency and urgency of 3-year duration. Urinalysis is negative on multiple occasions and cystoscopy 2 years before was reportedly normal. Filling defects are seen at point 1. At point 2, during an involuntary detrusor contraction, the filling defects are seen again and there is partial urethral obstruction by the tumor. At point 3, Pdetmax = 30 cm H2O, and Qmax = 10 mL/sec. F. Detrusor overactivity, urethral obstruction, low bladder compliance, and vesicoureteral reflux. Seventy-yearold woman who develops an enterovesical fistula after undergoing synthetic pubovaginal sling. After closure of the fistula, she develops refractory overactive bladder and recurrent febrile urinary tract infections. During bladder filling, a steep rise in pressure reaches 50 cm H2O at a bladder volume of 125 mL. At each arrow, the bladder infusion is temporarily stopped and the detrusor pressure falls, proving that the rise in pressure is due to compliance and not a detrusor contraction. At point 1 there is an involuntary detrusor contraction and she is incontinent. X-ray shows grade 2 right vesicoureteral reflux and obstruction at the bladder neck (Pdetmax = 48 cm H2O; Qmax = 2 mL/sec).
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Figure 7-13 ■ Urethral pressure profile demonstrating total urethral pressure, urethral closure pressure, and anatomic and functional urethral length. (From Karram MM. Urodynamics. In Benson JT, ed. Female Pelvic Floor Disorders: Investigation and Management. Norton Medical Books, New York, 1992, with permission.)
difficult to calibrate. More recent fiberoptic transducers have been introduced as a less-expensive alternative with simpler calibration. More experience in urodynamic applications is needed with fiberoptic catheters. Microtransducers are currently the most widely used catheters for urethral pressure studies in the United States. These catheters have two microtransducers mounted 6 cm apart. The distal transducer in the bladder measures bladder pressure, whereas the more proximal catheter is manually or mechanically withdrawn through the urethra. Microtransducers have an adequate response time for all aspects of urethral pressure profilometry. Some investigators have used multiple transducers along the urethra to assess stationary recordings of UPPs. Hilton and Stanton (1983) suggested a standard technique for performing UPPs, using microtransducer catheters. We use a similar technique (Fig. 7-14). 1. With the patient in the sitting position at maximum cystometric capacity (usually after filling cystourethrometry), the catheter is secured to a mechanical puller. The orientation of the transducer on the catheter is directed laterally to the 9 o’clock position. 2. As the proximal transducer is pulled through the urethra, the resting or static urethral pressure is recorded on graph paper that is moving at the same speed as the catheter. The urethral closure pressure (Pure – Pves) is recorded on a separate channel. The proximal sensor is then mechanically reinserted into the bladder, and a second profile is obtained to ensure consistency and reproducibility of results. A minimum of two profiles is averaged to obtain final results. 3. To perform a cough or stress pressure profile, the same procedure is repeated with the patient coughing
repetitively while the catheter is withdrawn through the urethra. The patient should cough at a consistent intensity, every 2 to 3 seconds, which corresponds approximately to every 2 to 3 mm of functional urethral length. It is important that the recorder be set so that the entire amplitude of each cough spike in the bladder and urethra remains on the chart paper. The external urethral meatus is visualized for involuntary loss of urine.
Interpretation Variables Urethral pressure is measured by inserting a transducer, mounted on a catheter into a normally coapted lumen. In reality, what is being measured is the force exerted by the walls of the urethra on the transducer. If the urethra were a tube with a circular lumen, the occlusive forces would be equal around its circumference; however, because the urethra is a collapsed tube with the anterior and posterior walls in apposition, the occlusive forces are unequally distributed around the urethra. Thus, certain factors must be taken into consideration to ensure the reproducibility of urethral pressure studies. Lack of standardization in catheter and patient characteristics have tremendously hampered the reproducibility of urethral pressure profilometry. Studies on orientation of the microtransducer within the urethral lumen have noted that the pressure is highest when the transducer is placed anteriorly and lowest when it is placed posteriorly. For this reason, most studies are performed with the transducer in the lateral positions, providing more standardized measurement. In addition, the pressure measurement depends on the size and stiffness of the catheter as well as the form of the
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technique. The values for normal urethral pressures in the literature are all taken from very small series. Abrams (1997) published values for maximum urethral pressure in patients who have no lower urinary tract abnormality noted on clinical or urodynamic assessment. He noticed a significant deterioration in closure pressure with an increase in age, noting a mean maximum urethral pressure of 90 cm H2O in patients less than age 25, with a significant decrease over time to a mean of 65 cm H2O in patients over age 64. This is similar to previous data published by Rud (1980), who noted that maximum urethral pressure decreases with changes in vascularization that are inevitable with increasing age. Also, previous studies indicate a trend toward lower urethral closure pressures and shorter functional length in stress incontinent patients than in patients who are stress continent.
Clinical Applications The clinical applications of urethral pressure studies are very controversial. Some investigators believe that urethral pressure studies are clinically useful in certain conditions, whereas others believe that they have no clinical use. DIAGNOSIS OF URODYNAMIC STRESS INCONTINENCE
Figure 7-14 ■ Technique of static urethral pressure profilometry with simultaneous measurement of bladder pressure. Study begins with both microtransducers in the bladder (top). As the catheter is mechanically withdrawn through the urethra (middle and bottom), urethral and bladder pressures are recorded.
pressure sensor. Catheter sizes ranging from 8 to 12 French and withdrawal speeds of 1 to 40 cm per minute do not significantly affect urethral pressure results. The position of the patient and bladder volume should also be standardized. Urethral pressure increases with increasing bladder volumes in continent, neurologically intact women. Most tests are performed in the supine or sitting position. The normal response to the assumption of a more upright posture is an increase in the maximum urethral closure pressure of about 23%. In some abnormal patients this increase may not occur, and, in women with neurogenic bladders, the increase in pressure may be excessive (greater than 100%). When performing stress pressure profiles, Schick (1985) noted that PTRs decrease as the strength of cough increases. Therefore, reproducibility requires comparable strengths of coughs during these tests. A normal female UPP is symmetric in shape, and asymmetry is generally caused by a faulty measurement
Over the years many investigators have attempted to use urethral pressure studies to explain the pathogenesis of urinary incontinence and to diagnose stress incontinence. However, the lack of consistent associations of UPP variables with diagnoses confirmed by video-urodynamic testing has limited its acceptance. Versi et al. (1990) examined 24 urethral pressure variables and used kappa statistical analysis to determine which variables were the most discriminatory. Although there was a significant difference in maximum urethral closure pressure between patients with stress incontinence and continent women, there was a large overlap between the two groups. They concluded that no single parameter of a urethral pressure study could be used to diagnose stress incontinence. PTR is a test of the dynamic response of the urethra to increases in intra-abdominal pressure. It requires simultaneous measurement of urethral and vesical pressures during coughing, allowing the calculation of the relative amounts of abdominal pressure transmitted to each structure. The PTR was, at one time, felt to be a useful test that could be used to quantitate urethral closure during stress. The PTR is calculated by dividing a cough-induced urethral pressure increase by the bladder pressure increase and multiplying by 100 (Bump et al., 1988; Rosenzweig et al., 1991). An extensive review of the published literature on urethral pressure profilometry concluded that parameters of urethral pressure profilometry (MUCP and PTR) cannot be consistently and reliably used to distinguish between continent and incontinent women (Weber, 2001). DIAGNOSIS OF INTRINSIC SPHINCTER DEFICIENCY Several studies have tried to identify a value of maximum urethral closure pressure (MUCP) that would serve as a clinically meaningful distinction between types of stress incontinence, that is, normal pressure (type II) versus low-pressure
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urethra (type III or ISD). McGuire (1981) and Hilton and Stanton (1983) reported that patients with recurrent incontinence after surgery had lower MUCP before surgery than those with successful surgery. Sand et al. (1987) retrospectively reported on 86 women undergoing Burch colposuspension and identified MUCP <20 cm of H2O as a cutoff predicting poor outcome (46% cure rate) compared with MUCP >20 cm of H2O (82% cure rate). However, this cutoff was established only in retrospect and was statistically significant only in women age 50 or less. For women over age 50, low urethral pressure did not influence the outcome. Other retrospective studies as well as a case-controlled study by Bowen et al. (1989) have shown higher failure rates in women with low MUCP, with the exception of the study by Richardson et al. (1991). However, all retrospective studies were uncontrolled and their relatively small patient populations were heterogeneous with respect to age, previous surgery, and other variables of importance in surgical outcomes. Two randomized trials have been reported (Quadri, 1999; Sand et al., 2000) that included only women with urethral hypermobility. Quadri et al. noted a 34% failure rate in 15 women with low urethral pressure who had undergone a Burch colposuspension and a 0% failure rate in 15 women undergoing a Marshall-Marchetti-Krantz procedure. Sand et al. compared a Burch colposuspension to a suburethral sling in women with low urethral pressure. They noted a 5% failure rate in the Burch group compared with a 0% failure rate in the sling group.
Urethral Function During Filling Cystometry When measurements of urethral pressure are performed during filling cystometry, fluctuations in urethral pressure are not uncommon. Artifactual pressure fluctuations caused by urethral catheter movement are common and should not be confused with the following conditions. The association between variations in urethral pressure (at the point of maximum urethral closure pressure at rest) and abnormal detrusor function has been examined. 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 no longer recommended by the ICS. If symptoms are seen in association with a decrease in urethral pressure, a full description should be given. Urethral relaxation incontinence is defined as leakage due to urethral relaxation in the absence of raised abdominal pressure or detrusor overactivity (Figs. 7-15 and 7-16). Although urethral relaxation is a well-documented cause of incontinence, it is very rare and its management is currently controversial. This form of incontinence may actually be a form of detrusor overactivity in which urethral pressure loss occurs, but the detrusor contraction is not perceived because the urethra is open and a urethral-vesical equilibrium exists. Tapp et al. (1988, British Journal of Urology) investigated the correlation between fluctuations in urethral pressure and clinical symptoms by comparing women with significant versus nonsignificant variations in mean urethral closure pressure. His analysis was carried out for absolute cutoff points and for the ratio change in mean urethral closure pressure to resting mean urethral closure pressure.
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He concluded that no significant difference was present in clinical symptoms between these two groups. Apparently, the actual significant level of fluctuation in mean urethral pressure and the overall clinical relevance of this entity are subject to debate. LOCAL PATHOLOGY IN THE URETHRA Urethral pressure measurements may be useful in diagnosing local pathology in the urethra, such as diverticula and strictures (Bhatia et al., 1981; Summitt et al., 1992).
LEAK POINT PRESSURES An alternative method to evaluate or objectively assess urethral resistance and function is the leak point pressure. Abdominal and detrusor leak point pressures determine urethral resistance to two different expulsive forces. These two forces (abdominal and detrusor pressures) are the sum total of the forces acting on the urethra to cause leakage.
Definitions An 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. A detrusor leak point pressure is defined as the lowest detrusor pressure of which urine leakage occurs in the absence of either a detrusor contraction or increased abdominal pressure. A detrusor leak point pressure is related to upper tract function in that a high detrusor leak point pressure (>40 cm/H2O) is associated with the propensity for upper tract deterioration. Abdominal and detrusor leak point pressures actually reflect outlet resistance at the time that these forces individually induce leakage. Neither leak point pressure reflects the strength or character of the detrusor contraction.
Methodology Ideally, the technique of performing an abdominal leak point pressure should be standardized and performed exactly the same way each time to allow comparison between patients and to make posttreatment studies meaningful. Many controversies exist regarding the technique of this test. These include catheter size, bladder volume, type of provocation, patient positioning, how the actual rise in pressure is determined, and how to best perform the test in the presence of genital prolapse. In abdominal leak point pressure measurements it is essential that the cystometrogram is stable (i.e., there is no significant increase in detrusor pressure during filling). If abnormal bladder compliance does exist, leak point pressure testing will underestimate urethral sphincter resistance. The technique we use for measuring abdominal leak point pressures is as follows. With a 6-French dual-sensor microtip transducer in the bladder, subtracted filling cystometry is performed to a bladder volume of 150 to 200 mL. Assuming no abnormalities in bladder compliance
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Figure 7-15 ■ Multichannel urodynamic tracing of a patient with urethral instability (uninhibited urethral relaxation). Note that bladder pressure remains stable and visual loss of urine occurs, simultaneous with drop in urethral pressure.
are present, leak point pressure measurements are performed at this volume. In the sitting position, the patient performs a gradually more vigorous Valsalva maneuver until leakage occurs. The lowest bladder pressure at which leaking occurs is considered the abdominal leak point pressure (Fig. 7-17, A). If a Valsalva maneuver cannot produce enough abdominal pressure to produce leakage or the patient is unable to strain on command, coughing is used as the provocative maneuver. Because coughing is a more “rapid” process than straining, attainment of accurate and reproducible values is more difficult. The patient is asked to cough repetitively, and the external urethral meatus is visualized for leakage. Once leakage has occurred, the strength of the cough is reduced until the cough that generates the minimal amount of abdominal pressure required to produce leakage is isolated (Fig. 7-17, B). These maneuvers are then performed several times in the
hope of documenting reproducible values. If patients do not leak with either a Valsalva maneuver or repetitive coughing, the catheter is removed from the bladder and the provocative maneuvers are repeated with the abdominal pressure being measured via an intravaginal or intrarectal catheter. Filling cystometry is then continued to maximum cystometric capacity, and the leak point pressure measurements are repeated. Although these numbers are usually significantly lower than those noted at 150 to 200 mL, they can be useful in objectively documenting and following the severity of the disease after various modes of nonsurgical or surgical therapy. To perform a bladder leak point pressure, the filling cystometrogram is performed at a slower filling rate, usually 25 mL/min. The patient is typically supine for this study. Filling continues to the point at which leakage occurs and is
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Figure 7-16 ■ Graphic representation to show difference between urethral instability (uninhibited urethral relaxation) and unstable urethral pressure. (From Karram MM. Urodynamics. In Benson JT, ed. Female Pelvic Floor Disorders: Investigation and Management. Norton Medical Books, New York, 1992, with permission.)
identified by either direct observation or fluoroscopy. The total bladder pressure (i.e., detrusor and abdominal pressures) is measured and recorded as the bladder leak point pressure. In some patients the pressure may occur at very large volumes and high pressures. Once a bladder pressure of 40 cm H2O is reached, the study should be terminated because ongoing filling above this pressure can be dangerous.
Interpretation Variables Variables in performing this study revolve around the lack of standardization. Multiple parameters have been shown to affect the abdominal leak point pressure measurements. These include catheter caliber, catheter location (vaginal versus intravesical), bladder volume, the use of coughing versus Valsalva maneuver as the provocation, patient position, and the use of an absolute or change in measured pressure. More subjects demonstrate urine loss during Valsalva maneuvers with a 3-French rather than 8-French transurethral catheter, and the abdominal leak point pressures obtained with the 3-French catheter are consistently lower. At least two investigators have shown that removal of the transurethral catheter and measurement of the intra-abdominal pressure rise with an intravaginal or intrarectal catheter consistently lowered abdominal leak point pressure by up to 20 cm H2O, suggesting that the transurethral catheters are obstructive. An inverse relationship exists between bladder volume and abdominal leak point pressures. Miklos et al. (1995) per-
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formed Valsalva leak point determination at various bladder volumes and found a 19-cm H2O fall in the leak point pressure as the volume increased from 150 mL to more than 400 mL. Although the effect of patient positioning on leak point pressure measurements has not yet been studied, one could postulate that if the patient moves from a supine to an upright position, the value of the leak point pressure diminishes, provided that a mechanical obstruction such as a large prolapse is not accentuated in the erect position. Another area of controversy concerns the use of coughing versus a Valsalva maneuver as the technique for provoking urine loss. Cough-induced leak point pressures are consistently higher than Valsalva-induced leak point pressures. A major concern with coughing is that it is technically more difficult to control the intensity of a cough and to pinpoint the absolute lowest value associated with urine loss. Unfortunately, some patients demonstrate incontinence only with coughing because Valsalva-induced incontinence has only a 70% to 80% sensitivity in detecting stress incontinence. Valsalva leak point pressures have been shown to have excellent reproducibility, with test-retest correlation coefficients of more than 0.9. The test-retest reliability of a cough-induced leak point pressure has not been studied. Finally, how should the actual number be determined? Some investigators have used a subtracted value or an increase in intravesical pressure over the baseline resting intravesical pressure, whereas others used the absolute increase in intravesical pressure, which reflects the increase plus the resting baseline pressure.
Clinical Applications The abdominal leak point pressure is being used as a severity measure for dysfunction of the urethral sphincteric mechanism, with implications regarding surgical management. Many urologists and urogynecologists use abdominal leak point pressures below 60 cm H2O to define ISD or type III stress incontinence. These concepts are not universally accepted and to date no surgical outcome data are available. These recommendations are based mostly on data published by McGuire et al. (1993), who performed leak point pressures on 125 women with urodynamic stress incontinence. They noted that 76% of patients who had a leak point pressure less than 60 cm H2O were noted to have type III incontinence on video-urodynamic testing. They defined type III incontinence as proximal urethral pressures less than 10 cm H2O or a nonfunctioning open internal sphincter. If leak point pressure measurements truly correspond to urethral function, then as urethral function worsens (manifested by worsening symptoms), leak point pressure should decrease. Two studies have correlated leak point pressures with subjective degrees of stress incontinence in women. Both studies defined severe incontinence due to ISD as loss of urine with minimal activity or gravitational incontinence. McGuire et al. (1993) noted that 81% of patients with leak point pressures less than 60 cm H2O had ISD, whereas Nitti and Combs (1996) noted that 75% and 50% of patients with ISD had leak point pressures less than 90 cm H2O and 60 cm H2O, respectively.
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Figure 7-17 ■ A. Graphic representation of Valsalva leak point pressure measurement at bladder volumes of 150 and 300 mL. Leak point pressures tend to decrease with increased bladder volume. B. Graphic representation of cough leak point pressure at bladder volumes of 150 and 300 mL. Note the difficulty involved in isolating the cough that generates the minimal amount of abdominal pressure required to produce leakage.
Theofrastous et al. (1996) reported women who leaked with Valsalva at lower bladder volumes had significantly worse measures of incontinence severity (incontinence episodes per week and quantitative pad test) compared with women who leaked at higher volumes and those who did not leak at all with Valsalva. Actual leak point pressure values were not analyzed relative to measures of incontinence severity. Cummings et al. (1997) analyzed the cumulative association of severity of symptoms and previous surgery with low leak point pressure (<65 cm H2O). Low leak point pressure was found in 8 of 17 (47%) patients with occult symptoms and no previous surgery, 12 or 22 patients (55%) with severe symptoms or previous surgery, and 15 of 18 (83%) patients with both severe symptoms and previous surgery.
CONTROVERSIES AND CORRELATIONS Urethral pressure and leak point pressure studies are two different urodynamic tests aimed at objectively quantifying urethral function. Until recently, intrinsic urethral sphincter deficiency was believed to be a condition that occurred only after injury
to the urethra. ISD was felt to commonly occur secondary to anterior vaginal wall surgery, previous bladder neck surgery, pelvic radiation, or thoracolumbar neurologic lesions. The diagnosis has recently become much more commonly used, based mostly on the more liberal use of these tests. Numerous investigators have attempted to correlate urethral pressures and leak point pressures. Two studies (Sultana, 1995; Swift and Ostergard, 1995a) noted a statistically significant but clinically weak correlation between maximum urethral closure pressure and Valsalva leak point pressure, measured as the absolute increase in intravesical pressure. These studies noted correlation coefficients around 0.5 to 0.6. However, studies by Bump et al. (1995a) and McGuire et al. (1993) noted no correlation between maximum urethral closure pressure and Valsalva leak point pressures. The inconsistencies in these findings are due, at least in part, to differences in the technique of performing Valsalva leak point pressure measurements. More recently, McLennan and Bent (1998) studied the relationship between a positive supine empty stress test, Valsalva leak point pressure, and maximum urethral closure pressure. They concluded that a positive supine empty stress test is a useful screening test for a low leak point pressure but not a low urethral closure pressure.
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SUMMARY The clinical applications of urethral pressure profilometry and abdominal leak point pressures are controversial. Until the techniques for performing these tests are standardized, clinical applicability will remain controversial. Based on a review of the currently available literature, no evidence supports the use of urethral pressure profilometry as a diagnostic test or as an objective measure of urethral function (Weber, 2001). Despite widespread use of leak point pressure testing in clinical practice, little data support its contribution to differential diagnosis in women with symptoms of stress incontinence. Leak point pressure values do seem to correspond on a continuum with severity of stress incontinence with lower leak point pressure values associated with worse symptoms. More research is needed to identify and validate a cutoff (assuming this would be clinically relevant) that identifies or correlates with severe urethral dysfunction. It would then need to be determined that identifying such a patient would alter clinical management.
Bibliography CYSTOMETRY Abrams P. Urodynamics, 2nd ed. Springer, London, 1997. 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. Arnold EP. Cystometry: postural effects in incontinent women. Urol Int 1974;29:185. Arnold EP, Webster JR, Loose H, et al. Urodynamics of female incontinence: factors influencing the results of surgery. Am J Obstet Gynecol 1973;117:805. Barnick CG, Cardozo LD, Benness C. Use of routine videocystourethrography in the evaluation of female lower urinary tract dysfunction. Neurourol Urodyn 1989;8:447. Bates CP, Whiteside CG, Turner-Warwick R. Synchronous cine/pressure/ flow cystourethrography with special reference to stress and urge incontinence. Br J Urol 1970;42:714. Bates P, Bradley WE, Glen E, et al. First report on the standardization of terminology of the lower urinary tract function. Urinary incontinence. Procedures related to the evaluation of urine storage: cystometry, urethral closure pressure profile, units of measurement. Br J Urol 1976;48:39; Eur Urol 1976;2:274; Scand J Urol Nephrol 1976;11:193; Urol Int 1976;32:81. Bergman J, Elia G. Effects of the menstrual cycle on urodynamic work-up: should we change our practice? Int Urogynecol J Pelvic Floor Dysfunct 1999;10:375–377. Bhatia NN, Bradley WE, Haldeman S. Urodynamics: continuous monitoring. J Urol 1982;128:963. Bhatia NN, Bradley WE, Haldeman S, et al. Continuous ambulatory urodynamic monitoring. Br J Urol 1982;54:357. Blaivas JG. Multichannel urodynamic studies. Urology 1984;23:421. Blaivas JG. Machines for measuring urodynamics. Contemp Obstet Gynecol 1990;35:99. Bradley WE, Timm GW, Scott FB. Cystometry: III. Cystometers. Urology 1975;5:843. Bradley WE, Timm GW, Scott FB. Cystometry: V. Bladder sensation. Urology 1975;6:654. Bump RC. The urodynamic laboratory. Obstet Gynecol Clin North Am 1989;16:795. 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;173:551–557. Cardozo L. Urogynecology. Churchill Livingstone, New York, 1997.
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Cass AS, Ward BD, Markland C. Comparison of slow and rapid fill cystometry using liquid and air. J Urol 1970;104:104. Colstrup H, Andersen JT, Walter S. Detrusor reflex instability in male intravesical obstruction. Fact or artifact? Neurourol Urodyn 1982; 1:183. Coolsaet BL, Blok C, Van Venrooij GE, et al. Subthreshold detrusor instability. Neurourol Urodyn 1985;4:309. DuBois P. Über den Druck in der Harnblase. Arch Klin Med 1876;17:248. Enhorning G. Simultaneous recording of intravesical and intraurethral pressure. Acta Chir Scand 1961;276(Suppl):1. Fossberg E, Beisland HO, Sauder S. Sensory urgency in females. Treatment with phenylpropanolamine. Eur Urol 1981;7:157. Gleason DM, Bottaccini MR, Reilly RJ. Comparison of cystometrograms and urethral profiles with gas and water media. Urology 1977;9:155. Jorgensen L, Lose G, Andersen JT. Cystometry: H2O or CO2 as filling medium? A literature survey of the influence of the filling medium on the qualitative and the quantitative cystometric parameters. Neurourol Urodyn 1988;7:343. Kulseng-Hanssen S, Klevmark B. Ambulatory urethro-cysto-rectometry: a new technique. Neurourol Urodyn 1988;7:119. Kulseng-Hanssen S, Klevmark B. Ambulatory urodynamic monitoring of women. Scand J Urol Nephrol 1996;179(Suppl 30):27. Lapides J, Friend CR, Ajemian EP. Denervation supersensitivity as a test for neurogenic bladder. Surg Gynecol Obstet 1962;114:141. Lewis LG. A new clinical recording cystometer. J Urol 1939;41:638. Massey A, Abrams P. Urodynamics of the female lower urinary tract. Urol Clin North Am 1985;12:231. McCarthy TA. Validity of rectal pressure measurements as indication of intraabdominal pressure changes during urodynamic evaluation. Urology 1982;20:657. McGuire EJ, Savastano JA. Stress incontinence and detrusor instability/urge incontinence. Neurourol Urodyn 1985;4:313. McGuire EJ, Woodside JR, Norden TA, et al. Prognostic value of urodynamic testing in myelodysplastic patients. J Urol 1981;126:205–209. Melzer M. The urecholine test. J Urol 1972;108:729. Merrill DC, Bradley WE, Markland C. Air cystometry. I. Technique and definition of terms. J Urol 1971;106:678. Merrill DC, Bradley WE, Markland C. Air cystometry. II. A clinical evaluation of normal adults. J Urol 1972;108:85. Merrill DC, Rotta JA. A clinical evaluation of detrusor denervation supersensitivity using air cystometry. J Urol 1974;111:27. O’Donnell PD. Urinary Incontinence. Mosby, St. Louis, 1997. Ouslander JG, Staskin D, Raz S, et al. Clinical versus urodynamic diagnosis in an incontinent geriatric female population. J Urol 1987;137:68. Penders L, De Leval J. Simultaneous urethrocystometry and hyperactive bladders: a manometric differential diagnosis. Neurourol Urodyn 1985;4:89. 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;1:57. Sand PK, Bowen LW, Ostergard DR. Uninhibited urethral relaxation: an unusual cause of incontinence. Obstet Gynecol 1986;68:645. Sand PK, Hill RC, Ostergard DR. Supine urethroscopic and standing cystometry as screening methods for the detection of detrusor instability. Obstet Gynecol 1987;70:57. Sutherst JR, Brown MC. Comparison of single and multichannel cystometry in diagnosing bladder instability. Br Med J 1984;288:1720. Torrens M, Abrams P. Cystometry: symposium on clinical urodynamics. Urol Clin North Am 1979;6:71. Van Waalwijk van Doorn ES, Gommer E. Ambulatory urodynamics. Curr Opin Obstet Gynecol 1995;7:378. Van Waalwijk van Doorn ES, Remmers A, Janknegt RA. Conventional and extramural ambulatory urodynamic testing of the lower urinary tract in female volunteers. J Urol 1992;147:1319. Wein AJ, Barrett DM. Voiding Function and Dysfunction. Mosby, Chicago, 1988. Weir J, Jaques PF. Large-capacity bladder: a urodynamic survey. Urology 1974;4:544.
URETHRAL PRESSURE PROFILOMETRY Abrams P. Urodynamics, 2nd ed. Springer, London, 1997. Abrams P, Blaivas JG, Stanton SL, et al. The standardization of terminology of lower tract function. Scand J Urol Nephrol 1988;114(Suppl):5.
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Asmussen M, Ulmsten U. Simultaneous urethrocystometry and urethral pressure profile measurement with a new technique. Acta Obstet Gynecol Scand 1975;54:385. Asmussen M, Ulmsten U. The role of urethral pressure profile measurement in female patients with urethral carcinoma. Ann Chir Gynecol 1982;71:122. Baker KR, Drutz HP. Retropubic colpourethropexy: clinical and urodynamic evaluation in 289 cases. Int Urogynecol J 1991;2:196. Bhatia NN, McCarthy TA, Ostergard DR. Urethral pressure profiles of women with diverticula. Obstet Gynecol 1981;58:375. Blaivas JG, Olsson CA. Stress incontinence: classification and surgical approach. J Urol 1988;139:727. Bonney V. On diurnal incontinence of urine in women. J Obstet Gynaecol Br Emp 1923;30:358. Bowen LW, Sand PK, Ostergard DR. Unsuccessful Burch retropubic urethropexy: a case controlled urodynamic study. Am J Obstet Gynecol 1989;160:452. Brown M, Wickham JE. The urethral pressure profile. Br J Urol 1969;41:211. Bump RC, Copeland WE, Hurt WG, et al. Dynamic urethral pressure profilometry pressure transmission ratio determinations in stress-incontinent and stress-continent subjects. Am J Obstet Gynecol 1988;159:749. 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. Bump RC, Hurt WG, Addison WA, et al. and the Continence Program for Women Research Group. Reliability and correlation of measurements during and after bladder neck surgery. Br J Urol 1998;82:628–633. Cardozo L. Urogynecology. Churchill Livingstone, New York, 1997. Edwards L, Malvern J. The urethral pressure profile: theoretical considerations and clinical applications. Br J Urol 1974;46:325. Enhorning G, Miller ER, Hinman F. Urethral closure studies with cine roentgenography and bladder urethral recording. Surg Gynecol Obstet 1964;118:507. Fantl AJ, Hurt WG, Bump RC, et al. Urethral axis and sphincteric function. Am J Obstet Gynecol 1986;155:554. Farghaly SA, Shah J, Worth P. The value of transmission-pressure ratio in the assessment of female stress incontinence. Arch Gynecol 1985;237(Suppl):366 (abstr 14.42.01). Ghoneim MA, Gottembourg JL, Freton J, et al. Urethral pressure profile. Standardization of technique and study of reproducibility. Urology 1975;5:632. Haeusler G, Tempfer C, Heinzi H, et al. Value of urethral pressure profilometry in the female incontinent patient: a prospective trial with an 8channel urethral catheter. Urology 1998;52:1113–1117. Hilton P. Unstable urethral pressure: toward a more relevant definition. Neurourol Urodyn 1988;6:411. Hilton P, Stanton SL. A clinical and urodynamic evaluation of the Burch colposuspension for genuine stress incontinence. Br J Obstet Gynaecol 1983;90:934. Horbach NS, Blanco JS, Ostergard DR, et al: A suburethral sling procedure with polytetrafluoroethylene for the treatment of genuine stress incontinence in patients with low urethral closure pressure. Obstet Gynecol 1988;71:648. Karlson S. Experimental studies in functioning of the female urinary bladder and urethra. Acta Obstet Gynecol Scand 1953;32:285. Kauppila A, Penttinen J, Haggman VM. Six-microtransducer catheter connected to computer in evaluation of urethral closure function of women. Urology 1989;33:159. Koonings PP, Bergman A, Ballard CA. Low urethral pressure and stress urinary incontinence in women: risk factor for failed retropubic surgical procedure. Urology 1990;36:245. Kujansuu E. The effect of pelvic floor exercises on urethral function in female stress urinary incontinence: a urodynamic study. Ann Chir Gynecol 1982;72:28. Kulseng-Hanssen S. Prevalence and pattern of unstable urethral pressure in one hundred seventy-four gynecologic patients referred for urodynamic investigation. Am J Obstet Gynecol 1983;146:895. McGuire EJ. Urodynamics findings in patients after failure of stress incontinence operations. Prog Clin Biol Res 1981;78:351. McGuire EJ, Lytton B, Pepe V, et al. Stress urinary incontinence. Obstet Gynecol 1976;47:255. Messelink EJ, Dabholwala NF, Vrij V, et al. Multichannel urethral pressure profiles: reproducibility and three-dimensional representation. J Endourol 1997;11:211–214.
Myers DL, Lasala CA, Hogan JW, et al. The effect of posterior wall support defects on urodynamic indices in stress urinary incontinence. Obstet Gynecol 1998;91:710–714. Millar HD, Baker LE. Stable ultraminiature catheter-tip pressure transducer. Med Biol Eng 1973;11:86. O’Donnell PD. Urinary Incontinence. Mosby, St. Louis, 1997. Plevnik S. Model of the proximal urethra: measurement of the urethral stress profile. Urol Int 1976;31:23. Quadri G, Magatti F, Belloni C, et al. Marshall-Marchetti-Krantz urethropexy and Burch colposuspension for stress urinary incontinence in women with low pressure and hypermobility of the urethra: early results of a prospective randomized clinical trial. Am J Obstet Gynecol 1999;181:12–18. Richardson DA, Ramahi A, Chaiss E. Surgical management of stress incontinence in patients with low urethral pressure. Gynecol Obstet Invest 1991;31:106–109. Richardson DA. Value of the cough pressure profile in the evaluation of patients with stress incontinence. Am J Obstet Gynecol 1986;155:808. Rosenzweig BA, Bhatia NN, Nelson AL. Dynamic urethral pressure profilometry pressure transmission ratio: what do the numbers really mean? Obstet Gynecol 1991;77:586. Rud T. Urethral pressure profile in continent women from childhood to old age. Acta Obstet Gynecol Scand 1980;59:331. Sand PK, Bowen LW, Ostergard DR. Uninhibited urethral relaxation: an unusual cause of incontinence. Obstet Gynecol 1986;68:645. Sand PK, Bowen LW, Panganiban R, et al. The low pressure urethra as a factor in failed retropubic urethropexy. Obstet Gynecol 1987;69:399. 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;182:30–34. Schick E. Objective assessment of resistance of female urethra to stress. Urology 1985;26:518. Summitt RL, Stovall TG. Urethral diverticula evaluation by urethral pressure profilometry, cystourethroscopy, and voiding cystourethrogram. Obstet Gynecol 1992;80(4):695. Swift SE, Rust PF, Ostergard DR. Intrasubject variability of the pressuretransmission ratio in patients with genuine stress incontinence. Int Urogynecol J Pelvic Floor Dysfunct 1996;7:312–316. Tanagho EA, Meyers FH, Smith DR. Urethral resistance: its components and implications. Invest Urol 1969;7:135. Tapp AJ, Cardozo L, Hills B, et al. Who benefits from physiotherapy? Neurourol Urodyn 1988;7:259. Tapp AJ, Cardozo L, Versi E, et al. The prevalence of variation of resting urethral pressure in women and its association with lower urinary tract function. Br J Urol 1988;61:314. Tapp AJ, Hills B, Cardozo L. Randomized study comparing pelvic floor physiotherapy with the Burch colposuspension. Neurourol Urodyn 1989;8:356. Ulmsten U, Hendriksson L, Iosif S. The unstable female urethra. Am J Obstet Gynecol 1982;144:93. Versi E. Discriminant analysis of urethral pressure profilometry data for the diagnosis of genuine stress incontinence. Br J Obstet Gynaecol 1990;97:251. Versi E, Cardozo L. Urethral instability: diagnosis based on variations of the maximum urethral pressure in normal climacteric women. Neurourol Urodyn 1986;5:535. Versi E, Cardozo L, Brincat M, et al. Correlation of urethral physiology and skin collagen in postmenopausal women. Br J Obstet Gynaecol 1988;95:147. Versi E, Cardozo L, Studd J. Distal urethral compensatory mechanisms in women with an incompetent bladder neck who remain continent, and the effect of the menopause. Neurourol Urodyn 1990;9:579. Ward GH, Hosker GL. The anisotropic nature of urethral occlusive forces. Br J Obstet Gynaecol 1985;92:1279. Weber AM. Is urethral pressure profilometry a useful diagnostic test for stress urinary incontinence? Obstet Gynecol Surv 2001;58:720–735. Weil A, Reyes H, Bischoff P, et al. Modification of urethral rest and stress profiles after different types of surgery for urinary stress incontinence. Br J Obstet Gynaecol 1984;91:46.
LEAK POINT PRESSURES Bump RC, Elser DM, Theofrastous JP, et al. 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.
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Cummings JM, Boulier JA, Parra RO, Wozniak-Petrofsky J. Leak point pressures in women with urinary stress incontinence: correlation with patient history. J Urol 1997;157:818–820. Decter RM, Harpster L. Pitfalls in determination of leak point pressure. J Urol 1992;148:588. Gray M, King CJ. Urodynamic evaluation of the intrinsically incompetent sphincter. J Urol Nurs 1993;13:67. Howard D, Miller JM, DeLancey OL, Ashton-Miller JA. Differential effects of cough, Valsalva, and continence status on vesical neck movement. Obstet Gynecol 2000;95:535–540. McCormack M, Pike J, Kiruluta G. Leak point of incontinence: a measure of the interaction between outlet resistance and bladder capacity. J Urol 1993;150:1452. McGuire EJ, Fitzpatrick CC, Wan J, et al. Clinical assessment of urethral sphincter function. J Urol 1993;150:1452. McGuire EJ, Woodside JR, Bordern TA, et al. Prognostic value of urodynamic testing in myelodysplastic patients. J Urol 1981;126:205. McLennan MT, Bent AE. Supine empty stress test as a predictor of low Valsalva leak point pressure. Neurourol Urodyn 1998;17(2):121–127. McLennan MT, Melick CE, Bent AE. Leak-point pressure clinical application of values at two different volumes. Int Urogynecol J 2000;11:136–141. Miklos JR, Sze EH, Karram MM. A critical appraisal of methods of measuring leak point pressures in women with stress incontinence. Obstet Gynecol 1995;86:86. Nitti VW, Combs AJ. Correlation of Valsalva leak point pressure with subjective degree of stress urinary incontinence in women. J Urol 1996;155:281. Noblett KL, Jensen JK, Ostergard DR. The relationship of body mass index to intra-abdominal pressure as measured by multichannel cystometry. Int Urogynecol J Pelvic Floor Dysfunct 1997;8:323–326.
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O’Connell HE, McGuire EJ. Leak point pressure. In O’Donnell PD, ed. Urinary Incontinence. Mosby, St. Louis, 1997. Siltberg H, Larsson G, Victor A. Cough-induced leak-point pressure?a valid measure for assessing treatment in women with stress incontinence. Acta Obstet Gynecol Scand 1998;77:1000–1007. Sultana CJ. Urethral closure pressure and leak-point pressure in incontinent women. Obstet Gynecol 1995;86:839. Swift SE, Ostergard DR. A comparison of stress-leak-point pressure in incontinent women. Obstet Gynecol 1995a;85:704. Swift SE, Ostergard DR. Evaluation of current urodynamic test methods in the diagnosis of genuine stress urine incontinence. Obstet Gynecol 1995b;86:85. Swift SE, Utrie JW. The need for standardization of the Valsalva leak point pressure. Int Urogynecol J Pelvic Floor Dysfunct 1996;7:227. Theofrastous JP, Bump RC, Elser DM, et al. and the Continence Program for Women Research Group. Correlation of urodynamic measures of urethral resistance with clinical measures of incontinence severity in women with pure genuine stress incontinence. Am J Obstet Gynecol 1995;173:407–414. Theofrastous JP, Cundiff GW, Harris RI, Bump RC. The effect of vesical volume on Valsalva leak-point pressures in women with genuine stress urinary incontinence. Obstet Gynecol 1996;7:13–19. Wan J, McGuire EJ, Bloom DA, et al. Stress leak point pressure: a diagnostic tool for incontinent children. J Urol 1993;150:700–702. Weber AM. Leak point pressure measurement and stress urinary incontinence: a review. Curr Womens Health Rep 2001;1:45–52.
Urodynamics: Voiding Studies
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Mickey M. Karram
UROFLOWMETRY 102 Definitions and Normal Parameters Factors Affecting Flow Rates 103 Interpretation 104 Clinical Applicability 106 PRESSURE-FLOW STUDIES 106 Definitions 106 Methodology 107 Interpretation 107 Clinical Applicability 111 The Pressure-Flow Plot 111 COMBINED STUDIES 112
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Normal micturition depends on a multitude of complex factors that must be coordinated to facilitate bladder emptying. Voiding consists of a combination of bladder contraction and outlet relaxation so that emptying is rapid and complete. The neurophysiologic mechanisms involved in micturition are complex and have been discussed elsewhere. Disturbances in any of the connections in the voiding mechanism can produce abnormal micturition. Various urodynamic techniques have been devised to study voiding. Uroflowmetry is the simplest and most commonly used of these investigations. Drake described one of the first clinically useful urinary flowmeters in 1948. A kymograph was attached to a receptacle for the voided urine and rotated at a known speed, and a tracing of voided urine volume against time was obtained. Drake was the first to record average flow rates in men and noted that flow rates increased significantly with increasing volumes. In 1956 von Garrelts described the first electronic urine flowmeters, which consisted of a tall urine-collecting cylinder with a pressure transducer in the base. The pressure transducer measured the pressure exerted by an increase in the column of urine as the patient voided. Because of the direct relationship between the volume voided and the pressure recorded, von Garrelts was able to produce electronically a direct recording of urine flow rate.
UROFLOWMETRY Uroflowmetry, or the measure of urine volume voided over time, is a simple and noninvasive test that is performed by
asking the patient to void in a special commode. Urine is funneled into a flowmeter that records volume versus time (Fig. 8-1). A representative flow pattern is important to obtain, and the pattern depends on several factors. First, the patient should understand the simple nature of the test and be as relaxed as possible to have a normal desire to void at the time of the study. Second, the patient should be allowed to void in private because tension and embarrassment can artificially reduce the maximum flow achieved. Third, if there is doubt about the accuracy of the test, it is important to ask the patient whether he or she felt it was representative. If the patient believes that the test was not typical, it should be repeated.
Definitions and Normal Parameters Urine flow may be described in terms of flow rate and flow pattern and may be continuous or intermittent. Flow rate (Q) is defined as the volume of fluid expelled via the urethra per unit time and is expressed in milliliters per second (mL/sec). Certain information is necessary in interpreting the tracing, including the volume voided, the environment and position in which the patient passed urine, whether the bladder filled naturally or by a catheter, and whether diuresis was stimulated by fluid or diuretics. If filling was by catheter, the type of fluid used should be stated; it should also be stated whether the flow study was part of another investigation. Maximum flow rate (Qmax) is the maximum measured value of the flow rate after correction for artifacts. Voided volume is the total volume expelled via the urethra. Flow time (Qtime) is the time over which measurable flow occurs. Average flow rate (Qave) is voided volume divided by flow time. The average flow should be interpreted with caution if flow is interrupted or if there is a terminal dribble. Time to maximum flow is the elapsed time from onset of flow to maximum flow. Drach et al. (1979) observed that the mean maximum flow rate in asymptomatic women was 26 ± 14 mL/sec, with an average voided volume of 224 mL. Flow time, maximum flow rate, and average flow rate all increase with corresponding increases in volume voided. Flow rates are higher in women than in men and in pregnant versus nonpregnant women. Little variation in flow rates with menstrual cycles, menopause, or increasing age has been reported.
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detrusor force and urethral resistance, and because these factors may vary considerably and still produce adequate bladder emptying, a precise definition of a normal or a low flow rate cannot be made. The maximum urinary flow rate (MUFR) and average urinary flow rate (AUFR) are the two most important uroflowmetry parameters. Post-void residual urine is the volume of urine remaining in the bladder immediately after the completion of micturition. It is most accurately measured via a transurethral catheter, but can also be estimated by ultrasound or radiographic studies. A consistently high residual urine volume generally indicates increased outlet resistance, decreased bladder contractility, or both. Absent post-void residual urine is compatible with normal urinary tract function, but it can also exist in the presence of significant filling and storage disorders (incontinence) or with disorders of emptying, in which the intravesical pressure is sufficient to overcome increased outlet resistance. What constitutes an abnormally high residual urine volume is not universally established. Previous investigators empirically have chosen volumes of 50 or 100 mL to indicate normal residual urine volumes. However, the residual urine volume is best stated only in the context of the total voided volume. Normality should be described as a percentage of the total voided volume. We believe that most asymptomatic women should void spontaneously at least 80% of their total intravesical volume.
Factors Affecting Flow Rates
Figure 8-1 flowmetry.
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Figure 8-2
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Graphic representation of normal uroflow curve.
Most experts agree that one can consider a study normal if the patient voids at least 200 mL over 15 to 20 seconds, and it is recorded as a smooth single curve with a maximum flow rate greater than 20 mL/sec (Fig. 8-2). Maximum flow rates of less than 15 mL/sec, with a voided volume greater than 200 mL, are generally considered abnormal. However, because flow rate is determined by the relationship between
The clinical usefulness of uroflowmetry has been hampered by the lack of absolute values defining normal limits. These normal limits would need to be over a wide range of voided volumes ideally in the form of nomograms. Haylen et al. (1989) performed uroflowmetry on 249 female volunteers between ages 16 and 63. Uroflowmetry was performed on each woman in a completely private environment, and a second uroflow study was obtained in 46 of those women. The MUFR and the AUFR of the first voids were compared with respective voided volumes. By using statistical formulations of both voided volumes and urine flow rates, relationships between the two variables were obtained. This allowed the construction of nomograms that are shown in Figure 8-3. The study also showed that repetitive voiding does not seem to have an effect on flow rates (Fig. 8-4). Fantl et al. (1983) found no significant difference between the first and up to the sixth void in the 60 women who were tested. The use of nomograms overcomes the dangers of referencing flow rates to any one voided volume. A maximum flow rate of 15 mL/sec might fall just within the fifth centile curve at 200 mL voided volume, although well below the same curve at 400 mL. The previously described nomograms refer to free flowmetry voids and are not applicable to flow rates obtained during a pressure-flow study, because all urethral catheters can be expected to have the effect of decreasing urine flow rates for the equivalent voided volume. In 1999 Haylen et al. completed a further study of 250 women who were consecutive referrals for urogynecologic assessment, which included urodynamics secondary to symptoms of lower urinary tract dysfunction. Flow data for these women were converted to centiles from the Liverpool nomograms. They noted a decreased flow rate in symptomatic women,
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in general, and specifically in women with genital prolapse. Also, the data have shown that women who have undergone a hysterectomy have lower flow rates. In contrast to asymptomatic women, there is a decline in flow rates with age, and final urodynamic diagnosis shows that women with various combinations of stress incontinence, overactive bladder, or voiding dysfunction have flow rates that are significantly different than those of asymptomatic women.
Curve patterns refer to the configuration of the uroflowmetric curve. Continuous flow that shows a rapidly increasing flow rate that reaches the maximum within one third of the total voiding time is usually considered normal (see Fig. 8-2; Fig. 8-5, A). Figure 8-5, B demonstrates what has been termed a superflow pattern in which there is a very rapid acceleration to a high MUFR. Flow is considered intermittent when the flow rate drops and subsequently increases. Intermittent flow rates are described as multiple-peak patterns when there is a downward deflection of the flow rate that does not reach 2 mL/ sec (Fig. 8-5, C). When the downward deflection of the flow rate reaches 2 mL/sec or less (Fig. 8-5, D), an interrupted pattern occurs. Uroflowmetric parameters can be obtained from multiple peak patterns by reconstructing the curve, as shown in Figure 8-6. The peak flow rate is determined by the highest horizontal segment that has a duration of at least 1 second. The peak flow rate is then connected to an ascending and descending limb. Deflections from the reconstructed curve are analyzed individually. Uroflowmetric parameters on curves with interrupted flow patterns are usually not estimated. Obstructed voiding patterns are much less common in women than in men and usually produce a low, flat tracing (Fig. 8-5, E). Abnormal flow tracings caused by detrusor underactivity with abdominal straining (see Fig. 8-5, D) or by intermittent urethral sphincter activity (see Fig. 8-5, C) are characterized by slow changes in flow rate, producing a wavelike tracing. Each rise or fall in flow rate represents either a contraction of the abdominal and diaphragmatic muscles or a contraction of the external striated sphincter. Abnormal uroflowmetric parameters can occur secondarily to factors that affect detrusor contractility, urethral resistance, or both.
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Figure 8-5 ■ Graphic representation of various uroflow patterns. A. Normal curve; voided volume of 145 mL; MUFR 23 mL/sec. B. Superflow pattern; voided volume of 330 mL; MUFR 49 mL/sec. C. Intermittent flow rate with multiple peak pattern. This tracing is characteristic of voluntary urethral sphincter activity. D. Intermittent flow rate with interrupted pattern. This is a characteristic pattern seen when abdominal pressure is used to expel urine. E. Reduced urine flow rate secondary to detrusor outflow obstruction.
Figure 8-6 ■ Uroflowmetric curve with multiple-peak pattern. Qmax, Maximum flow rate; TQmax, time to maximum flow rate; FT, flow time. (Adapted from Fantl AJ, Smith PJ, Schneider V, et al. Am J Obstet Gynecol 1983;145:1017, with permission.)
Detrusor contractility can be affected by neuropathic lesions, pharmacologic manipulation, intrinsic detrusor muscle or bladder wall dysfunction, or psychogenic inhibition. Urethral resistance can be altered by tissue trophic changes producing atrophy or fibrosis, drug effects such as α-adrenergic stimulators or blockers, neuropathic striated muscle contraction, pain or fear, and urethral axis distortion secondary to severe pelvic organ prolapse. Outlet obstruction secondary to an intraurethral lesion or stricture is exceedingly rare in women. Extraurethral lesions, such as vaginal masses or cysts, and large enterocele or rectocele may externally compress the urethra, resulting in obstructed voiding. Detrusor-external sphincter dyssynergia is a condition in which there is lack of coordination between the detrusor muscle and the external striated urethral sphincter. This leads to obstructed voiding and is always secondary to a neurologic lesion, most classically high spinal cord trauma. In the
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nervous and anxious but neurologically normal patient, the urethra may be closed by pelvic floor contracture. Urethral closure may be due to contraction of the intraurethral striated muscle or a contraction of the pelvic floor musculature. This condition has been termed detrusor sphincter pseudodyssynergia.
Clinical Applicability Flow studies are much less useful in women than in men. Over half of cases of lower urinary tract dysfunction in men are related to outflow obstruction, whereas only about 4% of cases of lower urinary tract dysfunction in women are related to voiding problems. Nevertheless, uroflowmetry is a simple urodynamic investigation that is useful as a preliminary screening test to distinguish patients who need more extensive studies from those who do not. Uroflowmetry is also an integral part of the full urodynamic studies performed for more complex problems. Some clinical situations in which spontaneous uroflowmetry may be useful are briefly discussed here. 1. Symptoms suggestive of voiding dysfunction: If uroflow measures are normal in patients complaining of symptoms consistent with voiding difficulty, further investigation is unnecessary. Abnormal flow rates may require further urodynamic testing. 2. Frequency and urgency syndromes: Determining the urodynamic abnormality that is responsible for the symptom complex of frequency, nocturia, urgency, and urge incontinence is often necessary. Flow studies are only preliminary to cystometry in this situation. Flow studies can be also used to evaluate treatment response. 3. Before pelvic surgery: Stanton et al. (1983) showed that symptoms are an unreliable guide to the presence of voiding difficulty. They recommended that women who undergo pelvic surgery, particularly suprapubic procedures for incontinence and radical pelvic surgery, and those who are elderly, have neurologic disease, or have had past pelvic surgery should have uroflowmetry performed because it may unmask preoperative voiding dysfunction or predict postoperative voiding dysfunction. On the other hand, Bhatia and Bergman (1986) noted that neither abnormal peak flow rates (defined as less than 20 mL/sec during uroflowmetry with voided volumes greater than 200 mL) nor high post-void residual urine volumes were predictive of prolonged postoperative voiding difficulties in patients who undergo surgery for stress incontinence. 4. Neurologic disease: When neurologic disease affects the lower urinary tract, various degrees of voiding dysfunction can result. Uroflowmetry is preliminary to more detailed urodynamic tests and, at times, can be helpful in the diagnosis, management, and prognosis of these patients.
contractile properties of the detrusor and on the volume of fluid in the bladder. A low flow rate may be associated with a high voiding pressure or a below-normal voiding pressure. Similarly, the finding of a normal flow rate does not exclude bladder outlet obstruction because normal flow may be maintained by a high voiding pressure. Some women have normal flow rates in the absence of a detrusor contraction. This may be because sphincteric relaxation, either alone or assisted by increased intra-abdominal pressure from straining, is sufficient to produce a normal flow rate. Pressure-flow studies are essential for a complete functional classification of lower urinary tract disorders and an objective assessment of the basis of a patient’s voiding dysfunction.
Definitions The following are definitions of standardized terminology proposed by the International Continence Society (ICS) (Fig. 8-7). ●
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Premicturition pressure is the intravesical pressure recorded immediately before the initial isovolumetric contraction. It should be the same as the resting pressure at maximum cystometric capacity. Opening pressure is the pressure recorded at the onset of measured urine flow. A delay of approximately 0.5 to 1 second occurs in the recording of flow because of the time taken for urine to reach the flowmeter.
PRESSURE-FLOW STUDIES Because urine flow studies can provide only limited information, pressure-flow studies represent a natural progression. Flow rate depends on both the outlet resistance and the
Figure 8-7 ■ International Continence Society terminology and specific parameters for pressure-flow studies (see text). (From Karram MM. Urodynamics. In Benson JT, ed. Female Pelvic Floor Disorders: Investigation and Management. Norton Medical Books, New York, 1992, with permission.)
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Opening time is the elapsed time from initial rise in detrusor pressure to onset of flow. Opening time is the initial isovolumetric contraction period of micturition. Maximum voiding pressure is the maximum value of the measured pressure during voiding. Pressure at maximum flow is the lowest pressure recorded at the time of maximum flow. Any delay in the recording of flow rate must be allowed for. Contraction pressure at maximum flow is the difference between the pressure at maximum flow and the premicturition pressure. Closing pressure is the pressure at the end of measured flow. After contraction describes the common findings of a pressure increase after flow ceases. The etiology and significance of this event are unknown. To formalize the relationship of pressure and flow, various urethral resistance factors have been proposed. Initially, urethral resistance (UR) was defined as UR = Pressure/Qmax.2 However, this calculation of resistance fell into dispute largely because it was based on the hydrodynamics of laminar flow through rigid straight tubes. In reality, the urethra is neither rigid nor straight, and flow is often turbulent not laminar. In 1987 the ICS recommended that pressure-flow data be presented graphically, plotting one quantity against the other (Rowan et al., 1987).
Methodology These studies are usually performed after a cystometric evaluation. In most patients it is clear when bladder filling should be stopped. However, if the patient has little sensation, it is important to use the functional bladder capacity from the frequency-volume chart as a guide to cystometric capacity. At this point, if a separate filling catheter is being used, it is removed and the intravesical catheter is left in place. An intravaginal or intrarectal catheter records intra-abdominal pressure to assess whether the patient uses a Valsalva maneuver to void and to electronically derive true detrusor pressure. Thus, these studies involve the monitoring of abdominal, intravesical, and true detrusor pressure synchronously with flow. External sphincter electromyographic (EMG) activity, as well as urethral pressure, may also be measured. To ensure that proper pressure transmission is occurring, the patient should be asked to cough before being allowed to void. With the patient in a sitting position, she is then instructed to void to completion if possible (Fig. 8-8). Respecting the patient’s privacy during the voiding phase is important. Few women are able to void in the presence of others, so it may be necessary for the practitioner to leave the room for her to initiate voiding. Once flow is initiated, the patient can be asked to interrupt the stream suddenly (stop test). This test attempts to establish voluntary control of micturition and obtains isometric detrusor pressure.
Interpretation Pressure-flow studies are invasive because the patient is asked to void around catheters, sometimes with EMG needles in
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Figure 8-8 ■ Technique for performing pressure-flow studies. The patient must be able to void around the catheters.
place. Appreciating the limitations of pressure-flow studies is important, as well as the differences between the patient’s performance during urodynamic testing and her normal voiding. The best way to judge this is by asking the patient and by comparing the noninstrumented urine flow rate with the flow rate obtained from the pressure-flow study. Voiding in a urodynamic laboratory can be affected by various factors. It has been estimated that approximately 30% of women who void without problems at home are unable to void on command in the urodynamic laboratory, which is hardly surprising because they are surrounded by complex equipment, have catheters in their bladder and vagina or rectum, and are usually being observed by strangers. Fast-filling or overfilling of the bladder may make normal voiding difficult. Studies that compared ambulatory urodynamics (natural bladder filling) with conventional urodynamics show that voiding pressures are higher with natural filling. This implies that the detrusor may be incompletely stimulated, partially inhibited, or mechanically less efficient if it is artificially filled, overfilled, or filled too fast. During the voiding phase, the detrusor muscle may be normal, acontractile, or underactive. Normal voiding is usually achieved by a voluntarily initiated continuous detrusor contraction that is sustained and can be suppressed. An underactive detrusor during micturition implies that the detrusor contraction is of inadequate magnitude or duration (or both) to effect bladder emptying within a normal time span. Detrusor areflexia is defined as acontractility caused by an abnormality of nervous control and denotes the complete absence of a centrally coordinated contraction. During voiding, urethral function may be normal or abnormal. A normal urethra opens during voiding and is continuously relaxed to allow the bladder to be emptied at a normal pressure. Abnormal urethral function may be secondary to urethral overactivity or a mechanical obstruction, such as a urethral stricture or tumor. Bladder outlet obstruction for whatever reason is characterized by increased detrusor pressure and reduced urine flow rate, seen by observing the synchronous values of flow rate and detrusor pressure during voiding. In mechanical obstruction, which is rare in women, the voiding pressures are constantly elevated. If the obstruction is caused by urethral overactivity, the voiding
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pressures may fluctuate. Urethral overactivity is characterized by the urethra contracting during voiding or failing to relax. In detrusor-sphincter dyssynergia, the patient’s phasic contractions of the intrinsic urethral striated muscle are simultaneous with the detrusor contraction. This produces a very high voiding pressure and an interrupted flow. The urodynamic characteristic of this type of urethral overactivity is a fall in flow rate accompanied by a rising detrusor pressure that then falls when the urethra relaxes, leading to a resumption of urine flow. Another form of urethral overactivity is
Table 8-1
■
called dysfunctional voiding, most commonly seen in children who are neurologically normal but complain of urinary incontinence or recurrent infections. The interrupted flow in these children is caused by pelvic floor overactivity rather than contractions of the intrinsic striated muscle. Depending on age, menopausal status, total voided volume, and the presence or absence of lower urinary tract dysfunction, women who are neurologically intact void by any combination of a detrusor contraction, abdominal straining, and urethral relaxation (Table 8-1 and Figs. 8-9 and 8-10).
Potential Voiding Mechanisms on Pressure-Flow Studies in Neurologically Intact Women
Urethral Relaxation
Bladder Contraction
Abdominal Straining
Present Present Present Present
Absent Present Absent Present
Absent Absent Present Present
Figure 8-9 ■ Pressure-flow study in a patient who voids with urethral relaxation and bladder contraction. Note minimal Valsalva effort.
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Figure 8-10 ■ Pressure-flow study in a patient who voids with urethral relaxation and Valsalva maneuver. Note that bladder contraction is absent.
Whether abdominal straining that occurs during a pressure-flow study is real or artifactually induced by the surroundings and presence of indwelling catheters is difficult to ascertain. The patient should always be asked to void normally and in as relaxed a way as possible. If the patient has an acontractile or areflexic detrusor, voiding can be achieved only by straining (see Fig. 8-10). If the detrusor contracts during voiding but the patient also strains, the tracing is more difficult to interpret. Understanding precisely what effect straining has on urine flow is also difficult to determine. In patients without obstruction, straining increases flow, but it does not produce the same increase in flow as that achieved by a detrusor pressure rise of the same magnitude. However, in obstructed patients, straining does not increase flow.
Although pressure-flow studies are an established and accepted urodynamic modality, what constitutes a normal voiding mechanism is incompletely understood, and the normal range for detrusor pressure during voiding in women has not been scientifically established. Most of the previously published literature has been derived from male subjects in whom pressures are abnormally high secondary to outflow obstruction. To better evaluate the detrusor during voiding, one may perform a stop-flow test (Fig. 8-11). In many patients, if voiding is suddenly interrupted by sphincter action, the detrusor pressure rises rapidly. This behavior reflects a fundamental myogenic property of the contracting detrusor: a trade-off between the pressure generated and the flow delivered. The
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Figure 8-11 ■ Pressure-flow study with stop test. Note isometric rise in detrusor pressure simultaneous with stoppage of flow.
detrusor pressure attained on stopping (isometric detrusor pressure) should be a more reliable measure of detrusor contractions than the detrusor pressure during voiding, which also depends on flow rate and urethral resistance. The routine clinical use of the stop test has some disadvantages. A high isometric detrusor pressure implies a good detrusor contraction, but a low or absent rise in pressure
does not necessarily imply lack of a detrusor contraction. The detrusor contraction may be reflexly inhibited when the urethra is closed, or flow may be interrupted by inhibiting the detrusor instead of increasing outlet resistance. Also, the patient may be unable to interrupt her stream completely on command. These situations can lead to a falsely low isometric detrusor pressure. For these reasons, the test is probably
Chapter 8
The main clinical use of pressure-flow studies is to document the mechanism of abnormal voiding. If a patient has symptoms and signs of abnormal voiding, has low flow rates, and voids with a high detrusor pressure, she is probably voiding against an obstruction. On the other hand, if a patient has low flow rates and voids with minimal or no rise in detrusor pressure, her voiding dysfunction is probably secondary to an acontractile or underactive detrusor (Fig. 8-12). The limiting factor is that no clear cutoff exists between normal and abnormally high detrusor pressure during voiding. The clinical setting in which pressure-flow studies are most useful in women is in the patient who has undergone pelvic surgery and has developed postoperative voiding dysfunction. The dysfunction may be secondary to denervation, resulting in an underactive or acontractile detrusor, but, more commonly, the dysfunction is secondary to increased outlet resistance produced from the anti-incontinence surgery. Voiding dysfunction or retention occurs in 3% to 20% of patients after various operations to correct stress incontinence. Whether urethrolysis or a takedown of the sling will restore normal voiding is always a clinical dilemma. Filling cystometry and pressure-flow studies are helpful in this setting. If the patient is able to void around a catheter and is noted to have a high detrusor pressure with a low flow rate, the patient is obstructed, and relieving the obstruction should improve voiding (Nitti & Raz, 1994). Bhatia and Bergman (1984) performed pressure-flow studies on 30 patients with stress incontinence before retropubic urethropexy. They noted that no patient who voided preoperatively with a detrusor contraction greater than 15 cm H2O required prolonged bladder drainage (more than 7 days). Eighty-four percent of patients who used significant abdominal straining in addition to urethral relaxation during
The Pressure-Flow Plot The voiding pressure-flow plot is a record of the voiding phase of the filling and voiding cystometrogram. These graphs plot the detrusor pressure during voiding and associated flow rate over time (typically delayed chronologically to allow synchrony between pressure and flow). The plot is commonly used to assess the presence or absence of significant bladder outlet obstruction in men. A schematic pressure floor tracing presented stage by stage is shown in Figure 8-13. The pressure-flow plot illustrates the relationship between the contracting detrusor, the driving force to
P (cmH2O)
Clinical Applicability
70 60 50 40 30 20 10 0
(i) (ii)
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2
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6
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10
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C
Figure 8-13 The pressure-flow (p-Q) plot. A. Start of micturition: (i) detrusor pressure rises; (ii) sphincter opens and flow starts (Pdet, open). B. Maximum flow (Qmax): (i) pressure and flow are synchronous; the urethral sphincter is maximally dilated; (ii) the “passive” phase of micturition begins. C. End of micturition: (i) micturition ceases at the lowest detrusor pressure that allows flow Pdet, close. (Adapted from Wagg AS, Malone-Lee JG. Pressure flow point analysis and voiding inefficiency in women with lower urinary tract symptoms. Neuro Urol Urodyn 1997;16:435.) ■
Figure 8-12 ■ Recommended presentation of pressure-flow relationships for normal and abnormal voiding. (From Walters MD. Mechanism of continence and voiding, with International Continence Society classification of dysfunction. Obstet Gynecol Clin North Am 1989;16:773, with permission.)
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voiding required prolonged postoperative catheterization. In another study, Kobak et al. (2001) found that higher preoperative post-void residual volumes predicted longer times to voiding after anti-incontinence surgery but not detrusor pressure or abdominal straining or pressure-flow study. Thus, voiding studies may be useful prognostically to predict difficulty in postoperative voiding in patients undergoing anti-incontinence surgery, although their exact prognostic value remains undetermined.
P (cmH2O)
more accurate when the urethra is physically occluded with a catheter or by elevation of the anterior vaginal wall.
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empty the bladder, and the modulation of that force by the outflow tract. Analysis of the pressure-flow plot requires an understanding of the muscle mechanisms involved in bladder-emptying and knowledge of the properties of the urethra during voiding. The use of nomograms developed for the identification of outlet tract obstruction in men is most likely not valid in women. However, data are accumulating that suggest that the pressure-flow plot can give useful information about physiologic changes in urinary tract function and the variation of urethral resistance with disease and clinically useful data relating to detrusor contractile function (Wagg & Malone-Lee, 1997). Its role in women is currently not fully known, but because a significant number of women have irritative bladder symptoms, even though obvious outflow obstruction is rare, the future may show a potential for use of such a concept to further elucidate these problems.
COMBINED STUDIES Pressure-flow studies performed under fluoroscopy can be a useful diagnostic urodynamic procedure. The size of the bladder and the presence of trabeculations, bladder diverticula, and vesicoureteral reflux can be visualized. Competence of the sphincter can be assessed, and the patient’s ability to initiate and stop micturition can be observed. The site of significant outflow obstruction can usually be detected. The technique of these studies is discussed in Chapter 7. When neurogenic voiding dysfunction is present or suspected, EMG activity of the external striated sphincter should be recorded. The techniques and applications of EMG related to voiding studies are discussed in detail in Chapter 11.
SUMMARY Any condition that affects detrusor contractility or urethral resistance can impair micturition. Uroflowmetry is a simple noninvasive test that can be used to objectively document voiding dysfunction. Because it does not provide direct information on expulsive forces or outlet resistance, it is probably best considered a screening test. Pressure-flow studies provide information on detrusor and abdominal pressure. They are helpful in differentiating voiding dysfunction secondary to obstruction from that secondary to an underactive detrusor. They may also give useful information to predict postoperative voiding dysfunction after slings and urethropexy and to diagnose bladder outlet obstruction after slings. However, these tests are invasive and unpredictable; 20% to 30% of patients are not able to void around the catheters, and artifacts are difficult to assess. More research is needed to define normal voiding parameters in women and to determine the value of these tests in clinical practice.
Bibliography Abrams P. Uroflowmetry. In Stanton SL, ed. Clinical Gynecologic Urology. Mosby, St. Louis, 1984.
Abrams P, Blaivas JG, Stanton SL, et al. Sixth report on the standardization 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; Scand J Urol Nephrol 1986;20:161. Abrams P, Cardozo L, Fall M, et al. The standardization of terminology of lower urinary tract function: report from the Standardisation SubCommittee of the International Continence Society. Am J Obstet Gynecol 2002;187:116. Abrams P, Torrens M. Urine flow studies. Urol Clin North Am 1979;6:71. Backman KA. Urinary flow during micturition in normal women. Acta Chir Scand 1965;130:357. Barnick CG, Cardozo LD, Benness C. Use of routine videocystourethrography in the evaluation of female lower urinary tract dysfunction. Neurourol Urodyn 1989;8:447. Bergman A, Bhatia NN. Uroflowmetry: spontaneous versus instrumented. Am J Obstet Gynecol 1984;150:788. Bergman A, Bhatia NN. Uroflowmetry for predicting postoperative voiding difficulties in women with stress urinary incontinence. Br J Obstet Gynaecol 1985;92:835. Bhatia NN, Bergman A. Urodynamic predictability of voiding following incontinence surgery. Obstet Gynecol 1984;63:85. Bhatia NN, Bergman A. Use of preoperative uroflowmetry and simultaneous urethrocystometry for predicting risk of prolonged postoperative bladder drainage. Urology 1986;28:440. Bhatia NN, Bergman A, Karram MM. Changes in urethral resistance following incontinence surgery. Urology 1989;34:200. Busch R, Groen J. Urethral resistance is related to type of incontinence: changing etiologic concepts in female incontinence. Neurourol Urodyn 1998;17:386. Bradley WE. Urologically oriented neurological examination. In Ostergard DR, ed. Gynecologic Urology and Urodynamics, 2nd ed. Williams & Wilkins, Baltimore, 1985. Chancellor MB, Killholma P. Urodynamic evaluation of patients following spinal cord injury. Semin Urol 1992;10:83. Cucchi A. Acceleration of flow rate as a screening test for detrusor instability in women with stress incontinence. Br J Urol 1990;65:17. Diokno AC, Normolle DP, Brown MB, et al. Urodynamic tests for female geriatric urinary incontinence. Urology 1990;36:431. Drach GW, Ignatoff J, Layton T. Peak urinary flow rate: observations in female subjects and comparison to male subjects. J Urol 1979;122:215. Drake WM. The uroflowmeter: an aid to the study of lower urinary tract. J Urol 1948;59:650. Enhorning G. Simultaneous recording of intravesical and intraurethral pressure. Acta Chir Scand 1961;276(Suppl):4. Fantl AJ. Clinical uroflowmetry. In Ostergard DR, ed. Gynecologic Urology and Urodynamics, 2nd ed. Williams & Wilkins, Baltimore, 1985. Fantl AJ, Smith PJ, Schneider V, et al. Fluid weight uroflowmetry in women. Am J Obstet Gynecol 1983;145:1017. Griffiths DJ. Uses and limitations of mechanical analogies in urodynamics. Urol Clin North Am 1979;6:143. Griffiths DJ. Basics of pressure-flow studies. World J Urol 1995;13:30. Haylen BT, Ashby D, Sutherst JR, et al. Maximum and average flow rates in normal male and female populations: the Liverpool nomograms. Br J Urol 1989;64:30. Haylen BT, Parys BT, Anyaegbunam WI, et al. Urine flow rates in male and female urodynamic patients compared with Liverpool nomograms. Br J Urol 1990;65:483. Haylen BT, Law MG, Frazer MI, Schulz S. Urine flow rates and residual urine volumes in urogynecology patients. Int Urogynecol J 1999;6:378. Karl C, Gerlach R, Hannappel J, et al. Uroflow measurements: their information yield in a long-term investigation of pre- and postoperative measurements. Urol Int 1986;41:270. Kobak WH, Walters MD, Piedmonte MR. Determinants of voiding after three types of incontinence surgery: a multivariable analysis. Obstet Gynecol 2001;97:86. Massey JA, Abrams PH. Obstructed voiding in the female. Br J Urol 1988;61:36. Massey A, Abrams P. Urodynamics of the female lower urinary tract. Urol Clin North Am 1985;12:231. Meunier P. Study of micturition parameters in healthy young adults using a uroflowmetric method. Eur J Clin Inv 1983;13:25. Mundy AP. Clinical physiology of the bladder, urethra and pelvic floor. In Mundy AP, Stephenson TP, Wein AJ, eds. Urodynamics: Principles, Practice and Applications. Churchill Livingstone, New York, 1984.
Chapter 8
Nitti VW, Raz S. Obstruction following antiincontinence procedures: diagnosis and treatment with transvaginal urethrolysis. J Urol 1994;152:93. Rowan D, James ED, Kramer AE, et al. Urodynamic equipment technical aspects. J Med Eng Technol 1987;11:57. Sakakibara R, Hussein IF, Swinn MJ, et al. Flow-pressure study in patients with neurologic diseases—a preliminary report. Neuro Urol Urodyn 1998;17:304. Saxton HM. Urodynamics: the appropriate modality for the investigation of frequency, urgency, incontinence, and voiding difficulties, Radiology 1990;175:307. Schäfer W, Abrams P, Limin L, et al. Good urodynamic practices: uroflowmetry, filling, cystometry, and pressure-flow studies. Neurourol Urodyn 2002;21:261. Stanton SL, Ozsoy C, Hilton P. Voiding difficulties in the female: prevalence, clinical and urodynamic review. Obstet Gynecol 1983;61:144. Susset JG, Brissot RB, Regnier CH. The stop-flow technique: a way to measure detrusor strength. J Urol 1982;127:489. Susset JG, Picker P, Kretz M, et al. Critical evaluation of uroflometers and analysis of normal curves. J Urol 1983;109:874. Tanagho EA. Urodynamics: uroflowmetry and female voiding patterns. In Ostergard DR, ed. Gynecologic Urology and Urodynamics, 2nd ed. Williams & Wilkins, Baltimore, 1985. Tanagho EA, McCurrey E. Pressure and flow rate as related to lumen caliber and entrance configuration. J Urol 1971;105:583.
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Tanagho EA, Miller ER. Initiation of voiding. Br J Urol 1970;42:175. von Garrelts B. Analysis of micturition: a new method of recording the voiding of the bladder. Acta Chir Scand 1956;112:326. von Garrelts B, Strandell P. Continuous recording of urinary flow-rate. Scand J Urol Nephrol 1972;6:224. Wagg AS, Lieu PK, Ding YY, Malone-Lee JG. A urodynamic analysis of age associated changes in urethral function in women with lower urinary tract symptoms. J Urol 1996;156:1984. Wagg AS, Malone-Lee JG. Pressure flow plot analysis and voiding inefficiency in women with lower urinary tract symptoms. Neuro Urol Urodyn 1997;16:435. Wagg AS, Ray R, Malone-Lee JG. Pressure flow plot analysis in women with detrusor instability and genuine stress incontinence. Neuro Urol Urodyn 1995;14:439. Walter S, Olesen KP, Nordling J, et al. Bladder function in urologically normal middle aged females. Scand J Urol Nephrol 1979;13:249. Walters MD. Mechanism of continence and voiding, with International Continence Society classification of dysfunction. Obstet Gynecol Clin North Am 1989;16:773. Yalla SV, Blunt KJ, Fam BA, et al. Detrusor-urethral sphincter dyssynergia. J Urol 1977;118:1026.
Endoscopic Evaluation of the Lower Urinary Tract
9
Geoffrey W. Cundiff and Alfred E. Bent
HISTORICAL PERSPECTIVE 114 INDICATIONS 115 INSTRUMENTATION 115 Rigid Cystoscopy 115 Rigid Urethroscopy 116 Flexible Cystoscopy 116 Light Sources and Video Monitors 117 Distending Media 117 Operative Instrumentation 117 Instrument Care 117 CYSTOURETHROSCOPIC TECHNIQUE 117 Diagnostic Urethroscopy 117 Diagnostic Cystoscopy 119 Intraoperative Assessment of Lower Urinary Tract Integrity Operative Cystoscopy 120 CYSTOURETHROSCOPIC FINDINGS 120 Normal Findings 120 Pathologic Findings 121
119
HISTORICAL PERSPECTIVE The first description of an endoscopic technique for evaluating the female urethra and bladder was by Bozzini, in 1805. His invention was a cumbersome cystoscope consisting of a stand that supported different-sized hollow funnels, a candle for illumination, and a reflector to direct the light into the funnel when it was placed into the urethra. Visibility with this device was limited by both poor illumination and the tendency of the operator to burn himself if the stand was tilted for a better view. Nineteenth-century refinements to this crude instrument included the addition of a surrounding cannula and, later, a lens system to provide magnification of the field of view. The greatest drawback of the early cystoscope was poor illumination, and innovators tried multiple techniques to overcome the problem, including reflective mirrors, an alcohol lamp, a platinum wire loop, and, finally, an incandescent light source. Even with these improvements in the cystoscope and illumination, visualization was still poor
without bladder distention. Consequently, by the end of the nineteenth century, cystoscopy was considered to be nothing more than an adjunct to the established method of urethral dilation and bimanual palpation of the bladder. Kelly’s (1894) principal innovation in cystoscopy was developing a technique that provided adequate bladder distention. The Kelly cystoscope, a hollow tube without a lens, was not innovative, but his technique was. The cystoscope was introduced using an obturator, with the patient in knee-chest position. The negative intra-abdominal pressure created by this position allowed air to distend the bladder when the cystoscope was introduced. A head mirror was used to reflect an electric light into the bladder for illumination. The technique was simple but provided an excellent view. Its simplicity dramatically enhanced the accessibility of cystoscopy to all physicians. Kelly’s fame as a genitourinary surgeon, and as the founder of the Johns Hopkins Hospital residency training program in gynecology, the first in the nation, established cystoscopy as a gynecologic technique. The twentieth century provided many innovations in the cystoscope. Hopkins and Kopany (1954) introduced both a fiber-optic telescope and, later, a rod lens system, which dramatically improved light transmission and resolution. This rod lens design is the system used in today’s rigid cystoscopes. Replacement of the air chamber with a series of glass rods with optically finished ends, separated by intervening air spaces, provides a wider viewing field and permits a change in the viewing angle. The innovation of angled telescopes improved the extent of visualization and facilitated more invasive procedures. Increasingly complex instruments were developed to perform operative procedures through a cystoscope, and, gradually, general surgeons developed the subspecialty of urology around this new technology. The development of the subspecialty of urology coincided with changes in gynecology. The combination of gynecology and obstetrics into a single training program deemphasized cystoscopy in gynecologic training, and gynecologists gradually became less skilled in the technique, whereas urologists continued to develop it. The most recent development in cystoscopy is the flexible cystoscope. A flexible cystoscope takes advantage of the flexibility of the fiber-optic lens system to create a cystoscope
Chapter 9
that bends, thereby increasing the range of the field of view. Some authors report an improved view of the bladder neck using a flexible fiber cystoscope, whereas others advocate flexible cystoscopy to limit the necessary instrumentation and improve patient tolerance. Robertson (1973), the father of urogynecology, reintroduced cystoscopy to gynecology with the development of the Robertson urethroscope. He addressed the deficiencies of the cystoscope for viewing the urethra by applying the rods lens technology of the Hopkins cystoscope to a shorter straighton telescope with a nonfenestrated sheath designed specifically for viewing the urethra. He subsequently outlined a technique—dynamic urethroscopy—for evaluating incontinent women using the Robertson urethroscope. Dynamic urethroscopy offered a simple office procedure that considerably improved the diagnostic evaluation of the lower urinary tract over the alternatives of the time.
INDICATIONS Cystourethroscopy, an invaluable procedure for today’s urogynecologist, has both diagnostic and operative indications. Diagnostic indications include hematuria, lower urinary tract symptoms, urinary incontinence, urethral diverticula, and urogenital fistulas. The differential diagnosis of hematuria is extensive but falls into conditions that are primarily renal or post-renal in origin. Endoscopy is useful in the diagnosis of the post-renal conditions, including neoplasms of the bladder and urethra, urethral polyps, chronic cystitis, recurrent cystitis, interstitial cystitis, urolithiasis, and foreign bodies. The differential diagnosis for lower urinary tract symptoms is extensive, including many nebulous conditions. Possible causes include acute cystitis, chronic cystitis, trigonitis, radiation cystitis, urethral pain syndrome, urethral diverticula, urethritis, and interstitial cystitis. Other conditions that may cause similar symptoms include detrusor overactivity, urolithiasis, partial urinary retention, and moderate to severe pelvic organ prolapse. Cystourethroscopy is indicated when the presenting symptoms strongly suggest a diagnosis of urethral diverticulum, interstitial cystitis, urolithiasis, or tumor, and for patients who do not respond to initial therapy. Endoscopy should be avoided in the presence of an active urinary tract infection. The general agreement is that cystoscopy is indicated for patients complaining of persistent incontinence or voiding symptoms following incontinence surgery, but less agreement exists about the role of cystoscopy in the baseline evaluation of patients with urinary incontinence. The refinement of urodynamic evaluation over the last three decades has demonstrated the superiority of this modality for diagnosing the common causes of urinary incontinence, such as urodynamic stress incontinence and detrusor overactivity. However, although urodynamic testing excels at providing an objective assessment of lower urinary tract function, it provides little information about lower urinary tract anatomy. Cystourethroscopy contributes an anatomic assessment of the urethra and bladder that is not achieved by urodynamic tests alone. Anatomic abnormalities, such as urethral diver-
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ticula, urogenital fistulas, and intravesical foreign bodies causing detrusor overactivity, might be suspected based on history or urodynamic tests but require an anatomic assessment for confirmation. Cystourethroscopy can also reveal unsuspected neoplasia in the incontinent patient. However, in women with stress incontinence, bladder lesions are found in only about 1% of patients. The Clinical Practice Guidelines of the Agency for Health Care Policy and Research in 1996 noted that the evidence does not support the routine use of cystoscopy in the evaluation of women with simple symptoms of incontinence (Fantl et al., 1996). For many urogynecologists, cystourethroscopy also has a role in the diagnosis of intrinsic sphincteric deficiency, a condition that does not have standardized diagnostic criteria. Some advocate a single urodynamic parameter to make the diagnosis. However, in the absence of validated standard criteria for diagnosing intrinsic sphincteric deficiency, an approach that combines clinical measures of severity, urodynamic evidence of poor urethral resistance, and an anatomic evaluation of urethral coaptation seems to be warranted. Cystourethroscopy is perhaps the simplest way to achieve such an anatomic evaluation of the urethrovesical junction (UVJ). Operative indications of cystourethroscopy in the female lower urinary tract include minor operative procedures performed through an operative cystoscope and intraoperative uses. Cystoscopy is an important adjuvant to surgery of the female genitourinary system and is commonly used to (1) perform and judge coaptation during periurethral injections and suburethral sling procedures, (2) facilitate surgical repair of urinary tract fistula and urethral diverticula, (3) ensure the safe placement of suprapubic catheters, and (4) evaluate the ureters and bladder mucosa for inadvertent damage at the time of surgery.
INSTRUMENTATION Rigid Cystoscopy The three components of the rigid cystoscope include the telescope, the bridge, and the sheath (Fig. 9-1). Each component serves a different function and is available with various options to facilitate its role under different circumstances.
Figure 9-1 ■ Rigid endoscopes in urology and urogynecology. (Top to bottom) Catheter-deflecting bridge; 30-degree telescope; 70-degree telescope; cystoscope sheath with bridge; obturator.
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The telescope transmits light to the bladder cavity and an image to the viewer. Telescopes designed for cystoscopy are available with several viewing angles, including 0-degree (straight), 30-degree (forward-oblique), 70-degree (lateral), and 120-degree (retro view). The different angles facilitate the inspection of the entire bladder wall. Although the zero-degree lens is ideal for adequate urethroscopy, it is insufficient for cystoscopy. The 30-degree lens provides the best view of the bladder base and posterior wall, and the 70-degree lens permits inspection of the anterior and lateral walls. The retro view 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 elevation of the UVJ. For operative cystoscopy, the 70-degree telescope is preferable. The angled telescopes have a field marker, visible as a blackened notch at the outside of the visual field opposite the angle of deflection, that helps facilitate orientation. The cystoscope sheath provides a vehicle for introducing the telescope and distending medium into the vesical cavity. Sheaths are available in various calibers, ranging from 17 to 28 French for use in adults and smaller calibers for use in pediatrics. When placed within the sheath, the telescope, which is 15 French, only partially fills the lumen, leaving an irrigation-working channel. The smallest sheath is better tolerated for diagnostic procedures, whereas the larger calibers 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 medium and another for removal. The distal end of the cystoscope sheath is fenestrated to permit use of instrumentation in the angled field of view. The cystoscope is also beveled, opposite the fenestras, to increase the comfort of introduction of the cystoscope into the urethra. Bevels increase with the diameter of the cystoscope, and larger sheaths may require an obturator for atraumatic placement. 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 that has a deflector mechanism at the end of an inner sheath (Fig. 9-2). When placed in the cystoscope sheath, the deflector mechanism is located at the distal end of the inner sheath within the fenestra of the outer sheath. In
Figure 9-2
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Deflector at the tip of an Albarran bridge.
this location, elevation of the deflector mechanism assists the manipulation of instruments within the field of view.
Rigid Urethroscopy The rigid urethroscope is a modification of the cystoscope designed exclusively for evaluation of the urethra (Fig. 9-3). Because it is primarily a diagnostic instrument, it does not have a bridge. The telescope is shorter and has a 0-degree viewing angle, which provides a circumferential view of the urethral lumen as the mucosa in front of the urethroscope is distended by the distention medium. The 0-degree lens is essential for adequate urethroscopy. The urethroscope sheath is designed to maximize distention 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-French and 24-French calibers. If tolerated, the larger sheath is useful because it provides the best view of the urethral lumen by providing more rapid fluid flow for maximal distention.
Flexible Cystoscopy Unlike the rigid cystoscope, the flexible cystoscope combines the optical systems and irrigation-working channel in a single unit. The coated tip is 15 to 18 French in diameter and 6 to 7 cm in length; the working unit makes up half the length. The optical system consists of a single image–bearing fiber-optic bundle and two light-bearing fiber-optic bundles. The fibers of these bundles are coated parallel coherent optical fibers that transmit light even when bent. The coating of the fibers results in a somewhat granular image, and the delicate 5- to 10-μm diameter makes them susceptible to damage. Gentle handling is essential to good visualization and instrument longevity. The flexibility of the fibers permits incorporation of a distal tip–deflecting mechanism, controlled by a lever at the eyepiece, that will deflect the tip 290 degrees in a single plane. The optical fibers are fitted to a lens system that magnifies and focuses the image, and a focusing knob is located just distal to the eyepiece. The irrigation-working port enters the instrument at the eyepiece opposite the deflecting mechanism. Many urologists prefer the flexible cystoscope because of improved patient comfort, but this applies primarily to male patients. The absence of a prostate and the short length
Figure 9-3
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Rigid urethroscope.
Chapter 9
of the female urethra make rigid cystoscopy well tolerated by women. This may offset any perceived advantage of flexible cystoscopy in female patients. Moreover, several disadvantages exist with the flexible cystoscope. The flow rate of the irrigation-working channel is approximately one fourth that of a similar-sized rigid cystoscope and is further curtailed by passage of instruments down the channel. Some tip deflection is also lost with use of the instrument channel. In addition, because the view afforded by the flexible cystoscope is not as clear as that of a rigid cystoscope, greater operator skill is required to completely visualize the vesical cavity. No difference is present in the post-procedural morbidity as compared with rigid cystourethroscopy.
Light Sources and Video Monitors Any light source that provides adequate illumination via a fiber-optic cable is sufficient. A high-intensity (Xenon) light source is often recommended for the use of video monitoring or photography, but, with recent innovations, the newest cameras require less light. The cable attaches to the telescope at the eyepiece. Light cables are either fiber-optic or fluid-filled. The fluid-filled cables tend to be more expensive and more durable, although they add a slight tint to the light. Fiber-optic cables use flexible optic fibers that are comparable to those of the flexible cystoscope and are similarly prone to damage. Although all cystoscopic procedures can be performed with direct visualization through the eyepiece, video monitoring eliminates awkward positioning required for direct visualization. It permits video documentation, which facilitates teaching, and often improves patient tolerance by providing distraction during the procedure. The video camera attaches directly to the eyepiece and should be maintained in an upright orientation. Changing the direction of view is accomplished by rotating the cystoscope without moving the camera itself.
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Operative Instrumentation A wide range of instrumentation is available for use through a cystoscope. Those most pertinent to urogynecology are grasping forceps, with either a rat tooth or alligator jaws, biopsy forceps, and scissors. These instruments can be obtained in semirigid or flexible varieties and come in various diameters. A flexible monopolar ball electrode is useful for electrocautery during operative cystoscopy.
Instrument Care Blood and debris should be removed promptly from the equipment to avoid accumulation in crevices and pitting of metal surfaces. The most common method of sterilization is immersion in a 2% activated glutaraldehyde solution (Cidex; Surgikos, Inc., Arlington, TX). Cystourethroscopic equipment should be soaked for 20 minutes and then transferred to a basin of sterile water until ready for use. Longer soaks shorten the life of the telescope by deteriorating the lens system and seals. If more permanent storage is desired, the scopes are cleaned with detergent and water, rinsed, and stored. Once a week the scopes are cleaned inside and out with alcohol and super oil is used for lubrication. The irrigating ports and locking mechanisms should also be lubricated regularly.
CYSTOURETHROSCOPIC TECHNIQUE A complete evaluation of the lower urinary tract includes both urethroscopy and cystoscopy. A convenient approach begins with urethroscopy followed by cystoscopy. Diagnostic urethroscopy provides an evaluation of the urethral mucosa and UVJ. Diagnostic cystoscopy permits evaluation of the vesical cavity and ureteral function.
Diagnostic Urethroscopy Distending Media The three types of distention media are nonconductive fluids, conductive fluids, and gases. Cystourethroscopy is feasible with carbon dioxide, but most practitioners prefer to use water or saline to distend the bladder and urethra. A liquid medium prevents the carbon dioxide bubbling and washes away blood or debris that can limit visualization. Moreover, the bladder volumes achieved using a liquid medium more accurately approximate physiologic volumes. The choice of liquid medium depends on the procedure for which it is to be used. For diagnostic cystourethroscopy, sterile water is an ideal medium that is readily available and inexpensive. If absorption of a large volume of fluid into the vascular space is anticipated, an osmotic solution, such as normal saline, should be used. Similarly, if electrocautery is to be used, a nonconducting solution, such as glycine, should be used. If a liquid medium is used, the water is instilled by gravity through a standard intravenous infusion set. The bag should be placed 100 cm above the patient’s pubic symphysis to provide adequate flow.
The urethral meatus is cleansed with a disinfectant, and, with the distention medium flowing, the urethroscope is advanced 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. The mucosa is normally pink and smooth, and a posterior longitudinal ridge, the urethral crest, may be seen. When the UVJ, typically round or horseshoe-shaped, is reached, flow is stopped and the area is observed for fronds (feathery structures with a central capillary) and polyps (bulbous structures). Dynamic urethroscopy is performed after the bladder has a volume of 300 mL. The urethroscope is withdrawn until the UVJ closes one third of the way and the response of the UVJ to “hold your urine” and “squeeze your rectum” commands is evaluated. The urethroscope is then withdrawn until the UVJ is two thirds closed and its response to Valsalva maneuver and cough is observed (Fig. 9-4). The normal response is UVJ closure with all of these commands.
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Figure 9-4 ■ Evaluating urethral hypermobility using dynamic urethroscopy. A. Urethroscope is positioned to view the urethrovesical junction (window cut away to visualize the urethrovesical junction). B. As the patient coughs, the urethrovesical junction descends and opens (the urethroscope is elevated to follow the urethrovesical junction visualized through cutaway).
Chapter 9
The urethroscope is then positioned so that the UVJ is one third closed and its response to bladder filling is observed. The bladder volumes at first sensation of filling, fullness, and maximum capacity are noted. The maneuvers at the UVJ are repeated, and the patient attempts to void. If voiding occurs, the urethra opens to the meatus and water escapes around the sheath. The normal UVJ should close over the urethroscope in response to a “hold your urine” command. The urethroscope is next withdrawn while a vaginal finger massages the urethra against the scope. Exudate or diverticular openings may be seen.
Diagnostic Cystoscopy Cystoscopy is performed using a 30- or 70-degree rigid telescope with a 17-French sheath. Topical anesthetics are typically avoided during urethroscopy because they can affect the color of the urethral mucosa. Following urethroscopy, however, 2% lidocaine jelly may be used on the cystoscope sheath as a lubricant and topical anesthetic. The cystoscope is placed into the urethral meatus with the bevel directed posteriorly and advanced to the bladder under direct vision. An obturator is not necessary when using a diagnostic 17-French sheath because downward pressure on the posterior lumen of the urethra with the blunt bevel is well tolerated by the majority of patients. The infusion of water is maintained at a slow rate until the patient reports fullness or a volume of approximately 400 mL is reached. Further infusion is not necessary 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 anteriorly an air bubble at the dome of the bladder. This serves as a landmark during the remainder of the examination. Beginning at the superior dome to the UVJ, the survey progresses in 12 sweeps, corresponding to the points of a clock (Fig. 9-5). Orientation is maintained by placing the field marker directly opposite the portion of the bladder to be inspected. The trigone and ureteral orifices are viewed by angling the scope downward at 30 degrees and laterally. Visualization of the bladder base can be difficult in patients with a large cystocele unless the prolapse is reduced with a vaginal finger. The
Figure 9-5 ■ Diagnostic cystoscopy. A survey of vesical cavity is made by making 12 sweeps clockwise from the superior bladder to the urethrovesical junction. The 5 o’clock sweep is demonstrated.
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mucosa is examined for color, vascularity, trabeculation, and abnormal lesions, such as plaques or masses. Once the survey is complete, the telescope is removed and the sheath is left in place. This allows the bladder to drain and permits measurement of the volume of drained fluid. The approach to diagnostic cystoscopy, using a flexible cystoscope, follows an approach similar to that described for rigid cystoscopy. Infection of the urinary tract is one of the potential causes of morbidity associated with cystourethroscopy, yet the actual rate of procedure-related bacteriuria is not well defined. In the literature, the rate of bacteriuria following cystoscopy ranges from 2.8% to 16.6%. The upper limit of the range represents significant factors of potential morbidity that have prompted many clinicians to use prophylactic antibiotics. Approaches vary considerably in terms of choice of antimicrobial agents and route of administration. Some practitioners use antibiotic bladder irrigation in lieu of oral antibiotics. The most common prophylactic regimen used for cystoscopy is probably oral nitrofurantoin. A double-blind randomized trial of nitrofurantoin prophylaxis for combined urodynamics and cystourethroscopy by Cundiff et al. (1999) showed no difference in rates of infection between those receiving nitrofurantoin and placebo.
Intraoperative Assessment of Lower Urinary Tract Integrity The majority of ureteral injuries today occur during gynecologic operations, and lower urinary tract injury is one of the most common reasons for medical litigation against gynecologists. Estimates of the incidence of injury to the ureters during major gynecologic surgery range from 0.4% to 2.5%. The incidence of lower urinary tract injury may be higher for urogynecologic and operative laparoscopic surgery. The approach to assessment of the integrity of the bladder mucosa following pelvic surgery is similar to the approach described for diagnostic cystoscopy. A thorough survey of the bladder is made with special attention to the portions of the bladder potentially jeopardized by the procedure. Inspection of the anterior and lateral aspects of the mucosa is important after a retropubic urethropexy and sling, whereas inspection
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of the trigone is warranted following a difficult vaginal hysterectomy or dissection of an enterocele from the bladder. Assessment of ureteral integrity should be considered after any retropubic suspension, vaginal apex suspension procedure, or culdoplasty and is warranted whenever a suspicion of ureteral injury is present. Intravenous administration of indigo carmine approximately 5 minutes before initiating cystoscopy facilitates visualization of the ureteral orifices during efflux by staining the urine blue. SUPRAPUBIC TELOSCOPY Suprapubic teloscopy is an alternative to transurethral cystoscopy for evaluating the lower urinary tract during pelvic surgery. Transurethral cystoscopy is well suited to pelvic surgery performed by a vaginal approach but is inconvenient in conjunction with an abdominal procedure. Valuable operative time is lost by closing the abdominal wound to permit repositioning and prepping for transurethral cystoscopy. Moreover, any significant cystoscopic findings mandate reopening the abdomen for surgical correction. Suprapubic teloscopy addresses this dilemma by providing a way to perform endoscopy from an abdominal approach. Because of the simplicity of the technique, suprapubic teloscopy compares favorably to the alternatives of open cystotomy or dissection of ureters in terms of required operating time and morbidity and is an easy transition for an endoscopist experienced in cystoscopy. Suprapubic teloscopy is an extraperitoneal technique that begins with closure of the anterior peritoneum to prevent contamination of the peritoneal cavity with spilled urine. If indigo carmine is to be used to help identify the ureteral orifices, it should be given at this juncture to permit time for renal excretion. The bladder cavity is filled to at least 400 mL through a triple-lumen transurethral Foley catheter. A 1- to 2-cm pursestring suture is placed into the muscularis layer of the dome of the bladder, using a 2–0 absorbable suture. Two absorbable stay sutures can be placed within the purse-string with a full-thickness purchase to facilitate introduction of the telescope. A stab incision made between the stay sutures provides an opening for insertion of the telescope. Because distention of the bladder is achieved through the transurethral catheter, the sheath and bridge are unnecessary and the telescope is inserted alone. The purse-string is tightened sufficiently to prevent leakage without limiting the movement of the telescope. A 30-degree telescope provides the best view of the trigone and ureteral orifices while also permitting a thorough bladder survey. Orientation can be achieved by identifying the transurethral Foley catheter bulb and locating the trigone beneath the bulb. If suprapubic catheterization is planned, the catheter can be placed through the same stab incision when teloscopy is completed.
Once the ureteral orifice is located, the ureteral catheter is advanced into the field of view. Although the deflecting mechanism of the Albarran bridge facilitates ureteral catheterization, it is usually not essential to its completion. The catheter is placed just outside the fenestrated end of the cystoscope, with the catheter tip oriented in the axis of the ureteral lumen. The tip is threaded into the ureteral orifice by advancing the entire cystoscope. Once the tip enters the ureteral orifice, the catheter is gently advanced until it meets resistance as it passes into the renal pelvis, which is generally 25 to 30 cm. If the catheter is to be left in place, it should be secured to a transurethral catheter and connected to a drainage device. Gentle technique is essential to preventing hematuria and resulting colic. Fluoroscopy with retrograde passage of contrast also facilitates safe catheter passage. Other potential complications include perforation and ureteral spasm, but with proper methods the risk of complication is small.
Operative Cystoscopy Operative cystoscopy is generally done by urologists. However, several minor procedures are easily performed in the office by urogynecologists during diagnostic cystoscopy. These include biopsy of mucosal lesions and removal of small foreign bodies or intravesical sutures. Because of the focal length of the optics, the best view is immediately in front of the telescope, where operative procedures should take place. Following introduction of the cystoscope into the bladder and instillation of a sufficient volume of fluid to view the entire vesical wall, the instrument is introduced into the operative port and advanced until it is visible just at the end of the cystoscope. Gross movements are made by moving the cystoscope, and minor adjustments are made by moving the instrument itself. This approach keeps the operation in the optimal field of view. Irrigation at a brisk rate helps keep the field from being obscured by blood. The bleeding that occurs with biopsy is usually minor, but if excessive hemorrhage occurs, it can be controlled by electrocautery. Because these procedures require a larger cystoscope sheath (larger than 22 French) and may cause some patient discomfort, anesthesia is recommended. Intravesical instillation of anesthetic is often sufficient but can be augmented by a bladder pillar block. For bladder instillation, the bladder is catheterized and drained; 50 mL of 4% lidocaine solution is instilled and left in place for 5 minutes. The bladder pillar block can be placed before the lidocaine is drained from the bladder. The block is performed by injecting submucosally 5 mL of 1% lidocaine solution at the bladder pillars. After placement of a bivalve speculum, the bladder pillars are located in the lateral fornices at 2 o’clock and 10 o’clock positions, with respect to the cervix.
CYSTOSCOPIC PASSAGE OF URETERAL CATHETERS The absence of efflux of urine from the ureteral orifices during pelvic surgery is an indication for the passage of ureteral catheters to evaluate for potential obstruction. Ureteral catheters are available in various sizes and with several specialized tips. The most useful catheters for assessing ureteral patency are the general-purpose catheter and the whistle-tip catheter. Although available from 3 to 12 French, the most useful catheter calibers are in the 4- to 7-French range. They have graduated centimeter markings for judging the length of insertion.
CYSTOURETHROSCOPIC FINDINGS Normal Findings The urethral mucosa is normally pink and smooth, with a posterior longitudinal ridge called urethral crest. The UVJ is typically round or an inverted horseshoe shape and is completely coapted until the irrigant opens the lumen. The
Chapter 9
UVJ normally closes briskly and has minimal mobility with Valsalva maneuver. In its normal state, the bladder mucosa has a smooth surface with a pale pink to a 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 reddened granular surface of the trigone is commonly covered by a thickened white membrane with a villous contour. Histologic evaluation of the layer reveals squamous metaplasia (Fig. 9-6). The trigone is triangular, 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 and runs between the ureteral orifices. The intramural portions of the ureters can often be seen as they course from the lateral aspect of the bladder toward the trigone and ureteral orifices. Marked variation is present in the ureteral orifices, but they are generally circular or slitlike openings at the apex of a small mound. 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, 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 bowel peristalsis is possible through the vesical wall.
Pathologic Findings URETHROSCOPIC PATHOLOGY In the urethral pain syndrome, the urethra is reddened and exudate can sometimes be expressed from the posterior urethral glands. Fronds or polyps, both of which can be seen in the proximal urethra or at the UVJ, have been associated with chronic inflammation. Urethral diverticula appear as ostia, usually along the lateral or posterior surface of the urethra, which may have expressed exudate on palpation (Fig. 9-7).
Figure 9-6
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Trigone demonstrating squamous metaplasia.
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Figure 9-7 ■ Urethroscopic view of the orifice of a suburethral diverticulum (arrow). The proximal urethral orifice is at the upper right side.
A stricture is a narrowing of the urethra that typically occurs at the meatus, although proximal or midurethral narrowing may also result from prior urethral surgery. Hypoestrogenism results in pale urothelium. A urethral lumen that is pale and rigid and is unresponsive to commands indicates fibrosis and may be expected in intrinsic sphincter deficiency. During dynamic urethroscopy the patient with urodynamic stress incontinence cannot close the UVJ to the “hold” and “squeeze” commands, and the UVJ generally opens and descends in response to coughs and Valsalva maneuvers. The patient with intrinsic sphincter deficiency may have a rigid, immobile urethra, with the UVJ unresponsive to commands. In severe cases, the urethral lumen may be visualized from meatus to bladder neck. CYSTOSCOPIC PATHOLOGY Pathology affecting the bladder can be categorized as mucosal lesions or structural variations. Mucosal lesions are either inflammatory or neoplastic, although their coexistence is not uncommon. Despite its common use to describe infection of the bladder, cystitis in its broadest definition refers to inflammation of the bladder mucosa, of which several varieties are known. Cystoscopy should be avoided in the presence of active infectious cystitis but, if performed inadvertently, may provide variable findings. In its mildest form, bacterial cystitis can be rather inconspicuous, with little more than pink or peachcolored macules or papules. With increasing severity, mucosal edema and hypervascularity are evident, with loss of the submucosal vascular pattern and marked vascular dilation. In hemorrhagic cystitis, this can progress to individual or confluent mucosal hemorrhages and may be associated with hematuria in addition to irritative voiding symptoms. The symptoms of hematuria and irritative voiding are typical of several other less common inflammatory conditions that can often be distinguished at cystoscopy. The hemorrhagic cystitis that follows bladder infusion with
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toxins, such as cyclophosphamide, is characterized by diffuse mucosal hemorrhage. In radiation cystitis, areas of hemorrhage are surrounded by pale mucosa, which may be fibrotic and hypovascular. A chronic indwelling urethral or suprapubic catheter produces an inflammatory reaction of the mucosa directly in contact with the catheter. Mucosal changes range from pseudopapillary edema and submucosal hemorrhage to vesical fibrosis. Interstitial cystitis, another form of chronic inflammation, is often associated with hematuria and fibrosis. The pathognomonic lesions appear on refilling the bladder, after initially filling to maximum cystometric capacity. General anesthesia is usually required to fill to maximum cystometric capacity because the associated fibrosis often makes filling intolerable. Glomerulations are the primary finding in very mild cases. These petechial hemorrhages are small red dots that may coalesce to form larger hemorrhagic areas. Rare petechiae are seen in normal patients, especially on the posterior wall and trigone, caused by cystoscope trauma. In contrast, interstitial cystitis patients have at least 10 to 20 glomerulations per field of vision. The classic Hunner’s ulcer is seen in more severe cases of interstitial cystitis. These ulcers appear as velvety red patches or linear cracks with a granulating base and surrounding vascular congestion. Recurrent or chronic inflammation can produce characteristic lesions as well. Inflammatory polyps are often identified at the UVJ if the cystoscope is retracted into the proximal urethra and the infusion interrupted to allow them to float into the field of view. They are usually translucent with a villous appearance but can become large enough to partially fill the urethral lumen. Cystitis cystica consists of clear mucosal cysts usually found in multiple areas over the bladder base. The cysts are formed by single layers of subepithelial transitional cells, which degenerate with central liquefaction. Cystitis glandularis has a similar appearance to cystitis cystica, but the cysts are not clear and have a less uniform contour. As in cystitis glandularis, the mechanism of formation is a glandular metaplasia. In cystitis glandularis, however, there is involvement of multiple layers, including the mucusproducing glandular epithelium. Both lesions are associated with chronic irritation of the bladder mucosa and are commonly surrounded by marked inflammation. The association of cystitis glandularis with adenovillous carcinoma of the bladder has led to the belief that cystitis glandularis may be a precursor of adenocarcinoma. A proposed metaplastic transformation from epithelial hyperplasia through cystitis glandularis and finally to adenocarcinoma is based on a case presented by Shaw et al. (1958) of a gradual transition of cystitis glandularis to adenocarcinoma over a 5-year period. Two subsequent reports are known of transformation of cystitis glandularis to adenocarcinoma. Although bladder cancer is twice as common in men, it is the most common genitourinary neoplasm in women. The vast majority of cases occur past the fifth decade. Transitional cell carcinoma is the most common histologic type, followed by adenocarcinoma and squamous cell carcinoma. Transitional cell carcinoma is usually carcinogen-induced. Tobacco, dyes, and organic chemicals are known carcinogens for the transitional epithelium. Adenocarcinoma is more common with bladder exstrophy. Squamous cell carcinoma has been reported with chronic indwelling catheters.
Cystoscopic appearance is variable, depending on histologic type and grade, but usually reveals a raised lesion with a villous feathery or papillary appearance. Circumferential inflammation is ubiquitous. Superficial transitional cell carcinoma may be multicentric or may have associated carcinoma in situ. Carcinoma in situ can be disturbingly inconspicuous, often mimicking the macules or plaques of infectious cystitis. Vesical and ureteral structural variations may be anatomic or functional anomalies. Auxiliary ureteral orifices are examples of rare anatomic anomalies, which are indicative of renal collecting anomalies. When present, they often enter the vesical wall slightly superior to the trigone close to the other ureteral orifice. Ureteroceles are caused by laxity of the distal ureteral lumen, with herniation into the vesical cavity during efflux. Trabeculations are considerably more common than auxiliary ureteral orifices or ureterocele. These smooth ridges become evident with distention of the bladder to volumes approaching maximum cystometric capacity. They appear as interlaced cords of different diameters with intervening sacculations and represent hypertrophied detrusor musculature associated with detrusor overactivity and functional or anatomic bladder obstruction. A bladder diverticulum can occur when high intravesical pressure produces an enlargement of the intervening sacculations. The thick muscular band that creates the neck varies in diameter and gives way to outpouchings of bladder mucosa. The interior of the diverticulum has been reported to be the site of neoplasm in approximately 7% of cases. Fistulas may also be encountered at cystoscopy. Approximately 75% are vesicovaginal fistulas (Fig. 9-8) that result from abdominal hysterectomies. They may also occur after vaginal hysterectomies, urologic procedures, radiation, foreign bodies, chronic indwelling catheters, cancer, and obstetric trauma. Post-hysterectomy fistulas are usually located in the bladder base, superior to the interureteric ridge and corresponding to the level of the vaginal cuff. The fistulous openings range from small to several centimeters in diameter. In the immediate postoperative state, the surrounding mucosa is edematous and hyperemic; in later stages the mucosa has a smooth appearance. In contrast, vesicoenteric
Figure 9-8
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Vesicovaginal fistula (bottom).
Chapter 9
fistulas uniformly have surrounding inflammatory reaction, often with bulbous edema, and the fistulous tract is not discernible in two thirds of cases. 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. Stones have 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.
Bibliography HISTORICAL PERSPECTIVE Gunning JE, Rosenzweig BA. Evolution of endoscopic surgery. In White RA, Klein SR, eds. Endoscopic Surgery. Mosby, St. Louis, 1991. Hopkins HH, Kopany NS. A flexible fiberscope, using static scanning. Nature 1954;179:39. Kelly HA. The direct examination of the female bladder with elevated pelvis: the catheterization of the ureters under direct inspection, with and without elevation of the pelvis. Am J Obstet Dis Women Child 1894;25:1. Ridley JH. Indirect air cystoscopy. South Med J 1951;44:114. Robertson JR. Office cystoscopy: substituting the culdoscope for the Kelly cystoscope. Obstet Gynecol 1966;28:219. Robertson JR. Air cystoscopy. Obstet Gynecol 1968;32:328. Robertson JR. Gynecologic urethroscopy. Am J Obstet Gynecol 1973;115:986.
INDICATIONS AND INSTRUMENTATION Aso Y, Yokoyama M, Fukutani K, et al. New trial for fiberoptic cystourethroscopy: the use of metal sheath. J Urol 1976;115:99. Bagley DH, Huffman JL, Lyon ES. Urologic Endoscopy: A Manual and Atlas. Little, Brown and Co., Boston, 1985. Clayman RV, Reddy P, Lange PH. Flexible fiber optic and rigid-rod lens endoscopy of the lower urinary tract: a prospective controlled comparison. J Urol 1984;131:715. Cundiff GW, McLennan MT, Bent AE. Randomized trial of antibiotic prophylaxis for combined urodynamics and cystourethroscopy. Obstet Gynecol 1999;93:749. Fantl JA, Newman DK, Colling J, et al. Urinary incontinence in adults: acute and chronic management. Clinical Practice Guideline, No. 2, 1996 Update. U.S. Department of Health and Human Services. Public Health Service, Agency for Health Care Policy and Research. AHCPR Publication No. 96-0682, Rockville, MD, March 1996. Figueroa TE, Thomas R, Moon TD. A comparison of rigid with flexible instruments. J LA State Med Soc 1987;139:26. Fowler CG. Fiberscope urethrocystoscopy. Br J Urol 1984;56:304. Fowler CG, Badenoch DF, Thakar DR. Practical experience with flexible fiberscope cystoscopy in out-patients. Br J Urol 1984;56:618. Groutz A, Samandarov A, Gold R, et al. Role of urethrocystoscopy in the evaluation of refractory idiopathic detrusor instability. Urology 2001;58:544. Hargreave TB. Practical Urological Endoscopy. Blackwell Scientific Publications, Oxford, 1988. Matthews PN, Bidgood KA, Woodhouse RJ. CO2 cystoscopy using a flexible fiberoptic endoscopy. Br J Urol 1984;56:188. Matthews PN, Skewes DG, Kothari JJ, et al. Carbon dioxide versus water for cystoscopy: a comparative study. Br J Urol 1983;55:364.
CYSTOURETHROSCOPIC TECHNIQUE Aldridge CW, Beaton JH, Nanzig RP. A review of office urethroscopy and cystometry. Am J Obstet Gynecol 1978;131:432. Clark KR, Higgs MJ. Urinary infection following out-patient flexible cystoscopy. Br J Urol 1990;66:503.
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Cundiff GW, Bent AE. The contribution of urethrocystoscopy to evaluation of lower urinary tract dysfunction in women. Int Urogynecol J Pelvic Floor Dysfunct 1996;7:307. Denholm SW, Conn IG, Newsam JE, et al. Morbidity following cystoscopy: comparison of flexible and rigid techniques. Br J Urol 1990;66:503. Fozard JB, Green DF, Harrison GS, et al. Asepsis and out-patient cystoscopy. Br J Urol 1983;55:680. Green LF, Khan AU. Cystourethroscopy in the female. Urology 1977;10:451. Manson AL. Is antibiotic administration indicated after out-patient cystoscopy? J Urol 1988;140:316. Marier R, Valenti AJ, Madri JA. Gram-negative endocarditis following cystoscopy. J Urol 1978;119:134. O’Donnell P. Water endoscopy. In Raz S, ed. Female Urology. WB Saunders, Philadelphia, 1983. Richards B, Bastable JR. Bacteriuria after outpatient cystoscopy. Br J Urol 1977;49:561. Robertson JR. Gas endoscopy. In Raz S, ed. Female Urology. WB Saunders, Philadelphia, 1983. Robertson JR. Dynamic urethroscopy. In Ostergard DR, ed. Gynecologic Urology and Urodynamics, 2nd ed. Williams & Wilkins, Baltimore, 1985. Romero RE, Hicks TH, Galindo GH, et al. Evaluation of the importance of cystoscopy in staging gynecologic carcinomas. J Urol 1979;121:64. Rosenzweig BA, Bhatia NN. The use of carbon dioxide laser in female urology. J Gynecol Surg 1991;7:11. Sand PK, Hill RC, Ostergard DR. Supine urethroscopic and standing cystometry as screening methods for the detection of detrusor instability. Obstet Gynecol 1987;70:57. Scotti RJ, Ostergard DR, Guillaume AA, et al. Predictive value of urethroscopy as compared to urodynamics in the diagnosis of genuine stress incontinence. J Reprod Med 1990;35:772. Uehling DT. The normal caliber of the adult female urethra. J Urol 1978;120:176.
CYSTOURETHROSCOPIC FINDINGS Anderson MJ. The incidence of diverticula in the female urethra. J Urol 1967;98:96. Bergman A, Karram M, Bhatia NN. Urethral syndrome: a comparison of different treatment modalities. J Reprod Med 1989;34:157. Davis BL, Robinson DG. Diverticula of the female urethra: assay of 120 cases. J Urol 1970;104:850. Edwards PD, Hurm RA, Jaesehke WH. Conversion of cystitis glandularis to adenocarcinoma. J Urol 1972;108:568. Hunner GL. A rare type of bladder ulcer in women: report of cases. Trans South Surg Gynecol Assoc 1914;27:247. Lee RA. Diverticulum of the urethra. Clinical presentation, diagnosis and management. Clin Obstet Gynecol 1984;27:490. Lyon RP, Smith DR. Distal urethral stenosis. J Urol 1963;89:414. MacDermott JP, Charpied GC, Tesluk H, et al. Can histological assessment predict the outcome in interstitial cystitis? Br J Urol 1991;67:44. Marshall FC, Uson AC, Melicow MM. Neoplasm and caruncles of the female urethra. Surg Gynecol Obstet 1960;110:723. Messing EM, Stamey TA. Interstitial cystitis: early diagnosis, pathology, and treatment. Urology 1978;12:381. Mufson MA, Belshe RB, Horrigan TJ, et al. Cause of acute hemorrhagic cystitis in children. Am J Dis Child 1973;126:605. Numazaki Y, Kumasaka T, Yano N, et al. Further study on acute hemorrhagic cystitis due to adenovirus type II. N Engl J Med 1973;289:344. Richardson FH. External urethroplasty in women: technique and clinical evaluation. J Urol 1969;101:719. Scotti RJ, Ostergard DR. The urethral syndrome. Clin Obstet Gynecol 1984;27:515. Shaw JL, Gislason GJ, Imbriglia JE. Transition of cystitis glandularis to primary adenocarcinoma of the bladder. J Urol 1958;79:815. Susmans D, Rubenstein AB, Dakin AR, et al. Cystitis glandularis and adenocarcinoma of the bladder. J Urol 1971;105:671. Walsh A. Interstitial cystitis. In Harrison JH, Gittes RF, Perlmutter AD, et al., eds. Campbell’s Urology, 4th ed. WB Saunders, Philadelphia, 1979.
Radiologic Studies of the Lower Urinary Tract and Pelvic Floor
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Mark D. Walters and Wen-Chen Huang
PLAIN FILM OF THE ABDOMEN 124 INTRAVENOUS AND RETROGRADE PYELOGRAPHY 124 CYSTOGRAPHY 125 VOIDING CYSTOURETHROGRAPHY 126 POSITIVE-PRESSURE URETHROGRAPHY 126 VIDEO-CYSTOURETHROGRAPHY 126 ULTRASOUND 127 Basic Procedure of Perineal Ultrasound 127 Normal Images of the Female Lower Urinary Tract 128 Applications in Female Lower Urinary Symptoms and Conditions 128 Conclusions and Future Investigation 133 COMPUTED TOMOGRAPHY 133 MAGNETIC RESONANCE IMAGING 133
Pelvic floor disorders include a broad array of interrelated clinical conditions that include urinary incontinence, pelvic organ prolapse, fecal incontinence, sensory and emptying abnormalities of the lower urinary tract, and defecatory dysfunction. A thorough evaluation, including physical examination, urodynamic and electrophysiologic investigations, and imaging studies of the lower urinary tract and pelvic floor as indicated, is crucial for understanding anatomy and function. Results of this evaluation can then guide the clinician to the appropriate management of bothersome symptoms. Radiologic studies are used in urogynecology and reconstructive pelvic surgery to diagnose various disorders. With new technological advancements over the past several decades, radiologic studies have evolved beyond their traditional diagnostic role to become important in our quest to understand the pathophysiology of pelvic floor disorders. The focus of this chapter is to describe the radiologic studies used in clinical practice and research in urogynecology and female urology.
PLAIN FILM OF THE ABDOMEN The flat plate of the abdomen, taken as a scout film for intravenous pyelogram (IVP) or as a plain radiograph, can screen
for urinary calculi. In addition, it may also reveal pelvic masses, bony lesions, and calculi in suburethral diverticula.
INTRAVENOUS AND RETROGRADE PYELOGRAPHY Despite the emergence of newer imaging techniques, IVP is still frequently used to evaluate the urinary tract (Fig. 10-1). IVP is safe, inexpensive, and widely available, and it provides information about the anatomy of the collecting system and functional status of the glomerular filtration apparatus. Computed tomographic (CT) IVP is gradually replacing conventional IVP because it gives more precise information about renal anatomy and function. One of the most common indications for performing an IVP in urogynecology is to detect possible ureteral obstruction caused by gynecologic cancer, pelvic mass, pelvic organ prolapse, or after gynecologic surgery. IVP, with delayed films and tomography, is also useful to help diagnose certain uncommon conditions, such as ectopic ureter and ureterovaginal fistula. Although IVP is safe, it is an invasive procedure and exposes patients to injection of iodine dye and to radiation; it is contraindicated in pregnant women or those with allergy to iodinated contrast media, renal insufficiency, and congestive heart failure. Because of these disadvantages, abdominal and Doppler ultrasounds have been used as a noninvasive and less expensive alternative to diagnose ureteral obstruction. If the pelvicaliceal or ureteric anatomy is not adequately visualized with IVP, or if there is a contraindication to IVP, an alternative approach is to perform a retrograde pyelogram, which is especially useful if there is a coexisting indication for cystoscopy. In retrograde pyelogram, the contrast medium is injected into the upper urinary tract through a cone-tipped catheter placed at cystoscopy under fluoroscopic guidance (Fig. 10-2). This approach is associated with a higher infection rate than antegrade pyelography and may be contraindicated in women with known allergic reaction to contrast media or very recent lower urinary tract trauma or surgery. The large amount of contrast medium injected and the pressure applied during retrograde pyelogram may
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result in anastomotic leak and extravasation, with systemic absorption of the contrast. Antegrade pyelography can provide excellent opacification of the renal collecting system. This approach involves placing a small-gauge needle into the renal pelvis; it is rarely performed for diagnostic indications only and is usually performed only when there is another indication for percutaneous puncture of the kidney. To perform an
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antegrade pyelography, the patient is placed in a prone position. A flexible 20- or 22-gauge needle is inserted into the collecting system under ultrasound or fluoroscopic control after administration of intravenous contrast medium. An obstructed renal collecting system should be decompressed before contrast medium is injected to avoid overdistention and urosepsis. Additional procedures, such as attempts of antegrade ureteral stenting, can then be performed to temporarily or permanently relieve the obstruction.
CYSTOGRAPHY Cystography is frequently performed to detect bladder injury after trauma, to diagnose fistulas between the bladder and the adjacent organs, and to confirm that a cystotomy or bladder fistula has healed after surgical repair. Vesicovaginal, vesicouterine, and vesicoenteric fistulas are diagnosed when contrast material from the bladder enters and opacifies the adjacent viscera (Fig. 10-3). Absence of contrast in the adjacent viscera does not always exclude a fistula because the connecting tract may not be large enough to allow passage of a sufficient quantity of contrast to be seen radiographically. To determine whether a cystotomy or fistula repair has healed, the bladder is filled slowly with contrast medium and then drained. A postvoid film is obtained to evaluate for extravasated contrast medium. Contrast from extraperitoneal leakage usually forms an irregularly shaped mass around the defect and remains there for a relatively long time. Contrast that has leaked from an intraperitoneal defect diffuses into
Figure 10-1 ■ Intravenous pyelogram showing duplication of the collecting system of the left kidney.
Figure 10-2
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Ureteral catheter used to perform retrograde pyelography.
Figure 10-3 ■ Retrograde contrast instillation into the bladder via a urethral catheter demonstrating a vesicovaginal fistula.
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the abdominal cavity and is rapidly absorbed through the peritoneal cavity.
VOIDING CYSTOURETHROGRAPHY Voiding cystourethrogram (VCUG) is a dynamic radiologic study that is used to diagnose structural bladder and urethral abnormalities with voiding and to evaluate for vesicoureteral reflux. VCUG is also used to investigate suspected bladder fistula or suburethral diverticula (Fig. 10-4) and to evaluate the integrity of the bladder or urethra after fistula or diverticula surgery. Because of recent advances, ultrasound and magnetic resonance imaging (MRI) technology have replaced VCUG as the primary imaging modality in diagnosing many of these conditions.
POSITIVE-PRESSURE URETHROGRAPHY Positive-pressure urethrography was first described and used by Davis and Cian in 1956 to evaluate the female urethra. Today, the primary indication for this diagnostic test is to search for possible suburethral diverticula not visualized on VCUG. The study requires a Tratner catheter, which has two balloons, with an opening in the lumen of the catheter between the two balloons for contrast injections. The distal balloon is placed into the bladder, and the proximal (sliding) balloon is positioned just outside the external urethral
Figure 10-4 ■ Voiding cystourethrogram demonstrating three small proximal suburethral diverticula (arrow).
meatus. The two inflated balloons create a temporary, closed system and allow the contrast injected into the urethra to opacify the diverticulum (Fig. 10–5). This radiologic test is often performed in conjunction with VCUG to maximize the diagnostic accuracy. It can also be used during surgery to help expand and identify urethral diverticula and to test the integrity of repairs after resection.
VIDEO-CYSTOURETHROGRAPHY Video-cystourethrography combines a fluoroscopic voiding cystourethrogram with simultaneous intravesical, intraurethral, and intra-abdominal pressures and urine flow rate. Urethral sphincter electromyography (EMG) is often done simultaneously to assess neurogenic voiding disorders. Videocystourethrography allows visual assessment of urethral sphincters and bladder function while synchronously recording urodynamic and EMG data and is considered the gold standard of urodynamic investigation against which other techniques are compared. Some controversy exists regarding the indications for video-cystourethrography and whether it should be performed routinely or selectively. Some common indications include complex cases with equivocal results after multichannel urodynamic studies, failed incontinence surgery, and voiding disorders associated with neurologic diseases.
Figure 10-5 ■ Positive-pressure urethrogram showing a large, multiloculated suburethral diverticulum.
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ULTRASOUND
BOX 10-1
After the introduction of real-time technology in the 1980s, ultrasound has been widely applied and has sometimes replaced radiography in the evaluation of pelvic floor disorders. It has the advantages of noninvasiveness, reproducibility, nonradiation exposure, and less expense. With use of high-resolution transducers, pelvic organs can be demonstrated clearly on ultrasonography. Moreover, three-dimensional technology with simultaneous axial, transverse, and coronal views of pelvic organs clearly displays the spatial orientation of the female lower urinary tract. Both color and power Doppler scanning not only can reveal the vascular flows of pelvic organs, but also can demonstrate the urinary flow. Color Doppler ultrasound analyzes the frequency shift of flow velocity information, whereas power Doppler technology uses the amplitude component of received signals to quantify the number of moving particles. Many approaches have been proposed for the evaluation of the lower urinary tract by ultrasound. These include transabdominal, transvaginal, transrectal, perineal (or translabial), and introital approaches. Because the lower urinary tract can be shaded by the acoustic shadow of the pubic symphysis, the transabdominal approach is used mainly to visualize the kidneys and pelvic organs, and for simple office measurement of bladder urine volume.
Patient’s position Bladder volume Liquid used for bladder filling Method of bladder filling Spontaneous Retrograde Simultaneous pressure measurement Cystometry Urethral pressure profile Voiding study Size of ultrasound transducer Ultrasound machine (type and manufacturer) Ultrasound frequency Picture orientation Method of performing ultrasound Introital Perineal/translabial Vaginal Rectal Abdominal
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EXAMINATION INFORMATION THAT SHOULD BE INCLUDED DURING ULTRASONOGRAPHIC EVALUATION OF THE FEMALE LOWER URINARY TRACT
Basic Procedure of Perineal Ultrasound For dynamic assessment, the transvaginal approach may exert a compressive effect on the lower urinary tract. Therefore, to prevent distortion of the anatomy of the lower urinary tract by probes, perineal (translabial) or introital approaches are used currently. The differences between perineal (translabial) and introital approaches are the site where the transducer is placed and the probe used in the ultrasonographic scanning: perineal (translabial) ultrasound uses a linear- or curved-array convex probe with frequency between 3.5 and 5 MHz; introital ultrasound uses a sector endovaginal probe with frequency between 5 and 7.5 MHz. The transducer is placed on the perineum in the perineal (translabial) approach; it is positioned between the labia minora just underneath the external urethral orifice in the introital approach. Both approaches have been proven to be devoid of potential morphologic artifacts resulting from distortion of the bladder neck or urethra. The information that should be obtained during ultrasonographic evaluation of the female lower urinary tract is shown in Box 10-1. Some disagreement exists regarding the optimal orientation of images. Some authors prefer an orientation as in conventional transvaginal ultrasound. However, others recommend showing superior structures above, inferior structures below, anterior structures on the right, and posterior structures on the left. The examination can be performed in dorsal lithotomy, semireclining, or standing position. No significant differences are present in the dynamic assessment of the bladder neck between the semireclining and the standing positions. The ultrasonographic evaluation of the lower urinary tract begins with the midsagittal plane. This results in an image including the symphysis pubis, urethra, bladder neck,
Figure 10-6 ■ Pelvic floor scanning by introital ultrasonography. sp, Symphysis pubis; bl, bladder; u, urethra; cx, cervix; v, vagina; r, rectum; a, anus.
vagina, cervix, rectum, and anal canal (Fig. 10-6). By moving the transducer to the left or to the right, periurethral structures can be assessed. The pressure exerted by the transducer should be kept low but still sufficient to obtain good images with high resolution. The presence of a full rectum may impair diagnostic accuracy and sometimes necessitates a repeat assessment after defecation. The bladder volume should be fixed on examination: 300 mL for the evaluation of dynamic changes of the bladder neck and less than 50 mL for the assessment of bladder wall thickness. The bladder volume can be estimated by either a transabdominal or transvaginal approach, although the accuracy is not reliable for bladder volumes less than 50 mL. In the transabdominal approach, three parameters, including height (H), depth (D), and width (W), are obtained from two perpendicular planes (sagittal and transverse). In sagittal scanning, height and depth
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correspond to the greatest superior-inferior measurement and the greatest anterior-posterior measurement, respectively. Thus, the bladder volume can be calculated from the formula: bladder volume (mL) = H × D × W × 0.7. The value of 0.7 is a correction factor for the nonspherical shape of a full bladder. The approximate error rate of the formula is 21%. Transvaginal ultrasound has also been recommended to measure bladder volumes in the range of 20 to 300 mL. Horizontal height and vertical depth are obtained in the sagittal scanning. The bladder volume can be estimated according to the formula: bladder volume (mL) = H × D × 5.9 − 14.6 (95% confidence limits around ± 37 mL).
Normal Images of the Female Lower Urinary Tract On ultrasonography, the symphysis pubis is displayed as an ovoid-shaped structure with homogenous hyperechogenic nature. Without signs of infection, the bladder content is uniformly echolucent. The bladder wall is smooth and intact in integrity. The normal bladder wall is no more than 6 mm thick and can be divided into the outer layer and the inner layer. On ultrasound, the outer layer contains adventitia (endopelvic fascia), and the inner layer is composed of the bladder mucosa and detrusor muscles. The former is more echogenic in nature than the latter. The thickness of the outer layer is fixed regardless of bladder volumes; however, the thickness of the inner layer varies with the degree of bladder distention. When the scan is deviated a little to the right or left parasagittal plane, two tiny nodules (ureter papilla), located at the junction of the trigone and bladder, can be visualized with peristalsis. The position of the ureteral orifices can be identified by urinary flow from each ureteral orifice (ureter jet phenomenon) displayed on color and power Doppler scanning. The urethra is a tubular structure with a central echolucent area and surrounding echogenic sphincters. Color and power Doppler ultrasonography can reveal blood supply signals within and around the urethra, whereas scant vascular signals are noted in the bladder wall. Less bladder neck hypermobility and funneling are noted in normal continent women than in women with stress urinary incontinence and pelvic organ prolapse. The normal range of bladder neck motion has not been defined, and a wide range of overlap is present between normal and abnormal values. In addition, the measurements of bladder neck position have been reported to be influenced by bladder filling, patient position, and catheterization. By the introital approach, Yang and Huang (2002) reported that in healthy continent women, the angles between bladder neck and midline of symphysis pubis are 81 ± 15 degrees at rest and 113 ± 27 degrees during straining, with the rotational angle of 30 ± 20 degrees; the distances between bladder neck and midline of symphysis pubis are 25.7 ± 4.9 mm at rest and 22.9 ± 3.3 mm during straining. Bader et al. (1995) reported that in women without stress incontinence and prolapse, the posterior urethrovesical angle is 97 degrees at rest and 108 degrees during stress.
Applications in Female Lower Urinary Symptoms and Conditions ULTRASONOGRAPHIC CHARACTERISTICS OF UROLOGIC AND PELVIC FLOOR DISORDERS (BOX 10-2) Cystitis. Without infection, urine is anechoic in nature with some occasional free floating particles on ultrasonography. With infection, the echogenicity of the urine increases or even forms a fluid-debris level. The bladder wall is focally or generally thickened. Intravesical blood clots, which are echogenic in nature, may be demonstrated in some rare conditions, such as surgical damage to the lower urinary tract, postoperative bladder bleeding, or hemorrhagic cystitis. Hemorrhagic cystitis is gross hematuria associated with bladder inflammation and may be caused by infection, medication, chemical toxins, or pelvic irradiation. Thickened and hypervascular bladder wall with active bleeding from the bladder wall, formation of intravesical blood clots, or both, is the usual finding on color or power Doppler ultrasonography. Calculi. Sonography can detect some, but not all, distal ureteral calculi or bladder stones. The sonographic characteristics of a distal ureteral calculus include unilateral dilation of the ureter, which is normally invisible, and presence of a hyperechogenic stone within the ureter accompanied by strong acoustic shadow and surrounding edematous tissue. Bladder calculi account for 5% of urolithiasis cases and usually occur as a result of foreign objects, obstruction, or infection. In situations of bladder calculi secondary to a suture from a bladder neck suspension, hyperechoic suture material and bladder stone sometimes can be clearly demonstrated on
BOX 10-2
SITUATIONS THAT CAN BE INVESTIGATED BY ULTRASOUND
Kidney/Ureter Size Anomalies Hydronephrosis/hydroureter Stones
Bladder Urinary tract infection Hemorrhagic cystitis Foreign bodies (suture or sling materials, stones) Bladder tumors (primary or metastatic) Bladder outlet obstruction Vesicovaginal and vesicouterine fistulas
Urethra Urethral stricture Urethral diverticulum Periurethral masses
Retropubic Hematoma/Pelvic Masses Pelvic Floor Dysfunction Pelvic floor relaxation Detrusor overactivity Stress urinary incontinence Voiding dysfunction Anal incontinence Levator ani dysfunction/defects
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ultrasonography, whereas radiography and cystoscopy may fail to identify the underlying pathogenesis of the stone. Ureteral Obstruction. The diagnosis of ureteral obstruction by abdominal (renal) ultrasound is inferred by the presence of pelvicaliceal dilation. However, calyceal dilation may be caused by obstructive and nonobstructive lesions. Even in acute obstruction, pelvicaliceal dilation may not appear for up to 48 hours after the onset of fever and costovertebral angle tenderness. Also, the degree of dilation on ultrasound correlates poorly with the extent of obstruction and abdominal ultrasound often cannot localize the obstruction site. A more direct approach to diagnose ureteral obstruction is to use transvaginal color Doppler ultrasound to demonstrate jets of urine entering the bladder from the ureteral orifice. If ureteric jets are absent, the diagnosis and the location of the obstruction should then be confirmed by an IVP or CT IVP. Bladder Wall Thickening or Tumors. Abnormalities of the bladder wall include focal or generalized thickening, loss of integrity, and abnormal vascularity. In addition to infection, pelvic radiation, pelvic surgery, bladder outlet obstruction, and neoplasm can cause bladder wall thickening. In patients with bladder outlet obstruction, thickened bladder wall with trabeculation or even formation of diverticulum, and high postvoid residual urine volume may be displayed on ultrasonography. Transvaginal ultrasonography has been reported to have 95% of accuracy in the detection of bladder wall invasion by cervical cancer. The movability of the bladder wall can be assessed by the ability of the bladder to slide along the uterine cervix when the probe is pushed up against the bladder from the anterior fornix. Movability suggests an intact bladder wall. With further invasion of cervical cancer into the bladder, the relationship of free movability between cervix and bladder is lost, the intactness of the endopelvic fascia is broken, and a tumor nodule may be formed and protrude into the bladder cavity. Ultrasonography is also a useful diagnostic modality for screening and detecting bladder tumors. On ultrasonography, the bladder tumors can have polypoid, sessile, or plaquelike shapes, with regular or irregular surface, with or without calcified foci (Fig. 10-7). Color and power Doppler ultrasonography may demonstrate neovascularization within the tumor, with a low resistance index of the tumor vessels. Fistulas. Vesicovaginal and vesicouterine fistulas can be displayed by transvaginal ultrasonography. Factors aiding in the visualization of vesicovaginal fistulas are edematous change of bladder and vaginal walls, accumulation of urine inside the vagina, and urine flow induced by coughing or Valsalva maneuver. A reverse urine flow from the fistula into the bladder may be induced by the increased intravaginal pressure secondary to reflex pelvic floor contraction or the inward motion of the vaginal probe during coughing. This should be differentiated from the urinary stream coming from the ureteral orifices (the ureter jet phenomenon). Urethral Strictures. Thirteen percent of cases with bladder outlet obstruction are secondary to urethral stricture, which appears as distortion of the central hypoechoic urethral mucosa on ultrasonography. Better delineation of a
Figure 10-7 ■ Bladder cancer. Cystoscopic (A) and three-dimensional (B) sonographic examinations revealing a polypoid mass protruding from the bladder wall.
urethral stricture can be achieved by increasing abdominal pressure on a full bladder, permitting pseudoantegrade filling of the proximal urethra. A hyperechoic structure around the urethral mucosa on ultrasonography indicates a fibrotic and nondistensible urethral segment, which is histologically consistent with spongiofibrosis, and is visible even in the presence of extensive stenosis; it is closely related to the ultimate prognosis of urethral stricture. Urethral Diverticula. Urethral diverticulum is an uncommon cause of female lower urinary tract symptoms. The reported incidence of female urethral diverticulum in normal women is 1% to 6%. Transvaginal ultrasound has been shown to be effective for evaluation of suspected urethral diverticulum, which is demonstrated as a single or multiple cystic lesions with hypoechogenicity or mixed echogenicity surrounding the urethra (Fig. 10-8).
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Real-time ultrasound can provide direct visualization of pelvic floor muscle contraction and may be a useful biofeedback technique for pelvic muscle exercises. Ultrasound allows the amount of movement of the bladder neck during pelvic muscle exercises to be quantified. PATHOPHYSIOLOGIC CHANGES OF PELVIC FLOOR DYSFUNCTION Detrusor Overactivity. Perineal ultrasound with simultaneous urodynamic recording can be used to evaluate the bladder and the urethra. The examination is performed with a patient in the sitting position. The bladder neck, the bladder base, and the upper two thirds of the urethra can usually be seen. Schaer et al. (1998) noted that this technique was as informative as videocystourethrography while avoiding radiation exposure. A well-known sonographic finding in patients with overactive bladder is wavelike detrusor contractions accompanied by bladder neck opening. Khullar et al. (1996) reported that an increase in mean bladder wall thickness is unique to detrusor overactivity. With a cutoff value of 5 mm, bladder wall thickness together with symptoms of overactive bladder had sensitivity of 84% and specificity of 89% for detecting detrusor overactivity, compared with videocystourethrography. The authors speculated that the increased bladder wall thickness in this disorder was secondary to detrusor hypertrophy associated with increased isometric detrusor contraction, urethral sphincter volume, and urethral closure pressure.
Figure 10-8 ■ Proximal (A) and distal (B) urethral diverticula. Transvaginal sonography showing the urethral diverticulum (d), an echolucent cystic mass surrounding the proximal urethra (A) or deviating the distal urethra toward symphysis pubis (B). sp, symphysis pubis; bl, bladder; u, urethra; eu, external urethral meatus.
Pelvic/Retroperitoneal Masses. Ultrasound can detect retroperitoneal hematoma following retropubic urethropexy or tension-free vaginal tape procedures, especially in patients with postoperative febrile and micturition problems. Retropubic hematoma is displayed as an echolucent cyst between the symphysis pubis and urethra and bladder. The size and progression of the hematoma can be determined by ultrasound. Thus, timely and sufficient management can be provided to alleviate the symptoms. Pelvic Organ Prolapse. Ultrasound is capable of identifying different compartmental defects of the pelvic floor. Pelvic organ prolapse can be quantified and staged with translabial ultrasound, and correlation with pelvic organ prolapse quantification (POPQ) measurements is good. Enteroceles, often difficult to recognize by clinical examination, are easily detected by perineal or introital ultrasound. The imaging of the cervix and vaginal apex may be incomplete with the presence of large rectoceles, and the extent of pelvic floor relaxation may be underestimated because of transducer pressure.
Stress Urinary Incontinence. Ultrasonography is not used for diagnosing stress urinary incontinence. Instead, together with clinical examination and urodynamic data, it can be used to detect anatomic alterations associated with stress incontinence, to help select the appropriate therapy, and to evaluate surgical outcomes and postoperative complications. The ultrasonographic studies for stress incontinence should provide quantitative measurements and qualitative descriptions of the lower urinary tract. Schaer et al. (1996), representing the German Association of Urogynecology, recommended both posterior urethrovesical angle and bladder neck position as the quantitative parameters in the ultrasonographic study. The three methods for the measurement of bladder neck position are determining bladder neck position by one distance and one angle (Fig. 10-9, A), by two distances (Fig. 10-9, B), and by measuring the height of bladder neck with reference to a horizontal line drawn at the lower border of the symphysis pubis (Fig. 10-9, C). The first two methods use the symphysis pubis with its central line and the inferior border of the bladder as references, and have been proven to have good reproducibility. The third method is reliable only when a stable position of transducer at rest and during straining is guaranteed. The differences between resting and stress bladder neck angles yield the rotational angle, which represents urethral or bladder neck mobility in a similar way as the Q-tip test. No values are defined for normal bladder neck descent or urethral mobility, possibly because of the methodologic variations, such as patient position, bladder filling, quality of Valsalva maneuver, and measurements of bladder neck position. Although the positions of the
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Bladder
cx
Dx
bl b
SP Dy
r
β
a V
u
sp
α
Urethra
a
A
B
Bladder
b
SP H
C
Horizontal line
Urethra
Lower border of sp
Figure 10-9 ■ Three methods for the measurement of bladder neck position recommended by the German Association of Urogynecology. A. Measurement of the bladder neck position by one distance and one angle. Schematic drawing shows the measurements of posterior urethrovesical angle (β) and the bladder neck position, by measuring the distance between bladder neck and inferior border of the symphysis (a) and the angle between this distance line and the central line of the symphysis. B. Measurements of the bladder neck position by using two distances. A rectangular coordinate system is set up with the origin at the lower border of the symphysis. The x-axis is determined by the central line of symphysis, which runs between its lower and upper borders. The y-axis is constructed perpendicularly to the x-axis at the lower symphysis border. Dx is the distance between the y-axis and the bladder neck, and Dy is the distance between the x-axis and the bladder neck. For precise localization of the bladder neck, the upper and ventral points of the urethral wall at the immediate transition into the bladder is used. C. Quantifying the bladder neck position by measuring the height of bladder neck. A horizontal line is drawn at the lower border of the symphysis. The height (H) of the bladder neck is determined as the distance between bladder neck and this horizontal line. For reliable measurements at rest, during Valsalva, and with pelvic floor contractions, the position of the transducer may not be changed. SP, Symphysis pubis; bl, bladder; u, urethra; cx, cervix; v, vagina; r, rectum; a, anus.
bladder neck in patients with stress incontinence are lower than those of continent women, an overlap exists between the two groups. Bladder neck funneling may also be observed and is seen in women with both stress and urge incontinence. It seldom occurs in normal continent women unless the bladder is
full. On some occasions, the opening of the bladder neck may be followed by egress of urine, which is manifested as a hyperechoic flow from the bladder through the urethra on real-time scanning. This can be confirmed by color or power Doppler ultrasonography. During straining, the bladder neck may move in a semicircular fashion with the tip of the
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symphysis pubis as the center (rotational descent) or move downward along the urethral axis (sliding descent). Burch colposuspension elevates and stabilizes the bladder neck and proximal urethra in a high retropubic position. On ultrasound, higher bladder neck position, smaller bladder neck angle at rest and during straining, and lesser rotational angle can be observed after both open and laparoscopic Burch colposuspension. Other reported ultrasonographic findings after colposuspension include decreased posterior urethrovesical angle, ventrocranial displacement of bladder neck, and reduced incidences of bladder neck funneling and bladder hypermobility. Successful colposuspension was found to be associated with a more anterior, although not necessarily more elevated, urethrovesical position. However, a trend that urethral support decreases with time has been noted on ultrasound in patients having undergone either open or laparoscopic Burch colposuspension. In patients developing posterior bladder or vaginal support defects, cystocele and enterocele may be detected on ultrasound. Urinary retention and late voiding difficulty occur in up to 20% of women after colposuspension. One of the precipitating factors is bladder neck overcorrection with elevation and fixation of the bladder neck. Viereck et al. (2004) showed that the differences of preoperative and postoperative vertical height of the bladder neck are associated with postoperative voiding complaints, such as urgency, de novo urge incontinence, or voiding difficulty. The tension-free vaginal tape (TVT) procedure is one of the most widely performed minimally invasive surgeries for treating female stress incontinence. The TVT is highly echogenic and easily identified posterior to the urethra on ultrasound. In general, bladder neck mobility remains unchanged after TVT. However, urethral angulation and ventrocaudal movement of the TVT tape toward the symphysis pubis have been visualized on ultrasound during straining in patients who have received TVT. The mode of action seems to be associated with dynamic kinking of the urethra during straining or compression of the urethra against the posterior surface of the symphysis pubis, or both (Fig. 10-10). Studies have reported variable effects of the TVT procedure on voiding function. The incidence of urinary retention or obstructive voiding symptoms has been reported to be 2.3% to 14% after the TVT procedure, and the postvoid residual urine volume is often increased postoperatively. Excessive angulation of midurethra at rest, suggesting overlift of the urethra by the tape, and acute narrowing of the central echolucent area of the urethra at rest are reported ultrasonographic findings implying postoperative obstructive voiding dysfunction. Voiding Dysfunction. Estimation of postvoid residual urine volume is best done by ultrasonography and is an important method of screening for voiding dysfunction. The cause of voiding dysfunction may relate to the bladder, the urethra, or both. Bladder factors include detrusor underactivity or areflexia; urethral causes consist of functional or mechanical obstruction, which can further be categorized as compressive or constrictive. On sonography, the urethra is shown as a tubular structure; a hypoechoic center represents the urethral mucosa (see Fig. 10–6). The hypoechoic nature is kept even when the urethral mucosa is prolapsed. Voiding dysfunction may result from dis-
Figure 10-10 ■ Dynamic change of the lower urinary tract in a case 8 months after TVT procedure: at rest (A) and during stress (B). Introital sonography shows the TVT, which is hyperechogenic and located posterior to the midurethra. During stress, hypermobility of the bladder neck and compression of the urethra against the posterior surface of the symphysis pubis occur. With a reference to the midline of the symphysis pubis, the bladder neck-pubic symphyseal angles are 87 degrees and 118 degrees at rest and during stress, respectively. The distances between bladder neck and inferior border of the symphysis pubis are 25 mm at rest and 23 mm during stress. The distances between inferior border of TVT and inferior border of the symphysis pubis are 13 mm at rest and 11 mm during stress, respectively. SP, Symphysis pubis; bl, bladder; u, urethra.
tortion of the anechoic urethral mucosa by intraluminal lesion (i.e., urethral stricture) or extramural factors, such as a diverticulum or an overlifted TVT. The pathophysiologic mechanism of voiding dysfunction secondary to an impacted pelvic mass, such as the retroverted gravid uterus or a fibroid in the posterior uterine wall, is different from that originated from the overelevation of bladder neck suspension procedure or secondary to genitourinary prolapse. Voiding dysfunction in cases of an impacted pelvic mass is caused by a displaced cervix compressing the lower bladder, obstructing the internal urethral orifice. The urethra itself is not compressed or distorted. Anal Incontinence. High-resolution ultrasound has emerged as the modality of choice in imaging anal sphincter defects and is integral in planning treatment for this distressing problem. The role of ultrasound in the diagnosis and management of anal incontinence is discussed in detail in Chapter 24.
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INTERVENTIONAL APPLICATION Minimally invasive methods of diagnosis and treatment are the trend for current and future health care. Transvaginal ultrasound provides high-resolution imaging of the lower urinary tract and may serve as an aid in the management of lower urinary tract disorders, with minimal invasiveness. With the combination of ultrasonography and flexible cystoscopy, percutaneous suprapubic cystostomy can be performed by a stab technique, with minimal risk to the surrounding pelvic organs. In the procedure of urethral dilation for urethral stricture, transvaginal ultrasound is helpful in preventing the hazard of urethral perforation and creation of a false passage, a possible sequela from the blind dilation. Even in the presence of extensive stenosis, the urethral mucosa appears as a hypoechoic area on ultrasonography. Thus, under ultrasonographic guidance, advancement of the dilator exactly through the echolucent part of the urethra ensures penetration of dilators into the correct tissue plane. Vesicovaginal fistula causes social inconvenience and psychological impact on women. The treatment of a vesicovaginal fistula includes bladder drainage and surgery, depending on the size and location of the fistula. Adequate and undisturbed drainage results in closure of small posthysterectomy fistulas in 12% to 80% of cases, but the outcome is unpredictable. Some suggest that 2 months are adequate for a vesicovaginal fistula to close spontaneously. If the fistula does not close, it must be repaired surgically. The timing of surgical intervention is most important and is best determined by periodic evaluation of tissue. Transvaginal sonography offers serial, noninvasive assessment of the condition of the bladder wall and fistula, and helps in determining the timing of surgical repair. After a major procedure in which surgical damage to the lower urinary tract or postoperative bladder bleeding is a possibility, it is required that the bladder is adequately drained and does not become overdistended. Cystoscopy may be helpful for determining the cause of blockage and evacuation of clots when bladder drainage fails because of obstruction, kinking, or displacement of catheter. However, severe hematuria may obscure the cystoscopic view and require high-flow irrigation, which carries a risk of bladder rupture. Transvaginal sonography has been reported to be an effective and safe tool in the treatment of acute urinary retention due to intravesical blood clots. It can help in identifying and localizing the clots without causing further instrumental injury to the bladder wall, and it can also aid in estimating the irrigating volume infused to prevent bladder overdistention. Intravesical suction and irrigation for removal of the clots may then be performed more efficiently.
Conclusions and Future Investigation A comprehensive evaluation of the female lower urinary tract is based on clinical history, physical examination, urodynamics, and imaging studies. Ultrasound is a valuable alternative to radiography and allows functional-morphologic documentations. With increasing knowledge of its application in the female lower urinary tract, more diagnostic and surgical procedures may be performed in a less invasive way with the aid of ultrasound. For female lower urinary tract disorders, performing transvaginal and introital sonography at the same time by using an endovaginal probe is more conve-
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nient to help diagnose both gynecologic or nongynecologic conditions. The levator ani muscles play an important role in supporting pelvic organs and maintaining normal pelvic floor function. With high-resolution images of the muscular tissues, MRI has been widely used for the morphologic investigation of the pelvic floor. However, MRI is currently not suitable for a large-scale survey because of its sophistication and expense. On the other hand, ultrasonography may be suitable for large-scale investigations owing to its availability and lower cost. Furthermore, three-dimensional ultrasound is able to perform volume calculation and scan simultaneously pelvic organs in axial, transverse, and coronal planes. With advances in technology and expertise, ultrasound may replace MRI in evaluating the morphology and function of levator ani muscles in the near future. Perineal and translabial ultrasound can be used to indirectly observe the function of levator ani muscles by viewing the displacement of pelvic structures (e.g., bladder neck or bladder base) with levator contraction. The bladder and urethra move upward and ventrally during pelvic floor contractions. Correlations between shift of bladder neck and palpation/perineometry have been shown to be good. However, the assessment of levator ani function is still regarded as inherently problematic in ultrasonography. Further studies will be needed to verify the reproducibility and validity of ultrasound in investigating levator ani muscles.
COMPUTED TOMOGRAPHY In urogynecology, CT IVP is primarily used in the evaluation of hematuria or to determine the etiology of ureteral obstruction when other imaging modalities cannot diagnose the underlying cause. CT IVP is valuable in assessing renal anatomy and function, evaluating for anomalies, and visualizing masses in the abdomen and pelvis. This diagnostic capability is due to its ability to provide cross-sectional visualization of the entire urinary tract. The helical CT technology allows rapid and continuous acquisition of scans through large areas of the body. The images are usually displayed in an axial twodimensional mode with capability for three-dimensional reconstruction. This additional capability provides even better anatomic detail of the urinary tract and its surrounding structures and allows helical CT to accurately characterize intrinsic and extrinsic causes of ureteral obstruction. Because of its ionization radiation, the length of time it takes to image pelvic organs, and its limited ability to contrast soft tissues, CT has not been used extensively to study pelvic floor disorders. It remains effective in imaging abdominal and pelvic masses and is an excellent technique to study suspected postoperative pelvic hematomas and abscesses (Fig. 10-11).
MAGNETIC RESONANCE IMAGING MRI is an increasingly important diagnostic and research tool. Its superb high-resolution images of soft tissues, multiplanar imaging capability, and high sensitivity in fluid detection allow it to evaluate areas and diagnose abnormalities not readily accomplished by other imaging modalities. In research, MRI
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Figure 10-11 ■ Pelvic CT scan of patient with a 10-cm hematoma (H) in the space of Retzius next to the bladder (B). (From Walters MD, Tulikangas PK, LaSala C, Muir TW. Vascular injury during tension-free vaginal tape procedure for stress urinary incontinence: a report of two cases and review of the literature. Obstet Gynecol 2001;98:957, with permission.)
has improved our understanding of normal and abnormal pelvic anatomy. In clinical urogynecology, MRI has been used to diagnose pelvic masses, ureteral obstruction, pelvic organ prolapse, levator abnormalities, anal sphincter defect, suburethral diverticulum, and other conditions. MRI can diagnose ureteral obstruction and its cause without using intravenous contrast material or ionizing radiation. Its disadvantages include inability to visualize ureteral calculi, the longer acquisition time for images and related difficulty with dynamic imaging, and the cost of the procedure. The use of MRI to diagnose ureteral obstruction should be reserved for patients with allergies to iodinated contrast material, contraindications to ionizing radiation, or renal failure. Strohbehn et al. (1996) compared MRI findings with periurethral and levator ani anatomy at dissection in female cadavers. The internal urethral anatomy visible on MRI was identified and confirmed histologically. The origin, lateral attachment, and insertion of the levator ani were confirmed during dissection. Their findings demonstrated that MRI images reflected actual anatomy. Kirschner-Hermanns et al. (1993) and Fielding et al. (2000) found that stress urinary incontinence was associated with atrophy, laxity, and thinning of the levator ani muscles on MRI. Klutke et al. (1990) used MRI to compare the periurethral anatomy of women with stress urinary incontinence with asymptomatic controls. They found that incontinent women have an oblique urethropelvic ligament, an inverted U-shaped vaginal lumen, and an increase in the distance between the symphysis pubis and the bladder neck. In contrast, asymptomatic controls have more horizontal urethropelvic ligaments, closer proximity of the bladder neck to the symphysis pubis, and an H-shaped vagina with the anterior vaginal wall conforming well to the urethra. Fast-scan MRI has been used to assess the presence and the severity of pelvic organ prolapse during Valsalva maneuvers. MRI findings in subjects with pelvic organ prolapse and urinary incontinence include focal changes in width, configuration, and signal intensity of the levator ani muscles; loss of
connection with urethra; and an increase in urogenital hiatus size, straining levator plate angle, and levator hiatus height. However, not all women with pelvic floor prolapse have abnormal morphologic features. A considerable variation in the size and configuration of the pelvic floor structures has been found in nulliparous asymptomatic women. It would require a study with a large sample size and strict inclusion criteria to define precisely the functional implications of specific MRI findings. Because the reference point for clinical prolapse staging (hymen) cannot be visualized on MRI, lines between anatomic landmarks, such as the inferior border of the symphysis pubis and last coccygeal joint, superior and inferior aspect of the symphysis pubis, and width of the levator hiatus, have been used as a reference to quantify prolapse. These lines were chosen for their closeness to the hymen and various other reasons. MRI can assess simultaneously all pelvic compartments and objectively grade prolapse severity. Accurate preoperative staging and identification of specific defects, such as rectocele versus enterocele and cystocele versus anterior enterocele, might allow for proper surgical planning and reduce the risk of failure. Defects, atrophy, and herniations of the levator muscles can be seen. Also, less common pelvic conditions, such as sigmoidocele, perineocele (Fig. 1012), and perineal descent, can be visualized and may thus improve surgical planning. However, MRI is not perfect in recognition of common prolapse conditions. A study by Kaufman et al. (2001) found that MRI failed to diagnose 6 of the 15 cystoceles, 8 of the 19 rectoceles, none of the 9 paravaginal defects, and none of the 2 rectal prolapses noted on clinical examination. MRI did diagnose four levator ani hernias that were not detected by pelvic examination. Kaufman et al. reported that physical examination, dynamic MRI, and dynamic cystocolpoproctography were concordant for rectocele, enterocele, cystocele, and perineal descent in only 41% of patients. The data suggest that MRI (and other imaging studies) should be used to diagnose specific conditions that are not commonly detected by clinical examination. At present, the indications and advantages of using MRI in the evaluation and management of pelvic organ prolapse remain to be determined, but it clearly is an excellent imaging tool for research in pelvic floor disorders. Hoyte et al. (2001) used reconstructed three-dimensional models of MRI to compare the pelvis of asymptomatic controls with women who have pelvic floor disorders. Their data demonstrated a statistically significant continuum in the angle, volume, shape, and integrity of levator ani, and levator-symphysis gap across groups of asymptomatic, stress urinary incontinence, and prolapse subjects. Their data also revealed that subjects with similar degree of prolapse often have different morphologic changes in their levator ani. The authors proposed that three-dimensional MRI may be used to identify a specific anatomic defect for each prolapse. Identification of anatomic defect could help guide therapy and possibly reduce the failure rate of reconstructive pelvic surgery. The authors also hypothesized that incontinent subjects with normal levator-symphysis gap (distance from the anterior-most part of the levator ani sling to the closest point of the symphysis pubis on axial view) and levator ani are more likely to respond to physiotherapy. In contrast, incontinent subjects whose levator has torn away from the symphysis probably would not be able to increase their levator tone with exercises.
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Figure 10-12 ■ Severe pelvic floor relaxation with perineocele (perineal hernia). A. Resting MRI. B. Straining MRI showing large hernia with small bowel prolapsing against the perineum.
MRI has become a valuable tool in studying the effects of childbirth on the pelvic floor. DeLancey et al. (2003) showed that 20% of parous women in their study had a visible defect in one or both levator ani muscles on MRI. Most of the abnormalities were in the pubovisceral portion of the muscle (pubococcygeus, puborectalis) with much fewer muscle defects (2%) in the ileococcygeus portion. Muscle defects were not seen in nulliparous controls. The authors further noted that stress incontinent primiparas were twice as likely to have a muscle abnormality. Despite its capability, MRI is expensive, time-consuming, and not widely available. Furthermore, findings from two- and three-dimensional MRI studies have not yet been fully validated clinically or surgically. However, they do further confirm the central role of levator ani in the pathogenesis of pelvic floor disorders and have been integral in assessing changes in the pelvic floor after childbirth and surgery. Imaging of soft tissue anatomy of the pelvis by MRI or ultrasound may allow much more precise understanding of anatomic defects and abnormalities in areas previously inaccessible except at surgery. Hopefully, this improved anatomic and functional information will eventually be used to improve patient care and surgical outcomes.
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Walters MD, Tulikangas PK, LaSala C, Muir TW. Vascular injury during tension-free vaginal tape procedure for stress urinary incontinence: a report of two cases and review of the literature. Obstet Gynecol 2001;98:957.
MAGNETIC RESONANCE IMAGING Butler H, Bryan PJ, LiPuma JP, et al. Magnetic resonance imaging of the abnormal female pelvis. Am J Roentgenol 1984;143:1259. Comiter CV, Vasavada SP, Barbaric ZL, et al. Grading pelvic prolapse and pelvic floor relaxation using dynamic magnetic resonance imaging. Urology 1999;54:454. Debaere C, Rigauts H, Steyaert L, et al. MR imaging of a diverticulum in a female urethra. J Belge Radiol 1995;78:345. DeLancey JO, Kearney R, Chou Q, et al. The appearance of levator ani muscle abnormalities in magnetic resonance images after vaginal delivery. Obstet Gynecol 2003;191:46. Fielding IR, Dumanli H, Schreyer AG. MR-based three-dimensional modeling of the normal pelvic floor in women: quantification of the muscle. Am J Roentgenol 2000;174:657. Gearhart SL, Pannu HK, Cundiff GW, et al. Perineal descent and levator ani hernia: a dynamic magnetic resonance imaging study. Dis Colon Rectum 2004;47:1298. Hodroff MA, Stolpen AH, Denson MA, et al. Dynamic magnetic resonance imaging of the female pelvis: the relationship with the pelvic organ prolapse quantification staging system. J Urol 2002;167:1353. Hoyte L, Schierlitz L, Zou K, et al. Two- and 3-dimensional MRI comparison of levator ani structure, volume, integrity in women with stress incontinence and prolapse. Am J Obstet Gynecol 2001;185:11. 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. Kester RR, Line L, Amendola MA, et al. Value of express T2-weighted pelvic MRI in the preoperative evaluation of severe pelvic floor prolapse: a prospective study. Urology 2003;61:1135. Khati NJ, Javitt MC, Schwartz AM, et al. MR imaging diagnosis of a urethral diverticulum. Radiographies 1998;18:517. Kirschner-Hermanns R, Wein B, Niehaus S, et al. The contribution of magnetic resonance imaging of the pelvic floor to the understanding of urinary incontinence. Br J Urol 1993;72:715. Klutke C, Golomb J, Barbaric Z, et al. The anatomy of stress incontinence: magnetic resonance imaging of the female bladder neck and urethra. J Urol 1990;143:563. Maubon A, Aubard Y, Berkane V, et al. Magnetic resonance imaging of the pelvic floor. Abdom Imaging 2003;28:217. Mostafavi MR, Saltzman B, Prasad PV. Magnetic resonance imaging in the evaluation of ureteropelvic junction obstructed kidney. Urology 1997;50:601. Regan F, Bohlman ME, Khazan R, et al. MR urography using HASTE imaging in the assessment of ureteric obstruction. Am J Roentgenol 1996;167:1115. Reuther G, Kiefer B, Wandl E. Visualization of urinary tract dilatation: value of single-shot MR urography. Eur Radiol 1997;7:1276. Siegelman ES, Banner MP, Ramchandani P, et al. Multicoil MR imaging of symptomatic female urethral and periurethral disease. Radiographics 1997;17:349. Singh K, Reid MN, Berger LA. Assessment and grading of pelvic organ prolapse by use of dynamic magnetic resonance imaging. Am J Obstet Gynecol 2001;185:71. Singh K, Reid WM, Berger LA. Magnetic resonance imaging of normal levator ani anatomy and function. Obstet Gynecol 2002;99:433. Singh K, Jakab M, Reid WM, et al. Three-dimensional magnetic resonance assessment of levator ani morphology features in different grades of prolapse. Am J Obstet Gynecol 2003;188:910. Strohbehn K, Quint LE, Prince MR, et al. Magnetic resonance imaging of the female urethra: a direct histologic comparison. Obstet Gynecol 1996;88:750. Tunn R, DeLancey JO, Howard D, et al. 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. Umek W, Kearney R, Morgan DM, et al. The axial location of structural regions in the urethra: a magnetic resonance study in nulliparous women. Obstet Gynecol 2003;102:1039.
Neurophysiologic Testing for Pelvic Floor Disorders
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Matthew D. Barber
ELECTRODIAGNOSTIC TESTING 138 Electromyography 139 Kinesiologic EMG 140 Concentric Needle EMG 141 Single Fiber EMG 145 NERVE CONDUCTION STUDIES 145 PNTML and PeNTML 145 Lower Extremities 147 SACRAL REFLEXES 147 AUTONOMIC TESTING 148 PELVIC FLOOR DISORDERS 148 Childbirth Injury 148 Stress Urinary Incontinence 149 Voiding Dysfunction 149 Fecal Incontinence 149 NEUROLOGIC CONDITIONS 151 Brain Lesions 151 Parkinson’s Disease/Multiple System Atrophy (MSA) Spinal Cord Lesions 151 Conus Medullaris and Cauda Equina Lesions 151 Lumbosacral Plexus Lesions 152 Peripheral Neuropathy 152 Pelvic Plexus Injury 153
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Gynecologists frequently encounter patients with abnormal bowel, bladder, and sexual function. Normal pelvic visceral function depends on the complex interactions of intact somatic and autonomic nervous systems. Several diseases or injuries of the central and peripheral nervous systems can result in alterations in pelvic visceral function (Box 11-1). The clinical evaluation of patients with urinary incontinence, fecal incontinence, voiding dysfunction, defecatory dysfunction, or pelvic organ prolapse should include a history and physical examination that includes a clinical neurologic evaluation. When this evaluation suggests the possibility of an underlying neurologic condition, several neurophysiologic tests can be performed to assist in diagnosis. Commonly
used tests to evaluate the autonomic function of the bladder and bowel include urodynamics and anal manometry. Tests that are used to directly investigate the integrity of the somatic innervation of the pelvic floor muscles and urinary and anal sphincters include electromyography (EMG), nerve conduction studies (e.g., the pudendal nerve terminal motor latency [PNTML]), and the electrophysiologic evaluation of the sacral reflexes. Neurophysiologic tests have played an important role in expanding our understanding of the relationship among vaginal childbirth, pelvic floor denervation, pudendal neuropathy, and the development of disorders of the pelvic floor such as urinary and fecal incontinence and pelvic organ prolapse. Recent studies suggest that neurophysiologic testing may have a prognostic role in predicting likelihood of success for certain therapies, such as Burch colposuspension for treatment of stress urinary incontinence and sacral neuromodulation for the management of refractory urge urinary incontinence and fecal incontinence. This chapter will review the common neurophysiologic tests used to investigate pelvic floor dysfunction, including EMG, nerve conduction studies, and sacral reflex studies.
ELECTRODIAGNOSTIC TESTING Common neurophysiologic tests used to investigate peripheral neurologic disease include EMG, nerve conduction studies, and spinal reflex testing. These tests are often performed together, because each provides unique information about the integrity of the nervous system. The results of electrodiagnostic testing should always be interpreted in the context of the patient’s clinical presentation and examination findings. Other tests that are often useful in evaluation of the patient with pelvic floor symptoms and suspected neurologic disease include urodynamics, anal manometry, magnetic resonance imaging (MRI) (lumbar and pelvic), dynamic proctography, and endo-anal ultrasound. The following section is intended to provide a fundamental overview of the neurophysiologic tests commonly used in the investigation of pelvic floor disorders. Some
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NEUROLOGIC CAUSES OF BOWEL AND BLADDER DYSFUNCTION
Brain Lesions Dementia Frontal lobe lesion Cerebrovascular accident Parkinson’s disease Multiple sclerosis Hydrocephalus Multiple systemic atrophy (Shy-Drager syndrome) Spinal Cord Lesions Spinal cord injury Intervertebral disk disease Multiple sclerosis Spinal stenosis Transverse myelitis Infections (Lyme’s disease, herpes zoster, AIDS, polio, tabes dorsalis) Neoplasm Infarction Cauda Equina Lesions Intervertebral disk disease (central herniation) Spinal stenosis Trauma Ankylosing spondylitis Peripheral Nerve Lesions Childbirth-related injury Radical pelvic surgery Trauma Guillain-Barré syndrome Radiation Diabetes mellitus Neoplasm Endometriosis ● ● ● ● ● ● ●
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BOX 11-2
INDICATIONS FOR NEUROPHYSIOLOGIC TESTING OF THE PELVIC FLOOR
Incontinence or voiding dysfunction associated with abnormal lower extremity or sacral neurologic examination Pelvic floor disorder in a patient with known neurologic disease (i.e., multiple sclerosis, Parkinson’s disease, etc.) Voiding dysfunction in young women Urinary retention in patient without obvious cause (i.e., advanced pelvic organ prolapse, previous anti-incontinence surgery) Diabetic patients with bowel or bladder disorders Evaluation for neurogenic fecal incontinence Prior to anal sphincter repair (for prognosis and/or sphincter mapping) Unexplained perineal numbness or pain For differentiation between early Parkinson’s disease and multiple systemic atrophy Bowel or bladder dysfunction unexplained after standard evaluation Potential Indications (under investigation): Prior to Burch colposuspension (for prognosis) Prior to sacral neuromodulation in patient with refractory urge urinary incontinence or fecal incontinence
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common indications for neurophysiologic testing of the pelvic floor are listed in Box 11-2.
Electromyography (EMG) The term electromyography is a general term that refers to methods of studying electrical activity of muscle. Various EMG techniques exist, each with its own indications, advan-
tages, and limitations. Of the many EMG techniques, only a few have use for the study of pelvic floor disorders. EMG techniques study neuromuscular activity of striated muscles, using a recording electrode that is inserted into or placed on the surface of a muscle. Bioelectric potentials generated by the depolarization of the skeletal striated muscle are picked up by this electrode and then filtered and amplified. They are displayed on an oscilloscope for visual analysis and fed
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through a speaker system so that they can be monitored acoustically. Modern computer-based equipment allows for conversion of the signal into digital data that can then be easily stored, processed, and analyzed. Electromyographic studies used to evaluate pelvic floor disorders can be separated broadly into two categories: kinesiologic EMG (kEMG) and motor-unit EMG. Kinesiologic EMG is used to simply assess the activity or inactivity of a muscle, usually the urethral or anal sphincter; it is used in conjunction with physiologic tests, such as urodynamics and anal manometry, to assess sphincter relaxation during voiding or defecation. Kinesiologic EMG is also used for biofeedback during pelvic muscle rehabilitation for treatment of urinary or fecal incontinence. In contrast, motor-unit EMG is a diagnostic test used to assess the neuromuscular function of a muscle. It can differentiate normal muscle from denervated/reinnervated or myopathic muscle. Common techniques used for motor-unit EMG are concentric needle EMG (CnEMG) and single-fiber EMG (SfEMG). Motor-unit EMG that uses computer-assisted digital analysis to obtain a faster, more standardized and detailed assessment of neuromuscular function than traditional needle EMG is known as quantitative EMG (qEMG). The general principles, techniques, interpretation, and limitations of each EMG technique as it applies to the investigation of pelvic floor disorders and sacral neurologic disease are outlined in the next section.
Kinesiologic EMG Kinesiologic EMG is used to assess the activity or inactivity of a muscle during a defined activity. The technique provides information on the timing of a muscle contraction by recording the increase in electrical activity that occurs during a contraction through surface or wire/needle electrodes placed on or within the specific muscle(s) being investigated. This increase in electrical activity correlates moderately with muscle strength and has been used by some as a surrogate for measuring this parameter. However, kEMG cannot be used to detect neuropathic or myopathic changes within a muscle. In the investigation of pelvic floor disorders, kEMG is used most frequently during urodynamic evaluations. Specifically, it is used to assess urethral sphincter and/or pelvic floor muscle activity during voiding. By simultaneously recording pelvic floor muscle activity using kEMG, and detrusor pressure using the urodynamic pressure catheters, detrusor/sphincter coordination can be assessed. The primary role of kEMG in this context is to detect the condition of detrusor sphincter dyssynergia in which a detrusor contraction is coupled with a simultaneous urethral sphincter contraction, resulting in abnormal voiding and frequent urinary retention. Similarly, kEMG can also be used to investigate coordinated relaxation of the levator ani muscles during defecation. This EMG technique has been used by some to diagnose anismus, a condition characterized by an inappropriate contraction of the levator ani complex, particularly the puborectalis muscle, during defecation resulting in obstructed evacuation. Another common use for kEMG is to provide visual and/or audio biofeedback of pelvic floor muscle activity during a pelvic
muscle exercise program for treatment of urinary or fecal incontinence. Pelvic floor rehabilitation using biofeedback has long been advocated as more effective than teaching pelvic muscle exercises with verbal instructions alone, although recent studies by Burgio et al. (2002) have called this into question. Kinesiologic EMG can be performed with various types of surface or intramuscular (needle or wire) electrodes. Surface electrodes measure the net electrical activity within a muscle. They have the advantage of being simple and noninvasive; however, they are prone to artifact and contamination from signals from other muscles. Because they measure net electrical activity of a muscle and are not capable of measuring individual motor unit potentials, surface electrodes cannot be used to diagnostically evaluate for denervation/reinnervation injury or myopathic diseases. Surface electrodes are used commonly for biofeedback for pelvic floor strengthening in the treatment of urinary or fecal incontinence. For measuring levator ani activity, two small circular skin electrodes are commonly applied on each side of the perineum at 1 cm anterior to the anus. Anal plugs with concentric ring electrodes are commonly used to assess external anal sphincter activity for biofeedback-assisted sphincter strengthening for the treatment of fecal incontinence. Similarly, ring electrodes placed on a Foley catheter at 1 cm distal from the balloon have been used to measure urethral sphincter activity. Electrical activity measured from surface or ring electrodes are amplified and visually displayed on a computer screen and/or audibly projected through a speaker system to provide the patient with immediate feedback during a contraction. Often surface electrodes are also placed on the gluteus or abdominal muscles so that patients can learn to appropriately contract their pelvic floor/sphincter muscles while avoiding simultaneous contraction from other surrounding muscle groups. To evaluate detrusor-sphincter coordination in a patient with voiding dysfunction, kEMG is performed in conjunction with a urodynamic evaluation. Either surface electrodes are applied to the perineum as described earlier, or a wire electrode is placed periurethrally into the urethral sphincter. The electrical activity of the pelvic floor/urethral sphincter is then recorded during the voiding phase of the study. In a neurologically intact subject, voiding is characterized by cessation of all sphincter EMG activity just before contraction of the detrusor muscle. In patients who have spinal cord lesions between the lower sacral segments and the upper pons, coordination between the detrusor muscle and the urethral sphincter can be lost. This detrusor sphincter dyssynergia is characterized by an increase in sphincter EMG activity during a detrusor contraction rather than a decrease, and these patients typically have severe voiding dysfunction and urinary retention. As a diagnostic test, except for the evaluation of detrusor-sphincter coordination, the relevance of kEMG is unclear, and no standardized method for performing or interpreting kEMG has been accepted. In the artificial setting of the urodynamic laboratory, many neurologically intact women will contract their urethral sphincter during voiding because of embarrassment and/or the discomfort of the urethral
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catheters and electrodes. Therefore, it is important to ask the patient whether she is trying to stop voiding voluntarily so that detrusor sphincter dyssynergia is not diagnosed in error. In a study of 550 consecutive patients, Blaivas et al. (1981) found that dyssynergia was found only in patients with welldefined lesions of the suprasacral spinal cord. Therefore, the diagnosis of detrusor sphincter dyssynergia made in the absence of other neurologic deficits consistent with this level of injury should be suspect. Inappropriate urethral contraction during voiding can also be a learned behavior resulting in dysfunctional voiding. As a method of biofeedback, kEMG is useful, but the limitations associated with surface electrodes still apply.
Concentric Needle EMG CnEMG is a widely used diagnostic test for evaluating the neuromuscular integrity of skeletal muscles. It can be used to differentiate normal muscle from muscle that is neuropathic or myopathic. A concentric needle electrode consists of a stainless-steel outer cannula within which runs a fine silver, steel, or platinum wire that is insulated except at its tip. The concentric needle is inserted into a muscle where the inner wire serves as a recording electrode, whereas the outer cannula serves as a reference electrode. Bioelectrical potentials are measured as voltage differences between the two electrodes that are then recorded, displayed, and analyzed. A CnEMG examination provides information on the insertional activity, spontaneous activity, motor-unit action potentials (MUAPs), and recruitment pattern (also known as interference pattern) of a muscle. Interpretation of each component provides the examiner with information about the presence and duration of neuropathic and/or myopathic injury to the examined muscle (see later). CnEMG can be performed on an individual muscle, as on the anal sphincter when evaluating isolated fecal incontinence, or systematically performed on several muscles to determine the level of a neurologic injury. All muscles that are innervated by one spinal segment (level) are referred to as a myotome. Using CnEMG to systematically evaluate several muscles in different myotomes often permits localization of a lesion to the spinal root, nerve plexus, or an individual peripheral nerve. In a patient with bowel or bladder dysfunction in which a neurologic cause is suspected, a thorough evaluation often requires EMG of the lower extremity as well as pelvic floor musculature. TECHNIQUE The clinical history and sacral neurologic examination should be reviewed carefully before beginning the EMG evaluation, because this will help determine which muscles should be examined. Ideally, the evaluation should be performed in a shielded room to prevent interference from other electronic devices or AC power cords. The patient is placed in a comfortable position that allows access to the pelvic floor musculature, usually the dorsal lithotomy or lateral decubitus positions. A grounding surface electrode is applied. Most laboratories do not use local anesthetics in any form before insertion of the needle electrodes, although some authors advocate
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using a topical anesthetic, particularly for examination of the urethral or anal sphincter. After wiping the skin overlying the appropriate muscle with alcohol, the concentric needle electrode is inserted until the insertional activity of the muscle is noted, confirming that the electrode is within the muscle. The EMG investigation consists of analysis of electrical activity at rest (assessment of spontaneous activity), at slight voluntary contraction (MUAP analysis), and at strong contraction (interference pattern analysis). Generally, the most painful portion of the examination is the initial insertion through the skin, so several sites within the muscle should be sampled by moving the tip of the needle without removing it from the skin. Depending on the muscle, more than one skin penetration may be necessary. Both the visual output on the screen of the EMG machine and the audio output from the speaker are used to assess the quality of the recording and to identify electrophysiologic phenomena. Commonly used settings for CnEMG evaluation of the pelvic floor muscles are filter settings 5 Hz to 10 kHz; horizontal sweep speed 10 msec/div; and gain setting 50–500 μV/div. ANAL SPHINCTER Both the subcutaneous and deep portions of the external anal sphincter (EAS) are accessible for CnEMG evaluation. To study the subcutaneous portion of the EAS, the needle electrode is inserted 1 cm outside the mucocutaneous junction of the anal orifice, to a depth of 3 to 6 mm beneath the skin. The deep portion of the EAS is assessed by inserting the needle at the mucocutaneous junction of the anus, at an angle of about 30 degrees to the anal canal axis, for a depth of 1 to 3 cm. Typically, the subcutaneous and/or deep portion of the EAS are sampled in at least four quadrants, roughly divided into the upper and lower, left and right portions of the sphincter. Ideally, 20 or more MUAPs should be sampled during the evaluation (Fig. 11-1). “Anal mapping” has been used in the past to identify the location of a sphincter defect before an anal sphincteroplasty in the treatment of fecal incontinence. To identify the precise location of a sphincter defect, more needle insertions are typically required, usually at 9 o’clock, 10 o’clock, 12 o’clock, 2 o’clock, 3 o’clock, and 6 o’clock positions. Endo-anal ultrasound has largely replaced anal mapping with EMG for the identification and localization of sphincter defects. URETHRAL SPHINCTER The external urethral sphincter can be studied by inserting the electrode into the sphincter muscle periurethrally or transvaginally. For the periurethral approach, the needle is inserted approximately 5 mm anterior to the external urethral meatus (12 o’clock) to a depth of about 1 to 2 cm. For the transvaginal approach, the posterior vaginal wall is retracted with a speculum, and the needle is inserted approximately 2 cm proximal to the external urethral meatus, off the midline and directed laterally into the urethral sphincter. Although slightly more painful, the periurethral approach provides superior sampling of the urethral sphincter, obtaining as many as twice the number of MUAPs as the transvaginal approach. At least 10 MUAPs should be recorded to adequately evaluate the urethra.
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or lumbosacral plexus. These lesions typically also affect innervation of the lower extremity. Therefore, whenever a patient’s history and examination suggest lower extremity involvement as well as bowel and/or bladder dysfunction, the electrophysiologic evaluation should include the muscles of the lower extremity as well as the pelvic floor. A detailed description of the CnEMG evaluation of the lower extremity musculature is beyond the scope of this text. However, muscles that are often useful in such an evaluation include quadriceps (L3, L4; femoral nerve); adductor longus (L4; obturator nerve); tibialis anterior (L4, L5; deep peroneal nerve); gastrocnemius (S1, S2; tibial nerve); gluteus maximus (S1; superior gluteal nerve); gluteus medius (L5; inferior gluteal nerve); adductor hallucis brevis (S1, S2; tibial nerve); and the paraspinal muscles from L3 to S1. INTERPRETATION
Figure 11-1 ■ Concentric needle EMG of the anal sphincter. The subcutaneous portion of the external anal sphincter (EAS) is examined by inserting the needle electrode (A) 1 cm outside the mucocutaneous junction of the anal orifice, to a depth of 3 to 6 mm beneath the skin. The deep portion of the EAS is assessed by inserting the needle (B) at the mucocutaneous junction of the anus, at an angle of about 30 degrees to the anal canal axis, for a depth of 1 to 3 cm. The subcutaneous and/or deep portion of the EAS are sampled in four quadrants, divided into the upper and lower, left and right portions of the sphincter (inset). (Reprinted with the permission of The Cleveland Clinic Foundation.)
BULBOCAVERNOSUS MUSCLE The bulbocavernosus muscle is a readily accessible perineal muscle that is innervated by the perineal branch of the pudendal nerve. The bulbocavernosus muscle can be reached either transmucosally, with a needle insertion medial to the labia minora, or through the skin lateral to the labia majora. LEVATOR ANI The iliococcygeus and pubococcygeus portions of the levator ani muscle complex are most easily investigated using a transvaginal approach. The muscles are localized by first inserting two fingers into the vagina and asking the patient to contract. One side of the levator complex is isolated, and the electrode is inserted using the opposite hand in at least two sites on the muscle. This is then repeated on the opposite side. Although there is no standardized location for needle insertion into the levator ani muscles, one technique that has been proposed uses the ischial spine as a fixed reference point and samples two sites relative to this easily identifiable landmark (Weidner et al., 2000). The first site is located 2 cm caudal and medial from the ischial spine. The second site is 2 cm farther medial. The puborectalis muscle can be accessed from a perineal approach. A 75-mm electrode is required and inserted approximately 1 cm posterior to the anus in the midline for a depth of approximately 3 cm. LOWER EXTREMITY Bladder and bowel dysfunction are not uncommon when there are lesions involving the lumbosacral nerve roots and/
CnEMG is a valuable tool for evaluating lower motor neuron disease and muscle disease. Lesions involving the upper motor neurons in isolation have a normal EMG evaluation. The initial assessment in any CnEMG examination is an evaluation for insertional activity. Insertional activity is the electrical activity that occurs when the needle electrode is first introduced into a muscle or is moved, is the result of mechanical stimulation or injury of the muscle fibers, and usually stops within about 2 seconds of movement. The presence of insertional activity confirms that the electrode has been placed within the muscle. Absence of insertional activity with an appropriately placed needle electrode usually means a complete atrophy of the examined muscle. Once the needle has been properly placed, the patient is asked to completely relax the muscle being examined, and the presence or absence of spontaneous activity is assessed. Denervated muscle fibers may produce rhythmic spontaneous electric potentials, such as fibrillation waves or positive sharp waves. The presence of this spontaneous activity in a resting muscle is a sign of denervation. In the urethral sphincter, the anal sphincter, and the levator ani muscles, which all tonically contract even in the resting state, the only normal spontaneous activity is normal MUAPs. In limb muscles and the bulbocavernosus muscle, which do not tonically contract, there should be a complete absence of spontaneous activity at rest. The pelvic floor muscles achieve complete electrical silence during voiding and defecation. Spontaneous activity that is found in pathologic conditions includes fibrillation potentials, positive sharp waves, complex repetitive discharges, fasciculations, myotonia, myokymia, and neuromyotonia (Fig. 11-2). Fibrillation potentials are biphasic muscle fiber potentials that occur spontaneously and typically have an amplitude of between 20 to 300 μV and a duration of less than 5 msec. They usually fire rhythmically at a rate of 2 to 20 Hz. Fibrillation potentials develop 2 to 30 days after an injury and can occur with a motor nerve lesion as well as with primary muscle diseases, such as acute muscle injury, muscular dystrophies, and inflammatory myopathies. Positive sharp waves are biphasic waves with an amplitude of 20 to 500 μV and a 1- to 5-msec duration. They are more common than fibrillations and have a similar clinical significance. Complex repetitive discharges (CRDs) are spontaneous high-frequency discharges
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Normal MUAP
Neuropathic MUAP
Nerve Injury
Myopathic MUAP Figure 11-2 ■ Examples of abnormal spontaneous activity seen during concentric needle EMG.
with a regular firing pattern beginning and ending abruptly that can be bizarre in appearance. They can be found after chronic partial denervation, muscular dystrophy, inflammatory myopathies, and in some metabolic disorders. The striated urethral sphincter appears to be particularly likely to develop CRDs, which have been found in association with urinary retention in young women (Fowler’s syndrome) and even in some neurologically normal women. The motor unit is the smallest functional unit of the motor system and consists of a motor neuron, its axon, and all of the muscle fibers innervated by the axon. The motor unit in a normal human limb muscle consists of several dozen muscle fibers lying within an area of 5 to 10 mm diameter. The MUAP is a compound potential representing the sum of the individual action potentials generated in the few muscle fibers of the motor unit that are within the pickup range of the recording electrode. After a determination about spontaneous activity is made, the patient is asked to slightly contract the muscle being examined, and attention is turned to MUAP analysis. The shape, amplitude, duration, number of phases, and stability of each MUAP should be assessed. Most EMG units have a trigger-and-delay mechanism that allows MUAPs to be “frozen” for more careful analysis. Ideally, 20 or more MUAPs should be sampled for each muscle. This is often difficult for striated urethral sphincter, where analysis of 10 MUAPs is often all that can be achieved due to the small size of the muscle. Muscles that have been denervated and reinnervated, and muscles that are myopathic, have distinct MUAP characteristics from those of normal muscle (Fig. 11-3). The morphology of a MUAP reflects, among other things, the number and local concentration of muscle fibers comprising a motor unit. After a neuronal injury, the muscle
Figure 11-3 ■ A normal motor unit (top left) consists of a motor neuron, its axon, and all of the muscle fibers that it innervates. A normal motor unit action potential (MUAP) (top) is characterized by its amplitude, duration, and number of phases (usually three to four). Denervation of a motor unit (middle) results in death of some motor fibers and reinnervation of others via collateral sprouting from an adjacent motor unit axon. This results in a more complex MUAP with greater amplitude, duration, and number of phases. Myopathy (bottom) results in death of muscle fibers without subsequent reinnervation, resulting in MUAPs with decreased amplitude.
fibers innervated by that neuron begin to atrophy. Adjacent nerve fibers attempt to reinnervate these denervated muscle fibers, resulting in a neuron that now supplies a greater number of muscle fibers. This creates a MUAP with larger amplitude, longer duration, and a greater number of phases and turns. Because these changes depend upon reinnervation by an adjacent motor neuron, large complex polyphasic MUAPs are not typically seen until 3 to 6 months after a nerve injury. In the setting of an acute nerve injury, reinnervation has not had time to occur and MUAP morphology is normal. Myopathic injury results in a loss of muscle fibers and therefore a motor unit with fewer muscle fibers. This results in a MUAP with shorter duration and smaller amplitude than normal. After performing MUAP analysis, the patient is asked to increase her contraction effort, and motor-unit recruitment is assessed. In normal muscle, as the force of voluntary contraction increases, motor units are recruited in a specific order that is determined by the thresholds inherent to the individual unit. Therefore, a sequential increase occurs in the firing rate of MUAPs as well as a sequential acquisition of new higher threshold MUAPs as the force of voluntary contraction increases. Analyzing this pattern of recruitment, often called an interference pattern, provides additional information about the health of a muscle and its innervation.
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Figure 11-4 ■ Normal interference pattern (top); neuropathic interference pattern characterized by increased amplitude, reduced number of MUAPs, and a rapid rate (middle); myopathic interference pattern characterized by decreased amplitude and a normal number of MUAPs (bottom); myopathic interference patterns become “full” at lesser degrees of muscle contraction.
An interference pattern is called “full” or “complete,” when the number and firing rate of the individual MUAPs becomes so great that they can no longer be distinguished and the baseline is obscured (Fig. 11-4). Recruitment is normal when a complete interference pattern occurs at maximal effort. In neuropathic disorders, a reduced number of motor units is present so a decreased recruitment and an incomplete interference pattern are present, although the remaining units fire rapidly. In myopathic disorders, muscle fibers are reduced and the number of motor units is normal. A complete interference pattern is seen, but it occurs at much less than maximal effort, and the amplitude to the MUAPs is reduced. The chronicity of a nerve lesion can be determined by the CnEMG features present. In an acute nerve lesion, reinnervation has not occurred so the MUAPs have normal morphology. The number of motor units is reduced, however, so recruitment is decreased. Between 2 and 30 days after an injury, spontaneous activity, such as fibrillation potentials and positive sharp waves, become apparent and insertional activity becomes longer. Between 3 and 6 months after an injury, reinnervation has occurred so the MUAPs become larger and more complex. The location of a nerve lesion is determined by the pattern of muscles demonstrating denervation. For instance, neuropathic CnEMG findings in the external anal sphincter, but normal findings in the levator ani muscle and bulbocavernosus muscle, suggest an isolated lesion involving the inferior rectal branch of the pudendal nerve. In contrast, if neuropathic findings were found in the external anal sphincter, the right levator ani muscle, the right gluteus maximus and gluteus medius muscles—but not on the left side or in the L5, S1 paraspinal muscles—this would suggest a right-sided lumbosacral plexus lesion. Traditionally, CnEMG has depended largely on an examiner’s auditory and visual impression for analysis. In an attempt to improve the accuracy, reliability, and speed with
which CnEMG can be performed, quantitative techniques have been developed. Although the first form of qEMG was introduced in the 1950s, it did not become widespread until recently, when newer EMG machines became computerized. The technical aspects of performing a qEMG evaluation are identical to conventional CnEMG described earlier. The difference is in the analysis, where computerized digital analysis is performed on the collected EMG data, allowing a much more detailed evaluation of neuromuscular function in a shorter period. Two complementary forms of qEMG are (1) analysis of multiple motor unit action potentials (multi-MUAP analysis) and (2) interference pattern analysis. In several recent studies, qEMG has been applied to the investigation of the pelvic floor muscles. In multi-MUAP analysis, the examiner identifies a period of crisp EMG activity during a slight-to-moderate muscle contraction. The computer uses a system of template matching to automatically extract, quantify, and sort any welldefined MUAPs according to their shape. This allows a rapid acquisition of data, such that the 20 to 30 MUAPs needed to adequately describe a muscle can be obtained in only a few minutes. Several MUAP parameters are then quantified, including amplitude, duration, area, number of phases, number of turns, rise time, and spike duration. Thickness (area/amplitude) and size index (2 × log [amplitude + area/ amplitude]) are automatically calculated by the computer and assist in differentiating between normal and myopathic or neuropathic muscles. Normative data for the external anal sphincter and levator ani muscles have been published and are available for comparison. Interference pattern analysis is a broad term used to describe one of several automatic quantitative techniques for evaluating muscle recruitment. Computerized analysis of interference patterns is particularly useful because the EMG signal recorded at even a moderate contraction is too dense to be accurately assessed by visual inspection. The most popular technique for interference pattern analysis is turns/ amplitudes cloud analysis (Fig. 11-5). This method of analysis is even faster than multi-MUAP analysis (2 to 3 minutes) and does not require a standardized force of contraction, eliminating an important source of variability. Although CnEMG is the most valuable tool for investigating lower motor neuron damage of the pelvic floor, it has several limitations. The primary limitation of needle EMG techniques in the evaluation of women with pelvic floor dysfunction is the lack of experience on the part of most gynecologists and the limited access to qualified experts with interest in studies of pelvic floor muscles and sphincters. The role of CnEMG in the day-to-day evaluation and management of patients with urinary and fecal incontinence or other pelvic floor disorders has yet to be established, and thus far appears to be limited. Techniques for EMG of the pelvic floor muscles have yet to be standardized, although some progress has been made by Podnar et al. (1999, 2000, 2002) and others toward standardization of the evaluation of the anal sphincter. The adoption of qEMG techniques has improved the speed, accuracy, and reliability of conventional CnEMG evaluations, but widespread applicability remains limited because of the specialized equipment and expertise needed. The concentric needle electrode is invasive and can be painful, although it is usually well tolerated in most patients.
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Amplitude (mV)
Neuropathy
Myopathy
Amplitude (mV)
Turns/second
Amplitude (mV)
Turns/second
Turns/second Figure 11-5 ■ Turn/amplitude cloud analysis is a quantitative method of analyzing interference patterns. Normal muscle (top) is characterized by all points being located within the “normal cloud” boundaries. Neuropathic muscle (middle) is characterized by MUAPs with greater amplitude and decreased turns/second, so points will be located above and to the left of the “normal cloud.” Myopathic muscle (bottom) is characterized by MUAPs with decreased amplitude, so points will be located below the “normal cloud.”
Single-Fiber EMG SfEMG is a specialized test that allows sampling of individual muscle fibers within a motor unit. An SfEMG electrode is slightly narrower than a CnEMG electrode and consists of a fine platinum of silver wire embedded in resin surrounded by an outer steel cannula. The inner wire serves as the recording electrode and exits a small aperture through the side of the electrode rather than at its tip. The pickup area of an SfEMG electrode is considerably smaller than a CnEMG electrode (300 μm vs 0.5 to 1 mm), allowing it to record only one to three individual muscle fibers within a muscle unit. The primary application of SfEMG in neurophysiologic investigation is for the diagnosis of diseases of the neuromuscular junction, such as myasthenia gravis and Eaton-Lambert syndrome; however, this application is not used in the investigation of pelvic floor muscles. The
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principal SfEMG parameter that has been applied to the pelvic floor is the measurement of fiber density. Fiber density is the mean number of muscle fibers belonging to an individual motor unit axon per detection site. A finding of increased fiber density suggests reinnervation after a denervation injury. Reinnervation of denervated muscle fibers is achieved by collateral sprouting from adjacent uninjured axons, so that an individual motor unit axon will supply more muscle fibers (i.e., increased fiber density). The measurement of fiber density requires sampling of at least 20 sites in a muscle. This usually implies four skin insertions of the electrode for each muscle, with adjustments of the position of the electrode within each insertion site. Amplifiers are set so that low-frequency activity is eliminated (500 Hz to 10 kHz) and each muscle fiber appears as a biphasic positive-negative action potential. The number of muscle fiber action potentials present at each detection site is averaged to determine fiber density. The normal fiber density of most limb muscles is approximately 2.0. The average fiber density for the anal sphincter is 1.5. Fiber density increases with both age and parity. The principal use of SfEMG and fiber density measurements in the investigation of the pelvic floor has been in the evaluation for neurogenic fecal incontinence. SfEMG is a sensitive test for detecting changes associated with reinnervation but is unable to detect changes associated directly with denervation, such as abnormal insertional activity and spontaneous activity. Therefore, SfEMG is not useful in the acute setting because 3 to 6 months are required for reinnervation to occur. Although it was used more commonly one to two decades ago, SfEMG is no longer widely used in neurophysiologic laboratories, except for the investigation of diseases of the neuromuscular junction.
NERVE CONDUCTION STUDIES PNTML and PeNTML The asymmetric distribution of ions between the inside (negative) and outside (positive) of a nerve cell creates a voltage potential, which, when breached (depolarization), allows the flow of current (electrons). Ohm’s law predicts that current, or nerve conduction, is inversely related to the resistance along the distance that the current travels. On an anatomic level, resistance is determined by the diameter of a neuron, the presence (or absence) of myelination, and the distance between nodes of Ranvier (bigger distances yield faster conduction velocities). Studies of nerve conduction all rely on the elementary formula: rate = distance/ time. The clinical significance of nerve conduction studies draws from the fact that nerve injury affects the rate at which a nerve impulse travels. For example, because resistance would increase with a demyelinating injury, conduction velocity would decrease. In a typical nerve conduction study, a voltage potential is applied between two points of known distance across a single nerve fiber. The time taken for the current to move between the two points is determined, and the rate or conduction is calculated from the aforementioned formula.
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Outside of the pelvis, both motor and sensory nerve conduction studies are performed as part of routine neurophysiologic investigation. Conduction studies can aid in the diagnosis of peripheral neuropathy and can distinguish between axonal loss and segmental demyelination. Conduction studies are also useful in localizing focal lesions to individual nerves, such as nerve entrapment syndromes (i.e., carpal tunnel syndrome). When applying these studies to pelvic floor function, two studies are performed: pudendal nerve terminal motor latency (PNTML) and perineal nerve terminal motor latency (PeNTML). The time taken for an applied stimulus to generate a motor or sensory response over a set distance is called latency (Fig. 11-6). For motor responses, the recorded contraction of a muscle in response to an electrical stimulus is called a compound motor action potential (CMAP). The amplitude of the CMAP is determined by the number of intact motor nerve fibers. However, CMAP amplitude can vary with the configuration of the test electrodes limiting its diagnostic value. Nerve latency is determined by the fastest conducting fiber stimulated. Nerve cell depolarization is an all-or-nothing event; therefore, across any one nerve fiber only a finite voltage potential can be established. A nerve is composed of many fibers, some more conductive than others. If a stimulus does not depolarize all of the fibers within the studied nerve, the latency could be falsely prolonged. In Figure 11-6 the arrangement for mea-
suring nerve conductions in the median nerve is displayed. Stimulated electrodes are placed distally and proximally, and the CMAPs are recorded from the abductor pollicis muscle. The distance is calculated between the two points of stimulation. The conduction velocity is calculated as the quotient of this distance divided by the differences in latencies from the two stimulating sites. Of importance is that the “time” portion of this equation is the distal latency subtracted from the proximal latency. Subtracting the distal latency removes the added conduction time attributed to the neuromuscular junction and muscle and allows calculation of the conduction velocity of the nerve alone. Currently, most clinicians use the St. Mark’s disposable electrode to perform PNTML and PeNTML. Figure 11-7 shows the appearance of a St. Mark’s electrode with its stimulating electrode at the tip of the second digit and receiving electrode at the base of the same digit. Commonly approached rectally, the stimulating tip is placed at the level of the ischial spine to stimulate the pudendal nerve. A receiving electrode situated at the level of the external anal sphincter detects the elicited CMAP. Stimuli of 0.1-msec duration are applied at 1-second intervals as the stimulating tip is positioned over the pudendal nerve. Current intensity is increased gradually until a supramaximal response is noted. The “ideal” location is determined at the point that the external anal sphincter muscle is felt to contract
PTML = T2 only D= unknown
D (mm) CV =
T1= unknown
T1−T2 (ms)
CV cannot be solved
Dmm Pudendal n. External anal sphincter m.
Distal Latency (T2) (ms)
Distal Latency (T2) (ms)
Proximal Latency (T1) (ms)
Figure 11-6 ■ A comparison of nerve conduction study techniques in the upper extremity and in the pelvis. Determination of nerve conduction in the median nerve, with motor responses measured from the adductor pollicis muscle (left). In this case, all components of the rate formula (Cv = conduction velocity, D = distance in millimeters, T1 and T2 = latency times in milliseconds between the two measured points) are available. Pudendal nerve terminal motor latency determination is presented (right), with motor responses measured from the external anal sphincter. In this case, neither the distance nor proximal latency can be determined, hence conduction velocity cannot be determined. ms, Milliseconds. (Reprinted with the permission of The Cleveland Clinic Foundation.)
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Figure 11-7 ■ St. Mark’s disposable pudendal electrodes fitted over the index finger of a disposable glove. Stimulating anode and cathode are positioned at the fingertip; the recording electrode is positioned at the base of the index finger.
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muscle. PNTML and PeNTML represent distal latencies; no proximal latency can be measured for the pudendal nerve. The differences in clinical information provided by PNTML and PeNTML and that of a typical nerve condition test used in the limbs cannot be underestimated. Any “prolonged” latency cannot be conclusively linked to nerve damage because conduction could be delayed due to differences in distance, neuromuscular junction transmission, muscle mass, and so forth. The American Gastroenterological Association recognized this problem in their position statement concluding that PNTML cannot discriminate between muscle weakness due to pudendal nerve injury and muscle weakness caused by muscle injury (Barnett et al., 1999). Furthermore, they condemned PNTML for (1) having poor correlation with clinical symptoms and histologic findings, (2) having lack of sensitivity and specificity for detecting external anal sphincter muscle weakness, (3) being operator-dependent, and (4) having no clear prognostic value in predicting surgical outcome.
Lower Extremities and CMAPs are maximal. PeNTML uses the same technique except that the receiving electrode is a modified bladder catheter that detects the CMAP associated with the striated urethral sphincter. The actual conduction velocity of a stimulus along these pelvic nerves is not calculated because the traveled distance is unknown; instead, only the latency is determined. Another method for measuring PNTML uses concentric needles placed in the bulbocavernosus or external anal sphincter muscles with bipolar stimulation of the perianal or perineal surfaces. Interestingly, this technique yields different results than the commonly used St. Mark’s technique. No universally agreed latency defines a patient as abnormal. Instead, each laboratory must establish its own normal values, with dysfunction typically defined as any values greater than two standard deviations from the mean. These values should consider the differences that have been demonstrated with age and sex. Additionally, each testing program should specify the patient positioning because this seems to affect the reproducibility of the technique. Generally, PNTML is considered prolonged (abnormal) when greater than 2.4 msec and PeNTML when greater than 2.6 msec. PNTML is perhaps the most common electrophysiologic test used in clinical practice for the diagnosis and management of pelvic floor disorders. This method is relatively simple and easy to learn, unlike many other neurophysiologic tests. Unfortunately, PNTML and PeNTML have significant limitations, causing some to advocate abandonment of these tests. Determination of nerve conduction requires knowledge of both the time it takes for a stimulus to generate a CMAP and the distance over which the stimulus travels. This distance should include only the studied nerve and not the neuromuscular junction or muscle, because passage through these structures would “add” time and obscure determination of conduction velocity. In measuring PNTML, the distance over which a stimulus is applied cannot be measured because of the inaccessible and circuitous route of the pudendal nerve. Moreover, the stimulus travels not only through the pudendal nerve but also through the neuromuscular junction and
When clinical evaluation suggests the possibility of a lesion involving the lumbosacral nerve roots, lumbosacral plexus, or a generalized peripheral neuropathy, nerve conduction studies of the lower extremities should be performed. Motor conduction studies of the peroneal (L4, L5) and tibial nerves (L5, S1, S2), and sensory conduction studies of the deep and superficial peroneal (L4, L5) and sural (L5, S1) nerves, can be performed. Detailed explanations of the technique and interpretation of these tests can be found in standard neurology and electrophysiology texts.
SACRAL REFLEXES The electrophysiologic testing of sacral reflexes evaluates the spinal cord reflex arc of the pudendal nerve and/or the pelvic plexus. Like the clinical examination, the two reflexes most commonly tested during neurophysiologic testing of the pelvic floor are the bulbocavernosus reflex and the anal reflex. A normal reflex implies intact efferent and afferent innervation and normal integration of the two in the sacral spinal cord (S2 to S4 level). The EMG assessment of the bulbocavernosus reflex has been found to be more sensitive than clinical assessment for detection of sacral neurologic disease. The bulbocavernosus reflex has also been called the clitoral-anal reflex, reflecting the site of the stimulating and recording electrodes, respectively. This reflex assesses the afferent and efferent branches of the pudendal nerve. It has been widely studied, is easy to learn and perform, and control data have been published by several groups. Stimulating visceral afferent neurons is possible in the lower urinary tract that travel within the pelvic plexus and cause a reflex contraction of the anal sphincter via pudendal efferent fibers. This autonomic/somatic reflex has been called the urethro-anal reflex and the bladder-anal reflex, depending upon the stimulation site. The primary goal of testing these reflexes is to evaluate for pelvic plexus pathology. The urethro-anal and bladder-anal reflexes are not as well tested
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as the somatic pudendal reflexes and have yet to be widely adopted. A recent study by Benson (2000), however, suggests that these tests may be useful in predicting the outcome of sacral neuromodulation. The bulbocavernosus reflex is assessed by applying an electrical, mechanical, or magnetic stimulus to the dorsal clitoral nerve and measuring the latency of the reflex response with recording electrodes within the anal sphincter or bulbocavernosus muscle. The strength of stimulus affects the latency (stronger stimulus results in shorter latencies) so the stimulus is slowly increased until it is about three times the patient’s sensory threshold. In some subjects, a paired stimulus 3 to 5 msec apart may be necessary to obtain a response. The bulbocavernosus reflex has two components. The first component has mean latencies of about 33 msec and is thought to be an oligosynaptic response. The second component, which is not always demonstrable, has a latency of about 70 msec and is thought to represent a polysynaptic suprasacral response. Like PNTML, individual labs are expected to define their own normal values, but, typically, a latency for the first component of the reflex is considered abnormal if it is greater than 45 msec. Stimulation can be performed on either side of the clitoris, allowing evaluation of both the right- and left-sided reflex arcs. The anal reflex is performed similarly to the bulbocavernosus reflex, but the stimulus is applied perianally. Normal latencies for the anal reflex are longer than those of the bulbocavernosus reflex, owing to the thinner myelinated nerve fibers in the afferent limb of the reflex arc. A prolonged or absent latency in either the bulbocavernosus or anal reflex implies a lesion somewhere along the reflex arc from the pudendal nerve to the conus medullaris. Urethral stimulation for the urethro-anal reflex is applied via an electrode mounted on a Foley catheter. Bladder stimulation for the bladder-anal reflex is applied by moving the ring electrode into an empty bladder. The electrical stimulus is slowly increased until it is approximately three times the patient’s sensory threshold, and latency is measured via a recording electrode as described previously. Normal latencies for these reflexes have been reported between 50 and 65 msec. A prolonged or absent urethro-anal or bladder-anal reflex latency with a normal bulbocavernosus reflex implies a pelvic plexus lesion or autonomic neuropathy, such as is seen in diabetic patients. Of all sacral reflexes, only the bulbocavernosus reflex is widely used; it is a relatively easy test to learn and to perform and (along with CnEMG) is probably the most useful and accepted of the neurophysiologic tests of the pelvic floor. Like all tests that rely on nerve conduction, the bulbocavernosus reflex is not sensitive to the detection of partial nerve lesions because the presence of only a few intact neurons can yield a normal latency. The urethro-anal and bladder-anal reflexes can be technically difficult to obtain and are not widely accepted. Furthermore, the sensitivity of these visceral-somatic reflexes for detecting pelvic plexus lesions is unknown.
AUTONOMIC TESTING Evaluation of the sympathetic and parasympathetic innervation of the pelvic viscera is an important part of the evalua-
tion of pelvic floor disorders. The integrity of the autonomic innervation of the bladder and anorectum is most frequently evaluated using urodynamics and anal manometry, respectively. These physiologic tests can provide information about visceral sensory innervation, as well as indirect evidence about the integrity and coordination of their sympathetic and parasympathetic innervations. A normal urodynamic or anal manometry evaluation implies a normally functioning autonomic innervation. However, abnormalities can reflect neurogenic or nonneurogenic dysfunction. When a pelvic plexus injury or a generalized autonomic neuropathy is suspected, methods to directly evaluate the integrity of the autonomic innervation of the pelvic viscera are needed. Methods that have been suggested for directly evaluating the pelvic autonomic innervation include assessment of the urethro-anal and bladder-anal reflexes (see previous text), the sympathetic skin response (SSR), and the quantitative sudomotor axon reflex test (QSART). The SSR and QSART evaluate the sympathetic sudomotor (sweat gland) innervation. The SSR is elicited by electrical stimulation to mixed nerve in the upper or lower extremity or the genitalia. This results in a reflex stimulation of sweat production on the hands, soles, and genitalia. Sweat production is quantified by measuring changes in electrical resistance on the skin. The absence of sweat production is considered abnormal. QSART assesses the integrity of the axon reflex arc involved in sweat production. Postganglionic sympathetic sudomotor (sweat) fibers are activated by iontophoresis of acetylcholine into the skin. QSART has greater sensitivity and specificity than SSR and, where available, has largely replaced it. The application of these autonomic studies in the evaluation of patients with pelvic floor disorders is currently unknown and is under investigation. Recent studies have demonstrated a relationship between sensation of the bowel and bladder and SSR of the palm, suggesting that autonomic testing may allow an objective confirmation of the subjective evaluation of visceral sensation obtained during urodynamics or anal manometry. Generalized autonomic neuropathy can be caused by diseases, such as diabetes, amyloidosis, Guillain-Barré syndrome, alcoholism, nutritional deficiencies, and certain metabolic syndromes. Testing for generalized autonomic dysfunction usually involves monitoring heart rate and blood pressure changes in response to deep breathing, the Valsalva maneuver, and tilt testing.
PELVIC FLOOR DISORDERS Childbirth Injury Numerous studies demonstrate an association between vaginal childbirth and the subsequent development of pelvic floor disorders, including stress urinary incontinence, fecal incontinence, and pelvic organ prolapse. A recent large cohort study by Rortveit et al. (2003) found that 50% of severe urinary incontinence was attributable to vaginal delivery. In addition to mechanical injury to the levator ani muscles, the urethral and anal sphincters, and pelvic connective tissue, many studies have demonstrated injury to the innervation of the pelvic floor after vaginal childbirth.
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The pudendal nerve, being fixed at the level of the pudendal canal, is thought to undergo stretch or traction injury with the descent of the fetal head. Additionally, distal nerve branches may be compressed directly. Neurophysiologic studies demonstrate prolonged PNTML, increased fiber density as measured by SfEMG, and CnEMG evidence of pelvic floor denervation after vaginal delivery. Snooks et al. (1984) found evidence of pudendal neuropathy after childbirth in 42% of women. Two months after delivery, pudendal nerve function recovered in 60% of the women. This denervation injury leads to decreased levator ani and anal sphincter squeeze strength, which is thought to contribute to the development of pelvic organ prolapse, stress urinary incontinence, and fecal incontinence. Even asymptomatic women can show evidence of pelvic floor nerve injury after uncomplicated deliveries. Multiple successive vaginal deliveries are associated with increased incidence of pudendal nerve injury, whereas cesarean section performed before the descent of the fetal head appears to be protective. Women who undergo elective cesarean section do not demonstrate neuropathic injury, whereas women who undergo cesarean section for second-stage arrest often do. Fynes et al. (1999) found prolongation of anal squeeze pressures and prolonged PNTML in women who underwent cesarean section after cervical dilation of 8 cm or greater. The relative contribution of pelvic floor denervation versus mechanical injury in the development of pelvic floor disorders after childbirth is currently unknown. The primary role of neurophysiologic testing in the setting of childbirth is as a research tool. Currently, no clinical application of this technology is known in the postpartum woman except for the investigation of symptomatic pelvic floor disorders or neurologic dysfunction.
Stress Urinary Incontinence Many studies have demonstrated an association between stress urinary incontinence and pudendal neuropathy with denervation of the urethral sphincter and/or levator ani muscles. Investigators have used PNTML, PeNTML, SfEMG, and CnEMG to demonstrate this relationship. Hale et al. (1999) correlated histologic analysis of urethral biopsies with CnEMG of the urethra and found that women with stress incontinence had greater histologic and CnEMG evidence of sphincter denervation than continent controls. Vaginal childbirth has often been implicated as the cause of this denervation injury, but aging and chronic straining may also contribute. The relative contribution of denervation injury versus direct mechanical injury in the pathogenesis of stress incontinence is unknown. A recent report has even suggested that urethral sphincter myopathy may play a role in some patients with stress incontinence due to intrinsic sphincteric deficiency. Although neurophysiologic testing has contributed to our understanding of the pathogenesis of stress urinary incontinence, its role in the diagnosis or management of patients with uncomplicated stress incontinence is unknown and thus far limited. However, two recent studies have suggested that EMG may be useful in predicting the success of Burch urethropexy for treatment of stress incontinence. Kenton et al. (2001) used preoperative qEMG of the urethral sphincter in 74 women who underwent Burch urethropexy
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and found that women who were cured had greater muscle recruitment than those who had unsuccessful surgery. Kjolhede and Lindehammar (1997) performed CnEMG on the pubococcygeus muscles of women after Burch urethropexy and found evidence of denervation significantly more often in the pubococcygeus muscles of women who had postoperative recurrent stress incontinence.
Voiding Dysfunction The most common use of neurophysiologic testing in the evaluation of patients with voiding dysfunction is to identify detrusor sphincter dyssynergia. As previously described, this is the primary role of kinesiologic EMG, which is performed to assess urethral relaxation/contraction during a urodynamic evaluation. Because true detrusor sphincter dyssynergia is very uncommon in patients without obvious neurologic dysfunction, performing kEMG during urodynamics is probably unnecessary if the clinical evaluation does not reveal preexisting or suspected neurologic dysfunction. Another instance where neurophysiologic testing appears to have clinical use is in the evaluation of young women with urinary retention. In 1988, Fowler et al. described a syndrome of painless urinary retention in premenopausal women often associated with polycystic ovary syndrome, called Fowler’s syndrome. CnEMG of the urethral sphincter of these women reveals complex repetitive discharges (CRDs) and decelerating bursts. The urethral sphincter is often hypertrophied and overactive. The typical patient is in her mid-20s and presents with painless urinary retention with bladder capacity of greater than 1 L. A recent report suggests that women with this condition respond well to sacral neuromodulation (Swinn and Fowler, 1998). The presence of CRDs in the urethral sphincter of a woman with urinary retention should suggest Fowler’s syndrome, but CRDs of the sphincter can be nonspecific and found in women with stress incontinence as well as voiding dysfunction.
Fecal Incontinence In the diagnosis and management of pelvic floor disorders, neurophysiologic testing has perhaps been most often applied to the patient with fecal incontinence. Common clinical applications for neurophysiologic testing in women with fecal incontinence include (1) sphincter mapping in a patient with a disrupted anal sphincter before surgical repair; (2) a prognostic tool in patients with a disrupted sphincter before surgical repair, and (3) evaluation for neurogenic incontinence. As previously mentioned, anal sphincter mapping has largely been replaced by endoanal ultrasound for the identification and characterization of anal sphincter disruption. This is primarily because of decreased discomfort and the ability to evaluate the internal as well as external anal sphincter with ultrasound. Several studies have found that women with fecal incontinence and a disrupted anal sphincter who have prolonged PNTML have a higher failure rate after surgical repair than women with normal latencies. This has led many authors to advocate routine preoperative PNTML testing before anal sphincteroplasty; however, several studies have failed to confirm this relationship (Table 11-1). These mixed results, and the limitations of PNTML
Overlapping Overlapping Ant. plication Overlapping Overlapping
Laurberg et al., 1988 Wexner et al., 1991 Engel et al, 1994 Londono-Schimmer et al., 1994 Simmang et al., 1994 Felt-Bersma et al., 1996 Nikiteas et al., 1996 Oliveira et al., 1996 Sitzler and Thomson, 1996 Sangwan et al., 1996 Chen et al., 1998 Gilliland et al., 1998 Buie et al., 2001
*Subgroup of 26 women with post-obstetric injury. †Proportion of subjects with either “excellent” or “good” outcomes. ns, Not significant; Ant. plication, anterior sphincter plication.
Overlapping Ant. plication Overlapping Overlapping
Overlapping Ant. plication
Procedure
Author, Year >2.4 >2.1 not specified not specified >2.3 not specified >2.5 >2.2 not specified >2.4 >2.2 >2.2 >2.2
Definition Prolonged (msec) 19 16 55 94 10 18 42 48 31 15 12 77 89
N 9–36 3–16 50 12–98 6 3–39 12–36 3–61 1–36 4–32 20–73 2–96 6–120
Follow-up (mo) 80 92 — 55 100 — 73* 73 67 100 100 63 61†
Normal PNTML
Prolonged PNTML and Outcomes from anal Sphincter Surgery for Fecal Incontinence
11 50 — 30 67 — 60* 38 63 14 64 16 56†
Prolonged PNTML
Success Rate (%)
.05 ns ns <.001 ns ns ns ns ns <.005 ns <.01 ns
P-value
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outlined previously, have led the American Society of Gastroenterology to discourage the routine use of this test. Diagnosing neurogenic causes of fecal incontinence remains an important role for neurophysiologic testing. CnEMG and sacral reflex testing are valuable tools for this endeavor. Additionally, recent studies suggest that CnEMG may have a role in predicting which patients with fecal incontinence will respond to sacral nerve modulation; however, the role of these tests as prognostic tools before surgery is currently unknown.
NEUROLOGIC CONDITIONS Brain Lesions Many conditions that affect the cerebrum can result in alterations in bowel and bladder function, including cerebrovascular accidents, dementia, tumors, hydrocephalus, multiple sclerosis, and lesions involving the anterior-medial frontal lobe. Alterations in continence can result from detrusor and rectal hyperreflexia, detrusor sphincter dyssynergia, and uninhibited sphincter relaxation. Additionally, conditions such as dementia and frontal lobe lesions can lead to socially inappropriate urination and defecation even with a normally functioning lower urinary and gastrointestinal tract. Urodynamics and anal manometry in conjunction with kinesiologic EMG can be helpful in characterizing the disturbances in these patients. CnEMG, nerve conduction studies, and sacral reflexes are typically normal.
Parkinson’s Disease/Multiple System Atrophy (MSA) Parkinson’s disease and multiple system atrophy (MSA) (formerly Shy-Drager disease) are distinct neurologic diseases with different pathology; however, in their early stages they can often be difficult to differentiate. Bowel and bladder dysfunction are common in both conditions, with as many as 50% to 80% of patients with either disease reporting bowel and/or bladder complaints. Urodynamic evaluation can reveal detrusor hyperreflexia, detrusor sphincter dyssynergia, or detrusor areflexia. Constipation is common in both conditions and is the result of decreased colonic motility, decreased rectal sensation, and paradoxical puborectalis contraction during defecation. One feature that distinguishes the two is the neuronal degeneration of Onuf ’s nucleus in MSA. This results in EMG abnormalities of the urethral and anal sphincter, including abnormal spontaneous activity and neuropathic MUAPs that are typically not present in patients with Parkinson’s disease. This has led Vodusek (2001) and others to recommend CnEMG of the anal sphincter as the test to distinguish the two diseases, particularly in the first 5 years after onset of symptoms.
Spinal Cord Lesions Bowel and bladder dysfunction is common in patients with spinal cord lesions and represents a major source of distress for the patients. The timing and location of the
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lesion or injury are the major determinants in the nature of the dysfunction. Immediately after an acute injury, the spinal shock phase occurs, resulting in bladder and bowel areflexia. Within several weeks, the recovery phase begins, and, if the injury is above the sacral cord, bladder activity often returns, albeit uninhibited. In a study that included 284 patients with spinal cord injury, Kaplan et al. (1991) found that in patients with cervical spine injuries, 15% had detrusor areflexia, 55% had detrusor sphincter dyssynergia, and 30% had detrusor hyperreflexia with a coordinated sphincter. In patients with a thoracic spine injury, 90% had detrusor sphincter dyssynergia. Lumbar spinal injuries resulted in detrusor hyperreflexia 30% of the time, detrusor sphincter dyssynergia in 30%, and areflexia in 40%. The relationship between the nature of bowel dysfunction and the location of spinal cord injury is less clear than with the bladder. Typically, patients have slow colon transit, increased rectal compliance, and decreased pelvic floor and anal sphincter function. The levator ani and anal sphincter may also demonstrate uncoordinated defecation, similar to detrusor sphincter dyssynergia. In a study of 115 patients after spinal cord injury, Glickman and Kamm (1996) found that constipation occurred in 17%, weekly fecal incontinence in 11%, and occasional fecal incontinence in 50%. Almost all of the patients in this study had to use at least one therapeutic method to induce defecation. Patients with spinal cord disease will demonstrate lower extremity hyperreflexia, sensory loss, and weakness consistent with the size and location of their injury. Urodynamics and anal manometry with kinesiologic EMG are useful for characterizing the nature of their bladder and/or bowel complaints. As injury to the spinal cord affects upper motor neurons rather than lower motor neurons, neurophysiologic studies, such as CnEMG, nerve conduction studies, and sacral reflexes, are usually normal unless the lower sacral cord (conus medullaris) is involved.
Conus Medullaris and Cauda Equina Lesions The terminal portion of the spinal cord, known as the conus medullaris, contains most of the nerve cell bodies that supply the pelvic floor and ends approximately at the level of the disk between the first and second lumbar vertebras. Nerve roots from the lower spinal cord travel from the conus medullaris at the L1–L2 level to their corresponding vertebral foramina in the lower lumbar vertebras and sacrum (Fig. 11-8). This portion of the cord is called the cauda equina (“horse’s tail”) and is particularly susceptible to damage from lumbosacral disk disease and other traumatic injury. Patients with lesions involving the conus medullaris or cauda equina classically present with so-called “saddle” anesthesia, lower extremity weakness, and bowel and bladder dysfunction. Lesions to the conus medullaris can result from L1–L2 disk disease, spinal stenosis, tumor compression, trauma, infarction, and multiple sclerosis. A common cause of cauda equina injury is central disk herniation of the lumbar spine, usually at the L4–L5 level. Central herniations, which represent less than 3% of herniations, preferentially compress the sacral nerve roots. Acute disk herniations are often dramatic and should be considered emergencies. Conditions such as spinal stenosis, ankylosing spondylitis, tumor compression, and chronic
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tal tone. In conus medullaris lesions, findings of denervation in the pelvic floor muscles and sphincters are expected but are often not seen in the lower extremities because weakness in these muscles is typically due to upper motor neuron injury. In cauda equina lesions, CnEMG often reveals denervation of muscles of the lower limbs and pelvic floor in an asymmetric pattern. Lower extremity motor nerve conduction studies demonstrate normal or prolonged conduction velocity with decreased amplitude, and PNTML and PeNTML are prolonged. These changes are bilaterally symmetric with conus lesions and have variable bilaterality with cauda equina lesions. Sensory nerve conduction studies of the lower extremity are normal for both conus medullaris and cauda equina lesions, as the dorsal root ganglion and distal sensory axon are spared in either case. MRI of the spine is the radiographic test of choice with these presentations.
Lumbosacral Plexus Lesions
Figure 11-8 ■ The sacral spinal cord, including the conus medullaris and cauda equina. (Reprinted with the permission of The Cleveland Clinic Foundation.)
central disk herniation may present less dramatically and be a greater diagnostic challenge. Because the conus medullaris represents the distal portion of the spinal cord and contains the anterior horn cells that supply the pelvic floor muscles and sphincters, lesions to this area result in a combination of upper and lower motor neuron symptoms. Typically, motor and sensory symptoms will be bilateral and symmetric. Sensory loss tends to be localized to the perianal region. In contrast, lesions of the cauda equina demonstrate only lower motor neuron symptoms that are often asymmetric and unilateral. Sensory loss is usually more variable and can be found from the soles of the feet to the perineum/ perianal region. Radicular pain to the back, buttock, perineum, and lower extremity can be found with both lesions, but tends to be more severe in cauda equina lesions. In both, weakness is often noted in the gastrocnemius, hamstring, and gluteal muscles (S1, S2 innervated muscles) as well as in the anal sphincter and levator ani muscles. A loss of anal sphincter resting tone and squeeze strength is present. Motor loss is symmetric in a conus lesion and often asymmetric in cauda equina lesions. Because of the upper motor neuron involvement in a conus medullaris lesion, the ankle reflex is increased and Babinski’s sign is positive, and the knee jerk is typically normal. In contrast, in cauda equina lesions, the knee and ankle reflexes are normal and Babinski’s sign is negative. The bulbocavernosus and anal wink reflexes are typically absent in both conditions. Urodynamics often reveal absent bladder sensation and a hypoactive detrusor with elevated postvoid residuals. As a result, the patient often has overflow incontinence that is worsened by a concurrent loss of urethral tone. Anal manometry also reveals absent sensation and lack of anorec-
Lesions of the lumbosacral plexus can result from pelvic trauma, radiation, diabetes, malignant neoplasms (colorectal, breast, sarcomas, multiple myelomas), radical pelvic surgery, and, rarely, obstetric injury. Depending upon the nature and location of the lesion, symptoms may be unilateral or bilateral and can include lower extremity weakness and sensory loss, and pain in the lower back, hip, buttock, and leg. Bowel and bladder dysfunction is common, particularly if the pelvic plexus is involved. When lower sacral nerve roots are involved, perineal anesthesia and loss of levator ani and sphincter tone and squeeze strength are noted. Knee jerk and ankle reflexes may be normal or decreased, and Babinski’s sign should be negative. Urodynamics and anal manometry will often reveal an areflexic bladder and anorectum. Neurophysiologic testing is useful to confirm a lumbosacral plexopathy and to distinguish it from a cauda equina lesion or generalized peripheral neuropathy. CnEMG will typically reveal denervation in the pelvic floor and lower extremity musculature in a distribution consistent with the nature of the lesion. Unlike cauda equina lesions, the L3–S1 paraspinal muscles should not be involved because these are innervated by the dorsal rami of the lumbosacral nerve roots and separate from the plexus. Lower extremity motor and sensory conduction studies will be abnormal in a distribution consistent with the lesion, and PNTML and PeNTML may be prolonged. Sacral reflexes will be unilaterally or bilaterally abnormal.
Peripheral Neuropathy Isolated injury to the distal pudendal nerve is the most common peripheral neuropathy seen in women with pelvic floor disorders. As described previously, distal pudendal neuropathy is commonly related to childbirth and has been implicated in the development of stress urinary incontinence, fecal incontinence, and pelvic organ prolapse. In an isolated pudendal nerve injury, CnEMG of the urethral and anal sphincters and/or bulbocavernosus muscle will reveal denervation, but the levator ani muscles and lower extremities will not. PNTML and PeNTML may be prolonged, and sacral reflexes are often prolonged or absent. In rare cases, perineal sensation will be altered. Injury to the levator ani nerve is
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also common after vaginal delivery, and denervation of the levator ani muscles can often be found in conjunction with distal pudendal neuropathy. Generalized peripheral neuropathies, including diabetic neuropathy, amyloidosis, Guillain-Barré syndrome, and some hereditary neuropathies can also cause bowel and bladder dysfunction. These disorders often affect the autonomic as well as the somatic nerves. Typically, clinical examination will reveal weakness and alterations in sensation of the lower extremities. If large fiber somatic nerves are involved, nerve conduction studies and CnEMG of the lower limbs will demonstrate the generalized and, typically, symmetric nature of these conditions.
Pelvic Plexus Injury Disruption of the autonomic pelvic plexus can occur with traumatic pelvic fractures, radical pelvic surgery, and, rarely, obstetric injury. Surgical procedures in women commonly implicated in pelvic plexus injury include abdominal perineal resection of the rectum for rectal carcinoma and radical hysterectomy for cervical carcinoma. Most commonly, the parasympathetic innervation is disrupted, resulting in urinary retention with elevated postvoid residuals. Occasionally, sympathetic injury will result in loss of tone of the internal urethral sphincter and stress incontinence. Bladder and rectal sensation may also be decreased. Typically, bladder dysfunction is transitory with normal voiding resuming within 6 months, although in some patients the dysfunction will be permanent. As mentioned previously, some generalized polyneuropathies, such as diabetic neuropathy, can cause autonomic dysfunction of the bowel and bladder. On clinical examination, this type of injury is characterized by normal perineal sensation, normal levator ani and anal sphincter squeeze strength, and normal bulbocavernosus and anal wink reflexes. Anal sphincter resting tone may be decreased. Urodynamics and anal manometry will often demonstrate areflexia with or without sphincter incompetence. Autonomic testing, such as urethro-anal and bladderanal reflexes and QSART, are typically abnormal. CnEMG of the pelvic floor muscles and sphincters, PNTML and PeNTML, and sacral reflexes will be normal if the injury is isolated to the pelvic plexus. In diseases like diabetes, which can affect both autonomic and somatic nerves, neurophysiologic testing of the pelvic floor and lower limbs will reflect the degree of somatic involvement.
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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. Rudy DC, Woodside JR. Non-neurogenic and neurogenic bladder: the relationship between intravesical pressure and the external sphincter electromyogram. Neurourol Urodyn 1991;10:169. Workman D, Cassisi J, Dougherty M. Validation of surface EMG as a measure of intravaginal and intra-abdominal activity: implications for biofeedback-assisted Kegel exercises. Psychophysiology 1993;30:120.
CONCENTRIC NEEDLE EMG Buchthal F. Introduction to electromyography. Scandinavian University Press, Copenhagen, 1957. FitzGerald MP, Blazek B, Brubaker L. Complex repetitive discharges during urethral sphincter EMG: clinical correlates. Neurourol Urodyn 2000;19:577. 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;297:1436. Gilad R, Giladi N, Korczyn AD, et al. Quantitative anal sphincter EMG in multisystem atrophy and 100 controls. J Neurol Neurosurg Psychiatry 2001;71:596. Olsen AL, Benson JT, McClellan E. Urethral sphincter needle electromyography in women: comparison of periurethral and transvaginal approaches. Neurourol Urodyn 1998;17:531. Podnar S, Rodi Z, Lukanovic A, et al. Standardization of anal sphincter EMG: technique of needle examination. Muscle Nerve 1999;22:400. Podnar S, Vodusek DB, Stalberg E. Standardization of anal sphincter electromyography: normative data. Clin Neurophysiol 2000;111:2200. Podnar S, Vodusek DB, Stalberg E. Standardization of anal sphincter electromyography: comparison of quantitative techniques of anal sphincter electromyography. Muscle Nerve 2002;25:83. Sanders DB, Stalberg EV, Nandedkar SD. Analysis of electromyographic interference pattern. J Clin Neurophysiol 1996;13:385. Sonoo M, Stalberg E. The ability of MUP parameters to discriminate between normal and neurogenic MUPs in concentric EMG: analysis of the MUP “thickness” and the proposal of “size index.” Electroencephalogr Clin Neurophysiol 1993;89:291. Stalberg E, Nandedkar SD, Sanders DB, Falck B. Quantitative motor unit potential analysis. J Clin Neurophysiol 1996;13:401. Tjandra JJ, Milsom JW, Schroeder T, Fazio VW. Endoluminal ultrasound is preferable to electromyography in mapping anal sphincter defects. Dis Colon Rectum 1993;36:689. Weidner AC, Sanders DB, Nandedkar SD, Bump RC. Quantitative electromyographic analysis of levator ani and external anal sphincter muscles of nulliparous women. Am J Obstet Gynecol 2000;183:1249. Weidner AC, Barber MD, Visco AC, 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;183:1390.
SINGLE FIBER EMG Kiff ES, Swash M. Slowed conduction in the pudendal nerves in idiopathic (neurogenic) fecal incontinence. Br J Surg 1984;71:614. Neill ME, Swash M. Increased motor unit fibre density in the external sphincter muscle in anorectal incontinence: a single fiber EMG study. J Neurol Neurosurg Psychiatr 1980;43:343. Osterberg A, Graf W, Eeg-Olofsson K, et al. Results of neurophysiologic evaluation of fecal incontinence. Dis Colon Rectum 2000;43:1256.
ELECTRODIAGNOSTIC TESTING
NERVE CONDUCTION STUDIES
Aminoff MJ. Clinical electromyography. In Electrodiagnosis in Clinical Neurology, 4th ed. Churchill Livingstone, New York, 1999, p. 243. Fowler CJ, Benson JT, Craggs MD, et al. Clinical neurophysiology. In International Consultation on Incontinence, 2nd ed. Health Publication Ltd., Plymouth, UK, 2002, p. 391. Vodusek DB. Clinical neurophysiological tests in urogynecology. Int Urogynecol J 2000;11:333.
Barnett JL, Hasler WL, Camilleri M. American Gastroenterological Association medical position statement on anorectal testing techniques. American Gastroenterological Association. Gastroenterology 1999;116:732. Lefaucheur J, Yiou R, Thomas C. Pudendal nerve terminal motor latency: age effects and technical considerations. Clin Neurophysiol 2001;112:472. Olsen AL, Rao SS. Clinical neurophysiology and electrodiagnostic testing of the pelvic floor. Gastroenterol Clin North Am 2001;30:33. Rogers J, Laurberg S, Misiewicz JJ, et al. Anorectal physiology validated: a repeatability study of the motor and sensory tests of anorectal function. Br J Surg 1989;76:607. Tetzschner T, Sorensen M, Rasmussen OO, et al. Reliability of pudendal nerve terminal motor latency. Int J Colorectal Dis 1997;12:280.
KINESIOLOGIC EMG Blaivas JG, Sinha HP, Zayed AA, Labib KB. Detrusor-external sphincter dyssynergia. J Urol 1981;125:542.
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SACRAL REFLEXES Benson JT. Sacral nerve stimulation results may be improved by electrodiagnostic techniques. Int Urogynecol J 2000;11:352. Henry MM, Swash M. Assessment of pelvic floor disorders and incontinence by electrophysiological recording of the anal reflex. Lancet 1978;i: 1290. Uher EM, Swash M. Sacral reflexes: physiology and clinical application. Dis Colon Rectum 1998;41:1165. Vodusek DB, Janko M, Lokar J. Direct and reflex responses in perineal muscles on electrical stimulation. J Neurol Neurosurg Psychiatr 1983;46:67.
AUTONOMIC TESTING Reitz A, Schmid DM, Curt A, et al. Electrophysiological assessment of sensations arising from the bladder: are there objective criteria for subjective perceptions? J Urol 2003;169:190. Shafik A, El-Sibai O, Shafik AA, Ahmed I. “Objective” assessment of rectal sensation: a novel approach. Front Biosci 2004;9:159. Shimada H, Kihara M, Kosaka S, et al. Comparison of SSR and QSART in early diabetic neuropathy?the value of length-dependent pattern in QSART. Auton Neurosci 2001;92:72.
PELVIC FLOOR DISORDERS Allen RE, Hosker GL, Smith AR, Warrell DW. Pelvic floor damage and childbirth: a neurophysiological study. Br J Obstet Gynaecol 1990;97:770. Altomare DF, Rinaldi M, Petrolino M, et al. Reliability of electrophysiologic anal tests in predicting the outcome of sacral nerve modulation for fecal incontinence. Dis Colon Rectum 2004;47:853. Anderson RS. A neurogenic element to urinary genuine stress incontinence. Br J Obstet Gynaecol 1984;91:41. Buie WD, Lowry AC, Rothenberger DA, Madoff RD. Clinical rather than laboratory assessment predicts continence after anterior sphincteroplasty. Dis Colon Rectum 2001;44:1255. Chen AS, Luchtefeld MA, Senagore AJ, et al. Pudendal nerve latency. Does it predict outcome of anal sphincter repair? Dis Colon Rectum 1998;41:1005. Engle AF, Kamm MA, Sultan AH, et al. Anterior anal sphincter repair in patients with obstetric trauma. Br J Surg 1994;81:1231. Felt-Bersma RJ, Cuesta MA, Koorevaar M. Anal sphincter repair improves anorectal function and endosonographic image. A prospective clinical study. Dis Colon Rectum 1996;39:878. Fynes M, Donnelly V, O’Connell PR, et al. Cesarean delivery and anal sphincter injury. Obstet Gynecol 1998;92:496. Fynes M, Donnelly V, O’Connell PR, O’Herlihy C. The effect of second vaginal delivery on anal sphincter function and faecal continence: a prospective study. Lancet 1999;354:983. Gilliland R, Altomare DF, Moreira H, et al. Pudendal neuropathy is predictive of failure following anterior overlapping sphincteroplasty. Dis Colon Rectum 1998;41:1516. Gregory WT, Lou J, Stuyvesant A, Clark AL. Quantitative electromyography of the anal sphincter after uncomplicated vaginal delivery. Obstet Gynecol 2004;104:327. Hale DS, Benson JT, Brubaker L, et al. Histologic analysis of needle biopsy of urethral sphincter from women with normal and stress incontinence with comparison of electromyographic findings. Am J Obstet Gynecol 1999;180:342. Kamm MA. Obstetric damage and faecal incontinence. Lancet 1994; 344:730. Kenton K, FitzGerald MP, Shott S, Brubaker L. Role of urethral electromyography in predicting the outcome of Burch retropubic urethropexy. Am J Obstet Gynecol 2001;185:51. Kjolhede P, Lindehammar H. Pelvic floor neuropathy in relation to the outcome of Burch colposuspension. Int Urogynecol J 1997;8:61. Laurberg S, Swash M, Henry MM. Delayed external sphincter repair for obstetric tear. Br J Surg 1988;75:786. Londono-Schimmer EE, Garcia-Duerly R, Nicholls RJ, et al. Overlapping anal sphincter repair for faecal incontinence due to sphincter trauma: five year follow-up functional results. Int J Colorectal Dis 1994;9:110. Nikiteas N, Korsgen S, Kumar D, Keighley MR. Audit of sphincter repair. Factors associated with poor outcome. Dis Colon Rectum 1996;39:1164. Noble JG, Dixon PJ, Rickards D, Fowler CJ. Urethral sphincter volumes in women with obstructed voiding and abnormal sphincter electromyographic activity. Br J Urol 1995;76:741.
Oliveira L, Pfeifer J, Wexner SD. Physiological and clinical outcome of anterior sphincteroplasty. Br J Surg 1996;83:502. Perucchini D, DeLancey JO, Ashton-Miller JA, et al. Age effects on urethral striated muscle. I. Changes in number and diameter of striated muscle fibers in the ventral urethra. Am J Obstet Gynecol 2002;186:351. Rortveit G, Daltvai AK, Hannestad YS, et al. Urinary incontinence after vaginal delivery or cesarean section. N Engl J Med 2003;348:900. Sangwan YP, Coller JA, Barrett RC, et al. Unilateral pudendal neuropathy. Impact on outcome of anal sphincter repair. Dis Colon Rectum 1996;39:686. Simmang C, Birnbaum EH, Kodner IJ, et al. Anal sphincter reconstruction in the elderly: does advancing age affect outcome? Dis Colon Rectum 1994;37:1065. Sitzler PJ, Thomson JP. Overlap repair of damaged anal sphincter. A single surgeon’s series. Dis Colon Rectum 1996;39:1356. Smith AR, Hosker GL, Warrel DW. The role of pudendal nerve damage in the aetiology of genuine stress incontinence in women. Br J Obstet Gynaecol 1989;96:29. Snooks SJ, Swash M. Abnormalities of the innervation of the urethral striated sphincter musculature in incontinence. Br J Urol 1984;56:401. Snooks SJ, Badenoch DF, Tiptaft RC, Swash M. Perineal nerve damage in genuine stress urinary incontinence. An electrophysiological study. Br J Urol 1985;57:422. Snooks SJ, Setchell M, Swash M, Henry MM. Injury to innervation of pelvic floor sphincter musculature in childbirth. Lancet 1984;2:546. 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. Swinn MJ, Fowler CJ. The clinical features of non-psychogenic urinary retention in young women (Fowler’s syndrome). Neurourol Urodyn 1998;17:304. Swinn MJ, Kitchen ND, Goodwin RJ, Fowler CJ. Sacral neuromodulation for women with Fowler’s syndrome. Eur Urol 2000;38:439. Takahashi S, Homma Y, Fujishiro T, et al. Electromyographic study of the striated urethral sphincter in type 3 stress incontinence: evidence of myogenic-dominant damages. Urology 2000;56:946. Tetzschner T, Sorensen M, Rasmussen OO, et al. Pudendal nerve damage increases the risk of fecal incontinence in women with anal sphincter rupture after childbirth. Acta Obstet Gynecol Scand 1995;74:434. Wexner SD, Marchetti F, Jagelman DG. The role of sphincteroplasty for fecal incontinence reevaluated: a prospective physiologic and functional review. Dis Colon Rectum 1991;34:22.
NEUROLOGIC CONDITIONS Andrew J, Nathan PW. Lesions of the anterior frontal lobes and disturbances of micturition and defecation. Brain 1964;87:233. Fowler CJ, Sakakibara R, Frohman EM, et al. Cauda equina disorders. In Neurologic Bladder, Bowel and Sexual Dysfunction. Elsevier Science, Amsterdam, 2001, p. 63. Glickman S, Kamm MA. Bowel dysfunction in spinal cord injured patients. Lancet 1996;347:1651. Hattori T, Yasuda K, Kita K, Hirayama K. Voiding dysfunction in Parkinson’s disease. Jpn J Psychiatry Neurol 1992;46:181. Kaplan SA, Chancellor MB, Blaivas JG. Bladder and sphincter behavior in patients with spinal cord lesions. J Urol 1991;146:113. Mathers S, Kempster P, Swash M, Lees A. Constipation and paradoxical puborectalis contractions in anismus and Parkinson’s disease: a dystonic phenomenon? J Neurol Neurosurg Psychiatry 1988;51:1503. Sakakibara R, Hattori T, Yasuda K, Yamanishi T. Micturitional disturbance after acute hemispheric stroke: analysis of the lesion site by CT and MRI. J Neurol Sci 1996;137:47. Sakakibara R, Hattori T, Uchiayama T, et al. Urinary dysfunction and orthostatic hypotension in multiple system atrophy: which is the more common and earlier manifestation? J Neurol Neurosurg Psychiatry 2000;68:65. Stocchi F, Badiali D, Vacca L, et al. Anorectal function in multiple system atrophy and Parkinson’s disease. Mov Disord 2000;15:71. Vodusek DB. Sphincter EMG and differential diagnosis of multiple system atrophy. Mov Disord 2001;16:600. Weber J, Dlanger T, Hanneqin D, et al. Anorectal manometric anomalies in seven patients with frontal lobe brain damage. Dig Dis Sci 1990;35:225.
Pathophysiology of Stress Urinary Incontinence
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James L. Whiteside and Mark D. Walters
ELEMENTS OF URINARY CONTINENCE 157 Muscular and Supportive Tissue Elements 157 Neurophysiologic Considerations 159 MECHANISMS OF FEMALE URINARY CONTINENCE AND INCONTINENCE 160 Historical Insights 160 Unifying Theories on the Causes of Urinary Incontinence Mechanisms of Injury 163 CONCLUSIONS 163
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The female continence mechanism and factors that contribute to its failure are not completely understood. Past theories of the mechanisms of stress urinary incontinence tended to focus on single factors to explain bladder neck and urethral incompetence. Advances in our knowledge of the histology, biochemistry, and neurophysiology that control bladder neck and urethral support and function have propelled our understanding beyond single factor concepts. We now believe that multiple physiologic factors make up the female continence mechanism. Defects alone, or in combination of any of these factors, can contribute to the presence and severity of stress incontinence in women. This chapter reviews the anatomic and physiologic mechanisms of urinary continence and the pathophysiology of stress incontinence in women. The historical theories explaining female urinary incontinence will be reviewed. Finally, unifying concepts regarding issues of urethral support defects and pelvic floor denervation are summarized to develop the current model of the mechanisms of urethral sphincteric incompetence.
ELEMENTS OF URINARY CONTINENCE The two functions of the lower urinary tract are the storage of urine in the bladder and the timely expulsion of urine from the urethra. The mechanisms that control urinary continence and voiding are complex. Normal function of the central and peripheral nervous systems, bladder wall, detrusor muscle, urethra, and pelvic floor musculature
is required. Dysfunction can occur at any of these levels, resulting in various types of lower urinary tract dysfunction. Simplistically, for a woman to remain continent, intraurethral pressure must be greater than intravesical pressure under both resting and stress conditions. At rest, urethral resistance is generated by the interaction of urethral smooth muscle, urethral wall elasticity and vascularity, and periurethral striated muscle. Each component contributes about one third of overall intraurethral pressure. The smooth muscle and vascular elastic tissue provide a constant amount of tension along the urethra; the periurethral striated urogenital sphincter muscles function prominently in the distal one half of the urethra. Multiple clinical factors, such as age and obstetric history, can affect the function of the urethral components.
Muscular and Supportive Tissue Elements BLADDER During physiologic bladder filling, little or no increase in intravesical pressure is observed, despite large increases in urine volume. This process, called accommodation, is caused primarily by passive elastic and viscoelastic properties of the smooth muscle and connective tissue of the bladder wall. As filling increases to a critical intravesical pressure, detrusor muscle contractility is probably inhibited by activation of a spinal sympathetic reflex that results in inhibition of parasympathetic ganglionic transmission and stimulation of β-adrenergic receptors in the bladder body. The net effect of these actions is filling and storage of urine within the bladder cavity, with little increase in intravesical pressure relative to volume. Abnormalities in the bladder wall, the detrusor muscle, or bladder innervation can result in incontinence (primarily detrusor overactivity, both idiopathic or neurogenic) or voiding dysfunction. URETHRA Urethral Support. Anterior vaginal wall support directly impacts urethral support (except for lateral attachments of the urethra to the levator ani [pubourethral ligaments]) as the urethra rests on the anterior vaginal wall. The anterior
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vaginal wall is attached to the arcus tendineus fasciae pelvis (ATFP) that is a condensation of levator ani fascia arising from the surface of the levator ani muscles. The arcus tendineus levator ani is the point of attachment between the levator ani and the obturator internus muscles and lies just cranial to the ATFP. This relationship between the urethra, vagina, and levator ani is a reoccurring theme in understanding the mechanisms of female urinary continence. Work by Jeffcoate and Roberts (1952), Hodgkinson (1953), and others emphasized the need for intact support of the bladder neck and proximal urethra in a retropubic position for maintenance of urinary continence under stress. This idea highlights urethral support by the anterior vaginal wall that can be altered by defects in vaginal attachments to the levator ani at the ATFP. A stable suburethral layer of anterior vaginal wall prevents urethral and bladder neck descent leading to urethral compression with straining. The emphasis on a retropubic urethra for urinary continence grew out of the success of retropubic operations (i.e., Marshall-Marchetti-Krantz urethropexy) to correct urinary incontinence. The concept is somewhat challenged, however, by the success of midurethral sling procedures that do not ordinarily maintain a retropubic urethra. DeLancey’s (1994) emphasis on the importance of a stable suburethral layer for effective urethral closure over the necessity of a retropubic urethra is perhaps borne from the efficacy of midurethral sling procedures. The pubourethral ligaments are lateral fascial and muscular attachments of the urethra to the levator ani. These structures, which are supportive of the female urethra and may contribute to urinary continence, are to be distinguished from the pubovesical muscles that probably play a role in voiding by opening the bladder neck. Pubovesical muscles can be seen during a retropubic dissection arching from the ATFP to insert on the urethra (Fig. 12-1); they are easily confused with the pubourethral ligaments that lie beneath. Some speculate that the pubourethral ligaments arise at the midurethra and may augment suburethral supports in promoting urethral compression with strain. Urethral Coaptation. The urethra is a pliable structure whose lumen must be completely sealed or coapted to maintain continence. The urethral wall must be sufficiently soft so that external forces can act on it to effect closure. Several studies by Zinner et al. (1980, 1983), using mechanical models, showed higher resistance to water flow when a softer lumen and a lubricating filler were used within the outflow tube. This finding makes clinical sense because a rigid urethra has poor closure properties, as can result from multiple surgeries or radiation. Because clinical scientific studies rarely address this issue, however, the actual importance of urethral softness and mucosal seal, as they pertain to continence, remains uncertain. Urethral Sphincter. Few pelvic organs are as misunderstood as the urethral sphincter. A simplistic understanding of urethral anatomy would expect that the urethral sphincter is analogous to the external anal sphincter, a circular muscle encompassing the urethral lumen. This expectation is met in only one of the three identified muscles of the female urethral sphincter, the rhabdosphincter. The other somatic muscles of the female urethral sphincter are the compressor
Figure 12-1 ■ Retropubic space with the proximal urethra and vagina transected at a level just below the bladder, revealing the attachment of the vagina to the levator ani muscles. PVP, Periurethral vascular plexus; R, rectum; VLA, vaginolevator attachment; VW, vaginal wall; PS, pubic symphysis; AFTP, arcus tendineus fasciae pelvis; ATLA, arcus tendineus levator ani; LA, levator ani; OIF, obturator internus fascia; PVM, pubovesical muscle; U, urethra. (From DeLancey JO, Starr RA. Histology of the connection between the vagina and levator ani muscles: implications for urinary tract function. J Reprod Med 1990;35:765, with permission.)
urethrae and urethrovaginal sphincter muscles that arch over the urethral lumen exerting downward compression with contraction against a stable suburethral base (anterior vaginal wall). Branches of the pudendal nerve (S2–S4) innervate all three muscles. LEVATOR ANI Recognition that the levator ani muscles can be made stronger with pelvic floor exercises and thereby improve female urinary continence has been known since before the 1950s. The levator ani muscles include the pubococcygeus, iliococcygeus, and puborectalis muscles. Of interest in urinary continence is the pubococcygeus muscle that, with contraction, pulls the pelvic floor tightly up and into the pelvic cavity (Fig. 12-2). This action renders a firm backboard for the urethra, particularly in light of the attachments between the urethra (pubourethral ligament), vagina (ATFP), and the levator ani. As discussed in Chapters 2 and 3, innervation of the levator ani does not come from the pudendal nerve. The nerve to the levator ani arises separately from S2–S4 and travels along the medial aspect of the levator muscles. Thus, a woman can possibly have functional levator ani and a dysfunctional urethral sphincter. The levator ani and periurethral striated muscles (rhabdosphincter, compressor urethrae, and urethrovaginal sphincter) have a dual role in maintaining urinary continence—they provide resting urethral tone and assist in support (slow-twitch fibers), and they contract rapidly with increased intra-abdominal pressure (fast-twitch fibers). The integration of these two somatic muscle groups is vital to normal urinary continence. During rapid increases in intraabdominal pressure and with interruption of urination, voluntary and reflex periurethral striated muscle contraction occurs, predominantly in the midurethra and distal urethra, augmenting urethral pressure. Constantinou and Govan
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Figure 12-2 ■ Levator ani muscles in a contracted state, narrowing the pelvic opening and supporting the pelvic organs. (Reprinted with the permission of The Cleveland Clinic Foundation.)
(1982) demonstrated that urethral pressure spikes precede, and are often greater than, intravesical pressure spikes during coughing in continent women. Using cinefluorography, Lund et al. (1959) observed two actions when a woman is asked to interrupt her urine stream. The first is a prompt constriction of the voluntary musculature that immediately interrupts the urine stream in the midurethra, presumably due to periurethral striated muscle contraction against a stable suburethral base. The urine distal to the constriction is voided, but the contents of the proximal urethra are forced back into the bladder. Simultaneously, the base of the bladder is seen to rise and is drawn cephalad, presumably due to levator contraction acting on levator attachments to the suburethral base and bladder (i.e., anterior vaginal wall). Both actions are characteristic of voluntary fast-twitch muscle contraction; in fact, the diameter of fast-twitch muscle in the levator ani has been correlated with urethral pressures during periods of stress. Emphasizing the role of levator support, Heidler et al. (1987) noted that with sneezing in dogs, pressure increases in the distal urethra decrease after transecting the pelvic muscles from the urethra. Taken together, normal urinary continence in women relies on multiple redundant interconnected mechanisms.
Neurophysiologic Considerations Chapter 3 describes in detail the neurophysiology of the lower urinary tract. Reexamining those concepts now is important to connect the aforementioned anatomic considerations with their neurologic connections. The disconnect between anatomy and function, which can appear in cases of complex urinary incontinence, perhaps stems from inadequate understanding of the neurologic basis of female continence. Furthermore, the fact that medications can affect stress-related urinary incontinence testifies to the role of nonanatomic elements in female urinary continence. EFFERENT AND AFFERENT PATHWAYS Bladder smooth muscle is innervated primarily by parasympathetic nerves while smooth muscle of the urethra and
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bladder neck are innervated by sympathetic nerves. Branches of the pudendal nerve innervate the skeletal muscles of the external urethral sphincter. These are the basic components of the efferent nerve pathways from the spinal cord to the lower urinary tract. The parasympathetic nerves that innervate the detrusor exit the spinal cord between S2 and S4. As with all parasympathetic nerves, the preganglionic neurotransmitter is acetylcholine (ACh), yet the postganglionic neurotransmitter varies with the target. Postganglionic parasympathetic neurotransmission to the urethral smooth muscle is via nitric oxide, while both ACh and adenosine triphosphate (ATP) serve in this role to the detrusor smooth muscle. The contribution of purinergic stimulation of the detrusor is likely minor under normal settings, although up-regulation under certain conditions may contribute to development of an overactive bladder (O’Reilly et al., 2002). The role of nitric oxide in urethral smooth muscle contraction is inhibitory. Parasympathetic efferent stimulation of detrusor smooth muscle cells is mediated by muscarinic receptors, of which there are two: M2 and M3. Although the M2 receptor is the most abundant, the M3 receptor appears to preferentially drive detrusor contraction. These subtype variations are significant when considering the effect(s) of anticholinergic medications on detrusor function. The sympathetic nervous system acts to relax the bladder and contract the urethra. Whereas ACh is shared as the preganglionic neurotransmitter with the parasympathetic system, postganglionic neurotransmission is via norepinephrine. Spinal cord input into the sympathetic control of the bladder arises from T10 to L2, with postganglionic delivery to the target organs via the hypogastric nerve. This nerve can be purposefully or inadvertently surgically transected, with resultant overexpression of parasympathetic drive to the lower urinary tract. Somatic nerve input to the lower urinary tract is primarily via the pudendal nerve that gets its spinal cord input from S2 to S4. Motor neurons in spinal cord segments S2 to S4 are located in Onuf ’s nucleus. The neurotransmitter ACh acts on nicotinic receptors in the striated muscle of the external urethral sphincter. Understanding of higher order control of urethral and bladder function has been greatly enhanced in recent years. The supraspinal elements of efferent control of the bladder have been referred to as the pontine micturition and storage centers. These sites serve as the final integrative centers taking input from afferent spinal cord nerves and other regions of the brain, ultimately acting to turn on or off the lower urinary tract. Central nervous system (CNS) excitatory neurotransmission is primarily via glutamic acid. The external urethral sphincter is activated via CNS glutamatergic transmission; suppression of this leads to urethral sphincter relaxation and voiding. Other supraspinal neurotransmitters that have garnered attention in recent years are serotonin and norepinephrine. As noted by Thor et al. (1990), both serotonin and norepinephrine stimulate the urethral sphincter, potentiating the effect of glutamate-induced activation. Serotonin and norepinephrine reuptake inhibitors are apparently effective because of the enhancement in glutamate activation of the external urethral sphincter at Onuf ’s nucleus. Given the prominence that serotonin and norepinephrine have in the
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development of clinical depression renders some insight into the recognized association of depression and urinary incontinence. The parasympathetic, sympathetic, and somatic efferent pathways also relay afferent sensory input from the lower urinary tract to the spinal cord and CNS. Parasympathetic sensory receptors (Aδ and C fibers) transmit information on both bladder volume during storage and contraction amplitude during voiding. These roles suggest that parasympathetic drive both initiates voiding and sustains bladder contraction during voiding. COORDINATING REFLEXES The common view that urinary incontinence neatly divides into anatomic-based causes and detrusor overactivity fades with a more complete understanding of the coordination between the anatomy and underlying neurologic circuitry. Pathways between the CNS and the lower urinary tract interact such that as one is activated, another may be inhibited. Parasympathetic activation with detrusor contraction and consequent urethral relaxation leads to reflex inactivation of sympathetic and somatic contraction of the urethral sphincter. The guarding reflex is a good example of coordination of the various nervous system inputs to the lower urinary tract. As the bladder fills, stretch receptors relay afferent input to the spinal cord where pudendal somatic efferent activation is stimulated. As the afferent stimulation increases with rising bladder volumes, the efferent stimulation to the external urethral sphincter is likewise increased to maintain continence. Meanwhile, detrusor contractile parasympathetic impulses are inactive with activation of sympathetic driven detrusor relaxation and urethral smooth muscle contraction. This sort of complex integration of nervous system input to the lower urinary tract is inadequately measured by urodynamic studies. To what extent that the autonomic nervous system is influencing detrusor and urethral sphincteric function cannot be measured. Because urethral resistance reflects not only any anatomic factors but also somatic and autonomic nervous system factors as well, the relative contribution of each is unknown. To assume that one factor is more important than another in causing urinary incontinence undoubtedly leads to the many treatments and to the variable treatment outcomes seen in clinical management.
MECHANISMS OF FEMALE URINARY CONTINENCE AND INCONTINENCE Historical Insights Historically, theories on the mechanisms of female urinary incontinence fell into two categories: dysfunctional urethral support and dysfunctional urethral sphincteric function. Unfortunately, many of these theories arose from how a particular therapy was perceived to remedy the problem. Although the problem of urinary incontinence had been recognized for years, it was not until Bonney introduced his paper in 1923, “On Diurnal Incontinence of Urine in Women,” that the problem was systematically examined. In
this paper Bonney noted many epidemiologic features that only later have been confirmed. He noted that urinary incontinence that occurs only with some kind of effort was found preferentially among parous women, also noting, however, that, “It does not as a rule begin until several years after labor . . . between forty and fifty years of age.” Bonney suggested that female urinary incontinence arose due to laxity in the vaginal support of the urethra. Predating the popularity of defect-based understanding of anterior vaginal support, Bonney claimed that incontinence was only associated with loss of distal anterior vaginal wall support. With the advent of bead-chain cystography in the 1930s, Stevens and Smith (1937) broke from Bonney’s ideas and emphasized the importance of the urethral sphincter over urethral support in the development of urinary incontinence. This idea echoed the importance that other prominent surgeons of the day placed on competent urethral sphincteric function in the maintenance of urinary continence. Based on findings from the development of newer diagnostic tools, Barnes (1940) proposed that urinary incontinence could stem from an increase in expulsive forces, a decrease in urethral resistance, or a combination of both. Although this idea seems obvious, it introduced concepts that still linger today. Pressure transmission theories arose from work by Barnes, and later Enhörning (1961), and held that continence stemmed from the equal transmission of intra-abdominal pressure to the bladder and urethra during periods of abdominal stress (Fig. 12-3). Hilton and Stanton (1983) found that subjects with stress incontinence had lower total urethral length, maximum urethral pressure, and pressure transmission ratios along the urethra than did continent controls. Furthermore, the total urethral length and maximum pressure decreased progressively with increasing severity of incontinence. Deficient pressure transmission ratios were noted in incontinent subjects, but not in continent controls, yet did not correlate with severity. These investigators concluded that the main pathophysiologic event causing stress incontinence is deficient pressure transmission to the urethra. Incontinence severity is determined by the degree of abnormalities in resting maximum urethral pressure, urethral and intra-abdominal pressure variations, and urethral response to sustained stress. Because no attempt was made to correlate pressure transmission ratios with measures of urethral mobility, it is unknown whether deficient pressure transmission results from urethral hypermobility, abnormal reflex urethral muscle contraction, or other undefined factors. Use of bead-chain cystourethrograms also contributed to the idea that an angle between the urethra and bladder between 90 and 100 degrees is the essential anatomic feature to female urinary stress continence. Arguably, the concept is merely a spin on urethral support ideas; however, here the emphasis is on how urethral support renders an effective posterior urethrovesical angle (PUV). Indeed, Green (1962) held that cystoceles and stress urinary incontinence were practically mutually exclusive. Based on the appearance of the beadchain cystourethrogram, stress urinary incontinence could be classified into two types: type I, representing complete loss of the PUV angle with preservation of the angle of inclination between the upper urethra to perpendicular, and type II, representing loss of both the PUV angle and the angle of
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Figure 12-3 ■ Pressure transmission concept for stress continence and incontinence. A. In continent women, rises in intra-abdominal pressure are transmitted equally to the bladder and urethra. B. In women with anterior vaginal support defects, the bladder base descends, and the urethra rotates during increases in intra-abdominal pressure. This can lead to decreased pressure transmission to the urethra relative to the bladder, which then results in stress urinary incontinence.
inclination. The distinction between the types served to predict surgical approach and outcome, with type II being associated with more failures. Green’s optimism—also shared with Hodgkinson (1953)—that an abnormal PUV angle was always associated with stress urinary incontinence, was later questioned by Fantl et al. (1981); the latter demonstrated the reliability of bead-chain cystourethrogram interpretation to be poor with no correlation between their findings and the diagnosis of true stress incontinence versus detrusor dysfunction. The idea that the normal urethra is an abdominal organ and that loss of this position leads to dysfunction falls into trouble with a paper that found no correlation between the intra-abdominal position of the bladder neck and urinary incontinence (Greenwald et al., 1967). Curiously, these concepts deemphasized, to some extent, the urethral support versus sphincteric function debate, focusing instead on conceptually simpler physical mechanisms. To understand that urinary incontinence follows conditions where urethral pressure is less than or equal to vesical pressure is important, but it disconnects the anatomic and neurophysiologic considerations that lead to these situations. The work by Snooks and Swash (1984) and others found that pudendal terminal motor latency, a measure of nerve conduction, was delayed in women with urinary incontinence, suggesting a neurogenic cause. Although pudendal nerve terminal motor latency may not be a good measure of nerve conduction, it appears to measure some nerve quality, and this appears to differ between women with and without urinary incontinence. Smith et al. (1989) confirmed this finding by demonstrating that partial denervation of pelvic floor muscles with subsequent reinnervation is a normal accompaniment of aging and is increased by childbirth. Women with stress urinary incontinence, fecal incontinence, or pelvic organ prolapse have significantly greater denervation of the pelvic floor than do asymptomatic women. The idea that urinary incontinence could stem from dysfunctional nerve and muscular function was in distinction from those who proposed that it
occurred from some kind of defective anatomy. Reconciliation of these two basic mechanisms for urinary incontinence did not largely result in a merging of these ideas. Instead of viewing urinary incontinence as arising from potentially multiple mechanisms that vary in kind and severity from one woman to the next, one or the other of the two mechanisms was seen as singularly operating in the incontinent woman. Intrinsic sphincteric deficiency came to be seen as that subset of stress urinary incontinence that arose from lost urethral sphincteric function, potentially as a result of neuromuscular injury. The problem with intrinsic sphincteric deficiency is that it is a clinical observation without a clear pathophysiologic mechanism to explain the observation. Theories regarding the mechanisms underlying stress urinary incontinence became further fractionated and clinically oriented during the 1980s. Efforts were made to define types of stress urinary incontinence to predict treatment outcome. These efforts include the work by Blaivas and Olsson (1988), who subdivided stress urinary incontinence into five types, based on fluoroscopic appearance of the bladder and urethra during urodynamic studies. Ultimately, the distinction of support versus sphincteric function underlies these clinical observations. This dichotomy neatly reconciles clinical observations and treatment outcomes, but the root of support loss (urethral, vaginal, pelvic floor) or sphincteric loss (neurogenic, myogenic, congenital, or acquired), and the extent to which each is contributing to dysfunction, is unresolved. Treatment efficacy, therefore, stems not from precise correction of continence anatomy but from blind compensation of one or more deficient continence mechanisms.
Unifying Theories on the Causes of Urinary Incontinence Two theories stand out in an attempt to merge the dichotomy of support versus sphincter as the root of female
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urinary incontinence. The Integral Theory, introduced by Petros and Ulmsten (1990), not only attempted to merge this dichotomy but also strove to explain urinary urge symptoms. This theory arose in conjunction with the introduction of the tension-free midurethral sling as a treatment for urinary incontinence. The second theory, the Hammock hypothesis, introduced by DeLancey (1994), merged the concepts of support versus sphincter from a culmination of anatomic work and stands out as conceptually simpler and more reflective of current understanding of the female pelvic anatomy. The stated position of the Integral Theory is that “stress and urge symptoms both arise from the same anatomic defect, a lax vagina” (Petros and Ulmsten, 1990). The theory posits that the vagina has a dual role in transmitting voluntary and involuntary muscle contractions involved in bladder neck and urethral closure as well as supporting “hypothesized” stretch receptors in the proximal urethra and trigone. The groundwork of this theory arises from the author’s perception of pelvic anatomy. Petros and Ulmsten saw the vagina as having two distinct anatomic segments that function together to render urinary continence and normal bladder sensation. Between the two segments is the pubourethral ligament that acts as a fulcrum. The hypothesized pubourethral ligament in this setting is not the same as the identified lateral attachments between the urethra and the levator ani mentioned earlier. Instead, the pubourethral ligament is purported to extend from the midurethra to the symphysis pubis. Beyond this, the theory holds that two normal urethral closure mechanisms are present—one at the urethra and the other at the bladder neck. A third urethral closure mechanism exists that is not normally necessary but which can be recruited with pelvic muscle exercises to assist in urinary continence if the normal mechanisms fail. The first urethral closure mechanism lies at the segment of the vagina between the urethral meatus and the pubourethral ligament, the “hammock.” The second and most important urethral closure mechanism lies between the pubourethral ligament and the bladder neck, the “supralevator vagina.” The hammock portion of the vagina is vertically oriented while the supralevator portion of the vagina is nearly horizontal. Note that the Integral Theory hammock and the Hammock hypothesis anatomic elements do not correspond. Urethral
closure relies on contraction of the pubococcygeus and external urethral sphincter muscles at the hammock portion of the vagina. Contraction of the pubococcygeus pulls ventrally the hammock portion of the vagina together with the urethra. A portion of the supralevator vagina is the “zone of critical elasticity” that lies below the presumed stretch receptors at the bladder base. Bladder neck closure relies on this elastic portion of the vagina that, with levator contraction, is pulled backward and downward, closing off bladder neck like a hinge. Attachments between the vagina, levators, and anus facilitate this hinge mechanism. The zone of critical elasticity needs to possess adequate integrity, however, to support the hypothesized stretch receptors. Loss of this integrity leads to abnormal activation of the stretch receptors and symptomatic detrusor overactivity. Overall, this complex interplay of anatomic structures contributing to urinary continence can be altered and made dysfunctional. Between the complexity and the imaginative anatomy, the Integral Theory falls short of its stated intentions. The anatomic elements of the Hammock hypothesis have been discussed earlier in this chapter. The urethra and bladder rest on the anterior vagina that is itself suspended by fascial attachments to the levator ani muscles at the ATFP. Loss of this hammock-like support leads to failed urethral compression during periods of increased abdominal pressure (Fig. 12-4). Furthermore, given the arrangement of the striated urethral sphincter muscles, lost vaginal support undermines a firm base for them to exert compression. In this sense, the Hammock hypothesis satisfies the observations of Bonney (1923) and other proponents of urethral support. Because the Hammock hypothesis dismisses the need for an intra-abdominal urethral position, it also reconciles those studies that challenged this concept. But the Hammock hypothesis also emphasizes the importance of the levator ani in continence (Fig. 12-5). Drawing on studies that document lower urethral pressures in patients with striated muscle blockade as well as those like Swash et al. (1985) and Smith et al. (1989) that linked nerve injury to stress incontinence, the Hammock hypothesis conjoins these by emphasizing the role of the external urethral sphincter and levator ani in rendering further urethral function and support. Although the Hammock hypothesis does not attempt to explain the
Figure 12-4 ■ Hammock hypotheses for stress continence and incontinence. A. Abdominal pressure (arrows) forces urethra against stable supportive layer (black) and compresses urethra closed. B. Unstable supportive layer (shaded) is ineffective in providing resistant backstop against which urethra can be compressed. C. Despite low extra-abdominal position of urethra and presence of cystourethrocele, supportive layer is firm and provides adequate backstop against which urethra may be compressed closed. (From DeLancey JO. Structural support of the urethra as it relates to stress urinary incontinence: the hammock hypothesis. Am J Obstet Gynecol 1994;170:1719, with permission.)
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urinary incontinence. The condition has come to imply a urethral sphincter that cannot maintain a watertight seal, even at rest. Despite the historical concepts regarding ISD, the bladder neck and urethra can be hypermobile, or fixed and nonmobile. The muscles involved in urethral closure can be very lax, or the urethral wall can be rigid and scarred. The causes of ISD are multifactorial, with likely changes in neurologic, muscular, and/or connective tissue function combined to create this clinical entity. ISD should not be seen as a distinct pathophysiologic process but rather a clinical diagnosis with multiple causes. Patients with ISD are often severely incontinent; leaking can occur with standing or with minimal exertion. Urodynamically, these patients tend to have lower maximum urethral closure (<20 cm H2O) and leak point pressures (<60 cm H2O). The challenges in how urethral resistance is measured and interpreted should temper the resolve that one has for the significance of this clinical entity. Figure 12-5 ■ Hammock hypothesis for stress continence. Lateral view of pelvic floor with urethra, vagina, and fascial tissues at level of bladder neck, indicating compression of urethra by downward force (arrow) against supportive tissues (levator ani muscles and vaginal hammock suspended by attachments to the ATFP), indicating influence of abdominal pressure on urethra. (From DeLancey JO. Structural support of the urethra as it relates to stress urinary incontinence: the hammock hypothesis. Am J Obstet Gynecol 1994;170:1718, with permission.)
etiology of symptomatic detrusor overactivity, its ability to reconcile the support versus sphincter debate and its truthful admission that urinary continence is “most likely related to a combination of interdependent factors” provide a stable platform on which to hang new investigation.
Mechanisms of Injury Having identified many of the elements of female urinary continence as well as a plausible framework of how they work together, it is fairly easy to imagine how they can be injured and lead to dysfunction. Although these elements are likely interdependent, a degree of redundancy appears to be present. Childbirth potentially impacts not only the structural elements of continence, but also the nerve and muscular elements. This obvious association, however, should not make other causes less likely or relevant. Any activity or injury to the pelvic floor bones, muscles, or nerves has the potential to singularly, or in combination with other injuries, lead to urinary incontinence and other pelvic floor disorders. It was DeLancey’s (1996) hope that by the year 2000 medical science would be able to accurately decipher those particular elements injured in the incontinent woman with therapy directed at that element alone. This hope has not yet been realized, yet it underscores the importance of thinking broadly (in structure, function, and timing) about the causes of any particular woman’s cause for incontinence. INTRINSIC SPHINCTER DEFICIENCY As mentioned earlier, the concept of intrinsic sphincter deficiency (ISD) evolved out of an attempt to reconcile the debate between sphincter versus support as the root of
CONCLUSIONS Multiple physiologic factors, only one of which is urethral support, make up the female urinary continence mechanism. Other important factors include levator muscle strength that is a function of both nerve and muscle integrity and urethral sphincter competence that reflects nerve, muscle, and soft tissue integrity. Different combinations of these factors can together become dysfunctional and create each woman’s “unique” incontinence problem. The etiology of stress urinary incontinence is more complex than the simple theories that evoke singular anatomic or neurologic injury during childbirth. Most likely, maternal characteristics, fetal size and position, labor characteristics, and obstetric management define the likelihood of anatomic or nerve injury. These injuries unmask a susceptibility to stress incontinence that is defined genetically (tissue strength and mechanical and anatomic relationships) and behaviorally (nutrition, smoking, and exercise). Although the Hammock hypothesis today presents the best agreement between how observed anatomy may interface with observed vaginal, urethral, and bladder function, the Integral Theory beguiles us to consider how anatomy may also promote bladder overactivity. Meanwhile, being overlaid on the form and function relationships of the bladder, urethra, and vagina are the neurophysiologic mechanisms that further blur the distinctions between stress and urge incontinence. The massive social, medical, and financial impact of urinary and fecal incontinence in women warrants a major commitment to the understanding of the pathophysiology of the disease. The relationship between pregnancy, childbirth, and incontinence will require longitudinal studies of the lower urinary tract and anal sphincter before, during, and after pregnancy in a large, heterogenous group of primiparous women. Unbiased subject selection and standardized ascertainment of history, physical examination, and diagnostic testing (cystometrogram, urethral pressure studies, endoanal ultrasound, pelvic MRI, studies of pudendal nerve function, and others) are critical. Results could then be correlated in multivariate analyses with demographic, morphometric, and obstetric variables.
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Ingrid Nygaard and W. Thomas Gregory
IMPACT OF CHILDBIRTH ON PELVIC MUSCLE AND NERVE FUNCTION 165 Anatomic Outcomes—Pelvic Floor Muscles 165 Anatomic Outcomes—Anal Sphincter Muscle 166 Neurologic Outcomes 167 Other Anatomic Findings 167 Summary 167 IMPACT OF CHILDBIRTH ON SPECIFIC PELVIC FLOOR DISORDERS 167 Fecal Incontinence 168 Urinary Incontinence 168 Pelvic Organ Prolapse 169 Pain 169 THE DEBATE OVER ELECTIVE PRIMARY CESAREAN DELIVERY CONCLUSION 170
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Labor has been called, and still is believed by many to be, a normal function … and yet it is a decidedly pathologic process. Everything, of course, depends on what we define as normal. If a woman falls on a pitchfork, and drives the handle through her perineum, we call that pathologic-abnormal, but if a large baby is driven through the pelvic floor, we say that it is natural, and therefore normal … —DeLee, 1920 DeLee’s words, written nearly a century ago, marked the beginning of our predecessors’ efforts to study and attempt to mitigate the impact of childbirth on the pelvic floor, an effort that continues to this day. Two facts are incontrovertible: Some women directly develop severe and devastating urinary incontinence, fecal incontinence, and pelvic organ prolapse (POP), as a result of childbirth. Also, most women deliver children via the vagina and do not suffer greatly from the burden of pelvic floor disorders. In this chapter, we will review some of the burgeoning information about the impact of childbirth on pelvic floor disorders.
IMPACT OF CHILDBIRTH ON PELVIC MUSCLE AND NERVE FUNCTION Anatomic Outcomes—Pelvic Floor Muscles Readers of this chapter have likely witnessed countless times the miracle of childbirth and have also likely considered the
“P’s”—that is, how the power pushes the passenger through the passage. In a classic review, Power (1946) described the mechanism by which the fetus negotiates the birth canal and is expelled through the pelvic diaphragm as follows: As the flexed fetal head strikes the pelvic floor, the levator ani muscle segments are funneled from behind and forward. The ischiococcygeus muscle is the first to receive the impact, but the head is often preceded by a dilating wedge of amniotic fluid and membranes that transfers most of the pressure onto the front of the pubococcygeus muscle. The anococcygeal raphe is pushed down until it becomes vertical. The ischiococcygeus assumes a vertical plane and acts as a deflecting surface for the descending head, which is deflected downward and forward onto the iliococcygeus. After the resistance of the ischiococcygeus is overcome, the head is shunted onto the pubococcygeus segment, which is stretched anteroposteriorly and peripherally. The perineal body is pushed downward as the head is propelled along the axis of the pelvic outlet. The rectovaginal septum fibers are stretched peripherally and longitudinally and often torn. As the outlet muscles—the bulbocavernosus, ischiocavernosus, transverse perinei, and periurethral muscles—are dilated, they are converted into a short muscular tube along the axis of the pelvic outlet. Finally, as the biparietal diameter of the fetal head reaches the transverse diameter of the pelvic outlet, the uterovaginal canal is converted into one continuous hiatus. The lateral ligaments of the cervix uteri (endopelvic fascia) are flattened peripherally and stretched vertically. The vagina is dilated spherically, and the pelvic diaphragm is changed from an oblique to a vertical plane. Power (1946) based his description on direct observation, the study of anatomy, and conjecture. Recently, Lien et al. (2004) used sophisticated imaging techniques to develop a biomechanical model to describe changes in levator ani muscles as the fetal head descends through the vagina (Fig. 13-1). The medial pubococcygeus muscle reached an impressive stretch ratio (defined as tissue length under stretch/ original tissue length) of 3.26. According to the authors, this exceeds the greatest stretch ratio (1.5) seen in passive striated muscle of nonpregnant women by 217%. Increasing the fetal head diameter by 9% increased medial pubococcygeus stretch by the same proportion. This model suggests that the medial pubococcygeus muscle has the greatest risk for injury of all the levator ani muscles during the second stage of labor. This supposition is supported by magnetic resonance imaging
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masked cohort study, he found higher rates of tissue damage in women delivered without episiotomy. Thirty-one percent and 24% of women delivered without episiotomy had levator atrophy and detached rectovaginal septum, respectively, compared with 12% and <1% of women, respectively, in whom a mediolateral episiotomy was made. Episiotomy appeared to protect the patient from pelvic tissue damage; thus some form of episiotomy became the standard in obstetric management for decades. Only with an emerging understanding of the importance of study design and analysis in drawing conclusions did modern obstetricians begin to reject routine “prophylactic” episiotomy. Recent studies confirm that pelvic floor muscle strength decreases after vaginal delivery. This is a consistent finding, regardless of the investigational techniques used, including vaginal cones, standardized assessment of pelvic muscle strength at physical examination, or intravaginal squeeze pressure measurement. In addition, histologic studies of cadavers confirm Gainey’s hypothesis that vaginal parity is associated with significant muscle replacement by fibrosis.
Anatomic Outcomes—Anal Sphincter Muscle
Figure 13-1 ■ 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 (round) located posteriorly and inferiorly to the pubic 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, grey, curved tube). The sequence of five images at right are front-left, threequarter views corresponding to those shown at left. (Courtesy, Biomechanics Research Lab, University of Michigan, Ann Arbor, MI.)
(MRI) studies that reveal abnormalities in this area in 20% of primiparous women after vaginal delivery. Between 1945 and 1955, Gainey (1955) systematically evaluated 2000 patients and compared the prevalence of postpartum pelvic tissue damage between women who were delivered with no episiotomy and those delivered via mediolateral episiotomy. In this nonrandomized, non-
No documented cases are known of sonographically detected anal sphincter disruption following cesarean delivery. However, cesarean delivery after labor onset is not entirely protective against postpartum fecal incontinence due to pelvic nerve damage, as discussed further in the next section. Injury to the anal sphincter during childbirth likely occurs either as a result of direct disruption of the muscles or due to injury to the pudendal nerves. The quoted incidence of sphincter laceration noted at the time of vaginal delivery ranges from 1% to 24%. The average incidence ranges from 6.5% (0.4% to 23.9%) in women with midline episiotomy, 1.3% (0.5% to 2.0%) in women with mediolateral episiotomy, and 1.4% (0% to 6.4%) in women without episiotomy. Endoanal ultrasound performed in the first months postpartum reveals that as many as 35% of primiparous women and up to 44% of multiparous women have evidence of sphincter disruption. Other anal function studies, such as anorectal manometry and anorectal sensation testing, also have demonstrated that vaginal delivery has an effect on anal function. Chaliha et al. (2001) showed that, compared to before delivery, vaginal delivery was associated with decreased anal squeeze pressures and resting pressures, whereas no change in anal sensation was noted. Risk factors for both overt and occult sphincter injuries include forceps, prolonged second stage, large birth weight, midline episiotomy, and occipitoposterior positions. Table 13-1 describes the typical adjusted odds ratios for predictors of anal sphincter disruption on multivariate analyses. In addition, Richter et al. (2002) reported that vaginal birth after cesarean delivery was an independent risk factor for anal sphincter disruption, compared to previous vaginal delivery (relative risk 5.46 [3.69–8.08]) after adjusting for primiparity, birth weight greater than 4000 g, forceps delivery, vacuum delivery, shoulder dystocia, and episiotomy. Randomized trials have also supported the association between episiotomy and anal sphincter disruption. Harrison et al. (1984) randomized 181 primigravid women to routine
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Table 13-1 ■ Predictors of Anal Sphincter Disruption After Vaginal Delivery Risk Factors
Adjusted Odds Ratios*
Midline episiotomy Nulliparity Operative delivery Birthweight ≥4000 g Occipitoposterior
4.9–16.5 2.5–4.0 2.5–3.5 1.5–2.5 1.2–1.8
* Numbers represent the minimum and maximum adjusted odds ratios reported in the medical literature.
mediolateral episiotomy or to restricted use of mediolateral episiotomy. The episiotomy group sustained rectal injury in 5 of 89 cases (5.6%), compared to no cases of rectal injury in the restricted group. Sleep et al. (1984) randomized 1000 women to liberal use of mediolateral episiotomy (51% of patients) or restricted mediolateral episiotomy (10% of patients). A liberal policy toward episiotomy resulted in significantly more maternal vaginal trauma and more suturing. The association between operative delivery and perineal trauma has also been studied in a randomized fashion. Yancey et al. (1991) randomly assigned uncomplicated, term gestations at 2+ station in occipitoanterior position to routine outlet forceps or to spontaneous delivery. Among patients delivered by outlet forceps, the incidence of third- or fourthdegree laceration was 30 of 165 (18%) versus 12 of 168 (7%) in women who delivered spontaneously. Midline episiotomy and outlet forceps were the only factors significantly associated with rectal trauma on multivariate analysis. Incidentally, defects that appear to be traumatic sphincter injuries on ultrasound may not always be the case. Threedimensional imaging and anatomic studies combined with MRI have shown that both the female and male anal sphincters have a variable natural gap occurring along its anterior length. The natural gap seen on ultrasound can be distinguished from a traumatic one by its anterior uniform hypoechogenicity, smooth and uniform edges, and symmetry.
Neurologic Outcomes Ample evidence links neurologic injury with pelvic floor disorders. It appears that labor and childbirth, but not pregnancy, are major risk factors for neurologic injury. For example, in a study by Sultan et al. (1994), the pudendal nerve terminal motor latency (PNTML) was not increased in pregnant non-laboring women compared with non-pregnant women. However, after vaginal delivery, Snooks et al. (1986) found that 42% of women had a prolonged PNTML, but this had eventually recovered in most women by 2 months postpartum. Single-fiber electromyography (EMG) of the anal sphincter revealed an increased fiber-density 2 months postpartum. These findings were most striking in multiparous women (suggesting a cumulative effect of vaginal delivery on the pelvic floor) and women delivered by forceps. No changes in these parameters were seen in women who had delivered by cesarean section. Five years after delivery, Snooks et al. (1990) reported that there was manometric
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and neurophysiologic evidence of weakness because of partial denervation of the pelvic floor striated sphincter musculature, with pudendal neuropathy, which was more marked in those women with incontinence. Other investigators have confirmed that latencies are prolonged after vaginal delivery and have also confirmed that the conduction time returns to normal in most women. In a prospective study by Allen et al. (1990), concentricneedle EMG was performed on the levator ani before delivery as well as 2 and 5 days after delivery. Following vaginal delivery, the duration of the motor unit potential was increased, consistent with nerve damage. Eighty percent of the women showed evidence of denervation with subsequent reinnervation after vaginal delivery. After elective cesarean delivery, however, the motor unit potentials were unchanged. In contrast to the findings after elective cesarean deliveries, the duration of the motor unit potentials was increased following emergency cesarean deliveries that were performed after labor onset. Similarly, other investigators have found the PNTML to be prolonged after a cesarean delivery performed in late labor (cervical dilation 8 cm or greater) but not in women delivered by cesarean before they reached 8 cm dilation.
Other Anatomic Findings The position of the perineum at rest and during straining is lower after vaginal delivery than either antepartum or after cesarean delivery. At 1 week postpartum, women are less able to elevate the bladder neck during voluntary levator ani muscle contraction. Most regain this ability after 6 to 10 weeks, but some women lose their ability to perform a voluntary pelvic muscle contraction. Other studies have also shown a loss of bladder neck support at rest and increased bladder mobility during straining after vaginal delivery, compared with women who had an elective cesarean delivery. Dietz and Bennett (2003) found that bladder neck descent was associated with cesarean deliveries done during labor, but not before the onset of labor, suggesting that labor itself contributes to changes in pelvic support.
Summary Immediately after vaginal delivery, women have less pelvic floor contraction strength, lower perineal and bladder neck support, more pelvic floor denervation, and more anal sphincter ruptures than women who delivered by cesarean delivery. Within the group of women that delivered by cesarean, these outcomes are more common in those that delivered after the onset of labor. This evidence, although suggestive, does not address what patients and providers want to know: Does the method of childbirth affect the risk of the actual pelvic floor disorders? In the following section, we highlight some of the evidence in this area.
IMPACT OF CHILDBIRTH ON SPECIFIC PELVIC FLOOR DISORDERS In this section, we discuss the role of childbirth on pelvic floor disorders most likely to affect women. The reader should bear
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in mind that in developing countries, vesicovaginal fistulas are epidemic and constitute a great societal problem. In the United States, the incidence of urogenital fistulas (such as uterovesical) has increased slightly as the cesarean delivery rate has increased; however, these remain rare and will not be addressed in this chapter.
Fecal Incontinence In large, prospective cohort studies of pregnant or newly postpartum women, incontinence to both flatus and stool ranged from 6% to 25%. Vaginal delivery by forceps, and, in some cases, vacuum delivery, increased the odds of postpartum fecal incontinence. As previously discussed, midline episiotomy is highly associated with sphincter injury but does not appear, in most studies, to be an independent risk factor for fecal incontinence. Studies assessing the prevalence of fecal incontinence at various postpartum intervals in women with known sphincter tears reveal prevalence of incontinence of flatus of 17% to 59% and incontinence to liquid and solid stool of 3% to 27%. Few studies have been designed to examine the difference in fecal incontinence after cesarean versus vaginal delivery. In a prospective study by Fynes et al. (1998), of 234 women attending a hospital antepartum clinic in Dublin, none of the 34 women who had a cesarean section reported fecal incontinence. Similarly, Abramowitz et al. (2000) reported that of 259 women who consecutively delivered at a single hospital, none of the 31 who delivered by cesarean reported fecal incontinence compared to 13% of primiparous women who delivered vaginally. In a large prospective study by Chaliha et al. (1999), of 549 nulliparous pregnant women, a greater proportion of women reported fecal urgency after vaginal delivery than after cesarean (7.3% vs 3.1%). The impact of delivery type on fecal incontinence appears to decline with age. In a retrospective study by Nygaard et al. (1997), the reported prevalence of fecal incontinence 30 years after delivery was similar, regardless of delivery type. Most studies have not separately examined the effect of a third-degree versus a fourth-degree laceration on future bowel control. In a recent retrospective single-site study by Fenner et al. (2003), 831 women (29% response rate) completed a bowel questionnaire 6 months after their first delivery. The incidence of worse bowel control than before pregnancy was nearly 10 times higher in women with fourthdegree lacerations (30.8%), compared with women with third-degree lacerations (3.6%). Although this difference may be due to increased participation from women with more symptoms, it is also possible that the higher incidence of fecal incontinence associated with fourth-degree lacerations may be due to the loss of some of the internal anal sphincter muscle. Further study is needed on the role of the internal anal sphincter in continence, and the best methods of repairing this muscle at the time of rupture. Although some degree of fecal incontinence after sphincter disruption is likely related to impaired neurologic control of continence, separation of the repaired muscles may also play a role. Fitzpatrick et al. (2000) examined 154 women at 3 months after primary repair of an anal sphincter disruption. One third had ultrasound evidence of a persistent, large
(larger than one quadrant) anal sphincter defect; this was not influenced by whether the repair was done in an end-to-end or overlapping fashion.
Urinary Incontinence Nulligravid pregnant women leak more often than nulliparous counterparts. Indeed, numerous cross-sectional studies reveal that 25% to 75% of women report symptoms of stress urinary incontinence (SUI) during pregnancy. In one of the few prospective studies with long-term follow-up, Viktrup et al. (1992) found that 32% of 305 primiparas developed SUI during pregnancy and 7% after delivery. By 1 year postpartum, only 3% had SUI. However, in a subsequent follow-up of the same women 5 years later, Viktrup and Lose (2001) reported that 19% of women with no symptom after the first delivery had SUI; of women with SUI at 3 months after delivery (most of whom had resolved by 1 year), 92% had SUI 5 years later. In a recent prospective cohort study of 523 women, Burgio et al. (2003) reported that 13% reported urinary incontinence at 12 months postpartum. This rate was similar to that at 3 months postpartum, but for most women the severity and frequency of leakage were lower 12 months later. Antepartum incontinence strongly predicted postpartum incontinence. Thus, it appears that the symptom of SUI occurs as a natural consequence of pregnancy and delivery and generally resolves or declines afterward in severity, but transient postpartum incontinence may be a marker for future persistent incontinence. Whether pregnancy itself or vaginal delivery is the risk factor for developing urinary incontinence in the majority of women is still unclear. Particularly in younger women, vaginal delivery roughly doubles a woman’s chance of experiencing urinary incontinence, after adjusting for other potential causes. Occasional urinary incontinence is common but often not bothersome; therefore, it may be more appropriate to examine the impact of vaginal delivery on more clinically significant leakage. In a recent large Norwegian populationbased study, Rortveit et al. (2003) found that women who delivered vaginally had a 2.2-fold higher risk of moderate or severe urinary incontinence compared to those who delivered solely by cesarean (after adjusting for other risk factors). These authors concluded that a woman’s risk of moderate or severe incontinence would be decreased from about 10% to about 5%, if all of her children were delivered via cesarean. Similarly, several other studies support a link between increasing parity and increasing prevalence of urinary incontinence, though the data are not wholly consistent. Similar to the population-based study mentioned previously, in a large study of Australian women, Chiarelli et al. (1999) found that parity was strongly associated with urinary incontinence in younger women. Although most studies do demonstrate a link between vaginal delivery and urinary incontinence in younger women, two facts warrant attention, as they help to put the debate of the role of “prophylactic” cesarean deliveries into perspective. First, in these studies, some women who delivered solely via cesarean also had moderate or severe incontinence. Second, the protective effect of cesarean delivery and nulliparity on urinary incontinence dissipates by age
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50 to 60, such that older women have the same rate of urinary incontinence regardless of their delivery status. Conflicting evidence exists about the role of other obstetric variables (besides vaginal delivery) on the development of SUI. Although some studies reported more SUI with prolonged second stage, increased head circumference, increased birth weight, epidural anesthesia, and oxytocin use, others did not. In prospective randomized trials, episiotomy did not protect women from developing SUI after delivery. Episiotomy also does not seem to affect PNTML, urethral closure pressure, or pelvic muscle strength. Only one randomized trial has assessed the difference in pelvic floor symptoms after planned elective cesarean delivery or planned vaginal birth: the Term Breech Trial, conducted by Hannah et al. (2002). Questionnaires were completed 3 months postpartum by 1596 women from 110 centers around the world. Although the conclusions are limited by the large number of women in the planned vaginal birth group who instead delivered by cesarean, the shortterm results are of interest. Women in the planned cesarean delivery group reported less urinary incontinence than those in the planned vaginal birth group (4.5% vs 7.3%; RR 0.62, 95% CI 0.41–0.93). Other outcomes did not differ. The lower rate of incontinence in this study, compared to others that assessed postpartum urinary incontinence, may be because women were queried about urinary incontinence symptoms only during the week before taking the questionnaire. In addition, women from different countries may interpret differently symptom questionnaires. Most studies that address the impact of subsequent deliveries on pelvic floor disorders are retrospective. In a recent prospective cohort study by Yip et al. (2003), in which women were followed for 4 years after their first vaginal delivery, the rates of SUI (defined as two or more episodes of incontinence occurring in the past month) were 21.1% in those with and 28.6% in those without a subsequent delivery, respectively. Thus, one interval delivery did not increase the short-term risk of SUI.
Pelvic Organ Prolapse Pelvic organ support defects appear to occur during pregnancy but before delivery. O’Boyle et al. (2002) found that nulligravid pregnant women were more likely to have POP than their nulliparous counterparts. Parity increases the risk for both POP and surgery for POP. In women participating in the Women’s Health Initiative, those who had borne at least one child were twice as likely to have uterine prolapse, rectocele, and cystocele as were nulliparous women, after adjusting for age, ethnicity, body mass index, and other factors. Similarly, in a study of 487 Swedish women, Samuelsson et al. (1999) reported that 31% had some degree of POP on examination; parity and age increased the risk of POP, after adjusting for other variables. In a British cohort study conducted by Mant et al. (1997) of 17,000 women, parity was the variable most strongly related to surgery for POP. The risk increased with each child, but the rate of increase declined once women had delivered two children. In a case-control study, Rinne and Kirkinen (1999) found that women under age 45 who underwent sur-
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gery for POP had more deliveries and heavier babies than age-matched controls operated for benign ovarian tumors. The impact of vaginal delivery and intrapartum management on the development or prevention of defects in the connective tissue and levator muscles that lead to POP has not been examined prospectively.
Pain The primary factor that influences pain after vaginal delivery appears to be episiotomy. In a randomized controlled trial by the Argentine Episiotomy Trial Collaborative Group (1993), perineal pain was less frequent with selective use of episiotomy. In another trial by Klein et al. (1994), women had pain-free intercourse earlier if no episiotomy was made than otherwise. In the 2006 Cochrane review on this subject, the authors concluded that restricting the use of episiotomy was associated with less posterior perineal trauma, less suturing, and further complications; no difference for most pain measures and severe vaginal or perineal trauma; but an increased risk of anterior perineal trauma with restrictive episiotomy.
THE DEBATE OVER ELECTIVE PRIMARY CESAREAN DELIVERY No chapter about the effect of childbirth on pelvic floor disorders is complete without mention of the current debate about the role of elective primary cesarean delivery. Those in favor of such a policy support their decision with factors, such as patient autonomy; concern over long-term adverse outcomes thought to be associated with vaginal delivery, particularly pelvic floor disorders; avoiding the higher morbidity associated with cesarean delivery after the onset of labor; preventing stillbirths that occur after 39 weeks by preemptively delivering via cesarean instead; and decreasing the incidence of traumatic birth injuries in neonates. Conversely, those opposed to allowing women a delivery choice cite the increased short-term morbidity, higher maternal mortality rate, greater neonatal respiratory complications, adverse effects on future pregnancies (in terms of both fertility and subsequent complications from repeated cesarean deliveries), greater cost associated with cesarean delivery, and dubious morality involved in turning a “natural” event into an invasive operation. Unfortunately, no current data are available that allow this debate to be entirely evidence-based. Most serious are concerns about higher mortality associated with cesarean delivery. It is difficult to tease out morbidity and mortality related to an elective cesarean delivery done before labor versus that done not only after active labor but also because of pregnancy complications that increase morbidity. Perhaps, more importantly, minimal information exists that allows us to judge risk over a woman’s entire reproductive career; the information that does exist suggests strongly that severe complications increase dramatically after two cesarean deliveries. At the time of this writing, the majority of affluent women in some countries (such as Brazil) are choosing to undergo cesarean, rather than vaginal, deliveries and these requests are being honored. Although a similar dramatic
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change has not been seen in the United States, women, partly fueled by news reports, are increasingly beginning to request delivery options. Before elective primary cesarean deliveries become widely accepted, it is imperative to investigate the risks and benefits of such practice over a woman’s entire reproductive career. Based on current available information about the strengths and limitations of both delivery types, a randomized clinical trial with long-term follow-up is necessary, feasible, and ethical.
CONCLUSION Childbirth increases the risk of pelvic floor disorders in young and middle-aged women. In most studies, vaginal delivery increases this risk more than does cesarean delivery. However, nulliparous women also develop pelvic floor disorders, though not at as high a rate as parous women. Further, most parous women do not have surgery for pelvic floor disorders. Both urinary and fecal incontinence increase with age; indeed, studies of older nulliparous women find the same or higher rates of these disorders as do studies of younger parous women. The fact that older women have high rates of urinary and fecal incontinence does not, however, mean that childbirth is not one of the causes of these disorders, but that in older women, other factors (such as functional impairment, medical problems, and even age itself) assume much greater importance, thereby minimizing the role of childbirth. In younger and middle-aged women, parity and vaginal delivery remain important risk factors for pelvic floor disorders. Further research is needed to identify the group of women most at risk for pelvic floor disorders, such that preventive efforts may be studied.
Bibliography 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; discussion 596. Allen RE, Hosker GL, Smith AR, et al. Pelvic floor damage and childbirth: a neurophysiological study. Br J Obstet Gynaecol 1990;97:770. Anderson RS. A neurogenic element to urinary genuine stress incontinence. Br J Obstet Gynaecol 1984;91:141. Argentine Episiotomy Trial Collaborative Group. Routine versus selective episiotomy: a randomized controlled trial. Lancet 1993;342:1517. Ballard RC, Gardiner A, Lindow S, et al. Normal female anal sphincter: difficulty in interpretation explained. Dis Colon Rectum 2002;45:171. Burgio KL, Zyczynski H, Locher JL, et al. Urinary incontinence in the 12-month postpartum period. Obstet Gynecol 2003;102:1291. Carroli G, Belizan J. Episiotomy for vaginal birth (review). Cochrane Database Syst Rev 2000;2:CD00081. Carroli G, Belizan J. Episiotomy for vaginal birth. Cochrane Pregnancy and Childbirth Group. Cochrane Database Syst Rev 2006:2. Chaliha C, Kalia V, Stanton SL, et al. Antenatal prediction of postpartum urinary and fecal incontinence. Obstet Gynecol 1999;94:689. Chaliha C, Sultan AH, Bland JM, et al. Anal function: effect of pregnancy and delivery. Am J Obstet Gynecol 2001;185:427. Chiarelli P, Brown W, McElduff P. Leaking urine: prevalence and associated factors in Australian women. Neurourol Urodyn 1999;18:567. Crawford LA, Quint EH, Pearl ML, et al. Incontinence following rupture of the anal sphincter during delivery. Obstet Gynecol 1993;82:527. Dietz HP, Bennett MJ. The effect of childbirth on pelvic organ mobility. Obstet Gynecol 2003;102:223. DeLancey JO, Kearney R, Chou Q, et al. The appearance of levator ani muscle abnormalities in magnetic resonance images after vaginal delivery. Obstet Gynecol 2003;101:46.
DeLee JB. The prophylactic forceps operation. Am J Obstet Gynecol 1920;1:34. Donnelly V, Fynes M, Campbell D, et al. Obstetric events leading to anal sphincter damage. Obstet Gynecol 1998;92:955. Fenner DE, Genberg B, Brahman P, et al. 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. Fitzpatrick M, Fynes M, Cassidy M, et al. Prospective study of the influence of parity and operative technique on the outcome of primary anal sphincter repair following obstetrical injury. Eur J Obstet Gynecol Reprod Biol 2000;89:159. Fornell EK, Berg G, Hallböök O, et al. Clinical consequences of anal sphincter rupture during vaginal delivery. J Am Coll Surg 1996;183:553. Fritsch H, Brenner E, Lienemann A, et al. Anal sphincter complex. Reinterpreted morphology and its clinical relevance. Dis Colon Rectum 2002;45:188. Fynes M, Donnelly VS, O’Connell PR, et al. Cesarean delivery and anal sphincter injury. Obstet Gynecol 1998;92:496. Gainey HL. Postpartum observation of pelvic tissue damage: further studies. Am J Obstet Gynecol 1955;70:800. Gordon H, Logue M. Perineal muscle function after childbirth. Lancet 1985;2:123. Green JR, Soohoo SL. Factors associated with rectal injury in spontaneous delivery. Obstet Gynecol 1989;73:732. Groutz A, Fait G, Lessing JB, et al. Incidence and obstetric risk factors of postpartum anal incontinence. Scand J Gastroenterol 1999;34:315. Handa VL, Harris TA, Ostergard DR. Protecting the pelvic floor: obstetric management to prevent incontinence and pelvic organ prolapse. Obstet Gynecol 1996;88:470. Hannah ME, Hannah WJ, Hodnett ED, et al. Outcomes at 3 months after planned cesarean vs planned vaginal delivery for breech presentation at term: The International Randomized Term Breech Trial. JAMA 2002;287:1822. Harrison RF, Brennan M, North PM, et al. Is routine episiotomy necessary? Br Med J 1984;288:1971. Heidkamp MC, Leong FC, Brubaker L, et al. Pudendal denervation affects the structure and function of the striated, urethral sphincter in female rats. Int Urogynecol J 1998;9:88. 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. Homsi R, Daikoku NH, Littlejohn J, et al. Episiotomy: risks of dehiscence and rectovaginal fistula. Obstet Gynecol Surv 1994;49:803. 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. Lien K, Mooney B, DeLancey JO, Ashton-Miller JA. Levator ani muscle stretch induced by simulated vaginal birth. Obstet Gynecol 2004;103:31. MacArthur C, Glazener CM, Wilson PD, et al. Obstetric practice and faecal incontinence three months after delivery. Br J Obstet Gynaecol 2001;108:678. 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. Meyer S, Schreyer A, de Grandi P, et al. The effect of birth on urinary continence mechanisms and other pelvic-floor characteristics. Obstet Gynecol 1998;92:613. Nodine P, Roberts J. Factors associated with perineal outcome during childbirth. J Nurse Midwifery 1987;32:123. Nygaard IE, Rao SS, Dawson JD. Anal incontinence after anal sphincter disruption: a 30-year retrospective cohort study. Obstet Gynecol 1997;89:896. O’Boyle AL, Woodman PL, O’Boyle JD, et al. Pelvic organ support in nulliparous pregnant and non-pregnant women: a case control study. Am J Obstet Gynecol 2002;187:99. Peschers U, Schaer G, Anthuber C, et al. Levator ani function before and after childbirth. Br J Obstet Gynaecol 1997;104:1004. Power RM. The pelvic floor during parturition. Surg Gynecol Obstet 1946;83:296. Richter HE, Brumfield CG, Cliver SP, et al. Risk factors associated with anal sphincter tear: a comparison of primiparous patients, vaginal births after cesarean deliveries, and patients with previous vaginal delivery. Am J Obstet Gynecol 2002;187:1194. Rieger N, Schloithe A, Saccone G, et al. The effect of a normal vaginal delivery on anal function. Acta Obstet Gynecol Scand 1997;76:769.
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Rinne KM, Kirkinen PP. What predisposes young women to genital prolapse? Eur J Obstet Gynecol Reprod Biol 1999;84:23. Rortveit G, Daltveit AK, Hannestad YS, Hunskaar S. Urinary incontinence after vaginal delivery or cesarean section. N Engl J Med 2003;348:900. Rortveit G, Hannestad YS, Daltveit AK, et al. Age- and type-dependent effects of parity on urinary incontinence: the Norwegian EPINCONT study. Obstet Gynecol 2001;98:1004. Samuelsson EC, Victor FT, Tibblin G, et al. Signs of genital prolapse in a Swedish population of women 20–59 years of age and possible related factors. Am J Obstet Gynecol 1999;180:299. Schuessler B, Hesse V, Dimpfel T, et al. Epidural anesthetic and avoidance of postpartum stress urinary incontinence. Lancet 1988;1:762. Shiono P, Klebanoff MA, Carey JC. Midline episiotomies: more harm than good? Obstet Gynecol 1990;76:765. Signorello LB, Harlow BL, Chekos AK, et al. Midline episiotomy and anal incontinence: retrospective cohort study. Br Med J 2000;320:86. Sleep J, Grant A, Elbourne D, et al. West Berkshire perineal management trial. Br Med J 1984;289:587. Sleep J, Grant A. West Berkshire perineal management trial: three year follow up. Br Med J 1987;295:749. 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. Snooks SJ, Swash M. Abnormalities of the innervation of the urethral striated sphincter musculature in incontinence. Br J Urol 1984;56:401. Snooks SJ, Swash M, Henry MM, et al. Risk factors in childbirth causing damage to the pelvic floor innervation. Int J Colorectal Dis 1986;1:20. Snooks SJ, Swash M, Mathers SE, et al. Effect of vaginal delivery on the pelvic floor: a 5-year follow-up. Br J Surg 1990;77:1358. Stanton SL, Kerr-Wilson R, Harris VG. The incidence of urological symptoms in normal pregnancy. Br J Obstet Gynaecol 1980;87:897. Swash M, Snooks SJ, Henry MW. Unifying concept of pelvic floor disorders and incontinence. J R Soc Med 1985;78:906.
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Sultan AH, Kamm MA, Hudson CN, et al. Anal-sphincter disruption during vaginal delivery. N Engl J Med 1993;329:1905. Sultan AH, Kamm MA, Hudson CN. Pudendal nerve damage during labour: prospective study before and after childbirth. Br J Obstet Gynaecol 1994;101:22. Tetzschner T, Sorensen M, Lose G, et al. Pudendal nerve function during pregnancy and after delivery. Int Urogynecol J 1997;8:66. Thorp JM, Bowes WA, Braune RG, et al. Selected use of midline episiotomy: effect on perineal trauma. Obstet Gynecol 1987;70:260. Thorp JM, Bowes WA. Episiotomy: can its routine use be defended? Am J Obstet Gynecol 1989;160:1027. Thorp JM, Norton PA, Wall LL, et al. Urinary incontinence in pregnancy and the puerperium: a prospective study. Am J Obstet Gynecol 1999;18:266. Viktrup L, Lose G, Rolff M, et al. The symptom of stress incontinence caused by pregnancy or delivery in primiparas. Obstet Gynecol 1992;79:945. Viktrup L, Lose G. The risk of stress incontinence 5 years after first delivery. Am J Obstet Gynecol 2001;185:82. Walker MP, Farine D, Rolbin SH, et al. Epidural anesthesia, episiotomy and obstetric laceration. Obstet Gynecol 1991;77:688. Wilcox LS, Strobino DM, Baruffi G, et al. Episiotomy and its role in the incidence of perineal laceration in a maternity center and a tertiary hospital obstetric service. Am J Obstet Gynecol 1989;160:1047. Woolley RJ. Benefits and risks of episiotomy: a review of the Englishlanguage literature since 1980. I and II. Obstet Gynecol Surv 1995;50:806. Wynne JM, Myles JL, Jones I, et al. Disturbed anal sphincter function following vaginal delivery. Gut 1996;39:120. Yancey MK, Herpolsheimer A, Jordan GD, et al. Maternal and neonatal effects of outlet forceps delivery compared with spontaneous vaginal delivery in term pregnancies. Obstet Gynecol 1991;78:646. Yip S, Sahota D, Chang A, et al. Effect of one interval vaginal delivery on the prevalence of stress urinary incontinence: a prospective cohort study. Neurourol Urodyn 2003;22:558.
Stress Urinary Incontinence and Pelvic Organ Prolapse: Nonsurgical Management
14
Holly E. Richter and Kathryn L. Burgio
THE BLADDER DIARY: A VALUABLE CLINICAL TOOL 172 BEHAVIORAL INTERVENTION: PELVIC FLOOR MUSCLE TRAINING AND EXERCISE 173 Teaching Daily Pelvic Floor Muscle Control 173 Using Muscles to Prevent Stress Accidents: Stress Strategies 174 Using Muscles to Prevent Urge Accidents: Urge Suppression Strategies 174 Adherence and Maintenance 175 Electrical Stimulation 175 BEHAVIORAL INTERVENTION: BLADDER TRAINING 175 BOWEL MANAGEMENT 176 WEIGHT LOSS AND INCONTINENCE 176 ESTROGEN AND STRESS INCONTINENCE 176 OTHER PHARMACOLOGIC THERAPIES 177 α-Adrenergic Agonists 177 β-Adrenergic Receptor Antagonists and Agonists 177 Tricyclic Antidepressants 177 Duloxetine 178 URETHRAL DEVICES 178 Urethral Inserts 179 Urethral Occlusive Devices 179 THE INS AND OUTS OF PESSARY USE 180 Pessary Placement and Management 183 Steps to Fitting a Pessary 183 Follow-Up Recommendations 183 Complications 183
Many advances in the treatment of stress urinary incontinence (SUI) have been in the arena of surgery. However, research and clinical practice have also seen significant advances in nonsurgical treatments for SUI and pelvic organ prolapse (POP). Most patients are not aware of the existence of nonsurgical treatment for prolapse and incontinence, and they are often relieved that treatment options, other than surgery, exist. Behavioral treatment, the current “gold standard” conservative approach for SUI, improves bladder control by changing the incontinent patient’s behavior, including teaching skills for preventing urine loss. Multicomponent
behavioral interventions include pelvic floor muscle training and exercise, biofeedback, bladder inhibition, and bladder training. As part of first-line treatment, estrogen optimizes urogenital tissue health and relieves some lower urinary tract symptoms. Other medications, including duloxetine, may offer effective treatment for mild to moderate stress incontinence. Pessaries stabilize the proximal urethra, and urethral inserts increase urethral pressure. Such devices provide valuable alternatives to patients. This chapter describes the full range of nonsurgical options for the treatment of SUI and POP, allowing us to offer a whole spectrum of less invasive treatment options in an individualized fashion. Optimal therapy for urinary incontinence depends on several factors, including the type and severity of incontinence, the presence of associated conditions such as prolapse or other abdominal pelvic pathology, prior surgical or nonsurgical therapy, the patient’s medical status, and her ability and willingness to cooperate with treatment.
THE BLADDER DIARY: A VALUABLE CLINICAL TOOL Before initiating nonsurgical treatment for incontinence, the patient is advised to complete a bladder diary for 5 to 7 days. At a minimum, the patient should record the time, volume, and circumstances of each incontinent episode (Fig. 14-1). The bladder diary assists the clinician in determining the type and severity of urine loss and in planning appropriate intervention. Using the diary, the circumstances of incontinence can be reviewed with the patient and instructions given that are specific to the patient’s situation. During treatment, the number of incontinent episodes can be monitored to determine the efficacy of treatment and to guide further intervention. Asking the patient to record the times she urinates during the day and night is useful. This can identify women who may benefit from more frequent urination to avoid a full bladder, especially during physical activity. It may also reveal cases in which voiding frequency is excessive and may be contributing
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Figure 14-1
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BLADDER DIARY
Sample bladder diary. Name
Date Urinated in toilet
Time up for the day: # of pads used today: Comments:
to reduced bladder capacity and urgency. These women may be targeted for interventions like bladder training that focus on increasing voiding intervals and bladder capacity. Though more burdensome, women are also encouraged to record voided volumes for a 24-hour period. This can identify patients with abnormal urine production, especially those with increased nighttime urine production resulting in nocturia. In addition to the value of the bladder diary to the clinician, completing a daily diary appears to directly benefit the patient. As a self-monitoring practice, it enhances the patient’s awareness of her voiding and incontinence patterns and often facilitates her recognition of the relationship between her activities and her incontinence. Specifically, understanding clearly the precipitants of urine leakage optimizes the patient’s readiness to implement the continence skills she learns through behavioral treatment.
BEHAVIORAL INTERVENTION: PELVIC FLOOR MUSCLE TRAINING AND EXERCISE Pelvic floor muscle training and exercise are the foundation of behavioral treatment for SUI. Kegel (1948), a gynecologist, first popularized it in the late 1940s. He asserted that
Small accident
Large accident
Reason for accident
Time to bed for the night: Number of accidents:
women with stress incontinence lack awareness and coordination of the pelvic muscles; with training and improved strength, stress incontinence can be prevented (Kegel, 1948, 1956). Through the years, this intervention has evolved both as behavior therapy and physical therapy, combining principles from both fields into a widely accepted conservative treatment for stress incontinence. Literature on outpatient behavioral treatment with pelvic muscle training and exercise has demonstrated that it is effective for reducing stress, urge, and mixed incontinence in most patients who cooperate with training. Behavioral treatments have been recognized for their efficacy by the 1988 Consensus Conference on Urinary Incontinence in Adults (1989) and by the Guideline for Urinary Incontinence in Adults developed by the Agency for Health Care Policy and Research (AHCPR) (Fantl et al., 1996). Although the majority of women are not cured with this approach, most can achieve significant improvement.
Teaching Daily Pelvic Floor Muscle Control The goal of behavioral intervention for stress incontinence is to teach patients how to improve urethral closure by contracting pelvic floor muscles during physical activities
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that cause urine leakage, such as coughing, sneezing, or lifting. The premise is that deliberate muscle contraction will increase intraurethral pressure and prevent urine loss caused by the brief rise in bladder pressure. Using biofeedback or other teaching methods, patients are taught to identify the pelvic muscles and to contract and relax them selectively (without increasing intra-abdominal pressure). Many women fail pelvic muscle exercise by religiously exercising the wrong muscles. It is an essential, yet often overlooked, step to help women identify and isolate the correct muscles. The most common approach to pelvic muscle training is to give women a pamphlet or brief verbal instructions to “lift the pelvic floor” or to interrupt the urinary stream during voiding. This approach is generally ineffective, most likely because the majority of women do not properly identify the pelvic muscles or persist long enough to reap the benefits of behavioral treatment. A much more effective way to begin treatment is to ensure that the patient understands which muscles to use, which is often accomplished by palpating the vagina during pelvic examination and guiding her with verbal feedback to find the proper muscles. Pelvic muscle control can also be taught using biofeedback or electrical stimulation. Biofeedback is a teaching technique that helps patients learn by giving them immediate feedback of their bladder or pelvic muscle activity. Kegel (1948) introduced a biofeedback device he called the perineometer, consisting of a pneumatic chamber that was placed in the vagina and a handheld pressure gauge that registered increased vaginal pressure generated by pelvic muscle contraction. This provided immediate visual feedback to the woman learning to identify her pelvic muscles and monitoring her practice. Most biofeedback instruments are now computerized. Pelvic muscle activity can be measured using vaginal or anal manometry or electromyography (EMG), with a probe or perianal surface electrodes. Signals are augmented through a computer, and muscle activity is displayed on a monitor where patients can receive immediate visual or auditory feedback. Patients learn better control through operant conditioning (trial and error learning) by observing the results of their attempts to control bladder and pelvic muscle responses. Biofeedback-assisted behavioral training has been tested in several studies, producing mean reductions of incontinence ranging from 60% to 85%. Patients can usually identify their pelvic floor muscles in a single session; treatment requires less repetition of biofeedback than was previously thought. The most common problem in identifying the pelvic floor muscles is that women tend to contract other muscles, typically the abdominal or gluteal muscles, instead of or in conjunction with pelvic muscles. Contracting abdominal muscles is counterproductive, because it increases pressure on the bladder rather than the urethra. Thus, it is important to notice this Valsalva response and to teach the patient to relax her abdominal muscles. Otherwise, her pelvic muscle exercises may be ineffective. Once patients learn to properly contract and relax selectively the pelvic muscles, a program of daily exercise is prescribed. The purpose of the daily regimen is not only to increase muscle strength, but also to enhance the skill of using the muscles through practice. The optimal exercise regimen has yet to be determined; however, good results are
generally achieved using 45 to 50 exercises per day. To avoid muscle fatigue, the exercises should be spaced across the day, usually in two to three sessions per day (Fig. 14-2). Patients generally find it easiest to at first practice their exercises in the lying position. Encouraging them to practice sitting or standing as well is important, so that they become comfortable using their muscles to avoid accidents in any position. To improve muscle strength, contractions should be sustained for 2 to 10 seconds, depending on the patient’s initial ability. Programs can be individualized, so patients begin by holding contractions for a brief period (1 to 2 seconds) and gradually progress to 10 seconds. Each exercise consists of contracting the muscle for up to 10 seconds followed by a period of relaxation using a 1:1 or 1:2 ratio. This allows the muscles to recover between contractions.
Using Muscles to Prevent Stress Accidents: Stress Strategies Although exercise alone can improve urethral support and continence status, optimal results depend on patients learning to use their muscles actively to prevent urine loss during physical exertion. With practice and encouragement, patients can develop the habit of consciously contracting the pelvic muscles to occlude the urethra before and during coughing, sneezing, or other activities causing urine loss. This skill has been referred to as stress strategy, counterbracing, and “the knack.” Some women will benefit simply from learning how to control their pelvic muscles and use them to prevent accidents. Others will need a more comprehensive program of pelvic muscle rehabilitation to increase strength as well as skill.
Using Muscles to Prevent Urge Accidents: Urge Suppression Strategies Traditionally, pelvic floor muscle training and exercise were used almost exclusively for stress incontinence. However, • Continue to keep your bladder diary. • Do 45 pelvic floor muscle exercises EVERY day: 15 at a time, 3 times per day. Do
lying down.
Do
sitting.
Do
standing.
• For each exercise squeeze your pelvic muscles as quickly and as hard as you can. Hold the squeeze for
seconds.
Relax completely between each squeeze for seconds. • Remember to relax all the muscles in your abdomen when you do these exercises and continue to breathe normally. • Once per day, practice stopping or slowing the stream of urine when you void. Figure 14-2
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Instructions for daily pelvic floor muscle exercise.
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voluntary pelvic muscle contraction can also inhibit detrusor contraction. Therefore, pelvic muscle training is now frequently used as a component in the behavioral treatment of urge incontinence as well. In addition to using pelvic muscles to occlude the urethra, patients learn to use pelvic muscle contractions and other urge suppression strategies to inhibit bladder contraction. Further, patients are taught a new way to respond to the sensation of urgency: Instead of rushing to the toilet, which increases intra-abdominal pressure and exposes patients to visual cues that can trigger incontinence, patients are encouraged to pause, sit down if possible, relax the entire body, and repeatedly contract pelvic muscles to diminish urgency, inhibit detrusor contraction, and prevent urine loss. When urgency subsides, patients are to proceed to the toilet at a normal pace. Behavioral training for urge incontinence has been tested in several clinical series using prepost designs. Mean reductions of incontinence range from 76% to 86%. In controlled trials using intention-to-treat models by Burgio et al. (1998, 2002), mean reductions of incontinence episodes range from 60% to 80%.
Adherence and Maintenance Pelvic muscle training and exercise require the active participation of a motivated patient. To remember to use muscles strategically in daily life is often challenging, as well as to persist in a regular exercise regimen to maintain strength and skill. This reliance on patient behavior change represents the major limitation of this treatment approach. In addition, improvement with behavioral treatment is gradual, usually evident by the fourth week of training and continuing for up to 6 months. Herein lies the challenge for behavioral treatment—to sustain the patient’s motivation long enough so that she will experience noticeable change in her bladder control. In initiating behavioral treatment, it is important to make it clear to the patient that her improvement will be gradual and will depend on consistent practice and use of her new skills. The patient who understands the usual course of treatment will be better prepared to persist until results are achieved. Clinicians can provide support by scheduling follow-up appointments to track and reinforce patient progress, to make adjustments to the exercise regimen, and to encourage persistence. The long-term effectiveness of pelvic floor muscle exercise in treating incontinence symptoms is still unknown because most studies follow patients for 1 or 2 years only. One study by Glazener et al. (2005) showed that, after 6 years of a postpartum pelvic muscle exercise program, initial improvements in SUI did not persist, and incontinence was similar to the control group. Only half the women were still performing the exercises.
Electrical Stimulation Pelvic floor electrical stimulation (PFES) has been used for the treatment of urinary incontinence since 1952 (Huffman et al., 1952). In this original study, PFES was added to pelvic muscle exercises to treat stress incontinence in women who had failed treatment with exercise alone. Seven of 17 women were cured. Fifteen years later, PFES was reported by Moore
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and Schofield (1967), using a vaginal probe, and has since become widely used. PFES stimulates pudendal nerve afferents, activating pudendal and hypogastric nerve efferents, causing contraction of smooth and striated periurethral muscles and striated pelvic floor muscles. This provides a form of passive exercise, with the goal of improving the urethral closure mechanism. In addition, PFES can be useful in teaching pelvic muscle contraction to women who cannot identify or contract these muscles voluntarily. Stimulation is generally applied via vaginal or anal probe for 15 minutes at a time one to three times per day. Research has demonstrated the efficacy of PFES compared to sham PFES (Sand et al., 1995; Yamanishi et al., 1997). Some evidence also shows that PFES yields similar results to pelvic muscle training (Hahn et al., 1991), although Bo et al. (1999) found pelvic muscle exercise to be superior. Several studies have combined PFES with various methods of pelvic muscle training and exercise and reported successful outcomes. One small study by Blowman et al. (1991) compared pelvic muscle exercise and exercise augmented with PFES in 14 patients and found that the addition of PFES improved outcomes as measured with bladder diaries and muscle strength. In another study by Sung et al. (2000), pelvic muscle exercises, augmented with both PFES and biofeedback, produced greater improvements compared with pelvic muscle exercises alone; however, the effect of PFES cannot be isolated from biofeedback. A third study by Goode et al. (2003) found that PFES did not significantly enhance the outcome of pelvic muscle training with biofeedback. Thus, although PFES shows promise in the treatment of stress incontinence, the role of electrical stimulation in combination with behavioral treatment with pelvic floor muscle training and exercise has not been clearly defined.
BEHAVIORAL INTERVENTION: BLADDER TRAINING Bladder training is a behavioral intervention developed originally for urge incontinence. In its earliest form, known as bladder drill, it was an intensive intervention often conducted in an inpatient setting. Patients were placed on a strict voiding schedule for 7 to 10 days to lengthen the interval between voids and to establish a normal voiding interval. Cure rates in women ranged from 82% to 86% (Frewen et al., 1979, 1982). Bladder training is a modification that is conducted more gradually in the outpatient setting. The premise of bladder training is that the habit of frequent urination can lead to reduced bladder capacity and detrusor overactivity, which, in turn, causes urge incontinence. The goal of the intervention is to break this cycle by encouraging patients to resist the sensation of urgency and postpone urination. Using consistent voiding schedules, the patient voids at predetermined intervals and, over time, gradually increases the voiding interval, which is believed to increase capacity and decrease overactivity, resulting in improved bladder control. Cure rates ranging from 44% to 90% have been demonstrated using outpatient bladder training or a mixture of
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inpatient and outpatient intervention. The first randomized trial of bladder training was reported by Fantl et al. (1991) and demonstrated an average 57% reduction of incontinence in older women. Interestingly, the training not only reduced urge incontinence, but also stress incontinence. The presumed mechanism for improving stress incontinence is that regular voiding helps avoid situations in which the bladder is full, making the patient less vulnerable to urine loss during physical activities. It is also possible that training leads the patient to greater awareness of bladder function, and postponing urination increases the use of pelvic muscles.
BOWEL MANAGEMENT Constipation and fecal impaction have been implicated as contributing factors in urinary incontinence. In severe cases, fecal impaction can obstruct normal voiding, contribute to overflow incontinence, or be an irritating factor in overactive bladder symptoms. Simple disimpaction can alleviate symptoms, especially common in nursing home patients. In outpatients who report that constipation aggravates urinary incontinence, it is often beneficial to implement a bowel management program, including instructions on normal fluid intake and dietary fiber (or supplements), to maintain normal stool consistency and regular bowel movements. When fiber is not enough, enemas can be used to stimulate a regular daily bowel movement.
WEIGHT LOSS AND INCONTINENCE Obesity is one of the major chronic health problems in America today. It contributes to more than 300,000 deaths per year and is associated with increased risk for hypertension, heart disease, diabetes, cancer, arthritis, respiratory disease, and depression. Over 50% of American women are currently overweight (body mass index [BMI] = 25–30 kg/ m2) or obese (BMI ≥ 30 kg/m2) (Mokdad et al., 2001). Obesity is a strong risk factor for incontinence. Data from the Heart and Estrogen-Progestin Replacement Study (HERS: 2763 women with coronary artery disease) and the Study of Osteoporotic Fractures (SOF: 9500 women at risk for fractures) revealed that of those complaining of incontinence, 65% to 75% were overweight or obese (Brown et al., 1996, 1999). Each five-unit increase of BMI was associated with a 60% increase in the risk of daily incontinence. Furthermore, obesity had the largest attributable risk for daily incontinence compared with other risk factors. Because many obese women are at risk for morbidity secondary to other chronic diseases, in addition to incontinence, weight loss should have a tremendous impact on quality of life. Weight loss has a positive effect on incontinence. Urinary symptoms can significantly improve in morbidly obese women with dramatic weight loss (45–50 kg) after bariatric surgery. Incontinence improves when women lose as little as 5% of their baseline weight, a reasonable goal for many overweight or obese women. In a small prospective cohort study with overweight and obese incontinent women enrolled in weight reduction programs, all patients with weight loss of
5% or greater had at least a 50% reduction in incontinence frequency. By comparison, only one in four women with less than 5% weight loss had a 50% or greater reduction in incontinence frequency. In a randomized trial, a very low-calorie liquid diet program was compared with no intervention in 42 overweight and obese women with incontinence (Subak et al., 2001). Women on the liquid diet lost an average of 1.4 kg over 3 months, and their frequency of incontinence episodes was reduced 60% compared with 4% in the controls. Although promising, these studies were small and outcomes were obtained over a short period. Larger studies with longer follow-up are needed, with appropriate investigation to study the mechanism by which weight loss reduces incontinence, to determine whether improvements are sustained and to identify predictors of improvement in incontinence associated with weight loss.
ESTROGEN AND STRESS INCONTINENCE Estrogen is discussed separately from other pharmacologic therapies for SUI because of the recent controversy over the effects of oral estrogen replacement therapy (ERT) on overall health and prevention of chronic disease. Despite this controversy, the benefits of oral and vaginal estrogen for urogenital health are undeniable. The prevalence of symptomatic urogenital atrophy in post-reproductive women may approach 50%. Since the lower urinary tract and vagina develop from the same embryologic origin, it is not surprising that estrogen receptors are present throughout the vagina, urethra, bladder trigone, pelvic connective tissue, and pelvic muscles. Decreased estrogen effect and resulting urogenital atrophy produce symptoms of vaginal dryness, pruritus, dyspareunia, vaginitis, recurrent urinary tract infections (UTIs), dysuria, urinary frequency, urinary urgency, nocturia, and incontinence. Painful urination or “urethral syndrome” secondary to decreased estrogen effect responds to local estrogen therapy, as do nocturia, irritative bladder symptoms, and recurrent UTI. Outcomes regarding the effect of estrogen on SUI have been mixed. Estrogen exerts beneficial effects in the urethra by increasing the concentration of α-adrenergic receptors in the urethra and bladder, improving vascularity and perfusion of the periurethral tissue and increasing thickness of the urethral epithelium. These changes facilitate coaptation and increase urethral pressure. Most of the nonrandomized studies, few with control groups, showed significant benefit of oral estrogen alone or in combination with progestin, in the treatment of SUI. Improvements have been reported on both subjective and objective parameters, including improved abdominal pressure transmission to the proximal urethra, increased functional urethral length, and increased maximal urethral closure pressure. Some studies found only subjective benefit. Large cohorts of women evaluated subjectively have had significant symptomatic improvement using vaginal estrogen. However, randomized controlled trials, with oral estrogen alone or combined with progestin, for the most part, showed no significant difference subjectively or objectively in SUI symptoms between groups. In one study by
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Grady et al. (2001), daily oral estrogen plus progestin was associated with worsening urinary incontinence. A recent questionnaire analysis of the Nurse’s Health Study participants by Grodstein et al. (2004) noted a significantly increased risk of developing urinary incontinence with use of postmenopausal hormone therapy. However, in randomized trials, ERT (oral and vaginal) combined with other therapies such as the α-adrenergic agonist, phenylpropanolamine (which is currently off the market due to increased risk of hemorrhagic stroke), pelvic muscle exercises, and surgery, have shown some benefit. Urogenital atrophy is an approved U.S. Food and Drug Administration (FDA) indication for estrogen therapy. Lower urinary tract symptoms associated with atrophy also significantly improve with hormonal therapy. Therefore, we strongly recommend optimizing urogenital tissue health as first-line with estrogen therapy, before or concurrent with behavioral therapy, pessary usage, or any other nonsurgical or surgical intervention for stress incontinence. Estrogen therapy may include standardized oral estrogen regimens, combined with a progestin when a uterus is present, as well as transdermal therapy. If oral estrogen is contraindicated, if the patient does not desire oral estrogen, or if oral estrogen does not improve urogenital symptoms, intravaginal treatment exists (Table 14-1). We typically recommend 0.5 g of vaginal estrogen cream for 4 to 6 weeks nightly, with maintenance doses of 0.5 g two to three times per week thereafter. The estrogen rings and tablets have standardized recommended regimens.
OTHER PHARMACOLOGIC THERAPIES Numerous medications have been used to treat SUI (Table 14-2); however, none are FDA approved for this primary indication. Efficacy has been seen in a few well-controlled trials when combined with other treatments (such as behavioral therapy). Recently, a new, centrally acting serotonin and norepinephrine reuptake inhibitor (SNRI) shows great promise for SUI as well as depression. The parasympathetic, sympathetic, and somatic nervous systems coordinated by the central nervous system control the bladder and urethra to maintain normal micturition and continence. Pharmacotherapy for SUI takes advantage of the effect of these medications on increasing urethral outlet resistance. Table 14-1
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α-Adrenergic Agonists The proximal urethra and bladder neck contain α-adrenergic receptors, which, when stimulated, result in increased smooth muscle tone and increased outlet resistance, both during bladder filling and voiding, continuously increasing urethral closure pressure. Several α-adrenergic agents have been studied, including phenylpropanolamine. The AHCPR Clinical Practice Guideline describes the results of eight randomized controlled trials for women with SUI (Fantl et al., 1996). Cure rates were 0% to 14%; reduction of incontinence episodes, 19% to 60%; side effects, 5% to 33%; and dropouts, 0% to 4.3%. However, phenylpropanolamine has been withdrawn from the market due to an increased risk of hemorrhagic stroke when used as an appetite suppressant. Midodrine is selective for a subtype adrenergic receptor, α-1. Midodrine produced subjective improvement but no significant changes in maximum urethral closure pressure at rest (Alhasso et al., 2004). Rarely is total dryness reported in patients with moderate to severe SUI when using this and other similar medications. Potential side effects of all α-adrenergic medications include hypertension, anxiety, hemorrhagic stroke, cardiac arrhythmias, palpitations, tremor, weakness, insomnia, and headache.
β-Adrenergic Receptor Antagonists and Agonists β-Adrenergic blocking agents theoretically should potentiate the activity of norepinephrine on α-receptors and increase urethral outlet resistance. Early studies demonstrated efficacy with propranolol in patients with SUI; however, subsequent randomized controlled trials have not been as successful. At this time, the role of β-adrenergic receptor antagonists for SUI is limited. Significant potential side effects include heart failure, lethargy, and pulmonary compromise. Animal studies have shown that β2-adrenergic agonists, such as clenbuterol, may prevent SUI by increasing the contractility of fast-contracting striated muscle fibers and suppressing slow-contracting fibers. A double-blind, placebo-controlled trial with clenbuterol was performed in 165 women with SUI (Yasuda et al., 1993). Significant effectiveness was observed over placebo with respect to subjective evaluation of incontinence frequency, pads per day,
Vaginal Estrogen Regimens
Product
Dosage
Manufacturer
Estradiol cream Estrace vaginal cream Conjugated estrogens cream Premarin vaginal cream Dienestrol cream Ortho-Dienestrol cream Estradiol vaginal ring Estring, Femring Estradiol vaginal tablets Vagifem
0.1 mg/g
Warner Chilcott, Inc., Rockaway, NJ Wyeth-Ayerst, Philadelphia, PA Ortho-McNeil, Raritan, NJ Pfizer, Inc., Warner Chilcott, Inc., Rockaway, NJ Novo Nordisk, Inc., Princeton, NJ
0.625 mg/g 0.1 mg/g 2 mg/3 mo 25 mcg/tablet
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Table 14-2
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Other Pharmacologic Therapy for Stress Incontinence
Drug Type
Drug Name
Dosage
Serotonin/norepinephrine reuptake inhibitor (pending FDA approval) α-Adrenergic agonist
Duloxetine
40 mg bid
Midodrine Pseudoephedrine hydrochloride Clenbuterol Propranolol Imipramine hydrochloride
2.5 mg tid 15 mg bid, 30 mg bid, tid, qid
β-Agonist/antagonist Tricyclic antidepressant
0.02 mg bid 10 mg bid to 40 mg tid 10 mg qhs (older patients), 25 mg tid, 75 mg bid
bid, Twice a day; tid, three times a day; qid, four times a day; qhs, at bedtime.
and global assessment. Maximum urethral closure pressure increased significantly in the continent patients.
Tricyclic Antidepressants Tricyclic antidepressants—in particular, doxepin and imipramine hydrochloride—improve SUI symptoms by decreasing bladder contractility and increasing urethral resistance. They are thought to exert central and peripheral anticholinergic effects at some sites. They block the active transport system in the presynaptic nerve ending responsible for the reuptake of norepinephrine and serotonin. They act as sedatives, presumably centrally, but potentially related to antihistaminic properties. No placebo-controlled trials exist of the effects of tricyclic antidepressants on SUI. Gilja et al. (1984) reported on 30 women with SUI who received imipramine 75 mg daily for 4 weeks. Subjective continence was reported in 21 participants. Mean maximum urethral closure pressures increased from 34.1 mm Hg to 48.2 mm Hg. Another study by Lin et al. (1999) reported on 40 women with SUI treated with imipramine 25 mg orally three times a day for 3 months. A 35% cure rate by pad testing was reported, and one quarter of the subjects described at least 50% improvement. Success in this study correlated with increased urethral closure pressures. A placebo-controlled trial with doxepin reported significant improvement on subjective and objective outcomes for mainly urge incontinence (Lose et al., 1989). Side effects associated with tricyclic antidepressants include dry mouth, blurred vision, urinary retention, constipation, orthostatic hypotension, sedation, tremors, sexual side effects, fatigue, rash, jaundice, and weakness. Elderly patients, in particular, are prone to side effects, including disorientation, falls, and heart rhythm abnormalities and decreased force of cardiac contraction. Lower doses should be used in older patients, whom we typically start on a 10-mg nightly dose, to determine tolerance and titrate up from there (see Table 14-2).
Duloxetine Serotonergic and noradrenergic reuptake inhibitors suppress parasympathetic activity and enhance sympathetic and somatic activity in the lower urinary tract, promoting urine storage. The dual SNRI, duloxetine, has shown clinical efficacy
for SUI in women in phases 2 and 3 studies. Following the completion of a phase 3 trial, the U.S. FDA issued an approval letter that should soon lead to the first pharmaceutical agent with a primary indication for the treatment of SUI; however, it is still currently not primarily approved for this indication. In a phase 2 study by Norton et al. (2002), 553 patients with SUI were randomized to receive duloxetine, 20 mg/day, 40 mg/day, 80 mg/day, or placebo for 12 weeks. At 80 mg/day, 50% of patients had a reduction in incontinence episode frequency of 64% or greater by pooled diary analysis, and 67% of patients reduced their incontinence episodes by 50% or more. A median decrease occurred in incontinence episode frequency of 41% for the placebo group, compared with 54%, 59%, and 64% with 20 mg/day, 40 mg/day, and 80 mg/ day, respectively. A phase 3 randomized, double-blind, placebo-controlled clinical trial for patients with SUI and stress-predominant, mixed incontinence showed significant decreases in incontinence episode frequency and improvement in Incontinence Quality of Life (I-QOL) and Patient Global Impression of Improvement (PGI-I) scales (Dmochowski et al., 2003). The trial involved 683 women ages 22 to 84, randomized to placebo or duloxetine (80 mg/day) for 12 weeks. Inclusion criteria included seven or more incontinence episodes per week. By intention-to-treat analysis, 51.4% of subjects taking duloxetine had a 50% to 100% decrease in incontinence episodes, compared with 33.5% of those taking placebo. Side effects associated with duloxetine include nausea, fatigue, dry mouth, and insomnia. Nausea was the most common reason for discontinuation in these trials. The phase 2 studies also identified other causes for discontinuation, including somnolence, dizziness, and menorrhagia.
URETHRAL DEVICES A urethral insert acts as a mechanical barrier to prevent urinary leakage by sealing the urethral lumen. The two main categories of devices include simple occlusive plugs or patches and the intraurethral prosthesis with valves (which is for chronic use and will not be addressed here). Urethral inserts are occlusive devices typically used episodically by more active women with SUI, usually during the day. Typically, they are self-inserted and used once.
Chapter 14
Urethral Inserts
Urethral Occlusive Devices Numerous external occlusive devices exist that essentially block urine loss through the external urethral meatus. Issues of ■
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179
cost, comfort, patient acceptability of manipulating the genitalia to apply the device, and concerns of lifelong dependence are at the forefront of deciding whether to use these products. Several reusable external urethral occlusive devices for SUI are available. These devices are noninvasive, silicon-domed caps, or patches that fit over the external urethral meatus, including the FemAssist (Apple/Insight Medical Corp., Bolton, MA), the CapSure Shield (CR Bard, Covington, GA), the MiniGard (Advanced Surgical Intervention, Dana Point, CA), the Continence Guard (Conveen, Marietta, GA), and the Impress Soft Patch (UroMed, Inc., Needham, MA). The FemAssist and CapSure shield are available by prescription and are held in place by a small amount of suction and ointment facilitating a watertight seal. Several studies exist with both objective and subjective outcomes, including standardized pad test, voiding diaries, and symptom-specific quality-of-life evaluation. These studies were typically small and had significant dropouts and short follow-up times (1 hour to 12 weeks). The largest of these studies (155 women) tested the efficacy of the FemAssist in women with SUI (Versi et al., 1998). Primary outcomes included assessing the efficacy of the device using visual analog scales, a quality-of-life questionnaire, 1- and 48-hour standardized pad tests, and a voiding diary. Secondary outcomes consisted of adverse effects and the clinical profile of patients willing to use the device. Patients were shown how to apply and remove the device and were given an opportunity to practice under nursing supervision. Using simple illustrations, patients were instructed on external anatomy, and correct placement was illustrated with the use of a mirror. Significant improvement in symptoms of stress incontinence, urgency, and urge incontinence was noted by visual analog scales. The score for irritation and discomfort increased. Diaries showed that 44% of patients were dry; in the 48-hour pad test, 44% were dry. Quality-of-life scores were significantly improved in 48% of patients by the Incontinence Impact Questionnaire and 32% of patients by the Urogenital Distress Inventory. Adverse events included symptomatic UTI, mucosal prolapse, and blood blisters. Thirty-nine percent of subjects chose to continue using the device.
The Reliance Urinary Control Insert (UroMed, Inc., Needham, MA) and FemSoft Urethral Insert (Rochester Medical Corp., Stewartville, MN) are safe, effective, and tolerable, producing marked improvement in quality of life. Patients using these devices require manual dexterity for placement. Specific training impacts on continued use and satisfaction with these devices. Studies on efficacy report significant dropout rates, which usually occur by the first followup visit. Issues related to early withdrawal from these studies are important to understand because they may impact on patient selection and satisfaction. Problems included inability to insert the device, protocol demands, dissatisfaction with the result, and inability to retain the device in or on the urethra. Comparisons of patients who withdrew from the study and those who continued did not reveal differences in demographics, incontinence severity or duration, or prior treatment (Vierhout and Lose, 1997). The most common side effects include urethral discomfort, hematuria, UTI, and bladder irritation (Table 14-3). Contraindications for the use of urethral inserts include pregnancy, significant urge incontinence and overactive bladder contractions, neuropathic bladder, a history of recurrent bladder infections, use of anticoagulants, and inflammatory or malignant lesions of the lower urinary tract. Factors noted to be important in patient compliance with these devices include a supportive and encouraging teaching program, for the patient to feel comfortable in her ability to correctly insert the device. The training can be accomplished in a single session, which typically includes a review of the female pelvic anatomy, hands-on practice, and supervised self-placement of the device, often with the use of a mirror. Telephone follow-up during the first week helps maintain patient motivation and compliance.
Table 14-3
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Urethral Insert Devices—Acute Use
Insert
Composite
Special Sizing Instrument Availability Reusable Efficacy
Reliance Insert Thermoplastic Inflating (UroMed, Inc., elastomer; meatal syringe Needham, MA) tab, rigid stem, and inflatable balloon at tip
Yes
No
FemSoft (Rochester Medical Corp., Stewartville, MN)
Yes
No
Silicon elastomer; silicon sleeve reservoir, proximal balloon tip distal shroud
Plastic stylet
f/u, Follow-up; IE, incontinence episodes; QOL, quality of life; UTI, urinary tract infection.
Complications
Prospective multicenter study, Symptomatic N = 135, 4-month outcome, bacteriuria, gross 80% dry (pad testing), another hematuria, device15% significant improvement. related mucosal Prospective multicenter trial, irritation N = 63, 1 year f/u 79% dry, another 16% improved Multicenter study, N = 150. Bacteriuria, UTI, Mean time 15 months. urinary symptoms Pad tests, voiding diaries, cystometrics, QOL, satisfaction. Significant reduction IE, 1.32 to 0.56 episodes/day. 93% women negative pad test at 12 months. Significant satisfaction.
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A larger multicenter study by Brubaker et al. (1999) evaluated the safety and efficacy of the Impress for mild-tomoderate stress or mixed incontinence. It included a 5-week baseline run-in, 12 weeks of using the device (as needed) for incontinence protection, and a 4-week follow-up period after discontinuation of device use. Diaries and standardized pad tests were used for outcomes. Eighty-four percent of patients completed the 21-week protocol. Patients subjectively reported significant improvement with the device. Average urine loss on the pad test decreased from 15.8 ± 26.5 mL before use to 6.9 ± 11.5 mL during device use. The mean number of daily incontinence episodes decreased from 14.2 ± 12.3 at baseline to 5.2 ± 7.3 after 8 weeks and 4.9 ± 6.9 after 12 weeks. After discontinuation of device use, the number of incontinence episodes increased to 9.4 ± 10.4. Adverse events included UTI and vulvar irritation.
THE INS AND OUTS OF PESSARY USE As the U.S. population continues to age, and women greater than age 65 will compose a significant proportion of this population, treatment seeking for SUI and POP will continue to increase. Historically, the use of pessaries has been reserved for those patients who decline surgery or are not surgical candidates due to significant medical comorbidities. Some practitioners extend indications for pessary use to pregnancy-related prolapse as well as prolapse and incontinence in elderly women. Two recent studies by Clemons et al. (2004) showed that age greater than 65, severe comorbidity, and maintenance of urinary continence were significant predictors of continued pessary use after 1 year for women with POP. Few literature-based reviews recommend pessaries as first-line therapy for women with SUI or POP, and little consensus exists regarding the choice of pessary and manage-
Figure 14-3
■
ment of pessary usage. Even urogynecologists have not come to consensus regarding indications for pessaries and their management. We rely primarily on descriptive and retrospective studies, relatively small prospective series, manufacturers’ recommendations, and our own clinical experience. Over 100 different kinds of pessaries have been described, with numerous materials used. Currently, according to Mylex Products, Inc. (Chicago, IL) brochures, there are six to nine sizes of 13 pessary models used for SUI and/or POP, the majority made of silicone or plastic (Fig. 14-3). Silicone is nonallergenic, does not absorb odors or secretions, is resistant to repeat cleansing and autoclaving, and is soft and pliable. If a pessary type contains latex, ensure that the patient does not have a latex allergy before using it. The pessary restores continence by stabilization of the proximal urethra and urethrovesical junction, facilitating pressure transmission to, or partially compressing, the urethra. Pessaries improve urinary incontinence in some women by increasing urethral functional length, urethral closure pressures, and cough profiles. Pessaries used for POP can also create or worsen SUI by supporting the prolapsed vagina and relieving bladder neck obstruction. This “occult” SUI occurred in 21% of the women who were successfully fitted with a pessary in the study by Clemons et al. (2004). Pessaries provide pelvic organ support by creating a functional obstruction within the vagina. Two categories of pessaries exist for prolapse: support and space-filling. The ring pessary (with diaphragm) is a commonly used support pessary, and the Gellhorn pessary is a commonly used space-filling pessary. Ring and other support pessaries are recommended for stages 1 and 2 prolapse, whereas space-filling pessaries are recommended for stages 3 and 4 prolapse. However, the Cochrane Review by Adams et al. (2004) shows no randomized controlled trials of pessary use in women with POP. Manufacturers’ recommendations for pessary selection can be found in Fig. 14-3 and Table 14-4 (LeKan-Rutledge et al., 2003).
Pessary types and indications. SUI, Stress urinary incontinence; UVJ, urethrovesical junction. (Courtesy of CooperSurgical, Inc.)
■
X X X X X X
Stage 3–4
Prolapse
X
X X X
X X
Sexually Active
X
Vaginal Wall
Guidelines for Pessary Selection
X
X
X
Stress Urinary Incontinence
Mid X
X X
Cystocele
Mid X Mid X Mid X
Rectocele
X
Incompetent Cervix
X
Retro Displacement
Ring Ring with support Shaatz Incontinence dish/ring Dish with support Hodge with support Donut Gellhorn (flex 95% rigid) Inflatoball Cube, tandem cube Gehrung Gehrung with knob Incontinence ring Hodge with knob Smith, Hodge, Risser
Most Commonly Used
■
Adapted from Milex Products, Inc., Chicago, IL.
X X X X X X
Stage 1–2
Table 14-4
Chapter 14 Nonsurgical Management
181
73 119 203
Clemons et al. (2004) Donnelly et al. (2004)
Fernando et al. (2006)
Prolapse
Prolapse Stress incontinence
Stress and mixed incontinence, prolapse
Stress incontinence
Stress or mixed incontinence
Stress and mixed incontinence
Prolapse Exercise incontinence Pessary vs. tampon vs. no device Stress incontinence Prolapse
Stress incontinence Stress incontinence
Indication
IIQ, Incontinence impact questionnaire; UDI, urogenital distress inventory.
100
38
Robert & Mainprize (2002)
Farrell et al. (2004)
70
11 110
Abu-Sitta et al. (1995) Wu et al. (1997)
Davila et al. (1999) (Introl device, UroMed, Needham, MA)
101 18
77
30 12
Bhatia & Bergman (1985) Suarez et al. (1991) (use of contraceptive diaphragm) Sulak et al. (1993) Nygaard (1995) (randomized trial)
Kondo et al. (1997) (bladder neck support prosthesis)
N
Investigators
Pessary Use for Incontinence and Prolapse
4 months
2 months 6 months
11 months
1 year
1 month
4 days 66% of those used at 1 month, continued for greater than 12 months 12 weeks
Mean 16 months None
None None
Time of Follow-up
Subjective pad test, 29% continent, 51% decreased severity by more than 50%, 81% combined subjective/objective some or maximum benefit 53/70 completed trial; significant improvement pad tests, diaries, high subjective improvement and quality of life 6/38 continued pessary use; pad test, voiding diary, IIQ, UDI 79% resolution symptoms 2 weeks; 55% of patients with stress, 63% of patients with mixed successfully fitted with pessary; 59% patients continued use 92% patient satisfaction 89% successful pessary fitting; 55 continued pessary usage for 6 months 75% retained pessary at 2 weeks; failure to retain pessary associated with higher parity and prior hysterectomy
50% continued use 36% pessary users continent; 58% tampon users continent Pad test, urine loss significantly decreased
Cough pressure profile 24/30 patients continent Subjective cure 9/12
Outcome
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Table 14-5
182 Management of Stress Urinary Incontinence and Pelvic Organ Prolapse
Chapter 14
Pessaries effectively manage SUI in women during exercise, as well as in a clinical setting. However, outcomes are short-term and study samples are small (Table 14-5). Satisfactory outcomes have been reported for stage 2 or greater prolapse using the Gellhorn and ring diaphragm pessary. After 2 to 6 months, 77% to 92% of women with successful pessary fitting were satisfied and, using intentionto-treat analysis, 44% to 67% of women who were treated initially with a pessary for prolapse were satisfied (Clemons et al., 2004).
Pessary Placement and Management Pessary placement involves consideration of several issues, primarily the patient’s motivation to use it. Typically, if she has had previous surgery or strongly desires to avoid surgery, she may be motivated enough for a primary attempt at pessary placement. Other issues include her medical and cognitive status, manual dexterity, current sexual function, type and duration of exercise, and status of the vaginal walls and cervix. We strongly recommend treatment of the vagina with estrogen, if the patient is hypoestrogenic, and maintenance of estrogen treatment using any of the many regimens discussed previously.
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longer (up to 6 to 8 weeks). Donut pessaries, which are very popular, are considered a space-fitting pessary for large vaginal vault prolapse or complete procidentia. Donut pessaries should be removed and cleaned every 2 to 3 days if possible.
Follow-Up Recommendations After the initial fitting, the patient should return in 1 to 3 days and then at 4 to 6 weeks, depending on her independence with the pessary, her proficiency in placement and removal, and her cognitive and motor abilities. After this initial follow-up, continued follow-up is at 6- to 12-month intervals at the discretion of the provider and depending on the patient’s ability to effectively insert and remove the pessary. If the patient has to return for removal and cleaning by a provider, 4- to 12-week intervals are more appropriate. On each return for follow-up, ensure proper placement of the pessary, with good support of the prolapse. If the patient is using the pessary for incontinence symptoms, check that her symptoms are resolved or stable. Since pessaries are fit by a process of trial and error, it is common to change the pessary size or type at least once after the initial fitting. Check the pessary’s integrity and the patient’s vaginal tissue for irritation, pressure sores, ulceration, and estrogen status.
Steps to Fitting a Pessary The patient should be examined in lithotomy position after emptying her bladder. We estimate the size of the pessary after digital examination and use of ring forceps to reduce the prolapse or bladder neck. After the approximate size is determined, the appropriate type is selected (see Fig. 14.3 and Table 14-4) based on the patient’s needs and activity level. The clinician should use a dry glove to better grasp the pessary and water-soluble lubricants as needed. On insertion, guide the pessary posteriorly to avoid the urethra. Proper size is ensured by being able to sweep the index finger between the pessary and the vaginal wall; the pessary should feel comfortable to the patient. When fitted, the patient is asked to stand, perform a Valsalva, and cough to ensure that the pessary is retained. The pessary should be assessed to ensure it is providing the desired urethral support and leakage control. Furthermore, the patient should be able to void with the pessary in place before being sent home. Insertion tips include use of a water-soluble lubricant for insertion; folding or collapsing the pessary to reduce its size; and, when the pessary is inside the vagina, pushing it high to an area behind the symphysis pubis. When instructing the patient to insert and remove the pessary, determine whether it is best done in a standing or supine position, depending upon the patient’s dexterity. Ring pessaries, with or without support, are the most commonly used. They are the easiest to fold, insert, and remove. Continence pessaries, rings, and dishes with support are also easy to fold, insert, and remove. Gellhorn and cube pessaries are typically more difficult to insert and remove. They are held in place by significant space occupation and suction and offer strong support. The suction of the cube pessary needs to be broken before removal. Cube pessaries should be removed daily; Gellhorns can stay in
Complications Vaginal discharge and odor may signal a possible complication of pessary use, such as infection or erosion. An increase in bacterial vaginosis has been seen with pessary usage. If the pessary does not stay in place, it is unlikely to cause erosion; conversely, the pessary may be too tight, which could lead to irritation or erosions. De novo or increased stress incontinence may occur with reduction of vaginal prolapse. Vaginal abrasions, erosions or ulcerations, rare vesicovaginal or rectovaginal fistulas, small bowel entrapment, bilateral hydronephrosis, and urosepsis have all been described. Another potential complication is the forgotten or incarcerated pessary. Therefore, whenever possible, the family or other health care professionals should help the debilitated or memory-impaired patient ensure adequate pessary care. Patient education is vital for successful pessary usage, and a review of female anatomy may be helpful before pessary placement. We also discuss, in an individualized fashion, the schedule of removal and cleaning of the pessary. Counseling the patient to call for concerns or problems related to pessary usage is important.
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BEHAVIORAL INTERVENTION: BLADDER TRAINING 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. Elder DD, Stephenson TP. An assessment of the Frewen regime in the treatment of detrusor dysfunction in females. Br J Urol 1980;52:467.
Fantl JA, Wyman JF, McClish DK, et al. Efficacy of bladder training in older women with urinary incontinence. JAMA 1991;265:609. Frewen WK. Role of bladder training in the treatment of the unstable bladder in the female. Urol Clin North Am 1979;6:273. Frewen WK. A reassessment of bladder training in detrusor dysfunction in the female. Br J Urol 1982;54:372. Jarvis GJ, Millar DR. Controlled trial of bladder drill for detrusor instability. Br Med J 1980;281:1322. Jarvis GJ. A controlled trial of bladder drill and drug therapy in the management of detrusor instability. J Urol 1981;53:565. Jarvis GJ. The management of urinary incontinence due to primary vesical sensory urgency by bladder drill. Br J Urol 1982;54:374. Jeffcoate TN, Francis WJ. Urgency incontinence in the female. Am J Obstet Gynecol 1966;94:604. Pengelly AW, Booth CM. A prospective trial of bladder training as treatment for detrusor instability. Br J Urol 1980;52:463. Svigos JM, Matthews CD. Assessment and treatment of female urinary incontinence by cystometrogram and bladder retraining programs. Obstet Gynecol 1977;50:9.
ELECTRICAL STIMULATION Blowman C, Pickles C, Emery S, et al. Prospective double blind controlled trial of intensive physiotherapy with and without stimulation of the pelvic floor in treatment of genuine stress incontinence. Physiotherapy 1991;77:661. Bo 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. Br Med J 1999;318:487. Caputo RM, Benson JT, McClellan E. Intravaginal maximal electrical stimulation in the treatment of urinary incontinence. J Reprod Med 1993;38:667. Erikson BC, Mjolnerod OK. Changes in urodynamic measurements after successful anal electrostimulation in female urinary incontinence. Br J Urol 1987;59:45. Fischer W. Physiotherapeutic aspects of urine incontinence. Acta Obstet Gynecol Scand 1983;62:579. Hahn I, Sommar S, Fall M. A comparative study of pelvic floor training and electrical stimulation for treatment of genuine female stress urinary incontinence. Neurourol Urodyn 1991;10:545. Huffman JW, Osborne SL, Sokol JK. Electrical stimulation in treatment of intractable stress incontinence. Arch Phys Med 1952;33:674. Montgomery E, Sheperd AM. Electrical stimulation and graded pelvic exercises for genuine stress incontinence. Physiotherapy 1983;69:112. Moore T, Schofield PF. Treatment of stress incontinence by maximum perineal electrical stimulation. Br Med J 1967;3:150. Olah KS, Bridges N, Denning J, Farrar DJ. The conservative management of patients with symptoms of stress incontinence: a randomized, prospective study comparing weighted vaginal cones and interferential therapy. Am J Obstet Gynecol 1990;162:87. Sand PK, Richardson DR, Staskin SE, et al. Pelvic floor stimulation in the treatment of genuine stress incontinence: a multicenter placebo-controlled trial. Am J Obstet Gynecol 1995;173:72. Sung MS, Hong JY, Choi YH, et al. FES-Biofeedback versus intensive pelvic floor muscle exercise for the prevention and treatment of genuine stress incontinence. J Korean Med Sci 2000;15:303. Yamanishi T, Yasuda K, Sakakibara R, et al. Pelvic floor electrical stimulation in the treatment of stress incontinence: an investigational study and a placebo controlled double-blind trial. J Urol 1997;158:2127.
WEIGHT LOSS AND INCONTINENCE Allison DB, Fontaine KR, Manson JE, et al. Annual deaths attributable to obesity in the United States. JAMA 1999;282:1530. 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. Brown J, 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. 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.
Chapter 14
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. Mokdad AH, Bowman BA, Ford ES, et al. The continuing epidemics of obesity and diabetes in the United States. JAMA 2001;286:1195. Subak LL, Johnson CE, Boban D, et al. Does weight loss improve incontinence in moderately obese women? Int J Urogynecol 2002;13:40. Subak LL, Whitcomb E, Shen H, et al. Weight loss: a novel and effective treatment for urinary incontinence. J Urol 2005;174:190.
ESTROGEN AND STRESS INCONTINENCE Ahlstrom K, Sandahl B, Sjoberg B, et al. Effect of combined treatment with phenylpropanolamine and estriol, compared with estriol treatment alone in postmenopausal women with stress urinary incontinence. Gynecol Obstet Invest 1990;30:37. Al-Badr A, Ross S, Soroka D, Drutz HP. What is the available evidence for hormone replacement therapy in women with stress urinary incontinence. J Obstet Gynaecol Can 2003;25:567. Beisland HO, Fossberg E, Moer A, Sander S. Urethral sphincteric insufficiency in postmenopausal females: treatment with phenylpropanolamine and estriol separately and in combination. A urodynamic and clinical evaluation. Urol Int 1984;39:211. Cardozo L, Bachmann G, McClish D, et al. Meta-analysis of estrogen therapy in the management of urogenital atrophy in postmenopausal women: second report of the Hormones and Urogenital Therapy Committee. Obstet Gynecol 1998;92(Suppl):722. Fantl JA, Bump RC, Robinson D, et al. and the Continence Program for Women Research Group: efficacy of estrogen supplementation in the treatment of urinary incontinence. Obstet Gynecol 1996;88:745. Fantl JA, Wyman JF, Anderson RL, et al. Postmenopausal urinary incontinence: comparison between non-estrogen-supplemented and estrogensupplemented women. Obstet Gynecol 1988;71:823. Grady D, Brown JS, Vittinghoff E, et al. Postmenopausal hormones and incontinence: the Heart and Estrogen/Progestin Replacement Study. Obstet Gynecol 2001;97:116. Grodstein F, Lifford K, Resnick NM, et al. Postmenopausal hormone therapy and risk of developing urinary incontinence. Obstet Gynecol 2004;103:254. Hilton P, Stanton SL. The use of intravaginal estrogen cream in genuine stress incontinence. Br J Obstet Gynaecol 1983;90:940. Hodgson BJ, Dumas S, Bolling DR, Heesch CM. Effect of estrogen on sensitivity of rabbit bladder and urethra to phenylephrine. Invest Urol 1978;16:67. Iosif CS, Batra S, Ek A, et al. Estrogen receptors in the human female lower urinary tract. Am J Obstet Gynecol 1981;141:817. Ishiko O, Hirai K, Sumi T, et al. Hormone replacement therapy plus pelvic floor muscle exercise for postmenopausal stress incontinence. A randomized, controlled trial. J Reprod Med 2001;46:213. Jackson S, Shepherd A, Brookes S. The effect of oestrogen supplementation on post-menopausal urinary stress incontinence: a double-blind placebo-controlled trial. Br J Obstet Gynaecol 1999;106:711. Karram MM, Yeko TR, Sauer MV, Bhatia NN. Urodynamic changes following hormonal replacement therapy in women with premature ovarian failure. Obstet Gynecol 1989;74:208. Keil K. Urogenital atrophy: diagnosis, sequelae, and management. Curr Womens Health Rep 2002;2:305. Kinn AL, Lindskog M. Estrogens and phenylpropanolamine in combination for stress urinary incontinence in postmenopausal women. Urology 1988;32:273. Lin HH, Sheu BC, Lo MC, et al. Comparison of treatment outcomes for Imipramine for female genuine stress incontinence. Br J Obstet Gynaecol 1999;106:1089. Larsson B, Andersson KE, Batra S, et al. Effects of estradiol on norepinephrine-induced contraction, alpha adrenoreceptor number and norepinephrine content in the female rabbit urethra. J Pharmacol Exp Ther 1984;229:557. Lovatsis D, Drutz HP. The role of estrogen in female urinary incontinence and urogenital aging: a review. Ostomy Wound Manage 1998;44:48. Palomba S, Napolitano V, Sammarcino A, et al. Effect of estriol treatment per vaginam before Burch colposuspension. J Minerva Ginecol 2001;53:141. Italian. Makinen J, Pitkanen YA, Salmi TA, et al. Transdermal estrogen for female stress urinary incontinence in postmenopause. Maturitas 1995;22:233.
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Rud T. The effects of estrogens and gestagens on the urethral pressure profile in urinary continent and stress incontinent women. Acta Obstet Gynecol Scand 1980;59:265. Sartori MG, Baracat EC, Girao MJ, et al. Menopausal genuine stress urinary incontinence treated with conjugated estrogens plus progestogens. Int J Gynaecol Obstet 1995;49:165. Suzuki Y, Oishi Y, Yamazuki H, et al. A study of the clinical effect of hormone replacement therapy for patients with stress incontinence. Nippon Hinyokika Gskkai Zasshi 1997;88:427. Schreiter E, Fuchs P, Stockamp K. Estrogenic sensitivity of receptors in the urethral musculature. Urol Int 1976;31:13. Versi E, Cardozo L, Brincat M, Studd J. Lower urinary tract symptoms, urodynamic findings and skin collagen in normal postmenopausal women. Maturitas 1984;6:204. Walter S, Kjaergaard B, Lose G, et al. Stress urinary incontinence in postmenopausal women treated with oral estrogen (estriol) and an alpha-adrenoreceptor-stimulating agent (phenylpropanolamine): a randomized double-blind placebo-controlled study. Int Urogynecol J 1990;1:74. Wilson PD, Faragher B, Butler B, et al. Treatment with oral piperazine oestrone sulphate for genuine stress incontinence in postmenopausal women. Br J Obstet Gynaecol 1987;9:528.
OTHER PHARMACOLOGIC THERAPIES Alhasso A, Glazener CM, Pickard R, et al. Adrenergic drugs for urinary incontinence in adults [Cochrane Review]. In Cochrane Library. John Wiley & Sons, Ltd., Chichester, England, 2004;2. Bartlett DM, Wein AJ. Voiding dysfunction: diagnosis, classification and management. In Gillenwater JY, Grayhack JT, Howards ST, Duckett JW, eds. Adult and Pediatric Urology, 2nd ed. Mosby, 1991, St. Louis, pp. 1001–1099. Cannon TW, Yoshimura N, Chancellor MB. Innovations in pharmacotherapy for stress urinary incontinence. Int Urogynecol J 2003;14:367. Dmochowski RR, Miklos JR, Norton PA, et al. Duloxetine versus placebo for the treatment of North American women with stress urinary incontinence. J Urol 2003;170:1259. Fellenius E, Hedberg R, Holmberg E, et al. Functional and metabolic effects of terbutaline and propanolol in fast and slow contraction skeletal muscle in vitro. Acta Physiol Scand 1980;109:89. Gilja I, Radej M, Kovacic M, et al. Conservative treatment of female stress incontinence with imipramine. J Urol 1984;132:909. Haeusler G, Leitich H, van Trotsenburg M, et al. Drug therapy of urinary urge incontinence: a systematic review. Obstet Gynecol 2002;100:1003. Kernan WN, Viscoli CM, Brass L, et al. Phenylpropanolamine and the risk of hemorrhagic stroke. N Engl J Med 2000;343:1826. 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. 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. Radley SC, Chapple CR, Bryan NP, et al. Effect of methoxamine on maximum urethral pressure in women with genuine stress incontinence: a placebo-controlled, double blind crossover study. Neurourol Urodyn 2001;20:43. Viktrup L, Bump RC. Pharmacological agents used for the treatment of stress urinary incontinence in women. Curr Med Res Opin 2003;19:485. Yasuda K, Kawabe K, Takimoto Y, et al. A double-blind clinical trial of a β-adrenergic agonist in stress incontinence. Int Urogynecol J 1993;4:146.
INTRAURETHRAL AND URETHRAL OCCLUSIVE DEVICES Bachmann G, Wiita B. External occlusive devices for management of female urinary incontinence. J Womens Health 2002;11:793. Bellin P, Smith J, Poll W, et al. Results of a multicenter trial of the CapSure continence shield on women with stress urinary incontinence. Urology 1998;51:897. Brubaker L, Harris T, Gleason D, et al. The external urethral barrier for stress incontinence: a multicenter trial of safety and efficacy. Obstet Gynecol 1999;93:932. Choe JM, Staskin DR. Clinical usefulness of urinary control urethral insert devices. Int Urogynecol J 1997;8:307.
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Eckford SD, Jackson SR, Lewis PA, et al. The continence control pad—a new external urethral occlusion device in the management of stress incontinence. Br J Urol 1996;77:538. Gallo M, Hancock R, Davila GW. Clinical experience with a balloon-tipped urethral insert for stress urinary incontinence. J Wound Ostomy Contin Nurs 1997;24:51. Miller J, Bavendam T. Treatment with reliance urinary control insert: oneyear experience. J Endourol 1996;10:287. Moore KH, Simons A, Powell C, et al. Efficacy and user acceptability of the urethral occlusive device for women with urinary incontinence. J Urol 1999;162:464. Nielson KK, Kromann-Andersen B, Jacobsen H, et al. The urethral plug: a new treatment modality for genuine urinary stress incontinence in women. J Urol 1990;144:1199. Rabin J. Clinical use of the FemAssist device in female urinary incontinence. J Med Syst 1998;22:257. Rovner ES. Treatment of urinary incontinence. Curr Urol Rep 2000;1:235. Sander P, Thyssen H, Lose G, et al. Effect of a vaginal device on quality of life with urinary stress incontinence. Obstet Gynecol 1999;93:407. 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. Staskin D, Bavendam T, Miller J, et al. Effectiveness of a urinary control insert in the management of stress urinary incontinence: results of a multi-center study. Urology 1996;47:624. Tincello DG, Bolderson J, Richmond DH. Preliminary experience with a urinary control device in the management of women with genuine stress incontinence. Br J Urol 1997;80:752. Versi E, Griffiths DJ, Harvey M-A. A new external urethral occlusive device for female urinary incontinence. Obstet Gynecol 1998;92:286. Vierhout ME, Lose G. Preventive vaginal and intra-urethral devices in the treatment of female urinary stress incontinence. Curr Opin Obstet Gynecol 1997;9:325.
INS AND OUTS OF PESSARY USE Abu-Sitta MI, Kapur G, Enhorning G. Stress incontinence alleviated by an intravaginal device. Int Urogynecol J 1995;6:95. Abrams P, Cardozo L, Khoury S, Wein A (Eds). Incontinence, 2nd International Consultation on Incontinence. Paris July 1–3, 2001, 2nd ed. Plymbridge Distribution, Ltd., London, 2002. Adams E, Thomson A, Maher C, Hagen S. Mechanical devices for pelvic organ prolapse in women [Cochrane Review]. In The Cochrane Library. John Wiley & Sons, Ltd., Chichester, UK, 2004;2. Alnaif B, Drutz HP. Bacterial vaginosis increases in pessary users. Int Urogynecol J 2000;11:219. Bash K. Review of vaginal pessaries. Obstet Gynecol Surv 2000;55:465.
Bhatia NN, Bergman A, Gunning JE. Urodynamic effects of a vaginal pessary in women with stress urinary incontinence. Am J Obstet Gynecol 1983;147:876. Bhatia NN, Bergman A. Pessary test in women with urinary incontinence. Obstet Gynecol 1985;65:220. Clemons JL, Aguilar VC, Tillinghast TA, et al. Risk factors associated with an unsuccessful pessary fitting trial in women with pelvic organ prolapse. Am J Obstet Gynecol 2004;190:345. Clemons J, Aguilar VC, Tillinghast TA, et al. 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. 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. Davila GW, Neal P, Horbach N, et al. A bladder-neck support prosthesis for women with stress and mixed incontinence. Obstet Gynecol 1999;93:938. Donnelly MJ, Powell-Morgan S, Olsen AL, Nygaard IE. Vaginal pessaries for the management of stress and mixed urinary incontinence. Int Urogynecol J 2004;15:302. Farrell SA, Singh B, Aldakhil L. Continence pessaries in the management of urinary incontinence in women. J Obstet Gynecol Can 2004;26:113. Fernando RJ, Thakar R, Sultan AH, et al. Effect of vaginal pessaries on symptoms associated with pelvic organ prolapse. Obstet Gynecol 2006;108:93. 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. LeKan-Rutledge D, Doughty D, Moore KN, Wooldridge L. Promoting social continence: products and devices in the management of urinary incontinence. Urol Nurs 2003;23:416. Nygaard I. Prevention of exercise incontinence with mechanical devices. J Reprod Med 1995;40:89. Palumbo MV. Pessary placement and management. Ostomy Wound Manage 2000;46:40. Poma PA. Nonsurgical management of genital prolapse. A review and recommendations for clinical practice. JRM 2000;45:789. Realini JP, Walters MD. Vaginal diaphragm rings in the treatment of stress urinary incontinence. J Am Board Fam Pract 1990;3:99. Robert M, Mainprize TC. Long-term assessment of the incontinence ring pessary for the treatment of stress incontinence. Int Urogynecol J 2002;13:326. Suarez GM, Baum NH, Jacobs J. Use of standard contraceptive diaphragm in management of stress urinary incontinence. Urology 1991;37:119. Sulak PJ, Kuehl TJ, Shull BJ. Vaginal pessaries and their use in pelvic relaxation. J Reprod Med 1993;90:919. Wu V, Farrell SA, Baskett TF, et al. A simplified protocol for pessary management. Obstet Gynecol 1997;90:990.
Retropubic Operations for Stress Urinary Incontinence
15
Mark D. Walters
INDICATIONS FOR RETROPUBIC PROCEDURES 187 SURGICAL TECHNIQUES 188 Operative Setup and General Entry Into the Retropubic Space 188 Burch Colposuspension 188 Paravaginal Defect Repair 189 General Intraoperative and Postoperative Procedures 190 CLINICAL RESULTS 190 MECHANISMS OF CURE 191 COMPLICATIONS 192 Short-Term Postoperative 192 Postoperative Voiding Difficulties 192 Overactive Bladder 193 Osteitis Pubis 193 Enterocele and Rectocele 193 ROLE OF HYSTERECTOMY IN THE TREATMENT OF INCONTINENCE 194 PREGNANCY AFTER RETROPUBIC SURGERY 194
Since 1949, when Marshall et al. first described retropubic urethrovesical suspension for the treatment of stress urinary incontinence (SUI), retropubic procedures have emerged as consistently curative. Although numerous terminologies and variations of retropubic repairs have been described, the basic goal remains the same: to suspend and to stabilize the anterior vaginal wall, and thus the bladder neck and proximal urethra, in a retropubic position. This prevents their descent and allows urethral compression against a stable suburethral layer. Selection of a retropubic approach (versus a vaginal approach) depends on many factors, such as the need for laparotomy for other pelvic disease, the amount of pelvic organ relaxation, the status of the intrinsic urethral sphincter mechanism, the age and health status of the patient, and the preference and expertise of the surgeon. Few data differentiate one retropubic procedure from another, although all have advantages and disadvantages. Historically, the three most studied and popular retropubic procedures are the Burch colposuspension, the MarshallMarchetti-Krantz (MMK) procedure, and the paravaginal defect repair. We no longer perform the MMK procedure, so this operation will not be described. We prefer the Burch colposuspension for urodynamic stress incontinence with
bladder neck hypermobility and adequate resting urethral sphincter function and combine it with a paravaginal defect repair, when the patient has stage 2 or 3 anterior vaginal prolapse or when a concurrent sacrocolpopexy is required. The surgical techniques described herein are contemporary modifications of the original operations: Tanagho (1976) described the modified Burch colposuspension; the paravaginal defect repair was described by Richardson et al. (1981) and Shull and Baden (1989) (paravaginal repair) and by Turner-Warwick (1986) and Webster and Kreder (1990) (vaginal obturator shelf repair). Although less critically studied, the paravaginal defect repair is regionally popular and widely performed in the United States. The operations described do not represent one correct technique but a commonly used and proven method. This chapter describes only retropubic suspension procedures that use an abdominal wall incision for direct access into the space of Retzius. The use of laparoscopy and miniincision laparotomy to enter the retropubic space and perform these and similar procedures is expanding, both in terms of clinical experience and research. The reader is encouraged to see Chapter 17 for a thorough critique of the use of operative laparoscopy for treatment of urinary incontinence and and pelvic organ prolapse.
INDICATIONS FOR RETROPUBIC PROCEDURES Retropubic urethrovesical suspension procedures are indicated for women with the diagnosis of urodynamic SUI and a hypermobile proximal urethra and bladder neck. These procedures yield the best results when the urethral sphincter is capable of maintaining a watertight seal at rest but cannot withstand the unequal transmission of abdominal pressure to the proximal urethra, relative to the bladder, with straining. Although retropubic procedures can be used for intrinsic sphincter deficiency with urethral hypermobility, other more obstructive operations, such as a sling, probably yield better long-term results (see Chapter 16). To diagnose urodynamic SUI, clinical and urodynamic (simple or complex) tests must be performed to evaluate bladder filling, storage, and emptying. Clinically, the urethra is shown to be incompetent by visually observing simultaneously the loss of urine and increases in intra-abdominal
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pressure. Urodynamic or radiologic methods may also be used for diagnosis. Abnormalities of bladder-filling function, such as overactive bladder, can coexist with urethral sphincter incompetence in up to 30% of patients and may be associated with a lower cure rate after retropubic surgery. Women with SUI should generally have a trial of conservative therapy before corrective surgery is offered. Conservative treatment comes in the form of pelvic muscle exercises, bladder retraining, pharmacologic therapy, functional electrical stimulation, and mechanical devices, such as pessaries. Eligible and willing postmenopausal patients with atrophic urogenital changes should be prescribed vaginal estrogen before surgery is considered.
SURGICAL TECHNIQUES Operative Setup and General Entry into the Retropubic Space In preparation of this technique, the patient is supine, with the legs supported in a slightly abducted position, allowing the surgeon to operate with one hand in the vagina and the other in the retropubic space. The vagina, perineum, and abdomen are sterilely prepped and draped in a fashion that permits easy access to the lower abdomen and vagina. A three-way 16- or 20-French Foley catheter with a 20- to 30-mL balloon is inserted sterilely into the bladder and kept in the sterile field. The drainage port of the catheter is left to gravity drainage, and the irrigation port is connected to sterile water, with or without blue dye. One perioperative intravenous dose of an appropriate antibiotic should be given as prophylaxis against infection. A Pfannenstiel or Cherney incision is made. During intraperitoneal surgery, the peritoneum is opened, the surgery is completed, and the cul-de-sac is plicated, if necessary. The retropubic space is then exposed. Staying close to the back of the pubic bone, the surgeon’s hand is introduced into the retropubic space and the bladder and urethra gently moved downward. Sharp dissection is not usually necessary in primary cases. To aid visualization of the bladder, 100 mL sterile water with methylene blue or indigo carmine dye may be instilled into the bladder after the catheter drainage port is clamped. If previous retropubic or other bladder neck suspension procedures have been performed, dense adhesions from the anterior bladder wall and urethra to the symphysis pubis are often present. These adhesions should be dissected sharply from the pubic bone until the anterior bladder wall, urethra, and vagina are free of adhesions and are mobile. If identification of the urethra or lower border of the bladder is difficult, one may perform a cystotomy, which, with a finger inside the bladder, helps define the bladder’s lower limits for easier dissection, mobilization, and elevation.
junction, thus protecting the delicate musculature of the urethra from surgical trauma. Attention is directed to the tissue on either side of the urethra. The surgeon’s nondominant hand is placed in the vagina, palm facing upward, with the index and middle fingers on each side of the proximal urethra. Most of the overlying fat should be cleared away, using a swab mounted on a curved forceps. This dissection is accomplished with forceful elevation of the surgeon’s vaginal finger until glistening white periurethral fascia and vaginal wall are seen (Fig. 15-1). This area is extremely vascular, with a rich, thin-walled venous plexus that should be avoided, if possible. The position of the urethra and the lower edge of the bladder is determined by palpating the Foley balloon and by partially distending the bladder to define the rounded lower margin of the bladder as it meets the anterior vaginal wall. Once dissection lateral to the urethra is completed and vaginal mobility is judged to be adequate by using the vaginal fingers to lift the anterior vaginal wall upward and forward, sutures are placed. No. 0 or 1 delayed absorbable or nonabsorbable sutures are placed laterally as far in the anterior vaginal wall as is technically possible. We apply bilaterally two sutures of No. 0 braided polyester on an SH needle (Ethibond; Ethicon, Inc., Somerville, NJ), using double bites for each suture. The distal suture is placed approximately 2 cm lateral to the proximal third of the urethra. The proximal suture is placed approximately 2 cm lateral to the bladder wall at or slightly proximal to the level of the urethrovesical junction. In placing the sutures, one should take a full thickness of vaginal wall, excluding the epithelium, with the needle parallel to the urethra (Fig. 15-2, inset). This maneuver is best accomplished by suturing over the surgeon’s vaginal finger at the appropriate selected sites. On each side, after the two sutures are placed, they are passed through the pectineal (Cooper’s) ligament so that all four suture ends exit above
Burch Colposuspension After the retropubic space is entered, the urethra and anterior vaginal wall are depressed. No dissection should be performed in the midline over the urethra or at the urethrovesical
Figure 15-1 ■ Dissection of the lateral retropubic space. After forceful elevation of the surgeon’s vaginal finger, the fat overlying the glistening white periurethral fascia is cleared in preparation for suture placement.
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the ligament (Fig. 15-2). Before the sutures are tied, a 1 × 4 cm strip of Gelfoam may be placed between the vagina and obturator fascia below Cooper’s ligament to aid adherence and hemostasis. As noted previously, this area is extremely vascular, and visible vessels should be avoided if possible. When excessive bleeding occurs, it can be controlled by direct pressure, sutures, or vascular clips. Less severe bleeding usually stops with direct pressure and after tying the fixation sutures. After all four sutures are placed in the vagina and through the Cooper’s ligaments, the assistant first ties the distal sutures and then the proximal ones, while the surgeon elevates the vagina with the vaginal hand. In tying the sutures, one does not have to be concerned about whether the vaginal wall meets Cooper’s ligament, so one should not place too much tension on the vaginal wall. A suture bridge is usually found between the two points. After the sutures are tied, one can easily insert two fingers between the pubic bone and the urethra, thus preventing compression of the urethra against the pubic bone. Vaginal fixation and urethral support depend more on fibrosis and scarring of periurethral and vaginal tissues over the obturator internus and levator fascia than on the suture material itself.
Paravaginal Defect Repair The object of the paravaginal defect repair is to reattach, bilaterally, the anterolateral vaginal sulcus with its overlying endopelvic fascia to the pubococcygeus and obturator internus muscles and fascia at the level of the arcus tendineus fasciae pelvis. The retropubic space is entered, and the bladder and vagina are depressed and pulled medially to allow visualization of the lateral retropubic space, including the obturator internus and levator muscles and the fossa containing the obturator neurovascular bundle. Blunt dissection can be carried dorsally from this point until the ischial spine
Figure 15-2 ■ Technique of Burch colposuspension. After the two sutures are placed on each side, they are passed through the pectineal (Cooper’s) ligament, so that all four suture ends exit above the ligament to facilitate knot tying. In placing the sutures (inset), one should take a full thickness of vaginal wall, excluding the epithelium, with the needle parallel to the urethra. This maneuver is best achieved by suturing over the vaginal finger.
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is palpated. The arcus tendineus fasciae pelvis is often visualized as a white band of tissue running over the pubococcygeus and obturator internus muscles from the back of the lower edge of the symphysis pubis toward the ischial spine. A lateral paravaginal defect representing avulsion of the vagina off the arcus tendineus fasciae pelvis or of the arcus tendineus fasciae pelvis off the obturator internus muscle may be visualized (Fig. 15-3). The surgeon’s nondominant hand is inserted into the vagina. While gently retracting medially the vagina and bladder, the surgeon elevates the anterolateral vaginal sulcus. Starting near the vaginal apex, a suture is placed, first through the full thickness of the vagina (excluding the vaginal epithelium) and then deep into the obturator internus fascia or arcus tendineus fasciae pelvis, 1 to 2 cm anterior to its origin at the ischial spine. After this first stitch is tied, additional (four or five) sutures are placed through the vaginal wall and overlying fascia and then into the obturator internus at about 1-cm intervals toward the pubic ramus (Fig. 15-3, inset). The most distal sutures should be placed as close as possible to the pubic ramus, into the pubourethral ligament; alternatively, Burch colposuspension sutures can be placed bilaterally at the level of the bladder neck and urethra if the patient has SUI. No. 2-0 or 0 nonabsorbable suture on a medium-sized, tapered needle is usually used for the paravaginal repair. This procedure leaves free space between the symphysis pubis and the proximal urethra but secures support so that rotational descent of the proximal urethra and bladder base is prevented with sudden increases in intra-abdominal pressure. According to Turner-Warwick (1986), the procedure avoids overcorrection and fixation of the periurethral fascia, which might compromise the functional movements of the urethra and bladder base and lead to obstruction and voiding difficulty. This principle may explain why the paravaginal defect repair usually results in spontaneous voiding on the first or second postoperative day. In fact, the vaginal obturator shelf repair has been used to correct patients with dysfunctional voiding symptoms after previous retropubic surgery.
Figure 15-3 ■ Lateral paravaginal defect and technique of paravaginal defect repair. Five or six sutures are placed (inset), first through the full thickness of the vagina (excluding the vaginal epithelium), and then into the obturator internus fascia or arcus tendineus fasciae pelvis, 3 to 4 cm below the obturator fossa.
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General Intraoperative and Postoperative Procedures If the surgeon is concerned that intravesical suture placement or ureteral obstruction may have occurred, cystoscopy—either transurethrally or through the dome of the bladder—or cystotomy may be performed to document ureteral patency and absence of intravesical sutures after retropubic procedures. Closed suction drains in the retropubic space are used only as necessary when hemostasis is incomplete and there is concern about postoperative hematoma. The bladder is routinely drained with a suprapubic or transurethral catheter for 1 to 2 days. After that time, the patient is allowed to begin voiding trials, and postvoid residual urine volumes are checked, either with the suprapubic catheter or by intermittent self-catheterization.
CLINICAL RESULTS Many studies report clinical experiences with retropubic urethral suspension procedures for SUI. Although most of these studies are methodologically flawed, increasing numbers of quality studies, including prospective randomized trials, have been or are being conducted. Currently, however, few prospective studies are available comparing the results of the various procedures for urodynamic SUI. Only a few studies have been done assessing the paravaginal defect repair for SUI. Early studies using subjective outcome measures reported that over 90% of women were continent after this procedure. However, in a prospective randomized trial, Columbo et al. (1996) found that only 61% of women were continent 3 years after a paravaginal defect repair compared with 100% of women who were continent after a Burch colposuspension. We currently believe that the paravaginal defect repair should be used for anatomic correction of anterior vaginal wall prolapse but not as primary treatment of SUI. The Burch colposuspension is the best-studied retropubic procedure. From 1980 to 1990, at least 18 studies reported using the Burch colposuspension in women with urodynamically proved SUI with objective measures of cure. Follow-up times ranged from 3 months to 7 years. At 3 to 24 months after surgery, 59% to 100% of patients became continent, for an overall average cure rate of 84%. At 3 to 7 years, continence rates ranged from 63% to 89%, for an average rate of 77%. Although objectively incontinent, a small percentage of additional patients were judged to be improved and satisfied with their surgical results. The overall reported absolute failure rate is 13.6% at 3 to 24 months and 14% at 5 to 7 years. In an excellent study, Eriksen et al. (1990) reported 91 women with urodynamically proved SUI, with or without bladder stability, who had undergone Burch colposuspension. Urodynamic evaluation was done on 76 patients after 5 years. Stress incontinence was cured in 71% of the patients with preoperative stable bladders and in 57% of those with stress incontinence and detrusor overactivity, a nonsignificant difference. After 5 years, only 52% of the study group
was completely dry and free of complications; about 30% needed further incontinence therapy. Several studies have been done that assessed women more than 10 years after undergoing a Burch procedure. Alcalay et al. (1995) followed a cohort of 109 women (out of 366 eligible women) who underwent Burch colposuspension between 1974 and 1983. The mean follow-up interval was 13.8 years. Both subjective and objective outcome measures were collected during the follow-up period. The cure of incontinence was found to be time-dependent, with a decline for 10 to 12 years and then a plateau at 69% (Fig. 15-4). Cure rates were significantly lower in woman who had had previous bladder neck surgery. Approximately 10% of patients required at least one additional surgery to cure their stress incontinence. Several review articles have been published comparing the cure rates of retropubic procedures with those of other procedures for the treatment of SUI. In 1994, Jarvis reviewed the studies after 1970 that addressed surgical treatment of SUI using objective outcome measures. As has been shown with other studies, the cure rates for surgical treatment of recurrent incontinence are generally somewhat lower than for first procedures. Jarvis noted that only the MMK procedure, the Burch colposuspension, endoscopic bladder neck suspension, and sling procedures produce mean continence rates above 85% for primary procedures and above 80% for repeat procedures. He also noted that the average cure rates of only colposuspension and sling procedures have tight confidence intervals, implying that studies describing these procedures have yielded the most consistent results. In 1996, Black and Downs published an excellent systematic review describing the effectiveness of surgery for stress incontinence in women. The methodological quality of studies was assessed, including all of the randomized controlled trials to that time. Only two randomized controlled trials of colposuspension were available. The study noted that different methods of performing colposuspension (e.g., Burch colposuspension and MMK procedure) have not been shown to be associated with significant differences in outcome. Preliminary evidence reveals that laparoscopic
100 Incontinence cure rate (%)
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90 80 70 60 50 0 0
2
4
6 8 10 12 14 Follow-up interval (years)
16
18
20
Figure 15-4 ■ Long-term cure rate after Burch colposuspension for stress urinary incontinence. (Modified from Alcalay M, Monga A, Stanton SL. Burch colposuspension: a 10–20 year follow up. Br J Obstet Gynaecol 1995;102:740, with permission.)
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colposuspension and open paravaginal defect repair may have somewhat lower cure rates than open Burch procedures. Colposuspension appears to be more effective than anterior colporrhaphy and needle urethropexy procedures in curing and improving stress incontinence. About 85% of women can expect to be continent 1 year after colposuspension, compared with 50% to 70% after anterior colporrhaphy and needle suspension. Primary procedures are generally more effective than repeat procedures. The benefit of Burch colposuspension is maintained for at least 5 years, whereas the benefits from anterior colporrhaphy and needle suspension diminish quite rapidly. Of the four prospective studies (done before 1996) comparing Burch colposuspension and sling procedures, none reported a difference in cure, however defined, regardless of whether the operations were carried out as primary or secondary operations. Similar outcomes were presented recently by the Cochrane Review (Lapitan et al., 2005). The American Urological Association convened the Female Stress Urinary Incontinence Clinical Guidelines Panel to analyze the literature up to 1993, regarding surgical procedures for treating SUI. The data from this meta-analysis indicate that after 48 months, retropubic suspensions and sling procedures seem to be more effective than transvaginal needle suspension procedures or anterior colporrhaphy. The panel’s opinion also noted that open retropubic suspensions and sling procedures are associated with slightly higher complication rates, including longer convalescence and postoperative voiding dysfunction. In a more recent prospective multicenter randomized trial of open Burch colposuspension and tension-free vaginal tape (TVT) procedure for urodynamic stress incontinence, Ward and Hilton (2002) found no significant difference between the surgeries for objective cure rates. Bladder injury was more common during the TVT procedure; delayed voiding, operation time, and return to normal activity were all longer after colposuspension. When these authors analyzed their data at 2 years and ignored subject withdrawals, no differences were seen between the procedures with objective cure rates of 81% for TVT and 80% for colposuspension. Clinical conditions that increase the risk of surgical failure for retropubic urethropexy are shown in Box 15-1. They include obesity, menopause, prior hysterectomy, and prior anti-incontinence procedures. Advanced age and concomitant hysterectomy do not appear to be associated with lower rates of cure after colposuspension. Urodynamic findings that increase the risk of surgical failure include signs of intrinsic urethral sphincter deficiency, abnormal perineal electromyography, and concurrent overactive bladder. Patients with intrinsic sphincter deficiency are probably better treated with a more obstructive operation, such as a sling procedure, if the urethra is hypermobile, or with periurethral injections of a bulking agent, if the urethra is nonmobile. Detrusor overactivity or urge incontinence may coexist in up to 30% of patients with urodynamic SUI. The term mixed incontinence has been used to describe this condition. In addition, about 15% of patients with urodynamic SUI who preoperatively have a stable cystometrogram develop de novo detrusor overactivity after a colposuspension procedure. The course of the overactive bladder after a retropubic repair in patients with mixed incontinence is unpredictable. Interestingly, some studies demonstrate that 50% to 60% of
BOX 15-1
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CONDITIONS THAT DECREASE THE CHANCE OF CURE OF INCONTINENCE AFTER RETROPUBIC BLADDER NECK SUSPENSION
Clinical Hypoestrogenic state Obesity Prior hysterectomy Prior procedures to correct SUI
Urodynamic Detrusor overactivity (preoperative or postoperative) Intrinsic urethral sphincter deficiency Lower maximum urethral pressure Lower leak point pressure Lower functional urethral length Open bladder neck at rest on videourodynamics Nonmobile bladder neck Abnormal perineal electromyography
Surgical Intraoperative blood loss greater than 1000 mL Concurrent abdominal sacrocolpopexy (?) SUI, Stress urinary incontinence.
patients with mixed incontinence are cured of their overactive bladder by surgical support of the bladder neck. A much smaller percentage (approximately 5% to 10%) have worsening of their urgency, with the remainder (20% to 30%) having persistence. Unfortunately, no preoperative urodynamic parameters have been identified that can accurately predict the course of overactive bladder after incontinence surgery. For this reason, we believe that women with mixed incontinence should initially receive nonsurgical therapy. Karram and Bhatia (1989) found that 32% of women with mixed incontinence became dry after nonsurgical therapy. The data suggest that initial nonsurgical therapy will save up to one third of patients the cost and morbidity of incontinence surgery.
MECHANISMS OF CURE Retropubic suspension procedures elevate and stabilize the bladder neck and proximal urethra in a high retropubic position. This results, at least partially, in mechanical compression of the urethra against the stable, elevated anterior vaginal wall or the posterosuperior aspect of the symphysis pubis during episodes of increased abdominal pressure. The principal urodynamic change in postoperative urethrovesical function is increased pressure transmission to the urethra, relative to the bladder, during elevations in intra-abdominal pressure. Resting urethral pressure and functional urethral length are unchanged, suggesting that the intrinsic function of the urethra is not altered appreciably by this type of surgery. The greater the difference in preoperative and postoperative pressure transmission ratios, the more likely that the patient will be continent after Burch colposuspension. If the retropubic procedure fails to elevate and stabilize the urethra, and postoperative pressure transmission ratios remain less than 100%, the patient may continue to have postoperative stress
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Figure 15-5 ■ Pressure transmission profiles in stress incontinent women before (—) and after (– – –) successful colposuspensions, compared with a group of 20 symptom-free women (- - -). (From Hilton P, Stanton SL. A clinical and urodynamic assessment of the Burch colposuspension for genuine stress incontinence. Br J Obstet Gynaecol 1983;90:934, with permission.)
incontinence. Appropriate elevation of the bladder neck and urethra, accompanied by pressure transmission ratios near 100%, result in continence in most patients. This concept is supported by a study by Penttinen et al. (1989, Arch of Gynecol Obstet), who noted a significant negative correlation between postoperative bladder neck mobility and pressure transmission ratios, indicating that correction of the urethrovesical anatomic disorder eliminates the functional disorder and restores continence. MMK and perhaps Burch procedures probably tend to overelevate and fix the urethra in a retropubic position. Hilton and Stanton (1983) found that pressure transmission profiles after successful Burch colposuspensions differed from those of continent control subjects, with pressure transmission ratios in the proximal half of the urethra significantly higher than 100% (Fig. 15-5). This observation suggests that an additional mechanism, probably partial outflow obstruction, results. Bump et al. (1988) determined that patients with postoperative voiding abnormalities and detrusor instability had pressure transmission ratios significantly greater than 100%, supporting the hypothesis that obstruction may play a role in post–continence-surgery voiding dysfunction and detrusor instability. Paravaginal defect repair procedures do not tend to overelevate the bladder neck and proximal urethra; thus, they may have somewhat lower cure rates for stress incontinence but with fewer postoperative problems, such as urgency and voiding dysfunction.
COMPLICATIONS Short-Term Postoperative Of the retropubic procedures, the MMK procedure was the most extensively studied with regard to complications, and
the data are probably similar to those for open Burch colposuspension. In a thorough review of the literature, Mainprize and Drutz (1988) summarized the postoperative complications (excluding urinary retention) of MMK procedures (Table 15-1). Wound complications and urinary infections are the most common surgical complications. Direct surgical injury to the urinary tract rarely occurs. Bladder lacerations occurred in 0.7% of patients; sutures through the bladder and urethra, and catheters sewn into the urethra, occurred in 0.3% of patients. Ureteral obstruction occurred in 0.1% of patients. Accidental placement of sutures into the bladder, during Burch colposuspension or paravaginal defect repair, can occur but is rare, resulting in vesical stone formation, painful voiding, recurrent cystitis, or fistula. Ureteral obstruction occurs rarely after Burch colposuspension and results from ureteral stretching or kinking after elevation of the vagina and bladder base. One study reported three unilateral ureteral obstructions and three bilateral ureteral obstructions in 483 Burch colposuspensions (1.2%). All patients were treated successfully with removal of sutures and ureteral stenting. No cases of transected ureters have been reported. Ericksen et al. (1990) found that 1 of 75 (1.3%) patients followed for 5 years after Burch procedures had absent unilateral renal function caused by presumed complete ureteral obstruction. This patient had developed only transient postoperative fever. Lower urinary tract fistulas are uncommon after retropubic procedures, with various types occurring after 0.3% of MMK procedures. Fistulas are probably less common after Burch and paravaginal defect repairs because the sutures are placed laterally several centimeters to the urethra.
Postoperative Voiding Difficulties The incidence of voiding difficulties after colposuspension varies widely, although patients rarely have urinary retention after 30 days. In our hands, the mean number of days to complete voiding after open Burch procedure is 7 days. Eriksen et al. (1990) found that only 2 of 91 patients had delayed spontaneous micturition after Burch colposuspension, when
Table 15-1
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Postoperative Complications in 2712 Marshall-Marchetti-Krantz Procedures
Type of Complication Wound, total Infection or hematoma Hernia or dehiscence Other Urinary tract infection Osteitis pubis Direct surgical injury to the urinary tract Bladder tears Urethral obstruction Sutures through bladder or urethra, with or without catheter sewn in Ureteral obstruction or hydronephrosis Fistula Death
Percent 5.5 3.4 1.8 0.3 3.9 2.5 1.6 0.7 0.5 0.3 0.1 0.3 0.2
Modified with permission from Mainprize TC, Drutz HP. The Marshall-MarchettiKrantz procedure: a critical review. Obstet Gynecol Surv 1988;43:724.
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the catheter was removed on the third postoperative day. Fifteen percent of the patients had residual urine volumes of 100 to 300 mL on the fifth day after surgery. In contrast, Korda et al. (1989) had a mean postoperative catheter drainage of 10 days (range, 5–60 days) for 174 patients after colposuspension. Twenty-five percent of the patients required catheter drainage for more than 10 days. Colposuspension can change the original micturition pattern and introduce an element of obstruction that can disturb the balance between voiding forces and outflow resistance, resulting in immediate postoperative as well as late voiding difficulties. Urodynamic findings that may occur after colposuspension include decreased flow rate, increased micturition pressure, and increased urethral resistance. Urodynamic tests may be used to predict early postoperative voiding difficulties, although their predictive value has not been demonstrated consistently. Bhatia and Bergman (1984) found that all patients with adequate preoperative detrusor contraction and flow rates were able to resume spontaneous voiding by the seventh postoperative day after Burch colposuspension. One third of patients who voided without detrusor contraction required bladder drainage for 7 days or longer. No patients with decreased flow rates and absent detrusor contraction during voiding were able to void in less than 7 postoperative days. These authors believed that use of a Valsalva maneuver during voiding may further lead to postoperative voiding difficulties, perhaps by intensifying obstruction at the bladder neck. In a study by Kobak et al. (2001), risk factors for prolonged voiding after Burch colposuspension included advanced age, previous incontinence surgery, increased first sensation to void, high postvoid residual volume, and postoperative cystitis. Abdominal straining during voiding was not associated with prolonged voiding after surgery.
Overactive Bladder Overactive bladder is a recognized postoperative complication of retropubic procedures. Detrusor overactivity, as demonstrated on cystometrogram, has been reported in 7% to 27% of patients with preoperative urodynamic SUI and stable bladders, with follow-up of up to 5 years after Burch colposuspension. Postoperative overactive bladder is more common in patients with previous bladder neck surgery and in those with mixed preoperative detrusor overactivity and urodynamic SUI. In a study of 148 patients with preoperative urodynamic SUI and stable bladders, Steel et al. (1986) reported that 24 (16.2%) patients had postoperative detrusor overactivity on cystometrogram 6 months after surgery. Ten of the 24 patients with overactive bladder were completely asymptomatic. Of the 14 symptomatic patients, 4 were improved with drugs aimed at correcting the urgency. The remaining 10 patients (6.8%) remained symptomatic with overactive bladder 3 to 5 years after surgery. The mechanism for this phenomenon is unknown. Some authors have suggested that postoperative onset of overactive bladder may be caused by disruption of the autonomic innervation of the bladder, although this relationship has not been proved. As noted previously, excessive urethral elevation or compression can lead to partial outflow obstruction and resulting urgency. Whatever the mechanism, postop-
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erative overactive bladder predictably occurs in a small but significant number of patients. Patients who undergo retropubic urethropexy should understand that the operation may cause urgency and urge incontinence, even if it cures their stress incontinence.
Osteitis Pubis Osteitis pubis is a painful inflammation of periosteum, bone, cartilage, and ligaments of structures of the anterior pelvic girdle and is a recognized postoperative complication of urologic and radical gynecologic procedures involving the prostate gland or urinary bladder. In urogynecology, osteitis pubis occurs after 0.74% to 2.5% of MMK procedures and very rarely after Burch procedures; the incidence is partially related to the diagnostic criteria used. It can also occur rarely after placement of artificial urinary sphincters and after radical pelvic surgery for gynecologic malignancies. The cause of osteitis pubis is unclear. It may result from infection, from trauma to the periosteum, or from impaired circulation in the vessels around the symphysis pubis. The disease typically occurs from 2 to 12 weeks postoperatively. Osteitis pubis is characterized by suprapubic pain radiating to the thighs and exacerbated by walking or abduction of the lower extremities, marked tenderness and swelling over the symphysis pubis, and radiographic evidence of bone destruction with separation of the symphysis pubis. The clinical course varies from prolonged, progressive debilitation over several months to spontaneous resolution after several weeks. Suggested conservative treatments include rest, physical therapy, steroids, and nonsteroidal anti-inflammatory agents. Whichever therapy is used, however, noninfectious osteitis pubis tends to be self-limiting. Recalcitrant cases may be due to pubic osteomyelitis. Diagnosis is made by bone biopsy and bacterial culture. Kammerer-Doak et al. (1998) found positive cultures in 71% of patients with clinical osteitis pubis who failed to respond to conservative therapy. Treatments are antibiotics, incision and drainage (if abscess formation occurs), or symphyseal wedge resection or debridement.
Enterocele and Rectocele Burch (1968) first reported that enteroceles occurred in 7.6% of cases after the Burch procedure, but only two thirds of these patients required surgical correction. Langer et al. (1988) reported that 13.6% of patients who had undergone Burch procedures, but no hysterectomy or cul-de-sac obliteration, developed an enterocele at 1 to 2 postoperative years. Alcalay et al. (1995) noted that 26% of patients, during a 10- to 20-year follow-up period after Burch colposuspension, underwent a rectocele repair and 5% underwent an enterocele repair. Although not all authors agree, performing a Burch colposuspension may increase the risk of developing apical or posterior vaginal prolapse in the future. Therefore, whenever possible, a cul-de-sac obliteration in the form of uterosacral plication, Moschcowitz procedure, or McCall culdoplasty should be performed at the time of retropubic colposuspension to prevent enterocele formation, although the true efficacy of this prophylactic maneuver is unknown. Rectocele repair should be done, as indicated, for
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symptomatic or large rectoceles, although care should be taken to avoid a resulting mid-vaginal ridge; the postoperative rate of dyspareunia may be as high as 38% when the two procedures are combined.
ROLE OF HYSTERECTOMY IN THE TREATMENT OF INCONTINENCE Gynecologists often perform hysterectomies at the time of retropubic or vaginal surgery for SUI. Although it was generally believed that the presence of a uterus somehow contributed to the genesis of sphincteric incompetence, few data support this theory. Langer et al. (1988) assessed the effect of concomitant hysterectomy during Burch colposuspension on the cure rate of SUI. Forty-five patients were randomly assigned to receive colposuspension only or colposuspension plus abdominal hysterectomy and cul-de-sac obliteration. Using urodynamic investigations 6 months after surgery, the rate of cure for stress incontinence between the two groups did not differ statistically (95.5% and 95.7% for the nonhysterectomy and hysterectomy groups, respectively). This study clearly showed that hysterectomy adds little to the efficacy of Burch colposuspension in curing SUI. In general, hysterectomies should be performed for specific uterine pathology only or for the treatment of uterovaginal prolapse.
PREGNANCY AFTER RETROPUBIC SURGERY Most physicians suggest that the patient finish her childbearing before surgical correction of stress incontinence is attempted. Few data demonstrate the continence status when pregnancy or vaginal delivery occurs after a retropubic repair. Thus, although surgical treatment for stress incontinence should generally be reserved for women who have finished their childbearing, no data convincingly demonstrate that a pregnancy and vaginal delivery would or would not be satisfactory for women after retropubic surgery. We believe that an elective cesarean delivery would be an acceptable option for these patients, if desired after careful review of the pertinent risks and benefits.
Bibliography SURGICAL TECHNIQUE Bhatia NN, Karram MM, Bergman A. Role of antibiotic prophylaxis in retropubic surgery for stress urinary incontinence. Obstet Gynecol 1989;74:637. Burch JC. Urethrovaginal fixation to Cooper’s ligament for correction of stress incontinence, cystocele, and prolapse. Am J Obstet Gynecol 1961;81:281. Gleason DM, Reilly RJ, Pierce JA. Vesical neck suspension under vision with cystotomy enhances treatment of female incontinence. J Urol 1976;115:555. Korda A, Ferry J, Hunter P. Colposuspension for the treatment of female urinary incontinence. Aust N Z J Obstet Gynaecol 1989;29:146. Krantz KE. The Marshall-Marchetti-Krantz procedure. In Stanton SL, Tanagho EA, eds. Surgery of Female Incontinence, 2nd ed. Springer-Verlag, New York, 1986. Lind LR, Gunn GC, Mattox TF, Stanford EJ. Mini-incision Burch urethropexy: a less invasive method to accomplish a time-tested procedure for treatment of genuine stress incontinence. Int Urogynecol J 2004;15:20.
Marshall VF, Marchetti AA, Krantz KE. The correction of stress incontinence by simple vesicourethral suspension. Surg Gynecol Obstet 1949;88:509. McGuire EJ, Lytton B, Pepe V, et al. Stress urinary incontinence. Obstet Gynecol 1976;47:255. Meltomaa SS, Haarala MA, Taalikka MO, et al. Outcome of Burch retropubic urethropexy and the effect of concomitant abdominal hysterectomy: a prospective long-term follow-up study. Int Urogynecol J 2001;12:3. Richardson AC, Edmonds PB, Williams NL. Treatment of stress urinary incontinence due to paravaginal fascial defect. Obstet Gynecol 1981;57:357. Shull BL. How I do the abdominal paravaginal repair. J Pelvic Surg 1995;1:43. Shull BL, Baden WF. A six-year experience with paravaginal defect repair for stress urinary incontinence. Am J Obstet Gynecol 1989;160:1432. Tanagho EA. Colpocystourethropexy: the way we do it. J Urol 1976;116:751. Timmons MC, Addison WA. Suprapubic teloscopy: extraperitoneal intraoperative technique to demonstrate ureteral patency. Obstet Gynecol 1990;75:137. Turner-Warwick R. Turner-Warwick vagino-obturator shelf urethral repositioning procedure. In Debruyne FM, van Kerrebroeck EV, eds. Practical Aspects of Urinary Incontinence. Dordrecht, The Netherlands, 1986, Martinus Nijhoff. Webster GD, Kreder KJ. Voiding dysfunction following cystourethropexy: its evaluation and management. J Urol 1990;144:670.
RESULTS AND MECHANISM OF CURE Alcalay M, Monga A, Stanton SL. Burch colposuspension: a 10–20 year follow up. Br J Obstet Gynaecol 1995;102:740. 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. 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. Bergman A, Koonings PP, Ballard CA. Primary stress urinary incontinence and pelvic relaxation: prospective randomized comparison of three different operations. Am J Obstet Gynecol 1989;161:97. Bidmead J, Cardozo L. Retropubic urethropexy (Burch colposuspension). Int Urogynecol J 2001;12:262. Black NA, Downs SH. The effectiveness of surgery for stress incontinence in women: a systematic review. Br J Urol 1996;78:497. 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. Burton G. A randomized comparison of laparoscopic and open colposuspension. Neurourol Urodyn 1994;4:497. Columbo M, Milani R, Vitobello D, et al. A randomized comparison of Burch colposuspension and abdominal paravaginal defect repair for female stress urinary incontinence. Am J Obstet Gynecol 1996;175:78. Columbo 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. 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 2003;14:104. Enhorning G. Simultaneous recording of intravesical and intraurethral pressure. Acta Chir Scand 1961;276(Suppl):1. Eriksen BC, Hagen B, Eik-Nes SH, et al. Long-term effectiveness of the Burch colposuspension in female urinary stress incontinence. Acta Obstet Gynecol Scand 1990;69:45. Feyereist J, Dreher E, Haenggi W, et al. Long-term results after Burch colposuspension. Am J Obstet Gynecol 1994;171:647. Gillon G, Stanton SL. Long-term follow-up of surgery for urinary incontinence in elderly women. Br J Urol 1984;56:478. Henriksson L, Ulmsten U. A urodynamic evaluation of the effects of abdominal urethrocystopexy and vaginal sling urethroplasty in women with stress incontinence. Am J Obstet Gynecol 1978;131:77. Herbertsson G, Iosif CS. Surgical results and urodynamic studies 10 years after retropubic colpourethrocystopexy. Acta Obstet Gynecol Scand 1993;72:298.
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Hertogs K, Stanton SL. Mechanism of urinary continence after colposuspension: barrier studies. Br J Obstet Gynaecol 1985;92:1184. Hilton P, Stanton SL. A clinical and urodynamic assessment of the Burch colposuspension for genuine stress incontinence. Br J Obstet Gynaecol 1983;90:934. Jarvis GJ. Surgery for genuine stress incontinence. Br J Obstet Gynaecol 1994;101:371. Karram MM, Bhatia NN. Management of coexistent stress and urge urinary incontinence. Obstet Gynecol 1989;73:4. Kjothede P. Long-term efficacy of Burch colposuspension: a 14-year followup study. Acta Obstet Gynecol Scand 2005; 84:767. Kujansuu E. Urodynamic analysis of successful and failed incontinence surgery. Int J Gynaecol Obstet 1983;21:353. Langer R, Golan A, Ron-El R, et al. Colposuspension for urinary stress incontinence in premenopausal and postmenopausal women. Surg Gynecol Obstet 1990;171:13. Langer R, Ron-El R, Neuman N, et al. The value of simultaneous hysterectomy during Burch colposuspension for urinary stress incontinence. Obstet Gynecol 1988;72:866. Lapitan MC, Cody DJ, Grant AM. Open retropubic colposuspension for urinary incontinence in women. Cochrane Database Syst Rev 2005;3: CD002912. Laursen H, Farlie R, Rasmussen KL, et al. Colposuspension Burch: an 18year follow-up study. Neurourol Urodyn 1994;13:445. 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. Liapis A, Papoulias I, Chryssicopoulos A, Creatsas G. Results of the colposuspension operation in pre and postmenopausal incontinent women. Maturitas 1998;31:69. Mainprize TC, Drutz HP. The Marshall-Marchetti-Krantz procedure: a critical review. Obstet Gynecol Surv 1988;43:724. Penttinen J, Käär K, Kauppila K. Colposuspension and transvaginal bladder neck suspension in the treatment of stress incontinence. Gynecol Obstet Invest 1989;28:101. Penttinen J, Lindholm EL, Käär K, et al. Successful colposuspension in stress urinary incontinence reduces bladder neck mobility and increases pressure transmission to the urethra. Arch Gynecol Obstet 1989;244:233. Richmond DH, Sutherst JR. Burch colposuspension or sling for stress incontinence? A prospective study using transrectal ultrasound. Br J Urol 1989;64:600. Rydhström H, Iosif CS. Urodynamic studies before and after retropubic colpourethrocystopexy in fertile women with stress urinary incontinence. Arch Gynecol Obstet 1988;241:201. Sand PK, Bowen LW, Ostergard DR, et al. Hysterectomy and prior surgery as risk factors for failed retropubic cystourethropexy. J Reprod Med 1988;33:171. Sand PK, Bowen LW, Panganiban R, et al. The low pressure urethra as a factor in failed retropubic urethropexy. Obstet Gynecol 1987;69:399. Stanton SL, Cardozo L, Williams JE, et al. Clinical and urodynamic features of failed incontinence surgery in the female. Obstet Gynecol 1978;51:515. Thunedborg P, Fischer-Rasmussen W, Jensen SB. Stress urinary incontinence and posterior bladder suspension defects. Acta Obstet Gynecol Scand 1990;69:55. van Geelen JM, Theeuwes AG, Eskes TK, Martin CB Jr. The clinical and urodynamic effects of anterior vaginal repair and Burch colposuspension. Am J Obstet Gynecol 1988;159:137. Ward K, Hilton P. Prospective multicentre randomized trial of tension-free vaginal tape and colposuspension as primary treatment for stress incontinence. Br Med J 2002;325:1.
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Ward K, Hilton P. A prospective multicenter randomized trial of tensionfree vaginal tape and colposuspension for primary urodynamic stress incontinence: two-year follow-up. Am J Obstet Gynecol 2004;190:324. Weil A, Reyes H, Bischoff P, et al. Modifications of the urethral rest and stress profiles after different types of surgery for urinary stress incontinence. Br J Obstet Gynaecol 1984;91:46. Wheelan JB. Long-term results of colposuspension. Br J Urol 1990;65:329.
COMPLICATIONS Applegate GB, Bass KM, Kubik CJ. Ureteral obstruction as a complication of the Burch colposuspension procedure: case report. Am J Obstet Gynecol 1987;156:445. Bhatia NN, Bergman A. Urodynamic predictability of voiding following incontinence surgery. Obstet Gynecol 1984;63:85. Bhatia NN, Bergman A. Use of preoperative uroflowmetry and simultaneous urethrocystometry for predicting risk of prolonged postoperative bladder drainage. Urology 1986;28:440. Burch JC. Cooper’s ligament urethrovesical suspension for stress incontinence. Am J Obstet Gynecol 1968;100:764. Cardozo LD, Stanton SL, Williams JE. Detrusor instability following surgery for genuine stress incontinence. Br J Urol 1979;51:204. Ferriani RA, Silva de MF, Dias de Moura M, et al. Ureteral blockage as a complication of Burch colposuspension: report of 6 cases. Gynecol Obstet Invest 1990;29:239. Galloway NT, Davies N, Stephenson TP. The complications of colposuspension. Br J Urol 1987;60:122. Kammerer-Doak DN, Cornella JL, Magrina JF, et al. Osteitis pubis after Marshall-Marchetti-Krantz urethropexy: a pubic osteomyelitis. Am J Obstet Gynecol 1998;179:586. Kjohede P, Noren B, Ryden G. Prediction of genital prolapse after Burch colposuspension. Acta Obstet Gynecol Scand 1996;75:849. Kobak WH, Walters MD, Piedmonte MR. Determinants of voiding after three types of incontinence surgery. Obstet Gynecol 2001;97:86. Kwon CH, Culligan PJ, Koduri S, et al. The development of pelvic organ prolapse following isolated Burch retropubic urethropexy. Int Urogynecol J 2003;14:321. Langer R, Ron-El R, Newman M, et al. Detrusor instability following colposuspension for urinary stress incontinence. Br J Obstet Gynaecol 1988;95:607. Lose G, Jorgensen L, Mortensen SO, et al. Voiding difficulties after colposuspension. Obstet Gynecol 1987;69:33. Maulik TG. Kinked ureter with unilateral obstructive uropathy complicating Burch colposuspension. J Urol 1983;130:135. Rebenack P, Thompson RJ, Wilf LH. Osteomyelitis pubis following a Burch retropubic urethropexy. J Gynecol Surg 1990;6:205. Rosenthal RE, Spickard WA, Markham RD, et al. Osteomyelitis of the symphysis pubis: a separate disease from osteitis pubis. J Bone Joint Surg 1982;64:123. Sand PK, Bowen LW, Ostergard DR, et al. The effect of retropubic urethropexy on detrusor stability. Obstet Gynecol 1988;71:818. Steel SA, Cox C, Stanton SL. Long-term follow-up of detrusor instability following the colposuspension operation. Br J Urol 1986;58:138. Turner-Warwick RT. The pathogenesis and treatment of osteitis pubis. Br J Urol 1960;32:464. Wang AC, Chen M. Comparison of tension-free vaginal taping versus modified Burch colposuspension on urethral obstruction: a randomized controlled trial. Neurourol Urodyn 2003;22:185. 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;182:1610. Wiskind AK, Creighton SM, Stanton SL. The incidence of genital prolapse after the Burch colposuspension. Am J Obstet Gynecol 1992;167:399.
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Mark D. Walters and Mickey M. Karram
HISTORICAL PERSPECTIVES 196 INDICATIONS 197 TYPES OF SLINGS 197 TECHNIQUES OF SUBURETHRAL SLING PROCEDURES 199 Proximal Suburethral Sling and Modifications 199 Synthetic Retropubic Midurethral Slings 201 Synthetic Transobturator Midurethral Sling 202 RESULTS 207 Pubovaginal Slings and Modifications 207 Tension-Free Vaginal Tape 208 COMPLICATIONS 208 Lower Urinary Tract Injury 208 Voiding Dysfunction and Retention 208 Detrusor Overactivity and Irritative Voiding Symptoms 209 Recurrent or Persistent Incontinence 209 Hemorrhage 209 Infection and Erosion 209 Nerve Damage 209 CONCLUSIONS 210
HISTORICAL PERSPECTIVES The vaginal approach for the surgical management of urodynamic stress urinary incontinence (SUI) associated with urethral hypermobility and intrinsic sphincter deficiency (ISD) has been comprised of a wide variety of procedures based on different surgical principles. Historically, suburethral sling procedures have been reserved for patients with severe stress incontinence, previous surgical failures, and patients who have significant ISD. Until recently, anterior colporrhaphy with Kelly’s plication and transvaginal needle suspension procedures were used for the transvaginal repair of primary stress incontinence and associated urethral hypermobility. Numerous studies, however, have shown that the objective success rate after anterior colporrhaphy and suburethral plication is significantly less than what could be achieved with retropubic colposuspension or a suburethral sling procedure. For this reason, suburethral plication should no longer be considered as a procedure for the correction of stress incontinence and should only
be performed as part of an anterior colporrhaphy or cystocele repair without incontinence or in the occasional elderly patient with mild incontinence in whom surgical morbidity should be kept low (see Chapter 19). Transvaginal needle suspension procedures were first described by Pereyra in 1959. The needle urethropexy underwent more than 20 modifications in an attempt to improve the cure rates and minimize complications. Modifications involved various amounts of dissection and different anchoring tissue and materials. Although extremely popular in the 1990s, these procedures are currently rarely done because several comprehensive reviews and prospective randomized trials have shown them to be significantly less effective than retropubic Burch colposuspension and suburethral sling procedures. The first suburethral sling procedure was described in 1907, and many variations of muscular and fascial slings have since been described to treat stress incontinence. The most popular and long-lasting sling variation was reported by Aldridge in 1942. He used two strips of rectus fascia sutured in the midline below the urethra via a separate vaginal incision. The fascial strips were brought down through the rectus muscle, behind the symphysis pubis, and united as a sling beneath the urethra. This provided a reliable cure for recurrent cases of stress incontinence and was the standard for five decades. To overcome the limitations of using autologous materials for slings, such as poor quality of fascial tissue, inadequate length, and need for harvesting procedures and their morbidity, synthetic materials began to be used for the sling graft. In spite of numerous refinements of technique and improvements in synthetic grafts, clear superiority of synthetic over autologous materials for pubovaginal slings has not been demonstrated. In fact, some trials reported an unacceptably high rate of erosion and infection with certain synthetic materials. The tension-free vaginal tape (TVT) procedure was developed in the 1990s by Petros and Ulmsten (1990, 1995). The concept behind this procedure is that stress incontinence results from the failure of the pubourethral ligaments in the midurethra. The “integral theory” for the management of stress incontinence was based on the model that continence is maintained at the midurethra
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and not at the bladder neck. The aim of the tape (sling) is to reinforce the functional pubourethral ligaments and hence secure proper fixation of the midurethra to the pubic bone, allowing simultaneous reinforcement of the suburethral vaginal hammock and its connection to the pubococcygeus muscles. This operation introduced two new concepts to the mechanism of cure for slings: placement at the midurethra, and placement without tension. Numerous cohort studies and a large clinical volume worldwide seem to show that the TVT procedure (and other variations of midurethral slings) is equivalent to other operations for cure of continence, with a quicker return to normal voiding and fewer postoperative complications. The other important innovation of the TVT was that it could be done under local anesthesia as an outpatient, and often patients could void the day of surgery and be discharged home without a catheter. Suburethral sling procedures, including proximal urethral and midurethral tension-free slings, are the most currently used operations for the surgical correction of urodynamic stress incontinence. This chapter will discuss the indications, types of available slings, surgical techniques, results, and potential complications of various methods of suburethral sling procedures.
INDICATIONS Traditionally a suburethral sling has been recommended for urodynamic SUI caused by ISD (or type III incontinence)— defined here as failure of the urethral sphincter to maintain a watertight seal regardless of bladder neck position. Patients with ISD usually present with severe stress incontinence, decreased vaginal pliability, low resting urethral closure pressure, and low Valsalva leak point pressures. Endoscopic or radiographic studies reveal an open bladder neck at rest. Recently, slings, especially tension-free midurethral slings, have been expanded for use with all types of SUI, regardless of urethral or leak point pressures. Based on the type and anatomic location of the sling, two mechanisms of continence are probably present after the suburethral sling. When placed at the proximal or midurethra, the first mechanism restores normal bladder neck or urethrovesical junction support and prevents descent with straining. The sling then functions as a backboard or stable suburethral base to effect urethral closure with increases in abdominal pressure. A second mechanism is a mechanical kinking that occurs over midurethral slings with increased abdominal pressure. Increased outflow resistance is created by slight upward displacement of the sling to cause urethral closure but may result in voiding dysfunction or even retention. Given this dual mode of action and good long-term outcomes, indications for suburethral slings have broadened over the last decade. They are currently used as a primary procedure in patients with hypermobility, as well as in patients with recurrent incontinence or ISD. Recent data indicate that, in experienced hands, the rate of postoperative voiding dysfunction and retention is not significantly greater (and may be less) than that of traditional retropubic suspensions.
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TYPES OF SLINGS Currently, suburethral sling procedures can be broadly classified into bladder neck and midurethral slings (Box 16-1; Fig. 16-1). Slings can be made of a biologic material and are placed at the level of the proximal urethra and bladder neck or a synthetic material placed either under the proximal or midurethra. The currently used biologic materials are divided into autologous tissue, which is harvested from the patient who is undergoing the sling; allograft material, which is most commonly cadaveric fascia lata; or xenografts, which are harvested from various animal sources. Proximal urethral slings are called pubovaginal slings when the arms of the material used are connected to the anterior rectus fascia on each side. Various modifications of a traditional pubovaginal sling have been described and involve various patch-type slings in which the sling materials are placed vaginally at the level of the proximal urethra and then attached to sutures that are passed suprapubically. Some surgeons believe in the importance of the arms of the sling penetrating the urogenital diaphragm and entering the retropubic space, whereas others feel that this is not necessary. Another type of proximal urethral sling is the in situ vaginal wall sling, in which an anterior vaginal wall patch under the proximal urethra is suspended to the anterior abdominal fascia via permanent bridging sutures. The TVT procedure was the first synthetic midurethral sling and was described by Petros and Ulmsten (1990, 1995). This ambulatory procedure was aimed at restoring the pubourethral ligament and suburethral vaginal hammock by using specially designed needles attached to a synthetic sling material. The synthetic sling material is made of polypropylene and is approximately 1 cm wide and 40 cm long. The sling material is attached to two stainless steel needles that are passed blindly from a vaginal incision made at the level of the midurethra through the retropubic space to exit at previously created stab wounds in the suprapubic area. After this midurethral sling became well-established, techniques to surgically correct stress incontinences via a suprapubic approach were described (SPARC procedure [American Medical Systems, Minnetonka, MN]; percutaneous vaginal tape [PVT]). This involved passage of a needle from the suprapubic area to exit in a previously created BOX 16-1
TYPES OF SLINGS
Proximal Urethral/Bladder Neck Slings Pubovaginal using rectus fascia Pubovaginal using allograft, xenograft, nonabsorbable graft Patch sling using suture bridges to rectus fascia Patch sling anchored to pubic bone Vaginal wall sling
Midurethral Slings Tension-free vaginal tape (TVT) Percutaneous vaginal tape (PVT), SPARC, others Transobturator slings Outside-in Inside-out
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Figure 16-1 ■ Cross-sectional view of suburethral sling modifications. A. Traditional pubovaginal sling. B. Modified patch sling, in which ends of sling do not enter the retropubic space. C. Patch sling, in which ends of sling are in the retropubic space. D. Patch sling, in which sutures are anchored into bone. E. Patch sling that is anchored directly into bone. F. In situ vaginal wall sling. G. Synthetic midurethral retropubic sling. H. Synthetic midurethral transobturator sling.
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incision in the vagina of the level of the midurethra. These procedures quickly became popular and were shown to be efficacious. Because they did require blind passage of the needle through the retropubic space, rare but serious complications were reported in the form of vascular and bowel injuries. These complications resulted in significant morbidity and rare cases of mortality. Delorme (2001) reported on the first transobturator synthetic midurethral sling and described that the passage of the needle completely avoided the retropubic space and avoided any potential for serious complications in the form of vascular or bowel injuries as well as the potential for injury to the lower urinary tract. The initial description of this procedure involved the passage of specially designed needles from the obturator region, through the obturator membrane, around the ischiopubic ramus to exit in the open portion of the vagina. Shortly after the initial description, a procedure that involved passage of the needle from the vaginal incision to exit the obturator space was described.
TECHNIQUES OF SUBURETHRAL SLING PROCEDURES Proximal Suburethral Sling and Modifications The optimal route and surgical technique of a suburethral sling procedure placed beneath the proximal urethra and bladder neck must be considered preoperatively. Most surgeons perform a pubovaginal sling procedure via a combined abdominal and vaginal route, with the majority of the dissection being done vaginally. The procedure can also be performed entirely via abdominal approach, with tunneling of the sling between the urethra and the vagina. However, this approach increases the likelihood of urethral trauma and is currently rarely used. More recently, sling procedures have been performed through an entirely vaginal route through which the sling material is either anchored to the back of the pubic bone or sutured into Cooper’s ligament via a special needle ligature passage. The choice of sling material, approach, and operative technique is at the discretion of the surgeon. To date, no randomized trial has compared these various modifications and sling materials. If the surgeon decides to use autologous tissue, it will most commonly be either fascia lata or rectus fascia. Harvesting of these tissues is usually performed before any vaginal dissection. The technique of harvesting fascia lata is determined by whether the surgeon prefers to do a complete pubovaginal sling, or whether a patch-type sling is performed. The fascia lata graft is usually approximately 4 × 6 cm in diameter. This can be obtained via a 3- to 4-cm transverse skin incision made approximately 8 cm above the midpatella, lateral to the knee and the lower thigh. Blunt dissection exposes the underlying fascial lata, and a piece of fascia is easily removed to serve as the patch for the sling procedure. Subcutaneous tissue is reapproximated, the skin is closed, and a pressure bandage is placed. If a full pubovaginal sling is used, a long piece of fascial lata can be obtained using a Wilson or Crawford fascial stripper. The technique for obtaining the full strip of fascia involves a blunt dissection of the fat away from the fascia lata all the way up the lateral side of the leg toward the greater trochanter.
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A 1-cm wide piece of fascia is usually removed using the fascial stripper. This will result in a 20-cm long piece of fascia. If a longer piece of fascia is desired, a second piece of fascia of a similar length can be obtained by repeating the same procedure. When this is performed, there should be a 1-cm wide area of fascia lata that remains between the two areas where the stripper has removed the tissue. In either case, closure of the fascia defect is not necessary. The other autologous tissue that is commonly used for pubovaginal sling is the fascia of the anterior abdominal wall of the anterior rectus fascia. To obtain this fascia, a low transverse abdominal incision is made approximately 4 cm above the pubic symphysis. Blunt dissection is performed in the subcutaneous tissues until the rectus fascia is visualized. An appropriately sized piece of rectus fascia is harvested in the transverse direction using sharp dissection or electrocautery. The size of the strip is usually approximately 1 cm wide and 20 cm long. The fascial incision is closed using No. 0 delayed absorbable sutures, and the abdominal incision is packed until the vaginal portion of the procedure is completed. The operative details for suburethral pubovaginal sling placed at the level of the proximal urethra are as follows: 1. The patient is placed in high stirrups in the dorsal lithotomy position and the vagina and lower abdomen are appropriately prepped and draped. Preoperative antibiotics are usually given on call to the operating room. 2. Hydrodissection of the anterior vaginal wall is usually used by injecting beneath the epithelium of the anterior vaginal wall at the level of the bladder neck. This facilitates dissection of the appropriate plane and may also have a hemostatic effect. 3. A midline vaginal incision or an inverted U vaginal incision is made at the level of the proximal urethra or bladder neck, which is easily determined by palpation of the anterior vaginal wall with a Foley catheter in place. The vaginal epithelium is carefully dissected off the underlying periurethral and perivesical fascia, using blunt and sharp dissection. This dissection is extended bilaterally to the inferior lateral aspects of the pubic rami. 4. The retropubic space is entered, using either blunt or sharp dissection (Fig. 16-2). Once the periurethral attachment of the urethra and the urogenital diaphragm has been penetrated on each side, one should be able to pass a finger along the backside of the pubic bone all the way to the inferior aspect of the rectus muscle. 5. If a traditional pubovaginal sling is to be performed, an abdominal incision is made at this time. The incision is usually made approximately 2 fingerbreadths or 4 cm above the level of the pubic symphysis, and is a transverse incision usually no more than 8 cm long. The incision is extended down to the rectus fascia. 6. The sling is brought into the field and is transferred from the vaginal incision, through the retropubic space, to above the anterior abdominal fascia. Each arm is transferred, using either a dressing forceps or some type of needle ligature carrier. Small incisions in the fascia allow each arm to come up through the
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Figure 16-2 ■ A. Technique of blunt dissection into retropubic space. With tip of index finger flexed anteriorly against posterior symphysis, periurethral attachment to pubic bone is perforated, completely detaching endopelvic fascia. B. Technique of vaginal entrance using Metzenbaum scissors; endopelvic fascia is perforated at inferior margin of pubic bone, as guided by surgeon’s index finger. Blades of scissors are separated, and dissection is completed by inserting a finger into space created, as shown in A.
fascia. The transfer of each arm of the sling is done under direct finger guidance. A full length pubovaginal sling should loosely sit at the level of the proximal urethra and is usually anchored there with several fine absorbable sutures (Fig. 16-3). 7. If a patch-type sling is used, the length of the patch is determined and the longitudinal edges of the patch are attached to permanent sutures and these sutures are passed into the anterior abdominal incision (Fig. 16-4). Bone fixation techniques can be done in which sutures, or the sling itself, are directly anchored into bone. 8. Cystourethroscopy is performed to ensure no inadvertent injury or passage of any material through the bladder. Also, visualization of the proximal urethra and bladder neck documents that the sling is in the appropriate position. Elevation on the arms of the sling or the sutures should elevate the level of the proximal urethra. If there is no mobility at this area, the sling is either placed in the wrong anatomic position or further periurethral dissection needs to be performed to create urethral mobility. 9. The final step involves appropriate tensioning of the sling. Unfortunately, no standardized method exists that can be used on all patients. One must individualize the patient based on the severity of her incontinence and the state of her pelvic tissue. In general, the sling should be placed loosely at the level of the proximal urethra and should act as a backboard to prevent descent of the proximal urethra during increases in intra-abdominal pressure. Thus, after tying of the sling, downward traction on a Foley catheter should document that this area has been appropriately supported with the previously mentioned backboard mechanism. The authors routinely place a right-angle clamp between the urethra and the sling material during tying, with the goal of maintaining zero tension at rest. A compressive
Figure 16-3 ■ Full-length suburethral sling, in which fascia or synthetic material is passed and tied above the anterior rectus fascia.
mechanism of a suburethral sling ideally should be activated only during increases in abdominal pressure. 10. After the sutures are tied, the anterior vaginal wall is closed, and a transurethral or suprapubic catheter is left in place. A vaginal packing is also commonly used.
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Figure 16-5 ■ Tension-free vaginal tape instrumentation, including (clockwise from top) a Foley catheter guide, needle introducer/handle, and specially designed needles attached to a synthetic suburethral sling tape. (Courtesy of Ethicon Inc., Somerville, NJ.)
Figure 16-4 ■ Patch sling using combined needle suspension sling procedure, in which a suburethral patch of fascia or synthetic material is suspended to the anterior rectus fascia with permanent sutures.
Synthetic Retropubic Midurethral Slings TVT The patient is brought to the operating room and one of general, regional, or local anesthesia with sedation is administered. Broad-spectrum preoperative antibiotics, such as cephazolin, should be used. The patient is positioned in the dorsal lithotomy position. The authors prefer to use candycane stirrups for this. Patients should be in the horizontal or in slight Trendelenburg position to displace bowel away from the pelvis. The instrumentation required for the procedure includes 30 mL of local anesthetic, such as lidocaine or Marcaine; a 22-gauge needle for infiltration; TVT kit (Fig. 16-5 [Ethicon Inc., Somerville, NJ]), which includes two 5-mm stainless steel needles connected by a 1.2-cm wide piece of polypropylene mesh; a nondisposable handle or introducer; an 18French Foley catheter; catheter guide; and absorbable sutures to close the incisions. Using a pen, the surgeon outlines the sites of the suprapubic stab incisions. These should be along the superior rim of the pubic bone, 2 fingerbreadths lateral to the midline, 0.5- to 1-cm long. The two suprapubic puncture sites should be anesthetized with local anesthesia. We prefer to use 1% lidocaine with epinephrine, 10 mL on each side. The injection should be taken down to the pubic bone to infiltrate the rectus fascia and muscle. An 18-French Foley catheter should be placed and the bladder drained. A Sims or weighted speculum is placed in the vagina. Local anesthesia (8 to 10 mL) is infiltrated in the anterior vaginal wall to achieve hydrodissection and vasoconstriction. A 1.5-cm midline incision is then made at the midurethra, as shown in Figure 16-10, A. Palpating the Foley bulb at the bladder neck may be helpful to ensure that the
incision is appropriately placed. With Allis clamps stabilizing the vaginal mucosa, the Metzenbaum scissors are used to dissect under the vaginal epithelium laterally to create a tunnel to the inferior pubic ramus. Unlike the bladder neck, at the midurethra the anterior vaginal wall and posterior urethra are fused and no natural plane of dissection is present. Hence, one must minimize creation of these tunnels to ensure that the tape stays in the proper position. Once the tunnels have been prepared, the sling may be passed. Two stab incisions can be made in the suprapubic region over the marked areas. The bladder is completely drained, and the guidewire is passed down the Foley. The catheter guide is directed to the ipsilateral side of trocar placement to displace the urethra and bladder neck in the contralateral direction. The TVT sling is made of a polypropylene mesh of approximately 40 × 1.1 cm. The mesh is encased in a plastic sheath that overlaps at the midpoint, allowing for easy removal once the sling is in place. The authors prefer to place a hemostat at the region of overlap to reduce slippage of the sheath during placement. The TVT sling is attached to a curved trocar that is then screwed on an introducer or handle, and the trocar tip is placed in the vaginal tunnel that has been created. The introducer should be held in the dominant hand while the thumb of the nondominant hand stabilizes the trocar; the index finger of the nondominant hand ensures that the vaginal mucosa is not perforated. The speculum is removed from the vagina, and while the catheter is moved to the ipsilateral side, the trocar is guided along the pubic bone initially directed toward the ipsilateral shoulder. Once the needle pierces through the urogenital diaphragm, it is then redirected to pass vertically through the space of Retzius along the back of the symphysis. Finally, it is brought out through the suprapubic stab incision. While the trocar is in place, the guidewire and catheter are removed and cystoscopy is performed to ensure no bladder injury. Examination with a 70-degree cystoscope is done with a full bladder. Once bladder integrity is confirmed, the introducer is removed from the trocar and the trocar is brought out through the abdominal incision. If a bladder perforation is noted, the introducer is backed out, the bladder is drained, and the procedure is repeated. Postoperatively, the authors do not routinely leave a catheter in place if a single perforation is noted; however, some surgeons may prefer to drain the bladder for 24 to 48 hours. The procedure is then
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repeated on the opposite side. Care is taken to ensure that the sling does not become tangled before placement. The next step is to properly tension the sling to stabilize, but not obstruct, the urethra. The trocars are cut from the sheath and Kelly clamps are placed at the sling ends. The sling is pulled to the urethra with the overlapping area at the midline. Mayo scissors or a right-angle clamp is initially placed between the posterior urethra and the mesh. If the patient is under local or regional anesthesia, she may be asked to cough or perform a Valsalva maneuver. With the bladder full of 250 to 300 mL of fluid, the sling should be tightened to ensure that only a few drops of urinary leakage are present with coughing. If the patient is under general anesthesia, adequate looseness should be present between the urethra and the mesh. If desired, Credé’s maneuver can be performed to simulate the Valsalva maneuver. Once the tensioning is secure, the sling sheath is removed while stabilizing the sling below the urethra. The remaining sling mesh is cut off at the abdominal skin. After ensuring hemostasis, the vaginal incision is closed using No. 3-0 Vicryl sutures in a running fashion. The skin incisions are closed using No. 4-0 Vicryl, Steri-Strip, or a skin adhesive. The Foley catheter is then replaced in the bladder, and the patient is taken to the recovery room. Correct orientation of the TVT trocar is critical to avoid cystotomy and damage to the bowel or bladder during retropubic placement. Cadaveric dissections by Muir et al. (2003) showed that a correctly placed TVT trocar is just lateral to the bladder and urethra and an average of 3.2 cm medial to the obturator neurovascular bundle, 3.9 cm medial to the superficial and inferior epigastric vessels, and 4.9 cm medial to the external iliac vessels. The orientation of the trocar and handle is best kept slightly lateral to the midline sagittal plane, directed to the ipsilateral shoulder during placement. Surgeons should be careful to minimize external or internal rotation of the device. Figure 16-6 shows the normal retropubic placement of the TVT trocar as well as the anatomic position of the device if it is placed into the bladder, or deviated cephalad or laterally, increasing the risk of vascular damage. ABDOMINAL APPROACH (TOP-DOWN) The positioning, infiltration, and dissection in the abdominal approach are performed similarly to the vaginal approach, with the exception of the vaginal tunnels that must be large enough to permit the tip of an index finger to touch the inferior pubic ramus. The bladder is drained completely with the Foley catheter. The abdominal guide needle handle is grasped in the surgeon’s dominant hand, with the nondominant hand stabilizing the base of the trocar or needle. The tip is placed in the suprapubic incision and advanced off the back of the pubic symphysis. A “pop” is usually felt as the needle pierces the rectus fascia. After penetration of the rectus fascia, the nondominant hand is placed in the vaginal tunnel on the ipsilateral side of the needle. The handle is then laid on the abdomen of the patient in a cephalad direction and the trocar or needle advanced down the back of the pubic symphysis until the tip is felt, by the index finger of the nondominant hand. Once the tip is felt, the needle is passed through the urogenital diaphragm to the vaginal incision. The procedure
is repeated on the opposite side; with both needles in place, a cystoscopy is performed to confirm no evidence of bladder injury. Once bladder integrity is determined, the sling is attached to the abdominal needles by a plastic connector (as per manufacturer’s recommendations) and the trocars are removed through the retropubic space into the abdominal wounds. The tape is cut from the trocars, and tensioning is performed as was described for the TVT.
Synthetic Transobturator Midurethral Slings The technique of placing a transobturator sling using the inside-out technique is as follows: 1. The patient is given general, regional, or local anesthesia with sedation. She is placed in lithotomy position in high candy-cane stirrups, with the hips sharply flexed and the buttocks to the end of the table. This is particularly important in obese women in whom the buttocks are large and the instrument needs to be correctly oriented in the plane of the dissection. A single dose of intravenous prophylactic antibiotic is given before surgery. 2. A Foley catheter is placed in the bladder, and the vaginal and perineal landmarks are examined, which include the suburethral area, bilateral periurethral area, and the upper inner thigh and lateral labia. The surgeon should keep in mind the obturator anatomy, as described in Chapter 2. The surgeon places an index finger into one vaginal fornix and the thumb lateral to the labia to palpate the ischiopubic ramus, including the medial margin of the obturator foramen at the level of the bladder neck and clitoris (Fig. 16-7). A pen is used to mark a line horizontally at the level of the clitoris (Fig. 16-8), at an area below the adductor longus muscle in a fold of skin at the most lateral portion of the labia majora. 3. If a cystocele repair or other reconstructive pelvic surgery is to be done, it is best to accomplish this before the transobturator sling through separate incisions. The vaginal incision of the cystocele repair would only extend to the level of the bladder neck; the bladder adventitia, but not the bladder neck, is plicated. Excess vaginal epithelium is trimmed and the vagina closed. The transobturator sling is then done through a separate suburethral incision. 4. One percent lidocaine with 1:200,000 epinephrine is injected bilaterally under the midurethra at the level of the bladder neck, raising a wheal at the fornix on each side. If the patient is under local anesthesia with sedation, 10 mL of lidocaine with epinephrine is also injected at the lateral labial incisions under the skin, into the muscle, and into the lateral portion of the ischiopubic ramus to the estimated area of the obturator membrane. After this is accomplished bilaterally, a 1-cm stab incision is made with a scalpel at the marked area of the lateral labia, where the sling device will be passed. 5. The angle of the lateral labial incision to the suburethral incision is approximately 30 to 40 degrees from the horizontal. Placement of the sling too anterior
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Figure 16-6 ■ Correct placement of the TVT trocar into the retropubic space. A. Placement of the TVT device through the bladder, typically at its lateral edge or slightly near the dome. B. Lateral deviation of the trocar, either due to aiming it laterally to the ipsilateral shoulder or due to external rotation of the device. C. Placement of the trocar too cephalad and lateral so that it approaches the obturator neurovascular bundle. D. Significant lateral deviation of the trocar, risking damage to the external iliac artery or vein.
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Figure 16-7 ■ Transobturator sling. The surgeon palpates the ischiopubic ramus and medial edge of obturator foramen.
Figure 16-8 ■ Transobturator sling. A horizontal line is drawn at the level of the clitoris to the lateral edge of the labia majora. This area is the point of entry or exit of the transobturator helical device.
on the labia or thigh will make passage of the helical device difficult because the ischiopubic ramus curves laterally at that point. Placement of the lateral labial incision too posterior will create a sling that is too flat and, possibly, less effective. 6. Several helical devices are marketed for passage of a transobturator sling (Monarc [American Medical Systems, Minnetonka, MN], Fig. 16-9; Obtryx [Boston
Figure 16-9 ■ Monarc helical device to pass transobturator sling. (Courtesy of Monarc® Subfascial Hammock, www.AmericanMedicalSystems.com.)
Scientific Corp, Natick, MA]; and others), and the surgeon should follow manufacturer’s recommendations for each sling kit. The helical sling device passes through the following tissue layers when going from lateral to medial: skin and subcutaneous fat, gracilis muscle, adductor brevis, obturator externus muscle, obturator membrane, obturator internus muscle, periurethral endopelvic fascia, and through the vaginal tunnel. The sling device is approximately 2.4 cm from the obturator neurovascular bundle as it exits the external obturator canal, based on dissections by Whiteside and Walters (2004). 7. A 2-cm midline incision is made under the midurethra with a scalpel (Fig. 16-10, A). Metzenbaum scissors are used to dissect bilaterally under the vaginal epithelium in the periurethral tissues, until the scissors tip meets the medial portion of the ischiopubic ramus. The scissors are spread slightly so that the surgeon’s finger can be gently placed into the tunnel to touch the bony landmark. The helical sling device is then oriented correctly and popped through the subcutaneous tissues and underlying muscles just lateral to the ramus. With the surgeon’s other index in the suburethral tunnel, the device is passed around the ramus, through the obturator muscles and membrane, until it meets the surgeon’s finger and is guided out laterally to the urethra (Fig. 16-10, B). The sling is connected to the helical device and pulled laterally through the periurethral tunnel and obturator membrane, and out the lateral labial incision. The device is disconnected from the sling. This procedure is repeated on the other side, and the sling is laid without tension under the urethra
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Figure 16-10 ■ Transobturator sling technique. A. A 1.5-cm midline vaginal incision is made at the midurethra. B. The helical device is passed around the ischiopubic ramus through the obturator membrane, and into the vaginal incision. C. Sling placement is complete.
and oriented without twisting or other distortion (Fig. 16-10,C). Cystoscopy is done to verify that the sling was not placed in the bladder lumen. 8. The plastic sleeves are removed bilaterally from the sling, again ensuring that no tension is on the sling. The sling ends are cut bilaterally below the level of the skin, and the vaginal and skin incisions are closed with No. 3-0 or 4-0 absorbable suture. 9. The patients are generally sent to the recovery room, where the Foley catheter is removed. Most patients are able to void the same day and are discharged home without a catheter. We generally check at least
one postvoid residual urine volume to ensure that they are emptying efficiently. If patients are unable to void the day of surgery, they are sent home with a Foley catheter and followed up in the clinic in several days for another voiding trial. Alternatively, they can be taught to catheterize themselves either in the recovery room or in the office in 1 to 2 days. The technique of placing a transobturator sling using the TVT Obturator System (Ethicon, Inc., Somerville, NJ) is shown in Figure 16-11. The patient is prepared as for other transobturator slings, including placement of a 2-cm incision
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Figure 16-11 ■ TVT Obturator sling technique. A. The helical device is placed through the suburethral tunnel. B. The device is popped through the TVT obturator membrane and then rotated sharply around the ischiopubic ramus to exit the skin (C). D. The sling is pulled through the skin incision and held.
below the midurethra, as described. Using manufacturer’s recommendations, the helical device is placed through the suburethral tunnel until the medial surface of the ischiopubic ramus is touched (Fig. 16-11, A). The device is popped through the obturator membrane and then rotated sharply around the ischiopubic ramus to exit out the skin (Fig. 16-11, B, C). The polypropylene sling is then pulled out through the skin incision and held (Fig. 16-11, D). The procedure is repeated on the
opposite side until the sling is in proper orientation and lying flat underneath the urethra. The sling is tensioned and the plastic sleeves removed, as with other transobturator slings, and the skin and vaginal incisions are closed. Complications with transobturator slings are generally few and include urinary tract infections, temporary voiding dysfunction, exposure of the suburethral mesh, and pain or bruising at the level of the lateral labial incision and inner
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thigh. Upper thigh obturator space hematomas or abscesses have been recorded but are extremely rare. Although cystotomy has been reported, especially in the presence of a large cystocele, it is quite rare, especially if the surgeon allows the helical device to touch the finger as it passes around the ischiopubic ramus. We generally perform a cystoscopy after the sling is placed to verify that a cystotomy or inadvertent placement of mesh into the bladder has not occurred. Other complications, such as ureteral injury, bowel injury, or catastrophic vascular injury, have not been reported.
RESULTS Pubovaginal Slings and Modifications The concept of supporting the bladder neck and urethra by a sling has been with urologists and gynecologists since the early 1900s. This procedure has undergone multiple revisions; however, it was not until 1942 that Aldridge used his fascial suburethral sling procedure, which is the forerunner of most modern sling procedures. He described the procedure as a salvage type operation for those women who had failed previous procedures. For the sling he used rectus fascial strips that remained attached to the anterior abdominal wall. In the majority of reported cases in the literature, the suburethral sling procedure has been used predominantly as a treatment for patients with recurrent SUI after previous failed bladder neck surgeries. Used for such an indication, the objective cure rates recorded in the literature range between 61% and 100% with a mean cure rate of 85%. The cohort literature related to the use of a suburethral sling (other than the TVT procedure) as a first procedure is limited, but a mean continence rate of 94% is quoted by Jarvis (1994). With the increasing popularity of sling procedures and escalating demand for minimally invasive techniques, numerous materials have become available for use in a suburethral sling. Current materials can be categorized as autologous fascia, allograft fascia, xenograft, and synthetic slings. Within these categories, different variants can be subgrouped into individual materials: autologous (rectus fascia, fascia lata, vaginal wall); allograft (freeze dried irradiated cadaveric fascia lata, solvent dehydrated cadaveric fascia lata, fresh frozen cadaveric fascia lata, cadaveric dermis); xenograft (porcine dermis, porcine subintestinal mucosa); and synthetic (polypropylene, Mersilene, silastic, expanded polytetrafluoroethylene). Autologous rectus fascia and fascia lata are probably the most common materials in use and the gold standard to which the outcome of other new materials should be compared. Application of newer technologies of harvesting tissue has made multiple human and animal-based materials available. The theoretical rationale for using allografts and xenografts for suburethral slings is reinforcement of inherently weak endopelvic fascia. Allogenic grafts harvested from cadaveric donors are widely used and do not seem to carry a significant risk of erosion or infection. The long-term durability of allograft fascia continues to be studied, and there seems to be wide variability in the quality of tissue depending on its source and processing. The type of sling material probably
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does not significantly affect cure rates, provided that the characteristics of the chosen material are considered carefully. Two large cohort studies have been done assessing the results of pubovaginal fascial sling for SUI. Morgan et al. (2000) reported a long-term follow-up of 247 women with types II and III incontinence after rectus fascia pubovaginal sling. These patients were followed urodynamically, as well as with quality-of-life questionnaires. At a mean follow-up of 51 (range, 22 to 68) months, continence rates were 88% overall, with a 91% cure rate for type II and 84% for type III stress incontinence. Preoperative urge incontinence resolved in 81 of 109 (74%), whereas de novo urgency developed in 7% of women. Secondary procedures were required in 14 patients for management of incontinence, and 5 required urethrolysis. Of the 247 women, 235 (95%) completed questionnaires, and 92% reported a high degree of satisfaction with low-symptom distress scores. In another study by Chaikin et al. (1998), 251 patients were followed for more than 1 year after a fascial sling; 92% of patients were objectively cured or improved. Most of the postoperative incontinence was urge incontinence. Permanent urinary retention developed in 2% of patients. Synthetic materials are readily available, allow the patient to avoid a harvesting procedure, and appear effective, but they have the disadvantage of potentially generating a foreign body inflammatory reaction. This may result in a slightly higher risk of erosion and fistula formation compared with autologous materials, although this has not been proved in a comparative trial. The most extensive experience has been obtained using Mersilene and polypropylene mesh. Several authors have reported short-term objective cure rates of 73% to 93%. Polypropylene mesh is also used in the TVT procedure, which will be reviewed later. The intermediate and long-term results for suburethral slings suggest that the 10-year continence rate is similar to the 1-year continence rate. In fact, Bidmead and Cardozo (2000) noted that if sling procedures are successful after 6 months, they are likely to remain successful for many years. As with Burch colposuspension, most of the chronic complications after sling procedures relate to voiding dysfunction and urge symptoms. The mean incidence of postoperative voiding disorders is 12.8% (range, 2% to 37%). Long-term self-catheterization has been reported in anywhere between 1.5% and 7.8% of patients, although a figure of 2% may be more realistic. Urge incontinence after slings, like colposuspension, occurs in 3% to 30% of cases and can be a persistence of preexisting urge symptoms or de novo development (about 7%). Vaginal and urethral erosions occur in up to 5% of patients, mostly after synthetic slings. Sling revision or removal is reported to occur in 1.8% to 35% of patients after synthetic slings. Modifications designed to achieve greater stabilization, such as anchorage to the pubic bone, do not seem to result in improvement over existing techniques and carry a risk of osteomyelitis at the site of anchorage. In the American Urological Association review by Leach et al. (1997), the general level of evidence for articles related to sling procedures was B or C by the Agency for Health Care Policy and Research (AHCPR) guidelines. However, many urologists in the United States are encouraged by the results of slings as primary and secondary procedures for SUI. This trend is illustrated by examining the results of two surveys in which American urologists were asked which procedure they
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used for SUI related to urethral hypermobility. In a 1996 report by Gee et al., 71% of urologists used needle suspensions and 25% used retropubic suspensions. In the 2001 report by Kim et al., 14% of urologists used needle suspensions, 17% used retropubic suspensions, and 68% used slings for type II SUI.
Tension-Free Vaginal Tape The recent swing toward sling procedures has been stimulated by the success of the polypropylene TVT. The procedure is based on a theory of pathophysiology of SUI presented by Petros and Ulmsten (1990, 1995). In their integral theory, impairment of the pubourethral ligaments is one of the primary causes of SUI. Following this view, a narrow strip of polypropylene mesh is placed at the midurethra to compensate for the inefficiency of the pubourethral ligaments. Long-term objective results of the TVT procedure for primary SUI were shown in a Nordic multicenter trial by Nilsson et al. (Int Urogynecol J, 2001); at a median followup of 56 months, 85% of patients were cured, 10.6% were improved, and 4.7% were regarded as failures. No cases existed of mesh erosion or permanent retention. Others have reported comparable statistics. The randomized trial comparing the results of TVT versus Burch colposuspension by Ward and Hilton (2002) showed similar objective and subjective cure rates from both procedures. In this study, where TVT and colposuspension were used as a primary procedure, the reporting of complete dryness in both groups was 38% and 40%, respectively. Dryness with stress was reported in 66% and 68% of women. Strict definitions of cure and the fact that nonattenders and patients with missing data were recorded as treatment failures explain the lower cure rates compared with other studies. The operating time of TVT is relatively short, and the majority of patients can undergo TVT without general anesthesia as an outpatient or overnight stay. Complications appear to be less severe and, possibly, less common than with pubovaginal fascial slings. In the multicenter study by Ward and Hilton (2002), intraoperative bladder perforation was recognized in 9% of procedures, but no long-term sequelae resulted. Nilsson et al. (2001) reported that 56% of patients with mixed incontinence had resolution of their urge symptoms after TVT, and 6% developed new symptoms of urge incontinence, findings that are similar to other sling procedures. Short-term voiding disorder is described in 4.3% of women, and retention requiring transection of the tape occurs in 1% to 2.8%. Mesh erosion into the vagina or urinary tract, as well as pelvic hematoma and bowel perforation, can occur but are very rare. Complications after TVT in 1 year in Finland are shown in Table 16-1. Transobturator slings, like TVT, can be performed as an outpatient with minimal postoperative pain and relatively rapid return to normal voiding. Although preliminary reports seem encouraging, long-term outcomes for transobturator slings are not yet available, and comparative trials to TVT, pubovaginal sling, or Burch procedure have not been done. The success of TVT has encouraged the introduction of similar products with modified methods of midurethral sling placement (retropubic “top-down” and transobturator). As with pubovaginal slings, the true comparison between the
Table 16-1
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TVT Complications in 1455 Patients in 38 Hospitals in Finland in 1999
Bladder perforation Minor voiding difficulties Retention Retropubic hematoma Major vessel injury Need for postoperative laparotomy for a complication
3.8% 7.6% 2.5% 1.9% 0.07% 0.3%
From 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, with permission.
outcome of these materials and modified methods compared with TVT can only be done in properly designed clinical trials.
COMPLICATIONS Lower Urinary Tract Injury Injury to the bladder or urethra can result from any of the vaginal procedures previously described for stress incontinence. This can occur during the dissection of the vaginal epithelium off the underlying adventitia or during the lateral dissection below the inferior pubic ramus, which is performed for certain needle procedures and suburethral sling procedures. Injury to the urethra and bladder are more common in patients who have had previous anterior vaginal wall or bladder neck surgery. Cystotomy and urethrotomy should be repaired in layers at the time of the injury and continuous bladder drainage instituted postoperatively for 7 to 14 days to allow adequate healing. Needle suspension-related injury to the bladder can occur during needle insertion or suprapubic transfer of suspension sutures. Inadvertent stitch or needle penetration into the bladder lumen can occur with procedures that entail blind passage of the needle ligature through the retropubic space. Intraoperative cystoscopy is mandatory and should identify bladder injury or inadvertent stitch penetration. If intravesical suture or mesh is noted, it should be removed and passed again under direct finger guidance. Unrecognized injury or suture penetration in the bladder lumen may result in postoperative detrusor overactivity, persistent urinary tract infection, or formation of a bladder calculi. Injury to the ureter during vaginal operations for stress incontinence is rare.
Voiding Dysfunction and Retention Voiding difficulty and even retention rarely occur in patients after various anti-incontinence surgeries. No consistent preoperative findings successfully predict which patients will develop postoperative voiding dysfunction. Patients with preoperative voiding dysfunction demonstrated by high postvoid residual urine volume, abnormal uroflowmetry, or absent or weak detrusor contraction on pressure-flow study may be more likely to develop postoperative voiding dysfunction or retention, although this has not been substantiated consistently in published reports. In our opinion, extensive
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dissection required for advanced anterior vaginal wall prolapse and the aggressiveness of the repair probably prolong the time to normal voiding. Because suburethral sling procedures can significantly increase urethral outlet resistance, most complications related to these procedures are secondary to obstruction and result in various forms of voiding difficulty and even permanent retention. The exact incidence of retention after pubovaginal sling procedures is unknown but is quoted in the literature as 2% to 10%. TVT and transobturator slings have lower rates of voiding dysfunction and retention, probably in the range of 1% to 3%. If severe voiding dysfunction or retention results from any anti-incontinence procedure, the surgeon and the patient must decide whether it would be best to undergo a second operation to take down the repair or loosen the sling in the hope of allowing spontaneous normal voiding. If it is decided to take down a procedure or loosen the sling material, this can be accomplished via vaginal or retropubic approach. This is discussed in detail in Chapter 30.
Detrusor Overactivity and Irritative Voiding Symptoms Postoperative detrusor overactivity and irritative symptoms with urgency, frequency, urge incontinence, or dysuria occur in 2% to 50% of patients after various operations for stress incontinence. This may be because of preexisting detrusor overactivity, now unmasked with increased bladder volumes caused by a return of outflow resistance, or de novo (new onset) overactivity possibly related to infection, foreign body reaction, denervation, or anatomic urethral obstruction. De novo detrusor overactivity is usually transient and responds well to bladder retraining and anticholinergic therapy.
Recurrent or Persistent Incontinence Postoperative incontinence after a vaginal anti-incontinence procedure may be caused by immediate surgical failure, development of de novo or worsening of preexisting detrusor overactivity, ISD, or fistula formation. The most common cause of recurrent or persistent incontinence after slings is probably either detrusor overactivity or ISD, but this has not been studied reliably. Fistulas are very rare after sling procedures. Patients with persistent incontinence after slings need re-evaluation with urodynamic studies and appropriate treatment.
Table 16-2
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Hemorrhage Bleeding complications can occur after all of the vaginal operations for incontinence mentioned in this chapter. Excessive bleeding and hematoma formation are more common after procedures that require vaginal entry into and needle passage through the retropubic space (i.e., invasive needle operations and suburethral sling procedures). Excessive intraoperative bleeding may occur during mobilization of the perivesical venous plexus and may be controlled with suture ligation, elevation of the bladder neck resulting in tamponade, or vaginal packing. When excessive bleeding occurs upward in the retropubic space, a technique described by Katske and Raz (1983) can be used in which a sponge-wrapped Foley catheter with a 30-mL balloon is placed into the bleeding space to achieve transvaginal tamponade. Vascular embolization or laparotomy and repair may be required if the bleeding persists. Meticulous surgical technique and knowledge of surgical anatomy are essential for the prevention and management of vascular injuries during these procedures.
Infection and Erosion A subset of complications, including erosion, infection, and sinus formation, occurs more commonly when synthetic materials are used for sling placement. A small proportion of patients may require removal of an eroded permanent suture. These problems are sometimes complicated further by coexisting infection. Although a few cases can be managed conservatively, the majority of the patients require removal of the foreign body or sling material. Because of complications specific to synthetic material, a growing trend occurs toward the use of autologous or donor-directed organic materials for pubovaginal sling procedures.
Nerve Damage Vaginal operations are performed with the patient in the dorsal lithotomy position, which can result in nerve damage from compression or stretch injuries. The nerve most often involved is the common peroneal nerve, but injury to the obturator, sciatic, femoral, or saphenous nerves can also occur (Table 16-2). These injuries usually resolve spontaneously over time. Early recognition and appropriate neurologic and physical medicine consultations are recommended.
Nerves Susceptible to Injury During Vaginal Surgery
Nerve
Location of Injury
Mechanism of Injury
Clinical Presentation
Common peroneal Sciatic
Fibular neck Sciatic notch
Obturator Femoral
Pubic ramus Inguinal ligament
Compression against brace Compression or stretching during hip flexion Compression Compression during hyperflexion of hips
Saphenous Ilioinguinal
Medial aspect of knee Stretching during hyperflexion of hips Lateral to pubic tubercle Nerve entrapment by suspension sutures
Footdrop Weakness during knee flexion or loss of common peroneal or tibial nerve function Weakness of ipsilateral thigh on adduction Quadriceps weakness, gait impairment, decreased sensation over anterior thigh and medial calf Burning or aching pain in medial calf Pain in medial groin, labia, or inner thigh
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Surgical injury to the ilioinguinal nerve can occur during placement and tying of sling material or suspension sutures on the abdominal wall during sling procedures. These patients present with characteristic complaints of pain in the medial groin and inner thigh. Miyazaki and Shook (1992) reported seven cases of ilioinguinal nerve entrapment in their series of 402 needle suspensions. Three patients were treated with surgical suture removal, whereas the remaining four had spontaneous resolution of their symptoms. However, long-term refractory groin pain can result. Because the nerve is most vulnerable to injury near its exit from the superficial inguinal ring, sutures or sling material should be attached and tied medially to the pubic tubercle or body of the symphysis pubis to prevent nerve entrapment.
CONCLUSIONS Long-term data suggest that Burch colposuspension and sling procedures, using autologous or synthetic materials, produce similar objective cure rates of approximately 80% and an additional improvement in about 10% of patients. These results are supported by a few randomized clinical trials as well as a large number of case-series (Strength of Evidence = Levels A and B). Anterior colporrhaphy, needle urethropexy, and paravaginal defect repair have lower cure rates for stress incontinence. However, the 2005 Cochrane Review on slings notes that the data are still too few to make reliable estimates of efficacy, especially compared with other treatments (Bezerra et al., 2005). For slings, in the presence of an increasing number of new (and unproven) materials, a need exists for more research to determine whether the choice of material influences the outcome. Data from a single randomized controlled trial demonstrate a similar success rate of TVT and open Burch colposuspension. However, TVT appears to be superior to laparoscopic Burch colposuspension, based on a recent randomized controlled trial by Paraiso et al. (2004). A relatively large number of cohort studies show cure rates for TVT of 80% to 85% and an overall cure plus improvement rate of about 94%. Long-term complications after pubovaginal slings and TVT are mostly related to voiding dysfunction and urgency. The TVT procedure seems to result in a more rapid return to voiding; although, as with other slings, a small number of cases still result in retention requiring sling transection.
Bibliography Abbas SS, Gasser RF, Chesson RR, Echols KT. The anatomy of midurethral slings and dynamics of neurovascular injury. Int Urogynecol J 2003;14:185. Abouassaly R, Steinberg JR, Lemieux M, et al. Complications of tension-free vaginal tape surgery: a multi-institutional review. BJU Int 2004;94:110. Aldridge AH. Transplantation of fascia for relief of urinary stress incontinence. Am J Obstet Gynecol 1942;44:398. Beck RP, McCormick RN, Nordstrom L. The fascia lata sling procedure for treating recurrent genuine stress incontinence of urine. Obstet Gynecol 1988;72:699. 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.
Bergman A, Elia G. Three surgical procedures for genuine stress incontinence: five-year follow-up of a prospective randomized trial. Am J Obstet Gynecol 1995;173:66. Bergman A, Kooning PP, Ballard CA. Primary stress urinary incontinence and pelvic relaxation: prospective randomized comparison of three different operations. Am J Obstet Gynecol 1989;161:91. Bezerra CA, Bruschini H, Cody DJ. Traditional suburethral sling operations for urinary incontinence in women. Cochrane Database Syst Rev 2005;3: CD001754. Bidmead J, Cardozo L. Sling techniques in the treatment of genuine stress incontinence. Br J Obstet Gynaecol 2000;107:147. Black NA, Downs SH. The effectiveness of surgery for stress incontinence in women: a systematic review. Br J Urol 1996;78:497. Breen JM, Geer BM, May GE. The fascia lata suburethral sling for treating recurrent urinary stress incontinence. Am J Obstet Gynecol 1997;177(6):1363. Bryans FE. Marlex gauze hammock sling operation with Cooper’s ligament attachment in the management of recurrent urinary incontinence. Am J Obstet Gynecol 1979;133:292. Carlin BI, Klutke JJ, Klutke CG. The tension-free vaginal tape procedure for the treatment of stress incontinence in the female patient. Urology 2000;56:28. Cetinel B, Demirkesen O, Onal B, et al. Are there any factors predicting the cure and complication rates of tension-free vaginal tape? Int Urogynecol 2004;15:188. Chaikin DC, Rosenthal J, Blaivas JG. Pubovaginal fascial sling for all types of stress urinary incontinence: long-term analysis. J Urol 1998;160:1312. 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. DeLancey JO. Structural support of the urethra as it relates to stress urinary incontinence: the hammock hypothesis. Am J Obstet Gynecol 1994;170:1713. Delorme E. Transobturator urethral suspension: mini-invasive procedure in the treatment of stress urinary incontinence in women. Prog Urol 2001;11:1306. French. Dietz HP, Ellis G, Wilson PD, Herbison P. Voiding function after tensionfree vaginal tape: a longitudinal study. Aust N Z J Obstet Gynaecol 2004;44:152. Farrell SA, Beckerson LA, Epp A, et al. Tension-free vaginal tape (TVT) procedure. J Obstet Gynaecol Can 2003;25:692. Gee WF, Holtgrewe HL, Albertsen PC, et al. Practice trends of American urologists in the treatment of impotence, incontinence and infertility. J Urol 1996;156:1778. 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. 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 follow-up of 1 year. J Urol 2001;165:159. 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. Hilton P, Stanton SL. Clinical and urodynamic evaluation of the polypropylene (Marlex) sling for genuine stress incontinence. Neurourol Urodyn 1983;2:145. Horbach NS, Blanco JS, Ostergard DR, et al. A suburethral sling procedure with polytetrafluoroethylene for the treatment of genuine stress incontinence in patients with low urethral closure pressure. Obstet Gynecol 1988;71:648. Jarvis GJ. Surgery for genuine stress incontinence. Br J Obstet Gynaecol 1994;101:371. 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. 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. Karram MM, Bhatia NN. Patch procedure: modified transvaginal fascia lata sling for recurrent or severe stress urinary incontinence. Obstet Gynecol 1990;75:461. Karram MM, Segal JL, Vassallo BJ, Kleeman SD. Complications and untoward effects of the tension-free vaginal tape procedure. Obstet Gynecol 2003;101:929.
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Katske FA, Raz S. Use of Foley catheter to obtain transvaginal tamponade. Urology 1983;21:627. Kelly HA, Dunn W. Urinary incontinence in women without manifest injury to the bladder. Surg Gynecol Obstet 1914;18:444. 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. Kleeman S, Goldwasser S, Vassallo B, Karram M. Predicting postoperative voiding efficiency after operation for incontinence and prolapse. Am J Obstet Gynecol 2002;187:49. 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. Klutke C, Siegel S, Carlin B, et al. Urinary retention after tension-free vaginal tape procedure: incidence and treatment. Urology 2001;58:697. Kobashi KC, Govier FE. Management of vaginal erosion of polypropylene mesh slings. J Urol 2003;169:2242. Krissi H, Adam JE, Stanton SL. MRI visualization of the female pelvis in the plane of the tension-free vaginal tape (TVT) procedure. Int Urogynecol J 2003;14:342. Kunde D, Varma R. Feasibility of performing TVT operation for stress urinary incontinence under general anaesthesia. J Obstet Gynaecol 2002;22:663. 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. 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. Lebret T, Lugagne PM, Herve JM, et al. Evaluation of tension-free vaginal tape procedure. Its safety and efficacy in the treatment of female stress urinary incontinence during the learning phase. Eur Urol 2001;40:543. 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. Liapis A, Bakas P, Salamalekis E, et al. Tension-free vaginal tape (TVT) in women with low urethral closure pressure. Eur J Obstet Gynecol Reprod Biol 2004;116:67. Liapis A, Bakas P, Lazaris D, Creatsas G. Tension-free vaginal tape in the management of recurrent stress incontinence. Arch Gynecol Obstet 2004;269:205. Lo TS, Chang TC, Chao AS, et al. Tension-free vaginal tape procedure on genuine stress incontinent women with coexisting genital prolapse. Acta Obstet Gynecol Scand 2003;82:1049. 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. 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. McGuire EJ. Urodynamic findings in patients after failure of stress incontinence operations. Prog Clin Biol Res 1981;78:351. McGuire EJ, Bennett CJ, Konnak JA, et al. Experience with pubovaginal slings for urinary incontinence at University of Michigan. J Urol 1987;138:525. McGuire EJ, Lytton B. Pubovaginal sling procedure for stress incontinence. J Urol 1978;119:82. McGuire EJ, O’Connell HE. Surgical treatment of intrinsic urethral dysfunction: slings. Urol Clin North Am 1995;22:657. Meltomaa S, Backman T, Haarala 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. Meschia M, Pifarotti P, Bernasconi F, et al. Tension-free vaginal tape: analysis of outcomes and complications in 404 stress incontinent women. Int Urogynecol J 2001;12(Suppl 2):S24. Minassian VA, Al Badr A, Drutz HP, Lovatsis D. Tension-free vaginal tape, Burch, and slings: are there predictors for early postoperative voiding dysfunction? Int Urogynecol J Pelvic Floor Dysfunct 2004;15:183. Miyazaki F, Shook G: Ilioinguinal nerve entrapment during needle suspension for stress incontinence. Obstet Gynecol 1992;80:246. Moran PA, Ward KL, Johnson D, et al. Tension-free vaginal tape for primary genuine stress incontinence: a two-centre follow-up study. BJU Int 2000;86:39.
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Morgan JE, Farrow GA, Steward FE. The Marlex sling operation for the treatment of recurrent stress urinary incontinence. A 16-year review. Am J Obstet Gynecol 1985;151:224. Morgan TO, Westney OL, McGuire EJ. Pubovaginal sling: 4-year outcome analysis and quality of life assessment. J Urol 2000;163:1845. Moss E, Toozs-Hobson P, Cardozo L, et al. A multicentre review of the tension-free vaginal tape procedure in clinical practice. J Obstet Gynaecol 2002;22:519. Muir TW, Tulikangas PK, Paraiso MF, Walters MD. The relationship of tension-free vaginal tape insertion and the vascular anatomy. Obstet Gynecol 2003;101:933. Mutone N, Brizendine E, Hale D. Factors that influence voiding function after the tension-free vaginal tape procedure for stress urinary incontinence. Am J Obstet Gynecol 2003;188:1477. Mutone N, Mastropietro M, Brizendine E, Hale D. Effect of tension-free vaginal tape procedure on urodynamic continence indices. Obstet Gynecol 2001;98:638. Nichols DH. The Mersilene mesh gauze hammock for severe urinary stress incontinence. Obstet Gynecol 1973;41:88. 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. 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. 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. Nilsson CG, Kuuva N, Falconer C, et al. Long-term results of the tensionfree vaginal tape (TVT) procedure for surgical treatment of female stress urinary incontinence. Int Urogynecol J 2001;12(Suppl 2):S5. Ogundipe A, Rosenzweig BA, Karram MM, et al. Modified suburethral sling procedures for treatment of recurrent or severe stress urinary incontinence. Surg Obstet Gynecol 1992;175:173. Olsson I, Kroon U. A three-year postoperative evaluation of tension-free vaginal tape. Gynecol Obstet Invest 1999;48:267. Paraiso MF, Walters MD, Karram MM, Barber MD. Laparoscopic Burch colposuspension versus tension-free vaginal tape: a randomized trial. Obstet Gynecol 2004;104:1249. Pereyra AJ. A simplified surgical procedure for the correction of stress incontinence in women. West J Surg 1959;67:223. Perk H, Soyupek S, Serel TA, et al. Tension-free vaginal tape for surgical treatment of stress urinary incontinence: two years follow-up. Int J Urol 2003;10:132. Parker RT, Addison WA, Wilson CJ. Fascia lata urethrovesical suspension for recurrent stress urinary incontinence. Am J Obstet Gynecol 1979;135:843. Petros P, Ulmsten U. An integral theory of female urinary incontinence, experimental and clinical considerations. Acta Obstet Gynecol Scand 1990;69(Suppl 153). Petros P, Ulmsten U. Intravaginal sling plasty. An ambulatory surgical procedure for treatment of female urinary stress incontinence. Scand J Urol Nephrol 1995;29:75. Poliak A, Daniller AI, Liebling RW. Sling operation for recurrent stress incontinence using the tendon of the palmaris longus. Obstet Gynecol 1984;63:850. Rackley RR, Abdelmalak JB, Tchetgen MB, et al. Tension-free vaginal tape and percutaneous vaginal tape sling procedures. Tech Urol 2001;7:90. Rafii A, Darai E, Haab F, et al. Body mass index and outcome of tension-free vaginal tape. Eur Urol 2003;43:288. Rardin CR, Kohli N, Rosenblatt PL, et al. Tension-free vaginal tape: outcomes among women with primary versus recurrent stress urinary incontinence. Obstet Gynecol 2002;100:893. 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. 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. 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. 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.
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Schatz H, Henriksson L. Pain during the TVT procedure performed under local anesthesia. Int Urogynecol J 2003;14:347. Stanton SL, Brindley GS, Holmes DM. Silastic sling for urethral sphincter incompetence in women. Br J Obstet Gynaecol 1985;92:747. Staskin DR, Choe JM, Breslin DS. The Gore-Tex sling procedure for female sphincteric incontinence: indications, technique, and results. World J Urol 1997;15:295. Staskin DR, Plzak L. Synthetic slings: pros and cons. Curr Urol Rep 2002;3:414. Stothers L, Chopra A, Raz S. Vaginal wall sling for anatomic incontinence and intrinsic sphincter damage: efficacy and outcome analysis. J Urol 1995;153:525. Tamussino KF, Hanzal E, Kolle D, et al. Tension-free vaginal tape operation: results of the Austrian registry. Obstet Gynecol 2001;98:732. Ulmsten U. The basic understanding and clinical results of tension-free vaginal tape for stress urinary incontinence. Urologe A 2001;40:269. Ulmsten U, Falconer C, Johnson P, et al. A multicenter study of tensionfree vaginal tape (TVT) for surgical treatment of stress urinary incontinence. Int Urogynecol J 1998;9:210. Ulmsten U, Henriksson L, Johnson P, Varhos G. An ambulatory surgical procedure under local anesthesia for treatment of female urinary incontinence. Int Urogynecol J 1996;7:81. Ulmsten U, Johnson P, Rezapour M. A three-year follow up of tension free vaginal tape for surgical treatment of female stress urinary incontinence. Br J Obstet Gynaecol 1999;106:345.
Vassallo BJ, Kleeman SD, Segal J, Karram MM. Urethral erosion of a tensionfree vaginal tape. Obstet Gynecol 2003;101:1055. Vassallo BJ, Kleeman SD, Segal JL, et al. Tension-free vaginal tape: a qualityof-life assessment. Obstet Gynecol 2002;100:518. Walsh K, Generao SE, White MJ, et al. The influence of age on quality of life outcome in women following a tension-free vaginal tape procedure. J Urol 2004;171:1185. Wang AC, Lo TS. Tension-free vaginal tape. A minimally invasive solution to stress urinary incontinence in women. J Reprod Med 1998;43:429. Ward K, Hilton P. Prospective multicentre randomized trail of tensionfree vaginal tape and colposuspension as primary treatment for stress incontinence. Br Med J 2002;325:1. Ward KL, Hilton P. 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;190:324. Whiteside JL, Walters MD. Anatomy of the obturator region: relations to a trans-obturator sling. Int Urogynecol J 2004;15:223. Williams TJ, TeLinde RW. The sling operation for urinary incontinence using Mersilene ribbon. Obstet Gynecol 1962;19:241. Young SB, Rosenblatt PL, Pingeton DM, et al. The Mersilene mesh suburethral sling: a clinical and urodynamic evaluation. Am J Obstet Gynecol 1995;173:1719.
Laparoscopic Surgery for Stress Urinary Incontinence and Pelvic Organ Prolapse
17
Marie Fidela R. Paraiso
LAPAROSCOPIC RETROPUBIC SURGICAL PROCEDURES 213 Indications 213 Anatomy 214 Operative Technique 214 Clinical Results and Complications 217 Technical Skill Development for Laparoscopic Colposuspension 220 LAPAROSCOPIC SURGERY FOR ENTEROCELE, VAGINAL APEX PROLAPSE, AND RECTOCELE 221 Indications 221 Anatomy 221 Operative Technique 221 Clinical Results and Complications 223 DISCUSSION 224
Since laparoscopic retropubic urethropexy was introduced in 1991, laparoscopic access and techniques have been applied to most abdominal-route and numerous vaginal-route surgical procedures for treatment of urinary incontinence and pelvic organ prolapse. Adoption of laparoscopic sacral colpopexy has increased in the past decade and has recently evolved to robotic assistance. The possible advantages of laparoscopic surgery are improved visualization of anatomy of the space of Retzius and peritoneal cavity because of laparoscopic magnification, insufflation effects, and improved hemostasis; shortened hospitalization resulting in potential cost reduction; decreased postoperative pain and more rapid recovery and return to work; and better cosmetic appearance of smaller incisions. Disadvantages of laparoscopic surgery include a steep learning curve in acquiring suturing skills, technical difficulty of retroperitoneal dissection, increased operating time early in the surgeon’s experience, and possible greater hospital cost secondary to increased operating room time and the use of disposable surgical instruments. These listed disadvantages, inadequate experience in advanced laparoscopy in residency and fellowship programs, and recently introduced minimally invasive midurethral sling and apical suspension procedures have thwarted widespread adoption of laparoscopic surgery for urinary incontinence and prolapse. The literature regarding these procedures consists of many case series from surgeons subspecializing in advanced laparoscopy. Comparative,
adequately powered studies regarding laparoscopic surgery for stress urinary incontinence and prolapse are rare.
LAPAROSCOPIC RETROPUBIC SURGICAL PROCEDURES In the first report, Vancaillie and Schuessler (1991) laparoscopically duplicated the conventional Marshall-MarchettiKrantz (MMK) procedure. Subsequently, Albala et al. (1992) published a case series of MMK and Burch procedures. Many investigators have modified the laparoscopic retropubic colposuspension using varying numbers and types of suture, synthetic mesh, staples, bone anchors, coils, tacks, fibrin sealant, and radiofrequency. Various suturing and needle devices have been used to simplify laparoscopic suturing and knottying, the most difficult skills to acquire. The Burch procedure can be performed via a small laparotomy incision with good long-term success and minimal morbidity. To replace this accepted and effective approach with laparoscopic access, there must be comparable efficacy and an equivalent or better complication rate. If one is to consider performing a laparoscopic retropubic bladder neck suspension, we believe that it should be performed exactly the same as the open procedure. Modifications to the open procedure represent essentially new operations, thus requiring further study and outcome analysis.
Indications After the patient has been diagnosed with urodynamic stress incontinence and has opted for surgical management, the choice of laparoscopic versus open retropubic colposuspension depends on numerous factors: history of previous pelvic or anti-incontinence surgery; history of severe abdominopelvic infection or known extensive abdominopelvic adhesions; patient age and weight; ability to undergo general anesthesia; need for concomitant abdominal, pelvic, or vaginal surgery; patient preference; and operator experience and preference. To date, most laparoscopic colposuspensions have been done for only primary stress incontinence because of difficulty in dissecting retropubic adhesions. Many patients
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choose laparoscopic surgery because of the smaller, more cosmetic incisions, shorter recuperation time, and rapid return to work. We explain to our patients that we perform the same procedure open and laparoscopically and that it is only the route that differs. We also state that the procedure outcomes appear to be comparable to open techniques in our hands based on short-term follow-up.
Anatomy Thorough knowledge of the anatomy of the anterior abdominal wall is mandatory for safe and effective trocar insertion. The umbilicus is approximately at the L3–L4 level, and the aortic bifurcation is at L4–L5. In obese women the umbilicus is caudal to the bifurcation. Thus, the intraumbilical trocar should be introduced at a more acute angle toward the pelvis in thin women and closer to 90 degrees in obese women. The left common iliac vein courses over the lower lumbar vertebras from the right side and may be inferior to the umbilicus. Common iliac arteries course 5 cm before bifurcating into the internal and external iliac arteries. The ureter crosses the common iliac artery at or above its bifurcation. The superficial epigastric artery, a branch of the femoral artery, courses cephalad and can be transilluminated. The inferior epigastric artery branches from the external iliac artery at the medial border of the inguinal ligament and runs laterally to and below the rectus sheath at the level of the arcuate line. Two inferior epigastric veins accompany this artery (Fig. 17-1). The median umbilical ligament, the embryonic urachus, is attached to the apex of the bladder and extends to the umbilicus. The urachus remains patent in some women and may be somewhat vascular. The medial umbilical folds, the peritoneum overlying the obliterated
umbilical arteries, are the lateral landmarks of dissection of the parietal peritoneum during transperitoneal surgery into the space of Retzius. The upper margin of the dome of the bladder is noted approximately 3 cm above the pubic symphysis when the bladder is filled with 300 mL of fluid. Before distention of the bladder, the upper margin of the dome lies several centimeters above the pubic symphysis. The important landmarks of the space of Retzius are Cooper’s ligaments; the accessory or aberrant obturator veins; the obturator neurovascular bundles, which are 3 to 4 cm above the arcus tendineus fasciae pelvis; the bladder neck, which is delineated by placing traction on the Foley bulb; and the arcus tendineus fasciae pelvis and arcus tendineus levator ani, which insert into the pubic bone (Figs. 17-2 and 17-3).
Operative Technique OPERATIVE SETUP AND INSTRUMENTATION The operating room setup is shown in Figure 17-4. The monitor screens should be placed laterally to the legs in direct view of the surgeon standing on the opposite side of the table. The scrub nurse should be in the center if two monitor screens are used; otherwise, the scrub nurse is located behind one surgeon and the electrosurgical unit or harmonic scalpel on the opposite side. After the three-way Foley catheter and uterine manipulator (if needed) have been placed, the vaginal tray with cystoscope is set aside, if desired, for later use. Ideal stirrups for combined laparovaginal cases are the Allen stirrups and Yellofins (Allen Medical Systems, Acton, MA) that have levers that can quickly convert the patient from low to high lithotomy position while preserving sterility of the field. A sterile pouch attached to each thigh is equipped with commonly used instruments, such as unipolar scissors,
External iliac artery and vein Rectus muscle Inferior epigastric artery
Superficial epigastric artery
Inferior epigastric artery and vein
Cooper's ligament
Obturator nerve
Superficial circumflex iliac artery
External iliac artery
Accessory branch Femoral artery
Obturator artery and vein
Pubic branches
10 or 5/12 mm port 5 mm port for all procedures, except 10 mm for colpopexy 5 mm ports, as required Figure 17-1 ■ Anatomy of the anterior abdominal wall and suggested laparoscopic trocar positions.
Figure 17-2
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Anatomy of the pelvic sidewall near Cooper’s ligament.
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Cooper's ligament
Arcus tendineus levator ani
Arcus tendineus fasciae pelvis
Obturator internus muscle and fascia
Obturator canal
Figure 17-3
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Retropubic space anatomy. X identifies suture placement during Burch procedure.
bipolar cautery, graspers, and laparoscopic blunt-tipped dissectors. The irrigation should be set up before making incisions for trocars. For standard suturing technique, needle holder preference is determined by comfort of the surgeon. Conventional and 90-degree self-righting German needle holders (Ethicon EndoSurgery, Inc., Cincinnati, OH) have ratchet spring handles, and the Talon curved needle drivers with spring handles (Cook OB/GYN, Spencer, IN) self-right the needle at an angle, either 45 or 90 degrees to the needle driver shaft, depending on the style chosen. The Storz Scarfi needle holder and notched assistant needle holder (Karl Storz Endoscopy, Culver City, CA) are most like conventional needle holders used during laparotomy. However, the handles are difficult to maintain and may pop open after extended use. The needle holder tips may become magnetized, which hampers needle grasping. Disposable suturing devices have been introduced that include the Endo-stitch (U.S. Surgical Corp., Norwalk, CT) and the Capio CL (Cooper’s ligaments) (Microvasive Boston Scientific, Inc., Natick, MA). Extracorporeal knot-tying is preferred because of technical facility and the ability to hold more tension on the suture. The choice of an open-ended or close-ended knot pusher for extracorporeal knot-tying depends on surgeon preference. Our suture of choice is the double-armed No. 0 Ethibond 36-inch suture on an SH or CT-2 needle (Ethicon, Inc., Somerville, NJ). Our alternative choice for suture is No. 0 Gore-Tex (W.L. Gore & Associates, Inc., Phoenix, AZ). A 48-inch suture is preferred when suturing from ports at the level of the umbilicus. Sterile steel thimbles may be used by the surgeon or assistant when elevating the vagina while the surgeon is placing the stitches in the vaginal wall. SKIN INCISIONS FOR TROCAR SITES
Figure 17-4
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Operating room setup for operative laparoscopy.
Intraumbilical or infraumbilical incisions are made depending on the anatomy of the umbilicus. Many variations of the accessory trocar sites have been described. We use two additional trocars: a 5/12-mm disposable trocar with reducer in the right lower quadrant (if knot-tying from the right) lateral to the right inferior epigastric vessels and a reusable 5-mm port or an additional 5/12-mm disposable trocar, with
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reducer in the left lower quadrant lateral to the left inferior epigastric vessels. Trocars are placed laterally to the rectus muscle, approximately 3 cm medial to and above the anterior superior iliac spine. Based on an anatomic study by Whiteside et al. (2003), we know that ilioinguinal and iliohypogastric nerve entrapment during fascial closure may be reduced if the ports are placed at least 2 cm cephalad to the anterior superior iliac spines. An additional 5-mm port may be placed on the principal surgeon’s side so that he or she can operate with two hands. Both reusable and disposable ports may be secured with circumferential screws to prevent port slippage. Versa Step Plus trocars (U.S. Surgical Corp., Norwalk, CT) allow easy introduction of needles, maintain pneumoperitoneum during extracorporeal knot-tying, and prevent port slippage because of the expandable sleeve. Port placement is shown in Figure 17–1. ROUTE: EXTRAPERITONEAL OR INTRAPERITONEAL The choice of extraperitoneal or intraperitoneal approach depends on whether concomitant intraperitoneal procedures are being performed, on whether the patient has had previous abdominal wall surgery, and on surgeon preference. Previous retropubic surgery is a contraindication for extraperitoneal approach, and low transverse or midline incisions make the dissection more difficult and prone to failure. Some surgeons report less operating time, easier dissection, and fewer bladder injuries with the extraperitoneal route. This route is sometimes easier because the balloon performs the majority of the dissection. We prefer the intraperitoneal approach because it allows a larger operating space for safe, secure, comfortable handling of the suture. Furthermore, a culdoplasty or other intraperitoneal surgery can be performed concomitantly. The intraperitoneal approach begins with insertion of the 0-degree laparoscope (5 mm or 10 mm) through a respective 5- or 10-mm intraumbilical or infraumbilical cannula followed by intra-abdominal insufflation. Inspection of the peritoneal cavity is performed, delineating the inferior epigastric vessels, abdominal and pelvic organs, pelvic adhesions, and coexisting abdominal or pelvic pathology. Two additional trocars (a 5-mm and a 5/12-mm or two 5/12-mm ports) are placed under direct vision, one on each side, as previously noted. All trocars are nondisposable except the 5/12-mm trocar through which 5- and 10-mm instruments are introduced. This site is used for introduction of the needles and sutures. Some surgeons backload the suture through 5-mm ports and introduce and remove needles through the skin incisions. This is easily accomplished in thinner patients. However, trauma to the subcutaneous tissues and inferior epigastric vessels may result with this technique. Furthermore, it is difficult to use this technique with sutures with double-armed needles. The bladder is filled with 200 to 300 mL sterile water or saline (indigo carmine or methylene blue is optional). Using sharp dissection with electrocautery or harmonic scalpel, a transverse incision 2 cm above the bladder reflection between the medial umbilical folds is made. Identification of the loose areolar tissue at the point of incision confirms a proper plane of dissection. Blunt and sharp dissection aiming toward the posterior-superior aspect of the pubic symphysis decreases
risk of bladder injury. Blunt dissection is then carried out inferolaterally on both sides to identify the pubic symphysis, Cooper’s ligaments, and bladder neck. Medial dissection over the urethra should be avoided. The extraperitoneal approach to the space of Retzius is best performed using a balloon dissector (Origin Medsystems, Menlo Park, CA; U.S. Surgical Corp., Norwalk, CT). This approach begins with an infraumbilical incision and modified open laparoscopy. After the anterior sheath of the rectus fascia is incised, a finger is swept around the rectus muscle over the posterior rectus sheath and into the preperitoneal space. Lubricated Hagar dilators can aid blunt dissection to the retropubic space. The space of Retzius is dissected by tunneling the tip of the dissector to the posterior superior aspect of the pubic symphysis. The balloon is subsequently inflated under video guidance. A 10-mm Hasson cannula or its modification (some alternatives have inflatable balloons on the shaft to decrease CO2 loss) is then placed, a 0-degree laparoscope is inserted, and CO2 is insufflated into the preperitoneal space. Further delineation of the retropubic anatomy is achieved with blunt dissection. Two additional ports are placed under direct vision laterally to the inferior epigastric vessels, taking special care to avoid entry into the peritoneal cavity. LAPAROSCOPIC BURCH COLPOSUSPENSION After the space of Retzius is exposed, the surgeon places two fingers in the vagina and identifies the urethrovesical junction by placing gentle traction on the Foley catheter. With elevation of the vaginal fingers, the vaginal wall lateral to the bladder neck is exposed by using a laparoscopic blunt-tipped dissector. As recommended by Tanagho (1976), no dissection is performed within 2 cm of the bladder neck to avoid bleeding and damage to the periurethral musculature and nerve supply. We place stitches in the vaginal wall, excluding the vaginal epithelium at the level of, or just proximal to, the midurethra and bladder neck (see Fig. 17-3). No. 0 nonabsorbable suture is placed in a figure-of-eight stitch incorporating the entire thickness of the anterior vaginal wall. The needle is then passed ipsilaterally through Cooper’s ligaments. If doublearmed suture is used, we make two passes through Cooper’s ligaments and subsequently tie above the ligaments. We place Gelfoam (Pharmacia Upjohn, Inc., Kalamazoo, MI) between the vaginal wall and the obturator fascia before knot-tying to promote fibrosis. With simultaneous vaginal elevation, the suture is tied with six extracorporeal square knots. Two granny half-hitches (equivalent to a surgical knot) and a flat square knot secure the stitch. Our technique for laparoscopic Burch procedure is illustrated in Color Plate 3. Sutures are tied as they are placed to avoid tangling. Midurethral stitches are placed first, although this is a matter of preference. Placing stitches from the contralateral port is easier. For example, a right-handed surgeon elevates the vagina with his or her left hand while simultaneously placing stitches on the patient’s right side through the lower left port. In this circumstance, the principal surgeon must switch sides with the assistant. If the lower quadrant ports are placed higher (at or slightly below the level of the umbilicus), placement of ipsilateral stitches is facilitated because the
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angle to the ipsilateral vaginal wall and Cooper’s ligaments is less acute. The appropriate level of bladder neck elevation is estimated with the assistant’s vaginal hand. The assistant elevates the vaginal wall to place the urethra and bladder neck in a high retropubic position, which does not result in kinking or compression of the urethra. The goal is to elevate bilaterally the vaginal wall to the level of the arcus tendineus fasciae pelvis so that the bladder neck is supported and stabilized by the vaginal wall that acts as a hammock between both “white lines.” In tying the sutures, the surgeon should not reapproximate the vaginal wall to Cooper’s ligaments or place too much tension on the vaginal wall. A suture bridge of 1.5 to 2 cm is common. When double-armed needles are used, application of two 5/12-mm ports can streamline the procedure. A surgeon can use one port for suture and needle introduction and the other port for needle exit and knot-tying. After introducing the first needle, the surgeon takes a stitch through the endopelvic fascia and vaginal wall, then through Cooper’s ligaments, and removes it through the opposite port. The second needle is introduced and an additional stitch is taken perpendicularly in the endopelvic fascia to the first stitch (resulting in a double throw), then through Cooper’s ligaments. The second stitch is removed and extracorporeal knot-tying is performed after placement of Gelfoam. This technique diminishes suture locking. Gore-tex suture is single armed and tends to slip through the tissue much easier than braided polyester suture. LAPAROSCOPIC PARAVAGINAL DEFECT REPAIR The laparoscopic approach to the space of Retzius for the paravaginal defect repair is identical to the Burch procedure. The dissection is carried out laterally with a blunt-tipped dissector until the obturator internus muscle, obturator foramen with neurovascular bundle, and arcus tendineus fasciae pelvis are delineated. A vaginal hand is used to elevate the vagina and medially retract the bladder, thus aiding in the dissection of the vagina and lateral landmarks. Blunt dissection is carried out dorsally until vaginal palpation of the ischial spine is visualized laparoscopically. Starting at the vaginal apex, a No. 2–0 nonabsorbable, 36- or 48-inch suture on a CT-2 needle is used to place a stitch into the full thickness of the vagina (excluding the vaginal epithelium) and then into the arcus tendineus fasciae pelvis, which is 3 to 4 cm below the obturator fossa (Color Plate 4). This is then tied extracorporeally. An additional three to five sutures are placed through the vaginal wall and into the arcus tendineus or fascia of the obturator internus muscle at 1- to 2-cm intervals until the defect is closed. The same procedure is performed on the opposite side. If this procedure is performed concomitantly with the Burch colposuspension, the paravaginal defect repair should be performed first because exposure of the lateral defect decreases after the Burch sutures are tied. We first place the stitch at the level of the ischial spine and then place subsequent distal stitches as needed. GENERAL INTRAOPERATIVE AND POSTOPERATIVE PROCEDURES The patient is instructed to take one bottle of magnesium citrate or equivalent bowel preparation and limit her diet to
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clear liquids on the day before surgery. Placing an orogastric or nasogastric tube to decompress the stomach at the time of surgery is also helpful. Patients receive prophylactic, intravenous antibiotic therapy 30 minutes before surgery. Pneumatic compression stockings are routinely used. The Burch procedure and paravaginal defect repair are performed under general anesthesia in the low lithotomy position. A 16-French three-way Foley catheter with a 20- to 30-mL balloon is attached to continuous drainage, and the irrigation port is connected to sterile water or saline. After all sutures are placed and tied, transurethral cystoscopy or suprapubic telescopy is done to document ureteral patency and absence of sutures in the bladder. A suprapubic catheter is placed, if desired. The surgeon must reinspect the space of Retzius for bleeding while reducing the carbon dioxide insufflation. Routine closure of the peritoneum is performed based on surgeon preference. All ports are removed under direct visualization, and the peritoneum and fascia of all 10- or 12-mm incisions are reapproximated with the fascial closure instrument (Karl Storz, Tuttingen, Germany) or the Grice needle (New Ideas in Medicine, Inc., Clearwater, FL). The skin is closed in a subcuticular fashion. The fascia and subcutaneous fat are infiltrated with a long-acting local anesthetic, such as bupivacaine hydrochloride 0.5%, if desired. Postoperative care consists of oral pain medication (intravenous, if needed), rapid diet advancement, ambulation, and continuation of pelvic muscle exercises. Voiding trials begin as soon as the patient is ambulatory. Intermittent self-catheterization protocols can begin immediately, especially if the patient was preoperatively taught the technique. Alternatively, the suprapubic tube is clamped when the patient is awake. The patient voids with urge or every 3 hours. Voids and post-void residuals are measured and recorded. The patient is allowed to unclamp the suprapubic tube at night and attach it to a catheter bag for drainage. Once the patient has voided more than two thirds of total bladder volume during two serial attempts (voids must be greater than 150 mL), the suprapubic catheter is removed. Many patients are able to go home on the same day if adequately counseled preoperatively. Preoperative teaching includes discussion of postoperative analgesics, the need for a caretaker at home during the immediate recovery period, instruction in catheter care or intermittent self-catheterization, and explanation of goals to be reached before outpatient discharge. Patients are instructed to refrain from sexual intercourse and lifting objects greater than 10 lb for at least 6 weeks. They are cautioned to heed to these instructions despite rapid recovery.
Clinical Results and Complications Numerous case series have reported laparoscopic Burch colposuspension with conventional suturing technique (Table 17-1). Liu (1994) reported the first large series; 132 patients were followed for 3 to 27 months with a 97% cure rate (completely dry) and 10% complication rate (4 bladder injuries, 4 patients with urinary retention, 1 with ureteral obstruction, 3 with detrusor overactivity, and 1 with gross hematuria caused by insertion of a suprapubic catheter). Continence rates among studies vary from 69% to 100%. Five of 14 studies reported objective data. Total operative time varied from 35 to 330 minutes, with means ranging
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Table 17-1
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Cohort Studies of Laparoscopic Burch Colposuspension Using Suturing Technique for Women with Urodynamic Stress Urinary Incontinence
Author (Year)
No. of Patients
Follow-Up (Mo)*
Subjective Data
Objective Data
Cure Rate (%)
Major Complication Rate (%)
Albala et al. (1992) Liu (1994)
10 132
Yes Yes
No Yes
100 96
0 7.4
Gunn et al. (1994) Nezhat et al. (1994) Langebrekke et al. (1995) Carter (1995) Radomski and Herschorn (1996) Flax (1996) Cooper et al. (1996) Lam and Rosen (1997)
15 62 8 50 34 47 113 107
7 18 (3–27) (4–9) (8–30) 3 (12–36) 17.3 (2–15) 8 (1–28) 16 (1.5–36)
Yes Yes Yes Yes No Yes Yes Yes
No Yes Yes No No No No Yes
100 100 87.5 100 85 73 87 98
0 10 25 6 11.8 12.8 23.8 7.4
Papasakelariou and Papasakelariou (1997) Lobel and Davis (1997) Ross (1998) Lee (2001)
32 35 48 160
Yes Yes Yes Yes
No No Yes No
90.6 68.6 89 91
6.3 22.9 6.3 17.2
24 34 24 46
*Single value denotes mean. Values in parentheses denote range.
from 90 to 196 minutes. Most authors reported less blood loss, shorter hospitalization, and less frequent postoperative voiding dysfunction and de novo detrusor overactivity when compared with the abdominal route. As a preliminary observation, many authors reported decreased incidence of urinary retention and detrusor overactivity associated with laparoscopic Burch. Reasons for less-frequent postoperative voiding dysfunction are unknown, and possible explanations include sutures not being tied as tightly, which is intentional or unintentional, as a result of technique variables; less dissection of the periurethral and paracolpium tissues by some surgeons; and less postoperative pain associated with smaller incisions. The largest series of laparoscopic Burch colposuspension for primary urodynamic stress incontinence was reported by Lee et al. (2001). With only 10 patients lost to follow-up at an average of 46 months (range 36 to 60), the authors reported a satisfaction rate of 96%. Complications included 3 (1.9%) bladder injuries that were repaired intraoperatively and 23 (15.3%) patients who required oxybutynin for detrusor overactivity. Moore et al. (2001) reported a 90% objective cure rate for recurrent stress urinary incontinence in 33 consecutive patients at 19 months average follow-up. Several case series have reported modifications of the retropubic urethropexy. Ou et al. (1993) first reported the use of hernia staples and polypropylene mesh in 40 patients who underwent a modified retropubic colposuspension with a cure rate of 100% at 6 months. Von Theobald et al. (1995) sutured Prolene mesh to the vagina and stapled it to Cooper’s ligaments in 37 patients, with 8% of patients experiencing complications (2 bladder injuries and 1 patient with pelvic pain requiring mesh removal 1 year later). Using subjective and objective measures, 70% of patients were completely dry and 16% were highly improved. Hannah and Chin (1996) reported 100 patients in whom mesh and staples or tacks were used. Follow-up ranged from 12 to 24 months, and the cure rate was 91% based on subjective outcome. Lyons
(1994) reported the Nolan-Lyons modification of suturing the vagina and stapling the suture to Cooper’s ligaments in 38 women with stress incontinence; a 92% cure rate at 12 months was found. Henley (1995) described his modification of using staples to secure permanent suture to the vagina and to Cooper’s ligaments in 60 patients; however, no follow-up data were reported. In the French literature, Grossmann et al. (1996) summarized 21 case series, which included a total of 578 patients with follow-up varying from 3 to 21 months (many studies did not include length of follow-up). They found a 96% success rate at 12 months, with a laparoconversion rate of 3.6% and average complication rate of 12.5%. No report has been made of subjective or objective data or a distinction between cure and improvement rates. The authors divided the patients into three groups, which all had similar success rates: intraperitoneal colposuspensions (304), extraperitoneal colposuspensions (171), and mixed vaginal-laparoscopic colposuspensions (69), in which Stamey or Pereyra needles were often used to place the stitches through Cooper’s ligaments. Multiple studies compare laparoscopic Burch colposuspension with other anti-incontinence procedures (Table 17-2). Five randomized controlled trials (RCTs) (Burton, 1999; Carey et al., 2000; Fatthy et al., 2001; Su et al., 1997; Summitt et al., 2000) comparing laparoscopic with open colposuspension show similar or lower cure rates associated with laparoscopic Burch. Moehrer et al. (2003) published a systematic review on laparoscopic colposuspension using the Cochran Incontinence Review Group’s specialized registrar of controlled trials. The authors’ meta-analysis of four RCTs demonstrated that subjective perception of cure showed no difference between groups and ranged from 85% to 96% in the laparoscopic group and 85% to 100% in the open group after 6 to 18 months of followup. When urodynamic studies were analyzed, a significantly lower success rate was shown for laparoscopic compared
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Table 17-2
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Comparative Studies of Laparoscopic Burch Colposuspension
Author (Year) Burton (1993)* Polascik et al. (1995) Lyons (1995) McDougall et al. (1995) Das and Palmer (1995) Ross (1995) Ross (1996) Su et al. (1997) Miannay et al. (1998) Saidi et al. (1998) Burton (1999)* Persson and Wollner-Hanssen (2000) Summitt et al. (2000)* Carey et al. (2001)* El-Toukhy and Davies (2001) Fatthy et al. (2001) Morris et al. (2001) Liang and Soong (2002) Zullo et al. (2001) Üstun et al. (2003) Ankardal (2004) Huang and Yang (2004) Paraiso et al. (2004)
Follow-Up (Mo)
No. of Patients
Lsc Burch Cure (%)
Open Burch Cure (%)
12 20.8/35.6
30/30 12/10
73 83
97 70
>12 12
10/10/10 10/8/23
90 78 †
90
10
10/10/10
12 12 >12 24
30/32 35/34 46/46 36/36
94 91 80 † 68
12.9/16.3 60 12
70/87 30/30 83/78
91 57 83
92 93
12
28/34
93
88
6
104/96
89
94
32
38/49
18
34/40
88
85
72
38/35
77
48
18/23
23/22
77 †
12
30/30
89
11/14
23/23
83
12
120/120
12
82/75
89
21
36/26
81
100
Lsc Modification Cure (%)
Lsc MMK Cure (%)
Raz Cure (%)
75
82
TVT Cure (%)
90 90 ‡
100
93 94 § 96 64
58 †
79
62 ‡
83 73 § 83 92
74 §
84 97
Lsc, Laparoscopic; MMK, Marshall-Marchetti-Krantz; Raz, needle suspension; TVT, tension-free vaginal tape. *Published in abstract form. † Lsc 1 stitch, Burch. ‡ In this modification, bone anchors were used with one stitch on each side. § The staple/tack-mesh modification was used.
with open colposuspension (relative risk [RR] 0.89; 95% confidence interval [CI] 0.82–0.98), with an additional 9% risk of failure for laparoscopic versus open colposuspension. When one poor quality trial was excluded from the analysis for objective cure, the cure rate for stress urinary incontinence was lower but not significantly so for the laparoscopic compared with the open colposuspension (RR 0.91; 95% CI 0.82–1.01), with 8% more failures for laparoscopy compared with open procedures. Based on a single trial by Persson and Wollner-Hanssen (2000), two stitches placed on each side of the bladder neck are better than one. When further analyzing the methods of the RCTs, Carey et al. (2000), Fatthy et al. (2001), and Summitt et al. (2000) performed identical procedures by both routes and showed similar cure rates; however, Fatthy
et al. (2001) used only one polypropylene suture on each side. The main criticisms of Burton’s (1999) trial are that he had not gained sufficient experience with laparoscopic colposuspension before initiating the study and that the suture used was absorbable with a smaller needle, which may have included insufficient thickness of tissue. Similarly, Su et al. (1997) used three absorbable sutures in the open Burch compared with a single nonabsorbable suture in the laparoscopic procedure. Unfortunately, three of the five RCTs,—those of Burton, Carey et al., and Summitt et al.—have been published as abstracts only. Several cohort studies (Miannay et al., 1998; Ross, 1995; Saidi et al., 1998) have shown similar cure rates between laparoscopic and open colposuspension (see Table 17-2). Huang and Yang (2004) used ultrasound cystourethrography to compare laparoscopic and open Burch
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and found that resting and straining positions at 12 months were similar. Three studies, thus far, compare tension-free vaginal tape (TVT) procedure with laparoscopic retropubic procedures (see Table 17-2). In a prospective randomized trial comparing TVT and laparoscopic Burch urethropexy, Üstun et al. (2003) showed 83% cure in both groups. Longer operative times, hospital stay, and duration of catheterization were reported in the laparoscopic Burch group. In a two-center randomized trial comparing TVT and laparoscopic Burch colposuspension, Paraiso et al. (2004) found a higher cure rate of 97% for TVT versus 81% for laparoscopic Burch, based on urodynamic studies at 1 year (p = .056). Postoperative subjective symptoms of incontinence (stress, urge, and any) were reported significantly more often in the laparoscopic Burch group than in the TVT group (p < .04 for each category). Operative times were significantly longer for the laparoscopic Burch group. Hospital stay, total cost, and duration of catheterization did not differ between groups. In a prospective nonrandomized study comparing TVT with single-stitch laparoscopic bladder neck suspension, Liang and Soong (2002) showed no difference in subjective and objective cure. Operative time and time to resumption of spontaneous urination was significantly lower in the TVT group. Moehrer et al. (2003) reported that trends (no statistical difference) were shown toward a higher complication rate (bladder injury, obturator vein laceration, retropubic hematoma, wound infection, voiding difficulties, cystitis), less postoperative pain, less analgesic requirement, shorter hospital stay, and shorter time to return to normal function for laparoscopic compared with open colposuspension. Operating time is longer for laparoscopic than for open colposuspension in most studies. Estimated blood loss was higher, and duration of catheterization was longer in the open colposuspension group when compared to the laparoscopic group. In general, major intraoperative and short-term complications (urinary tract injury, bowel injury, inferior epigastric and other major vessel injury, blood loss requiring transfusion, and abscess formation in the space of Retzius) are noted in 0% to 25% of cases (see Table 17-1). Bladder injury is the most common major complication but occurs less frequently with increased experience. Laparoscopic bladder injury is detected by direct observation of urine or fluid in the operating field or by gaseous distention of the urinary bag. Most studies do not differentiate between major and minor complications. Major operative and early postoperative complications include urinary tract and bowel injury, inferior epigastric and other major vessel injury, blood loss requiring transfusion, and abscess formation of the space of Retzius. Long-term problems include failure of the procedure requiring resuspension, new-onset urethral intrinsic sphincter deficiency, de novo detrusor overactivity requiring long-term medical management, urinary retention requiring permanent catheterization, voiding pain with or without suture material in the bladder, vesicovaginal fistula, ureteral obstruction requiring reoperation, posterior and apical compartment compensatory defects requiring surgery, small bowel obstruction in a postoperative peritoneal defect, and incisional hernias. No deaths have been reported.
Two cases of foreign body erosions (tacks) into the bladder have been reported after modification of laparoscopic colposuspension using mesh and tacks (Kenton et al., 2002). Modifications of laparoscopic colposuspension using mesh and tacks or staples and diminishing the number of sutures to decrease operating time are not recommended because of compromise to the procedure. Generalizability of the data regarding laparoscopic Burch colposuspension is a concern because the majority of investigations were carried out by expert laparoscopists. Despite the steep learning curve associated with laparoscopic colposuspension, implementation of modifications should be avoided. Three investigations evaluated cost of open and laparoscopic Burch colposuspension. Kung et al. (1996) found total charges for the open Burch urethropexy ($5692) to be significantly higher than for the laparoscopic route ($2398). Average hospitalization was significantly higher for the open group (11.2 days) than for the laparoscopic group (3.6 days). However, the prolonged hospital stay in the open group of this Canadian study is not standard care in the United States. Loveridge et al. (1997) reviewed 49 consecutive patients who underwent laparoscopic (26) and open (23) colposuspension and found that overall in-hospital costs were similar because the increase in operating time in the laparoscopic group offset the longer hospital stay in the open group. Kohli et al. (1997) compared open (21 patients) and laparoscopic (17 patients) colposuspension and found that although mean length of stay was significantly different (2.1 days versus 1.3 days), the total hospital charges were significantly higher for the laparoscopic group ($4960) than for the open group ($4079). This difference was attributed to longer operating time. Ostrzenski (1998) has reported a prospective series of 28 patients who underwent laparoscopic paravaginal defect repair for urodynamic stress incontinence. Mean operative time was 2 hours and 45 minutes, and all patients were discharged on the same day. The cure rate was 93% based on subjective and objective data for minimum follow-up of 24 months. The efficacy of laparoscopic paravaginal defect repair requires additional investigation.
Technical Skill Development for Laparoscopic Colposuspension Before performing laparoscopic retropubic procedures, the surgeon should have adequate experience in performing these procedures by laparotomy and experience in performing operative laparoscopic procedures (adnexectomy, hysterectomy). The technique of laparoscopic suturing may be learned in a stepwise fashion. A surgeon can begin to develop suturing skills on inanimate models in pelvic trainers. Using laparoscopes, cameras, and video monitors to simulate operative conditions and improve depth perception is optimal. The next step involves performing laparoscopic retropubic procedures on pigs or goats in animal labs. Cadaver laboratories are ideal but less accessible. A surgeon should perform initial cases of laparoscopic bladder neck suspensions with an experienced and advanced laparoscopist who is proctoring and assisting. In our experience, a surgeon gains the most proficiency during the first 20 cases.
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LAPAROSCOPIC SURGERY FOR ENTEROCELE, VAGINAL APEX PROLAPSE, AND RECTOCELE Indications The indications for laparoscopic enterocele, vaginal apex prolapse, and rectocele repairs are identical to those for vaginal and abdominal routes. The choice of laparoscopic route is determined by surgeon and patient preference and the laparoscopic skill of the surgeon. Additional factors that should be considered include a history of pelvic or anti-incontinence surgery, previous failed transvaginal colpopexy, a short vagina, severe abdominopelvic adhesions, patient age and weight, need for concomitant pelvic surgery, and the patient’s ability to undergo general anesthesia.
Anatomy When considering the anatomy of the repair of pelvic organ support, a surgeon must keep in mind the three levels of support of the vagina. The upper fourth of the vagina (level I) is suspended by the cardinal/uterosacral complex, the middle half (level II) is attached laterally to the arcus tendineus fasciae pelvis and the medial aspect of the levator ani muscles, and the lower fourth (level III) is fused to the perineal body. The endopelvic fascia (also referred to as the anterior pubocervical fascia and posterior rectovaginal fascia) contributes to the integrity of the wall of the vagina. All pelvic support defects—whether anterior, apical, or posterior—represent a break in the continuity of the endopelvic fascia and/or a loss of its suspension, attachment, or fusion to adjacent structures. The goals of pelvic reconstructive surgery are to correct all defects, thus reestablishing vaginal support at all three levels, and to maintain or restore normal visceral and sexual function. The anatomic landmarks during laparoscopic enterocele repair are the pubocervical fascia, the rectovaginal fascia, the uterosacral ligaments, and the ureter, which courses along the pelvic sidewall and is approximately 1 to 1.5 cm lateral to the uterosacral ligament as it passes underneath the uterine artery. If a uterosacral ligament vaginal vault suspension is performed, the portion of the uterosacral ligaments proximal to their break from previous attachment to the vagina is delineated. Richardson (1995) describes breaks in the endopelvic fascia and uterosacral/cardinal ligaments rather than attenuation and stretching of tissue as the cause of vaginal apex prolapse. The key anatomic landmarks of sacral colpopexy are the middle sacral artery and vein; the sacral promontory with anterior longitudinal ligament; the aortic bifurcation and the vena cava, which are at the L4–L5 level; the right common iliac vessels and right ureter, which are at the right margin of the presacral space; and sigmoid colon, which is at the left margin. The left common iliac vein is medial to the left common iliac artery and can be damaged during dissection or retraction. The anatomic landmarks of laparoscopic rectocele repair are the rectovaginal septum, made up of Denonvilliers’ fascia, and its lateral attachment to the medial aspect of the levator ani muscles. Denonvilliers’ fascia is the endopelvic
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fascia attached superiorly to the uterosacral cardinal ligament complex, laterally to the superior fascia of the levator ani muscle, and inferiorly to the perineal body. The rectovaginal septum is the posterior point of attachment of the sacral colpopexy mesh. Rectovaginal fascia, rectovaginal septum, and Denonvilliers’ fascia are synonymous. The pubocervical fascia is the anterior point of mesh attachment during sacral colpopexy.
Operative Technique LAPAROSCOPIC MOSCHCOWITZ AND HALBAN PROCEDURES The Moschcowitz procedure is performed laparoscopically exactly as during laparotomy. A No. 0 nonabsorbable 36-inch suture is stitched in the peritoneum around the cul-de-sac in a purse-string fashion and subsequently tied extracorporeally. Additional sutures are placed as needed. The ureters should be examined carefully during and after the Moschcowitz procedure. The peritoneum medial to the ureters may be incised to prevent ureteral kinking. The Halban procedure is performed by suturing No. 0 nonabsorbable suture starting at the posterior vagina and proceeding longitudinally over the cul-de-sac peritoneum and then over the inferior sigmoid serosa. These sutures are tied as they are placed. Sutures should be approximately 1 cm apart. Little risk of ureteral compromise is present with this procedure; however, it is important to visualize the ureters after all sutures are tied. LAPAROSCOPIC ENTEROCELE REPAIR The enterocele sac is dissected laparoscopically or vaginally so that the endopelvic fascial defects are identified and the pubocervical fascia and rectovaginal fascia are delineated. If the enterocele is large, the surgeon excises redundant peritoneum and vagina by the vaginal route, taking care not to foreshorten or narrow the vaginal apex. A vaginal obturator, sponge stick, or equivalent vaginal manipulator (EEA sizer by U.S. Surgical Corp., Norwalk, CT; the CDH by Ethicon Endo-Surgery, Inc., Cincinnati, OH) may be used for delineation of the vaginal apex or rectum when performing the dissection laparoscopically. The pubocervical and rectovaginal fascial edges are reapproximated with a No. 0 nonabsorbable suture in interrupted stitches until the fascial defect is closed. Extracorporeal knot-tying is performed after each stitch is placed, which is often performed concomitantly with a uterosacral ligament vaginal vault suspension so that level I suspension is reestablished. LAPAROSCOPIC UTEROSACRAL LIGAMENT AND VAGINAL VAULT SUSPENSION To suspend the vaginal apex to the uterosacral ligament, the surgeon must dissect and delineate the pubocervical and rectovaginal fascias. The surgeon sutures the full thickness of the uterosacral ligament at the proximal portion of its break with a No. 0 nonabsorbable suture and reattaches it to the vaginal apex with a full thickness stitch incorporating the uterosacral/cardinal ligament complex and rectovaginal fascia, excluding the vaginal epithelium. This stitch is tied extracorporeally, and the opposite uterosacral ligament is reattached in the same fashion. Two or three additional
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stitches are taken more proximally in the uterosacral ligaments on each side to reattach it to the rectovaginal fascia (Color Plate 5). Plication of the uterosacral ligaments is not necessary. If concomitant enterocele repair is performed, the uterosacral ligaments may be tagged before dissection of the posterior vagina and rectovaginal septum so that they are easily identified for subsequent suspension. To protect the ureters, peritoneal incisions may be made laterally to the uterosacral ligaments. The apical vault repair described by Ross (International Urogynecology Journal, 1997) reestablished the lateral and posterior paracervical rings of endopelvic fascia by bringing the rectovaginal septum and cardinal/uterosacral ligaments together. After the peritoneum is dissected off the vaginal apex and the pubocervical fascia and rectovaginal septum are identified, a No. 0 nonabsorbable suture is used to incorporate the left and right uterosacral and cardinal ligaments, the rectovaginal septum, and posterior vaginal wall in purse-string stitches, thus plicating the uterosacral ligaments. The first stitch is placed in the uterosacral ligament approximately 3 to 4 cm proximal to the vaginal apex. Three or more successive stitches are placed until the vaginal apex is reached. The final suture incorporates the pubocervical fascia into the repair. This repair differs from the uterosacral ligament vaginal vault suspension by placement of purse-string sutures resulting in uterosacral ligament plication. LAPAROSCOPIC SACRAL COLPOPEXY In addition to the intraumbilical port, a 5/12-mm trocar should be placed in both lower quadrants for suture introduction. One or two additional 5-mm ports are placed at the level of the umbilicus, lateral to the rectus muscle for simultaneous suturing and/or retraction (see Fig. 17-1). After the ancillary ports are placed, dissection of the peritoneum between the vaginal apex and rectum is performed to delineate the rectovaginal fascia (Color Plate 6). Anterior dissection is performed (taking care to avoid damage to the bladder) if a mesh is stitched to the pubocervical fascia or if enterocele repair is needed. A vaginal obturator, sponge stick, or equivalent vaginal manipulator is used for delineation of the vaginal apex or rectum. If exposure of the sacral promontory and presacral space is not adequate, the patient should be tilted to her left and a reusable snake retractor (Snowden Pencer, Tucker, GA) or fan retractor (Origin Medsystems, Menlo Park, CA) placed through an ancillary port. The peritoneum overlying the sacral promontory is incised longitudinally with laparoscopic scissors or harmonic scalpel (Gynecare, Inc., Somerville, NJ) and extended to the cul-de-sac. A laparoscopic dissector or hydrodissection is used to expose the periosteum of the sacral promontory. If blood vessels are encountered during the dissection, coagulation or clip placement is used to achieve hemostasis. Some surgeons prefer to first dissect the presacral space, thus eliminating the most technically difficult portion of the procedure. A Halban procedure or Moschcowitz culdoplasty may be performed based on surgeon preference or when a deep cul-de-sac is noted. When a concomitant culdoplasty is performed, it is completed after posterior mesh placement.
A 12- × 3.5-cm polypropylene mesh or biologic tissue is introduced through a 5/12-mm port. When a T-shaped mesh is used, a 4- × 3.5-cm mesh is sutured to the larger piece of mesh with a No. 0 nonabsorbable suture before intraperitoneal placement. The mesh is sutured anteriorly to the vaginal apex, with two to three pairs of No. 0 nonabsorbable sutures, and into the posterior vaginal apex and rectovaginal septum, with three to four similar rows of suture. When a T-shaped mesh is used, it is easier to first suture the anterior portion so that the cephalad portion of the mesh may be retracted anteriorly while the posterior rows of sutures are being placed. A second technique used to incorporate a Tshaped mesh is suturing separately two pieces of mesh. The larger piece of mesh is sutured into the posterior wall of the vagina, and the smaller piece of mesh is sutured to the anterior wall. We then sew both pieces together into the vaginal apex and trim the excess anterior mesh. A third technique incorporates two pieces of 12- × 3.5-cm polypropylene mesh or biologic tissue. We first sew on the posterior mesh. The most caudal stitch is placed on the posterior vaginal wall and rectovaginal fascia. After placement of the first stitch, the mesh is threaded through the stitches before introducing the mesh into the peritoneal cavity. The corresponding contralateral stitch is taken and threaded through the mesh to anchor the inferior border of the mesh to the rectovaginal septum or perineum. (Note that a 15- to 18-cm mesh length may be required for laparoscopic sacral colpoperineopexy.) The sutures are tied extracorporeally as they are placed. Care is taken to place the stitches through the entire thickness of the vaginal wall, excluding the epithelium. The surgeon sutures the mesh to the longitudinal ligament of the sacrum in two rows of two No. 0 nonabsorbable sutures (Color Plate 7). No undue tension is placed on the mesh. Titanium tacks or hernia staples may also be used to attach the mesh to the anterior longitudinal ligament of the sacrum. The redundant portion of the mesh is excised, and the peritoneum is reapproximated over the mesh with a No. 2–0 polyglactin suture. If the mesh remains exposed, sigmoid epiploic fat may be sutured over it. A concomitant laparoscopic Burch colposuspension is performed, if the patient has urethral hypermobility with urodynamic stress incontinence. A paravaginal defect repair is performed, if needed, to treat anterior vaginal wall defects. If rectal prolapse is present, a rectopexy with or without sigmoid resection can be performed laparoscopically. We perform these combined cases with our colorectal surgery colleagues. Our technique for sacrohysteropexy (sacrocervicopexy) involves dissection of the rectovaginal space approximately one third to one half of the length of the posterior vaginal wall. A 3.5- × 12-cm polypropylene mesh or biologic tissue graft is stitched to the posterior vaginal wall with a No. 0 nonabsorbable suture in several rows along the rectovaginal fascia and posterior cervix to the level of the internal os of the cervix. Peritoneal closure of the mesh is then performed. LAPAROSCOPIC RECTOCELE REPAIR The rectovaginal septum is opened using electrocautery, harmonic scalpel, or laser. Blunt dissection with blunt-tipped dissectors or dolphin-tipped dissectors, hydrodissection, or sharp dissection may be used to open the rectovaginal space
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down to the perineal body. This dissection should follow surgical planes and be bloodless. The perineal body is sutured to the rectovaginal septum. The rectovaginal fascial defects are closed with a No. 0 nonabsorbable suture. If the rectovaginal fascia is detached from the iliococcygeus fascia, it is reattached with a No. 0 nonabsorbable suture. The medial aspects of the levator ani muscles may also be plicated, but care should be taken to avoid a posterior vaginal ridge. Lyons and Winer (1997) have reported the use of polyglactin mesh in extensive rectocele repairs. Most surgeons prefer rectocele repair by vaginal route.
Clinical Results and Complications The current gynecologic literature for laparoscopic pelvic reconstruction is sparse and consists of descriptive studies with short-term follow-up. Several reports of laparoscopic rectopexy in the colorectal surgery literature are beyond the scope of this chapter. No reports evaluate clinical results and complications of uterosacral shortening and culdoplasty, although these techniques have been described by a few authors. Lyons and Winer (1995) reported 276 enterocele repairs or prophylaxis with Halban or Moschcowitz procedures and noted no complications other than trocar site infections. Cadeddu et al. (1996) described a modified Moschcowitz procedure, approximating the posterior vaginal fascia with the anterior wall of the rectum. Koninckx et al. (1995) used the carbon dioxide laser for vaporization of the enterocele sac, followed by uterosacral shortening and suspension of the posterior vaginal wall. Lyons and Winer (1997) evaluated prospectively, at 3-month intervals for 1 year, 20 patients who underwent laparoscopic rectocele repair with polyglactin mesh and concomitant reparative procedures. An objective telephone interviewer asked a series of questions with regard to bowel and sexual function. The mean operative time for rectocele repair was 35 minutes (range, 20 to 48 minutes). Estimated blood loss was minimal and hospital stay was less than 24 hours. Eighty percent of patients had symptomatic relief of digital defecation and prolapse at 1 year. A small number of reports is documented of laparoscopic repair of vaginal apex prolapse. Nezhat et al. (1994) reported a series of 15 patients who underwent laparoscopic sacral colpopexy in whom the mean operative time was 170 minutes (range, 105 to 320 minutes) and mean blood loss was 226 mL (range, 50 to 800 mL). The mean hospital stay was 2.3 days, excluding a case converted to laparotomy for presacral hemorrhage. The cure rate for apical prolapse was 100% at 3 to 40 months. Lyons (1995) reported 4 laparoscopic sacrospinous fixations and 10 laparoscopic sacral colpopexies, with operative times comparable to vaginal and abdominal approaches. He reported less intraoperative and postoperative morbidity with the laparoscopic route; this was attributed to a superior anatomic approach and visualization of anatomic structures. Nezhat et al. (1994) and Lyons (1995) used mesh and suture, and, at times, they stapled the mesh into the longitudinal ligament of the anterior sacrum. Ross (Journal of the American Association of Gynecologic Laparoscopists, 1997) evaluated 19 patients with prospective posthysterectomy vaginal apex prolapse with extensive preoperative and postoperative testing, including multichan-
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nel urodynamics and transperineal ultrasound. All patients underwent sacral colpopexy, Burch colposuspension, and modified culdoplasty. Paravaginal defect repair and posterior colporrhaphy were added as indicated. The author reported seven complications: three cystotomies, two urinary tract infections, one seroma, and one inferior epigastric vessel laceration. Five patients had recurrent defects that were all less than grade 2 (two paravaginal defects and three rectoceles). Vaginal length ranged from 10.8 to 12.1 cm and all sexually active patients reported no sexual dysfunction. All patients but four voided spontaneously and none required more than 4 days of catheterization. All were discharged within 24 hours. The cure rate at 1 year was 100% for vaginal apex prolapse and 93% for stress incontinence, although two patients were lost to follow-up. In another study, Ross (2004) prospectively analyzed 51 cases of laparoscopic sacral colpopexy for grade III or IV apical vaginal prolapse. Forty-three patients demonstrated an objective cure rate of 93% at the vaginal apex during their 5-year follow-up visit. Complications included one partial small bowel obstruction secondary to bowel adherence to the mesh and two locally treated mesh erosions. The author concluded that patient recovery was greatly enhanced with the majority of patients requiring only an overnight hospitalization. Gadonneix et al. (2004) reported the use of two separate meshes for laparoscopic sacral colpopexy with or without Burch colposuspension in 46 consecutive patients with primary vaginal apex prolapse, with or without primary stress incontinence. Mean operating time was 171 minutes and mean hospital stay was 4 days. Median follow-up was 24 months (range, 12 to 60). Eleven percent of patients required conversion to laparotomy. Complications included de novo urge incontinence in 5% of patients, laparoscopically treated bladder injury in 7% of patients, and 12% recurrence of rectoceles (occurring only in women who had undergone laparoscopic Burch colposuspension compared with no colposuspension; P = .036). One patient developed obstructed defecation, which the authors attributed to excessive mesh tension. At the Cleveland Clinic we compared our first 56 consecutive laparoscopic sacral colpopexies to 61 consecutive open sacral colpopexies performed during the same period (Paraiso et al., 2005). Mean follow-up was 14 and 16 months in the laparoscopic and open groups, respectively. Laparoscopic sacral colpopexy and concomitant procedures required a significantly longer operating time when compared with open sacral colpopexy, with mean operating times of 269 versus 218 minutes. However, mean hospital stay was significantly longer in the open group than the laparoscopic group: 4 versus 1.8 days. We found similar clinical outcomes and reoperation rates. Our sample size was too small to determine differences in complications. Long-term outcomes of laparoscopic sacral colpopexy were reported by Higgs et al. in 2005. One hundred and three women with a median follow-up of 66 months were contacted and asked to complete questionnaires. Sixty-six patients underwent physical examination with the POPQ system. Overall, 79% reported subjective cure or improvement of prolapse symptoms, whereas 38% still complained of prolapse. Among those examined, 92% were cured at the vaginal apex, whereas 42% had a recurrence of prolapse in at least one vaginal segment.
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The literature regarding laparoscopic uterosacral ligament suspension is equally as sparse with no comparative studies. Miklos et al. (1998) reported a series of 17 women who underwent laparoscopic uterosacral ligament identification with site-specific vaginal repair of enterocele and rectocele. They reported mild asymptomatic apical prolapse in 12% of patients at a mean of 6 months (range, 1 to 17). More recently, Seman et al. (2003) reported their 2-year experience with laparoscopic pelvic reconstruction. They retrospectively assessed 73 consecutive women who underwent various laparoscopic procedures for genital prolapse with a mean follow-up of 8 months (range, 0 to 26). Fortyseven patients underwent uterosacral vaginal vault suspension with an objective success rate of 100%.
DISCUSSION Laparoscopy is a means of less-invasive surgical access, not a unique procedure, and its use is expanding rapidly in all surgical specialties. We believe that the laparoscopic and open Burch procedures should be identical in operative techniques. Bladder injury is probably more common with laparoscopy, but the risk of cystotomy decreases with surgical experience. Complications associated with open Burch bladder neck suspension, such as wound infection and hernias, are rare with the laparoscopic route. The benefits of improved visualization of anatomic structures and the small incisions associated with the laparoscopic approach are desirable, particularly in obese patients. The advantages of less postoperative pain, shorter hospitalization, shortened recovery period, and earlier return to work are very popular with patients, but these advantages are partially offset by increased operating time and, possibly, increased cost. The operating time and cost will probably decrease as surgeons gain experience with the advanced laparoscopic techniques of suturing and knot-tying. However, the technical ease and clinical success associated with midurethral sling procedures and the steep learning curve in development of laparoscopic suturing skills may deter many gynecologic surgeons from performing retropubic procedures by this approach. Although over 50 articles are published on laparoscopic colposuspension, the data are influenced by many confounding variables. A meta-analysis by Moehrer et al. (2003) of the randomized clinical trials comparing laparoscopic and open colposuspensions shows similar subjective cure rates with an additional 8% risk of objective failure for laparoscopic compared with open colposuspension. Although it is possible that no difference exists between laparoscopic and open colposuspension, a trend appears to be moving toward lower cure rates with the laparoscopic Burch procedure. One- to two-year follow-up data from one randomized clinical trial and one nonrandomized prospective trial show similar cure rates of TVT to laparoscopic colposuspension. One recently published randomized trial (Paraiso et al., 2004) demonstrated similar subjective improvement and patient satisfaction after both laparoscopic Burch colposuspension and TVT. However, TVT resulted in significantly greater subjective cure rates for stress incontinence
than the laparoscopic Burch colposuspension. Also, substantially more subjects demonstrated urodynamic stress incontinence during urodynamic testing 1 year after surgery in the laparoscopic Burch colposuspension group than in the TVT group (Absolute risk increase 15.6%; P = .056). Multiple outcome measures were analyzed, which confirmed the superior efficacy of the TVT procedure. The evidence for laparoscopic Burch colposuspension is limited by short-term follow-up, small numbers, and poor methodology in some studies; therefore, the value of this procedure cannot be determined. Further well-designed and adequately powered randomized trials are required. We do not recommend the staple/tack-mesh modification because of multiple comparative trials showing significantly lower cure rates compared with standard laparoscopic and open Burch colposuspension and because of the increased potential of staple- and mesh-related complications. The principles of laparoscopic reparative procedures for enterocele, rectocele, and vaginal apex prolapse are not new; the difference is the route by which they are performed. Adequate laparoscopic suturing skills are essential in performing these procedures. The increase in operating time may increase the cost of the procedure, especially early in a surgeon’s experience. A review regarding innovations in prolapse surgery by Deval and Haab (2003) stated that laparoscopic approaches for pelvic organ prolapse are the least used because of the great degree of technical difficulty associated with laparoscopic suturing. However, the greatest potential for laparoscopic advances and innovations may be for surgeries for prolapse. We believe that laparoscopic sacral colpopexy will gain popularity because the abdominal sacral colpopexy remains the most proven and effective surgery for cure of severe apical prolapse. Pelvic floor surgeons in specialized centers will strive to offer their patients pelvic reconstruction by laparoscopic route. Many centers are applying robotic assistance to laparoscopic sacral colpopexies with some success. More comparative studies and prospective clinical trials with long-term follow-up are warranted.
Bibliography LAPAROSCOPIC RETROPUBIC SURGICAL PROCEDURES Albala DM, Schuessler WE, Vancaillie TG. Laparoscopic bladder suspension for the treatment of stress incontinence. Semin Urol 1992;10:222. Ankardal M, Ekerydh A, Crafoord K, et al. A randomized trial comparing open Burch colposuspension using sutures with laparoscopic colposuspension using mesh and staples in women with stress urinary incontinence. BJOG 2004; 111:974 Aslan P, Woo HH. Ureteric injury following laparoscopic colposuspension. Br J Obstet Gynaecol 1997;104:266. Birken RA, Leggett PL. Laparoscopic colposuspension using mesh reinforcement. Surg Endosc 1997;11:1111. Burton G. A randomised comparison of laparoscopic and open colposuspension (abstract). Neurourol Urodyn 1993;13:497. Burton G. A three-year prospective randomised urodynamic study comparing open and laparoscopic colposuspension (abstract). Neurourol Urodyn 1997;16:353. Burton G. A five-year prospective randomized urodynamics study comparing open and laparoscopic colposuspension (abstract). Neurourol Urodyn 1999;18:295–296. Carey M, Rosamilia A, Maher C, et al. Laparoscopic versus open colposuspension: a prospective multicentre randomized single-blind study (abstract 8). Neurourol Urodyn 2000;19:389. Carter JE. Laparoscopic bladder neck suspension. Endosc Surg 1995;3:81.
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Classi R, Sloan PA. Intraoperative detection of laparoscopic bladder injury. Can J Anaesth 1995;42:415. Cooper MJ, Cario G, Lam A, et al. A review of results in a series of 113 laparoscopic colposuspensions. Aust N Z J Obstet Gynaecol 1996;36:44. Das S, Palmer JK. Laparoscopic colpo-suspension. J Urol 1995;154:1119. Dorsey JH, Cundiff G. Laparoscopic procedures for incontinence and prolapse. Curr Opin Obstet Gynecol 1994;6:223. Dorsey JH, Sharp HT, Chovan JD, et al. Laparoscopic knot strength: a comparison with conventional knots. Obstet Gynecol 1995;86:536. El-Toukhy TA, Davies AE. The efficacy of laparoscopic mesh colposuspension: results of a prospective controlled study. BJU Int 2001;88:361. Fatthy H, El Hao M, Samaha I, Abdallah K. Modified Burch colposuspension: laparoscopy vs laparotomy. J Am Assoc Gynecol Laparosc 2001;8:99. Flax S. The gasless laparoscopic Burch bladder neck suspension: early experience. J Urol 1996;156:1105. Frankel G, Kantpong M. Sixteen-month experience with video-assisted extraperitoneal laparoscopic bladder neck suspension. J Endourol 1993;9:259. Grossmann T, Darai E, Deval B, et al. Place de l’endoscopie dans la chirurgie de l’incontinence urinaire. Ann Chir 1996;50:896. Gunn GC, Cooper RP, Gordon NS, et al. Use of a new device for endoscopic suturing in the laparoscopic Burch procedure. J Am Assoc Gynecol Laparosc 1994;2:64. Hannah SL, Chin AL. Laparoscopic retropubic urethropexy. J Am Assoc Gynecol Laparosc 1996;4:47. Henley C. The Henley staple-suture technique for laparoscopic Burch colposuspension. J Am Assoc Gynecol Laparosc 1995;2:441. Huang WC, Yang JM. Anatomic comparison between laparoscopic and open Burch colposuspension for primary stress urinary incontinence. Urology 2004;63:671. Kenton K, Fitgerald MP, Brubaker L. Multiple foreign body erosions after laparoscopic colposuspension with mesh. Am J Obstet Gynecol 2002;157:252. Kiilholma P, Haarala M, Polvi H, et al. Sutureless colposuspension with fibrin sealant. Tech Urol 1995;1:81. Kohli N, Jacobs PA, Sze EH, et al. Open compared with laparoscopic approach to Burch colposuspension: a cost analysis. Obstet Gynecol 1997;90:411. Kung RC, 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. Lam AM, Jenkins GJ, Hyslop RS. Laparoscopic Burch colposuspension for stress incontinence: preliminary results. Med J Aust 1995;162:18. Lam AM, Rosen DM. Laparoscopic Burch colposuspension for urinary stress incontinence: results from 109 consecutive cases. Gynaecol Endosc 1997;6:109. Langebrekke A, Dahlstrom B, Eraker R, et al. The laparoscopic Burch procedure: a preliminary report. Acta Obstet Gynecol Scand 1995;74:153. Lee CL, Yen CF, Wang CJ, et al. Extraperitoneal approach to laparoscopic Burch colposuspension. J Am Assoc Gynecol Laparosc 2001;8:374. Liang CC, Soong YK. Tension-free vaginal tape versus laparoscopic bladder neck suspension for stress urinary incontinence. Chang Gung Med J 2002;25:360. Liu CY. Laparoscopic retropubic colposuspension (Burch procedure): a review of 58 cases. J Reprod Med 1993;38:526. Liu CY. Laparoscopic treatment of genuine urinary stress incontinence. Clin Obstet Gynecol 1994;8:789. Lobel RW, Davis GD. Long-term results of laparoscopic Burch urethropexy. J Am Assoc Gynecol Laparosc 1997;4:341. Loveridge K, Malouf A, Kennedy C, et al. Laparoscopic colposuspension. Is it cost-effective? Surg Endosc 1997;11:762. Lyons TL. Minimally invasive retropubic urethropexy: the Nolan-Lyons modification to the Burch procedure. Gynecol Endocrinol 1994;3:40. Margossian H, Pollard RR, Walters MD. Small bowel obstruction in a peritoneal defect after laparoscopic Burch procedure. J Am Assoc Gynecol Laparosc 1999;6:343. McDougall EM, Lutke CG, Cornell T. Comparison of transvaginal versus laparoscopic bladder neck suspension for stress urinary incontinence. Adult Urol 1995;45:641. Miannay E, Cosson M, Querleu D, et al. Compariaison entre la colposuspension par coelioscopie et laparotomie dans le traitement de l’incontinence urinaire d’effort. Etude comparative a partir de 72 cas apparies. Contracept Fertil Sex 1998;26:376.
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Moehrer B, Carey M, Wilson D. Laparoscopic colposuspension: a systematic review. Br J Obstet Gynaecol 2003;110:230. Moore RD, Speights SE, Miklos JR. Laparoscopic Burch colposuspension for recurrent stress urinary incontinence. J Am Assoc Gynecol Laparosc 2001;8:389. Morris AR, Reilly ET, Hassan A, et al. 5–7 year follow up of a randomized trial comparing laparoscopic colposuspension and open colposuspension in the treatment of genuine stress incontinence (abstract). Int Urogynecol J 2001;12(Suppl 3):S6. Nezhat CH, Nezhat F, Nezhat CR, et al. Laparoscopic cystourethropexy. J Am Assoc Gynecol Laparosc 1994;14:339. Ostrzenski A. Genuine stress urinary incontinence in women: new laparoscopic paravaginal reconstruction. J Reprod Med 1998;43:477. Ou CS, Presthus J, Beadle E. Laparoscopic bladder neck suspension using hernia mesh and surgical staples. J Laparoendosc Surg 1993;3:563. Papasakelariou C, Papasakelariou B. Laparoscopic bladder neck suspension. J Am Assoc Gynecol Laparosc 1997;4:185. Paraiso MF, Falcone T, Walters MD. Laparoscopic surgery for genuine stress incontinence. Int Urogynecol J 1999;10:237. Paraiso MF, Walters MD, Karram MM, et al. Laparoscopic Burch colposuspension versus tension-free vaginal tape: a randomized clinical trial. Obstet Gynecol 2004;104:1249. Persson J, Wollner-Hanssen P. Laparoscopic Burch colposuspension for stress urinary incontinence: randomized comparison of one or two sutures on each side of the urethra. Obstet Gynecol 2000;95:151. Polascik TJ, Moore RG, Rosenberg MT, et al. Comparison of laparoscopic and open retropubic urethropexy for treatment of stress incontinence. Urology 1995;45:647. Raboy A, Hakim LS, Ferzli G, et al. Extraperitoneal endoscopic vesicourethral suspension. J Laparoendosc Surg 1995;3:505. Radomski SB, Herschorn S. Laparoscopic Burch bladder neck suspension: early results. J Urol 1996;155:515. Ross JW. Laparoscopic Burch repair compared to laparotomy Burch for cure of urinary stress incontinence. Int Urogynecol J 1995;6:323. Ross JW. Multichannel urodynamic evaluation of laparoscopic Burch colposuspension for genuine stress incontinence. Obstet Gynecol 1998;91:55. Ross JW. Two techniques of laparoscopic Burch repair for stress incontinence: a prospective randomized study. J Am Assoc Gynecol Laparosc 1996;3:351. Saidi MH, Gallagher MS, Skop IP, et al. Extraperitoneal laparoscopic colposuspension: short-term cure rate, complications, and duration of hospital stay in comparison with Burch colposuspension. Obstet Gynecol 1998;92:619. Smith AR, Stanton SL. Laparoscopic colposuspension. Br J Obstet Gynaecol 1998;105:383. Speights SE, Moore RD, Miklos JR. Frequency of lower urinary tract injury at laparoscopic Burch and paravaginal repair. J Am Assoc Gynecol Laparosc 2000;7:515. 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. Summitt RL, Lucente VL, Karram MM, et al. Randomised comparison of laparoscopic and transabdominal Burch urethropexy for the treatment of genuine stress incontinence (abstract). Obstet Gynecol 2000;95(4 Suppl 1):S2. Tanagho EA. Colpocystourethropexy: the way we do it. J Urol 1976; 116:751. Üstun Y, Engin-Üstun Y, Gungor M, et al. Tension-free vaginal tape compared with laparoscopic Burch urethropexy. J Am Assoc Gynecol Laparosc 2003;10:386. Vancaillie TG, Schuessler W. Laparoscopic bladder neck suspension. J Laparoendosc Surg 1991;1:169. Von Theobald P, Guillaumin D, Levy G. Laparoscopic preperitoneal colposuspension for stress incontinence in women: technique and results of 37 procedures. Surg Endosc 1995;9:1189. Wallweiner D, Grischke EM, Maleika RA, et al. Endoscopic retropubic colposuspension: “Retziusscopy” versus laparoscopy: a reasonable enlargement of the operative spectrum in the management of recurrent stress incontinence? Endosc Surg 1995;3:115. Wattiez A, Boughizane S, Alexandre F, et al. Laparoscopic procedures for stress incontinence and prolapse. Curr Opin Obstet Gynecol 1995;7:317. Whiteside JL, Barber MD, Walters MD, et al. Anatomy of ilioinguinal and iliohypogastric nerves in relation to trocar placement and low transverse incisions. Am J Obstet Gynecol 2003;189:1574.
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Zullo F, Palomba S, Piccione F, et al. Laparoscopic Burch colposuspension: a randomized controlled trial comparing two transperitoneal surgical techniques. Obstet Gynecol 2001;98:738.
LAPAROSCOPIC SURGERY FOR ENTEROCELE, VAGINAL APEX PROLAPSE, AND RECTOCELE Cadeddu JA, Micali S, Moore RG, et al. Laparoscopic repair of enterocele. J Endourol 1996;4:367. DeLancey JO. Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 1992;166:1717. Deval B, Haab F. What’s new in prolapse surgery? Curr Opin in Urol 2003;13:315. Dorsey JH, Sharp HT. Laparoscopic sacral colpopexy and other procedures for prolapse. Baillieres Clin Obstet Gynaecol 1995;9:749. 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. Higgs PJ, Chua HL, Smith AR. Long-term review of laparoscopic sacrocolpopexy. BJOG 2005;112:1134. Koninckx PR, Poppe W, Deprest J. Carbon dioxide laser for laparoscopic enterocele repair. J Am Assoc Gynecol Laparosc 1995;2:181. Lyons TL. Minimally invasive treatment of urinary stress incontinence and laparoscopically directed repair of pelvic floor defects. Clin Obstet Gynecol 1995;38:380. Lyons TL, Winer WK. Vaginal vault suspension. Endosc Surg 1995;3:88.
Lyons TL, Winer WK. Laparoscopic rectocele repair using polyglactin mesh. J Am Assoc Gynecol Laparosc 1997;4:381. 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. Nezhat CH, Nezhat F, Nezhat C. Laparoscopic sacral colpopexy for vaginal vault prolapse. Obstet Gynecol 1994;84:885. Paraiso MF, Walters MD, Rackley RR, et al. Laparoscopic and abdominal sacral colpopexies: a cohort study. Am J Obstet Gynecol 2005;192:1752. Richardson AC. The rectovaginal septum revisited: its relationship to rectocele and its importance in rectocele repair. Clin Obstet Gynecol 1993;35:976. Richardson AC. The anatomic defects in rectocele and enterocele. J Pelvic Surg 1995;1:214. Ross JW. Apical vault repair, the cornerstone of pelvic floor reconstruction. Int Urogynecol J 1997;8:146. Ross JW. Techniques of laparoscopic repair of total vault eversion after hysterectomy. J Am Assoc Gynecol Laparosc 1997;4:173. Ross JW. The role of laparoscopy in the treatment of severe vaginal vault prolapse: 6 to 10 year outcome (abstract). J Am Assoc Gynecol Laparosc 2004;11:S4. Seman EI, Cook JR, O’Shea RT. Two-year experience with laparoscopic pelvic floor repair. J Am Assoc Gynecol Laparosc 2003;10:38. Vancaillie TG. The role of laparoscopy in the management of pelvic floor relaxation. J Am Assoc Gynecol Laparosc 1997;4:147.
Urethral Injection of Bulking Agents for Intrinsic Sphincter Deficiency
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Alfred E. Bent
INDICATIONS AND CONTRAINDICATIONS EVALUATION 228 MATERIALS 228 TECHNIQUES 229 Periurethral Method 229 Transurethral Method 229 Insertion Devices 230 Post-Injection Follow-up 230 COMPLICATIONS 230 SAFETY 231 EFFECTIVENESS 231 FUTURE CONSIDERATIONS 232
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In 1938 Murless reported the use of morrhuate sodium for injection management of urinary incontinence. Since the use of injectable polytetrafluoroethylene (PTFE) in the 1970s for treatment of urinary incontinence, a number of materials for this purpose have gradually emerged. The ideal material is biocompatible, nonimmunologic, and hypoallergenic. It retains its bulking characteristics for a prolonged interval and therefore should not biodegrade or migrate (particle size over 80 μm). The material should be easy to prepare and easy to inject, and the ideal material is safe, readily obtainable, inexpensive, efficacious, durable, and induces minimal tissue reaction. The theory on how injectable materials treat incontinence is by mucosal coaptation with subsequent increased urethral resistance to outflow of urine. Although transmission of pressure to the urethra during increased intra-abdominal pressure may not occur in these patients, the pressure forcing the urine from the bladder through the urethra is resisted by the bulking of the mucosa in the immediate proximal urethra. This essentially prevents involuntary bladder neck opening.
INDICATIONS AND CONTRAINDICATIONS The ideal patient for urethral bulking has both limited mobility of the bladder neck and a poorly functioning sphincteric mechanism. More often she is older; because repeat injec-
tions are usually required over time to maintain effect, this could mean many injections in a young patient. Although some reports indicate equal effectiveness in patients with hypermobility of the bladder neck, others have noted that bulking is not as effective in these patients. The Medicare guidelines for reimbursement were first published in 1994 and then revised in 1996, and indicated that immobility of the bladder neck had to be present. It was not specified as to how immobility was to be determined, but most physicians use a Q-tip test with a straining value of less than 30 to 40 degrees as the cutoff value for hypermobility. In one study, hypermobility was determined radiologically by a standing stress test with 2 cm or greater descent of the bladder neck determined to be hypermobile. The other requirement was initially a leak point pressure of 65 cm H2O or less that was later changed to 100 cm H2O. The measurement of leak point pressure required at least 150 mL of bladder filling, but no requirement was present regarding position of the patient, size of urethral catheter, or kind of effort used to increase the intra-abdominal pressure. One standard method is to do the test in the sitting position, with 200 mL in the bladder, using an 8-French catheter, and asking to patient to gradually strain harder and harder until urine leakage is observed. Certain patients respond better to periurethral bulking. Should the procedure provide no relief after two injections, subsequent ones are usually futile. A suburethral sling can be performed after periurethral bulking without concern for residual material. It may be preferable to use a nonsynthetic sling in those patients who have bulking agents that do not biodegrade, although no study has shown this. If a surgery has first been performed, either an anti-incontinence procedure or other pelvic floor surgery, and stress incontinence persists or recurs, no contraindication to using a bulking agent is known, and often it is very effective. This may be done as early as 6 weeks after surgery. As stated, bulking agents are not generally indicated for patients with urethral hypermobility. In some cases in highrisk patients with prolapse and stress incontinence, a pessary has provided excellent control of pelvic organ prolapse, and some temporary stabilization of bladder neck mobility has been present. Periurethral bulking may be used in this patient to treat the potential stress incontinence that was unmasked after the prolapse was reduced.
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Contraindications to the use of periurethral bulking include active urinary tract infection, high residual urine (>100 mL), severe detrusor overactivity, and reduced bladder capacity (<250 mL). Periurethral bulking can be done after radiation therapy, but results have not been encouraging.
EVALUATION Evaluation before therapy includes a history, physical examination, neurologic screen, 24-hour voiding diary, postvoid residual urine determination, and urinalysis and/or culture. A cystometrogram with leak point pressure determination and cystoscopy complements this. The procedure needs to be fully explained to the patient, including the predicted effectiveness and the probable need for repeat injections.
MATERIALS (see Box 18-1) Contigen (C R Bard Inc., Covington, GA) was approved by the U.S. Food and Drug Administration (FDA) in Washington, DC, in 1993. The material is prepared by a glutaraldehyde cross-linking of bovine dermal collagen, which is dispersed in phosphate-buffered physiologic saline that may comprise up to 65% of the total volume. The material contains 95% of type I collagen and 1% to 5% of type III collagen. It requires a skin test to be placed 30 days before injection to ensure absence of an allergic response, which occurs in 2% to 5% of women. The material biodegrades in 3 to 19 months, which is why repeat injections are usually required to maintain efficacy. However, patients have been satisfactorily managed by one injection for as long as 6 years. The material is readily available and was the only injectable agent approved in the United States until 1999. The material comes in 2.5-mL syringes; injects through a 22-gauge needle; and requires one to three syringes injected transurethrally, and more as a periurethral injection. Durasphere (Carbon Medical Technologies Inc., St. Paul, MN) was approved by the FDA in 1999. It consists of pyrolytic carbon-coated zirconium oxide beads suspended in a waterbased carrier gel containing beta glucan. The newer preparation (Durasphere EXP) has a particle size of 95 to 200 μm compared with the older material that had particle size of 251 to 300 μm. The material is nonbiodegradable, is radiopaque, and requires injection with an 18-gauge needle. The material comes in 1-mL syringes and requires 2 to 4 syringes for injection.
BOX 18-1
Tegress (CR Bard Inc., Covington, GA) is an ethylene vinyl copolymer dissolved in dimethyl sulfoxide (DMSO) that was recently approved by the FDA. Upon contact with a liquid medium, diffusion of DMSO occurs, and a solid polymer precipitates. It comes in 1-mL syringes, and up to 2.5 mL of material can be injected at a total of three sites, with no more than 1 mL at any one site. Calcium hydroxylapatite (Coaptite; Bioform Medical Inc., San Mateo, CA) consists of 100-μm hydroxylapatite spheres suspended in an aqueous gel of sodium carboxylmethylcellulose. The material is a natural constituent of bones and teeth and has been used in dental and orthopedic applications for several years. Calcium hydroxylapatite was approved for clinical use in the United States by the FDA in 2006. It is injected via a 21-gauge needle, requires only 2.5 mL on initial injection, and can be visualized radiographically or by ultrasound. The best materials will probably come from tissue engineering and autologous cell bioimplants. This was briefly studied in the past by the use of autologous ear cartilage and in vitro expansion of cells for implant. The technology was not advanced because of cost and use of other readily available and cheaper products. Macroplastique (Uroplasty BV, Geleen, The Netherlands) is approved for use in Europe but remains in study protocols in the United States. The material is made from highly textured polydimethyl-siloxane macroparticles suspended in a bioexcretable carrier hydrogel of polyvinylpyrrolidone. It consists of silicone microimplants of 73 to 100 μm and is prepared in 2.5-mL syringes. It requires a special injection apparatus for transurethral injection, but it recently has been applied periurethrally by use of an implantation device. The silicone name will most likely inhibit ease of approval in the United States. Zuidex gel (Q-Med AB, Uppsala, Sweden) is a combination of dextranomer (cross-linked polysaccharides) and hyaluronic acid. Dextranomer has been used in wound treatment for several years. Nonanimal stabilized hyaluronic acid is similar to natural hyaluronic acid found in the body. The material is prepared in 0.7-mL syringes and used transurethrally with an implantation device (Implacer) and the injection of four syringes of material (see Fig 18-3). The material is in current use in the United States for ureterovesical reflux and is marketed as Deflux. Permacol (Tissue Science Laboratories plc [TSL], Aldershot, Hampshire, UK) is approved for use in Europe and is currently under study protocol in the Unites States. Permacol is a sterile injectable suspension of acellular crosslinked porcine collagen matrix.
INJECTABLE AGENTS IN NORTH AMERICA
Trade Name
Company
Approval
Contigen Durasphere EXP Tegress Macroplastique Zuidex Coaptite
CR Bard Inc., Covington, GA Carbon Medical Technologies Inc., St. Paul, MN CR Bard Inc., Covington, GA Uroplasty BV, Geleen, The Netherlands Q-Med AB, Uppsala, Sweden Bioform Medical Inc., San Mateo, CA
1993 1999 2005 FDA trials ongoing FDA trials ongoing 2006
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Urethral Injection of Bulking Agents for Intrinsic Sphincter Deficiency
TECHNIQUES The methods of injection to be described will relate to use in the current bulking materials. In some cases (Macroplastique), a need exists for a special delivery device, but, in most cases, the materials are injected through spinal needles—disposable injection needles that fit the operating channel of a cystoscope sheath—or through a special channel in an operating sheath and bridge set. The amount of material injected is usually greater for periurethral techniques, although the efficacy of periurethral versus transurethral injections is the same. A limit exists to the amount of some materials injected, such as Tegress, which is restricted to 2.5 mL per session. Various transurethral injection sites are known, including just the 3 o’clock and 9 o’clock positions; 4 o’clock, 8 o’clock, and 12 o’clock positions; or the circumferential techniques using material at the 3 o’clock, 6 o’clock, 9 o’clock, and 12 o’clock positions. The bulking materials are intended for injection into the superficial urethral muscle adjacent to the submucosa.
Periurethral Method The sites for injection of local anesthesia are selected at the level of the Skene duct opening on either side of the urethra; a 27-gauge needle is used to inject 1.0 mL of 1% lidocaine solution 0.5 to 1.0 cm from the urethral meatus (Fig. 18-1). Xylocaine 2% gel may be placed in the urethra at the start of the procedure. The scope with 0-degree lens is inserted to the urethrovesical junction and then withdrawn to observe the proximal urethra. A syringe with 1% lidocaine solution and an attached 22-gauge spinal needle, with or without a small amount of indigo carmine to stain the tissues, is inserted and guided parallel to the urethra directing the needle bevel medially toward the urethral lumen. This allows the injecting material to be viewed more easily as the position of the needle is determined. The cystoscope is used to observe the advancing needle, and the syringe is moved in short strokes to allow the needle tip to be seen under the tissue at the proximal urethra until the desired location is found. The syringe is replaced with a syringe of bulking agent, and the material is injected until the entire syringe has been injected or until adequate effect has been noted with urethral bulking. The process is repeated on the opposite site; the second side may Figure 18-1 ■ Periurethral bulking technique. Urethroscopic-guided periurethral injection of collagen 1 cm distal to the bladder neck.
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be more difficult due to distortion of the proximal urethra caused by the initial injection. The amount of Contigen averages 3.75 mL for each of two sites. Durasphere EXP comes with its own injection needle, 18-gauge and angled, to aid accurate submucosal placement.
Transurethral Method The transurethral method has normally required the use of a cystoscope with a 12- or 25-degree lens, with the appropriate sheath (20 or 21 French with no fenestration) and operating channel to allow the passage of a 5-French thermoplastic injection catheter and beveled 22-gauge disposable injection needle. Alternatively, some physicians use a 0- or 30-degree lens, but this makes simultaneous viewing of the needle puncture site and impact of the injection difficult. A built-in needle delivery system is found with some products, and the delivery mechanism is spring-loaded to allow advancement of the needle into the urethral submucosa for shallow or deep injection, and then removal of the needle just by releasing the thumb-operated mechanism. The various materials for injection may dictate injection systems, such as the pressure gun required for injection of Macroplastique. On the other hand, material like Tegress can be injected through a 25-gauge needle. The procedure begins with optional placement of 2% Xylocaine gel in the urethra for 5 to 10 minutes. The injection needle may be preloaded with 1% lidocaine solution (0.4 mL fills the 22-gauge disposable injection needle used for Contigen), which is injected into the selected site. The selected site may be as much as 2 cm distal to the bladder neck, but the needle bevel extends 1 cm from the hub, and the site of injection ends up 1 cm distal to the bladder neck. The injection should gradually cause distension of the urethral mucosa, and this is observed by appropriate angling of the cystoscope lens during the injection (Fig. 18-2). Should the injection be too superficial, there will be blanching or superficial appearance of the injection material under the urethral mucosa, and the needle must be repositioned. Discussion is widespread as to whether the needle bevel should turn toward the urethral lumen or away from it. The needle inserts better into the tissue if the bevel is turned away from the lumen during insertion, and then it can be rotated according to visualized effect. After injecting the first side, lidocaine is flushed through
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Post-Injection Follow-Up
A
B
C
Figure 18-2 ■ Transurethral injection of bulking agent. A. Bladder neck open. B. Submucosal placement of material results in partial closure of bladder neck. C. Injection is complete, and bladder neck closed.
the injecting needle to clear the remaining collagen. The second syringe of Contigen is attached, and the injection at the second site commences as the lidocaine solution is first delivered to provide anesthesia, followed by the collagen. The urethral mucosa should swell with the injection and the injection sites meet gradually in the midline as the bladder neck is occluded. The injection of Tegress is volumelimited (2.5 mL), and the midline occlusion is not seen with this material. A modified injection technique has been described for Durasphere, which consists of a single needle stick at the 4 o’clock position; hydrodissection with 1.5 mL of 1% lidocaine, gradual withdrawal, advancement, or rotation of the needle tip after resistance is noted; and holding the needle in position for 10 seconds after coaptation is achieved, to prevent leakage of material from the injection site.
Insertion Devices The Macroplastique implantation device is currently in use in North America for the FDA-approved Macroplastique trials and has previously been shown to have success rates comparable to endoscopic techniques. Also, a device for Zuidex, called an Implacer, allows transurethral injection without visualization of the injection site (Fig. 18-3).
Immediately after injection, the patient should not have any pain. She may have urethral burning with urination, which lasts for only part of a day and can be controlled with phenazopyridine generic (Pyridium). Antibiotics are not mandatory but are usually given immediately before and/or 1 or 2 days after injection because the rate of post-procedure urinary tract infection is high. The patient is allowed to void after the injection, and she should be prepared to stay in the clinic area for 1 to 2 hours to allow the initial swelling from the injection to diminish enough to allow voiding. If voiding does not occur or is associated with high residual urine (over 200 mL as determined by bladder scan, ultrasound, or straight catheter), then the patient either needs to be instructed in self-catheterization or have an 8- to 10-French Foley catheter placed, using no more than 5 mL in the balloon. One technique is to teach most patients self-catheterization before the injection, but this means that as many as 70% to 80% of patients are taught unnecessarily. One can resort to teaching those who need it after the injection. The other alternative is to insert a small Foley catheter (8 to 10 French) for 48 hours and then have the patient return for voiding assessment. Those who use self-catheterization should do so after attempts at voiding, four or five times a day. Continuing to perform self-catheterization after voiding commences is not necessary, when residual urine amounts are less than 100 mL or less than 25% of voided volumes of greater than 100 mL. Voiding dysfunction usually resolves in 12 hours. Patients should be called the day following the injection to be sure that no continuing problem is present. A follow-up appointment should be made for 1 to 4 weeks, and, at that time, in addition to patient history, assessment is made for voiding function, urinary tract infection, and swelling at the suburethral injection site. The effectiveness of the injection is then assessed, and overactive bladder symptoms are addressed, if appropriate. Repeat injections can be scheduled as needed for persistent symptoms of stress incontinence.
COMPLICATIONS The main advantage of injectables is their safety profile even in very ill patients. The most common complication during the injection is pain during the procedure. For those having treatment in a clinic or office setting, this can be minimized with intraurethral topical anesthetic gel and/or injection of 0.4 to 0.8 mL of local anesthetic, such as 1% lidocaine solution, into the submucosal injection site. This can be accomplished by preloading a disposable 22-gauge injection needle, which holds 0.4 mL of solution. Another complication is extrusion of material during injection, and this can be avoided by submucosal placement of the needle approximately 1 cm into the tissue and then observing the injection effect on the urethral lining. If the injection is too superficial, and the lining distends rapidly, then an alternative site should be selected. A small amount of bleeding may occur from the injection site, or the material may start to extrude from the puncture site. In this case, when using a disposable needle, the hub should be pressed against the lining of the urethra, and this will usually
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Urethral Injection of Bulking Agents for Intrinsic Sphincter Deficiency
A
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B
Figure 18-3 ■ Implantation device. A. Implacer device with syringes in position before urethral insertion. B. Device activated and needles ready to be advanced into submucosal site. (Courtesy of Q-med AB, Seminariegatan 21, SE-752 28 Uppsala, Sweden.)
control the situation. After injection, a small amount of material may leak from the site, but this is seldom a problem unless the material used is Tegress. In this situation, the extruded material needs to be removed because it is permanent and will lead to recurrent irritative voiding and infections. After the injection, the most common complications in the immediate period are urinary retention and voiding dysfunction. It is important to assess voiding after the injection is complete, and this can be accomplished by comparing the amount voided to the amount of fluid infused during the procedure, using a bladder scanner, or placing a straight catheter. Most of the time, if 200 mL is placed during the procedure, and the patient is able to void 100 mL or greater within the hour after injection, little concern exists regarding retention. Voiding discomfort occurs in some patients, and this has already been discussed. Urinary tract infection occurs in 10% to 15% of cases; antibiotic treatment should be given after the injection, and the urine should be checked for infection at the initial postoperative visit. Few delayed complications exist, but one rare one is formation of a suburethral abscess. This is associated with increasing voiding dysfunction with or without pain. A more common problem is recurrent urinary tract infections requiring prophylactic antibiotics. Cystoscopy may be required to be certain that there is no bulking material resting in the urethra. In the Durasphere randomized study by Lightner et al. (2001), urinary urgency and urinary retention were more common in the Durasphere group than in the Contigen group, but the urgency had mostly resolved by the end of the study, and the retention resolved within 7 days of the injection.
Macroplastique was associated with a high incidence of dysuria for 48 hours, and one patient required catheter drainage for 6 weeks after injection.
SAFETY Inherent in the discussion of indications, contraindications, and complications is the theme that the products used for urethral bulking are safe. The most common event is urinary tract infection, which often occurs remotely from the injection procedure. Allergic responses may occur with Contigen, but these potential events are screened by skin testing before the procedure. Permanent voiding dysfunction has not been reported, and there appears to be little risk of obstructive uropathy. Suburethral abscess has been reported, but the incidence is far less than 1%. This abscess is usually sterile and may present as a simple bulge under the urethra, without any symptoms. Other rare events include tissue necrosis at the injection site, urethral prolapse, delayed hypersensitivity with systemic arthralgia, osteitis pubis, pseudocysts or collagen polyps, urethral diverticulum, and vesicovaginal fistula. The study on Tegress has shown a moderate incidence of material extrusion in the urethra, and this can cause irritative voiding or recurrent infection. Because the material is permanent, large projections should be removed by dislodging with a scope, and smaller areas will usually cover over with epithelium. Prevention is the best approach, so material should not be injected too close to the urethral lumen or around prominent sites of prior injection.
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Table 18-1
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Results of Injectable Urethral Bulking Agents in Women (minimum 60 patients)
Investigator
Agent
Cross et al., 1998 Groutz et al., 2000 Herschorn et al., 1992 Monga et al., 1995 Smith et al., 1997 Swami et al., 1997 Lightner et al., 2001
Collagen Collagen Collagen Collagen Collagen Collagen Durasphere
No. of Patients
Follow-Up (mo)
139 63 187 60 96 111 61
18 (6–36) 12 (1–32) 22 (4–69) 24 14 (6–21) 40 12
Mean/Volume of Injections (mL) NR 2.1/3.1 2.5/9.6 1.6/19 2.1/11.9 NR –/4.8
Dry/Improved/ Failed (%) 74/20/6 13/27/60 23/52/25 48/20/32 38/29/33 25/40/35 —/80/20
NR, Not reported.
One case of long-term retention and its management has been described for Durasphere. Migration of Durasphere particles along the lymphatic chain of the pelvis has been reported, but the clinical significance is unknown.
EFFECTIVENESS No standardized manner exists to evaluate effectiveness of therapy. Most of the FDA-approved trials use voiding diaries, pad tests, and subjective data, such as the Stamey scoring system. Urodynamic testing and leak point pressures have not proved useful in evaluating effectiveness. Definitions of cure, improvement, and failure vary in the literature. In the Cochrane review from 2003, randomized trials suggest, but do not prove, that periurethral injection of established bulking agents results in objective and subjective short-term improvement of symptomatic stress incontinence in women. They would like to see randomized trials involving placebo and conservative treatment arms. Many of the study papers on Contigen included patients with severe incontinence (leak point pressures less than 65 cm H2O) and minimal urethral mobility precluding operative intervention other than potentially obstructive slings. Several of these patients were significantly improved, and, although injection therapy may last only 12 months, repeat injections are generally reproducible. As stated earlier, for women with extensive comorbidity, injection therapy may represent a useful option for relief of symptoms for a 12-month period, although two or three injections will likely be needed to achieve a satisfactory result. The statement from the 2nd International Consultation on Incontinence (2002) quoted a cure rate of 48% after periurethral bulking (defined in 15 articles as completely dry), and a success rate of 76%, although most of the studies were of short-term follow-up and relatively small numbers of women. Patients may require two injections to provide continence or significant improvement, and these can be performed as close together as 1 month. If there is no improvement after two injections, a response is unlikely. Cure or improvement occurs in 70% to 80% of patients, with total continence in around 40%. Repeat injections are required at varying intervals to maintain the effect. Table 18-1 shows the results of the larger studies on urethral bulking for stress incontinence.
The effectiveness of Durasphere was reported at 1 year in a randomized, controlled study compared with Contigen (Lightner et al., 2001). The Durasphere group had an 80% (49 of 61) cure or improvement at 1 year, compared with the Contigen group with a 69% (47 of 68) cure or improvement. The effectiveness of Macroplastique at 3 months after a single injection was 40% dry (16 of 40), 33% improved, and 27% no better. A second injection cured four of the improved group. After 3 years, 40% remained dry and 18% were improved. Few data exist on calcium hydroxylapatite, and the initial journal publication included only 10 patients. However, a subsequent multicenter study was reported at the International Continence Society annual meeting in 2003 and showed 6 months’ data for 100 patients with equivalent or slightly better results than Contigen, and 12-month outcomes on 46 patients showed similar results.
FUTURE CONSIDERATIONS Contigen remains the bulking agent of choice, at least in the United States. The reason is because of a good safety profile for the 10 years of use, ease of injection, and its effectiveness in providing relief of symptoms in a large proportion of patients. Durasphere will increase in popularity as long as the injection technique is made user-friendly. The newer products with recent FDA approval may be equally effective, but long-term data are required to determine durability. The ideal material has not been found, and, in spite of prolonged search, nothing financially feasible as yet appears to be better than Contigen. Only autologous injection of either muscle cells or collagen may prove to be better, and this remains a long way off. Studies have illustrated that skeletal muscle proliferates and appears to persist favorably following injection into the bladder and urethral smooth muscle. These preliminary studies indicate that autologous skeletal muscle injection may come to represent a viable alternative to other injectable agents currently available.
Bibliography Bent AE. Periurethral collagen injections. In Gershenson DM, ed. Operative Techniques in Gynecologic Surgery, vol. 1, no. 1. Philadelphia, 1997, WB Saunders Co.
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Bent AE, Foote J, Siegel S, et al. Collagen implant for treating stress urinary incontinence in women with urethral hypermobility. J Urol 2001;166:1354. 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. Chancellor MB, Yokoyama T, Tirney S, et al. Preliminary results of myoblast injection into the urethral and bladder wall: a possible method for the treatment of stress urinary incontinence and impaired detrusor contractility. Neurourol Urodyn 2000;19:279. Cross CA, English SF, Cespedes RD, McGuire EJ. A follow-up on transurethral collagen injection therapy for urinary incontinence. J Urol 1998;159:106. Dmochowski RR, Appell RA. Injectable agents in the treatment of stress urinary incontinence in women: where are we now? Urology 2000;56 (Suppl 6A):32. Faerber GJ, Belville WD, Ohl DA, Plata A. Comparison of transurethral versus periurethral collagen injection in women with intrinsic sphincter deficiency. Tech Urol 1998;4:124. Gross M, Appell RA. Periurethral injections. In Bent AE, Ostergaard DR, Cundiff GW, Swift SE, eds. Ostergard’s Urogynecology and Pelvic Floor Dysfunction, 5th ed. Philadelphia, 2003, Lippincott Williams & Wilkins, pp 495. 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. Harriss DR, Iacovou JW, Lemberger RJ. Peri-urethral silicone microimplants (Macroplastique) for the treatment of genuine stress incontinence. Br J Urol 1996;78:726. Hartano VH, Lightner DJ, Nitti VW. Endoscopic evacuation of Durasphere. Urology 2003;62:135. Henalla SM, Hall V, Duckett JR, et al. A multicentre evaluation of a new surgical technique for urethral bulking in the treatment of genuine stress incontinence. Br J Obstet Gynaecol 2000;107:1035. Herschorn S, Radomski SB, Steele DJ. Early experience with intraurethral collagen injections for urinary incontinence. J Urol 1992;148: 1797. Herschorn S, Steele DJ, Radomski SB. Follow-up of intraurethral collagen for female stress urinary incontinence. J Urol 1996;156:1305. Kobashi KC, Leach GE. Injection therapy for female stress urinary incontinence. Infect Urol 2002;15:9. Lightner D, Calvosa C, Anderson R, et al. A new injectable bulking agent for treatment of stress urinary incontinence: results of a multicenter, randomized, controlled, double-blind study of Durasphere. Urology 2001;58:12. Madjar S, Covington-Nichols C, Secrest CL. New periurethral bulking agent for stress urinary incontinence: modified technique and early results. J Urol 2003;170:2327.
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Mayer R, Lightfoot M, Jung I. Preliminary evaluation of calcium hydroxylapatite as a transurethral bulking agent for stress urinary incontinence. Urology 2001;57:434. McLennan MT, Bent AE. Suburethral abscess: a complication of periurethral collagen injection therapy. Obstet Gynecol 1998;92:650. Medicare Coverage Issues Manual: Incontinence Control Devices. Department of Health and Human Services, Health Care Financing Administration, June 1994, Transmittal No. 70. Section 65–69. Medicare Coverage Issues Manual: Incontinence Control Devices. Department of Health and Human Services, Health Care Financing Administration, September 1996, Transmittal No. 89. Section 65–69. Monga AK, Robinson D, Stanton SL. Periurethral collagen injections for genuine stress incontinence. A 2-year follow-up. Br J Urol 1995;76: 156. 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. Murless BC. The injection treatment of stress incontinence. J Obstet Gynaecol Br Emp 1938;45:521. Pannek J, Brands FH, Senge T. Particle migration after transurethral injection of carbon coated beads for stress urinary incontinence. J Urol 2001;1350. Pickard R, Reaper J, Wyness L, et al. Periurethral injection therapy for urinary incontinence in women (Cochrane Review). In The Cochrane Library. Update Software, Oxford, 2003, Issue 2. Politano VA, Small MP, Harper JM, et al. Periurethral Teflon injection for urinary incontinence. J Urol 1974;111:180. Smith AR, Daneshgari F, Dmochowski R, et al. Surgical treatment of incontinence in women. In Abrams P, Cardozo L, Khoury S, Wein A, eds. Incontinence. 2nd International Consultation on Incontinence. Health Publication Ltd, 2002. Smith DN, Appell RA, Winters JC, et al. Collagen injection therapy for female intrinsic sphincteric deficiency. J Urol 1997;157:1275. 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. Swami S, Batista JE, Abrams P. Collagen for female genuine stress incontinence after a minimum 2-year follow-up. Br J Urol 1997;80:757. Sweat SD, Lightner DJ. Complications of sterile abscess formation and pulmonary embolism following periurethral bulking agents. J Urol 1999;161:93. Von Heland M, Mantovani F, Zanetti G, et al. Urethral implantation of collagen in the treatment of urinary incontinence. Comparison of transurethral and periurethral approach. Minerva Urol Nefrol 1998;50:213. Yokoyama T, Yoshimura N, Dhir R, et al. Persistence and survival of autologous muscle derived cells versus bovine collagen as potential treatment of stress urinary incontinence. J Urol 2001;165:271.
Surgical Correction of Anterior Vaginal Wall Prolapse
19
Mark D. Walters
ANATOMY AND PATHOLOGY 234 EVALUATION 235 History 235 Physical Examination 236 Diagnostic Tests 237 SURGICAL REPAIR TECHNIQUES 237 Anterior Colporrhaphy 237 Vaginal Paravaginal Repair 240 Abdominal Cystocele Repair 241 Cystoscopy 241 RESULTS 241 COMPLICATIONS 244
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 prolapse progresses, symptoms may develop and worsen, and treatment becomes indicated. This chapter reviews the anatomy and pathology of anterior vaginal prolapse and describes methods of surgical 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, the term anterior vaginal prolapse is preferred over cystocele. The reason is because information obtained at the physical examination does not allow the exact identification of structures behind the anterior vaginal wall, although, in fact, it is usually the bladder. The ICS grading system for prolapse is discussed fully in Chapter 5. The cause 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, as discussed in Chapter 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. Pathologic loss of that support may occur with damage to the pelvic muscles, connective tissue attachments, or both. Nichols and Randall (1996) described two types of anterior vaginal prolapse: distention and displacement. Distention was thought to result from overstretching and attenuation of the anterior vaginal wall, caused by overdistention 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 distention cystocele, with urethral hypermobility, or with apical prolapse. Rugal folds may or may not be preserved. Another related theory ascribes most cases of anterior vaginal prolapse to disruption or detachment of the lateral connective tissue attachments at the arcus tendineus fasciae pelvis or white line, resulting in a paravaginal defect and corresponding to the displacement type discussed earlier. This was first described by White in 1909 but disregarded until reported by Richardson in 1976. Richardson also 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 19-1. Few systematic or comprehensive descriptions of anterior vaginal prolapse have emerged 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, DeLancey (2002) described paravaginal defects
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Paravaginal defect
Midline defect
Transverse defect Figure 19-1 Three different defects can result in anterior vaginal wall prolapse. Lateral or paravaginal defects occur when there is a separation of the endopelvic 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 endopelvic fascia separates from the vaginal cuff or uterosacral ligaments. (From Karram MM. Vaginal operations for prolapse. In Baggish MS, Karram MM, eds. Atlas of Pelvic Anatomy and Gynecologic Surgery. WB Saunders, Philadelphia, 2001, with permission.) ■
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. (1995) 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 19-2, the posterior pubourethral ligaments (bilateral attachment of arcus tendineus fasciae pelvis to posterior aspect of the pubic symphysis) are seen clearly. In the two subjects with clinically apparent paravaginal defects, lateral detachments were evident (Fig. 19-3). 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, ultimately, may guide the choice of surgical repair.
EVALUATION History When evaluating women with pelvic organ prolapse or urinary or fecal incontinence, attention should be paid to all
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Figure 19-2 ■ 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. (From 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, with permission.)
Figure 19-3 ■ Axial T1-weighted image from a 57-year-old 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. (From 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, with permission.)
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 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.
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 reexamined in the standing position. The grading systems for prolapse and measurement of urethral hypermobility are described in Chapters 5 and 6. 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 forceps placed in the anterolateral vaginal sulci directed toward the ischial spine. Bulging of the anterior vaginal wall in the midline between the forceps blades implies a midline defect; blunting or descent of the vaginal fornices on either side with straining suggests lateral paravaginal defects. Studies have shown that the physical examination technique to detect
Physical Examination The physical examination should be conducted with the patient in the lithotomy position, as for a routine pelvic
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paravaginal defects is not particularly reliable or accurate. In a study by Barber et al. (1999) 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 unexpected 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. (2004) 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.
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 does not usually change management in women for whom surgical repair is planned. Therefore, routine imaging of the kidneys and ureters is not necessary. 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. (1988), 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 situation is reported to occur in 17% to 69% of women with stage III or IV prolapse. In this situation, the surgeon should choose an anti-incontinence procedure in conjunction with anterior vaginal prolapse repair. If sphincteric incompetence is not present even after reduction of the prolapse, an anti-incontinence procedure may not be indicated.
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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-French 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 diamondshaped 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 layers of the vaginal muscularis, and gently forced upward while being partially opened and closed (Fig. 19-4, A, B). 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 19-4, C. 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. Using sharp dissection is also important to mobilize the bladder base from the vaginal apex, as shown in Figure 19-5. In most cases, even if the patient does not suffer from urinary incontinence, plicating sutures at the urethrovesical
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A
B
D
C Figure 19-4 ■ 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 facilitates dissection of the bladder off the vaginal wall. D. Mobilization of the cystocele off the vaginal wall is completed. (From Karram MM. Vaginal operations for prolapse. In Baggish MS, Karram MM, eds. Atlas of Pelvic Anatomy and Gynecologic Surgery. WB Saunders, Philadelphia, 2001, with permission.)
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A
Figure 19-5 ■ Cystocele repair. Sharp dissection is used to mobilize the bladder base from the vaginal apex during anterior colporrhaphy.
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 is 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 nonabsorbable suture. The first plicating stitch is placed into the periurethral endopelvic fascia and tied (Fig. 19-6, A). 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. 19-6, B). 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.
B Figure 19-6 ■ 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 with preferential support of the bladder neck when compared with the bladder base (inset). (From Karram MM. Vaginal operations for prolapse. In Baggish MS, Karram MM, eds. Atlas of Pelvic Anatomy and Gynecologic Surgery. WB Saunders, Philadelphia, 2001, with permission.)
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 aide in support in the anterior vagina. This can be done in several ways and the surgical techniques continue
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to evolve. One modification is to place a piece of polyglactin 910 mesh into the fold of imbricated bladder wall below the trigone and 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 nonabsorbable suture. The anchor points are usually at or near the arcus tendineus fasciae pelvis or bilateral obturator fascia, as shown in Figure 19-7. Biologic materials that have been used include segments of rectus fascia, fascia lata, cadaveric fascia, or other allograft or xenograft materials. Permanent (usually polypropylene) mesh may be used, although nonabsorbable material carries a risk of infection or erosion, with a need for subsequent revision or removal in 2% to 12% of cases. A more recent innovative approach is to anchor an allograft or polypropylene mesh without tension via strips placed through the obturator foramen with a special device (Perigee, American Medical Systems, Minneapolis, MN). The 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 judgment is required to perform the bladder plication tightly enough to sufficiently reduce the anterior vaginal prolapse, 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 completed.
Vaginal Paravaginal Repair The objective 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 white line or
Figure 19-7 ■ 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.
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arcus tendineus fasciae pelvis. This can be accomplished using a vaginal or retropubic approach. Retropubic paravaginal defect repair is discussed in Chapter 15, 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. 19-8, A). In patients who have had a hysterectomy, marking sutures are also placed at the vaginal apex. If an apical suspension is being performed, the stitches are placed (not tied) until the 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 laterally dissecting the vaginal muscularis. The dissection is performed bilaterally until the 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 of the spine can be followed to the back of the symphysis pubis. After dissection is complete, midline plication of vaginal muscularis can be performed (Fig. 19-8, B), 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. With a No. 0 nonabsorbable suture, the first stitch is placed around the tissue of the white line just anterior to the ischial spine. A Capio device (Boston Scientific Inc., Watertown, MA) works well to facilitate suture placement. If the white line is detached from the pelvic sidewall or clinically not felt to be durable, 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. 19-8, D). Starting with the most anterior stitch, the surgeon picks up the edge of the periurethral tissue (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 stitches are placed on one side, the same procedure 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
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(Fig. 19-8, F). 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 of 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 a No. 0 delayed absorbable suture. The vaginal flaps are trimmed and closed with a running subcuticular or interlocking delayed absorbable suture.
Abdominal Cystocele Repair Abdominal repair of mild anterior vaginal prolapse can be accomplished at the time of abdominal hysterectomy. 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 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 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.
Cystoscopy Cystoscopy is usually performed after cystocele repair, especially if slings or apical suspension procedures are also being done. The purpose is to ensure that no sutures or mesh have been placed in the bladder and to verify patency of both ureters.
RESULTS 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 series. Definitions of recurrence vary and sometimes are not stated, and loss to follow-up is often not stated. In our review of surgical techniques for the correction of anterior vaginal prolapse (Weber and Walters, 1997), reported failure rates ranged from 0% to 20% for anterior colporrhaphy and 3% to 14% for paravaginal defect repair. Weber et al. (2001) 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 an optimal or satisfactory anatomic result; anterior colporrhaphy with polyglactin 910 mesh overlay had a 42% optimal or satisfactory result, and ultralateral plication under tension had 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.
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Marking sutures at bladder neck
Vaginal wall
Marking sutures at vaginal apex
A
B Bilateral paravaginal defects Midline cystocele repair
Detached edge of pubocervical fascia
Illiococcygeus muscle
C Obturator internus muscle
D
Arcus tendineus fasciae pelvis (white line)
Ischial spine
Figure 19-8 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 multiple sutures are passed through the arcus tendineus fasciae pelvis (white line). ■
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E
F Figure 19-8 ■ Cont’d 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. (From Karram MM. Vaginal operations for prolapse. In Baggish MS, Karram MM, eds. Atlas of Pelvic Anatomy and Gynecologic Surgery. WB Saunders, Philadelphia, 2001, with permission.)
(2001) noted fewer recurrent cystoceles when polyglactin 910 mesh was incorporated into the imbrication of the repair. Prosthetic augmentation of cystocele repair is a promising although evolving innovation. Many variations in techniques and materials are used, but few quality studies exist to date; one technique variation is shown in Figure 19-7. Biologic prosthetic materials placed over a midline cystocele plication as a simple overlay and anchored laterally has been done but does not seem to offer significant lasting improvement over standard repair. However, anchoring the mesh to the obturator fascia in the paravaginal space, the addition of suburethral slings, and anchoring of the prosthesis to the apical portion of the repair may significantly improve longterm results. Placement of nonabsorbable mesh into an anterior vaginal prolapse repair is a promising, although more controversial, variation. Polypropylene mesh has limited foreign body reaction in general, and is probably the best choice. Technique variations include mesh overlays, modified fourcorner attachments, transobturator attachments, and anterior flaps as part of an apical mesh procedure. Cure rates appear high (Table 19-1), but comparative trials with more traditional sutured repairs have not been done. Vaginal mesh erosions continue to be a problem; they occur in 2.1% to 13% of cases, a significant number of which require reoperation for mesh removal. Creation of vaginal flaps that are
thicker with 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 is less effective than Burch colposuspension and most slings (Glazener and Cooper, 2002). These findings hold irrespective of the coexistence of pelvic organ prolapse. However, as noted previously, suburethral plication may be satisfactory for some women with mild symptoms of stress incontinence who do not desire a sling, who have significant preoperative voiding dysfunction, or 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, placement of a TVT results in significantly higher objective postoperative continence rate compared with suburethral plication (92% vs. 56%; P < .01; Meschia et al., 2004). Thus, placement of a TVT, or perhaps a transobturator sling, is recommended for all women with potential stress incontinence, with the possible exception of very elderly patients and those with significant voiding dysfunction. Paravaginal defect repair, using the transvaginal approach, has been used infrequently as an isolated procedure for treatment of stress urinary incontinence. Evidence suggests that
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Literature Review of Anterior Vaginal Wall Prolapse Repair with Nonabsorbable Mesh*
Author (year)
Mesh
Julian (1996) Nicita (1998) Flood et al. (1998) Mage (1999)
Marlex Polypropylene Marlex Mersuture (Ethicon, Issy-les-Moulineaux, France) Mixed fiber† Polypropylene Polypropylene Polypropylene Polypropylene
Migliari and Usai (1999) Migliari et al. (2000) Hardiman et al. (2000) Salvatore et al. (2002) De Tayrac et al. (2005)
N 12 44 142 46 15 12 18 32 87
Follow-Up (mo)
Success Rate (%)
Vaginal Erosion
24 14 36
100 93.2 94.4
1 (8.3%) 1 (2.3%) 2 (2.1%)
26 23.4 20.5 1.5 17 24
100 93 75 100 87 91.6
1 (2.2%) 0 0 2 (11.1%) 4 (13%) 7 (8.3%)
*Definitions of success and surgical techniques vary. † 60% Polyglactin 910 and 40% polyester.
it has less than satisfactory results when used in this capacity. In a report by Mallipeddi et al. (2001), 57% of subjects with anterior vaginal prolapse and stress incontinence and 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, although 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. (1991), 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 studied specifically. Vaginal prolapse recurs with increasing age, but the actual frequency is unknown. Recurrence may represent a failure to identify and repair all support defects, or may be due to weakening, stretching, or breaking of patient’s 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 severity of initial prolapse, 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. 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 to 14 days to allow adequate healing. Ureteral damage or obstruction occurs rarely (0% to 2%), usually with very large cystoceles or apical prolapse. Other rare complications include intravesical or urethral suture placement (and associated urologic problems), and fistula, 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%. Urinary tract infections occur commonly (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. 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 Skibsted (1988) studied 55 sexually active women who underwent various 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 worsen function if vaginal stiffness, mesh erosions, or draining sinuses result. More data with careful anatomic and functional follow-up after surgery are needed.
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Bibliography ANATOMY AND PATHOLOGY 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. DeLancey JO. Fascial and muscular abnormalities in women with urethral hypermobility and anterior vaginal wall prolapse. Am J Obstet Gynecol 2002;187:93. Nichols DH, Randall CL. Vaginal Surgery, 4th ed. Williams & Wilkins, Baltimore, 1996. Richardson AC, Lyon JB, Williams NL. A new look at pelvic relaxation. Am J Obstet Gynecol 1976;126:568. White GR. A radical cure by suturing lateral sulci of vagina to white line of pelvic fascia. JAMA 1909;21:1707. White GR. An anatomical operation for the cure of cystocele. Am J Obstet Dis Women Child 1912;65:286.
EVALUATION 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. Beverly CJ, Walters MD, Weber AM, et al. Prevalence of hydronephrosis in women undergoing surgery for pelvic organ prolapse. Obstet Gynecol 1997;90:37. Bhatia NN, Bergman A. Pessary test in women with urinary incontinence. Obstet Gynecol 1985;65:220. 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. de Gregorio G, Hillemanns HG. Urethral closure function in women with prolapse. Int Urogynecol J 1990;1:143. Richardson DA, Bent AE, Ostergard DR. The effect of uterovaginal prolapse on urethrovesical pressure dynamics. Am J Obstet Gynecol 1983;146:901. Tulikangas PK, Lukban JC, Walters MD. Anterior enterocele: a report of three cases. Int Urogynecol J 2004;15:350. Whiteside JL, Barber MD, Paraiso MF, et al. Clinical evaluation of anterior vaginal wall support defects: interexaminer and intraexaminer reliability. Am J Obstet Gynecol 2004;191:100.
SURGICAL REPAIR TECHNIQUES AND COMPLICATIONS Barber MD. Surgical correction of paravaginal defects. In Vasavada S, Appell R, Sand P, Raz S, eds. Female Urology, Urogynecology and Voiding Dysfunction. Marcel Dekker, New York, 2005. Beck RP, McCormick S. Treatment of urinary stress incontinence with anterior colporrhaphy. Obstet Gynecol 1982;59:269. Black NA, Downs SH. The effectiveness of surgery for stress incontinence in women: a systematic review. Br J Urol 1996;78:497. 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. Flood CG, Drutz HP, Waja L. Anterior colporrhaphy reinforced with Marlex mesh for the treatment of cystoceles. Int Urogynecol J 1998;9:200. Gandhi S, Goldberg RP, Kwon C, et al. A prospective randomized trial using solvent dehydrated fascia lata for the prevention of recurrent anterior vaginal wall prolapse. Am J Obstet Gynecol 2005;142:1649. Gardy M, Kozminski M, DeLancey J, et al. Stress incontinence and cystoceles. J Urol 1991;145:1211. Glazener CM, Cooper K. Anterior vaginal repair for urinary incontinence in women (Cochrane Review). In The Cochrane Library. Update Software, Oxford, 2002, Issue 3. 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.
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Gomelsky A, Rudy DC, Dmochowski RR. Porcine dermis interposition graft for repair of high grade anterior compartment defects with or without concomitant pelvic organ prolapse procedures. J Urol 2004;171:1581. Haase P, Skibsted L. Influence of operations for stress incontinence and/or genital descensus on sexual life. Acta Obstet Gynecol Scand 1988;67:659. Hardiman P, Oyawoye S, Browning J. Cystocele repair using polypropylene mesh. Br J Obstet Gynaecol 2000;107:825. (Abstract). 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. Karram MM. Vaginal operations for prolapse. In Baggish MS, Karram MM, eds. Atlas of Pelvic Anatomy and Gynecologic Surgery. WB Saunders Co., Philadelphia, 2001. Kobak WH, Walters MD, Piedmonte MR. Determinants of voiding after three types of incontinence surgery. Obstet Gynecol 2001;97:86. 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. Macer GA. Transabdominal repair of cystocele, a 20-year experience, compared with the traditional vaginal approach. Am J Obstet Gynecol 1978;131:203. Mage P. Interposition of a synthetic mesh by vaginal approach in the cure of genital prolapse. Gynecol Obstet Biol Reprod (Paris) 1999;28:825. (in French). Mallipeddi PK, Steele AC, Hohli N, Karram MM. Anatomic and functional outcome of vaginal paravaginal repair in the correction of anterior vaginal prolapse. Int Urogynecol J 2001;12:83. 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. Migliari R, De Angelis M, Madeddu G, Verdacchi T. Tension-free vaginal mesh repair for anterior vaginal wall prolapse. Eur Urol 2000;38:151. Migliari R, Usai E. Treatment results using a mixed fiber mesh in patients with grade IV cystocele. J Urol 1999;161:1255. Natale F, Marziali S, Cervigini M. Tension-free cystocele repair (TCR): longterm follow-up. Int Urogynecol J 2000;11:S51. (Abstract). Nicita G. A new operation for genitourinary prolapse. J Urol 1998;160:741. Palma P, Riccetto C, Dambros M, Netto NR. New trends in the transobturator management of cystoceles. BJU Int 2006;97:201. Pelusi G, Bacchi P, Demaria F, et al. The use of Kelly plication for the prevention and treatment of genuine stress urinary incontinence in patients undergoing surgery for genital prolapse. Int Urogynecol J 1990;1:196. Salvatore S, Soligo M, Meschia M, et al. Prosthetic surgery for genital prolapse: functional outcome. Neurourol Urodyn 2002;21:296. (Abstract). 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. 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. Stanton SL, Norton C, Cardozo L. Clinical and urodynamic effects of anterior colporrhaphy and vaginal hysterectomy for prolapse with and without incontinence. Br J Obstet Gynaecol 1982;89:459. Symmonds RE, Jordan LT. Iatrogenic stress incontinence of urine. Am J Obstet Gynecol 1961;82:1231. Weber AM, Walters MD. Anterior vaginal prolapse: review of anatomy and techniques of surgical repair. Obstet Gynecol 1997;89:311. Weber AM, Walters MD, Piedmonte MA, Ballard LA. Anterior colporrhaphy: a randomized trial of three surgical techniques. Am J Obstet Gynecol 2001;185:1299. Young SB, Daman JJ, Bony LG. Vaginal paravaginal repair: one-year outcomes. Am J Obstet Gynecol 2001;185:1360. Zacharin RF. Free full-thickness vaginal epithelium graft in correction of recurrent genital prolapse. Aust N Z J Obstet Gynaecol 1992;32:146.
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Tristi W. Muir
ANATOMY AND PATHOPHYSIOLOGY 246 EVALUATION 247 History 247 Physical Examination 248 Diagnostic Tests 249 SURGICAL REPAIR TECHNIQUES 250 Posterior Colporrhaphy 250 Site-Specific Defect Repair 253 Graft Augmentation 253 Abdominal Sacral Colpopexy (Colpoperineopexy) Endorectal Repair 257 Perineorrhaphy 258 Postoperative Instructions 258 ANALYSIS OF OUTCOMES 258 COMPLICATIONS 259 CONCLUSION 260
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Pelvic organ prolapse is very common. Annually, approximately 200,000 women undergo prolapse surgery in the United States. Approximately three fourths of women with prolapse have a rectocele. Although rectocele repair has been commonly performed for over a century, the longterm functional and anatomic outcomes and ideal procedure have not been determined. This chapter will review the anatomy, pathophysiology, evaluation techniques, and surgical management of rectoceles and perineal body defects.
ANATOMY AND PATHOPHYSIOLOGY “The gynecologist, searching for a means of holding up and maintaining sagging structures and organs, has placed reliance on a mythical support of his own creation.” (Ricci and Thom, 1954) The terminology of the anatomic tissue that is present under the vaginal epithelium has been the subject of debate for most of the past century. The term fascia was introduced by Emmet in 1883. The histology of the apical portion of the
posterior vaginal wall consists of mucosa (which includes the epithelium of the posterior wall and the lamina propria), a superficial and deep muscularis layer, and adventitia. This fibromuscularis has been named rectovaginal fascia and perirectal fascia, perhaps giving the surgeon an illusion of sturdier tissue than is actually present. Comparisons of the histology of women with and without prolapse have shown that the smooth muscle content of the posterior vaginal wall of women with prolapse is disorganized and significantly reduced in comparison to women without prolapse. Prolapse of the posterior vaginal wall may be secondary to the presence of an enterocele, sigmoidocele, or rectocele, or a combination of these entities. A rectocele is an anterior protrusion of the rectal wall to the posterior vaginal wall. The rectovaginal space exists between the vaginal tube and the rectum. This potential space, occupied by areolar tissue, allows the vagina and rectum to function independently of each other. Support of the posterior vaginal wall is provided by a complex interaction of the integrity of the vaginal tube, the connective tissue support, and muscular support of the pelvic floor. DeLancey (1996) divided the connective tissue support of the vagina into three levels. All three levels of support should be evaluated and addressed during surgical management of the posterior vaginal wall. At level I, the apical portion of the posterior vaginal wall is suspended and supported primarily by the cardinaluterosacral ligaments. This mesentery of support originates at the sacrum and the pelvic sidewalls and inserts onto the posterior cervix and upper vagina. With normal support, the apical posterior wall of the vagina is dorsally directed to lie upon the rectum in a horizontal fashion overlying the levator ani muscles. With increases in abdominal pressure, the vaginal tube is closed top-to-bottom and supported by the pelvic floor muscles. Level II includes the support for the middle half of the vagina. This support is provided by the endopelvic fascia attaching the lateral posterior vaginal wall to the aponeurosis of the levator ani on the pelvic sidewall. Most of the fibers of the endopelvic fascia connect the lateral edge of the vaginal tube to the pelvic sidewall. Very few of the fibers actually run like a sheet from sidewall to sidewall. This lateral attachment, the arcus tendineus fasciae rectovaginalis, is dorsal to the arcus tendineus fasciae pelvis for the distal
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Figure 20-1 ■ Level II support of the posterior vaginal wall includes attachment to the pelvic sidewall from the arcus tendineus fasciae rectovaginalis in the distal half of the vagina and from the proximal arcus tendineus fasciae pelvis, which is attached to the ischial spine near the apex. ATFP, arcus tendineus fasciae pelvis; ATFR, arcus tendineus fasciae rectovaginalis; IS, ischial spine. (Reprinted with the permission of The Cleveland Clinic Foundation.)
half of the posterior wall (Fig. 20-1). The sidewall attachment of the posterior vaginal wall converges with the sidewall attachment of the anterior wall approximately midway in the vaginal canal. The proximal half of the posterior vagina is supported by bilateral endopelvic attachments to the arcus tendineus fasciae pelvis. The role of the perineal body is to resist caudally directed forces by the rectum and to provide a physical barrier between the vagina and rectum. The perineal body is thicker (approximately 3 cm long) and more defined in women. It includes interlacing muscle fibers of the bulbospongiosus, transverse perinei, and external anal sphincter. The perineal body is anteriorly attached to the vaginal epithelium and muscularis of the posterior vaginal wall. Laterally, the perineal body is attached to the ischiopubic rami through the transverse perinei muscles and the perineal membrane. Anteriorly, the perineal membrane spans the anterior half of the pelvic outlet and is comprised of dense fibromuscularis. The perineal body extends cranially in the posterior wall of the vagina to approximately 2 to 3 cm proximal to the hymenal ring. This dense, fused level of support represents level III. Posteriorly, the perineal body includes the anterior portion of the external anal sphincter and its attachment to the longitudinal fibrous sheath of the internal anal sphincter. The perineal body is suspended by and attached to the puborectalis muscle. Interruption in the support of the perineal body will allow the posterior vaginal wall, perineal body, and the distal portion of the anterior rectal wall to descend with increased abdominal and rectal pressure. The puborectalis also provides a sling of support for the vaginal tube. This sling leads to an angulation of the midposterior wall of approximately 45 degrees from vertical. The proximal portion of the vagina lies upon (and is supported by) the pubococcygeus and iliococcygeus muscles. The puborectalis helps close the potential space of the vagina and close the levator hiatus. With a healthy pelvic floor, little
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stress and strain are placed on the connective tissue support system. The levator hiatus has been shown to be larger in women with prolapse than in those with normal support. In a woman with an intact pelvic floor, the puborectalis is in a chronic state of contraction. This contraction closes the vaginal canal, and the anterior and posterior vaginal walls are in direct apposition. With defecation, the increased pressure placed on the posterior vaginal wall is equilibrated by the opposing anterior vaginal wall, and minimal stress is placed on the endopelvic fascial attachments (Fig. 20-2, A). If there is muscular and/or neurologic damage to the puborectalis, the levator hiatus widens and the vaginal canal opens. The increased rectal pressure and distension associated with defecation places strain on the endopelvic fascial attachments and the fibromuscularis of the posterior vaginal wall and can result in rectocele and perineal descent (Fig. 20-2, B,C). Any condition or event that damages the support of the posterior vaginal wall can lead to prolapse. Vaginal delivery, particularly in the occipitoposterior position, is associated with an increased risk for posterior vaginal wall and perineal body trauma. Magnetic resonance images in the postpartum period show changes in intensity within the levator ani muscle. These changes likely reflect the recovery process following neurologic or muscular damage related to childbirth. Aging may also affect the levator ani muscles, leading to muscle atrophy and devascularization. Chronic strain and constipation have been associated with (but do not necessarily cause) rectocele, perineal descent, and fecal incontinence. With chronic straining, a stretch is placed in the pudendal nerve and the nerve to the levator ani muscle. Meschia et al. (2002) found that fecal incontinence was more prevalent in women with a rectocele that extended beyond the hymen (31%) than in women with prolapse inside the hymenal ring (19%). Increasing body mass index has been strongly associated with incident rectocele but not with prolapse of other areas of the vagina (cystocele or uterine prolapse). Pelvic surgery can predispose a woman to develop prolapse. Alterations of the connective tissue support, and injury to the innervation and vascularization to the pelvic floor muscles, occur with pelvic surgery. Alterations of the axis of the vagina may increase the forces placed on the connective tissue supports. Overelevation of the anterior vaginal wall, as with a retropubic urethropexy or needle suspension procedure, alters the distribution of force on the vaginal walls and can open the posterior wall to the development of an enterocele or rectocele.
EVALUATION History Many women with a rectocele or a perineal body defect are asymptomatic. However, women may complain of symptoms associated with prolapse, such as bulging of the vagina and pressure, which worsens by the end of the day and improves when lying down. Sexual dysfunction also occurs in some women with prolapse. A woman may reduce sexual activity due to the discomfort of the prolapse or the embarrassment
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of the urinary or anal incontinence, which may accompany her prolapse. A woman with a perineal body defect, which leads to a widened genital hiatus, may describe loss of sensation for herself and her partner during intercourse. Defecatory dysfunction and pelvic organ prolapse are both common in women. It is often difficult to determine whether there is a causal link between the posterior wall prolapse and defecatory dysfunction or whether they are separate, concurrent disorders. Many women state that they are constipated. It is important to determine what a woman means when she states that she is constipated. Constipation includes excessive straining; hard, lumpy stools; splinting; feeling of incomplete emptying; and infrequent stools. Infrequent defecation is not likely related to a rectocele and may require additional evaluation. Women with a large rectocele may trap stool within this rectal pocket, leading to feeling of incomplete emptying, which can result in soiling. Splinting, or placing manual pressure in the vagina, over the rectum, or on the perineum to reduce the prolapse and facilitate emptying of the rectum, is commonly described. Anal incontinence is commonly seen in patients with posterior wall and perineal body defects. Many women are reluctant to initiate the conversation about anal incontinence due to embarrassment, so it is important to ask about accidental loss of solid or liquid stool or gas. An important part of the history to obtain from your patient is an understanding of her management desires. If the patient requires and is willing to undergo surgical management, having her express her expectations of surgery can be illuminating.
Physical Examination
Figure 20-2 ■ Pathophysiology of rectocele. A. Normal posterior wall support provided by the levator ani muscles holds the vagina closed. When abdominal pressure is increased, pressure on the posterior vaginal wall is equilibrated by pressure on the anterior vaginal wall (upper arrows). Stress on the connective tissue supports is avoided. Distally, the pressure in the rectum is resisted by the perineal body. ARW, anterior rectal wall; PB, perineal body; PVW, posterior vaginal wall. B. When the levator ani no longer holds the vagina closed, the anterior wall pressure no longer balances the posterior wall pressure. The pressure in the rectum is not counterbalanced by atmospheric pressure in the open vagina, and stress is placed on the connective tissue support. As this gives way (or in the presence of a connective tissue defect), a rectocele may develop (arrow). C. Increased distal abdominal pressure on a damaged perineal body may result in severe rectocele and perineal descent (arrow). (Reprinted with the permission of The Cleveland Clinic Foundation.)
The patient is generally examined in the dorsal lithotomy or semirecumbent position. An excellent correlation exists in the evaluation of prolapse between the supine and standing positions in women performing maximal Valsalva maneuver. If the prolapse observed in the lithotomy position does not recreate the degree of prolapse that the patient described, a standing examination should be performed. However, it is physically more difficult to make measurements of the prolapse in this position. To stage the severity of prolapse the posterior vaginal wall is visualized with the posterior blade of a bivalve speculum or a Sims speculum. The retractor elevates the anterior wall and reduces any uterine or apical prolapse. The patient is asked to increase abdominal pressure with a Valsalva maneuver or cough. The Pelvic Organ Prolapse Quantification (POPQ) system is a standardized, validated tool for measuring and staging pelvic organ prolapse (see Chapter 5). Measurements of the posterior vaginal wall are documented at maximal strain, 3 cm proximal to the hymen (Ap), at the most dependent portion of the posterior vaginal wall proximal to this mark (Bp), and at the vaginal cuff (C) or cul-de-sac, if the uterus is present (D). The genital hiatus (GH) and perineal body (PB) are measured with the patient straining. Evaluation for and staging of concurrent anterior wall and apical prolapse should be performed. The perineal body should be evaluated for descent. It may be difficult to measure perineal descent, but documentation of its presence or absence can be helpful in planning your
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surgery. Descent of the perineal body occurs with a lack of continuity from the suspensory support at the apex (level I) to the perineal body (level III). It may also occur because of a mass effect of the rectum or small bowel herniating into the perineal body, a perineocele. Perineal descent has also been associated with fecal incontinence. Nerve stretch and subsequent neuromuscular damage is one of the proposed mechanisms of fecal incontinence. Perform a careful rectovaginal examination evaluating the posterior vaginal wall and perineal body. If the area of anterior rectal wall bulging and the posterior wall prolapse is the same, this provides clinical confirmation of the presence of a rectocele. Palpation of loops of small bowel confirms an enterocele; a sigmoidocele is diagnosed if sigmoid colon is palpated. Performing a rectovaginal examination in the standing position may increase the detection of an enterocele by allowing the bowel to enter the enterocele sac. This search for an enterocele should continue in the operating room. If an enterocele is missed, posterior wall prolapse may persist following surgical management. Elevating the rectal finger up to the posterior vaginal wall helps identify an area with less support, although the clinical examination has not been shown to be accurate in comparison to the surgical identification of site-specific defects of the posterior vaginal wall. Last, pressure on the posterior wall of the vagina, directed downward toward the rectum, may facilitate identification of rectal prolapse or intussusception. Because anal incontinence commonly occurs with rectocele, assessment of the anal sphincter should be performed. This includes evaluation of anal tone, squeeze, and symmetry. If a symptomatic woman is found (or suspected) to have a disrupted anal sphincter on examination, further testing is indicated. A focused neurologic examination includes evaluation of sensation, motor function, and reflexes of sacral nerves 2–4. The patient is asked to discriminate between sharp and dull on the perineum. Assess pelvic floor muscle strength with the patient contracting and relaxing the pelvic floor muscles around the examiner’s fingers. Reflex testing includes the bulbocavernosus reflex and anal wink (see Chapters 6 and 11).
Diagnostic Tests A number of imaging techniques have been used to evaluate rectoceles. Defecography provides a two-dimensional view of the efficiency of rectal emptying and quantification of rectal parameters. The size of the rectocele is determined by measuring the distance between the line of the anterior border of the anal canal and the maximal point of the bulge of the anterior rectal wall into the posterior vaginal wall. Rectoceles have been described in nulliparous women. Anything less than 2 cm is considered normal, whereas a rectocele is considered large if the anterior rectal wall protrudes more than 3.5 cm. Contrast in the small and large bowels may also reveal the presence of an enterocele, sigmoidocele, or perineocele. Rectal intussusception and perineal descent may also be identified, although the clinical significance of rectal intussusception has not been determined. The dynamic nature of the study allows for insight into the defecation process. Retention of more than
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10% of the barium following defecation is referred to as barium trapping. This examination is done in an artificial environment, which may make the patient more prone to incomplete emptying. A situation in which defecography may convert a surgical procedure to one managed conservatively is the identification of pelvic floor dyssynergia. Defecation is effective through the coordination of relaxation of the levator ani and external anal sphincter and contraction of the colon. If the puborectalis or external anal sphincter is paradoxically contracted during defecation, this situation might respond to more conservative measures, such as the use of enemas or biofeedback. An electrophysiologic analysis of the puborectalis may also lead to this diagnosis. Another situation in which defecography might influence treatment is the identification of a sigmoidocele; the surgical approach to prolapse management might also include a sigmoid resection. Rectoceles that retrain contrast tend to be larger than those that do not. However, fluoroscopic evidence of barium trapping does not relate to patient symptoms. In the symptomatic, elderly population, Savoye-Collet et al. (2003) found no association between the abnormalities demonstrated by defecography and symptoms. Defecography performed following surgical management of rectoceles has generally shown a reduction in the size of the rectocele and improvement in emptying. The limitations of defecography include that it requires special equipment, exposes the patient to radiation, does not show the rectum and adjacent soft tissue structures simultaneously, and is uncomfortable and poorly accepted by patients. Dynamic magnetic resonance imaging (MRI) provides high-quality images of the pelvic soft tissues and viscera. MRI is noninvasive and does not require ionizing radiation or significant patient preparation. However, poor correlation exists between MRI grading of prolapse and clinical staging. To accomplish a dynamic MRI at most facilities, the woman is placed in the dorsal supine position with her legs together. MRI defecography has also been performed in the dorsal supine position with a sonographic transmission gel placed in the rectum and vagina. Images are obtained resting and while performing a Valsalva maneuver and with evacuation. However, during a Valsalva maneuver in this position, the true extent of the prolapse may not be exhibited because this is not a normal position for defecation and may not simulate that woman’s ability to defecate. An upright evaluation has been described but requires an open configuration MRI unit that is available in only a few medical centers. The limitations of this method of imaging include a lack of standardization of grading of prolapse, high cost, and relatively limited availability. At this time, there is a lack of a standardized method of establishing a radiologic diagnosis of rectocele. Clinical examination has good sensitivity for the detection of a rectocele; therefore, radiologic confirmation of the presence or absence of a rectocele is not worthwhile. Although defecatory dysfunction is common in women with prolapse, the extent of the prolapse does not necessarily correlate with the extent of bowel symptoms. If the woman’s primary complaint is defecatory dysfunction or fecal incontinence and not a bulge, surgical correction of the rectocele or perineal body defect may not correct her symptoms. Ancillary testing
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is then pursued based on the woman’s complaints. Validated functional and quality-of-life questionnaires are now available. These may be performed preoperatively and postoperatively to provide a standardized method of evaluating the surgical outcomes. The patient’s preoperative symptoms and surgical goals will guide the provider in the selection of additional testing. A woman who describes lifelong infrequent bowel movements (less than one per week) and an absence of a daily urge to defecate is unlikely to be cured of her constipation with a rectocele repair. A colon transit study may be helpful in identifying patients with slow-transit constipation. Dietary modifications, including fiber and laxatives, should be encouraged in any woman whose main complaint is constipation (see Chapter 25). In women with symptoms of anal incontinence, an evaluation and attempt at medical management should be performed before rectocele repair. An endoanal ultrasound provides anatomic detail of the integrity of the external and internal anal sphincters; EMG study of the external anal sphincter can provide neurologic information. Urodynamic testing with prolapse reduction may be useful in women with stage III or stage IV posterior wall prolapse. With retraction of the posterior wall prolapse (simulating correction of the prolapse), women may develop stress incontinence or have an increase in leak volumes. If potential or occult stress urinary incontinence or intrinsic sphincter deficiency is uncovered, this observation should be factored into preoperative surgical recommendations and surgical planning.
SURGICAL REPAIR TECHNIQUES Current repair techniques address connective tissue defects. The dysfunctional levator ani, which widens the levator hiatus, increases the stress and strain on the connective tissue, and is a likely key contributor to the development of pelvic organ prolapse. Currently, pelvic floor muscle exercises (with or without biofeedback) are our primary method of strengthening the remaining innervated pelvic floor muscles but do not address deinnervated or damaged muscle. The goals of rectocele repair are to provide anatomic correction, relieve prolapse symptoms, and restore normal bowel and sexual function without creating new symptoms. Evaluation of prolapsed posterior vaginal wall in the operating room should include a careful inspection for an enterocele or sigmoidocele, and for associated apical support defects. To compare various techniques for repair of posterior vaginal prolapse and anterior rectal wall prolapse is difficult because the indications for surgery and the standardized definitions of bowel function symptoms are not frequently reported. The definition of anatomic or functional cure also varies from study to study. Few prospective, randomized studies compare surgical procedures to correct rectoceles. The gynecologist typically approaches repair of a rectocele through a transvaginal incision. The patient is placed in the dorsal lithotomy position with her legs in high leg holders. The colorectal surgeon often performs an endoanal
repair of the rectocele, with the patient in the prone position. Patients are given preoperative prophylactic antibiotics and mechanical bowel preparation.
Posterior Colporrhaphy The posterior colporrhaphy was introduced in the nineteenth century. The goals of this procedure were to narrow the vaginal tube and genital hiatus and to create a shelf of support. The posterior colpoperineorrhaphy was thought to be the key component of all prolapse surgery (including correction of anterior wall and uterine prolapse). When postoperative results revealed that posterior colporrhaphy with perineorrhaphy treated a rectocele but was less effective for anterior wall or uterine prolapse, it continued to be the treatment of choice. Currently, it has remained a commonly performed surgical procedure for posterior wall prolapse. The traditional posterior colporrhaphy has an anatomic cure rate of 76% to 96% (Table 20-1). The posterior colporrhaphy is a plication of the vaginal wall in the midline, decreasing the width of the posterior vaginal wall and increasing the fibromuscularis in the midline. It purposely narrows the vaginal tube. To estimate adequate caliber, Allis clamps are placed on the posterior hymen and, when brought together in the midline, allow for a three-fingerbreadth genital hiatus. Traditionally, a perineorrhaphy is included in this repair. To begin the procedure, subepithelial injection of saline or local anesthetic with dilute epinephrine may be done to aid dissection. A triangular incision is made into the perineal skin with the base of the triangle at the hymen (Fig. 20-3, A). The skin is dissected away from the perineal body. The vaginal epithelium is opened in the midline, extending the incision to the vaginal apex (Fig. 20-3, B). The posterior vaginal epithelium is dissected bilaterally, away from the underlying fibromuscularis and extended to the levators (Fig. 20-3, C). Remaining in a plane close to the epithelium is important to avoid injury to the rectum. The posterior vaginal wall, stripped of its epithelium, is plicated in the midline with interrupted vertically or transversely placed lateral sutures incorporating a generous purchase of the fibromuscularis. Plication begins proximally and progresses toward the hymenal ring (Fig. 20-4). Care should be taken during the plication to ensure that each plication suture is in continuity with the previous one. If continuity is not maintained, ridging of the posterior vaginal wall may occur and be a source of dyspareunia. The vaginal epithelium is trimmed, if necessary, and closed with a running No. 2-0 absorbable suture. Care should be taken to avoid trimming too much vaginal epithelium, particularly in women with atrophy. The caliber of the vagina at the conclusion of the vaginal reconstruction should be three fingerbreadths in sexually active women. The plication of the fibromuscularis can include plication of the levator ani muscles. Interrupted sutures are placed in the muscular sidewall of the posterior wall and brought to the midline. This provides a sturdy posterior shelf but may further constrict the vaginal caliber and be a source of postoperative pain and/or dyspareunia; however, it is effective for elderly women with a wide levator hiatus who do not expect to be sexually active.
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42
231 171
87
12
12 >12
70 67
38 38
183 183
30 34
76 24
100 4
100 5
64 31
21 4
Vaginal Bulge (%)
100 16
33
50 0
20
Vaginal Digitation (%)
17 18
3 0
4 11
8 8
36
Fecal Incontinence (%)
Modified with permission from Cundiff GW, Fenner D. Evaluation and treatment of women with rectocele: focus on associated defecatory and sexual dysfunction. Obstet Gynecol 2004;104:1403 *Prospective study. † Definitions of “cure” and “dyspareunia” vary among studies.
82
90
12
22 33
100 88
75 54
Constipation (%)
8 17
37 5
26
16
8
23
Dyspareunia (%)†
■
53 53
76
96
12
25 25
Anatomic Cure (%)†
80
Mean FollowUp (Mo)
29 24
N
Posterior Colporrhaphy: Anatomic and Functional Results
Arnold et al. (1990) Preoperative Postoperative Mellgren et al. (1995)* Preoperative Postoperative Kahn and Stanton (1997) Preoperative Postoperative Weber et al. (2000)* Preoperative Postoperative Sand et al. (2001)* Preoperative Postoperative Maher et al. (2004)* Preoperative Postoperative Abramov et al. (2005) Preoperative Postoperative
Study (Year)
Table 20-1
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252
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B
C Figure 20-3 ■ Surgical repair of rectocele. A. A triangular incision is made in the epithelium of the overlying posterior fourchette and perineal body. B. The vaginal epithelium is opened in the midline. C. Dissection of the posterior vaginal wall is completed bilaterally, exposing the fibromuscularis from sidewall to sidewall. (Reprinted with the permission of The Cleveland Clinic Foundation.)
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Figure 20-5 ■ Locations of site-specific defects in the posterior vaginal wall. Defects in the posterior wall fibromuscularis may be found in the lateral sidewalls (L), midline (M), or in a transverse orientation (T) at the apex or distally near the perineal body. Combinations of defects may be identified. (Reprinted with the permission of The Cleveland Clinic Foundation.)
Figure 20-4 ■ Posterior colporrhaphy includes midline plication of the vaginal fibromuscularis over the rectum. (Reprinted with the permission of The Cleveland Clinic Foundation.)
Site-Specific Defect Repair The site-specific defect repair relies upon the theory advocated by Richardson (1976), that herniation of the rectum into the vagina is the result of identifiable defects in the fibromuscularis (rectovaginal fascia). Defects of the posterior vaginal wall may occur as an isolated defect in the lateral, distal, midline, and superior portions of the wall or as a combination of defects (Fig. 20-5). The anatomic cure rate of the site-specific posterior repair is 56% to 100%, as shown in Table 20-2. Most studies report no change or a decrease in dyspareunia in the series involving defect-specific rectocele repairs. The vaginal epithelium is opened with a transverse incision at the posterior fourchette (Fig. 20-6, A). The posterior vaginal epithelium is incised in the midline to a level proximal to the bulge and dissected away from the underlying fibromuscularis (Fig. 20-6, B). The dissection is extended laterally to the endopelvic fascial attachments of the posterior vaginal wall to the arcus tendineus fasciae pelvis and arcus tendineus fasciae rectovaginalis. The fibromuscularis is carefully inspected to identify breaks. Irrigation and a rectal examination may accentuate the defects to aid identification (Fig. 20-7). Defects are individually isolated and repaired with delayed-absorbable or nonabsorbable No. 0 or 2-0 suture (Fig. 20-8). If a distal defect is present, such as a separation of the fibromuscularis from the perineal body, absorbable suture is used for repair in an attempt to reduce the incidence of postoperative dyspareunia. Repair of perineal body defects is also addressed with interrupted sutures. A levator plication is not performed. Repeating the
rectal examination should confirm repair of the rectocele. The vaginal epithelium is closed with a running No. 2-0 absorbable suture. Currently, this is the technique of choice in a sexually active woman in whom the goals are to reduce the bulge, potentially improve rectal emptying, and avoid de novo dyspareunia.
Graft Augmentation Approximately one third of women undergoing surgery for prolapse or urinary incontinence will undergo a subsequent procedure for recurrence. In an effort to improve the anatomic durability of the rectocele repair, placement of a mesh to augment support of the posterior vaginal wall can be performed. Graft materials that have been used include allografts, xenografts, and permanent synthetic materials. The graft is used as a sheet to reinforce the posterior colporrhaphy or site-specific repair or to reinforce the existing posterior vaginal wall. The graft can also be placed through a perineal incision in the rectovaginal space between the posterior vaginal wall and the anterior rectal wall. A gynecologist typically places the graft through a vaginal incision as another layer of support upon completion of the rectocele repair. The graft is placed after plication of the fibromuscularis is completed (in the posterior colporrhaphy) or after the site-specific defects are closed (Fig. 20-9). The graft is attached bilaterally to the levator fascia. If the patient is concurrently undergoing an apical suspension procedure (with or without mesh), the apical portion of the graft can be attached to the apical support sutures. The graft material is attached bilaterally to the endopelvic attachment on the levator ani muscles in a proximal to distal fashion, ensuring that no tension is placed on the graft material. Delayedabsorbable or nonabsorbable No. 0 suture is used. The graft
82 90 100 92 56
6 12 3 18
125 72
66 46
67 67
42 33
124 124 >12
82
Anatomic Cure (%)†
12
Mean FollowUp (mo)
69 61
N
33 37
41 57
60 50
46 13
Constipation (%)
100 11
78 7
86 9
38 14
100 18
Vaginal Bulge (%)
30 15
24 21
39 18
Vaginal Digitation (%)
15 19
9 5
30
24 21
13 8
Fecal Incontinence (%)
Modified with permission from Cundiff GW, Fenner D. Evaluation and treatment of women with rectocele: focus on associated defecatory and sexual dysfunction. Obstet Gynecol 2004;104:1403. *Prospective study. † Definitions of “cure” and “dyspareunia” vary among studies.
Cundiff et al. (1998) Preoperative Postoperative Porter et al. (1999) Preoperative Postoperative Kenton et al. (1999) Preoperative Postoperative Glavind and Madsen (2000)* Preoperative Postoperative Singh et al. (2003)* Preoperative Postoperative Abramov et al. (2005) Preoperative Postoperative
Study (year)
Site-Specific Defect Rectocele Repair: Anatomic and Functional Results
8 16
31 15
12 3
28 8
67 46
29 19
Dyspareunia (%)†
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Table 20-2
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Figure 20-6 ■ Opening the posterior vaginal epithelium for a site-specific defect repair. A. A transverse incision at the level of the hymen can be done if there is no perineal body defect. B. The epithelium is opened in the midline. The dissection is extended proximally to the defect. (Reprinted with the permission of The Cleveland Clinic Foundation.)
A Figure 20-7 A finger is placed in the rectum to elevate the anterior rectal wall toward the posterior vaginal wall. Areas of weakness or defects in the fibromuscularis can be identified, as shown on the left. (Reprinted with the permission of The Cleveland Clinic Foundation.) ■
Figure 20-8 ■ Site-specific rectocele defects: identification and surgical repair. A. Midline defect of the fibromuscularis.
(Continued)
B
C
D
E
F
G
Figure 20-8 ■ Cont’d B. Left lateral defect of the fibromuscularis. C. Repair of left lateral defect with interrupted sutures. D. Distal transverse defect, separating the fibromuscularis of the posterior wall from the perineal body. E. Proximal transverse defect in the fibromuscularis near the apex. Repair of the proximal transverse defect is done as with a distal defect. If a level I vaginal vault suspension procedure is done, the distal portion of the break in the fibromuscularis may be incorporated in the apical repair. F. The distal defect is repaired with interrupted sutures. These sutures should reestablish continuity of the vaginal fibromuscularis with the perineal body. G. The epithelium of the posterior vagina and perineum is closed with running absorbable suture. (Reprinted with the permission of The Cleveland Clinic Foundation.)
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Figure 20-9 ■ Graft-augmented rectocele repair. A graft is trimmed and placed over a posterior colporrhaphy or site-specific defect repair. (Reprinted with the permission of The Cleveland Clinic Foundation.)
is trimmed and the distal portion of the graft is attached to the perineal body with interrupted, absorbable No. 0 sutures. The vaginal epithelium is closed and a perineorrhaphy is performed, if needed. The variety of graft materials available and methods of placement make it difficult to summarize the efficacy of graft augmentation. Long-term efficacy and safety have not been established. Randomized trials comparing posterior colporrhaphy and site-specific defect repair, with and without graft placement, are needed.
Abdominal Sacral Colpopexy (Colpoperineopexy) An abdominal or laparoscopic approach to rectocele repair can be performed when the rectocele is accompanied by apical prolapse. Suspension of the posterior vaginal wall is accomplished through a sacral colpopexy or sacral colpoperineopexy (in the case that the posterior support defect continues to the level of the perineal body). Mesh is placed on the posterior vaginal wall, posterior to the vaginal tube and bridged to the anterior longitudinal ligament of the sacrum. Various meshes have been used in sacral colpopexy procedures, but most evidence supports the use of polypropylene. To perform the procedure, the patient is placed in low leg holders with a Foley catheter in the bladder throughout the procedure. An end-to-end anastomosis (EEA) sizer may be placed in the vagina and one in the rectum to aid in identification of tissue planes. The procedure is accomplished through a Pfannenstiel incision into the peritoneal cavity or may be performed laparoscopically (see Chapter 17). If the laparoscopic procedure is performed, a reusable 5- or 10-mm port is placed at the umbilicus for operation of the laparoscope. Two 5/12-mm disposable ports are placed in the right and left lower quadrants for suture and mesh introduction. An additional 5-mm reusable port is placed on the left side lateral to the umbilicus. To access the presacral space, the sigmoid colon may be retracted to the left with a laparoscopic snake retractor.
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The surgical steps of the procedure are the same if performed through an open incision or laparoscopically. The right ureter is identified. The peritoneum is opened from the sacral promontory to the cul-de-sac lateral to the right side of the colon and medial to the right ureter. Sharp and blunt dissection is used to expose the anterior longitudinal ligament of the sacrum over S1 to S2. Hydrodissection of the presacral space may also be performed by placing a suction-irrigator underneath the peritoneum and inserting water into the space. The rectovaginal space is identified with an EEA sizer in the vagina (elevating the vagina toward the anterior abdominal wall) and one in the rectum (deflecting the rectum posteriorly). The rectovaginal space is entered sharply between the vagina and rectum. This avascular space is dissected with sharp and blunt dissection. The dissection proceeds to the perineal body for correction of a distal rectocele or significant perineal descent. Cautery is used sparingly in this dissection to preserve vascularization of the vagina (and potentially decrease the risk of mesh erosion). Laparoscopically, the posterior mesh (approximately 3 cm wide × 15 cm long) is introduced into the abdomen through a lower quadrant port. The mesh is attached to the posterior vaginal wall with a series of three to five pairs of No. 2-0 or No. 0 nonabsorbable sutures. The posterior mesh is then laid over the sacrum to determine the length of the mesh bridge. The mesh should provide support of the posterior vaginal wall without tension. The mesh is then attached to the anterior longitudinal ligament with three No. 0 nonabsorbable sutures. The excess mesh is trimmed, and the peritoneum is closed with No. 2-0 absorbable suture.
Endorectal Repair Endorectal repair of distal rectoceles was first recommended by Sullivan et al. in 1968. A colorectal surgeon typically approaches the rectocele repair from this end. The success rate for repair of a distal rectocele is 47% to 82% (Cundiff and Fenner, 2004). An endorectal approach allows for simultaneous correction of other anorectal pathology, such as hemorrhoids and mucosal rectal prolapse. Ayabaca et al. (2002) reported that 53% of women who underwent a rectocele repair also had rectal mucosa prolapse and 41% had hemorrhoids. Repair of proximal (high) rectoceles is difficult with the endorectal approach because of inadequate exposure. This procedure is done in the prone jackknife position, with the buttocks spread and taped. An anal retractor is inserted to expose the anterior rectal wall. A transverse incision is made in the rectal mucosa at or proximal to the dentate line. Two vertical incisions are made in parallel. A flap is developed, including a portion of the muscular wall of the rectum to a level proximal to the rectocele (usually approximately 7 cm long). Vertical plication sutures are placed with No. 3-0 polyglycolic acid suture. One or two transverse sutures are placed to buttress the vertically plicated area. Levator ani plication can also be done with the endorectal approach. The rectal mucosal flap is trimmed, and the rectal mucosa is closed with a running No. 5-0 polyglycolic acid suture. The use of the circular stapler for closure of the rectocele and treatment of the redundant rectal mucosa has been described.
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Perineorrhaphy A perineorrhaphy, when indicated, completes the vaginal approach to a rectocele repair. Allis clamps are placed on the posterior hymen and brought together in the midline. Preservation of three fingerbreadths at the genital hiatus is important for comfortable future coital activity. A triangular incision is made medial to the Allis clamps, extending to the midline of the perineal skin, with the base of the triangle at the posterior hymen. The bulbospongiosus muscles are plicated in the midline of the perineal body with an interrupted Vicryl No. 0 suture. The transverse perinei muscles are plicated (Fig. 20-10). An anal sphincteroplasty may be performed, as indicated, for anal incontinence and an external/internal anal sphincter defect. The skin is closed with a running No. 2-0 Vicryl suture. Extensive dissection and repair is required for women with an absent perineal body, most commonly as a result of difficult vaginal delivery or surgical trauma. A transverse semicircular incision is made in the layer separating the posterior vaginal wall and the anterior rectal wall. Dissection is extended laterally and proximally. To facilitate proximal dissection in the rectovaginal space without injury to the rectal mucosa, the surgeon may insert a finger of the nondominant hand into the rectum. The internal anal sphincter is plicated
in the midline with No. 3-0 absorbable suture. The rectal mucosa is reapproximated, as needed, with a running absorbable No. 3-0 suture, and extended to the skin overlying the external anal sphincter. Dissection of the anus is performed to identify the retracted ends of the external anal sphincter. Care should be taken with this step to avoid extensive lateral and posterior dissection and injury to the inferior hemorrhoidal nerves and vessels. The scarred ends of the external anal sphincter are identified and reapproximated in an overlapping fashion with vertical mattress sutures of No. 0-delayed absorbable suture. The scar on the ends of the external anal sphincter is left intact and used for suture placement. The transverse perinei and bulbospongiosus muscles are plicated in the midline. With midline construction of the perineal body, the transverse portion of the initial incision becomes vertically oriented. The vaginal epithelium is closed with a No. 2-0 absorbable suture. The skin of the perineal body is closed in an inverted Y shape with interrupted absorbable No. 2-0 sutures. The patient is instructed that superficial wound breakdown on the perineum may occur. In most cases, this superficial wound breakdown will respond to conservative management rather than require aggressive debridement. The use of absorbable sutures in the perineal body and distal vagina may decrease the incidence of entrance dyspareunia, but care should be taken to avoid ridging the introitus with a tight plication of the bulbocavernosus muscles. A perineorrhaphy will increase slightly the functional length of the posterior vaginal wall.
Postoperative Instructions A vaginal pack and Foley catheter are usually placed after the surgery and removed the next morning. The patients are discharged with instructions to avoid lifting anything greater than 10 lb and to take stool softeners to avoid straining for 3 months. Pelvic rest (avoiding the use of tampons, douching, or sexual intercourse) is recommended for at least 6 weeks. Patients who undergo an anal sphincteroplasty as part of their perineal body repair are placed on broad-spectrum antibiotic coverage for 1 week.
ANALYSIS OF OUTCOMES
Figure 20-10 ■ Perineorrhaphy. Following the completion of the repair of the rectocele, the perineal body may need to be reconstructed. The bulbospongiosus and the transverse perinei muscles are plicated in the midline with absorbable sutures. (Reprinted with the permission of The Cleveland Clinic Foundation.)
The patient’s surgical goals should be elicited preoperatively. If the goal of the surgery is correction of the bulge, this may be accomplished through various techniques. To compare the various surgical repairs is difficult because the definition of cure has varied with each study. In some studies, functional resolution or improvement is defined as a cure, while others define cure as strictly anatomic but vary at which point anatomic cure lies. Cundiff and Fenner (2004) reviewed the literature and summarized the anatomic and functional outcomes after posterior colporrhaphy, site-specific defect repair, transanal repair, and rectocele repair with graft materials. Anatomic cure ranges from 76% to 96% for posterior colporrhaphy and from 56% to 100% for site-specific defect repair. The data are summarized and updated in Tables 20-1 and 20-2. The sensation of a vaginal bulge is generally relieved, as
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is vaginal digitation to assist emptying, but disorders of defecation, such as constipation and fecal incontinence, are often not significantly improved. Maher et al. (2004) reported on 38 women with symptomatic rectoceles (stage II or greater) and obstructed defecation treated with midline rectovaginal fascial plication. Seventy-nine percent of women had anatomic cure after 24 months, and 87% no longer experienced obstructed defecation. In this study, the rate of dyspareunia actually improved, possibly due to minimal trimming of vaginal epithelium, and 97% of women were very satisfied. Rates of cure after transanal repair range from 70% to 98%. A recent Cochrane Review of surgical management of pelvic organ prolapse (Maher et al., 2004, Cochrane Database Syst Rev) reported that, for posterior vaginal wall prolapse, the transvaginal approach is associated with a lower rate of recurrence for rectocele and/or enterocele than the transanal approach (RR 0.24; 95% CI, 0.09–0.64). However, a higher blood loss and more pain occur with the vaginal approach. The Cochrane Review noted that insufficient data exist on the effect of surgery on bowel symptoms and on whether one variation of vaginal repair (posterior colporrhaphy vs. sitespecific defect repair vs. graft augmentation) is superior to others. Risk factors for failure of rectocele repairs have not been systematically studied. Genetic predisposition, severe childbirth trauma with levator muscle dysfunction, chronic straining of stool, and other factors probably increase a patient’s risk of recurrence. For prolapse repairs in general, younger women with more severe disease (stage III or IV prolapse) are more likely to experience recurrence after surgery. Few studies have reported clinical results after graftaugmented rectocele repairs. In a prospective randomized surgical trial, Sand et al. (2001) showed no improvement in cure, with addition of polyglactin 910 mesh to posterior colporrhaphy. Recently, Altman et al. (2005) reported a 38% recurrence (greater than stage II) after rectocele repair with porcine dermis graft overlay. Further studies are needed to determine the role of grafts for treatment of rectoceles. Correction of anatomy is not always equivalent to symptomatic cure or patient satisfaction. In general, satisfaction seems to be high for relief of symptoms of prolapse. However, correction of function is more complicated because of multiple confounding factors, such as coexisting bowel and sexual dysfunction. Randomized, prospective trials comparing different procedures, which include anatomic and functional preoperative and postoperative data, are underway.
COMPLICATIONS Short-term complications associated with rectocele repair include pain, temporary urinary retention, and constipation. Hematoma, infection, inclusion cyst formation, fecal impaction, injury to the rectum with the development of a rectovaginal or a rectoperineal fistula may occur but are uncommon. Anal incontinence has been reported to occur in up to 19% of women who undergo a rectocele repair. A significant association exists between fecal incontinence and more than one prior posterior colporrhaphy. A rectocele
Surgical Treatment of Rectocele and Perineal Defects
259
may be associated with altered rectal sensation and/or anal sphincter defect related to prolonged straining or trauma. Anal sphincter function may be improved if identified preoperatively and corrected at the time of rectocele repair. However, anal sphincter function may be damaged by a rectocele repair, particularly with the dilation associated with an endoanal repair. It is important to determine whether a woman with recurrent posterior wall prolapse has a history of fecal incontinence and to consider ancillary testing to anatomically evaluate the anal sphincter (endoanal ultrasonography) and neurologic function (EMG) of the external anal sphincter. Postoperative sexual dysfunction has been a significant concern for several decades with the surgical management of rectoceles and perineal body defects. Francis and Jeffcoate (1961) observed a high rate of sexual dysfunction following prolapse surgery. Seventy of 140 (50%) sexually active women reported apareunia or dyspareunia after an anterior and posterior colporrhaphy and perineorrhaphy. On postoperative examination, 43 of the 70 women were found to have a significantly narrowed vagina that would admit one finger only. Haase and Skibsted (1988) noted increased or de novo dyspareunia in 21% of woman who underwent an anterior and posterior colpoperineorrhaphy. Kahn and Stanton (1997) routinely plicated the levator muscles and attributed an increase in sexual dysfunction from 18% to 27% to pressure atrophy of the levator muscles and associated scar formation. Arnold et al. (1990) found similar rates of dyspareunia among women who underwent a transvaginal approach (23%) versus an endoanal approach (21%). In a prospective observational study of sexual function after prolapse repairs, Weber et al. (2000) found that performance of a posterior colporrhaphy, especially a posterior colporrhaphy with Burch colposuspension, were the only variables that predicted postoperative dyspareunia. Vaginal dimensions, in general, did not predict dyspareunia, and pain was often due to ridging in the posterior vaginal wall. The attractiveness of the site-specific defect rectocele repair is that sexual function was often found to improve (or not worsen) following surgical correction of a rectocele. In general, avoidance of sutures that constrict the mid- or distal vagina and care to not over-trim the vaginal epithelium before closing will help keep postoperative dyspareunia to a minimum. Venkatesh and Ramanujam (1996) reported a 50% (6/12) rate of persistent perineal pain following a perineal body reconstruction in women with a preoperative perineal pain and a cloaca. The patients with persistent postoperative perineal pain described dyspareunia and dissatisfaction with the surgical results, despite excellent anatomic reconstruction of the perineal body. Rectocele repairs that include a biologic or synthetic meshes have complications related to the specific mesh material that is used. The potential complications that have been described with the use of graft material are erosion into the surrounding tissue (in this case, the vagina and rectum); infection; scarring (which may increase the occurrence of dyspareunia); allergic reaction to the material used; and failure. A thorough understanding of the mesh material and its risks and benefits is important before its use is recommended as part of rectocele repairs.
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Risks associated with abdominal sacral colpoperineopexy include bleeding from the sacral vessels, mesh infection/erosion, bowel injury/obstruction, stress urinary incontinence, and recurrent prolapse. The risk of mesh erosion with an abdominal sacral colpopexy is approximately 3% to 8%, with the majority occurring within the first 2 postoperative years. This rate is increased if the mesh (40%) or sutures (16%) are introduced vaginally and then secured to the sacrum. The risk of mesh erosion will also differ with the type of mesh used. Polypropylene and Mersilene are commonly used synthetic mesh materials.
Olsen AL, Smith VJ, Bergstrom JO, et al. Incidence and clinical characteristics of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 1997;89:501. Ricci JV, Thom CH. The myth of a surgically useful fascia in vaginal plastic reconstructions. Q Rev Surg Obstet Gynecol 1954;11:253. Stern R, Bernstein P, Sherer DM. Spontaneous delivery through the rectovaginal septum and perineal body: an unusual complication of persistent occiput posterior position. J Matern Fetal Med 1998;7:194. Uhlenhuth E, Nolley GW. Vaginal fascia, a myth? Obstet Gynecol 1957;10:349. Ward GG. Technique of repair of enterocele (posterior vaginal hernia) and rectocele. JAMA 1922;79:709. Woodman PJ, Graney DO. Anatomy and physiology of the female perineal body with relevance to obstetrical injury and repair. Clin Anat 2002;15:321.
CONCLUSION
EVALUATION
Our population is aging. People over age 65 are estimated to comprise 20% of the population in 2030. The demand for the treatment of prolapse will increase as the population ages. To provide superior care for our patients, it is imperative that we perform clinical research studies in women with rectoceles to determine the most efficacious procedure associated with the fewest complications.
Bibliography Department of Health and Human Services, Administration on Aging: Older Population by Age: 1900–2050. Accessed May 9, 2004, from http://www. aoa.gov/prof/Statistics/online_stat_data/AgePop2050.asp.
ANATOMY AND PATHOPHYSIOLOGY Boreham MK, Wai CY, Miller RT, et al. Morphometric properties of the posterior vaginal wall in women with pelvic organ prolapse. Am J Obstet Gynecol 2002;187:1501. Boyles SH, Weber AM, Meyn L. Procedures for pelvic organ prolapse in the United States, 1979–1997. Am J Obstet Gynecol 2003;188:108. Cundiff GW, Fenner D. Evaluation and treatment of women with rectocele: focus on associated defecatory and sexual dysfunction. Obstet Gynecol 2004;104:1403. DeLancey JO. Standing anatomy of the pelvic floor. J Pelvic Surg 1996; 2:260. DeLancey JO. Structural anatomy of the posterior pelvic compartment as it relates to rectocele. Am J Obstet Gynecol 1999;180:815. DeLancey JO, Hurd WW. Size of the urogenital hiatus in the levator ani muscles in normal women and women with pelvic organ prolapse. Obstet Gynecol 1998;91:364. Emmet TA. A study of the etiology of perineal laceration, with a new method for its proper repair. Trans Am Gyn Soc 1883;8:210. 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. Hudson CN, Sohaib SA, Shulver HM, Reznek RH. The anatomy of the perineal membrane: its relationship to injury in childbirth and episiotomy. Aust N Z J Obstet Gynaecol 2002;42:193. Leffler KS, Thompson JR, Cundiff GW, et al. Attachment of the rectovaginal septum to the pelvic sidewall. Am J Obstet Gynecol 2001;185:41. Meschia M, Buonaguidi A, Pifarotti P, et al. Prevalence of anal incontinence in women with symptoms of urinary incontinence and genital prolapse. Obstet Gynecol 2002;100:719. Morren GL, Beets-Tan RG, van Engelshoven JM. Anatomy of the anal canal and perianal structures as defined by phased-array magnetic resonance imaging. Br J Surg 2001;88:1506. Oelrich TM. The striated urogenital sphincter muscle in the female. Anat Rec 1983;205:223. Oh C, Kark AE. Anatomy of the perineal body. Dis Colon Rectum 1973;16:444. Oladokun A, Babarinsa IA, Adewole IF. The deficient perineum: oblique presentation of a clinically obvious anomaly. Afr J Med Sci 2002;31:267.
Agildere AM, Tarhan NC, Ergeneli MH, et al. MR rectography evaluation of rectoceles with oral gadopentetate dimeglumine and polyethylene glycol solution. Abdom Imaging 2003;28:28. Bartram C. Dynamic evaluation of the anorectum. Radiol Clin North Am 2003;41:425. 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. Burrows LJ, Sewell C, Leffler KS, Cundiff KS. The accuracy of clinical evaluation of posterior vaginal wall defects. Int Urogynecol J 2003;14:160. Cortes E, Reid WM, Singh K, Berger L. Clinical examination and dynamic magnetic resonance imaging in vaginal vault prolapse. Obstet Gynecol 2004;103:41. Henry MM, Parks AG, Swash M. The pelvic floor musculature in the descending perineum syndrome. Br J Surg 1982;69:470. Hullfish KL, Bovbjerg VE, Gibson J, Steers WD. Patient-centered goals for pelvic floor dysfunction surgery: what is success, and is it achieved? Am J Obstet Gynecol 2002;187:88. Johansson C, Nilsson BY, Holmström B, et al. Association between rectocele and paradoxical sphincter response. Dis Colon Rectum 1992;35:503. Kenton K, Shott S, Brubaker L. The anatomic and functional variability of rectoceles in women. Int Urogynecol J 1999;10:96. Mimura T, Roy AJ, Storrie JB, Kamm MA. Treatment of impaired defecation associated with rectocele by behavioral retraining (biofeedback). Dis Colon Rectum 2000;43:1267. Myers DL, LaSala CA, Hogan JW, Rosenblatt PL. The effect of posterior wall support defects on urodynamic indices in stress urinary incontinence. Obstet Gynecol 1998;91:710. Rentsch M, Paetzel C, Lenhart M, et al. Dynamic magnetic resonance imaging defecography. Dis Colon Rectum 2001;44:999. Savoye-Collet C, Savoye G, Koning E, et al. Defecography in symptomatic older women living at home. Age Ageing 2003;32:347. Steiner RA, Healy JC. Patterns of prolapse in women with symptoms of pelvic floor weakness: magnetic resonance imaging and laparoscopic treatment. Curr Opin Obstet Gynecol 1998;10:295. Swift SE, Herring M. Comparison of pelvic organ prolapse in the dorsal lithotomy compared with the standing position. Obstet Gynecol 1998;91:961. 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;189:372. Segal JL, Karram MM. Evaluation and management of rectoceles. Curr Opin Urol 2002;12:345. Tunn R, DeLancey JO, Howard D, et al. MR imaging of levator ani muscle recovery following vaginal delivery. Int Urogynecol J 1999;10:300. Weber AM, Walters MD, Ballard LA, et al. Posterior vaginal prolapse and bowel function. Am J Obstet Gynecol 1998;179:1446.
SURGICAL TECHNIQUES AND COMPLICATIONS Abramov Y, Gandhi S, Goldberg RP, et al. Site-specific rectocele repair compared with standard posterior colporrhaphy. Obstet Gynecol 2005;105:314. Altman D, Zetterström J, López A, et al. Functional and anatomic outcome after transvaginal rectocele repair using collagen mesh: a prospective study. Dis Colon Rectum 2005;48:1.
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Altomare DF, Rinaldi M, Veglia A, et al. Combined perineal and endorectal repair of rectocele by circular stapler. Dis Colon Rectum 2002;45:1549. Arnold MW, Stewart WR, Aguilar PS. Rectocele repair: four years’ experience. Dis Colon Rectum 1990;33:684. Ayabaca SM, Zbar AP, Pescatori M. Anal continence after rectocele repair. Dis Colon Rectum 2002;45:63. Cogan JE, Harris JW. Rectal complications after perineorrhaphy and episiotomy. Arch Surg 1966;93:634. Cundiff GW, Weidner AC, Visco AG, et al. An anatomic and functional assessment of the discrete defect rectocele repair. Am J Obstet Gynecol 1998;179:1451. 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;177:1345. Francis WJ, Jeffcoate TN. Dyspareunia following vaginal operations. J Obstet Gynaecol Br Commonw 1961;68:1. Fox SD, Stanton SL. Vault prolapse and rectocele: assessment of repair using sacrocolpopexy with mesh interposition. Br J Obstet Gynaecol 2000;107:1371. Glavind K, Madsen H. A prospective study of the discrete fascial defect rectocele repair. Acta Obstet Gynecol Scand 2000;79:145. Hakelius L. Reconstruction of the perineal body as treatment for anal incontinence. Br J Plast Surg 1979;32:245. Haase P, Skibsted L. Influence of operations for stress incontinence and/or genital descensus on sexual life. Acta Obstet Gynecol Scand 1988;67:659. Jeffcoate TN. Posterior colpoperineorrhaphy. Am J Obstet Gynecol 1959;77:490. Kahn MA, Stanton SL. Posterior colporrhaphy: its effects on bowel and sexual function. Br J Obstet Gynaecol 1997;104:82. Kenton K, Shott S, Brubaker L. Outcome after rectovaginal fascia reattachment for rectocele repair. Am J Obstet Gynecol 1999;181:1360. Kenton KS, Woods MP, Brubaker L. Uncomplicated erosion of polytetrafluoroethylene grafts into the rectum. Am J Obstet Gynecol 2002;187:233. Khubchandani IT, Clancy JP, Rosen L, et al. Endorectal repair of rectocele revisited. Br J Surg 1997;84:89. Kohli N, Miklos JR. Dermal graft-augmented rectocele repair. Int Urogynecol J 2003;14:146. López A, Anzén B, Bremmer S, et al. Cystodefecoperitoneography in patients with genital prolapse. Int Urogynecol J 2002;13:22. Maher C, Baessler K, Glazener CM, et al. Surgical management of pelvic organ prolapse in women. Cochrane Database Syst Rev 2004;4: CD004014. Maher CF, Qatawneh AM, Baessler K, et al. Midline rectovaginal fascial plication for repair of rectocele and obstructed defecation. Obstet Gynecol 2004;104:685.
Surgical Treatment of Rectocele and Perineal Defects
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Mellgren A, Anzén B, Nilsson B, et al. Results of rectocele repair: a prospective study. Dis Colon Rectum 1995;38:7. Miklos JR, Moore RD, Kohli N. Laparoscopic surgery for pelvic support defects. Curr Opin Obstet Gynecol 2002;14:387. Nichols DH. Posterior colporrhaphy and perineorrhaphy: separate and distinct operations. Am J Obstet Gynecol 1991;164:714. Olsen AL, Smith VJ, Bergstrom JU, et al. Incidence and clinical characteristics of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 1997;89:501. Porter WE, Steele A, Walsh P, et al. The anatomic and functional outcomes of defect-specific rectocele repairs. Am J Obstet Gynecol 1999;181:1353. Richardson AC, Lyon JB, Williams NL. A new look at pelvic relaxation. Am J Obstet Gynecol 1976;126:568. Rovner ES, Ginsberg DA. Posterior vaginal wall prolapse: transvaginal repair of pelvic floor relaxation, rectocele, and perineal laxity. Tech Urol 2001;7:161. Sand K, 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. Singh K, Cortes E, Reid WM. Evaluation of the fascial technique for surgical repair of isolated posterior vaginal wall prolapse. Obstet Gynecol 2003;101:320. Sullivan ES, Leaverton GH, Hardwick CE. Transrectal perineal repair: an adjunct to improved function after anorectal surgery. Dis Colon Rectum 1968;11:106. Sehapayak S. Transrectal repair of rectocele: an extended armamentarium of colorectal surgeons. A report of 355 cases. Dis Colon Rectum 1985;28:422. Van Dam JH, Hop WC, Schouten WR. Analysis of patients with poor outcome of rectocele repair. Dis Colon Rectum 2000;43:1556. 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;42:204. Venkatesh KS, Ramanujam P. Surgical treatment of traumatic cloaca. Dis Colon Rectum 1996;39:811. Visco AG, Weidner AC, Barber MD, et al. Vaginal mesh erosion after abdominal sacral colpopexy. Am J Obstet Gynecol 2001;184:297. 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;183:257. Weber AM, Walters MD, Piedmonte MA. Sexual function and vaginal anatomy in women before and after surgery for pelvic organ prolapse and urinary incontinence. Am J Obstet Gynecol 2000;182:1610. Whiteside JL, Weber AM, Meyn LA, et al. Risk factors for prolapse recurrence after vaginal repair. Am J Obstet Gynecol 2004;191:1533.
Surgical Treatment of Vaginal Vault Prolapse and Enterocele
21
Mickey M. Karram and Mark D. Walters
PATHOLOGY OF PELVIC ORGAN PROLAPSE 262 PREVALENCE AND DEMOGRAPHICS 263 ENTEROCELE 263 Definition and Types 263 Diagnosis 264 Surgical Repair Techniques 265 VAGINAL PROCEDURES THAT SUSPEND THE APEX 267 Sacrospinous Ligament Suspension 267 Endopelvic Fascia Repair (Modified McCall Culdoplasty) 275 Iliococcygeus Fascia Suspension 276 High Uterosacral Ligament Suspension 276 Infracoccygeal Sacropexy 279 ABDOMINAL PROCEDURES THAT SUSPEND THE APEX 279 Abdominal Sacral Colpopexy 279 High Uterosacral Ligament Suspension 284 SURGICAL APPROACHES—VAGINAL VERSUS ABDOMINAL 284 UTERINE PRESERVATION DURING SURGERY FOR UTEROVAGINAL PROLAPSE 285 SUMMARY 285
In recent years, the problem of pelvic organ prolapse has been given much more attention. Many women are living longer, and more interest exists in maintaining self-image of femininity and the capacity of sexual activity beyond menopause. The management of pelvic organ prolapse can be difficult; several support defects often coexist, and simple anatomic correction of the various defects does not always result in normal function of the vagina and surrounding organs. To accomplish the goals of pelvic reconstruction, the surgeon must thoroughly understand normal anatomic support and physiologic function of the vagina, bladder, and rectum. These goals are to restore anatomy, maintain or restore normal bowel and bladder function, and maintain vaginal capacity for sexual intercourse. This chapter discusses the pathology and surgical correction of enterocele, uterovaginal prolapse, and posthysterectomy apical prolapse. Normal anatomy of the pelvic diaphragm is discussed in detail in Chapter 2. The evaluation of patients with pelvic organ prolapse, especially regarding their symptoms, physical examination, and diagnostic tests, is discussed in Chapters 5 and 6.
PATHOLOGY OF PELVIC ORGAN PROLAPSE Pelvic organ prolapse can result when normal pelvic organ supports are subjected chronically to increases in intraabdominal pressure or when defective genital support responds to normal intra-abdominal pressure. Individual organs that pass through the pelvic floor can lose support singly or in combination, resulting in various degrees and combinations of pelvic organ prolapse. This loss of support occurs as a result of damage to any of the pelvic supportive systems. These systems include the bony pelvis, to which the soft tissues ultimately attach; the subperitoneal retinaculum and smooth muscle component of the endopelvic fascia (the cardinal and uterosacral ligament complex); the pelvic diaphragm, with the levator ani muscles and their fibromuscular attachments to the pelvic organs; and the perineal membrane. The perineal body and the walls of the vagina can lose tone and weaken from pathologic stretching from childbirth and attenuating changes of aging and menopause. Loss of support or integrity of the anterior and posterior vaginal walls results in cystocele and enterorectocele, respectively. Uterovaginal prolapse occurs with damage or attenuation of endopelvic fascia that supports the uterus and upper vagina over the pelvic diaphragm. Furthermore, when the muscles within the pelvic diaphragm weaken as a result of congenital factors, childbirth injury, pelvic neuropathy, or aging, the levator ani lose resting tone and fail to contract quickly and strongly with increases in intra-abdominal pressure. Muscle atrophy and a wider levator hiatus result; weaker and less rapid muscle contractions with rises in intra-abdominal pressure contribute to related symptoms of urinary and fecal incontinence. A useful approach to understanding the pathophysiology of prolapse was described by Bump and Norton (1998). They proposed considering risk factors for the development of prolapse as predisposing, inciting, promoting, or decompensating events. Predisposing factors are genetic, race, and gender; inciting factors are pregnancy and delivery, surgery such as hysterectomy for prolapse, myopathy, and neuropathy; promoting factors are obesity, smoking, pulmonary disease, constipation, and recreational or occupational activities; and decompensating factors are aging, menopause,
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Surgical Treatment of Vaginal Vault Prolapse and Enterocele
debilitation, and medications. Depending on the combination of risk factors in an individual, prolapse may or may not develop over her lifetime. With further research on the human genome project, risk factors will continue to be identified. Eventually, we may be able to predict those at highest risk for developing prolapse. Modifiable risk factors can be altered to decrease the likelihood of subsequent prolapse. Obesity is one of the modifiable risk factors identified so far. Although increased parity is a risk factor for prolapse, nulliparity does not provide absolute protection against prolapse. Data from the Women’s Health Initiative (Hendrix et al., 2002) noted that almost one fifth of nulliparous women had some degree of prolapse. These data contradict those who enthusiastically promote cesarean delivery for all women to prevent prolapse. Normally, the vaginal axis in an erect woman is nearly horizontal in the upper half of the vagina, with the uterus and upper 3 or 4 cm of the vagina lying over the levator plate in the hollow of the sacrum (Fig. 21-1). Funt et al. (1978) found that the vagina is directed toward the S3 and S4 vertebras and extends approximately 3 cm past the ischial spines in most nulliparous women. Increases in intra-abdominal pressure compress the vagina anteriorly to posteriorly over the contracted levator muscles in the midline (levator plate). Diminished muscle tone may result in loss of stability of the levator plate, widening of the levator hiatus, and loss of an adequate base to support the upper vagina and uterus in the normal axis. Distortion of the normal vaginal axis during reconstructive pelvic surgery predisposes women to the development of pelvic organ prolapse at an anatomic site opposite to where the repair was performed. Examples of this are the development of posterior vaginal wall prolapse after colposuspension procedures for stress incontinence and the development of anterior vaginal wall prolapse after suspension of the vaginal apex to the sacrospinous ligament. Connective tissue defects have been found in women with uterine prolapse and stress incontinence. In several studies, Mädakinen et al. (1986, 1987) identified abnormal histologic changes in the pelvic connective tissue in 70% of women with uterine descent, compared with 20% of normal
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controls. Decreased cellularity (fibroblasts) and an increase in collagen fibers were observed. Ulmsten et al. (1987) reported 40% less total collagen in the skin and round ligaments of women with stress incontinence when compared with that of continent women. These studies and others suggest that abnormal connective tissue may be associated with pelvic organ prolapse and stress urinary incontinence.
PREVALENCE AND DEMOGRAPHICS Because the prevalence of pelvic organ prolapse increases with age, the changing demographics of the world’s population will result in even more affected women. Based on projections from the U.S. Census Bureau, the number of American women age 65 and over will double in the next 25 years to more than 40 million women by 2030. One study by Luber et al. (2001) noted that the demand for health care services, related to pelvic floor disorders, will increase at twice the rate of the population itself. Using data from a large U.S. Northwest health maintenance organization database, Olsen et al. (1997) reported the risks of pelvic organ prolapse or urinary incontinence surgery by age 80 as 11.1%. Surgery for pelvic organ prolapse with continence surgery (22%) or without (41%) accounted for 63% of this risk, or a lifetime risk of 7%. Boyles et al. (2003) reported that over a nearly 24-year period reviewed, the rate of procedures to correct prolapse decreased slightly, but not significantly, and that the surgical indication for approximately 7% to 14% of hysterectomies is listed as pelvic organ prolapse. Data from the U.S. National Hospital Discharge Survey (NHDS) indicate that approximately 200,000 women undergo surgery for pelvic organ prolapse annually. A study by Brown et al. (2002), using data from the NHDS for surgical rates, indicated that approximately 22.7 per 10,000 women had some form of pelvic organ prolapse surgery in a year. As expected, surgical rates vary with age peaking in the sixth decade, with an average age of surgery of 55 years. Racial differences were also reported, with Caucasian women having a threefold greater rate of pelvic organ prolapse surgery than African American women. Pelvic organ prolapse is common worldwide. Samuelsson et al. (1999) reported a prevalence of pelvic organ prolapse of 30.8% among Swedish women ages 20 to 59, with 2% having prolapse to the introitus. In the United Kingdom two hospitalizations per 1000 person-years for pelvic organ prolapse occur by age 60 (Mant et al., 1997). Sajan and Fikree (1999) reported that 19.1% of women in Pakistan who were under age 30 reported feeling symptoms of prolapse.
ENTEROCELE Definition and Types
Figure 21-1 ■ Normal vaginal axis of nulliparous woman in the standing position. Note that the upper third of the vagina is nearly horizontal and is directed toward the S3 and S4 sacral vertebras. (From Funt MI, Thompson JD, Birch H. Normal vaginal axis. South Med J 1978;71:1534, with permission.)
Enterocele is a hernia in which peritoneum and abdominal contents displace the vagina and may even be in contact with vaginal mucosa. The normal intervening endopelvic fascia is deficient or absent, and small bowel fills the hernia sac. Generally, enteroceles have been divided into four types: congenital, traction, pulsion, and iatrogenic. Congenital
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Management of Stress Urinary Incontinence and Pelvic Organ Prolapse
enterocele is rare. Factors that may predispose to the development of congenital enterocele include neurologic disorders, such as spina bifida and connective tissue disorders. Traction enterocele occurs secondary to uterovaginal descent, and pulsion enterocele results from prolonged increases in intraabdominal pressure. The two latter types of enterocele may coexist with apical vaginal prolapse, cystocele, or rectocele. Iatrogenic enterocele occurs after surgical procedures that elevate the normally horizontal vaginal axis toward a vertical direction; examples include colposuspension and needle urethropexy operations for stress incontinence, or hysterectomy, with or without repair, when the vaginal cuff and cul-de-sac are not managed effectively. Clinically, enteroceles are best classified based on their anatomic location. Apical enteroceles herniate through the
apex of the vagina, posterior enteroceles herniate posteriorly to the vaginal apex, and anterior enteroceles herniate anteriorly to the vaginal apex (Fig. 21-2).
Diagnosis Enteroceles may commonly occur in association with rectocele and/or cystocele. When these hernias coexist with rectoceles, the rectovaginal examination may demonstrate the rectocele as distinct from the bulging sac that arises from a higher point in the vagina. Visual inspection of the posterior vaginal wall may reveal a transverse furrow between the two hernias. However, in many posthysterectomy prolapse patients, it is difficult to preoperatively determine whether an enterocele sac coexists with a large rectocele or cystocele.
Figure 21-2 ■ Cross-section of pelvic floor showing various anatomic locations of enteroceles. A. Anterior enterocele—defect in the pubocervical fascia near its attachment to the vaginal apex. The peritoneal sac with its contents protrudes anterior to the vaginal cuff. B. Apical enterocele—defect at the vaginal apex; the peritoneal sac protrudes between the pubocervical fascia anterior and the rectovaginal fascia posterior. C. Posterior enterocele—defect posterior to the vaginal cuff. The peritoneal sac protrudes through the defect in rectovaginal fascia, posterior to the vaginal cuff.
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Surgical Treatment of Vaginal Vault Prolapse and Enterocele
For this reason, in cases of advanced anterior or posterior vaginal wall prolapse, the surgeon should attempt to determine whether a portion of the prolapse is secondary to an enterocele. This should include routine dissection of the vagina from its underlying structures all the way to the apex of the vagina. The enterocele sac can usually be visually or digitally identified as a sac of peritoneum separate and distinct from the wall of the bladder or rectum. At times, a finger in the rectum or retrograde filling of the bladder may assist the surgeon in safely isolating and entering an enterocele sac.
Surgical Repair Techniques Surgical repair of enterocele can be performed vaginally or abdominally. No data exist comparing the various types of repairs. The approach and type of procedure performed depend on the surgeon’s preference and whether there is concomitant vaginal or abdominal pathology. Vaginal surgical techniques described herein are the traditional vaginal enterocele repair and the McCall culdoplasty, and abdominal approaches discussed include the Moschcowitz procedure, Halban procedure, and uterosacral ligament plication. VAGINAL ENTEROCELE REPAIR Patients rarely have an isolated enterocele; hence, concurrent vaginal vault suspension, with or without cystocele and rectocele repair, is often necessary. The technique of vaginal repair of an apical or posterior enterocele is as follows: 1. The patient is positioned as for a posterior colporrhaphy. A midline posterior vaginal wall incision is made over the enterocele sac up to the vaginal apex and extended to the perineum, if a rectocele is also present. Dissection of the posterior vaginal wall from the enterocele sac, the anterior rectal wall, and the rectovaginal fascia is accomplished sharply and bluntly. The dissection should extend laterally to the medial margins of the levator ani muscles (Fig. 21-3, A). 2. The enterocele sac should be mobilized from the vaginal walls and rectum. When the enterocele sac is difficult to distinguish from the anterior rectum, differentiation is aided by a rectal examination with simultaneous dissection of the enterocele sac from the anterior rectal wall (Fig. 21-3, B). At times, distinguishing the enterocele sac from a large cystocele may prove difficult. In this situation, placement of a probe into the bladder or transillumination with a cystoscope may prove helpful. 3. After the enterocele sac has been dissected from the vagina and rectum, traction is placed on it with two Allis clamps and the sac is entered sharply (Fig. 21-3, C). The enterocele sac is explored digitally to ensure that no small bowel or omental adhesions are present (Fig. 21-3, D); if encountered, they are dissected to the level of its neck. 4. Under direct visualization, two or three circumferential, nonabsorbable, purse-string sutures are used to close the enterocele sac (Fig. 21-3, E). The cardinaluterosacral ligaments are incorporated as well. Once
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placed, the sutures are tied in sequence. Care should be taken to avoid kinking the ureter. 5. Posterior colporrhaphy and vaginal vault suspension are performed as indicated (Fig. 21-3, F). MCCALL CULDOPLASTY McCall (1957) described the technique of surgical correction of enterocele and a deep cul-de-sac at the time of vaginal hysterectomy. The advantage of the McCall culdoplasty is that it not only closes the redundant cul-de-sac and associated enterocele but also provides apical support and lengthening of the vagina. Many authors advocate using this procedure as part of every vaginal hysterectomy, even in the absence of enterocele, to minimize future hernia formation and vaginal vault prolapse. The technique is as follows (Fig. 21-4): 1. After the vaginal hysterectomy is completed, the surgeon places a finger into the posterior cul-de-sac to evaluate vaginal depth. Lateral traction is placed on the previously tagged uterosacral ligaments. 2. With the patient in Trendelenburg’s position, a large pack is placed intraperitoneally to prevent descent of the omentum or bowel into the field. A permanent suture is initially passed through one uterosacral ligament as high as possible. Successive bites are then taken at 1- to 2-cm intervals through the anterior serosa of the bowel, until the opposite uterosacral ligament is reached. This suture is left untied, and successive identical sutures are placed as needed, progressing toward the posterior vaginal cuff. The number of internal McCall sutures placed depends on the size and depth of the enterocele or cul-desac. The goal is obliteration of the entire dependent portion of the cul-de-sac. 3. After all of the internal permanent sutures have been placed and their ends held laterally without tying, one or two sutures of delayed absorbable No. 0 suture are placed. These are inserted from the vaginal lumen just below the middle of the cut edge of the posterior vaginal cuff, through the peritoneum, and through the right uterosacral ligament. Successive bites are taken across the cul-de-sac as before and into the left uterosacral ligament. This suture is passed through the peritoneum and vaginal epithelium, adjacent to the point of entry. 4. The permanent sutures are tied in sequence. The vaginal cuff is then closed. Finally, the delayed absorbable sutures are tied in a manner to bring the posterior vagina up to the level of the uterosacral ligaments. The complications as reported by Given (1985) after McCall culdoplasty are shown in Table 21-1. He reported ureteral injury in 1 of 48 McCall culdoplasty procedures. Stanhope et al. (1991) also found that culdoplasty sutures were implicated in ureteral obstruction after vaginal surgery. To ensure ureteral patency, cystoscopy should be routinely considered after the McCall culdoplasty. When there is excessive redundancy of the posterior vaginal wall and peritoneum, a modification of the McCall
Figure 21-3 ■ Dissection and vaginal repair of enterocele. A. The enterocele sac has been completely mobilized of the vaginal epithelium. B. A finger in the rectum facilitates sharp dissection of the enterocele sac off the anterior wall of the rectum. C. The enterocele sac is sharply entered. D. The peritoneum has been excised and the cul-de-sac is exposed. E. A series of purse-string sutures incorporating the distal ends of the uterosacral ligaments are placed to close the defect at its neck. F. The vaginal apex is attached to the plicated uterosacral ligaments.
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include the ureter in the purse-string sutures or to allow the ureter to be kinked medially when tying the sutures. Halban described a technique to obliterate the cul-desac using sutures placed sagittally between the uterosacral ligaments. Four or five sutures are placed sequentially in a longitudinal fashion through the serosa of the sigmoid, into the deep peritoneum of the cul-de-sac, and up the posterior vaginal wall (Fig. 21-6, B). The sutures are tied, obliterating the cul-de-sac. Transverse plication of the uterosacral ligaments can be used to obliterate the cul-de-sac (Fig. 21-6, C). Three to five sutures are placed into the medial portion of one uterosacral ligament, into the back wall of the vagina, and into the medial portion of the opposite uterosacral ligament. The lowest suture incorporates the anterior rectal serosa to bring the rectum adjacent to the uterosacral ligaments and vagina. Care must be taken to avoid entrapment or kinking of the ureter. Relaxing incisions can be made in the peritoneum lateral to the uterosacral ligaments to release the ureters, if necessary.
Figure 21-4 ■ McCall culdoplasty technique. Internal and external McCall sutures are placed. The lowest suture (external McCall) incorporates the posterior vaginal wall, providing additional support.
Table 21-1
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Complications After McCall Culdoplasty*
Complication Removal of silk suture Postoperative cuff infection High rectocele Partial prolapse of vaginal vault Shortened vagina Introital stenosis Pulmonary emboli Nerve palsy Ureteral obstruction
Percent of Patients (N = 48) 10 4 4 4 4 2 2 2 2
*Follow-up was 2 to 22 (average 7) years. From Given FT. “Posterior culdeplasty”: revisited. Am J Obstet Gynecol 1985;153:135, with permission.
culdoplasty, in which a wedge of posterior vaginal wall and peritoneum is excised, can be considered (Fig. 21-5). ABDOMINAL ENTEROCELE REPAIRS Three techniques of abdominal enterocele repair have been described: Moschcowitz and Halban procedures and the uterosacral ligament plication. The Moschcowitz procedure is performed by placing concentric purse-string sutures around the cul-de-sac to include the posterior vaginal wall, the right pelvic side wall, the serosa of the sigmoid, and the left pelvic side wall (Fig. 21-6, A). The initial suture is placed at the base of the cul-de-sac. Usually, three or four sutures completely obliterate the cul-de-sac. The purse-string sutures are tied so that no small defects remain that could entrap small bowel or lead to enterocele recurrence. Care should be taken not to
VAGINAL PROCEDURES THAT SUSPEND THE APEX When mild forms of isolated uterovaginal prolapse (descent of the cervix not beyond the midportion of the vagina) are present, vaginal hysterectomy and culdoplasty, with anterior and posterior colporrhaphy, are usually sufficient to relieve the patient’s symptoms and restore normal vaginal function. However, more severe apical prolapse requires separate operations to re-suspend the apex. In Figure 21-7, A an isolated apical enterocele is shown with a wells-supported anterior and posterior vaginal walls. In such a case, no formal vaginal vault suspension is necessary because simple excision and closure of the enterocele sac will result in a wellsupported vagina of adequate length. As more of the anterior and posterior vaginal walls become everted, the more complex the repair becomes (Fig. 21-7, B, C).
Sacrospinous Ligament Suspension SURGICAL ANATOMY To perform this procedure correctly and safely, the surgeon must be familiar with pararectal anatomy as well as the anatomy of the sacrospinous ligament and its surrounding structures (Fig. 21-8). The sacrospinous ligaments extend from the ischial spines on each side to the lower portion of the sacrum and coccyx. Nichols and Randall (1989) described the sacrospinous ligament as a cordlike structure lying within the substance of the coccygeus muscle. However, the fibromuscular coccygeus muscle and sacrospinous ligament are basically the same structure and thus called the coccygeus-sacrospinous ligament (C-SSL). The coccygeus muscle has a large fibrous component that is present throughout the body of the muscle and on the anterior surface, where it appears as white ridges. The C-SSL can be identified by palpating the ischial spine and tracing posteriorly and medially the flat triangular thickening to the sacrum The fibromuscular
Figure 21-5 ■ Modified McCall culdoplasty. A. The cul-de-sac is digitally palpated, and excessive peritoneum and posterior vaginal wall are noted. B. A wedge of tissue (dotted line), which includes full thickness vaginal wall and peritoneum, is excised to decrease the caliber of the upper portion of the posterior vaginal wall. C. External McCall stitches are placed in a traditional fashion. D. Tying of these sutures obliterates the cul-de-sac, supports the vaginal cuff, and increases posterior vaginal wall length.
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Figure 21-6 plication.
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Techniques of enterocele repair via the abdominal route. A. Moschcowitz procedure. B. Halban procedure. C. Uterosacral ligament
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Ischial spine
Vaginal length = 9 cm
coccygeus is attached directly to the underlying sacrotuberous ligament. Posterior to the C-SSL and sacrotuberous ligament are the gluteus maximus muscle and the fat of the ischiorectal fossa. The pudendal nerves and vessels lie directly posterior to the ischial spine. The sciatic nerve lies superiorly and laterally to the C-SSL. Also superiorly lies an abundant vascular supply that includes inferior gluteal vessels and hypogastric venous plexus. SURGICAL TECHNIQUE
A
Vaginal length = 4.5 cm
B
Level of ischial spine
Urethra
Cystocele
C Rectocele
Enterocele with vault eversion
Figure 21-7 ■ Various degrees of vaginal vault eversion. A. Isolated enterocele with well-supported anterior and posterior vaginal walls. Note that surgical repair would only require excision of the sac and closure of the defect because the vaginal cuff is already at the level of the ischial spine. B. Note that vaginal cuff is at –4.5 cm; thus, surgical repair should ideally require suspension of vaginal cuff to or above the level of the ischial spine. C. Note complete eversion of the vagina, with the vaginal cuff prolapsed well beyond the hymen; also note coexistent cystocele and rectocele. Surgical repair becomes much more complicated if the goal is to create a well-supported vagina of sufficient length.
Before this operation is initiated, one should have preoperatively recognized the ischial spine and C-SSL on pelvic examination. Preoperative estrogen replacement therapy should be given liberally, if appropriate. We prefer to use a preoperative vaginal estrogen cream for 4 to 6 weeks. The performance of this operation almost always requires simultaneous correction of the anterior and posterior vaginal walls and enterocele repair. Displacing the prolapsed vaginal apex to the sacrospinous ligament to see whether the anterior and posterior vaginal wall prolapse disappears with a Valsalva maneuver helps determine whether cystocele and rectocele repairs are needed. The patient should be consented routinely for these repairs because many times it is difficult preoperatively to discern the extent of the various defects. The technique of unilateral sacrospinous fixation is as follows: 1. With the patient in dorsal lithotomy position, the vaginal area is prepped and draped. Prophylactic perioperative antibiotics are given routinely. 2. The apex of the vagina is grasped with two Allis clamps, and downward traction is used to determine the extent of the vaginal prolapse and associated pelvic support defects. The vaginal apex is then reduced to the sacrospinous ligament intended to be used. Although bilateral sacrospinous fixations have been described, most surgeons prefer unilateral fixation of the vaginal vault. At times, the apex of the vagina is foreshortened and will not reach the intended area of fixation. This is commonly associated with a shortened anterior vaginal wall and a prominent enterocele. The apex should be moved to a portion of the vaginal wall over the enterocele, thus allowing sufficient vaginal length for suspension to the sacrospinous ligament. The intended apex is tagged with two sutures for its later identification. 3. If the patient has complete eversion of the vagina and requires anterior vaginal wall repair and/or bladder neck suspension, we prefer doing this portion of the operation first. During this procedure, one can separate the bladder base away from the vaginal apex, thus lowering the risk of cystotomy. After these procedures are completed, the anterior vaginal wall is closed with a continuous running suture. 4. The posterior vaginal wall is then incised. After a transverse perineal incision, a midline posterior vaginal wall incision is made just short of the apex of the vagina, leaving a small vaginal bridge approximately 3 or 4 cm wide. In the majority of cases, an enterocele sac is present. This sac should be dissected off the posterior vaginal wall and closed with a high purse-
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Figure 21-8 ■ Close-up view of the coccygeussacrospinus complex to demonstrate close proximity of various nerves and blood vessels. Hypogastric artery and vein Inferior gluteal artery Hypogastric plexus
Sciatic nerve
External iliac artery and vein
Sacrospinous ligament
Obturator neurovascular bundle
Ischial spine
5.
6. 7.
8.
string suture, as previously described (see Fig. 21-3). Once the enterocele has been incised and ligated, one is ready to begin the sacrospinous fixation. The first step is entry into the perirectal space. The right rectal pillar separates the rectovaginal space from the right perirectal space. The rectal pillar is areolar tissue that extends from the rectum to the arcus tendineus fasciae pelvis and overlies the levator muscle. It has two layers and may contain a few small muscle fibers and blood vessels. In the majority of cases, entry into the perirectal space is best achieved by breaking through the fibroareolar tissue just lateral to the enterocele sac at the level of the ischial spine. This maneuver can usually be accomplished bluntly by mobilizing the rectum medially. At times, however, the use of gauze on the index finger or a tonsil clamp is necessary to break through into this space. Once the perirectal space is entered, the ischial spine is identified and, with dorsal and medial movement of the fingers, the C-SSL is palpated. Blunt dissection is used to further remove tissue from this area. The surgeon should take great care to ensure that the rectum is adequately retracted medially. At this time, we recommend performing a rectal examination to ensure that no inadvertent rectal injury has occurred. Two techniques have been popularized for the actual passage of sutures through the ligament (Fig. 21-9). The first is the technique of Randall and Nichols (1971), using a long-handled Deschamps ligature carrier and nerve hook (Fig. 21-10, A). Long, straight retractors are used to expose the coccygeus muscle. Heaney retractors or Breisky-Navratil retractors (Fig. 21-10, B) are preferred. One must
Pudendal artery and vein
take great care not to let the tip of the retractor be pushed across the anterior surface of the sacrum, risking potential damage to vessels and nerves. If the right sacrospinous ligament is to be used, the middle and index fingers on the left hand are placed on the medial surface of the ischial spine and, under direct vision, the tip of the ligature carrier penetrates the C-SSL at a point two fingerbreadths medial to the ischial spine. When pushing the ligature carrier through the body of the C-SSL, considerable resistance should be encountered; this must be overcome by forceful yet controlled rotation of the handle of the ligature carrier. If visualization of the C-SSL is difficult, the muscle and ligament can be grasped in the tip of a long Babcock or Allis clamp, which helps isolate the tissue to be sutured from underlying vessels and nerves. After suture passage, the fingers of the left hand are withdrawn. The retractor is suitably repositioned, and the tip of the ligature carrier is visualized. The suture is then grasped with a nerve hook (see Fig. 21-10, A). A second suture is similarly placed 1 cm medial to the first. To avoid a second passage of the ligature carrier, the original long suture can be cut in the center and each end of the cut loop paired with its respective free suture. This obtains two sutures through the ligament, with only one penetration of the ligature carrier. To ensure that an appropriate bite of tissue has been obtained, one should be able to gently move the patient with traction of the sutures. A second technique that has been popularized for passing the sutures through the C-SSL is the technique of Miyazaki (1987), using a Miya hook ligature carrier (Fig. 21-11). The
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Figure 21-9 ■ A. Passage of Deschamps ligature carrier with suture through C-SSL. Note that the needle-tip is passed in superior direction. Retrieval of suture is with nerve hook. B. Passage of Miya hook through C-SSL. Note that needletip is passed inferiorly. Retrieval of suture is facilitated by using notched speculum.
Figure 21-11 ■ Miya hook, notched speculum, and suture hook for use during sacrospinous ligament fixation.
Figure 21-10 ■ A. Long-handled Deschamps ligature carrier and nerve hook. Note slight bend near the tip to facilitate suture placement into the C-SSL. B. Breisky-Navratil retractors, various sizes.
proposed advantage of this technique is that it is safer and easier because the ligature carrier enters the C-SSL under direct palpation of distinct landmarks and is then pulled down into the safe perirectal space below. To perform this modification, the right middle fingertip is placed on the C-SSL just below its superior margin, approximately two fingerbreadths medial to the ischial spine. The Miya hook, in the left hand in a closed position, is slid along the palmar surface of the right hand. The hook point should come to rest just beneath the previously positioned tip of the right middle finger. The handles are then opened and lowered to a near horizontal position. This points the
hook into the C-SSL at about a 45-degree angle. If a high perineum prevents lowering the handle, an episiotomy should be performed. With the tip of the middle finger, the hook point is placed two fingerbreadths medial to the ischial spine, approximately 0.5 cm below the superior edge. With experience, the hook point can be passed above the superior edge. With the middle and index fingers, apply firm pressure downward just behind the hook hump so that the hook point penetrates the C-SSL (see Fig. 21-9, B). Downward pressure with two fingers on the top, plus traction with the back of the thumb on the back handle, produces enough force to penetrate the ligament. Close and elevate the handles of the Miya hook, and, with the index and middle fingers, push the tissue from the hook point to make the suture clearly visible. If too much tissue is in the hook, simply back out the hook a little and take a smaller bite. An assistant should hold the elevated handles in a closed position. A long retractor is then placed medially to mobilize the rectum, and a notched speculum is inserted by palpation underneath the hook point. A nerve hook is then used to retrieve the suture. In addition to these techniques, two instruments have been designed to facilitate passage of a suture through the ligament. These are shown in Figure 21-12.
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remains in the vagina. We recommend a No. 0 delayed absorbable suture. After the sutures have been brought out through the vagina, the upper portion of the posterior vaginal wall is closed with interrupted or continuous No. 3-0 sutures. The vaginal vault suspension stitches are then tied, thus elevating the apex of the vagina to the C-SSL. It is important that the vagina comes into contact with the coccygeus muscle and no suture bridge exists, especially if delayed absorbable sutures are being used. While tying these sutures, it may be useful to perform a rectal examination to detect any suture bridges. Figure 21-12 ■ Two specially designed instruments to facilitate passage of sutures through the sacrospinous ligament. A. Capio Device (Boston Scientific, Natick. Capio is a trademark of Boston Scientific Corp., Waltertown, MA). B. Nichols-Veronikis ligature carrier. (Courtesy of CooperSurgical, Trumbull, CT.)
9. Now the surgeon is ready to bring the stitches out to the apex of the vagina. Again, two methods have been popularized for this maneuver (Fig. 21-13). The first involves bringing the vaginal apex to the surface of the C-SSL with the use of a pulley stitch. After the stitch has been placed in the ligament, one end of the suture is rethreaded on a free needle, sewn into the full thickness of the fibromuscular layer of the undersurface of the vaginal apex, and tied by a single half-hitch, while the free end of the suture is held long (see Fig. 21-13, A). Traction of the free end of the suture pulls the vagina directly onto the muscle and ligament. A square knot then fixes it in place. With this type of fixation, a permanent suture should be used because the suture is not exposed through the epithelium of the vagina. Some surgeons prefer a second technique, especially if the vaginal wall is thin or if greater vaginal length is desired. This method inserts each end of the suture through the vaginal epithelium (see Fig. 21-13, B). When this method is used, a delayed absorbable suture should be used because the knot
10. After the sutures are tied, the posterior colpoperineorrhaphy is completed, as needed, and the vagina is packed with a moist gauze for 24 hours. RESULTS AND COMPLICATIONS The results of sacrospinous fixation are difficult to evaluate because few studies report long-term follow-up (Table 21-2). The largest published series to date is by Nichols (1982), who performed the operation on 163 patients and followed them for at least 2 years. He reported only a 3% incidence of recurrent vaginal eversion and did not specify whether other pelvic support defects recurred. Morley and DeLancey (1988) reported on 100 patients who underwent sacrospinous fixation, with or without anterior and posterior vaginal wall repairs. Subjective 1-year follow-up was available on 71 patients; only 3 had recurrent vaginal vault prolapse. These authors did note, however, that 22 patients had recurrent or persistent mild-to-moderate anterior vaginal wall relaxation or symptomatic cystoceles. Shull et al. (1992) reported the results of sacrospinous ligament fixation, as well as other pelvic reconstructive surgery, in 81 patients. The authors performed preoperative sitespecific analysis of pelvic support defects and at consecutive postoperative visits. The findings at 6 postoperative weeks and at subsequent visits were noted for each of five sites: urethra, bladder, vaginal cuff, cul-de-sac, and rectum. The most common site for recurrent prolapse was the anterior vaginal wall. Sze et al. (1997) reported on 75 women who underwent sacrospinous ligament fixation in conjunction with other
Figure 21-13 ■ Technique of fixing vaginal apex to C-SSL. A. Pulley stitch. Permanent sutures should be used. B. Stitches are placed through the vaginal epithelium and tied in the vaginal lumen. Delayed absorbable sutures should be used.
163 92 11 31 48 61 51 22 155 81 23 63§ 76 36 24 30 14 75 1137
≥2 yr 1 mo–11 yr 8–21 mo
6 mo–5.6 yr — 2–5 yr — 2 mo–1 yr — 15–79 mo 4–26 mo Median = 48 mo 3–6 mo 7–72 mo 1 mo–11 yr
8 mo–3.2 yr 1 mo–8.6 yr
81
1–10 yr
?/4 20/36
3/5 0/0
5/5 3/3 1/1 2/6 0/1 1/1 0/0 0/0 0/4 0/1 2/2 1/1
2/2
Vault
?/1 4/25
0/1 4/6
0/1 0/0 0/0
4/20 0/1 0/16 ?/1 1/3 0/0 0/2 ?/16 7/96
0/2 0/2 0/0 0/2
0/0 0/0
0/10
Posterior Wall
0/5 0/6 0/3 0/1
2/11 0/0
0/12
Anterior Wall
From Sze EH, Karram MM. Transvaginal repair of vault prolapse: a review. Obstet Gynecol 1997;89:466, with permission. *Subjective assessment, based on telephone interview or questionnaire; objective assessment, based on findings from pelvic examination. †Cure rate applies to vaginal vault support only; does not include support defect at other site. ‡Extrapolated from text. §Includes 11 patients whose uteri were preserved. ||Includes 33 patients with anterior vaginal wall defects, 3 vaginal vault prolapses, and 8 posterior vaginal wall relaxations.
Richter and Albright (1981) Richter (1982) Nichols (1982) Morley and DeLancey (1988) Brown et al. (1989) Keetel and Herbertson (1989) Cruikshank and Cox (1990) Monk et al. (1991) Backer (1992) Heinonen (1992) Imparato et al. (1992) Shull et al. (1992) Kaminski et al. (1993) Carey and Slack (1994) Porges and Smilen (1994) Holley et al. (1995) Sauer and Klutke (1995) Peters and Christenson (1995) Elkins et al. (1995) Sze et al. (1997) Total
Investigator
?/1 0/57
0/1
0/2 0/33||
0/11 0/6
0/3
Unspecified/ Multiple Sites
Surgical Repair Required/Recurrent Pelvic Relaxation (n)
158 (97)† 75 (82) 10 (91) 25 (81) 40 (83) 52 (85) 48 (94) 19 (86) 140 (90) 53 (65) 20 (87) 46 (73) — 3 (8) 15 (63) 23 (77) 12 (86) 53 (71)
57 (70)
No. Cured (%)
Subjective/objective Objective Subjective/objective Objective‡ Objective Objective Objective Objective Objective Objective Objective Objective‡ Objective Objective‡ Subjective/objective Objective‡ Objective‡
Objective
Cure Assessment
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Duration of Follow-Up
Table 21-2 ■ Long-Term Complications, Follow-Up, and Recurrence of Prolapse After Sacrospinous Ligament Suspension Surgical Repair Required/Recurrent Pelvic Relaxation (n)
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reconstructive surgery. Fifty-four of the women had stress incontinence and also underwent a needle suspension procedure. Patients were objectively followed for an average of 2 years. The rate of recurrence of symptomatic prolapse was 33% in the needle suspension group and 19% in the remainder of the patients. Table 21-2 reviews these and other studies that have reported the long-term follow-up and recurrence of prolapse after sacrospinous ligament suspension. Miyazaki (1987) reported on 74 cases of sacrospinous fixation, using the Miya hook. Results with regard to treatment of the prolapse were not discussed, but the safety of the technique was documented. No patients had injuries to the bladder, rectum, nerves, or blood vessels, and no blood transfusions were performed. Average blood loss was approximately 75 mL. To date there have been three randomized trials for the management of apical vaginal prolapse that included sacrospinous suspension. All three trials compared unilateral or bilateral sacrospinous suspension to abdominal sacral colpopexy. Benson et al. (1996) and Lo and Wang (1998) reported a higher success with abdominal sacral colpopexy, whereas Maher et al. (2004) reported similar success in the two groups. These studies are discussed, in more detail, in the section on surgical approaches (vaginal vs abdominal). Although infrequently reported, serious intraoperative complications can occur with sacrospinous fixation. Potential complications of the procedure follows. Hemorrhage. Severe hemorrhage can result from overzealous dissection superior to the coccygeus muscle or lateral to the ischial spine. This can result in hemorrhage from the inferior gluteal vessels, hypogastric venous plexus, or internal pudendal vessels. Hemorrhage from these vessels can be difficult to control. For this reason, we prefer using the Capio device or the technique described by Miyazaki in which the needle tip is passed downward into the safe ischiorectal space, rather than the technique using the Deschamps ligature carrier in which the needle tip is passed superiorly toward an abundant vasculature. If severe bleeding occurs in the area around the coccygeus muscle, we recommend initially packing the area. If this does not control the bleeding, visualization and attempted ligation with clips or sutures should be performed. This area is difficult to approach transabdominally, so bleeding should be controlled vaginally, if possible. Buttock Pain. It has been our experience that approximately 10% to 15% of patients experience moderate-tosevere buttock pain on the side on which the sacrospinous suspension was performed. The probable cause is injury of a small nerve that runs through the C-SSL. This nerve injury is always self-limiting and should resolve completely by 6 postoperative weeks. Reassurance and anti-inflammatory agents are usually all that are necessary. Nerve Injury. Because of the close proximity of the sciatic nerve to the C-SSL, the potential for its injury is present. Although it is rarely reported, if this injury occurs, reoperation with removal of suture material may be necessary. Rectal Injury. Rectal examination should be performed frequently during this operation because of the close prox-
275
imity of the rectum to the C-SSL. Rectal injury can occur during entering of the perirectal space as well as during mobilization of tissue off of the C-SSL. If a rectal injury is identified, it can usually be repaired primarily transvaginally by conventional techniques. Stress Urinary Incontinence. This may occur after vaginal vault suspension procedures and is probably secondary to straightening of the vesicourethral junction coincident with restoration of vaginal length and depth. Stress incontinence should be tested preoperatively by performing a stress test in the standing position with reduction of the vaginal prolapse. Vaginal Stenosis. Stenosis may occur if too much anterior and posterior vaginal wall tissue is trimmed or if too tight a posterior colporrhaphy is performed. We recommend postoperative use of estrogen vaginal cream in these patients in the hope of preventing or decreasing the incidence of this problem. Recurrent Anterior Vaginal Wall Prolapse. As mentioned earlier, the pelvic support defect that recurs with the highest incidence is that of the anterior vaginal wall. Approximately 20% of patients return with a moderate anterior vaginal wall prolapse within a year after surgery. This defect probably results from the alteration of the vaginal axis in an exaggerated posterior direction.
Endopelvic Fascia Repair (Modified McCall Culdoplasty) Between 1952 and 1981, two groups of investigators performed a total of 367 surgeries for vaginal eversion by suturing the prolapsed vagina to the endopelvic fascia with few complications (Lee and Symmonds, 1972; Phaneuf, 1952; Symmonds and Pratt, 1960; Symmonds and Sheldon, 1965; Symmonds et al., 1981). More recently, Webb et al. (1998) reported on 660 women who underwent primary endopelvic fascia repair for posthysterectomy vault prolapse between 1976 and 1987. The technique of this repair is as follows: 1. An elliptical wedge of vaginal mucosa is excised initially from the anterior and posterior walls of the prolapsed vagina to narrow the vault and to allow access to the lateral apical supports of the vagina and rectum. The width and length of the excised wedge are determined by the desired dimensions of the reconstructed vagina. 2. The enterocele sac is isolated and excised, and the ureters are identified by palpation or dissection. 3. Up to three modified McCall stitches are placed (see Fig. 21-5). Each suture incorporates the full thickness of the posterior vaginal wall, the cul-de-sac peritoneum, the remains of the uterosacral-cardinal complex laterally, and the fascial tissue lateral and posterior to the upper vagina and rectum. 4. Sutures are then tied, resulting in fixation of the prolapsed vaginal vault to the uppermost portion of the endopelvic fascia as well as high closure of the culde-sac peritoneum.
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The results and complications of this technique were discussed in a review article by Sze and Karram (1997). Of the initial studies reporting 367 patients, 322 (88%) received postoperative follow-up ranging from 1 to 12 years, with a cure rate of 88% to 93%. Thirty-four (11%) patients developed recurrent pelvic relaxation, including 9 with vaginal vault prolapse, 2 with anterior vaginal wall defects, 11 with posterior vaginal wall relaxations, and 12 patients with pelvic support defects at multiple or unspecified sites. The subsequent study by Webb et al. (1998) reported results on 660 women, most of whom were followed up with a questionnaire. Information about recurrent prolapse was available on 504 women (72.7%). Fifty-eight (11.5%) patients complained of a “bulge” or “protrusion” at the time of questioning. The question about satisfaction with the operation was answered by 385 patients, and 82% indicated that they were satisfied. Forty-two of 189 (22%) sexually active women complained of dyspareunia.
Iliococcygeus Fascia Suspension In 1963, Inmon described bilateral fixation of the everted vaginal apex to the iliococcygeal fascia just below the ischial spine in three patients with atrophied uterosacral ligaments. The technique of this repair is as follows: 1. The posterior vaginal wall is opened in the midline as for a posterior colporrhaphy, and the rectovaginal spaces are dissected widely to the bilateral levator muscles. 2. The dissection is extended bluntly toward the ischial spines. 3. With the surgeon’s nondominant hand depressing the rectum downward and medially, an area 1 to 2 cm caudad and posterior to the ischial spine in the iliococcygeus muscle and fascia is exposed (Fig. 21-14). A single No. 0 delayed absorbable suture is placed deeply into the levator muscle and fascia. Both ends of the suture are then passed through the ipsilateral posterior vaginal apex and held with a hemostat. This is repeated on the opposite side. 4. The posterior colporrhaphy is completed, and the vagina is closed. Both sutures are tied, elevating the posterior vaginal apices. This repair is often done in conjunction with a culdoplasty or uterosacral suspension. From 1981 to 1993, Shull et al. (1993) and Meeks et al. (1994) used the Inmon technique to treat 152 patients with posthysterectomy vault prolapse or total uterine procidentia. Four intraoperative complications occurred, including one rectal and one bladder laceration and two cases of hemorrhage requiring transfusion. Thirteen (8%) patients developed recurrent pelvic support defects at various sites at 6 weeks to 5 years after the initial procedure; two had vault prolapse, eight had anterior vaginal wall relaxation, and three had posterior wall defects. More recently, Maher et al. (2001) performed a matched case control study to compare iliococcygeus suspension and sacrospinous colpopexy for vaginal vault prolapse. They
found the procedures to be equally effective with similar complication rates.
High Uterosacral Ligament Suspension A relatively new approach to the management of enterocele and vault prolapse is based on the anatomic observations of Richardson (1995), who believed that the connective tissue of the vaginal tube does not stretch or attenuate but rather breaks at specific definable points. This repair may be superior to previously discussed repairs in that it can be performed vaginally, abdominally, or laparoscopically, and it suspends the apex of the vagina into the hollow of the sacrum and thus does not create any significant distortion of the vaginal axis. 1. The vaginal apex is grasped with two Allis clamps (Fig. 21-15, A) and incised with a scalpel. The vaginal epithelium is dissected off the enterocele sac up to the neck of the hernia. The enterocele is opened, and the hernia sac is excised (Fig. 21-15, B). 2. Numerous moist tail sponges are placed in the posterior cul-de-sac. A wide Deaver retractor is used to elevate the packs and the intestines out of the operative field. 3. The ischial spines are palpated transperitoneally. The remnants of the uterosacral ligaments are found posteriorly and medially to the ischial spine, and the ureter can usually be palpated along the pelvic side wall, anywhere from 2 to 5 cm ventral and lateral to the ischial spine. 4. Upward traction on Allis clamps placed at approximately the 4 o’clock and 7 o’clock positions allows easy palpation of the uterosacral ligaments (Fig. 2115, C). 5. Usually, two to three delayed absorbable sutures are passed through the ligament on each side. To ensure adequate vaginal length, the highest suture should be close to the level of the ischial spine (Fig. 21-15, D). 6. The distal remnants of the uterosacral ligaments are plicated across the midline, with one to three permanent sutures. Tying of these sutures completely obliterates the cul-de-sac (Fig. 21-15, D). 7. The delayed absorbable sutures that had been passed high up through the uterosacral ligaments are then passed through the full thickness of the posterior vaginal wall (Fig. 21-15, E). 8. If necessary, an anterior colporrhaphy is performed. The vagina is trimmed and closed with a 3-0 delayed absorbable suture (Fig. 21-15, F, G). 9. Tying of the vault suspension sutures elevates the vagina high up into the hollow of the sacrum (Fig. 21-15, H, Fig. 21-16, A, B). In 2000, Shull et al. reported on 298 patients; 35 (12%) had evidence of an anterior wall defect in the form of cystocele or urethrocele. However, 25 of these defects were noted to be only grade 1. Eleven (4%) patients developed posterior wall defects. In all, 38 patients (13%) had development of one or more support defects; however, 24 of these were grade 1 only. Two patients required another surgery for recurrent prolapse.
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Ischial spine
Site of vaginal fixation
Needle placed deep into levator muscle and fascia Cystocele
A
Fingers pressing rectocele
Bilateral iliococcygeus fixation
B Figure 21-14 ■ Iliococcygeus fascia suspension. A. With the surgeon’s finger pressing the rectum downward, the right iliococcygeus fascia suture is placed. Approximate location of the iliococcygeus fascia sutures (inset). B. Bilateral iliococcygeus fascia suspension.
Small intestine
Uterosacral ligament
Ureter (phantom)
Peritoneum Posterior vaginal wall Peritoneum Sigmoid colon
C A
B
Vaginal wall
Traction on uterosacral ligaments
Cystocele Anterior vaginal wall
Obliteration of posterior cul-de-sac
D
F
E Anterior vaginal wall Midline plication
G
H
Figure 21-15 ■ High uterosacral ligament suspension. A. Apex of the vagina is grasped with two Allis clamps. Level of vaginal cuff is marked (dotted line). B. Enterocele sac has been dissected off the vaginal wall and sharply entered. C. Bowel is packed and lifted out of the cul-de-sac with a large retractor. Traction on Allis clamps placed at approximately 4 o’clock and 7 o’clock allows palpation of uterosacral ligaments. D. Numerous (usually two to three on each side) delayed absorbable sutures are passed through the uterosacral ligaments. Ideally, the highest suture should be at the level of the ischial spine to ensure adequate vaginal length. Permanent sutures are used to plicate the cul-de-sac distal to the uterosacral suspension sutures. E. The delayed absorbable uterosacral suspension sutures are individually passed through the full thickness of the posterior vaginal wall. The previously placed permanent sutures are tied, obliterating the distal portion of the cul-de-sac. F. If a cystocele is present, a midline anterior vaginal wall dissection is initiated. G. Repair of the cystocele has been completed. H. The anterior vaginal wall and vaginal cuff are closed with a 3-0 delayed absorbable suture. Tying of the uterosacral suspension sutures suspends the vagina high up into the hollow of the sacrum (inset).
Vaginal apex
Pubocervical fascia Peritoneum
A
Rectovaginal fascia
Vaginal apex
B
Figure 21-16 ■ A. Cross-section of pelvis demonstrating enterocele and vaginal vault prolapse. B. Cross-section of pelvis after excision of enterocele sac and suspension of vaginal apex to uterosacral ligaments.
Barber et al. (2000) reported on 46 women who underwent vaginal site-specific repair with suspension of the vaginal cuff to the proximal uterosacral ligaments. Symptomatic prolapse (two apical, one anterior, and one proximal) developed in four patients (10%), and three of them underwent reoperation. Karram et al. (2001) reported on 202 patients; 168 patients were available for follow-up either by phone or by office visit; 89% of patients indicated that they were happy or satisfied with the procedure; the reoperation rate was 5.5%. The most commonly reported complication of this procedure is ureteral injury or kinking. Karram et al. (2001) reported a 2.4% risk, Barber et al. (2000) reported an 11% risk (with most obstructions relieved intraoperatively), and Shull et al. (2000) reported a 1% risk. It is imperative that intraoperative cystoscopy be done to ensure ureteral patency. If ureteral spill is not observed, then the suspension sutures on that side should be cut and removed and the ureter reevaluated. Often, the suture can be replaced using a more medial placement into the uterosacral ligament complex. Other rare complications have included pelvic abscess, hemorrhage with subsequent transfusion, bowel and bladder injury, and postoperative small bowel obstruction.
Infracoccygeal Sacropexy The infracoccygeal sacropexy was initially described as a minimally invasive surgical option to restore vaginal vault support (Petros, 1997). The first prospective study using this procedure reported cure rates of 94% for vault prolapse, with a 5.3% tape erosion rate (Petros, 2001). In 2002 Farnsworth reported on 93 infracoccygeal sacropexy procedures performed on patients with advanced vaginal vault prolapse. Cure of prolapse was stated to be 87% but was not explicitly defined. Complications included one rectal perforation and one mesh erosion into the rectum. The technique of the procedure involves subjects undergoing placement of a U-shaped mesh using a tunneler (trocar device) in an effort to establish artificial uterosacral neoligaments. The trocar is
introduced through two small buttock incisions, into the ischiorectal fossa and through the levator ani muscles toward the ischial spine (Fig. 21-17). The trocar tip is then deviated medially, where it briefly passes through the perirectal space and into the posterolateral aspect of the vagina, beneath the vaginal epithelium (Fig. 21-18). A mesh tape is introduced onto the trocar tip and pulled back through the trocar’s path. A similar passage is performed on the opposite side, completing the U-shape. The intravaginal mesh is sutured to the apex of the vagina in the precise bilateral position of the atrophied uterosacral ligaments, in an effort to reestablish support for the vagina apex. The vaginal epithelium is then closed. The two ends of the tape are gently stretched at the buttock incisions and are left in a tension-free fashion. The guidelines used to adjust tension on the tape are unclear. So far, no comparative trials of efficacy have been performed using the infracoccygeal sacropexy. Since the original description of the infracoccygeal sacropexy, complete vaginal mesh repairs have been described. Several kits are currently available to facilitate the performance of these procedures. In the authors’ opinions the benefits of the techniques are not yet proven, and the procedure introduces the risk of bilateral perirectal needle insertion into the ischiorectal fossa. Vaginal mesh erosions of 5% to 12% have been reported. More data on efficacy and risk are needed.
ABDOMINAL PROCEDURES THAT SUSPEND THE APEX Abdominal Sacral Colpopexy Suspension of the vagina to the sacral promontory via the abdominal approach is an effective treatment for uterovaginal prolapse and vaginal eversion and can offer several advantages over vaginal surgical approaches. This approach is the procedure of choice for patients who have other indications for abdominal surgery, such as ovarian masses. The laparotomy
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Figure 21-17 ■ Lithotomy view demonstrating the infracoccygeal sacropexy trocar passing from the skin surface at insertion point into the ischiorectal fossa through the inferior rectal branches of the pudendal vessels. It is bordered medially by the external anal sphincter, pubococcygeus, iliococcygeus, and rectum; laterally by the ischial tuberosity and obturator internus; and inferiorly by the gluteus maximus and sacrotuberous ligament (not shown). (Reprinted with the permission of The Cleveland Clinic Foundation.)
incision also offers the advantage of performing simultaneous retropubic procedures, such as the Burch colposuspension and the paravaginal defect repair. Sacral colpopexy can also be done laparoscopically as discussed in Chapter 17. Many different materials, both autologous and synthetic, have been used for the graft in the sacral colpopexy. Natural materials that have been used include fascia lata, rectus fascia, and dura mater. Synthetic materials include polypropylene mesh, polyester fiber mesh, polytetrafluoroethylene mesh, Dacron mesh, and Silastic silicone rubber. A recent randomized trial (Culligan et al., 2005), comparing objective anatomic outcomes after sacral colpopexy performed with cadaveric fascia lata and polypropylene mesh, noted Prolene mesh to be superior to fascia lata in terms of Pelvic Organ Prolapse Quantification (POPQ) points, POPQ stage, and objective anatomic failure rates. As was noted earlier, the normal vaginal axis directs toward sacral segments S3 and S4 in the nulliparous woman. Although some authors have advocated connecting the graft
material at this level, Sutton et al. (1981) encountered lifethreatening hemorrhage from presacral vessels at this low level on the sacrum. As these authors suggest, we recommend fixing the graft to the upper one third of the sacrum, near the sacral promontory, thus improving safety without sacrificing outcome or future vaginal function. The technique of abdominal sacral colpopexy using graft placement is as follows (Figs. 21-19 and 21-20): 1. The patient should be placed in Allen stirrups or in frog-leg position so that the surgeon has digital access to the vagina during the operation. A sponge stick or end-to-end anastomosis (EEA) sizer can be placed in the vagina for manipulation of the apex, if desired. A Foley catheter is placed into the bladder for drainage. Prophylactic perioperative antibiotics are used during this procedure. 2. A laparotomy is performed through a low transverse or midline incision. The small bowel is packed into
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Figure 21-18 ■ Upright-oblique view of the pelvis illustrating the pathway of the infracoccygeal sacropexy trocar through the inferolateral vagina. Mean total vaginal length was 8.7 cm and mean vaginal entry depth was only 4.8 cm from the hymenal ring. (Reprinted with the permission of The Cleveland Clinic Foundation.)
the upper abdomen, and the sigmoid colon is packed into the left pelvis as much as possible. The ureters are identified bilaterally for their entire course into the bladder. If the uterus is present, a hysterectomy should be performed and the vaginal cuff closed. The depth of the cul-de-sac and the length of the vagina are estimated when completely elevated. 3. While the vagina is elevated cephalad with a sponge stick or EES sizer, the peritoneum over the vaginal apex is incised transversely and the bladder dissected from the anterior vaginal wall (this may have already been done if the uterus was removed). The peritoneum over the posterior vaginal wall into the cul-de-sac is incised longitudinally and dissected bilaterally for several centimeters. The vaginal apex is elevated bilaterally with clamps or guide sutures. 4. Five to eight pairs of nonabsorbable No. 0 sutures are placed transversely in the posterior vaginal wall, 1 to 2 cm apart. Sutures are placed through the full fibromuscular thickness of the vagina but not into the vaginal epithelium. The sponge stick is
removed to ensure that no sutures have perforated the sponge. Sutures are then fed through the graft in pairs and tied. The graft should extend at least halfway down the length of the posterior vaginal wall. We prefer to attach a second smaller piece of mesh to the upper part of the anterior vaginal wall. This piece of mesh is then sewn to the posterior piece of mesh, which will be attached to the sacrum (see Fig. 21-19). Other potential configurations of mesh attachment are reviewed in Figure 21-20. 5. A Moschcowitz or Halban procedure is performed to obliterate the lower cul-de-sac (see Fig. 21-6). 6. A longitudinal incision, approximately 6 cm long, is made in the peritoneum over the sacral promontory. At this point, the surgeon should carefully palpate the aortic bifurcation and common and internal iliac vessels and mobilize the sigmoid colon and right ureter so that these structures can be avoided. The left common iliac vein is medial to the left common iliac artery and is particularly vulnerable to damage during this procedure. The middle sacral artery and vein should be identified.
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Figure 21-19 ■ Abdominal sacral colpopexy. Note that Halban technique is used to obliterate cul-de-sac below graft. Graft connects vagina to sacrum and lies without tension in the deep pelvis (inset).
7. Blunt and sharp caudal dissection may be used to create a subperitoneal tunnel into the full depth of the cul-de-sac so that the graft can then be tunneled retroperitoneally or placed above the previous Halban or Moschcowitz cul-de-sac closure. The surgeon can then extraperitonize the mesh by sewing the serosa of the sigmoid colon to the lateral peritoneum of the cul-de-sac. 8. The bony sacral promontory and anterior longitudinal ligaments are directly visualized for approximately 4 cm by using blunt and sharp dissection through the subperitoneal fat. Special care should be taken to avoid the delicate plexus of presacral veins that is often present, especially as one dissects caudally. 9. With stiff but small half-curved tapered needle with permanent No. 0 suture, two to four sutures are placed through the anterior sacral longitudinal ligament, over the sacral promontory. The graft should be trimmed to the appropriate length. The sutures are then fed through the graft in pairs and tied. The appropriate amount of vaginal elevation should provide gentle tension without undue traction on the vagina. 10. The peritoneum over the presacral space is closed with a running absorbable suture. The bladderflap peritoneum is also closed transversely over the graft.
11. When appropriate, retropubic urethropexy or paravaginal repair should be accomplished at this time, followed by placement of a suprapubic catheter, if desired, and closure of the abdomen. 12. Posterior colporrhaphy and perineoplasty can be performed to treat any remaining rectocele and perineal defect. If attention has been paid to repairing all of the support defects of the vagina at the time of sacral colpopexy, recurrences of vaginal vault prolapse are uncommon. Addison et al. (1989) reported three cases of recurrent vaginal prolapse after the sacral colpopexy with Mersilene mesh. In two patients, the mesh separated from the vaginal apex. In the remaining patient, the posterior vaginal wall ruptured distally to the attachment of the mesh to the vagina. These authors and others believe that failures of this procedure can be minimized by suturing the suspensory mesh to the posterior vagina and anterior vaginal apex over as extended an area as possible. This is the justification for suturing the graft to the posterior vagina, with numerous pairs of permanent sutures. Some investigators (Cundiff et al., 1997) advocated attaching the mesh along the entire posterior vaginal wall and fixing the mesh to the perineum (see Fig. 21-20, E), thus performing an abdominal sacral colpoperineopexy. A recent review of abdominal sacral colpopexy (Nygaard et al., 2004) noted the success rate when defined as lack of
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Figure 21-20 ■ A. Cross-section of the pelvis demonstrating large enterocele and vaginal vault prolapse. B. EEA sizer placed in vagina to elevate apex. (C–F) Obliteration of cul-de-sac with examples of various configurations for mesh attachment to the vagina. C. Mesh attached to upper half of posterior vaginal wall. D. Mesh attached as in C; second piece of mesh attached to upper part of anterior vaginal wall and sewn to posterior piece of mesh E. Mesh attached along entire length of posterior vaginal wall and fixed to perineum. F. Vaginal end of mesh is divided and fixed to upper parts of the anterior and posterior vaginal walls.
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postoperative apical prolapse ranged from 78% to 100%. The median reoperation rates for pelvic organ prolapse and for stress urinary incontinence in the studies that reported these outcomes were 4.4% (range, 0% to 18.2%) and 4.9% (range, 1.2% to 30.9%), respectively. No data either supported or refuted the contentions that concomitant culdoplasty or paravaginal repair decreased the risk of failure. Few studies rigorously assessed pelvic symptoms, bowel function, or sexual function. To date, two out of three randomized controlled trials have reported significantly better outcomes with abdominal sacral colpopexy when compared with vaginal sacrospinous suspension (Benson et al., 1996; Lo and Wang, 1998), whereas one study (Maher et al., 2004) reported similar outcomes between the two procedures. Intraoperative complications are uncommon but can be life threatening. When bleeding occurs from presacral vessels, hemostasis can be difficult to achieve because of the complex interlacing of the venous network, both beneath and on the surface of the sacral periosteum. When these veins have been damaged, they can retract beneath the bony surface of the anterior sacrum and recede into the underlying channels of cancellous bone. Communications with adjacent pelvic veins, especially the left common iliac vein, can be particularly troublesome. Packing of the presacral space may temporarily control bleeding, but it often recurs when the pack is removed, and packing may further lacerate delicate veins. Sutures, metallic clips, cautery, and bone wax should be used initially. If these measures are not successful, sterilized stainless steel thumbtacks can be placed on the retracted bleeding presacral vein to treat lifethreatening hemorrhage that has not responded to other measures. Other complications that have been reported after abdominal sacral colpopexy tend to be similar to those of procedures that require laparotomy, retropubic surgery, and extensive pelvic dissection. The complications include enterotomy, ureteral damage, cystotomy, proctotomy, extrafascial wound infections, and persistent granulation tissue in the vaginal vault. Remarkably, graft rejections are exceedingly rare. Lansman (1984) reported a small bowel obstruction after colpopexy that was caused by a loop of ileum adherent to a hole in the posterior peritoneum, near the side wall of the pelvis. The median rate (when reported) of small bowel obstruction requiring surgery is 1.1% (range, 0.6% to 8.6%). This problem underscores the importance of reperitonization to prevent small bowel from getting trapped in the cul-de-sac or behind the graft. The most common long-term complication is erosion of synthetic mesh through the vagina, which has been reported to occur in 3.4% of cases. This complication almost always requires partial or complete removal of the mesh. Mesh erosion after sacral colpopexy is further discussed in Chapter 40.
High Uterosacral Ligament Suspension The vaginal and laparoscopic approaches to this repair have been discussed previously. The abdominal repair involves the same concepts.
1. The remnants of the uterosacral ligaments are identified and tagged at the level of ischial spines. 2. The ureters are identified on each side, and the enterocele is addressed by abdominal obliteration of the cul-de-sac. 3. The peritoneum over the apex of the vagina is opened, and the endopelvic fascia of the anterior and posterior vaginal walls are identified and approximated. 4. Nonabsorbable sutures are then used to suspend the prolapsed vagina with its fascia to the uterosacral ligaments.
SURGICAL APPROACHES—VAGINAL VERSUS ABDOMINAL To date, very little scientific evidence is available to base the decision on which route of surgery to perform for advanced uterovaginal or posthysterectomy vaginal vault prolapse. Benson et al. (1996) randomly assigned 88 women to undergo either sacrocolpopexy or bilateral sacrospinous vault suspension. Numerous concomitant procedures were performed based on the surgeon’s judgment. Outcomes were termed optimal when women were free of prolapse symptoms, the vaginal apex remained above the levator plate, and no part of the vagina prolapsed beyond the hymen; satisfactory when women were free of prolapse symptoms and the prolapse was improved from the preoperative status but did not meet the criteria for optimal surgical effectiveness; and unsatisfactory if they had symptomatic vaginal apex descent more than 50% of its length or vaginal protrusion beyond the hymen. Enrollment was halted earlier than planned when interim analysis showed disparity in outcomes between the groups. Mean follow-up was 2.5 years. The vaginal group experienced 29% optimal, 38% satisfactory, and 33% unsatisfactory surgical outcomes compared with the abdominal group that had 58% optimal, 26% satisfactory, and 16% unsatisfactory outcomes. Surgical failures occurred sooner in the vaginal group, with a mean of 11.2 months, compared with the abdominal group with a mean of 22.1 months. Lo and Wang (1998) randomly assigned 138 women with stage III or greater vaginal vault or uterine prolapse to either a unilateral sacrospinous ligament suspension or to abdominal sacrocolpopexy. Optimal effectiveness was defined as postoperative prolapse less than stage III. Optimal effectiveness was significantly less in the vaginal group (80.3%) than in the abdominal group (94.2%). Maher et al. (2004) randomly allocated 95 women with posthysterectomy vaginal vault prolapse, to or beyond the hymen, to undergo either abdominal sacrocolpopexy or sacrospinous ligament suspension. Objective success was defined as no vaginal prolapse beyond the halfway point of the vagina during examination, using the POPQ system. Women with no symptoms of prolapse were considered subjective successes. The investigators found no statistically significant difference in either objective or subjective success 2 years after the procedure, with respective rates of 76% and 94% in the abdominal group, and 69% and 91% in the vaginal group. Mean patient satisfaction with the
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surgery was 85% in the abdominal group and 81% in the vaginal group. A recent Cochrane Database Review (Maher et al., 2005) noted abdominal sacral colpopexy to be associated with a lower rate of recurrent vault prolapse and dyspareunia than the vaginal sacrospinous colpopexy. These benefits must be balanced against a longer operating time, longer time to return to activities of daily living, and increased cost of the abdominal approach. Women with prolapsed foreshortened vaginas, previous vaginal failures, and young women with advanced prolapse are probably better managed with abdominal sacral colpopexy. Roovers et al. (2004) randomized 82 women undergoing surgical correction of uterine prolapse stages II to IV to either vaginal hysterectomy (combined with anterior and/or posterior colporrhaphy and possible needle suspension) to sacrocolpopexy with uterine preservation, culdoplasty, and possible Burch colposuspension. Their main outcome measure was the domain scores of the Urogenital Distress Inventory (UDI) at 1 year after surgery. Scores on the discomfort/pain domain, overactive bladder domain, and obstructed micturition domain were significantly higher in the abdominal group than in the vaginal group. Reoperation was performed or planned in 9 of the 41 patients who underwent abdominal surgery and in 1 of the 41 patients who underwent vaginal surgery. This study concluded that vaginal hysterectomy with repairs is preferable to abdominal sacral colpopexy, with uterine preservation in patients with stages II to IV uterine prolapse.
UTERINE PRESERVATION DURING SURGERY FOR UTEROVAGINAL PROLAPSE Traditionally, uterine preservation in women with uterovaginal prolapse was considered only if future fertility was desired. Recently, more women are requesting uterine preservation for other reasons, most notably the perception that sexual function is improved if the cervix is not removed. Vaginal, abdominal, and laparoscopy techniques have all been described. A recent literature search on this topic (Diwan et al., 2004) concluded that uterine preservation during surgery for uterovaginal prolapse may be an option in appropriately selected women who desire it; however, prospective randomized trials are needed to corroborate this. Recent studies have reported excellent results with laparoscopic suture hysteropexy (Krause et al., 2005; Maher et al., 2001) and sacrospinous hysteropexy (van Brummen et al., 2003).
SUMMARY The prevalence of vaginal prolapse appears to be increasing, partly because of the increased longevity of women and also probably as a result of inadequate recognition and repair of pelvic organ support defects when pelvic surgery has been performed. The standard use of cul-de-sac plication and uterosacral ligament suspension to provide appropriate support of the vaginal apex at the time of hysterectomy would most likely decrease the prevalence of later entero-
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cele and posthysterectomy apical prolapse. More education and research into the understanding of the anatomy of vaginal support and the pathogenesis of prolapse, and in the principles of pelvic and vaginal reconstructive surgery, are needed to improve care to all affected women.
Bibliography PATHOLOGY OF PELVIC ORGAN PROLAPSE Bump RC, Norton PA. Epidemiology and natural history of pelvic floor dysfunction. Obstet Gynecol Clin North Am 1998;25:723. DeLancey JO. Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 1992;166:1717. Funt MI, Thompson JD, Birch H. Normal vaginal axis. South Med J 1978;71:1534. Harrison JE, McDonagh JE. Hernia of Douglas pouch and high rectocele. Am J Obstet Gynecol 1950;60:83. Heit M, Rosenquist C, Culligan P, et al. Predicting treatment choice for patients with pelvic organ prolapse. Obstet Gynecol 2001;101:1279. 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. Kuhn RJ, Hollyock MD. Observations on the anatomy of the rectovaginal pouch and septum. Obstet Gynecol 1982;59:445. Mädakinen J, Kähäri V, Soderstrom K, et al. Collagen synthesis in the vaginal connective tissue of patients with and without uterine prolapse. Eur J Obstet Gynecol Reprod Biol 1987;24:319. Mädakinen J, Soderstrom K, Kiilholma P, et al. Histologic changes in the vaginal connective tissue of patients with and without uterine prolapse. Arch Gynecol 1986;239:17. 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. Milley PS, Nichols DH. A correlative investigation of the human rectovaginal septum. Anat Rec 1969;163:443. Nichols DH. Posterior colporrhaphy and perineorrhaphy: separate and distinct operations. Am J Obstet Gynecol 1991;164:714. Nichols DH, Randall CL. Vaginal Surgery, 3rd ed. Williams & Wilkins, Baltimore, 1989. Richardson AC. The anatomic defects in rectocele and enterocele. J Pelvic Surg 1995;1:215. Richardson AC, Lyon JB, Williams NL. A new look at pelvic relaxation. Am J Obstet Gynecol 1976;126:568. 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.
DEMOGRAPHICS AND PREVALENCE Boyles SH, Weber AM, Meyn L. Procedures for pelvic organ prolapse in the United States, 1979–1997. Am J Obstet Gynecol 2003;188:108. Brown JS, Waetjen LE, Subak LL, et al. Pelvic organ prolapse surgery in the United States, 1997. Am J Obstet Gynecol 2002;186:712. 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 2004;175:10. 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. Luber KM, Boero S, Choe JY. The demographics of pelvic floor disorders: current observations and future projections. Am J Obstet Gynecol 2001;184:1496. Olsen AL, Smith VJ, Bergstrom JO, et al. Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 1997;89:501. Sajan F, Fikree FF. Perceived gynecological morbidity among young evermarried women living in squatter settlements of Karachi, Pakistan. J Pak Med Assoc 1999;49:92. Samuelsson EC, Arne Victor FT, Tibblin G, Svardsudd KF. Signs of genital prolapse in Swedish population of women in 59 years of age and possible related factors. Am J Obstet Gynecol 1999;180(2 Pt 1):299.
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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. Subak LL, Waetjen LE, van den Eeden S, et al. Cost of pelvic organ prolapse surgery in the United States. Obstet Gynecol 2001;98:646. Swift SE. The distribution of pelvic organ support in a population of female subjects seen for routine gynecologic health care. Am J Obstet Gynecol 2000;183:277. U.S. Census Bureau. U.S. Interim Projections by Age, Sex, Race, and Hispanic Origin. Retrieved June 28, 2005, from http://www.census.gove/ipc/www/ usinterimproj.
ENTEROCELE Francis WJ, Jeffcoate TN. Dyspareunia following vaginal operations. Br J Obstet Gynaecol 1961;68:1. Given FT. “Posterior culdeplasty”: revisited. Am J Obstet Gynecol 1985;153:135. Haase P, Skibsted L. Influence of operations for stress incontinence and/or genital descensus on sexual life. Acta Obstet Gynecol Scand 1988;67:659. Harris RL, Cundiff GW, Theofiastous JP, et al. The value of intraoperative cystoscopy in urogynecologic and reconstructive pelvic surgery. Am J Obstet Gynecol 1997;177:1367. McCall ML. Posterior culdoplasty. Obstet Gynecol 1957;10:595. Moschcowitz AV. The pathogenesis, anatomy, and cure of prolapse of the rectum. Surg Gynecol Obstet 1912;15:7. Stanhope CR, Wilson TO, Utz WJ, et al. Suture entrapment and secondary ureteral obstruction. Am J Obstet Gynecol 1991;164:1513. Torpin R. Excision of the cul-de-sac of Douglas for the surgical care of hernias through the female caudal wall, including prolapse of the uterus. J Int Coll Surg 1955;24:322. Tulikangas PK, Lukban JC, Walters MD. Anterior enterocele: a report of three cases. Int Urogynecol J 2004;15:350. Waters EG. Vaginal prolapse: technique for correction and prevention at hysterectomy. Obstet Gynecol 1956;8:432.
VAGINAL PROCEDURES THAT SUSPEND THE APEX Amreich I. Atiologie und operation des scheiden stump prolapses. Wien Klin Wochenschr 1951;65:74. Backer MH. Success with sacrospinous suspension of the prolapsed vaginal vault. Surg Gynecol Obstet 1992;175:419. Barber MD, Visco AG, Weidner AC, et al. Bilateral uterosacral ligament vaginal vault suspension with site specific endopelvic fascia defect repair for treatment of pelvic organ prolapse. Am J Obstet Gynecol 2000;183:1402. Brown WE, Hoffman MS, Bouis PJ, et al. Management of vaginal vault prolapse: retrospective comparison of abdominal versus vaginal approach. J Fla Med Assoc 1989;76:249. Burrows LJ, Meyn LA, Walters MD, Weber AM. Pelvic symptoms in women with pelvic organ prolapse. Obstet Gynecol 2004;104:982. Carey MP, Slack MC. Transvaginal sacrospinous colpopexy for vault and marked uterovaginal prolapse. Br J Obstet Gynaecol 1994;101:536. Cruikshank SH. Sacrospinous fixation: should this be performed at the time of vaginal hysterectomy? Am J Obstet Gynecol 1991;164:1072. Cruikshank SH, Cox IN. Sacrospinous fixation at the time of vaginal hysterectomy. Am J Obstet Gynecol 1990;162:1611. DeLancey JO. Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 1992;166:1717. Elkins TE, Hopper JB, Goodfellow K, et al. Initial report of anatomic and clinical comparison of the sacrospinous ligament fixation to the high McCall culdoplasty for vaginal cuff fixation at hysterectomy for uterine prolapse. J Pelvic Surg 1995;1:12. Farnsworth BN. Posterior intravaginal slingplasty (infracoccygeal sacropexy) for severe posthysterectomy vaginal vault prolapse—a preliminary report on efficacy and safety. Int Urogynecol 2002;13:4. Farrell SA, Scotti RJ, Ostergard DR, et al. Massive evisceration: a complication following sacrospinous vaginal vault fixation. Obstet Gynecol 1991;78:560. Funt MI, Thompson JD, Birch H. Normal vaginal axis. South Med J 1978;71:1534. Heinonen PK. Transvaginal sacrospinous colpopexy for vaginal vault and complete genital prolapse in aged women. Acta Obstet Gynecol Scand 1992;71:377.
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. Imparato E, Aspesi G, Rovetta E, et al. Surgical management and prevention of vaginal vault prolapse. Surg Gynecol Obstet 1992;175:233. Inmon WB. Pelvic relaxation and repair including prolapse of vagina following hysterectomy. South Med J 1963;56:577. Kaminski PF, Sorosky JI, Pees RC, et al. Correction of massive vaginal prolapse: an older population. J Am Geriatr Soc 1993;41:42. Karram MM, 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. Keetel LM, Hebertson RM. An anatomic evaluation of the sacrospinous ligament colpopexy. Surg Gynecol Obstet 1989;168:318. Kovac SR, Cruikshank SH. Successful pregnancies and vaginal deliveries after sacrospinous uterosacral fixation in five of 19 patients. Am J Obstet Gynecol 1993;168:1778. Lee RA, Symmonds RE. Surgical repair of posthysterectomy vault prolapse. Am J Obstet Gynecol 1972;112:953. Mädakinen J, Söderström K, Kiilholma P, et al. Histologic changes in the vaginal connective tissue of patients with and without uterine prolapse. Arch Gynecol 1986;239:17. Maher CF, Murray CJ, Carey MP, et al. Iliococcygeus or sacrospinous fixation for vaginal vault prolapse. Obstet Gynecol 2001;98:40. Maher CF, Cary MD, Slack MC, et al. Uterine preservation or hysterectomy at sacrospinous colpopexy for uterovaginal prolapse. Int Urogynecol J 2001;12:381. McCall ML. Posterior culdoplasty. Obstet Gynecol 1957;10:595. Meeks GR, Washburne JF, McGeher RP, et al. Repair of vaginal vault prolapse by suspension of the vagina to ileococcygeus (prespinous) fascia. Am J Obstet Gynecol 1994;171:1444. Miyazaki FS. Miya hook ligature carrier for sacrospinous ligament suspension. Obstet Gynecol 1987;70:286. Monk BJ, Ramp JF, Montz FJ, et al. Sacrospinous fixation for vaginal vault prolapse. Complications and results. J Gynecol Surg 1991;7:87. Morley G, DeLancey JO. Sacrospinous ligament fixation for eversion of the vagina. Am J Obstet Gynecol 1988;158:872. Nagata I, Kato K. Sacrospinous ligament fixation of vaginal apex for repair operation of uterine prolapse: operative procedure and postoperative outcome evaluated with score system and x-ray subtraction colpography. Acta Obstet Gynaecol Jpn 1986;38:29. Nichols D. Massive eversion of the vagina. In Gynecologic and Obstetric Surgery. Mosby, St. Louis, 1993. Nichols DH, Randall CL. Vaginal Surgery, 3rd ed. Williams & Wilkins, Baltimore, 1989. Peters WA, Christenson ML. Fixation of the vaginal apex to the coccygeus fascia during repair of vaginal vault eversion with enterocele. Am J Obstet Gynecol 1995;172:1894. Petros PE. New ambulatory surgical methods using an anatomical classification of urinary dysfunction improve stress, urge, and abnormal emptying. Int Urogynecol J 1997;8:270. Petros PE. Vaginal prolapse II: restoration of dynamic vaginal supports by infracoccygeal sacropexy. An axial day-case vaginal procedure. Int Urogynecol J 2001;12:296. Phaneuf TE. Inversion of the vagina and prolapse of the cervix following suprapubic hysterectomy and inversion of the vagina following total hysterectomy. Am J Obstet Gynecol 1952;64:739. Porges RF, Smilen SW. Long-term analysis of the surgical management of pelvic support defects. Am J Obstet Gynecol 1994;171:1518. Randall C, Nichols D. Surgical treatment of vaginal inversion. Obstet Gynecol 1971;38:327. Richardson DA, Scotti RJ, Ostergard DR. Surgical management of uterine prolapse in young women. J Reprod Med 1989;34:388. Richter K. Massive eversion of the vagina: pathogenesis, diagnosis, and therapy of the “true” prolapse of the vaginal stump. Clin Obstet Gynecol 1982;25:897. Richter K, Albright W. Long-term results following fixation of the vagina on the sacrospinal ligament by the vaginal route. Am J Obstet Gynecol 1981;151:811. Ridley JH. A composite vaginal vault suspension using fascia lata. Am J Obstet Gynecol 1976;126:590. Sauer HA, Klutke CG. Transvaginal sacrospinous ligament fixation for treatment of vaginal prolapse. J Urol 1995;154:1008.
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Surgical Treatment of Vaginal Vault Prolapse and Enterocele
Seigworth GR. Vaginal vault prolapse with eversion. Obstet Gynecol 1979;54:255. Sharp TR. Sacrospinous suspension made easy. Obstet Gynecol 1993;82:873. Shull BL, Bachofen C, Coates KW, Kuehl TJ. 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. Shull BL, Capen CV, Riggs MW, et al. Preoperative 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. Shull BT, Capen CV, Riggs MW, et al. Bilateral attachment of the vaginal cuff to ileococcygeus fascia: an effective method of cuff suspension. Am J Obstet Gynecol 1993;168:1669. Symmonds RE, Pratt JH. Vaginal prolapse following hysterectomy. Am J Obstet Gynecol 1960;79:899. Symmonds RE, Sheldon RS. Vaginal prolapse after hysterectomy. Obstet Gynecol 1965;25:61. Symmonds RE, Williams TJ, Lee RA, et al. Posthysterectomy enterocele and vaginal vault prolapse. Am J Obstet Gynecol 1981;140:852. Sze EH, Karram MM. Transvaginal repair of vault prolapse: a review. Obstet Gynecol 1997;89:466. Sze EH, Miklos JR, Partoll L, et al. Sacrospinous ligament fixation with transvaginal needle suspension for advanced pelvic organ prolapse and stress incontinence. Obstet Gynecol 1997;89:94. Thakar R, Stanton S. Management of genital prolapse. Br Med J 2004; 324:1258. Thompson JD, Rock JA, eds. TeLinde’s Operative Gynecology, 7th ed. JB Lippincott, Philadelphia, 1992. van Brummen HJ, van de Pol, Aulders CI, et al. Sacrospinous hysteropexy compared to vaginal hysterectomy as primary surgical treatment for a descensus uteri: effects on urinary symptoms. Int J Urogynecol 2003;14:350. Webb MJ, Aronson MP, Ferguson LK, et al. Posthysterectomy vaginal vault prolapse: primary repair in 693 patients. Obstet Gynecol 1998;92:281.
ABDOMINAL PROCEDURES THAT SUSPEND THE APEX Addison WA, Livengood CH, Parker RT. Posthysterectomy vaginal vault prolapse with emphasis on management by transabdominal sacral colpopexy. Postgrad Obstet Gynecol 1988;8:1. 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. Addison WA, Timmons CM, Wall LL, et al. Failed abdominal sacral colpopexy: observations and recommendations. Obstet Gynecol 1989;74:480. Angulo A, Ligman I. Retroperitoneal sacrocolpopexy for correction of prolapse of vaginal vault. Surg Gynecol Obstet 1989;169:319. Bai SW, Kim EH, Shin JS. A comparison of different pelvic reconstruction surgeries using mesh for pelvic organ prolapse patients. Yonsei Med J 2005;46:112. Baker KR, Beresford JM, Campbell C. Colposacropexy with Prolene mesh. Surg Gynecol Obstet 1990;171:51. 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. Carey MP, Dwyer PL. Genital prolapse: vaginal versus abdominal route of repair. Curr Opin Obstet Gynecol 2001;13:499. Cowan W, Morgan HR. Abdominal sacral colpopexy. Am J Obstet Gynecol 1980;138:348. Creighton SM, Stanton SL. The surgical management of vaginal vault prolapse. Br J Obstet Gynaecol 1991;98:1150. Culligan PJ, Blackwell L, Goldsmith LJ. A randomized controlled trial comparing fascia lata and synthetic mesh for sacral colpopexy. Obstet Gynecol 2005;106:29. 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;177:1345. Diwan A, Rardin CR, Kohli N. Uterine preservation during surgery for uterovaginal prolapse: a review. Int J Urogynecol 2004;15:286.
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Drutz HP, Cha LS. Massive genital and vaginal vault prolapse treated with abdominal-vaginal sacropexy with use of Marlex mesh: review of the literature. Am J Obstet Gynecol 1987;156:387. Feldman GB, Birnbaum SJ. Sacral colpopexy for vaginal vault prolapse. Obstet Gynecol 1979;53:399. Given FY, Muhlendorf TK, Browning GM. Vaginal length and sexual function after colpopexy for complete uterovaginal eversion. Am J Obstet Gynecol 1993;169:284. Grunberger W, Grunberger V, Wierrani F. Pelvic promontory fixation of the vaginal vault in sixty-two patients with prolapse after hysterectomy. Surg Gynecol Obstet 1994;178:69. Iosif CS. Abdominal sacral colpopexy with use of synthetic mesh. Acta Obstet Gynecol Scand 1993;72:214. Kohle N, Walsh P, Roat TW, et al. Mesh erosion following abdominal sacral colpopexy. Obstet Gynecol 1998;92:999. Krause HG, Groh JT, Sloane K, et al. Laparoscopic sacral suture hysteropexy for uterine prolapse. Int Urogynecol J 2006;17:378. Lansman HH. Posthysterectomy vault prolapse: sacral colpopexy with dura mater graft. Obstet Gynecol 1984;63:577. Lo T-S, Wang AL. Abdominal colposacropexy and sacrospinous ligament suspension for severe uterovaginal prolapse: a comparison. J Gynecol Surg 1998;14:59. Maher CF, Qatawney 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. Maher CF, Carey MP, Murray CJ. Laparoscopic suture hysteropexy for uterine prolapse. Obstet Gynecol 2001;97:1010. Maher C, Bassler K, Glazener CM, et al. Surgical management of pelvic organ prolapse in women. The Cochrane Database of Systemic Reviews; The Cochrane Library Oxford Press, vol. 4, 2005. Maloney JC, Dunton CJ, Smith K. Repair of vaginal vault prolapse with abdominal sacropexy. J Reprod Med 1990;35:6. Nichols DH. Fertility retention in the patient with genital prolapse. Am J Obstet Gynecol 1991;164:1155. Nygaard IE, McCreery R, Brubaker L, et al. for the Pelvic Floor Disorders Network. Abdominal sacrocolpopexy: a comprehensive review. Obstet Gynecol 2004;104:805. Paraiso MF, Walters MD, Rackley RR, et al. Laparoscopic and abdominal sacral colpopexies: a comparative cohort study. Am J Obstet Gynecol 2005;192:1752. Roovers JP, van der Vaart CH, van der Bom JG, et al. A randomized controlled trial comparing abdominal and vaginal prolapse surgery: effects for urogenital function. BJOG 2004;111:50. Rust JA, Botte JM, Howlett RJ. Prolapse of the vaginal vault. Improved techniques for management of the abdominal approach or vaginal approach. Am J Obstet Gynecol 1976;125:768. Snyder TE, Krantz KE. Abdominal-retroperitoneal sacral colpopexy for the correction of vaginal prolapse. Obstet Gynecol 1991;77:944. Sutton GP, Addison WA, Livengood CH, et al. Life-threatening hemorrhage complicating sacral colpopexy. Am J Obstet Gynecol 1981;140:836. Tancer ML, Fleischer M, Berkowitz BJ. Simultaneous colpo-recto-sacropexy. Obstet Gynecol 1987;70:951. Timmons MC, Addison WA, Addison SB, et al. Abdominal sacral colpopexy in 163 women with posthysterectomy vaginal vault prolapse and enterocele. J Reprod Med 1992;37:323. Timmons MC, Kohler MF, Addison WA. Thumbtack use for control of presacral bleeding, with description of an instrument for thumbtack application. Obstet Gynecol 1991;78:313. Todd JW. Mesh suspension for vaginal prolapse. Int Surg 1978;63:91. Traiman P, De Lucia LA, Silva AA, et al. Abdominal colpopexy for complete prolapse of the vagina. Int Surg 1992;77:91. Valaitis SR, Stanton SL. Sacrocolpopexy: a retrospective study of a clinician’s experience. Br J Obstet Gynaecol 1994;101:518. van Lindert AC, Groenendijk AG, Scholten PC, et al. Surgical support and suspension of genital prolapse, including preservation of the uterus, using Gore-Tex soft tissue patch. Eur J Obstet Gynecol Reprod Biol 1996;50:133. Visco AG, Weidner AC, Barber MD, et al. Vaginal mesh erosion after abdominal sacral colpopexy. Am J Obstet Gynecol 2001;184:297. Vitranen H, Hirvonen T, Makinen J, et al. Outcome of thirty patients who underwent repair of posthysterectomy prolapse of the vaginal vault with abdominal sacral colpopexy. J Am Coll Surg 1994;178:283.
Obliterative Procedures for Vaginal Prolapse
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William Andre Silva and Mickey M. Karram
HISTORICAL PERSPECTIVES 288 PREOPERATIVE EVALUATION 288 LE FORT PARTIAL COLPOCLEISIS 289 TOTAL COLPECTOMY AND COLPOCLEISIS 290 URINARY FUNCTION AFTER OBLITERATIVE PROCEDURES QUALITY OF LIFE AND REGRET OF LOSS OF SEXUAL FUNCTION 293 CONCLUSION 294
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As women live longer and healthier lives, pelvic floor disorders are becoming even more prevalent and an increasingly important health and social issue. An estimated 63 million women will be 45 years old or greater by 2030, and 33% of the population will be postmenopausal by 2050. Over 10% of women will undergo surgery for pelvic organ prolapse or incontinence in their lifetime; the reoperation rate for failure is approximately 30%. Due to an increasing number of women entering the eighth and ninth decades of life, many of these individuals will present with pelvic organ prolapse, often after unsuccessful trials of conservative treatment or surgeries. These women frequently have concomitant medical issues and are not sexually active, making extensive surgery not suitable. This chapter discusses the use of obliterative procedures as a surgical option for pelvic organ prolapse in this patient population.
HISTORICAL PERSPECTIVES Before the introduction of operative procedures, uterine prolapse had been treated unsuccessfully with various techniques, including vaginal packing and instillation with caustic substances. Early forms of surgical treatment were later promoted in the form of introital narrowing and/or excision of the prolapsing areas. Gerardin of Metz, in 1823, first described the reapproximation of denuded vaginal mucosa as an obliterative procedure. As noted by Tauber (1947), the procedure was first performed by Neugebauer of Warsaw, in 1867, by suturing the anterior and posterior vaginal walls together after removing a 6 × 3 cm rectangu-
lar area of vaginal mucosa in each segment. Leon Le Fort of Paris popularized the procedure in 1877 and modified the previous description by Neugebauer by creating a narrower and longer area of mucosal removal and the addition of a posterior colpoperineoplasty at 8 postoperative days (Taft, 1889). In 1881, Berlin reported the first three American cases performed at the New England Hospital for Women. In the early twentieth century, reports in the literature were mainly technical descriptions with brief mention of outcome data. Baer and Reis, in 1928, reported a 100% success rate in a group of 14 women who received Le Fort colpocleisis. Phaneuf, in 1935, had two vault recurrences and one anterior vaginal prolapse in a total of 20 patients. In 1936, Adair and DaSef published their series of 38 patients, one of whom developed a recurrence of uterine prolapse through a lateral channel, and two had recurrence of cystoceles. Collins and Lock (1941) had a 94% success rate in 31 patients, whereas Mazer and Israel (1948) reported a 97% success rate in 38 women. Martin (1898) from Europe has been credited for the initial use of hysterectomy and complete vaginectomy for the correction of uterovaginal prolapse. Total colpocleisis with levator plication was first reported in 1901 in the English literature by Edebohls. He described four cases of panhysterocolpectomy, which involved vaginal hysterectomy, vaginectomy, and visceral reduction via purse-string sutures. The incorporation of levator plication into the procedure was described by Phaneuf, in 1935, in five subjects. Masson and Knepper, in 1938, published a case series of 23 patients who underwent vaginectomy, with or without hysterectomy, purse-string reduction of the viscera, levator plication, and perineorrhaphy. No recurrences were observed in a series of 60 cases of vaginal hysterectomy with vaginectomy and levatorplasty by Williams in 1950.
PREOPERATIVE EVALUATION The evaluation and staging of pelvic organ prolapse are described in Chapters 5 and 6. Most gynecologists would
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agree that optimal treatment is contingent upon obtaining a thorough history and physical examination findings as well as an understanding of the relationship between pelvic prolapse and coexisting functional derangements. This may commonly require ancillary testing. The role of preoperative imaging to detect hydronephrosis or ureteric compromise in the setting of advanced prolapse is controversial. Beverly et al. (1997) showed that the prevalence of hydronephrosis increases with worsening stage of prolapse. In women with severe prolapse, preoperative imaging may document preexisting hydronephrosis or ureteric obstruction that might otherwise be confused with iatrogenic ureteric injury at time of surgery. In addition, if preoperative radiographic studies demonstrate complete ureteric obstruction, a pessary with or without a ureteral stent may be placed if definitive surgery cannot take place promptly. The role of urodynamic testing in the medically fragile population, with severe prolapse, has not been determined. Occult or “potential” stress incontinence can be masked by the presence of pelvic organ prolapse. Not infrequently, incontinent women may note the decrease or disappearance of stress incontinence episodes as the degree of prolapse worsens. The office demonstration of the sign of urine loss is facilitated by the use of a speculum or pessary to reduce the prolapse while a stress maneuver is performed. Its presence may influence management options given to the patient. However, the method to reduce vaginal prolapse to evaluate latent incontinence is not universally agreed upon or standardized at this time. Some authors have not incorporated voiding diaries and urodynamics in their assessment because of the advanced age of their population and lack of compliance. In contrast, others advocate routine urodynamic testing in the setting of preoperative urinary symptoms or selective usage, depending on mitigating medical issues or excessive patient travel time. In a study by von Pechmann et al. (2003), 75 of 92 subjects underwent multichannel preoperative urodynamics; 36 (48.0%) had stress incontinence, 13 (17.3%) had detrusor overactivity, and 16 (21.3%) had mixed incontinence. Thus, treatment for clinical stress and urge incontinence must be incorporated into the treatment plan. In addition, FitzGerald and Brubaker (2003) found that 27% of patients without preoperative symptoms of stress incontinence developed new onset stress incontinence after surgery. Last, elderly patients with advanced prolapse are at higher risk for voiding dysfunction and retention when an anti-incontinence procedure, such as a suburethral sling, is performed.
LE FORT PARTIAL COLPOCLEISIS An obliterative procedure in the form of a Le Fort partial colpocleisis is an option if the patient has her uterus and is no longer sexually active. Because the uterus is retained, it will be difficult to evaluate any future uterine bleeding or cervical pathology. Therefore, endovaginal ultrasound, endometrial biopsy, and Papanicolaou smear must be done before surgery. Denehy et al. (1995) reported two patients who were considered for a Le Fort procedure but were found to have stage IA endometrial carcinoma during the work-up phase.
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The procedure is started by placing the cervix on traction to evert the vagina. The vaginal mucosa is injected with 0.025% bupivacaine or 2% lidocaine with 1:200,000 epinephrine just below the epithelium. A Foley catheter with a 5- to 10-mL balloon is placed in the bladder for identification of the bladder neck. A marking pen is used to mark out the areas that are to be denuded anteriorly and posteriorly. The area should extend from about 2 cm from the tip of the cervix to 4 to 5 cm below the external urethral meatus. A mirror image on the posterior aspect of the cervix and vagina should also be marked out. The previously marked areas are removed by sharp dissection (Fig. 22-1, A,B). The surgeon should leave the maximum amount of muscularis behind on the bladder and rectum. Hemostasis is an absolute must. After reducing the cervix 3 to 4 cm, the cut edges of the anterior and posterior vaginal walls are sewn together with interrupted delayed absorbable sutures (Fig. 22-1, C). The knots should be turned into the epithelium-lined tunnels that were created bilaterally. The uterus and vaginal apex are gradually turned inward. After the vagina has been inverted, the superior and inferior margins of the incisions can be sutured together (Fig. 22-1, D). In the author’s opinion, a plication of the bladder neck should be routinely performed because of the high incidence of postoperative stress incontinence (Fig. 22-1, A, inset). Also, because there is no real support to the repair, an aggressive perineorrhaphy with a distal levator plication should be done to narrow the introitus and build up the perineum. In general, about 90% to 95% of patients have relief of symptoms and good anatomic results. Complete breakdown or partial recurrence can be expected in 2% to 5% of patients. This is due to mostly either poor hemostasis with hematoma formation or infection. Goldman et al. (1985) reported on results and complications from a modified Le Fort procedure in 118 patients. Ninety-one percent of patients had good anatomic results, whereas 85% had relief of symptoms, 2.5% had recurrence of their prolapse, 10.2% developed incontinence or worsening of their incontinence, and 1.8% had late vaginal bleeding. These patients typically have other medical problems that may need to be addressed and closely monitored. Denehy et al. (1995) compared two cohorts of medically compromised women, of whom 21 received a modified Le Fort partial colpocleisis with Kelly plication and posterior colpoperineoplasty and 42 received a vaginal hysterectomy, anterior colporrhaphy, and posterior colpoperineoplasty. No differences were present in median hospital stay or postoperative decrease in hemoglobin. Complications among the patients in the Le Fort group included one arrhythmia, three urinary tract infections, and one death at 42 postoperative days due to end-stage biliary cirrhosis. The hysterectomy group consisted of one pulmonary embolus, three urinary tract infections, and one arrhythmia (Denehy et al., 1995). Glavind and Kempf (2005) presented the results of 25 patients who underwent Le Fort colpocleisis and 17 patients who had colpectomy. The colpocleisis group experienced one case of postoperative bleeding that required resuturing in the operating theater and one case of severe vaginal discharge. No reported complications were found in the colpectomy group.
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Figure 22-1 ■ Technique of Le Fort partial colpocleisis. A. Anterior vaginal wall has been removed, and suburethral plication stitch is placed at the bladder neck, as indicated (inset). B. Posterior vaginal wall is removed. C. Cut edge of anterior vaginal wall is sewn to cut edge of posterior vaginal wall in such a way that the cervix, uterus, and remaining vagina are inverted. The inset shows that tunnels in the vaginal wall are created bilaterally. D. After the uterus is completely reduced and the anterior and posterior vaginal walls sutured together, a perineorrhaphy is done, and the vaginal epithelium is closed.
TOTAL COLPECTOMY AND COLPOCLEISIS For patients with posthysterectomy vaginal vault prolapse who do not desire coital function and where operative time is to be kept at a minimum, a colpectomy and partial or complete colpocleisis can be done to effectively treat the prolapse.
Colpocleisis can also be performed concurrently with an initial vaginal hysterectomy and closure of the vaginal apex. To perform this operation for complete vaginal vault eversion, the vaginal epithelium is completely excised from the underlying vaginal muscularis and endopelvic fascia (Fig. 22-2, A,B). A series of purse-string sutures are used to
Chapter 22
invert the prolapse (Fig. 22-2, C). Once the prolapse is reduced, a suburethral plication (if indicated), posterior colpoperineorrhaphy, and levator plication are done (Fig. 22-2, D). In cases of vaginal colpectomy, no attempt is made to enter the enterocele sac. The concern regarding the recurrence of apical prolapse in the absence of an enterocele repair has been raised; however, an enterocele does not protrude below the pelvic floor because the vaginal canal is com-
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pletely obliterated after surgery. In addition, the entry into an enterocele may involve a theoretical increase in the rate of postoperative infection, ileus, and other complications. We and others advocate plication of the levator ani with narrowing of the levator hiatus during colpectomy. The levator hiatus is invariably widened in this patient population. The puborectalis and pubococcygeus muscle may be approximated in the midline with delayed absorbable sutures to
Figure 22-2 ■ Technique of vaginal colpectomy. A. The vagina is circumscribed by an incision several centimeters from the hymen. It can be marked in quadrants and portions of the vagina removed sharply, as shown. B. The posterior vaginal wall epithelium is sharply removed. The peritoneal cavity is not entered. C. A series of purse-string sutures are placed, sequentially inverting the vagina by tying sutures 1, then 2, then 3. The apex of the soft tissue is inverted by the tip of a forceps as each purse-string suture is tied. D. A perineorrhaphy is usually performed, and the vaginal epithelium is closed.
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create a shelf above the rectum, thus creating a further barrier to visceral descent (Fig. 22-3). A variation of the procedure involves the performance of separate anterior and posterior colporrhaphies, with two purse-string sutures to close the anterior and posterior segments together, and an extensive perineorrhaphy. Cespedes et al. (2001) reported 38 cases of this multicompartment colpocleisis. No significant complications were present in their series. Mean operating time was 145 minutes; however, some of the patients required an additional anti-incontinence proce-
dure (pubovaginal sling, Kelly plication). At a mean follow-up duration of 24 months, no recurrence in prolapse was noted. Complications of total colpectomy and colpocleisis are similar to those of Le Fort partial colpocleisis and are often related to the fragile medical condition of the patient. Stepp et al. (2005) found that, among women over age 75 with prolapse who underwent a full range of surgeries, including colpectomy, most complications (after bladder infections and blood transfusions) were medical. The most common postoperative medical complications were pulmonary edema
C Figure 22-3 ■ Technique of posterior colporrhaphy and levator plication. A. Widened genital hiatus and vaginal opening, as shown, is frequently found in women with severe pelvic organ prolapse. The inset shows the widened atrophic levator muscles. B. To accomplish the perineorrhaphy, a triangular incision is made in the skin of the perineal body and a midline posterior vaginal incision is done. The vaginal flaps are dissected bilaterally off the rectum until the levator muscles are seen. Inset: Delayed absorbable sutures are used to plicate the distal levator muscles. C. The plication creates a shelf over the rectum and perineal body, narrowing the vaginal introitus (inset) and providing additional support to a prolapse repair. As with other obliterative procedures, a tight levator plication should be done in only women who are not, or are not planning to be, sexually active.
Chapter 22
and congestive heart failure. Preoperative risk factors for complications included length of surgery, coronary artery disease, and peripheral vascular disease. DeLancey and Morley (1997) performed total colpocleisis on 33 women and reported a worsening of congestive heart failure in two women, urinary tract infection in two women, and pneumonia in one woman. Recurrent eversion developed in one patient a year later and required repeat colpocleisis. Harmanli et al. (2003) analyzed the complication rates in 41 women who underwent total colpocleisis, of whom 12 received a vaginal hysterectomy at the same time. Complications occurred at a low rate: febrile morbidity (19.5%), bladder injury (2.4%), and late rectal bleeding (9.8%). No patients required blood transfusion or sustained ureteral or intestinal injury. Von Pechmann et al. (2003) reported on 92 subjects who had total colpocleisis with high levator plication, of whom 37 (40.2%) underwent a simultaneous vaginal hysterectomy. Concurrent hysterectomy was associated with a statistically significant decrease in hematocrit (11.9% vs. 9.5% change; P = .01) and increase in transfusion requirement (35.1% vs. 12.7%; P = .02). Von Pechmann et al. (2003) reported two cases of rectal prolapse after total colpocleisis and high levator plication in 92 patients. It was unclear whether the concurrent risk factors for the development of rectal prolapse (advanced age, female sex, chronic constipation) or the levator plication itself (intra-abdominal pressure finding the path of least resistance) contributed to the development (or unmasking) of rectal prolapse. A small risk (0–2%) of ureteric occlusion or injury may exist with total colpectomy, usually due to kinking in the distal ureter from the purse-string sutures. The majority of cases will resolve with removal of the purse-string or plication stitches. Rare cases of obstruction secondary to intramural ureteral edema, from preoperative placement of ureteric stents, have been reported and they resolved after a second passage of stents. Also, if there is no flow of urine from one ureter after surgery, the possibility of long-standing severe preexisting hydronephrosis from the prolapse, leading to renal cortical atrophy and diminished or absent function, must be considered. Preoperative or intraoperative imaging studies to assess renal function may be helpful in women with long-standing severe prolapse, especially if their serum creatinine is elevated. Rare reports of postoperative infection or vaginal evisceration have been reported in the literature. Kohli et al. (1996) described a patient with pyometra at 8 months postLe Fort that required subsequent hysterectomy. Small bowel evisceration through the vagina at 3 years after colpocleisis has also been reported.
URINARY FUNCTION AFTER OBLITERATIVE PROCEDURES The challenge for the pelvic surgeon is to provide effective treatment for pelvic organ prolapse while maintaining or restoring lower urinary tract function. De novo stress incontinence is a recognized phenomenon after obliterative surgery. In addition, the risk of worsening any preexisting
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urinary retention with an anti-incontinence procedure must be weighed against the risk of post-colpocleisis stress incontinence if an anti-incontinence procedure is not performed. Surprisingly, many elderly women with advanced prolapse have normal urinary tract function but are at high risk for postoperative irritative symptoms and retention, if suburethral sling is performed. Fitzgerald and Brubaker (2003) retrospectively reviewed the results of colpocleisis with particular attention to perioperative stress incontinence. They demonstrated a 36% incidence of elevated postvoid residual volumes (>100 mL) in 64 patients. Stress incontinence was diagnosed in 78% of those tested, and an occult incontinence rate of 33% was noted. Autologous fascial slings were inserted concurrently in 33% of patients, whereas 19% had a Kelly plication as they opted not to undergo a formal anti-incontinence procedure. At a median follow-up time of 12 weeks, all patients with preoperative elevated postvoid residual volumes had normal residual volume after surgery. However, urinary retention persisted in three patients after a sling (14%), and all patients required takedown of the sling. Stress incontinence persisted in six (28%) of the subjects, three who had a sling and three who underwent Kelly plication. The rate of de novo stress incontinence was 27%; one patient had a suburethral plication, and seven had no extra bladder neck procedure. Moore and Miklos (2003) described their experience with 30 women who had colpocleisis and tension-free vaginal tape (TVT) under local anesthesia for stress incontinence and severe uterovaginal prolapse. No intraoperative complications occurred; however, one woman developed a postoperative myocardial infarction. At an average followup period of 19.1 months, 94% were cured of their stress incontinence. One patient required suburethral release of the sling after experiencing acute urinary retention for 5 weeks. The authors concluded that the TVT sling was safe and effective for the concurrent treatment of stress incontinence in a woman having colpocleisis. The use of other midurethral slings, including transobturator slings or transurethral collagen injection in the setting of obliterative surgery, is likely to be effective but remains to be studied. The majority of studies do not describe the outcomes of urgency and urge incontinence after obliterative procedures or make any attempt to differentiate stress from urge incontinence. In their series of 33 women who underwent total colpocleisis, DeLancey and Morely (1997) reported cure of stress incontinence in 4 of 5 women (1 lost to follow-up) who had a concurrent anti-incontinence procedure. Of the six women with preoperative urge incontinence who were available for follow-up, three were either cured or improved.
QUALITY OF LIFE AND REGRET OF LOSS OF SEXUAL FUNCTION Barber et al. (2006) found that obliterative surgery for stage III or IV pelvic organ prolapse significantly improves quality of life, as measured by several standardized questionnaires. Preoperative counseling should involve the discussion of the sexual implications of vaginal obliteration. Harmanli et al. (2003) reported no postoperative cases of regret after 41
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consecutive cases of total colpocleisis. However, von Pechmann et al. (2003) reported regret over loss of coital ability in eight women (12.9%), of whom four stated that they would have still had the procedure if asked again, three were unsure, and one would not have had the procedure. No significant risk factors (age, number of previous prolapse surgeries) were identified for regret in this study. In another study by DeLancey and Morley (1997), 1 of 33 women expressed remorse, stating she had “accepted” her loss of sexual function.
CONCLUSION Obliterative procedures for advanced pelvic organ prolapse are increasing in popularity due to a growing number of women entering the eighth and ninth decades of life, of whom many have concomitant medical issues that make more extensive surgery less suitable. Optimal treatment is contingent upon a thorough assessment of historical and physical examination findings and an understanding of the relationship between advanced pelvic prolapse and coexisting visceral abnormalities. Obliterative surgeries generally have very high rates of cure and satisfaction; most of the morbidity is due to coexistent medical conditions.
Bibliography HISTORICAL PERSPECTIVES Adair F, DaSef L. The Le Fort colpocleisis. Am J Obstet Gynecol 1936;32:218. Adams HD. Total colpocleisis for pelvic eventration. Surg Gynecol Obstet 1951;2:321. Anderson GV, Deasy PP. Hysterocolpectomy. Obstet Gynecol 1960;16:344. Baer J, Reis R. Immediate and remote results in two hundred twelve cases of prolapse of the uterus. Am J Obstet Gynecol 1928;16:646. Berlin F. Three cases of complete prolapsus uteri operated upon according to the method of Leon Le Fort. Am J Obstet Gynecol 1881;14:866. Collins C, Lock F. The Le Fort colpocleisis. Am J Surg 1941;53:202. Edebohls GM. Panhysterocolpectomy: a new prolapsus operation. Med Rec N Y 1901;60:561. Martin A. Ueber estirpatio vaginae. Berl Klin Wschr 1898;35:910. Masson JC, Knepper PA. Vaginectomy. Am J Obstet Gynecol 1938;36:94. Mazer C, Israel S. The Le Fort colpocleisis: an analysis of 43 operations. Am J Obstet 1948;56:944. Phaneuf L. The place of colpectomy in the treatment of uterine and vaginal prolapse. Am J Obstet Gynecol 1935;30:544. Pratt J, Baker R. Urinary incontinence following the Le Fort operation: report of a case. Obstet Gynecol 1960;16:722. Ridley JF. Evaluation of the colpocleisis: a report of fifty-eight cases. Am J Obstet Gynecol 1972;113:1114. Taft C. Le Fort’s operation for complete procidentia of the uterus, with a report of a case. Am J Med Sci 1889;98:128. Tauber R. The modern technique of the Le Fort operation. Ann Surg 1947;125:334.
Thomsen H. Vaginal evisceration trods kolpokleise og kolpoperineoplastik. Ugeskr Laeger 1988;150:867. Ubachs JM, Van Sante TJ, Schellekens LA. Partial colpocleisis by a modification of Le Fort’s operation. Obstet Gynecol 1973;42:415. Williams JT. Vaginal hysterectomy and colpectomy for prolapse of the uterus and bladder. Am J Obstet Gynecol 1950;59:365.
EVALUATION, SURGICAL TREATMENT, AND COMPLICATIONS Barber M, Amundsen C, Paraiso M, et al. Quality of life after surgery for prolapse in elderly women: obliterative vs. reconstructive surgery, 2006. In press. Beverly C, Walters MD, Weber AM, et al. Prevalence of hydronephrosis in patients undergoing surgery for pelvic organ prolapse. Obstet Gynecol 1997;90:37. Cespedes RD, Winters JC, Ferguson KN. Colpocleisis for the treatment of vaginal vault prolapse. Tech Urol 2001;7:152. DeLancey JO, Morley GW. Total colpocleisis for vaginal eversion. Am J Obstet Gynecol 1997;176:1228. Denehy TR, Choe JY, Gregori CA, Breen JL. Modified Le Fort partial colpocleisis with Kelly urethral plication and posterior colpoperineoplasty in the medically compromised elderly: comparison with vaginal hysterectomy, anterior colporrhaphy, and posterior colpoperineoplasty. Am J Obstet Gynecol 1995;173:1697. Falk HC, Kaufman SA. Partial colpocleisis: the Effort procedure. Obstet Gynecol 1955;5:617. FitzGerald MP, Brubaker L. Colpocleisis and urinary incontinence. Am J Obstet Gynecol 2003;189:1241. Fitzgerald MP, Richter HE, Siddique S, et al. Colpocleisis: a review. Int Urogynecol J Pelvic Floor Dysfunct 2006;17:261–271. Glavind K, Kempf L. Colpectomy or Le Fort colpocleisis—a good option in selected elderly patients. Int Urogynecol J 2005;16:48. Goldman J, Ovadia J, Feldberg D. The Neugebauer-Le Fort operation: a review of 118 partial colpocleises. Eur J Obstet Gynaecol Reprod Biol 1985;12:13. Hanson GE, Keettel WC. The Neugebauer-Le Fort operation: a review of 288 colpocleisis. Obstet Gynecol 1979;34:352. Harmanli OH, Dandolu V, Chatwani AJ, Grody MT. Total colpocleisis for severe pelvic organ prolapse. J Reprod Med 2003;48:703. Kohli N, Sze E, Karram M. Pyometra following Le Fort colpocleisis. Int Urogynecol J 1996;7:264. Lee RA. Atlas of Gynecologic Surgery. WB Saunders Co., Philadelphia, 1992, p. 68. Moore RD, Miklos JR. Colpocleisis and tension-free vaginal tape sling for severe uterine and vaginal prolapse and stress urinary incontinence under local anesthesia. J Am Assoc Gynecol Laparosc 2003;10:276. Nichols DH, Randall CL. Vaginal Surgery, 3rd ed. Williams & Wilkins, Baltimore, 1989. Olsen AL, Smith VJ, Bergstrom JO, et al. Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 1997;89:501. 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. Stepp KJ, Barber MD, Yoo EH, et al. Prevalence of perioperative complications of urogynecologic surgery in elderly women. Am J Obstet Gynecol 2005;192:1630. von Pechmann WS, Mutone M, Fyffe J, Hale DS. Total colpocleisis with high levator plication for the treatment of advanced pelvic organ prolapse. Am J Obstet Gynecol 2003;189:121.
The Use of Biologic Tissue and Synthetic Mesh in Urogynecology and Reconstructive Pelvic Surgery
23
Marie Fidela R. Paraiso
PROPERTIES OF THE IDEAL GRAFT MATERIAL 295 BIOLOGIC PROPERTIES OF HOST TISSUE 296 PROPERTIES OF SYNTHETIC MATERIAL 296 PROPERTIES OF BIOLOGIC TISSUE 299 UROGYNECOLOGIC PROCEDURES INVOLVING THE USE OF SYNTHETIC MESH AND/OR BIOLOGIC TISSUE 302 CLINICAL RESULTS AND COMPLICATIONS ASSOCIATED WITH SYNTHETIC MESH 302 CLINICAL RESULTS AND COMPLICATIONS ASSOCIATED WITH BIOLOGIC TISSUE 303 CONCLUSION 304
Pelvic organ prolapse and urinary incontinence are common phenomena in women. Eleven percent of the female population will undergo surgery for prolapse or stress incontinence in their lifetime (Olsen et al., 1997). Approximately 30% of these women will need a repeat operation for recurrent prolapse. No standard surgical approach is available to patients who suffer from recurrent pelvic organ prolapse and/or incontinence. Multiple surgical techniques for recurrence, some incorporating surgical implants of synthetic or biologic graft material, have evolved. Some investigators have recommended the use of graft material or prosthesis for recurrent prolapse. Currently, the use of implants, both synthetic and biologic, in reconstructive pelvic surgery is expanding rapidly in spite of a paucity of data supporting their use. Indications for the use of graft implantation in reconstructive pelvic surgery include nonexistent or suboptimal autologous tissue; need to augment weak or absent endopelvic tissue; connective tissue disorder; unavoidable stress on the repair (chronic lifting, chronic obstructive pulmonary disease [COPD], chronic straining to defecate, obesity); need to bridge a space; concern about vaginal length or caliber; and denervated pelvic floor. Some surgeons choose augmentation with graft implants routinely in reconstructive pelvic surgery.
Good evidence supports the use of implantation of synthetic material for abdominal treatment of pelvic organ prolapse, as noted in Chapter 21. Suburethral sling procedures using synthetic materials have been shown to have similar cure rates compared with autologous rectus fascia (ARF) slings. The tension-free vaginal tape (TVT) procedure, a polypropylene mesh midurethral sling, has gained widespread popularity and has proven effectiveness comparable to Burch colposuspension. However, the use of synthetic or biologic implants in transvaginal reconstructive procedures is less clear. Although multiple studies have examined the use of implants for vaginal repair of anterior or posterior compartment prolapse, most are case series or cohort studies, with very few randomized surgical trials. Presently, several manufacturers promote various types of synthetic and biologic materials. No adequate studies comparing implants are known. In this chapter, we will review properties of the ideal graft material, host tissue, and available implants. The surgical procedures that involve mesh implantation, associated clinical results, and complications will also be summarized.
PROPERTIES OF THE IDEAL GRAFT MATERIAL Authors have proclaimed a need for ideal graft materials since the mid-twentieth century, and the search continues today. The ideal graft would be chemically and physically inert, noncarcinogenic, mechanically strong, sterilizable, not physically modified by body tissue, readily available, inexpensive, and have minimal risk of infection and rejection (Box 23-1). In prolapse and incontinence surgery, the optimal implant, once healed, would restore normal anatomy and function to the vagina and surrounding pelvic organs. It would be biocompatible and, if biodegradable, persist long enough to allow a durable and adequate repair and incorporation of the
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BOX 23-1
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PROPERTIES OF THE IDEAL GRAFT MATERIAL
Chemically and physically inert Noncarcinogenic Nonimmunogenic Mechanically strong Not modifiable by host Generally available Inexpensive Resistant to infection Resistant to shrinkage Pliable Various shapes and configurations
surrounding tissue. It would be resistant to mechanical stress or shrinkage and easy to work with and be pliable. Other desired criteria include availability in the desired shapes for various operations, prevention of adhesions at visceral surfaces, and a better, or at least equal, response to implantation compared with autologous tissue. Unfortunately, at present, none of the synthetic or biologic tissue implants meet all of these criteria. To date, no published human articles are known that directly compare synthetic and biologic implants in human subjects, except for two randomized trials: one that compares porcine dermal sling to the TVT procedure; (Arunkalaivanan and Barrington, 2003) and another that compares polypropylene mesh to solvent dehydrated cadaveric fascia lata (Culligan et al., 2005). Literature regarding the physical properties of these materials is confined to animal studies and is rarely comparative, mostly analyzing abdominal wall implantation. Furthermore, few studies are known of the biomechanical properties of graft materials or vaginal wall after implantation. Walter et al. (2003) were successful in using a rabbit vagina model to study graft material tensile strength after implantation.
BIOLOGIC PROPERTIES OF HOST TISSUE Before discussing properties of various implants, the role of connective tissue in the pelvic floor must be described. Cervigni and Natale (2001) eloquently summarized the biologic properties of host connective tissue. This supportive structure contains fibrous elements (collagen and elastin) and a viscoelastic matrix containing proteoglycans (large polysaccharides attached to proteins). Connective tissue cells determine the biomechanical properties of soft tissue and are embedded in the extracellular matrix, which comprises 20% of the tissue volume. Collagen, a protein produced by fibroblasts, is composed of glycine, proline, and hydroxyproline. Glycine allows collagen to form a tight helix while proline and hydroxyproline form cross-links to stabilize the collagen chains. Tensile strength of tissues is attributed to collagen fibers. Two fibers found in tissue that require strength and flexibility are type I (the most plentiful and strongest) and type III (less common and randomly organized with type I). Elastin and laminin are glycoproteins that are thought to play a role in a tissue’s ability to stretch. Several authors have
shown that the metabolism of collagen and/or elastin is disrupted in various pelvic floor disorders. After reconstructive surgery, fibrous protein synthesis and remodeling reestablish tissue strength with collagen playing a central role in wound healing. Immature fibroblasts synthesize and secrete collagen and proteoglycans within 24 hours of surgery. During the first 2 weeks after reparative surgery, type III collagen is the principal type found. With maturation of scar tissue, a stronger type I collagen replaces type III collagen. Elastin is not synthesized and remodeled to the extent that collagen is by humans. Scar tissue resulting from wound healing after surgical repair is never as strong as the original tissue that it replaces. For the scope of this chapter it is important to summarize the reaction of host tissue to implanted materials. Biocompatibility is defined as the capability of a material to cause a favorable reaction in a living system, thus performing, augmenting, or replacing a natural function in the host. Williams (1973) described four types of soft tissue response: (1) minimal response with a thin layer of fibrosis around the implant, (2) chemical response with severe and chronic inflammatory reaction around the implant, (3) physical response with an inflammatory reaction to certain materials and the presence of giant cells, and (4) necrosis resulting from in situ exothermic polymerization. Four stages of histologic reaction to graft implantation have been described by Kaupp et al. (1979). They are: Stage 1—During week 1, an intense inflammatory infiltrate around the implant, capillary proliferation, granular tissue, and the presence of giant cells ensue. Stage 2—Within 2 weeks, granular tissue remains and foamy histiocytes appear. The number of giant cells with foreign body graft fibers may increase or decrease. Stage 3—Up to week 4, the acute inflammation disappears, capillaries are reduced, and the number of foamy histiocytes and giant cells increase. Stage 4—After week 4, a few collections of giant cells are present on the surface of the implant, and dense fibrous tissue is present.
PROPERTIES OF SYNTHETIC MATERIAL The available absorbable synthetic mesh implants are polyglycolic acid (Dexon, Davis & Geck, American Cyanamid, Danbury, CT) and polyglactin 910 (Vicryl, Ethicon Inc., Somerville, NJ). Absorbable implants may be desirable because they promote postoperative fibroblast activity, are not threatened by infection, do not undergo rejection, and are not known to be harmful to viscera. Lamb et al., (1983) showed that fibrous deposition into polyglactin mesh cannot take place before its absorption. Polyglactin 910 starts to hydrolyze during the third week after implantation and loses the majority of its mechanical value after 30 days. Polyglycolic acid requires 90 days for absorption. Macrophage activation results in mesh absorption and subsequent recycling of byproducts into new collagen fibers (Levasseur et al., 1979). The resultant scar tissue is not as strong as the reinforced tissue, as evidenced in animal studies (Klinge et al., 2001).
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297
Synthetic
Absorbable
Polyglactin 910
Non-absorbable Multi
Polyglycolic acid
Mixed Mono
Vipro Vipro II
Figure 23-1
Table 23-1
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Synthetic graft materials.
Types and Characteristics of Synthetic Graft Materials
Material
Brand Name
Company
Key Properties
Type
Sizes (cm × cm)
Polyglycolic acid
Dexon
Multifilament
17.5 × 22.5
Polyglactin 910
Vicryl
Davis & Geck, American Cyanamid, Danbury, CT Ethicon, Inc., Somerville, NJ
Multifilament
15 × 15
Absorbable
Nonabsorbable Polypropylene
Atrium
Monofilament
I
Marlex
Atrium Medical, Canton, OH CR Bard, Cranston, RI
Monofilament
I
Prolene Prolene-soft Gynemesh PS
Ethicon, Inc., Somerville, NJ Gynecare, Somerville, NJ
Monofilament
I I I
Boston Scientific, Natick, MA
Polyester
Trelex Surgipro Mersilene
Ethicon, Inc., Somerville, NJ
Monofilament Woven polypropylene Multifilament woven Dacron
Polytetrafluoroethylene (PTFE)
Teflon Surgical Membrane
CR Bard, Haverhill, MA; WL Gore, Flagstaff, AZ
Expanded PTFE
Gore-Tex
WL Gore, Flagstaff, AZ
Polypropylene
Surgipro
Monofilament
I III III
7.5 × 15 15 × 15 5 × 10 5 × 30 2.5 × 10 6 × 11 12 × 15 10 × 15 20 × 20 6 × 11
III Configured for apical prolapse Woven polypropylene
II II
5 × 13 5 × 17
III
Composites Expanded PTFE
Dual-Mesh
PTFE
MycroMesh
Silastic mesh Polypropylene
Pelvitex
CR Bard, Covington, GA
Cellguard Preclude pericardial membrane Preclude dura mater substitute
Nonabsorbable (permanent) synthetic mesh implants are either monofilament or multifilament (Fig. 23-1 and Table 23-1). The most important physical properties of synthetic implants are pore size and porosity. Some authors have noted small intrafiber pores (interstices of less than 10 μm) as a theoretic disadvantage of multifilament mesh
Macroporous one side/ II other microporous, antibiotic impregnated Perforated PTFE, III antibiotic impregnated IV Coated with hydrophilic I porcine collagen, lightweight Polypropylene sheeting IV
10 × 15
IV IV
in comparison to monofilament mesh (Brun et al., 1992; Neel, 1983). Most bacteria are less than 1 μm in diameter in comparison to granulocytes and macrophages, which are greater than 10 μm in diameter. The pore size plays an important role in mesh infection prevention and fibrous ingrowth of surrounding tissues. When describing the characteristics
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of synthetic mesh, Bobyn et al. (1982) listed type of polymer, weave, type of filament, weight, and pore size as important. The authors emphasized that the pore size is the key factor in determining inflammatory response, fibrocollagenous tissue ingrowth, angiogenesis, flexibility (or stiffness), and strength. Best mechanical anchorage with collagen infiltration was noted with pore size between 50 and 200 μm. Pourdeyhimi (1989) noted that exact pore sizes of various meshes cannot be quoted because measurement is technique-dependent. Marlex reportedly has the highest flexural rigidity when compared with Mersilene, Teflon, and Prolene. Both Marlex and Prolene are monofilament; however, Prolene is more flexible due to its larger pore size. Magnified views of six types of synthetic mesh are displayed in Figure 23-2. Synthetic mesh has been reclassified as types I to IV, with respect to pore size, as described by Amid (1997). Refer to Table 23-1 for various grafts and associated properties. Type I is macroporous (pore size >75 μm). Type II is microporous (pore size <10 μm) in at least one of its three dimensions. Type III is a macroporous material with multifilamentous or microporous components.
Type IV is submicronic (pore size <1 μm); this type of mesh is often associated with type I mesh for adhesion prevention in intraperitoneal implantation. All types of synthetic mesh have high tensile strength (more than 50 newtons [N]). Type I mesh acts as a scaffold for tissue ingrowth (fibroblastic cell infiltration). Pore size of greater than 90 μm reduces inflammation, and type I mesh has been associated with reduced rates of infection. Lower inflammatory responses should decrease erosion. Marlex mesh has a smaller pore size and thus has poor tissue ingrowth; therefore, all polypropylene mesh is not type I. Type II and III meshes result in greater foreign body reaction when compared to type I mesh. Klinge et al. (1999) noted that microporous mesh had ongoing perimesh inflammatory reaction at 18 months. Microporous and macroporous multifilament meshes appear to be associated with greater infection rates and poor tissue ingrowth that is attributed to fiber makeup or less surface tension. Microporous multifilament mesh, such as Gore-Tex, is associated with a high infection rate and foreign body reaction. Implant structure has been eloquently outlined by Cosson et al. (2003). The mechanical properties depend on
Figure 23-2 ■ Pore configuration of various synthetic implants. A. Marlex. B. Mersilene. C. Prolene. D. Gore-Tex. E. Gynemesh-PS. F. IVS (Figures A–D reprinted with permission from Iglesia CB, et al. The use of mesh in gynecologic surgery, Int Urogynecol J 1997;8:105.)
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the structure of the fabric and the thread. These materials can be woven, knitted, or unwoven. Plain, twill, and satin are the three types of woven materials, and their advantages are strength and good memory (Fig. 23-3, A). The disadvantages of woven structures are fraying and poor conformity. Knitted fabrics consist of warp knit, interlock, and circular knit (Fig. 23-3, B). The advantages of knitted materials are flexibility, versatility, and high conformity. The unwoven materials are well-absorbed but have the disadvantages of no conformity and poor visibility. Composite structures have two surfaces, one of which prevents adhesions. The disadvantages of these fabrics are that they are rigid and poorly visible. Implants can have perforations and be molded into various shapes: kidney, umbrella, or a plug. Materials can be structured from monofilament or multifilament fibers, which can be twisted, coated, braided, or double-braided (Fig. 23-4). Cosson et al. (2003) reported mechanical properties of eight types of synthetic implants available in Europe from a study performed in collaboration with the engineering department of Institut Catholique des Arts et Métiers (ICAM); however, they acknowledge that no current recommendations are known regarding desired resistance or elasticity of various implants. Certain materials had differing values based on orientation (lengthwise or widthwise); however, too little is known about how various mechanical properties of mesh contribute to the function and longevity of a reparative procedure. A composite mesh has recently been introduced in the United States for use in pelvic reconstructive surgery. This mesh is comprised of a monofilament polypropylene mesh coated with a hydrophilic porcine collagen (Pelvitex, C.R. Bard Inc., Covington, GA). The hydrophilic, absorbable coating protects the viscera from risk of adhesion formation during the first 10 to 14 days after surgery when inflammatory processes peak. Although no data are available regarding the use of this mesh in pelvic floor procedures, adhesion formation has been minimized in abdominal hernia repair (Mutter et al., 2000; Balique et al., 2000). This mesh is also a lightweight monofilament polypropylene thought to maintain strength, increase flexibility, and decrease mesh load on
Figure 23-3 ■ A. Woven mesh. B. Knitted fabric. (Adapted with permission from Cosson M, Debodinance P, Boukerrou M, et al. Mechanical properties of synthetic implants used in the repair of prolapse and urinary incontinence in women: which is the ideal material? Int Urogynecol J 2003;14:169.)
299
Figure 23-4 ■ Fiber structure. (Adapted with permission from Cosson M, Debodinance P, Boukerrou M, et al. Mechanical properties of synthetic implants used in the repair of prolapse and urinary incontinence in women: which is the ideal material? Int Urogynecol J 2003;14:169–178.)
the tissues. A lighter weight and load of mesh may decrease erosion.
PROPERTIES OF BIOLOGIC TISSUE Autologous grafts can be harvested, but allograft, xenograft, and synthetic materials are widely available, and the morbidity associated with autologous tissue procurement can be undesirable in some patients. Although synthetic materials eliminate the morbidity associated with the donor site, they may have a higher risk of erosion compared to allografts (biologic tissue procured from a source other than the recipient) and xenografts (biologic tissue procured from a source or species foreign to the recipient). Some surgeons routinely use biologic tissue because they consider the host tissue impaired or insufficient for successful reconstruction (although for slings, host tissue is well proven to be effective). The biologic grafts include cadaveric dermis, cadaveric fascia lata (CFL), and collagen matrix laminates—usually from porcine dermis, porcine small intestine submucosa, or bovine pericardium (Fig. 23-5; Table 23-2). Each product differs in the type of processing and sterilization techniques, giving biologic graft materials varying biomechanical and physiologic properties. Various abbreviations for biologic tissue used in this chapter are listed in Box 23-2. Implantation of xenografts has gained popularity in reconstructive pelvic surgery because of concerns regarding availability of human allograft tissue and risk of viral transmission. Porcine dermal allografts (DAs) have been used in cardiothoracic and general surgery for many years. The
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Biologic Allografts Autologous
Xenografts Donor
Porcine
Dermis
Dermis
Dermis
Fascia
Fascia
Intestinal Submucosa
Bovine Pericardium
Rectus or Fascia Lata Figure 23-5
Table 23-2
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Biologic tissue implants.
Types and Characteristics of Biologic Tissue Implants
Biologic Tissues
Brand
Company
Properties/Processing/ Sizes (cm × cm)
Cadaveric fascia lata
Tutoplast Suspend
Mentor, Santa Barbara, CA
Bard Fascia Lata
CR Bard, Covington, GA
AlloDerm Repliform
LifeCell Corporation, Branchburg, NJ Boston Scientific, Natick, MA
Bard Dermal Allograft
CR Bard, Murray Hill, NJ
Axis
Mentor, Santa Barbara, CA
Pelvicol Pelvisoft PelviLace
CR Bard, Murray Hill, NJ
InteXen Symphasis Stratasis TF FortaGen Veritas
AMS, Minnetonka, MN Cook Urological, Inc., Bloomington, IN Organogenesis, Canton, MA Synovis Surgical Innovations, St. Paul, MN
Solvent dehydrated Γ-irradiated, preserved 4 × 7, 2 × 12, 2 × 18, 6 × 8 Freeze-dried, Γ-irradiated 4 × 7, 2 × 12, 4 × 12, 8 × 12 Freeze-dried, Γ-irradiated Viral inactivation, 3 × 6, 3 × 15 Freeze-dried Cryopreservation without ice crystal damage Freeze-dried Cryopreservation without ice crystal damage Freeze-dried 2 × 7, 2 × 12 Solvent dehydrated Γ-irradiated Acellular collagen matrix HMDI cross-linked Acellular collagen biomesh Biourethral support system Freeze-dried Freeze-dried Cross-linked with HMDI
Cadaveric dermis
Porcine dermis
Porcine small intestinal submucosa (SIS) Bovine pericardium Preclude dura mesh
Non–cross-linked 2 × 8, 2 × 18, 4 × 7, 4 × 15, 6 × 8
Γ, gamma; HMDI, hexamethylene di-isocyanate; EDC, 1-ethyl-3(3-dimethylaminopropol) carbodimide hydrochloride.
BOX 23-2
ARF AFL CFL DA SD FD SIS BCM
BIOLOGIC TISSUE ABBREVIATIONS
Autologous rectus fascia Autologous fascia lata Cadaveric fascia lata Dermal allograft Solvent dehydrated Freeze-dried Small intestinal submucosa Bioengineered collagen matrix
intended goal of human allograft and xenograft tissue is to provide a scaffold of acellular biocompatible material to allow infiltration and subsequent replacement of graft tissue by the regenerated functional host cells. This acellular material consists of a bioactive and absorbable extracellular tissue matrix consisting of proteins, collagen, elastin, and various growth
factors. Acellularity is a desired quality rendering the tissue incapable of eliciting an inflammatory response by its implantation (nonimmunogenic), thus decreasing risk of infection and erosion after graft implantation. However, published data refute that various biomaterials are cell-free. Zheng et al. (2005) recently showed the presence of porcine DNA in small intestinal submucosa (SIS) implants for tendon repair. This cellular characteristic may increase risk of rejection and infection after implantation. Fitzgerald and Brubaker (2000) reported that freeze-dried (FD) and Tutoplast CFL retain donor HLA class I and II antigens. Choe and Bell (2001) proved that FD gamma-irradiated CFL and acellular cadaveric DA tissue contained intact DNA. Hathaway and Choe (2002) used extraction techniques and DNA amplification to show that all four commercially processed human allografts (SD-CFL Tutoplast, Mentor Corp., Santa Barbara, CA; DA, Musculoskeletal Transplant Foundation, Edison, MJ; DA, Regeneration Technologies Inc., Alachua, FL; and cryopre-
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served CFL Repliform, Life Cell Corp., Woodlands, TX) contained intact genetic material. This is of particular concern because of the theoretical transmission of prions during allograft implantation. Prions are small proteinaceous infectious particles, which resist inactivation by procedures that modify nucleic acids. Despite the previous findings of intact DNA and antigens, there have been no reported cases of disease transmission after allograft implantation. Tissue processing is very important; however, no consensus is known on the methods that should be implemented to produce the ideal biomaterial. Materials are sterilized by various processes, which include freeze-drying, solvent dehydration, or γ-irradiation. A recent investigation by Grimes et al. (2005) emphasized that little is known regarding the effect of sterilization techniques on the structure, mechanical strength, and biocompatibility of biomaterials. The authors showed that all sterilizing methods of SIS (ethylene oxide, gamma irradiation, and e-beam irradiation) resulted in an increase in the rate of sample degradation. They hypothesized that sterilization techniques resulted in the release of extractable growth factors. Fitzgerald et al. (1999) reported a 17% early sling failure rate with FD-CFL, although numerous investigators have refuted their findings with the use of similar biomaterials. Biomaterials are often “cross-linked” to delay reabsorption, a property that various industries promote for success of graft augmentation procedures (despite lack of supporting data). The following is a summary of animal studies regarding cross-linking of biologic tissue. A potential longterm problem with aldehyde cross-linked implants is that they may develop foci of mineralization (calcification) that can become extensive. Calcification of implants prompted one publication by Jorge-Herrero et al. (2001) that evaluated the influence of two anticalcification pretreatments on glutaraldehyde cross-linked bovine pericardium in rats. Currently marketed bovine pericardium (Veritas, Synovis, St. Paul, MN) is not cross-linked with glutaraldehyde. Aldehydes are also cytotoxic at higher levels. One porcine dermis product is cross-linked and stabilized with hexamethylene di-isocyanate (HMDI), making it more permanent and resistant to breakdown by collagenases produced by inflammatory cells and fibroblasts. Animal studies in rats have shown no evidence of mineralization after HMDI cross-linked porcine dermal graft implantation at 2 years (Oliver, 1987). In conclusion, whether cross-linking, despite prolonging a graft’s existence, renders it more effective in reconstructive surgery is unknown. Aldehyde cross-linked implants should be avoided because of mineralization. Some biologic tissues are fenestrated to ensure porosity and to enhance fibrocollagenous ingrowth and angiogenesis. Fenestrations are thought to decrease the risk of seroma formation and infection associated with graft implantation. Therefore, some companies recommend fenestration/perforation of the graft before surgical implantation. The following is a summary of the data regarding histologic properties of various types of biologic tissue after implantation. Fokaefs et al. (1997) showed that ARF persists, neovascularizes, and remodels consistent with noninflammatory scar tissue. Once implanted, the ideal biologic tissue (allograft or xenograft) would be physiologically identical to ARF. However, in animal studies ARF has shown shrink-
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age by 50% and reduction in tensile strength in up to 30%. Although the histologic fate of autologous fascia lata (AFL) has not been reported, some authors have shown tissue remodeling in patients who underwent sling revision. Animal data showed that FD-CFL remodels and are replaced with parallel bundles of host collagen at 12 weeks (Walter et al., 2003). Histologic studies for solvent dehydrated (SD) have not been published. In animal studies, DA has been shown to have greater thickness than SIS at 4 months after implantation. Most investigations of biomechanical properties of various biologic tissue and mesh measure tensile strength as an end point. Whether this is an adequate test is unknown for comparison of the biomechanical properties of biomaterials once implanted in the pelvis. We are currently developing a model that measures compliance and burst strength of the vagina because we believe this is more physiologic. Decter (1993) showed greater tensile strength with AFL when compared with ARF because of longitudinal versus transverse fibers. The maximum load to failure of ARF was consistent with solvent dehydrated (SD) CFL and cadaveric dermal allograft (DA). FD-CFL (gamma-irradiated) has less tensile strength than aforementioned biologic tissues and has been shown to lose 90% of its tensile strength after implantation in the rabbit model. Choe et al. (2001) compared autologous tissues (dermis, rectus fascia, and vaginal mucosa), cadaveric tissues (decellularized dermis, and FD gamma-irradiated CFL), and synthetic materials (Gore-Tex and polypropylene mesh) used in sling procedures and evaluated full strip slings versus patch suture slings. They found that in rank order for the full strip slings, cadaver allografts had the strongest tensile strength followed by the synthetics and autologous tissues (P <.05). The tensile strength for the full strip slings was significantly greater than for the patch suture slings. In rank order for the patch slings, the synthetics and dermal tissues (autograft and allograft) had the highest tensile strength followed by AFL, ARF, and vaginal mucosa (P <.05). They concluded that when a patch sling is constructed from autograft and allograft tissues, the risk of suture pull-through and recurrent stress incontinence must be considered. Dora et al. (2004) investigated six materials for comparison of tensile strength, stiffness, shrinkage, and distortion after implantation in rabbit rectus fascia: two types of CFL (Tutoplast, Mentor Corp., Santa Barbara, CA; LifeNet, Virginia Beach, VA), porcine SIS (Stratasis, Cook Urological Inc., Spencer, IN), deepithelialized dermis (Derm Matrix, Carbon Medical Technologies, Saint Paul, MN), polypropylene mesh (SPARC, American Medical Systems, Minnetonka, MN), and ARF. The authors showed that human cadaveric fascia and porcine allografts showed a marked decrease (60%–89%) in tensile strength and stiffness from baseline. Polypropylene mesh and autologous fascia did not differ in tensile strength from baseline. Comparison of TVT and CFL in an in vivo rat model showed that TVT mesh has a greater break load and maximum average load than CFL (Spiess et al., 2004). In conclusion, porcine SIS and FD-CFL have the lowest tensile strength before implantation when compared with other biologic tissues and synthetic mesh. Patch slings are more susceptible to suture pull-through than full-length slings. Autologous fascia and polypropylene mesh are the only graft materials in comparative animal studies that do not
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weaken after implantation. None of these findings, however, can be extrapolated to clinical outcome data in humans.
UROGYNECOLOGIC PROCEDURES INVOLVING THE USE OF SYNTHETIC MESH AND/OR BIOLOGIC TISSUE Most synthetic materials have been used in sacral colpopexy and suburethral sling procedures, and the best evidence for their use is in these procedures. Implantation of biologic tissues has also been reported with these procedures, however, to a much lesser degree. Synthetic meshes and biologic tissues have been incorporated by abdominal, vaginal, and laparoscopic surgery, or a combination of routes in reconstructive surgery. Both synthetic and biologic materials have been used in repair of anterior and posterior vaginal wall defects. The question remains whether something stronger than the native tissue is desired or whether damaged structures need to be “bridged” with regenerated tissue. In general, grafts are indicated when the host tissue is insufficient for proper repair and in certain situations in which the patient is at high risk for surgical failure. Indications for graft augmentation in anterior or posterior vaginal prolapse may include recurrence, connective tissue disorder, chronic straining or increases in abdominal pressure, concomitant perineal descent, denervation of the pelvic floor, chronic constipation, or surgeon preference. According to the Third International Consultation for Incontinence Committee for Pelvic Organ Prolapse review, insufficient data preclude any definitive conclusions with regard to the role of prosthetic materials in primary or recurrent prolapse surgery. Because of the paucity of baseline data regarding the efficacy of traditional anterior and posterior vaginal repairs, the efficacy of adding prosthetic materials is difficult to assess. Although there is a suggested theoretical advantage with graft augmentation, this must be balanced against potential morbidity and cost. Additional procedures in which graft implantation has been described are shown in Box 23-3. The use of a CFL bridge to the sacrospinous ligament for vaginal vault prolapse in a patient with a neovagina and pelvic kidneys has been reported (Muir and Walters, 2004). The use of biologic tissue in fistula repair, repair of vaginal evisceration following colpocleisis, and vaginoplastic procedures for dyspareunia and apareunia has also been reported. The use of biologic tissue has also been reported in urethral reconstruction procedures, augmentation cystoplasty, repair of bladder exstrophy, ureteral overlay, and ureteral segment interposition. Further discussion of these procedures is beyond the scope of this chapter.
CLINICAL RESULTS AND COMPLICATIONS ASSOCIATED WITH SYNTHETIC MESH A recent review of 98 articles regarding sacral colpopexy by Nygaard et al. from the Pelvic Floor Disorders Network (2004) showed success rates for apical support and support
of all segments to range from 78% to 100% and 58% to BOX 23-3
OTHER UROGYNECOLOGIC SURGICAL PROCEDURES USING GRAFTS
Creation of a neovagina, with or without vaginal suspension Fistula repair Repair of vaginal evisceration Vaginoplastic procedures for sexual dysfunction Urethral reconstruction Augmentation cystoplasty Repair of bladder exstrophy Ureteral overlay Ureteral segment interposition
100%, respectively. The mean rate of mesh erosion was 3.4%. Culligan et al. (2005) recently published a clinical trial comparing CFL and polypropylene mesh for sacral colpopexy. At 1 year, 89 of 100 patients followed up, and objective cure was superior in the synthetic mesh group compared with the CFL group: 91% versus 68% (P = .007). Iglesia et al. (1997) published a review of synthetic mesh and summarized cure and complication rates of various materials. Sacral colpopexy resulted in 68% to 100% cure, and sling procedures varied from 61% to 100% cure. For slings, complications included urethral erosion of 3% to 6% and sling removal rate of 1% to 35%. For sacral colpopexy, rates of mesh erosion vary by technique of mesh placement. Visco et al. (2001) retrospectively analyzed Mersilene mesh erosion rates in 273 women who underwent sacral colpopexy or sacral colpoperineopexy. Overall risk of erosion was 3.2% for abdominal sacral colpopexy and 4.5% for sacral colpoperineopexy (introducing abdominally the graft and sutures). Erosion increased to 16% if sutures were placed vaginally and attached to an abdominally introduced mesh during sacral colpoperineopexy. If mesh were introduced vaginally, erosion rate peaked at 40%. The median times to mesh erosion were 15.6 months, 12.4 months, 9.0 months, and 4.1 months, respectively. Refer to Chapter 21 for a comprehensive review of clinical results and complications after synthetic mesh implantation in abdominal sacral colpopexy. The new generation of suburethral sling procedures placed under no tension at the midurethra has been associated with much lower rates of urethral erosion in comparison to traditional slings using other synthetic materials. Mesh materials for the TVT, SPARC, Monarc, and similar procedures, either retropubic or transobturator, are macroporous and associated with little inflammation. The mechanism(s) contributing to decreased erosion associated with the midurethral slings is (are) unknown. However, they include type of mesh material, plastic sleeves used for mesh introduction, smaller incisions, minimal dissection, shorter procedure times, and low sling tension. Refer to Chapter 16 for a comprehensive review of clinical results and complications after synthetic mesh implantation in suburethral and midurethral sling procedures. The use of synthetic nonabsorbable mesh in anterior vaginal repairs has been associated with high cure rates and high rates of erosion. In the study by Julian (1996), three patients suffered mesh-related complications of an erosion
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that failed primary closure, persistent granulation tissue with spotting, and painful intercourse for the partner secondary to fiber perforation that resolved with trimming the mesh. Augmentation with absorbable mesh (Vicryl) has shown no difference in one randomized clinical trial (Weber et al., 1999) and lower rates of recurrent cystocele in another randomized trial (Sand et al., 2001). A few case series are known regarding synthetic mesh interposition in rectocele repair with short-term follow-up. Despite paucity of data, there is an increase in adoption of tension-free vaginal mesh procedures involving procedural kits that include disposable insertion needles, retrieval devices, and polypropylene mesh. Those available at the present time include Anterior, Posterior, and Total Prolift (Gynecare, Somerville, NJ), and Apogee and Perigee (American Medical Systems, Minnetonka, MN). Porcine dermis grafts with polypropylene arms are also available with Apogee and Perigee. Analysis of the first 100 tensionfree vaginal mesh procedures revealed a 17.5% erosion rate, which fell to 2.7%, with the avoidance of T-shaped colpotomies, concomitant hysterectomy, and perineal incisions (Berrocal et al., 2004).
CLINICAL RESULTS AND COMPLICATIONS ASSOCIATED WITH BIOLOGIC TISSUE To date, most investigations that involve biologic tissues are animal studies or short-term retrospective analyses. Many investigations are industry-sponsored, thus at risk for research bias. One prospective trial is known, comparing patients who underwent anterior repair, with and without allograft patch augmentation. No prospective studies have directly compared various types of biologic tissue in humans. There have been no studies comparing cost of procedures involving tissue implantation with traditional surgical procedures. The most obvious advantages of biologic tissue implantation are avoidance of donor site morbidity and reduction in operative time. Walter et al. (2003) showed increased operative time and postoperative pain with AFL. Fifty percent of patients reported continued donor site pain at 25 months, with 13% of patients reporting dissatisfaction with the procedure. Surgical outcome with AFL is similar to ARF. Wright et al. (1998) reported higher morbidity associated with an increase in operative time and hospital stay with ARF compared to cadaveric tissue. Some investigators have shown an increased risk of ventral hernia after procurement of ARF. Suburethral sling procedures using ARF have been associated with a long-term cure rate of 87% (Chaikin et al., 1998; Smith et al., 2005). In a survey of the International Urogynecological Association (IUGA) in 2002, 12% of members reported the use of CFL for suburethral sling material. CFL has been shown to be equally effective in short-term surgical outcome to ARF and AFL (Elliot and Boone, 2000; Handa et al., 1996; Walsh et al., 2002; Wright et al., 1998). One institution reported a 38% failure rate at 11 months after bone-anchor pubovaginal sling in 154 patients and thus abandoned the use of CFL in all sling procedures (Carbone et al., 2001). Intermediate and long-term surgical outcome in
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most investigations show greater cure rates with autologous tissue when compared with allografts (Almeida et al., 2004; Kassardijian, 2004; O’Reilly and Govier, 2002; Soergel et al., 2001). Simsiman et al. (2005) compared CFL (80), porcine dermis (83), and autologous (78) slings. The authors found that CFL and porcine dermis slings had much higher failure rates than autologous fascia slings at a minimum mean follow-up of 17 months, 52% and 51% versus 29%, respectively. McBride et al. (2005) recently published a retrospective cohort of 71 full-length AFL sling procedures and 39 fulllength SD-CFL sling procedures with minimum follow-up of 2 years. Urodynamic stress incontinence was demonstrated in 41.7% of SD-CFL patients compared with 0% of autograft patients (P = .007), despite no difference in subjective quality of life measures, subjective continence rates, maximum urethral closure pressures, and bladder neck mobility. However, one institution showed enduring beneficial effects on lower urinary tract symptoms and quality of life at 48 months in 102 women who underwent CFL sling procedures (Richter et al., 2003). Variability in tissue processing or host factors may account for some failures with CFL slings. Some authors have reported an 85% to 95% short-term cure rate with CDA suburethral slings. The disadvantages of CFL and CDA include availability, possible risk of infection, and possible reduced durability. FD-CFL use in sacral colpopexy has been associated with high rates of failure in one series (Fitzgerald et al., 1999), although a recent investigation showed 95% cure at the vaginal apex in 19 patients at 1 year (Flynn et al., 2005). Fitzgerald et al. (1999) reported a high reoperation rate (13 of 102) after sacral colpopexy (67) and suburethral sling (35) procedures in which FD-irradiated CFL was implanted. Histologic specimens showed graft autolysis and rejection. The authors concluded that risk of failure outweighs the benefits of decreased erosion risk associated with biologic materials for this procedure. The authors expressed their concerns regarding freeze-drying or gamma-irradiation processing of allografts as factors increasing the risk of autolysis. Blander and Zimmern (2000) found that the histology of failed CFL sling procedures demonstrated collagen with almost complete acellularity, with no evidence of capillary or fibroblast ingrowth. Kammerer-Doak et al. (2002) reported vaginal erosion of CFL in 23% and 27% of patients following 11 abdominal sacrocolpopexies and 22 suburethral sling procedures, respectively. Fifty percent of patients required surgical intervention under local anesthesia. The authors noted an association with perioperative febrile morbidity. The use of cadaveric dermis in pubovaginal sling procedures proved to be disappointing with intermediate follow-up (Owens and Winters, 2004). Gandhi et al. (2005) did not show significantly improved outcomes after 2 cm × 4 cm SD-CFL augmentation of anterior in a randomized clinical trial of 154 patients, 76 with and 78 without an allograft patch, with median follow-up of 13 months. Recurrence of anterior vaginal wall prolapse was seen in 21% of the patch group and 29% of the control group. Logistic regression showed that the fascial patch did not reduce recurrent anterior prolapse (OR 0.70); however, the presence of a transvaginal Cooper’s ligament sling did reduce recurrent anterior prolapse (OR 0.105; P <.001). In a multicenter follow-up of cadaveric prolapse repair with sling (CaPS), using
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SD-CFL in 132 patients, Kobashi et al. (2002) reported a 10% apical failure rate and 18% recurrence of stress incontinence at a mean of 12.4 months. Satisfaction or overall improvement was reported by 71% of patients. Groutz et al. (2001) used SD-CFL (Tutoplast) for cystocele repair, with and without pubovaginal sling in 21 patients and reported 100% cure for the anterior wall at 20 months, with 9% of patients developing a mild recto-enterocele at 4 to 6 months. Preliminary data have shown that cadaveric dermal allograft (CDA) (AlloDerm) graft interposition in cystocele repair is associated with an 84% cure rate in 19 patients at 28 months (Chung et al., 2002). Vaginal paravaginal defect repair with CDA (AlloDerm) resulted in a 41% failure rate at 18 months in 33 patients (Clemons et al., 2003). Kohli and Miklos (2003) reported a 93% cure rate at 13 months in 30 patients who underwent site-specific defect posterior repair augmented with CDA (AlloDerm). Altman et al. (2005) recently published a prospective cohort of 32 patients who underwent rectocele repair with porcine dermis. At 12 months follow-up 24% had rectoceles (greater than stage II) by clinical examination, and 52% had rectocele during defecography. The authors concluded that augmentation with collagen mesh improved anatomic support, but that there was substantial risk of recurrence with unsatisfactory anatomic and functional outcome 1 year after surgery. They recommended further evaluation before adoption of rectocele repair augmentation into clinical practice. Complications of wound healing have been reported with porcine dermis. Moore et al. (2003) reported a graftrelated complication rate of 20% in posterior repair interposition. Cole et al. (2003) reported a case of encapsulation of a porcine dermal suburethral sling, which showed no histologic evidence of tissue ingrowth. A recent publication by Gandhi et al. (2005) summarized histopathology of extirpated HMDI cross-linked porcine dermis grafts (Pelvicol) from patients who experienced urinary retention after transvaginal Cooper’s ligament suburethral sling procedures or tissue specimens from those who failed the procedure. Tissue reaction to the xenograft varied, including (1) limited remodeling, (2) foreign body type reaction, and (3) complete replacement of graft by fibroconnective tissue and moderate neovascularization in cases of recurrent stress incontinence. The authors concluded that variability in tissue reaction after implantation may result in unpredictable clinical outcomes in different patients, raising questions about the overall tolerability and efficacy of HMDI porcine dermis grafts in pelvic reconstructive surgery. Processed SIS has been used in bone-anchor pubovaginal sling series with cure rates up to 93% (Rutner et al., 2003). No published randomized trials are known involving vaginal repair augmentation with SIS. We are currently completing a trial comparing traditional posterior colporrhaphy and defect-specific repairs of posterior vaginal wall prolapse, with and without graft augmentation.
CONCLUSION Few prospective studies are known that compare graft augmentation techniques with traditional repairs for anterior
and/or posterior vaginal wall prolapse. Given the relatively low cure rates associated with traditional repairs for defects in these vaginal segments, innovation could result in much needed improvement. The greatest potential for macroporous synthetic grafts and biologic tissue may be seen in augmentation of deficient or weak endopelvic fascia and vaginal muscularis. When bridging a space to support an organ, as in the sacral colpopexy procedure, the evidence supports a loosely placed polypropylene mesh with few indications, if any, for biologic tissue. For traditional suburethral sling procedures, autologous fascia placed loosely is associated with high long-term cure rates and low rates of erosion. The macroporous midurethral tension-free slings may make fascial slings obsolete. No synthetic or biologic graft material is perfect. Randomized trials are urgently needed. New procedures should be evaluated prospectively, ideally with controlled trials. Random introduction of new materials may be unethical and potentially crippling. Synthetic and biologic mesh usage in urogynecology and reconstructive pelvic surgery will continue to increase, despite high costs of graft material and lack of evidence. Cure rates associated with synthetic mesh implantation must be equal to or better than cure associated with use of autologous tissue. The benefits of decreasing donor site morbidity must balance the risks of complications associated with synthetic mesh. With the increasing use of prolapse “kits” that involve tension-free implantation of larger pieces of macroporous polypropylene mesh by vaginal route, improved cure rates and shorter operative times must outweigh the risks of infection, erosion, and de novo dyspareunia associated with synthetic implants. Biologic tissue implantation must also result in equal or better cure rates when compared to conventional procedures. The decrease in operative time should justify the cost of the biomaterial. The data are sparse and surgical series vary with respect to type and size of graft used, location of implantation in the vaginal wall, location of lateral attachments of the graft, and whether the graft is secured with suture or is tension-free. Materials of the future will be impregnated with antibiotics and/or growth factors. Tissue or mesh impregnated with growth factors will result in active control of tissue regeneration. Gene therapy will likely play a role in future management of pelvic organ prolapse. We are a long way from the ideal biomaterial. Rigorous investigation of surgical implants in urogynecology and reconstructive pelvic surgery is warranted so that repair is safe, effective, and durable.
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Kobashi KC, Leach GE, Chon J, Govier FE. Continued multicenter follow-up of the cadaveric prolapse repair with sling. J Urol 2002;168:2063. Kohli N, Miklos JR. Dermal graft-augmented rectocele repair. Int Urogynecol J Pelvic Floor Dysfunct 2003;14:146. Lamb JP, Vitale T, Kaminski DL. Comparative evaluation of synthetic meshes used for abdominal wall replacement. Surgery 1983;93:643. Levasseur JC, Lehn E, Tignier P. Etude experimentale et utilization clinique d’un nouveau materiel dans les eviscerations graves post-operatoires. Chirurgie 1979;105:577. Liapis A, Bakas P, Creatsas G. Burch colposuspension and tension-free vaginal tape in the management of stress urinary incontinence in women. Eur Urol 2002;41:469. 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. Mantovani F, Trinchieri A, Castelnuovo C, et al. Reconstructive urethroplasty using porcine acellular matrix. Eur Urol 2003;44:600. Mavrilas D, Sinouris EA, Bynios DH, Papgeorgakopoulou N. Dynamic mechanical characteristics of intact and structurally modified bovine pericardial tissues: J Biomech 2005;38:761. McBride AW, Ellerkmann RM, Bent AE, Melick CF. Comparison of longterm outcomes of autologous fascia lata slings with Suspend Tutoplast fascia lata allograft slings for stress incontinence. Am J Obstet Gynecol 2005;192:1677. Migliare R, Usai E. Treatment results using a mixed fiber mesh in patients with grade IV cystocele. J Urol 1999;161:1255. McPherson JM, Sawamura S, Armstrong R. An examination of the biologic response to injectable glutaraldehyde cross-linked collagen implants. J Biomed Res 1986;20:93. Miklos JR, Kohli N. Rectovaginal fistula repair utilizing a cadaveric dermal allograft. Int Urogynecol J 1999;10:405. Miklos JR, Kohli N, Moore R. Levatorplasty release and reconstruction of rectovaginal septum using allogenic dermal graft. Int Urogynecol J 2002;13:44. Moore RD, Miklos JR. Repair of a vaginal evisceration following colpocleisis utilizing an allogenic dermal graft. Int Urogynecol J 2001;12:215. Moore RD, Miklos JR, Kohli N. Posterior repair with Pelvicol dermal graft augmentation. Int Urogynecol J 2003;14:S2. Moore RD, Miklos JR, Kohli N. Rectovaginal fistula repair using a porcine dermal graft. Obstet Gynecol 2004;104:1165. Morgan JE, Farrow GA, Stewart FE. The Marlex sling operation for the treatment of recurrent stress urinary incontinence: a 16 year review. Am J Obstet Gynecol 1985;106:369. Muir TW, Walters MD. Surgical management of vaginal vault prolapse in a woman with neovagina and pelvic kidneys. Obstet Gynecol 2004;104:1199. Mutter D, Jamali FR, Moody DL, et al. The concept of protected mesh to minimize adhesion formation in intraperitoneal abdominal wall reinforcement: preclinical evaluation of a new composite mesh. Hernia 2000;4(Suppl):S3–S9. Neel HB III. Implants of Gore-Tex. Arch Otolaryngol 1983;109:427. Nilson CG, Falconer C, Rezapour M. Seven-year follow-up of the tensionfree vaginal tape procedure for treatment of urinary incontinence. Obstet Gynecol 2004;104:1259. Norton P, Boyd C, Deak S. Collagen synthesis in women with genital prolapse or stress urinary incontinence. Neurourol Urodyn 1992;11:300. Nygaard I, McCrary R, Brubaker L, et al. Abdominal sacrocolpopexy: a comprehensive review. Obstet Gynecol 2004;104:805. O’Connor RC, Hollowell CM, Steinberg GD. Distal ureteral replacement with tubularized porcine small intestine submucosa. Urology 2002;60:697. Oliver RF. Scar and collagen implantation. Burns 1987;13:S49. Olsen AL, Smith VJ, Bergstrom JO, et al. Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 1997;89:501. O’Reilly KJ, Govier FE. Intermediate term failure of pubovaginal slings using cadaveric fascia lata: a case series. J Urol 2002;167:1356.
Owens DC, Winters JC. Pubovaginal sling using Duraderm graft: intermediate follow-up and patient satisfaction. Neurourol Urodyn 2004;23:115. Petros P, Ulmsten U. An integral theory and its method for the diagnosis and management of female urinary incontinence. Scand J Urol Nephrol 1993;153:1. Petros P, Ulmsten U. Urethral pressure increase on effort originates from within the urethra, and continence from musculovaginal closure. Neurourol Urodyn 1995;14:337. Pourdeyhimi B. Porosity of surgical mesh fabrics: new technology. J Biomed Mater Res 1989;23:145. Richter HE, Burgio KL, Holley R, et al. Cadaveric fascia lata sling for stress urinary incontinence: a prospective quality-of-life analysis. Am J Obstet Gynecol 2003;189:1590. Rutner AB, Levine SR, Schmaelzle JF. Processed porcine small intestine submucosa as a graft material for pubovaginal sling: durability and results. Urology 2003;62:805. Safir MH, Gousse AE, Rovner ES, et al. 4-Defect repair of grade 4 cystocele. J Urol 1999;161:587. 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. Scales JT. Materials for hernia repair. Proc R Soc Med 1953;46:647. Simsiman AJ, Powell CR, Stratford R, Menefee SA. Suburethral sling materials: best outcome with autologous tissue. Am J Obstet Gynecol 2005;193(6):2112–2116. Smith AR, Daneshgari F, Dmochowski R, et al. Surgery for urinary incontinence in women. In Abrams, Cardozo, Koury, eds. The 3rd International Consultation on Incontinence. Health Publications, Paris, 2005. Soergel TM, Shott S, Heit M. Poor surgical outcomes after fascia lata allograft slings. Int Urogynecol J 2001;12:247. Spiess PE, Rabah D, Herrera C, et al. The tensile properties of tension-free vaginal tape and cadaveric fascia lata in an in vivo rat model. BJU Int 2004;93:171. Uitto J, Perejda A. Connective Tissue Disease: Molecular Pathology of the Extracellular Matrix. Marcel Dekker, New York, 1986. Visco AG, Weidner A, Barber MD, et al. Vaginal mesh erosion after abdominal sacral colpopexy. Am J Obstet Gynecol 2001;194:297. Voyles CR, Richardson JD, Bland SM, et al. Emergency abdominal wall reconstruction with polypropylene mesh: short-term benefits versus long-term complications. Ann Surg 1981;194:219. 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. Walter AJ, Morse AN, Leslie KO, et al. Changes in tensile strength of cadaveric fascia lata in a rabbit vagina model. J Urol 2003;169:1907. Ward K, Hilton P. Prospective multicenter randomized trial of tension-free vaginal tape and colposuspension as a primary treatment for stress incontinence. Am J Obstet Gynecol 2004;190:324. 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;183:257. Weber AM, Walters MD, Piedmonte MR, Ballard LA. Anterior colporrhaphy: a randomized trial of three surgical techniques. Am J Obstet Gynecol 2001;185:1299. Williams DF. The response of the body environment to implants. In Williams DF, Roaf R, eds. Implants in Surgery. WB Saunders Co. Ltd., London, 1973, pp. 203–297. Wright EJ, Iselin CE, Carr LK, Webster GD. Pubovaginal sling using cadaveric allograft fascia for the treatment of intrinsic sphincter deficiency. J Urol 1998;160:759. Zheng MH, Chen J, Kirilak Y, et al. Porcine small intestine submucosa (SIS) is not an acellular collagenous matrix and contains porcine DNA: possible implications in human implantation. J Biomed Mater Res 2005;73:61.
Fecal Incontinence Tracy L. Hull and Massarat Zutshi
EPIDEMIOLOGY 309 ETIOLOGY 309 EVALUATION 310 History 310 Physical Examination 310 Scoring Scales for Fecal Incontinence 311 Diagnostic Testing 311 NONSURGICAL TREATMENT 312 Medical Treatments 312 Biofeedback and Pelvic Muscle Exercises 312 Bowel Management 314 SECCA PROCEDURE 314 SURGICAL TREATMENT 315 Sphincteroplasty 315 Postanal Pelvic Floor Repair 317 Muscle Transposition Procedures 317 Artificial Anal Sphincter 318 Sacral Neuromodulation 318 Colostomy or Ileostomy 318 CONCLUSION 318
EPIDEMIOLOGY The inability to control feces is a devastating problem. Many people find this problem socially incapacitating and stay home, thus minimizing social contact to avoid an embarrassing situation. To estimate the number of people afflicted with fecal incontinence is difficult because many do not mention the problem to their caregivers. In a study by Johanson and Lafferty (1996), only about a third of patients discussed their incontinence with their physicians. Others incorrectly describe their symptoms and may refer to their incontinence as “diarrhea,” making it difficult for the physician to understand the problem without careful questioning. Thus, estimates probably grossly underreport the prevalence, which ranges from 0.1% to 18%. Studies in the United States found an overall prevalence of 18.4%, with a higher prevalence of 26% in patients who visited a gastroenterologist. Definitions
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of fecal incontinence also vary from report to report, making comparisons difficult. Caring for incontinent patients is a tremendous financial responsibility. Over $400 million is spent annually on adult diapers, and fecal and urinary incontinence are primary reasons for nursing home placement (outnumbering senile dementia). Fecal incontinence probably increases progressively with age, although it can affect all ages, even children. It affects men as well as women, and some studies find men affected more commonly than women.
ETIOLOGY Defecation is a complex process that involves an intricate interaction between anal function and sensation, rectal compliance, stool consistency, stool volume, colonic transit, and mental alertness. An alteration in any of these can lead to incontinence. Box 24-1 lists some common causes of fecal incontinence. A large component of continence is the function of the anal sphincter complex. It consists of the internal anal sphincter (IAS) muscle, the external anal sphincter (EAS) muscle, and the puborectalis (PR). The smooth muscle of the IAS is innervated by the autonomic nervous system. The IAS is responsible for more than half of the resting tone. The striated muscle of the EAS is innervated by the inferior branch of the pudendal nerve and is responsible for about a third of the resting tone. Defecation is a result of voluntary relaxation of the EAS and PR that are innervated by the S3 to S4 nerves in response to rectal distension that is dictated by receptors in the pelvic floor and the anal transition zone. Anatomical disruption of the sphincter complex or disruption due to neurologic reasons is a common cause of fecal incontinence. Childbirth is increasingly being recognized as commonly injuring the mother’s sphincter complex. In a study by Sultan et al. (1993), women were evaluated before and after childbirth, with interviews, anal physiology testing, and anal endosonography. They found that 35% of primiparous women and 44% of multiparous women
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BOX 24-1
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CAUSES OF FECAL INCONTINENCE
Anal Injury Obstetric (vaginal delivery/trauma) Surgical (fistulotomy, hemorrhoidectomy, sphincterotomy, stretch) Irradiation Trauma Congenital (e.g., imperforate anus)
Intestinal Colitis or proctitis Colon, rectum, or small bowel resection Tumors Fecal impaction Decreased rectal compliance Rectal prolapse
Neurologic Central nervous system Dementia Neoplasm Stroke Trauma Multiple sclerosis Peripheral (e.g., diabetes)
Other Diarrhea Combinations of anal and rectal causes Myopathy (e.g., scleroderma) Functional
had sphincter defects after delivery. The IAS was injured more often than the external sphincter—sometimes when no breach occurred in the perineal skin. A strong correlation was found between sphincter defects and the development of bowel symptoms, although only about a third of women with sphincter defects developed bowel symptoms. Incontinence may not appear until decades after the obstetric injury, so it remains to be seen how many of these women develop incontinence later in life. In the past, these patients, particularly women with delayed symptoms years after childbirth injury, were labeled with idiopathic incontinence. However, with the advent of more sophisticated evaluation techniques, defects in the sphincter complex have been found. Fecal incontinence also appears to be associated with urinary incontinence and pelvic organ prolapse. In one study by Jackson et al. (1997), a third of women presenting to a urogynecologist for urinary incontinence also had fecal incontinence, and 7% of women with isolated pelvic organ prolapse had fecal incontinence. In another study by Tetzscher et al. (1996), 18% of women who had a previous obstetric anal sphincter disruption had both urinary and fecal incontinence. Besides obstetric injury, other causes thought to possibly contribute to both conditions include chronic constipation with straining at stool, aging, and relaxation of pelvic support.
EVALUATION History Evaluation of a patient with fecal incontinence starts with a comprehensive history. Important questions to ask include duration of the problem, frequency of incontinence, time of day of incontinence, quality of stool lost, ability to control flatus, use of pads, frequency of bowel motions, problems with constipation or diarrhea, and effects of incontinence on daily life. To differentiate incontinence from urgency is important. Urgency may reflect inability of the rectal reservoir to store stool (as with diarrhea or proctitis) rather than a true sphincter problem. Equally important is to differentiate diarrhea from incontinence because many patients incorrectly interchange the two problems. The quality of stool lost gives clues to the severity of the incontinence. Flatus is more difficult to control than liquid stool, and solid stool is the most easily controlled. Patients with incontinence of solid bowel motions without knowledge of the loss of stool are usually more distressed and reclusive than those with incontinence of flatus only. Additionally, the physician should obtain a thorough obstetric history: number of vaginal deliveries, duration of second stage of labor, previous episiotomy, use of forceps, perineal tears or infections, weight of babies, and unusual presentations at birth. A sexual history, including the effect of incontinence on sexual behavior, should be obtained. Other medical and surgical conditions must be ascertained, including back injuries, previous anorectal or abdominal surgeries, irradiation history, diabetes, multiple sclerosis, and scleroderma. Medications, food intolerance, and activity restrictions may add information.
Physical Examination The physical examination starts with inspection of the anal area, looking for soilage of stool on the skin, and evidence of skin irritation. Sometimes the underwear also gives evidence of stool soilage. The anus is inspected, looking for gaping of the muscles and any scarring. The patient is asked to squeeze and to simulate holding in a bowel movement to look for uniform circular contraction of muscle. Next, asking the patient to strain may show exaggerated perineal descent or prolapse of hemorrhoids or even the rectum. The anocutaneous reflex can be checked by rubbing the perianal skin gently (a Q-tip works well) and looking for the reflex contraction of the anal sphincter mechanism. Sensation to pinprick can also be checked. Both of these give a crude assessment of sphincter innervation. Palpation of the sphincter is next done with digital examination. The initial tone reflects the internal sphincter and should be noted. Then the patient is asked to squeeze on the index finger in the anus as if she were holding in a bowel movement. Strength, defects in the circle of muscle, and early fatigability are assessed. Scars or masses are appreciated. A digital rectal examination checks for masses, occult or gross blood, fistula, and the presence of a rectocele. The physical examination is usually completed with a sigmoidoscopy or proctoscopy; this rules out proctitis or neoplasm as a source of the problem.
Chapter 24
Scoring Scales for Fecal Incontinence Qualifying fecal incontinence has been difficult because many scoring systems have been introduced. A validated questionnaire for measuring quality of life, the Fecal Incontinence Quality of Life (FIQL), was reported in 2000 by Rockwood et al. and has 29 items that relate to four scales: lifestyle, coping/ behavior, depression/self-perception, and embarrassment. In the same year, Reilly et al. (2000) developed a questionnaire to assess epidemiology of fecal incontinence and associated risk factors. This assessed general bowel habits, assessed presence and severity of fecal incontinence, measured symptoms related to pelvic floor dysfunction, and assessed risk factors for fecal incontinence. The FIQL is currently used routinely to assess quality of life during patient’s follow-up after any mode of treatment. The American Society of Colon and Rectum Fecal Incontinence Severity Index (FISI) is a severity rating score and consists of questions that rate continence to gas, mucus, solid, and liquid stool. The FISI is commonly used in conjunction with the FIQL as a tool to measure the efficacy of treatment. The other popular tool is the Wexner score that uses lifestyle alterations and wearing of a pad, in addition to incontinence to solids, liquid, and gas. In this score, zero is a score for perfect continence and 20 for complete incontinence. See Chapter 39 for further discussion of these outcome questionnaires.
Diagnostic Testing The use of additional testing depends on the severity of the problem and the amount of distress it causes the patient. Further tests may be helpful in establishing the diagnosis and in planning the most appropriate treatment. These tests are discussed individually. ENEMA To determine whether the patient is truly having incontinence, an enema may help clarify the problem. About 100 mL of tap water is given, and it is noted whether the patient can hold this for more than a few minutes. Because liquid is more difficult to control than solid stool, patients who can hold a tap water enema probably do not have significant incontinence. They may need to be questioned more carefully to fully understand their symptoms. ANORECTAL PHYSIOLOGY TESTING Many methods are available to assess anorectal physiology. Manometry, electromyography (EMG), rectal compliance, and pudendal nerve studies may all be helpful. Manometry provides quantitative information regarding the resting and squeeze pressures of the sphincter muscles. The resting pressures reflect the constant tone of the internal sphincter muscles. The squeeze pressures reflect the pressure generated by the external sphincter muscle. The length of the anal canal can be determined by the measured distance of these pressures. A shortened anal canal length may reflect injury to the muscle. Positive rectoanal inhibitory reflex rules out Hirschsprung’s disease (see Chapter 25). Rectal compliance can be determined by inserting a balloon and determining the minimal volume that the rectum
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can sense, then sequentially inflating the balloon to a volume that cannot be tolerated. Decreased compliance signals a rectal reservoir that does not appropriately store stool and may push the fecal bolus past sphincter muscles, even if the sphincter muscle pressures are adequate. Note that normal manometric findings do not exclude incontinence, and normal people without symptoms of fecal incontinence may have abnormal manometry. EMG is used to study the innervation of the external sphincter complex and to examine for reinnervation seen in pelvic neuropathy. Traditionally, needle EMG has been used with concentric or single-fiber electrodes, although this is quite painful for the patient. An increase in fiber density implies compensatory reinnervation after denervation of the external sphincter. Surface electrodes (attached to the skin overlying the subcutaneous portion of the external anal sphincter) give a less precise EMG but still provide some information. Pudendal nerve terminal motor latency can be determined using an electrode attached to a glove inserted into the anal canal. A prolonged conduction in the pudendal nerve may signal damage to the innervation of the external sphincter and puborectalis muscle. DEFECOGRAPHY Defecography is indicated if rectal prolapse or internal intussusception (occult prolapse) is suspected. See Chapter 27 for a more thorough discussion. COLONOSCOPY AND BARIUM ENEMA Proctoscopy, sigmoidoscopy, colonoscopy, and barium enema are appropriate in some patients, particularly if diarrhea and blood are associated or contributing symptoms. Colitis and neoplasms can be ruled out with these tests. ENDORECTAL ULTRASONOGRAPHY (ERUS) Endosonography is recognized as a valuable tool in the assessment of fecal incontinence. A probe is inserted into the rectum and withdrawn through the anal canal allows for a 360degree visualization of the internal and external anal sphincters. Particularly in patients with surgical or obstetric injury who did not develop incontinence until many years (even decades) after the insult, endosonography allows visualization of defects in the sphincter muscle, which, in turn, can lead to surgical correction. In the past, many of these patients would have been diagnosed with idiopathic incontinence, and surgical repair may have not been considered (Fig. 241). Additionally, the pictures obtained from endosonography provide a “road map” for repair of the sphincter. For instance, in some patients who become incontinent after a sphincterotomy for a fissure, it gives visualization of the ends of the internal sphincter muscle and the amount of gap between those ends. This allows planning of the surgical incision. Similarly, in patients with a past obstetric injury, the gap in the internal and external sphincter muscles can be noted and allows planning of the surgical procedure. A recent study by Oberwalder et al. (2004) measured perineal body thickness ultrasonographically and concluded that a perineal body thickness less than 10 mm is abnormal;
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NONSURGICAL TREATMENT Treatment begins with correction of underlying medical and surgical problems. Preliminary surgical treatments may include cancer resection, treatment of inflammatory bowel disease, repair of rectal prolapse, and removal of impactions.
Medical Treatments
Figure 24-1 ■ Anal endosonography in a woman with “idiopathic incontinence” decades after the birth of her children. The internal anal sphincter is intact (straight arrows). The external anal sphincter has an anterior defect (curved arrows). MID AC, Midanal canal.
patients with perineal body thickness greater than 12 mm are unlikely to have a defect, whereas those between 10 and 12 mm are associated with a defect in the sphincters in about a third of the patients. The use of three-dimensional (3D) ultrasound is yet to prove its superiority, whereas magnetic resonance imaging (MRI) with endorectal coil has results that are similar to the two-dimensional (2D) ERUS. Although use of MRI is still controversial, it is less operator-dependent and is superior in defining EAS defects, whereas IAS defects are visualized more clearly with ERUS. CONCLUSION What tests are essential for treating patients with fecal incontinence? A suggested algorithm for the diagnosis and treatment of fecal incontinence is shown in Figure 24-2. Many excellent caregivers use few of these tests, although, recently, more testing is being used. To rule out colitis, proctitis, and neoplasia, evaluation of the colon and rectum by endoscopy or barium enema is needed. Defecography may or may not be needed for evaluation of rectal prolapse but may be necessary to diagnose internal intussusception (or occult prolapse). The enema test is easy and inexpensive and helps determine whether a patient has true fecal incontinence. Many clinicians do not have access to an anorectal physiology laboratory or endosonography machine. Additionally, it takes experienced personnel to perform and interpret the results of these tests. Even for some surgical procedures these tests are not mandatory but may be helpful for planning surgery and predicting success. For complicated surgical repairs or previously failed repairs, anal physiology testing and endosonography have significant value in planning an appropriate repair or determining why a previous repair failed. As caregivers become aware of this previously silent group of patients, more testing will be needed to study these patients in an effort to understand their problem. Then, as incontinence becomes analyzed more accurately, these tests and others yet to be discovered will allow more precise treatment planning.
In patients with minor incontinence, the use of bulking agents, such as Metamucil, Citrucel, or Konsyl, can change the consistency of the stool, making it firmer and more easily controlled. Starting with a teaspoon daily and working up to a tablespoon up to three times daily helps decrease side effects, such as abdominal distension and bloating. If one agent gives these side effects, sometimes switching to another agent produces fewer side effects. Restricting the amount of fluid taken with these products may enhance their ability to increase stool bulk, especially if diarrhea is a problem. Agents designed to slow down the intestinal tract may also help with stool control. Even in patients without diarrhea, these agents may slightly constipate patients, allowing them to better control their stool. Loperamide hydrochloride (Imodium) is often prescribed in this capacity. It prolongs intestinal transit time, allowing fecal volume to be reduced (secondary to the increased time allowed for removal of fluid from stool) and bulk density to be increased. It also increases rectal compliance, which decreases urgency. Side effects are rare, and physical dependence does not occur. The dosage must be individualized for each patient. If patients have particular trouble after meals, 2 to 4 mg may be given before a meal to decrease the chance of stooling. The maximum daily dosage is 16 mg. Some patients with diarrhea require the maximum dosage, but patients with mild incontinence who use it to mildly decrease the intestinal transit may need only two or three 2-mg doses daily, or as needed. Diphenoxylate hydrochloride (Lomotil) is another agent used in this capacity, especially if diarrhea is a primary contributor to the incontinence. Diphenoxylate hydrochloride is less expensive than Imodium but is a Schedule V substance (under the Controlled Substances Act). It has minimal potential for physical dependence. Side effects are rare but may include abdominal distension, drowsiness, dizziness, depression, restlessness, nausea, headache, blurred vision, and dry mouth. The dosing is similar to that of Imodium. One or two 2.5-mg tablets are used up to four times daily. As with Imodium, the dosing must be individualized. Other agents that focus on control of diarrhea include tincture of opium, paregoric, and codeine. Side effects and the risk of physical dependence make them less attractive. Amitriptyline has been used to improve symptoms in patients with idiopathic fecal incontinence. It acts by decreasing intrarectal pressures by reducing the amplitude and frequency of rectal motor complexes, possibly through an anticholinergic mechanism.
Biofeedback and Pelvic Muscle Exercises Successful treatment of fecal incontinence has been achieved with biofeedback and pelvic muscle exercises. Jensen and Lowry (1997) showed that functional outcomes after
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Fecal incontinence
History, physical examination, and evaluation of bowel
Normal
Abnormal
Medical therapy plus pelvic muscle exercise
Treat colitis, proctitis, neoplasm, other
Cured or satisfied with improvement
Not improved
Repeat anal examination With or without endoanal ultrasound With or without anorectal physiology evaluation*
Sphincter defect
No sphincter defect
Endoanal ultrasound (if not already done) Anorectal physiology evaluation* (if not already done) Biofeedback
Anal sphincteroplasty
Not improved
Cured or satisfied with improvement
Not improved
Endoanal ultrasound Anorectal physiology evaluation*
Sphincter defect
Cured or satisfied with improvement
Consider: Muscle transposition procedure Artificial anal sphincter Colostomy
No sphincter defect
Redo anal sphincteroplasty with or without stoma or biofeedback *Could include anal manometry, electromyography, rectal compliance studies, and pudendal nerve studies. Figure 24-2
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Algorithm for diagnosis and treatment of fecal incontinence.
sphincteroplasty improved in patients who initially did not experience optimal results from surgery and were then treated with biofeedback. Biofeedback is indicated for alert, motivated patients because it is labor-intensive and requires a dedicated therapist. Reported results are difficult to compare because three methods of biofeedback therapy are available, and most reports do not distinguish the type, duration, and exact method of performing the biofeedback. The three types are (1) external anal sphincter strengthening, (2) coordina-
tion of rectal distension and anal sphincter contraction, and (3) improving sensation of stool in the rectum. For all three, the initial setup is similar. A balloon is placed in the rectum to simulate stool. Anal sphincter contraction is measured with a different balloon in the anal canal, by an anal plug, or by perianal surface electrodes. When contraction of the sphincter muscles is initiated, the patient observes this on the monitor. Visual (and in some systems, auditory) feedback is given regarding contraction of the external sphincter. For sphincter strengthening, patients are encouraged when
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the proper sphincter response is made. They are encouraged to exercise the muscle by replicating this type of contraction outside the therapy session. The goal is to increase the strength of the striated muscle. Rectoanal coordination uses the same equipment. The goal is to train the patients to achieve maximum voluntary squeeze in less than 1 second after the balloon is inflated in the rectum by consciously contracting the sphincter muscles. This method is customized for each patient. Patients may need one or more sessions to be able to perform the maneuver at home in the correct way. Rectal sensory perception is used to teach the patients to sense smaller volumes of stool. The patients are urged to defecate with the balloon in the rectum. The patients observe this on the monitor. Gradually, the volume in the balloon is decreased, and patients learn to sense smaller volumes with less rectal distension. Improvement has been reported in 63% to 90% of patients after biofeedback. As stated earlier, most studies do not elaborate on exactly the type and how the biofeedback was taught. In one study, Rao et al. (1996) found that anal squeeze pressures improved, the duration of squeeze increased, and the capacity to retain liquid increased. These findings correlated with a decrease in the number of episodes of fecal incontinence. No known studies definitively show that pelvic muscle– strengthening exercises (Kegel exercises) alone benefit patients with fecal incontinence. However, they are safe and cost nothing. Therefore, they should be discussed with most patients afflicted with fecal incontinence. They may particularly benefit patients who have early fatigability of the sphincter muscle on digital examination when asked to squeeze. Sometimes biofeedback is used to assist patients in performing these exercises by giving visual feedback when the correct muscles are contracted. When using biofeedback, we attempt to have patients hold the contraction for a full 10 seconds while watching a screen that tells them when the contraction decreases. Consultation with an interested physical therapist may optimize results. The scientific evidence supporting the use of biofeedback and/or sphincter exercises for the treatment of fecal incontinence in adults was reported in a Cochrane Review in 2002. Only five eligible studies, with relatively poor methodologic quality, were reviewed. Suggestions made were that rectal volume discrimination training improves continence more than sham training and that anal biofeedback combined with exercises and electrical stimulation provide more short-term benefits than vaginal biofeedback and exercises for women with obstetric-related fecal incontinence (Norton et al., 2002). One recent study questioning biofeedback was reported by Norton (2004). She assigned 171 patients to two groups: those with an intact sphincter and those with a disrupted sphincter. Subjects were further randomized to four treatment groups: the first received standard care; the second received standard care, verbal instruction, and a leaflet explaining pelvic exercises; the third received standard care and computer-assisted biofeedback at each session; and the fourth received standard care plus a home EMG biofeedback device. The results showed that overall, 75% patients recorded improvement, with equal numbers (54% vs 53%)
in the biofeedback and nonbiofeedback groups. The study concluded that no significant differences were present between the treatment groups and leads one to wonder whether standard diet, bowel management counseling, and verbal instructions may be sufficient.
Bowel Management Some patients find that daily enemas with approximately 2 pints of tap water, usually at the same time each morning just after eating, induce a bowel motion and empty the rectum. Sometimes a cone-tipped catheter (the same type used for colostomy irrigation) may be needed for incontinent patients to instill an enema so that it does not run out with instillation. Some advocate inserting a glycerine or bisacodyl (Dulcolax) suppository 20 to 30 minutes after eating along with abdominal massage to induce a bowel motion daily. With either method, bulking agents can be used, in addition to medications, to stop stooling in between desired defecation.
SECCA PROCEDURE The U.S. Food and Drug Administration (FDA) has approved a new procedure, the Secca procedure, in patients without a sphincter defect, or with pudendal neuropathy. The procedure is an outpatient procedure done under conscious sedation and local anesthesia. Contraindications include a history of depression or psychiatric illness, inflammatory bowel disease, collagen vascular disease, a history of pelvic radiation, and anal infections like abscesses or fistulas. The Secca procedure uses radiofrequency energy that is delivered to the anal sphincter (Figs. 24-3 and 24-4). This creates 64 lesions in the muscle where the thermal energy triggers collagen contraction (Fig. 24-5). Over time the deposition of collagen and remodeling of tissues causes improvement of the
Figure 24-3 ■ Radiofrequency energy is delivered through this anoscope device, which has needles that protrude at the area indicated by the arrow. These needles penetrate to the muscle to deliver energy that achieves a target temperature of 85°C for 1 minute. (Reproduced with permission from Springer-Verlag and Efron JE, Corman ML, Fleshman J, et al. Safety and effectiveness of temperature-controlled radio frequency energy delivery to the anal canal [Secca procedure] for the treatment of fecal incontinence. Dis Colon Rectum 2003;46:1606.)
Chapter 24
Figure 24-4 ■ The device is inserted into the anal canal. A light source is present and the barrel is clear to allow exact placement and then deployment of the needles. (Reproduced with permission from Springer-Verlag and Efron JE, Corman ML, Fleshman J, et al. Safety and effectiveness of temperature-controlled radio frequency energy delivery to the anal canal [Secca procedure] for the treatment of fecal incontinence. Dis Colon Rectum 2003;46:1606.)
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Figure 24-6 ■ Sphincteroplasty repair. The patient is in the prone jackknife position. The buttocks are taped apart. A curved incision is made anteriorly, avoiding the pudendal nerves, which approach the external sphincter from a deep posterolateral position.
continued postoperatively for variable periods, at the discretion of the surgeon. For surgery to correct a defect secondary to an injury, the tissue must be soft and pliable, and at least 3 to 6 months should elapse after the injury for the inflammation to subside. A Foley catheter is placed. Patients may be positioned in the lithotomy position or prone jackknife position for procedures directly performed on the sphincter muscle. For muscle wraps or the artificial sphincter, the prone jackknife position is indicated. We prefer the prone jackknife position for almost all anal procedures because it allows the buttock muscles to fall out of the way and gives the surgical assistants optimal viewing of the surgical field. For simple procedures, such as sphincteroplasty or postanal repair, general, epidural, or spinal anesthesia may be used. For complicated sphincter wraps, general anesthesia is needed. Figure 24-5 ■ Graphic representation of the location of four rings of treatment, 64 total lesions, beginning at the dentate line and moving proximally in 5-mm intervals. (Reproduced with permission from SpringerVerlag and Efron JE, Corman ML, Fleshman J, et al. Safety and effectiveness of temperature-controlled radio frequency energy delivery to the anal canal [Secca procedure] for the treatment of fecal incontinence. Dis Colon Rectum 2003;46:1606.)
fecal incontinence. A pilot trial showed improvement in 8 out of 10 patients at 2 years. Currently, a trial is ongoing in the United States to further assess this procedure.
SURGICAL TREATMENT For sphincter repairs, the bowel is completely cleansed with an agent, such as polyethylene glycol. Prophylactic antibiotics, such as intravenous metronidazole and a third-generation cephalosporin, are given preoperatively. These antibiotics are
Sphincteroplasty When a defect is detected in the sphincter complex, reapproximation of the two ends is attempted. Usually, these defects are secondary to obstetric injury, fistula repair, or lateral internal sphincterotomy. Occasionally, defects after hemorrhoidectomy can be repaired successfully. An arc type of incision is made over the injury, usually about 1 to 1.5 cm beyond the anal verge (Fig. 24-6). For obstetric injuries, this arc spans anteriorly about 200 degrees. It is important to remember that the branches of the pudendal nerves that innervate the external sphincter approach the muscle from the posterolateral position. To avoid nerve injury, the arc of the incision should not extend to the extreme posterolateral position. We prefer to initially dissect down the rectovaginal septum to avoid injury to any remaining muscle and to avoid buttonhole defects into the anal canal or rectum. Sometimes the only remaining perineal body is the vaginal and anal mucosa, so dissection is difficult. The dissection is carried laterally to the ischiorectal fat.
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Placing a finger in the vagina or rectum and dissecting from lateral to medial may facilitate the dissection. Any tears in the anal mucosa are repaired with No. 4-0 chromic suture. The ends of the sphincter are usually approximated with scar in the midline (or midportion of the injury). This scar is divided in the middle, leaving two ends of sphincter with scar attached. Dividing the scar is important but not trimming it from the ends of the sphincter because it will provide tensile strength when the repair is done. If both the internal and external muscles are injured, we prefer to leave them intact and repair them as one unit. If the internal sphincter is not disrupted, we divide and repair the external sphincter only. The levator ani muscles may be plicated, at this point, using No. 0 or 2-0 delayed absorbable sutures. This may lengthen the anal canal. The vagina should be checked after the levator plication to ensure that a ridge or narrowing did not occur with levator plication because this may contribute to dyspareunia. If the internal anal sphincter was not injured and hence not divided for the overlapping repair, plication can be done before the sphincteroplasty, if there is redundant internal sphincter (Fig. 24-7). The sphincter ends that have been sufficiently mobilized to allow overlapping of the muscle are grasped. Some advocate merely approximating the muscles, but, if possible, we
prefer to overlap the muscle ends. We use No. 2-0 polyglactin sutures and place mattress sutures for the sphincteroplasty. Approximately six sutures (three on each side) are used (Fig. 24-8). The repair is performed to tighten the anal canal so that just an index finger is admitted. During the procedure, irrigation of the wound is carried out with antibiotic solution. The skin edges are closed in a V-Y fashion, starting laterally and leaving the center open for drainage (Fig. 24-9). If a significant amount of “dead space” is present, a half-inch Penrose drain can be inserted and then removed on postoperative day 2. Postoperatively, patients are kept on intravenous antibiotics for 2 to 3 days, and oral intake is withheld. We do not use constipating agents, and we also do not use Sitz baths because we feel that they macerate the skin edges; however, showers are permitted. The Foley catheter is removed on postoperative day 2, and the patient is allowed a high-fiber diet just before discharge. At discharge, patients are placed on daily Metamucil, Citrucel, or Konsyl. Additionally, they take 1 ounce of mineral oil each morning. If they do not move their bowels by postoperative day 7, they take 1 ounce of milk of magnesia twice daily until their bowels move. Because they undergo a complete bowel cleansing before surgery, patients may not move their bowels for several days after surgery.
Figure 24-7 ■ If the internal anal sphincter (long arrow) is intact, it can be plicated before the external anal sphincter (short arrows) is overlapped. The levator muscles can also be plicated (curved arrow).
Figure 24-8 ■ The sphincter ends are identified and overlapped. Three mattress sutures are placed on each side to hold the muscle ends in place.
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Collectively, these studies have shown that less than 40% of patients who undergo a repair report long-term satisfactory fecal continence 5 to 10 years after surgery.
Postanal Pelvic Floor Repair
Figure 24-9 ■ The skin edges are closed in a V-Y fashion starting laterally and leaving the center open for drainage.
Diverting stoma is used at the discretion of the surgeon. Preoperatively, we discuss the possibility of using a stoma in patients who have had previous failed repairs, have concomitant inflammatory bowel disease or severe diarrhea, or need an extremely complicated repair. A stoma does not ensure success but may aid a successful outcome in such patients. Initial functional improvement can be anticipated in 80% to 90% of patients. Pudendal nerve damage is associated with suboptimal results. Age does not seem to significantly affect results, although erratic bowel problems, such as urgency and diarrhea, may lead to continued incontinence. Wound infection occurs in up to a quarter of patients but does not adversely affect the outcome unless the sphincter repair sutures become disrupted. Complete disruption of the skin sutures usually heals by secondary intention with adequate wound care. For patients who do not improve after overlapping repair, repeat evaluation of the sphincters should be done, usually with anal ultrasound. If a persistent defect is present, a repeat sphincter repair can be performed. In patients undergoing repeat overlapping sphincter repair, the improvement rate is similar to those who have initially had the defect corrected. Even when patients have excellent initial improvement in fecal incontinence after sphincter repair, several studies have found that long-term results are disappointing.
The postanal repair has been advocated for patients with incontinence without a sphincter defect or with neuropathic incontinence. This procedure is designed to reestablish the anorectal angle, increase the length of the anal canal, and tighten the anal canal. Optimal results seem to be in patients with incontinence from anal sphincter stretch or loss of anorectal angulation. Patients with neurogenic incontinence usually do not have significant improvement. Preoperative preparation has been described previously. A posterior, inverted V incision is made 5 to 6 cm from the anal verge. Flaps are raised and the intersphincteric plane is identified. Dissection is carried in this plane cephalad to Waldeyer’s fascia, which is divided to expose the mesorectal fat. Figure-of-eight, No. 2-0 polypropylene sutures are placed to draw the two sides of the iliococcygeus muscle together. The sides will not approximate because of the distance, so the sutures are tied with minimal tension to form a lattice. The pubococcygeus muscle is the next muscle encountered. Sutures are placed and tied to again form a lattice, especially posteriorly, although anteriorly the ends may also be approximated. The last layer plicated is the puborectalis and external sphincter. The skin is closed with absorbable suture in a V-Y fashion. Postoperative care is similar to the sphincteroplasty repair. Original results by Parks (1975) demonstrated postoperative improvement in incontinence in 80% of patients; however, this degree of success has not been achieved by others. Recent studies have shown that long-term continence is restored in perhaps 30% of patients who undergo the postanal repair.
Muscle Transposition Procedures In some patients, repair of the sphincter does not relieve symptoms. Additionally, some patients have had traumatic loss of sphincter muscle, making approximation of the ends impossible. Transposition of the gracilis muscle has been advocated for these patients. This procedure, however, is not available to patients in the United States because the generator to stimulate the muscle is no longer available. To perform dynamic graciloplasty, the gracilis muscle is mobilized from the inner thigh, proximally preserving the neurovascular bundle. The tendon of insertion is divided at the knee, preserving as much tendon as possible. The muscle is wrapped around the anus, and the tendon is sewn to the opposite ischial tuberosity. An electrical stimulator is placed at an optimal site on the abdomen. Leads are tunneled from the stimulator and placed onto the proximal portion of the nerve. The entire procedure is done under cover of a stoma and usually in several stages. The expected lifespan of the stimulator is approximately 7 years. Patients appropriate for this procedure include those with incontinence caused by obstetric injury, idiopathic incontinence, traumatic loss of sphincter muscle, and congenital anal sphincter problems. Contraindications include neurologic
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disease, such as multiple sclerosis. This operation carries a high morbidity and has a significant learning curve. Surgeons with considerable experience, such as Baeten et al. (1995), achieve excellent results, especially considering that the only alternative for many of these patients is a permanent stoma. In their 1995 study, about 23% achieved perfect continence for solid and liquid stool and flatus. An additional 50% had continence for solid and liquid stool but not flatus. Others have achieved complete continence in 46% to 65% of patients. As more experience is gained with this procedure, surgeons hope that the technical and learning problems will be remedied.
Artificial Anal Sphincter As success with the artificial urinary sphincter was attained, efforts turned toward using a modified version of this device for fecal incontinence. This fully implantable device incorporates a balloon that, when fully inflated, occludes the anus. The device is indicated for patients in whom conventional management of fecal incontinence has failed. Few centers in the world perform this procedure, and many technical challenges are associated with its implantation. Wong et al. (1996) reported the results from a combined study of the University of Minnesota and The Royal Infirmary in Edinburgh, Scotland. They found infectious or mechanical complications in 33% of patients. Seventy-five percent had improvement in their incontinence, although some of the patients with improvement, at times, experienced incontinence of flatus, mucus, or liquid stool. As with the muscle transpositions, a considerable learning curve is present with this operation. However, it also holds promise for patients with severe fecal incontinence. In a recent study from Spain (Casal et al., 2004), continence was restored in the immediate postoperative period in 100% of patients for solid stool, 16% for liquid stool, and 44% for gas. However, only 22% patients retained this at 29 months and 60% patients had postoperative complications. Parker et al. (2003) reported their experience of 45 patients who were divided into two groups: one group was viewed retrospectively and the other prospectively. They concluded that although infection was a major complication and a reason for revision and explantation, once the artificial sphincter stabilized its function remained stable for many years.
Sacral Neuromodulation Currently, stimulation of the sacral nerve is under investigation for fecal incontinence and voiding disorders. The same procedure has been approved previously by the FDA for certain forms of urinary. As for patients with urinary symptoms, the procedure consists of two parts; the first places a temporary sacral stimulation lead. The patient keeps a diary and, if improvement is demonstrated, a permanent device is implanted. In Europe there has been tremendous enthusiasm and positive results for fecal incontinence with this procedure (see Chapter 31).
Colostomy or Ileostomy Fecal diversion, in the form of an end colostomy or, occasionally, an ileostomy, sometimes can offer a much better lifestyle for patients with incapacitating incontinence when
repairs fail or have no chance of succeeding. They allow patients trapped in their homes the opportunity to leave their “prisons” free from fear of an episode of incontinence.
CONCLUSION Fecal incontinence is a complex problem with many causes. Even though it is not a life-threatening problem, it can be life-devastating. Evaluation is tailored to the patient, and treatment depends on the findings from history, physical examination, and diagnostic testing. Many patients can obtain improvement or cure from nonsurgical treatment, and newer techniques like the Secca procedure and sacral neuromodulation hold some hope for those without a demonstrable sphincter defect. Others with a demonstrable defect in the sphincter mechanism may be candidates for sphincter repair. New frontiers with the artificial anal sphincter and other techniques are emerging for patients who fail sphincter repair or are not suitable candidates for other procedures. Significant disappointments and failures after surgery for incontinence still exist, and fecal diversion is still the appropriate treatment for some.
Bibliography 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. Casal E, San Ildefonso A, Carracedo R, et al. Artificial bowel sphincter in severe anal incontinence. Colorectal Dis 2004;6:180. Den KI, Kumar D, Williams JG, et al. The prevalence of anal sphincter defects in faecal incontinence: a prospective endosonic study. Gut 1993;34:685. Devesa JM, Vicente E, Enriquez JM. Total fecal incontinence—a new method of gluteus maximus transposition: preliminary results and report of previous experience with similar procedures. Dis Colon Rectum 1992;35:339. Efron JE, Corman ML, Fleshman J, et al. Safety and effectiveness of temperature-controlled radio frequency energy delivery to the anal canal (Secca procedure) for the treatment of fecal incontinence. Dis Colon Rectum 2003;46:1606. Gordon PH. Anal incontinence. In Gordon PH, Nivatvongs S, eds. Principles and Practice of Surgery for the Colon, Rectum, and Anus. Quality Medical Publishing, St. Louis, 1992. Gutierrez AB, Madoff RD, Lowry AC, et al. Long-term results of anterior sphincteroplasty. Dis Colon Rectum 2003;47:727. Hay-Smith J, Herbison P, Morkved S. Physical therapies for prevention of urinary and faecal incontinence in adults (Cochrane Review). In The Cochrane Library, Oxford, Update Software, Issue 3, 2002. Jackson SL, Weber AM, Hull TL, et al. Fecal incontinence in women with urinary incontinence and pelvic organ prolapse. Obstet Gynecol 1997;89:423. Jensen LL, Lowry AC. Biofeedback improves functional outcome after sphincteroplasty. Dis Colon Rectum 1997;40:197. Johanson JF, Lafferty J. Epidemiology of fecal incontinence: the silent affliction. Am J Gastroenterol 1996;91:33. Jorge JM, Wexner SD. Etiology and management of fecal incontinence. Dis Colon Rectum 1993;36:77. Madoff RD, Parker SC, Varma M, Lowry AC. Fecal incontinence in adults. Lancet 2004;364:621. Madoff RD, Williams JG, Caushaj PF. Fecal incontinence. N Engl J Med 1992;326:1002. Meyenberger C, Bertschinger P, Zala GF, et al. Anal sphincter defects in fecal incontinence: correlation between endosonography and surgery. Endoscopy 1996;28:217. Morren GL, Hallbook O, Nystrom PO, et al. Audit of anal sphincter repair. Colorectal Dis 2001;3:17. Norton C. Behavioral management of fecal incontinence in adults. Gastroenterology 2004;126:S64.
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Norton C, Hosker G, Brazzelli M. Biofeedback and/or sphincter exercises for the treatment of faecal incontinence in adults (Cochrane Review). In The Cochrane Library, Oxford, Update Software, Issue 3, 2002. Oberwalder M, Thaler K, Baig MK, et al. Anal ultrasound and endosonographic measurement of perineal body thickness. Surg Endosc 2004;18:650. Oliveira L, Pfeifer J, Wexner SD. Physiological and clinical outcome of anterior sphincteroplasty. Br J Surg 1996;83:502. Parker SC, Spencer MP, Madoff RD, et al. Artificial bowel sphincter: longterm experience at a single institution. Dis Colon Rectum 2003;46:722. Parks AG. Anorectal incontinence. Proc R Soc Med 1975;68:681. Rao SS, Welcher KD, Happel J. Can biofeedback therapy improve anorectal function in fecal incontinence? Am J Gastroenterol 1996;91:2360. Reilly WT, Talley NJ, Pemberton JH, Zinsmeister AR. Validation of a questionnaire to assess fecal incontinence and associated risk factors. Dis Colon Rectum 2000;43:3174. Rockwood TH. Incontinence severity and QOL scales for fecal incontinence. Gastroenterology 2004; Suppl 126:S106.
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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. Sultan AH, Kamm MA, Hudson CN, et al. Anal-sphincter disruption during vaginal delivery. N Engl J Med 1993;329:1905. Tetzscher T, Sorensen M, Lose G, et al. Anal and urinary incontinence in women with obstetric anal sphincter rupture. Br J Obstet Gynaecol 1996;103:1034. Vaizey CJ, Norton C, Thornton MJ, et al. Long-term results of repeat anterior anal sphincter repair. Dis Colon Rectum 2004;47:858. Wexner SD, Gonzalez-Padron A, Rius J, et al. Stimulated gracilis neosphincter operation: initial experience, pitfalls, and complications. Dis Colon Rectum 1996;39:957. Wexner SD, Schmitt SL. Fecal incontinence: surgical therapy. In Brubaker LT, Saclarides TJ, eds. The Female Pelvic Floor. FA Davis, Philadelphia, 1996. Wong WD, Jensen LL, Bartolo DC, et al. Artificial anal sphincter. Dis Colon Rectum 1996;39:1345.
Constipation J. Eric Jelovsek
DEFINITION AND ETIOLOGY 320 EPIDEMIOLOGY 321 EVALUATION 322 History 322 Psychiatric Evaluation 323 Physical Examination 323 Testing 323 NONSURGICAL TREATMENT 324 Medications 324 Biofeedback 327 SURGICAL TREATMENT 327 Slow-Transit Constipation (Colonic Inertia) Anorectal Outlet Obstruction 328 CONCLUSION 328
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DEFINITION AND ETIOLOGY Constipation is a broad term that is defined as difficult evacuation of feces, infrequent defecation, or inadequate defecation. Our understanding of the etiology of constipation has improved, resulting in an evolving definition. One commonly used definition is based upon bowel frequency of fewer than three stools per week. This definition is based on interviews of factory workers in the United Kingdom that found that 99% of the working population reported frequency of bowel movements between three per day and three per week. The problem with this definition is that it ignores the symptoms reported by most patients who consider themselves constipated (i.e., straining, hard stools); it does not assist in separating out those patients with disorders of slowed intestinal transit and those with disorders of defecation, and it may not apply to patients who are taking laxatives. Although physicians and patients often refer to constipation as a single disorder, it should be viewed as a symptom that means different things to different people. In 1987, Sandler and Drossman reported on the bowel habits of over a thousand adults. The patients were asked how they define the term constipation. Fifty-two percent said “straining at stool,” 44% reported “hard stools,” 34% reported “a sense of wanting to defecate but cannot,” 32% reported “infrequent
25 stools,” 20% reported “abdominal discomfort,” 19% reported “a sense of incomplete evacuation,” and 11% said “spending too much time on the toilet.” Therefore, simply asking a patient whether he or she has constipation is neither sensitive nor specific. However, there appears to be a large percentage of individuals who feel that they have constipation yet do not complain of any symptoms physicians typically use to define constipation. This difference in definition between patientcentered self-report of constipation and objective criteria indicates that reliance on stringent symptom-based criteria may miss a large population who believe that they have constipation, whether they do or do not, based on those criteria. Because most constipation becomes a problem only when the patient complains of it, and because symptoms of constipation may occur in the absence of any physiologic abnormalities (i.e., stool frequency does not necessarily correlate with transit time), a symptom-based definition still holds some value and has become the standard. This led to the development of the ROME criteria (Drossman et al., 2000). The criteria are expert consensus guidelines for making the clinical diagnosis of the various types of functional bowel disorders, including constipation. The criteria have become the standard for the definition of constipation. The ROME III criteria divide patients complaining of symptoms of constipation into two major groups: functional bowel and functional anorectal disorders. Functional bowel disorders include: (1) functional constipation and (2) irritable bowel syndrome with constipation (IBS-C). Subjects with functional constipation often complain of fewer than three bowel movements per week, hard or lumpy stools, straining, feeling of incomplete emptying after a bowel movement, a sensation that stool cannot be passed, or a need to press on or around their bottom or vagina to complete a bowel movement. Functional constipation may include patients who demonstrate slowed transit times on colonic transit studies or patients with idiopathic constipation because it is a symptom-based diagnosis. The diagnostic criteria for functional constipation are seen in Box 25-1. Patients with IBS-C have the same symptoms, except they often have abdominal pain. This pain is associated with improvement after a bowel movement, change in the number of bowel movements, or change in consistency of stools. Some experts felt that
Chapter 25
BOX 25-1
ROME III DIAGNOSTIC CRITERIA FOR FUNCTIONAL CONSTIPATION
Must fulfill both criteria: 1. Must include two or more of the following: Straining ≥25% of defecations Lumpy or hard stools ≥25% of defecations Sensation of incomplete evacuation ≥25% of defecations Sensation of anorectal obstruction/blockage ≥25% of defecations Manual maneuvers to facilitate ≥25% of defecations Less than three defecations per week 2. May not meet the criteria for the diagnosis of irritable bowel syndrome. Loose stools are rarely present without the use of laxatives and make 3. There are insufficient criteria for irritable bowel syndrome. From Longstreth GE. Thompson WG, Chey WD, et al. Functional bowel disorders. Gastroenterology 2006;130:1480.
constipation could be broken down into further subtypes based on the reported predominant evacuation symptoms, including IBS-outlet and outlet-type constipation. A subcategory of patients who fulfilled criteria for either constipationpredominant IBS or functional constipation also report one of the following evacuation symptoms: a sensation that stool cannot be passed when having a bowel movement, a need to press on or around their bottom or vagina to try to remove stool to complete a bowel movement, or difficulty relaxing or letting go to allow the stool to come out at least one quarter of the time. These subtypes are now referred to as functional defecation disorders. Functional defecation disorders (often referred to as evacuation disorders, outlet dysfunction or delay, or pelvic floor dysfunction) have been incorporated into the ROME III criteria and include (1) dyssynergic defecation and (2) inadequate defecatory propulsion. The diagnostic criteria for functional defecation disorders are: 1. The patient must satisfy diagnostic criteria of functional constipation 2. During repeated attempts to defecate must have at least two of the following: a. Evidence of impaired evacuation, based on balloon expulsion test or imaging b. Inappropriate contraction of the pelvic floor muscles (e.g., anal sphincter or puborectalis) or less than 20% relaxation of basal resting sphincter pressure by manometry, imaging, or EMG c. Inadequate propulsive forces assessed by manometry or imaging The problem with most gynecologic literature is that investigators have not clearly separated out these different types of disorders and have just placed these patients as being or not being “constipated.” Physiologically, patients with slow-transit constipation typically have decreased number of high amplitude propagated contractions of the bowel. Those with defecation disorders, may have normal or slightly slowed transit studies but have preferential storage of stool in the rectum. They also have higher defecatory sensation thresholds and may tolerate higher volumes in the rectum. Based on the Cleveland Clinic experience, outlet-type symptoms of constipation seems to be
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the predominate subtype seen in patients with pelvic organ prolapse and incontinence. Patients with dyssynergic defecation (the older term for this is anismus) have paradoxical contraction or failure to relax the pelvic floor muscles during attempts to defecate. Physical examination may reveal a failure to relax the puborectalis or paradoxical contraction during an attempted defecation, and they have laboratory testing showing evidence of inappropriate contraction or failure of relaxation of the pelvic floor during attempts to defecate. The pathophysiology of constipation continues to evolve. Investigators have attempted to examine the relationships between slow transit disorders and external neuropathy conditions, such as spinal cord injury patients, Parkinson’s disease, multiple sclerosis, and diabetes. The premise behind these disorders is that the symptoms of constipation result from motor and sensory disturbances, ultimately leading to delayed transit or physiologic disorders of the colon and pelvic floor. Neuropathy of the enteric nervous system may also occur in patients with Chagas’ disease secondary to infection from Trypanosoma cruzi, Hirschsprung’s disease, or chronic laxative abuse. Studies of the pathophysiology of disorders of defecation have examined altered anorectal motor and sensory function. These include studies involving perceptual responses to controlled rectal distension, alterations to visceral sensation, and pudendal nerve terminal motor latencies. For example, there is evidence that dyssynergia of the puborectalis and external anal sphincter muscles during defecation, leading to outlet dysfunction and constipation in patients with multiple sclerosis, is due to a spinal lesion. Mathers et al. (1989) showed that this functional abnormality also occurred in patients suffering from Parkinson’s disease, and that in Parkinson’s disease it was responsive to dopaminergic medication. De Groat et al. (1990) showed that interruption of pathways in the spinal cord can result in detrusor sphincter dyssynergia, and it is therefore likely that paradoxical puborectalis contraction in multiple sclerosis is due to interruption of spinal pathways by demyelination. The data provide evidence that functional bowel disorders may be more intimately associated with the neurologic system than is commonly thought. Despite these advances, our knowledge of neuroanatomy and its relationship to functional disorders of the bowel remains in its infancy.
EPIDEMIOLOGY Constipation is a commonly encountered problem in medical practice and is expected to increase dramatically. The U.S. population is becoming older and more likely to be living with chronic neurologic disease and to reside in nursing homes. Estimates of incidence and prevalence vary depending upon the definition used (i.e., self-reported constipation or ROME criteria) and the population studied. The data available on incidence of constipation are few. Talley et al. (1992) showed the onset of constipation of 40 per 1000 person-years in white residents of a single county in Minnesota. The symptom remission rate was 309 per 1000 person-years. Stewart et al. (1999), in a large U.S. epidemiologic study containing over 10,000 individuals, found an overall constipation prevalence of 14.7% in the general population. Higgins et al. (2004), in a systematic review of the epidemiology of constipation in North America, concluded that a conservative estimate of
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15% of the North American population, or 42 million individuals in the United States alone, suffer from constipation. Subtypes of constipation among the U.S. population in men and women showed functional constipation in 4.6%, constipation-predominant IBS in 2.1%, outlet subtype constipation in 4.6%, and IBS-outlet subtype in 3.6% (Stewart et al., 1999). Overall, women had higher rates of outlet disorders. However, when these constipation subtypes were broken down among gender, the only statistical difference was in women being more likely to have IBS-outlet subtype of constipation. Higgins et al. (2004), in the large systematic review, concluded that the prevalence of constipation stratified by gender showed constipation to be approximately 2.2-fold more frequent in women. Most of the studies that stratified by age found consistent trends of increasing prevalence of constipation with age, with significant increases after age 70. Interestingly, when Sandler et al. (1987) stratified by subtypes of constipation in women by age, the prevalence of constipation actually decreased as they got older. Most data suggest similar racial differences in the prevalence of constipation, with an average prevalence of 1.17- to 2.89-fold more frequent in non-Caucasians than in Caucasians. Outlet-type constipation was also more prevalent among nonwhites in the data from Sandler et al. (1987). At our institution, over 300 women who presented to a urogynecology clinic for either pelvic organ prolapse or incontinence had an overall prevalence of constipation of 36%, as defined by the ROME II criteria. When this sample was stratified by subtype, 5% had functional constipation, 19% outlet type, 5% constipation-predominant IBS, and 7% IBS-outlet type (Fig. 25-1). Given recent population shifts in North America, constipation and its associated outlet disorders make this a condition with which gynecologists and urologists should be familiar.
EVALUATION Patients who report constipation often have features of both slow-transit disorders and defecatory (outlet-type) disorders. 20 POP/UI
18
U.S. population
Prevalence (%)
16 14 12 10 8 6 4 2 0 Functional type
Outlet type
IBS type
IBS-outlet
Type of constipation
Figure 25-1 ■ One study of prevalence of subtypes of constipation in 302 consecutive patients presenting to the Cleveland Clinic Foundation for pelvic organ prolapse (POP) and urinary incontinence (UI) versus the U.S. population data. (From Stewart WF, Liberman JN, Sandler RS, et al. Epidemiology of constipation [EPOC] study in the United States: relation of clinical subtypes to sociodemographic features. Am J Gastroenterol 1999;94:3530.)
When attempting to evaluate constipation, it is convenient to try to separate out these two pathophysiologic mechanisms and tailor the treatment accordingly. A thorough history and physical examination is the first step toward treatment. Laboratory, radiologic, and other tests are done based on the history and physical examination.
History The history begins with clarification of the nature of the defecation problem, such as number of stools per week, difficulty expelling stool or a feeling of incomplete defecation, pain with defecation, consistency of stool (including hard or lumpy stools), and duration of the problem. Some patients experience rectal pressure or fullness. Others may need to use their fingers to expel stool or stabilize the vagina or perineum, referred to as splinting, during defecation. They may be embarrassed to admit some of these practices and may need to be encouraged to tell this information. Additionally, a dietary history, including questions about the amount of dietary fiber and fluid consumed daily, is necessary. Ruling out associated medical problems that may lead to secondary constipation (Box 25-2) is important. Constipation is more common in people with neurologic disease, such as multiple sclerosis and spinal cord injury. Diabetes may also be associated with constipation. Recent changes in routine,
BOX 25-2
POSSIBLE CONTRIBUTORS TO CONSTIPATION
Personal Habits Low physical activity Low calorie diet Employment status Obstructive Colon Neoplasm Benign stricture (i.e., diverticula) Rectal prolapse Anal outlet obstruction Pain (i.e., anal fissure) Stenosis Rectocele Pelvic floor dyssynergia Medications Narcotics Antidepressants Mineral supplements (i.e., iron, calcium) Anticholinergics Beta-blockers, calcium channel blockers Endocrine Hypothyroidism Hypercalcemia Hypokalemia Diabetes mellitus Uremia Neurologic Aganglionosis (congenital: Hirschsprung’s disease; acquired: Chagas’ disease) Central nervous system or spinal cord trauma or disease (Parkinson’s disease, multiple sclerosis) Pregnancy Psychiatric Causes Other
Chapter 25
such as levels of diet and exercise, may contribute to constipation. Self-reported constipation is higher in individuals with the least exercise (odds ratio [OR] = 1.2–3.3). Sandler et al. (1987) found that decreased caloric intake favored constipation with an OR of 1.15. In patients with severe constipation and no obvious cause, histories of physical and/or sexual abuse may be found. Past surgeries may provide clues and should be elicited. Some debate exists as to whether hysterectomy causes constipation. In 1992, Prior et al. reported on 200 subjects who underwent hysterectomy and found that 5% developed constipation-predominant IBS. In 2004, Altman et al. reported on 120 consecutive patients who underwent either vaginal or abdominal hysterectomy. No statistical difference was present in preoperative and postoperative bowel emptying difficulties, or incomplete bowel evacuation.
Psychiatric Evaluation The interplay between the emotional being and the colon and anus is not well understood. Some problems with abnormally holding in stool during childhood may be attributed to problems between children and their parents over bowel function. Patients who have experienced sexual trauma or abuse can have defecation problems. Some patients complain of infrequent stools and constipation, but a transit study may be normal; these two findings are not compatible because there must be bowel function to eliminate the markers. Additionally, patients with psychosis, depression, or eating disorders can have severe constipation from various causes. The clinician needs to be alert to possible cues from the patient and, if suspicious, refer him or her for a psychiatric assessment.
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tionnaire assessment of bowel function with standardized examinations, using the Pelvic Organ Prolapse Quantification (POPQ) method. In 26.6% it was rare to require straining to have a bowel movement, in 49.6% straining was sometimes required, in 14% straining was usually required, and in 9.8% straining was always required. Thirty-one percent needed to help stool come out by pushing with a finger in the vagina or rectum. Severity of prolapse was not related to bowel dysfunction. In a Swedish population of 491 women, when a rectocele was present, 18% reported problems with emptying the bowel at defecation compared with 13% in the nonrectocele group (Samuelsson et al., 1999). However, constipation was not related to prolapse in this population. Patients greater than ages 40 to 50 should be considered for colonoscopy or sigmoidoscopy. This examination rules out neoplasms, a solitary rectal ulcer (erythema or ulceration on the lower anterior rectal wall thought to be from trauma secondary to internal rectal prolapse), or melanosis coli (brown-black discoloration of the mucosa from chronic use of certain laxatives).
Testing Further testing depends on the severity of symptoms and findings on physical examination. At this stage, the majority of patients require no further testing, and the physician can proceed to medical therapy. A therapeutic trial of fiber is warranted if no cause has been found. Patients who do not respond may require further diagnostic evaluation to identify the subgroups of constipation. The tests chosen depend on the patient’s characteristics and severity of symptoms. LABORATORY TESTING
Physical Examination The physical examination is tailored to the patient. The abdominal examination is usually normal, but masses, palpable stool in the colon, and surgical scars and hernias should be noted. The perineal examination starts with an inspection, looking for anal fissures or abnormalities. Asking the patient to strain may demonstrate perineal descent, widening of the perineal body, rectal prolapse, or a large rectocele protruding into the vagina. Digital examination rules out fecal impaction, anal stenosis or stricture, external or internal rectal prolapse, pelvic or rectal masses, and rectocele. The examiner should note the consistency of stool in the rectum. The tone of the levator ani muscles on vaginal and rectal examination should be assessed at relaxation and with straining. Paradoxical contraction may be suspected if the patient’s failure to relax the puborectalis is noted. These patients often have a history of excessive straining before elimination. Even soft stools and enema fluid are difficult to pass. Digital examination has been shown to have excellent negative predictive values (96%, 96%, and 80%, respectively) when examining patients for rectocele, pelvic floor dyssynergia, and/or rectal intussusception (i.e., if it is not found on examination, it is unlikely to be present). Pain on the border of the puborectalis is a feature of some anorectal pain disorders, causing spasm. Few clinicians would dispute the association between vaginal prolapse and symptoms of constipation, although a direct relationship between the two is not clear. In 1998, Weber et al. described 143 women who completed a ques-
Blood work to assess levels of potassium, calcium, renal function, and glucose are performed initially. Thyroid function tests screening for hypothyroidism are also drawn, if a problem is suspected. ANATOMIC STUDIES OF THE COLON A barium enema or colonoscopy will diagnose anatomic abnormalities, such as stricture or cancer. At times barium enema is preferred because it defines the borders of the colon and may show a redundant or chronically dilated colon (megacolon) or rectum (megarectum). Defecography is performed by placing a paste of contrast material into the rectum to simulate stool. Radiographs are taken at rest and during straining. During the examination, the patient sits on a commode behind a curtain, and fluoroscopy is performed to obtain the pictures. The items examined include the angle between the anal canal and rectum is measured at rest, strain, and squeeze. The ability to evacuate contrast material, presence of a rectocele, and evidence of intussusception should be noted. During normal defecation, the anal canal becomes straighter, which, in turn, lengthens the angle. If this does not occur, the puborectalis muscle may be inappropriately contracting and may prohibit the expulsion of the contrast (and stool). The amount of descent of the perineum is noted because this may be associated with anal outlet obstruction and constipation. Additionally, enfolding of the walls of the rectum with defecation, as is seen with internal prolapse, is evaluated. Defecating proctogram may be useful
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in establishing the diagnosis of internal rectal prolapse or rectoceles. These studies help delineate the rectoceles that are displaced anteriorly, not fully emptying, and may require repair (Fig. 25-2). Also, enteroceles and sigmoidoceles can be seen. Note that this test is embarrassing for the patient and complicated for the radiologist to perform. Therefore, the results may not always demonstrate the abnormality or may not be totally accurate. Defecography is useful for assessing rectal evacuation. It provides functional or morphologic features of the defecatory maneuver. However, there is a poor correlation between studies of defecography and electromyography (EMG) or manometry for diagnosing pelvic floor dyssynergia. FUNCTIONAL STUDIES OF THE COLON The colonic transit study is an important test to evaluate the colon for slow transit. Patients must stop all laxatives 48 hours before the study. They should also consume a highfiber diet (30 g daily) and refrain from using enemas. Many variations of this study are known, but, basically, patients consume a commercially prepared capsule that contains a certain number of radiopaque markers. Radiographs are then taken daily or every other day and compared. The mouth-to-cecum time is 3.6 hours. Material usually lasts around 12 hours each from the right colon, left colon, and sigmoid colon. This gives an overall transit of approximately 36 hours. Normally, 80% of the markers are passed by the fifth day, and all markers should be passed by the seventh day. Some people divide the colon into right, left, and rectosigmoid to determine the transit time of each segment. This allows distinction between whole gut dysmotility, as seen by evenly distributed markers throughout the colon to the rectum, versus anal outlet obstruction, in which the markers progress quickly through the colon and are held up in the rectal sigmoid region. In another pattern, markers proceed
through the colon and accumulate in the left colon and stop. This signals left colonic dysfunction. Anal physiology testing can be helpful in patients with defecation disorders. The balloon expulsion test has been used to exclude patients with constipation suspected of having outlet dysfunction. In 2004, Minguez et al. identified patients with functional constipation, both with and without pelvic floor dyssynergia. Balloon testing was performed, showing a specificity and negative predictive value of balloon testing for excluding defecation disorders of 89% and 97%. This may be a useful screening test in clinical practice because patients with a normal balloon expulsion test result, independent of the frequency of distal symptoms, do not need other functional studies that are more expensive and difficult to perform to rule out pelvic floor dyssynergia. Normally, rectal distension is simulated with a fluid-filled balloon, usually a lubricated latex condom, in the rectum. This is tied to a catheter that is introduced into the rectum. Water is instilled into the balloon, and total volume is measured when the patient has a sustained feeling of necessity of defecation. Distension leads to reflexive internal sphincter relaxation. This is called the rectal anal inhibitory reflex. In patients with Hirschsprung’s disease, this does not occur. Compliance of the rectum can be calculated by measuring the sensitivity and maximal volume tolerated in a fluid-filled balloon. An increased compliance can be seen in patients with constipation and signals a megarectum or insensitive rectum. Manometry is useful in the measurement of rest and attempted defecation intrarectal and anal pressures. These pressures are helpful in categorizing defecation disorders into those of dyssynergic defecation and those of inadequate propulsion. A normal pattern is increased intrarectal pressure and relaxation of the anal sphincter. Dyssynergic defecation is characterized by adequate propulsion (intrarectal pressure ≥45 mm Hg) and increased anal pressure or adequate propulsion and absent or insufficient (<20%) relaxation of basal anal sphincter pressure. Inadequate propulsion is defined as an intrarectal pressure less than 45 mm Hg and insufficient relaxation or contraction of the anal sphincter. EMG is done with surface electrodes or needles placed directly in the puborectalis and external sphincter. EMG done during straining should reveal a decrease in electrical activity of these muscles; that is, the muscles should relax to allow passage of stool. If paradoxical contraction or nonrelaxation is seen in these muscles during straining, this may be a cause of pelvic floor dyssynergia. The EMG is an important test to distinguish patients with slow transit constipation from spastic pelvic floor problems. However, patients may have both disorders.
NONSURGICAL TREATMENT Medications
Figure 25-2 ■ Defecating proctogram demonstrating a rectocele (arrow) during the defecation.
The majority of patients with constipation can be treated nonsurgically. If possible, it is important to correct associated medical or gastrointestinal abnormalities. These include problems such as hypothyroidism and hypokalemia. Hyperparathyroidism should be ruled out in patients with elevated calcium levels. Conditions, such as Hirschsprung’s
Chapter 25
disease require surgical intervention. Treating fissures and anal or colonic stenosis may resolve associated constipation. Medications that are known to cause constipation sometimes can be modified to relieve the symptoms. Patients without these obvious or correctable problems should be started on medical management. Dispelling the myth that a daily bowel movement is “normal” initiates medical treatment. Many laxative manufacturers suggest that daily bowel movements are essential for a happy life in an effort to sell their products. However, this is not simply true. Next, a careful dietary history may provide clues to easily correctable problems that do not require specific drug treatment. Encouraging most patients to drink at least six 8-oz glasses of fluid daily is important. BULK-FORMING LAXATIVES AND FIBER Low fiber is not the main determinant of constipation. A large British study by Connell et al. (1965) showed no relationship between dietary fiber intake and whole gut transit time. Constipated patients on the average do not eat less fiber than their nonconstipated controls. Finally, patients who are constipated have lower stool weights and longer transit times than controls, whether or not treated with wheat bran. Despite this, fiber does work and is recommended, if treatment is needed. Fiber is the nondigestible segment of plants. Humans should consume 20 to 35 g of fiber daily for bowel health; however, the average American consumes only 11 g daily. These agents promote evacuation of the bowel by increasing bulk volume and water content of feces. The mechanism of action using fiber may be done in four proposed ways. First, stool is 30% to 50% bacteria. Fiber provides substrate to increase the growth of bacteria and hence increase stool volume. Second, undigested hydrophilic components of fiber absorb fluid and can increase the fluidity of stool. Third, fermentation of fiber produces short chain fatty acids that decrease transit time in the colon. This allows less time for the colonic mucosa to be in contact with the luminal contents to reabsorb water, thus increasing the fluidity of stool. Finally, the weight of the stool is increased simply by the nondigested components in fiber. The use of fiber is dosedependent in its effect on stool weight. It requires a week to reach steady state, and patients who have slow transit require more fiber. Box 25-3 is a guide to the commonly used laxatives. They are grouped according to the U.S. Food and Drug Administration Classification. Natural fiber is classified as soluble or insoluble fiber and foods contain a mixture of these types. Stool size increases from the insoluble component of fiber. Foods high in insoluble fiber and their fiber content are listed in Box 25-4. BOX 25-3
CLASSIFICATION OF LAXATIVES
Bulk Hyperosmotic Lubricant Saline Stimulant Stool softeners From the U.S. Food and Drug Administration, Rockville, MD.
BOX 25-4
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INSOLUBLE FIBER CONTENT OF SELECTED FOODS
Food (Total Fiber) (g) One pear (4.2) One banana (3.9) One cup strawberries (3.5) One apple with skin (2.9) Half cup frozen boiled peas (10.3) Half cup cooked lima beans (5.5) Half cup frozen broccoli (4.0) Half cup cooked green beans (2.4) Half cup raw tomatoes (1.9) One cup chopped lettuce (0.9)
Insoluble Fiber (g) 2.9 1.6 3.0 2.8 3.2 5.5 2.1 1.2 1.0 0.5
Data from Dubuc MB, Lahaie LC. Nutritive Value of Foods. National Library, Ottawa, 1987, pp. 16–158.
Bulk laxatives are thought to be among the safest laxatives. These include familiar product names, such as Metamucil, Konsyl, Citrucel, and FiberCon. Dosage varies among products. Bulk laxatives should be taken with sufficient fluids to avoid esophageal bolus obstruction and bowel obstruction from fecal impaction. The optimum quantity of “sufficient fluids” is unknown, but in adults, a full 8-oz glass of fluid is recommended. For diabetic individuals, sugar-free varieties are manufactured. Side effects of bulk laxatives include increased flatus, distension, poor taste, and bloating. Compliance with fiber may be as low as 50%. Generally, patients are instructed to start with a teaspoon of Metamucil, Citrucel, or Konsyl daily for a week, then to increase to a tablespoon daily. This can be further increased, if needed. These agents take 12 to 72 hours to exert an effect, so patients should be encouraged to try the product for 1 to 2 weeks. Sometimes the problems of increased flatus and bloating decrease with continued use. If these symptoms are too distressing, the patient should switch to another bulk laxative because the side effects may not be as distressing with another product. HYPEROSMOTIC LAXATIVES Hyperosmotic agents contain poorly absorbed substances that remain in the intestinal lumen, increasing the intraluminal osmotic pressure by drawing water into the lumen. The volume increases as the consistency decreases. The increased volume induces peristalsis. Lactulose is a synthetic disaccharide that is not digested by gastrointestinal enzymes and is not significantly absorbed in the small intestine. Lactulose is metabolized by colonic bacteria to short-chain organic acids. The osmotic activity of the nonabsorbable short-chain organic acids draws water into the lumen. Lactulose is a syrup and the dosage is 15 to 30 mL daily, increased to 60 mL daily, if necessary. It may take up to 2 days to produce stool. Use as an enema in a 25% to 30% solution has been reported. Side effects include diarrhea, and the dosage must be titrated to each patient. Increased flatus and intestinal cramps can occur but usually subside with time. Lactulose contains galactose and lactose in small amounts and may alter serum glucose in diabetic persons. Sorbitol, another poorly absorbed carbohydrate, can cause chronic diarrhea in people who consume sugarless candy and gum that contain it. It works similarly to lactulose
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by reaching the colon as an active osmol. It can be administered orally or as an enema to treat constipation. Glycerin suppositories promote fecal evacuation 15 to 30 minutes after administration by stimulating rectal evacuation as a hyperosmotic agent drawing fluid into the rectum. Possible side effects are abdominal cramping, rectal discomfort, and irritation of the rectal mucosa. LUBRICANT LAXATIVES Mineral oil is the most common lubricant laxative. A nondigested hydrocarbon with limited absorption, mineral oil decreases the absorption of water from stool and penetrates the stool to lubricate and soften. It can be used orally (15–45 mL daily in single or divided doses for adults) or in an enema (120 mL). Major concerns come with long-term use (more than 4 months) of this product. Oral use for more than 2 weeks coats the small intestine and may interfere with vitamin absorption, especially vitamins A, D, E, and K (fatsoluble vitamins). For this reason, mineral oil should not be taken with meals. Additionally, many feel that it should not be administered at bedtime to reduce the occurrence of aspiration of the mineral oil, which can produce lipoid pneumonia. Administration with docusate salts may enhance absorption of mineral oil, which can form lipoid granulomas in the reticuloendothelial system; therefore, administration of both together is usually avoided. Other side effects include pruritus ani, anal leakage, and diarrhea. SALINE LAXATIVES Saline laxatives are usually used to prepare patients for diagnostic bowel procedures and testing. They contain a magnesium cation or phosphate anion. Some believe that the nonabsorbed ion produces an osmotic effect, which increases the intraluminal fluid and thus increases the volume of stool. However, recent studies suggest that their method of action may be to stimulate the release of cholecystokinin, which stimulates small bowel motility and inhibits absorption of fluid and electrolytes from the small intestine. Saline laxatives can produce an evacuation within 2 to 6 hours if given orally or 15 minutes if given rectally. Oral administration should be accompanied by sufficient amounts of fluid to decrease holdover in the stomach and limit the possible effect of dehydration. Examples of these agents are magnesium citrate, milk of magnesia (magnesium hydroxide), magnesium sulfate, Phospho-soda (sodium phosphate and biphosphate), and Fleet enema (sodium biphosphate and phosphate). These agents should be used cautiously in patients with impaired renal function because magnesium and phosphate may cause electrolyte abnormalities. The sodium salts may cause congestive heart failure in susceptible patients. Electrolytes should be monitored in selected patients with use of these products. Additionally, enema preparations can cause rectal irritation. STIMULANT LAXATIVES Stimulant laxatives produce their effect by irritating the intestinal mucosa or by selective action on the enteric nervous system. This reduces the water absorption and increases secretions, probably through prostaglandins. They are extremely potent and should be used for short-term treat-
ment only. These are the most popular laxatives and the most likely to be abused. Long-term use may lead to cathartic colon syndrome (a dilated and atonic colon following extensive and prolonged use of laxatives), melanosis coli (dark pigmentation of the colonic mucosa), or neuronal degeneration. Classes of stimulant laxatives include anthraquinones (cascara, senna [Senokot], and aloe), polyphenolic derivatives (phenolphthalein [Feen-a-Mint, Correctol, Ex-Lax] and bisacodyl [Dulcolax, Carter’s Little Pills]), and castor oil. Oral and some rectal preparations are available for these medications. The anthraquinones and polyphenolic derivatives work in 6 to 8 hours. Short-term side effects include cramps, nausea, and abdominal pain. Castor oil works in 2 to 6 hours and is used mainly as a preparation for colonic procedures or radiologic studies. STOOL SOFTENER LAXATIVES Stool softeners exert a detergent-type effect through their hydrophilic and hydrophobic properties, which break down surface barriers, allowing water and lipids to enter the stool. This softens the stool and increases the fecal mass. Onset of action may take several days when administered orally because it may take that long for the softened stool to reach the rectum. Rectal administration produces an effect in 2 to 15 minutes. Examples include docusate calcium (Surfak), docusate potassium (Dialose, Kasof), and docusate sodium (Colace, Comfolax, Modane Soft). Preparations of these in combination with stimulant laxatives include Feen-a-Mint, Correctol, Peri-Colace, and Doxidan. These agents have been suggested to decrease jejunal absorption and to damage villi, resulting in increased absorption of substances, such as mineral oil and phenolphthaleins. However, no serious adverse action is usually seen if these agents are taken alone. Side effects include diarrhea and mild abdominal cramping. OTHER AGENTS Prokinetic agents enhance normal propulsive action of the bowel. Metoclopramide and domperidone have not been found to have significant colonic effects. Tegaserod maleate (Zelnorm) is an approved medical treatment for women with constipation-predominant IBS and chronic idiopathic constipation. The approved dosage is 6 mg twice a day and has been shown in randomized, double-blind, placebocontrolled trials to produce significant improvements in global assessment of relief and number of bowel movements. This 5-HT4 agonist triggers the release of neurotransmitters from sensory neurons stimulating peristalsis and secretion and may inhibit visceral sensitivity. Patients with intractable constipation may benefit from daily administration of liquid polyethylene glycol solutions, such as GoLYTELY or Colyte. A daily dosage of 8 to 16 oz has been shown to improve stool frequency in chronically constipated patients. Another form of polyethylene glycol (MiraLax) has been shown in placebo-controlled trials to increase bowel movement frequency. This medication is available in a powder form (17 g added to 8 oz of water) and may be useful for patients with slow-transit constipation. These compounds are not absorbed and do not cause a net ion gain or loss, thus are safe for patients with concerns of fluid overload or renal insufficiency.
Chapter 25
Neurotrophin-3 belongs to a family of protein growth factors known as neurotrophins. It plays an essential role in the development of the enteric nervous system. This medication was used in the treatment of neurologic disorders, including diabetic patients with peripheral sensory neuropathy. Incidentally, investigators noticed an association with an increase in the frequency of bowel movements and softening of stools. In 2003, Parkman et al. performed a randomized, double-blind, placebo-controlled study showing an increase in spontaneous, complete bowel movements and dose-related softening of stool and improved ease of passage in patients who met the ROME II criteria for functional constipation. Enemas or suppositories used on an intermittent basis may relieve some patients of constipation. Some patients find that daily tap water enemas eliminate their need for oral laxatives. Many suppository and enema preparations are available. If long-term enema use is considered, the tap water variety may be the least irritating to the rectal mucosa. Potential side effects of enemas include electrolyte depletion, water intoxication, and colonic perforation. A systematic review in 1997 performed by Tramonte et al. examined 36 randomized controlled trials, using 25 different laxative or dietary therapies. Seventy percent of these were done in women. Tramonte et al. reported data showing an increase in mean bowel movements per week from 3.5 to 5 (95%, CI 1.1–1.8). Nine of 11 trials showed improvement in symptoms, and 8 of 11 showed improvement in stool consistency. The data support using bulk laxatives in most patients with constipation. However, this is not necessarily true for certain populations, and which type of bulk laxative to use is unclear. A systematic review in 2001 by Kenny et al. assessed the effectiveness of dietary fiber in older adults with constipation. The authors concluded that no strong or consistent evidence exists for the effectiveness of treating constipation in institution-dwelling older adults with dietary fiber. A lack of evidence resulted, making it difficult to determine differences between classes of laxatives.
Biofeedback Patients with rectal evacuation problems manifested only by a hold-up of markers in the rectum during the colonic transit study as well as those patients with pelvic floor dyssynergia defecation disorders may benefit from pelvic floor training with biofeedback. Neither of these conditions responds to current surgical treatment, and medication therapy often is not effective. Biofeedback allows patients to be more aware and responsive to biologic information provided to them. Bassotti et al. (2004) reported that approximately 70% of patients with dyssynergic defecation are likely to benefit. However, most of the data are from a single center and uncontrolled. Many different treatment protocols are available, making comparison of results difficult. Success rates vary from 18% to 100%. However, because this treatment is painless and harmless and can have a reasonable chance of improvement in patients otherwise difficult to treat, biofeedback should be considered. An alternative approach to biofeedback and surgical therapy involves modifying the neural control of the lower bowel and pelvic floor through sacral nerve stimulation. Cases have been reported using this technique, and larger studies are anticipated.
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SURGICAL TREATMENT Surgical treatment is required for patients with constipation caused by Hirschsprung’s disease. Surgery is also considered for patients with idiopathic constipation in whom an adequate course of medical therapy has failed. However, Pemberton et al. (1991) found that only 15% of constipated patients referred to them fall into the category that may benefit from surgery. Preoperative evaluation is essential in determining which patients will benefit from surgery and which surgical procedure to perform.
Slow-Transit Constipation (Colonic Inertia) NORMAL SIZE COLON AND RECTUM Severely constipated patients with colonic inertia demonstrated on colonic transit studies, a normal caliber colon and rectum, and a normal defecography may benefit from colectomy. When properly selected, this group of patients experienced a 70% improvement with surgery. Operative choices include colectomy with ileosigmoid, ileorectal, or cecorectal anastomosis. Cecorectal anastomosis, preserving the ileocecal valve, seems preferable. However, persistent constipation may be slightly more common with cecorectal and ileosigmoid anastomoses than with ileorectal anastomosis. Despite the entire colon being removed, subsets of patients still have constipation and require enemas. In addition, diarrhea can be a new problem after surgery (seen in 30%) along with fecal incontinence (seen in 0% to 38%). Slow-transit constipation that coexists with paradoxical puborectalis muscle contractions creates a dilemma. Which problem should be treated first? Many favor biofeedback to treat the nonrelaxing puborectalis because the slow transit can be a result of the abnormal pelvic muscle problem. If patients respond and demonstrate relaxation of the puborectalis with straining, colectomy may be offered. Some surgeons would offer colectomy to those without demonstrated relaxation of the puborectalis, contending that the liquid stool resulting after colectomy is easier to pass and not as problematic for the patient. Dyssynergic defecation is seen preoperatively, biofeedback treatment is tried initially. Patients are counseled that this operation might not improve their constipation and will probably produce diarrhea. For patients with marginal sphincters detected on preoperative evaluation, an ileostomy may be a better option because of the diarrhea that can result from the colectomy. Even those with normal anal sphincters are warned about the possible postoperative problem of fecal incontinence. If abdominal pain and bloating are part of their preoperative constellation of symptoms, patients are warned that these may not improve after a colectomy. MEGACOLON AND MEGARECTUM In some patients with constipation, preoperative studies may demonstrate a megacolon and/or megarectum. Hirschsprung’s disease is initially ruled out. In patients with a megacolon and normal-sized rectum, colectomy with ileorectal anastomosis is the preferred treatment. In patients with a rectum more than 6.5 cm in diameter at the pelvic brim and a normal transit time, the Duhamel’s operation
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may be an option. (In this operation, the colon is removed and the rectal stump is closed. After presacral dissection, the posterior wall of the rectum is anastomosed to the end of the proximal bowel.) However, if the transit time is prolonged, a proctocolectomy and pelvic pouch are reasonable. Some advocate anorectal myomectomy to treat megarectum not associated with Hirschsprung’s disease. This procedure has been used successfully in the pediatric population, but more positive data are needed before this approach can be recommended in adults. LEFT COLONIC DYSFUNCTION In the select group of patients who exhibit delayed passage of markers in the left colon (i.e., distal to the splenic flexure), a left colectomy and proctectomy with low colorectal or coloanal anastomosis has been done. The proximal colon was preserved in an attempt to decrease diarrhea. Conflicting results regarding success have been reported in the literature and reflect only small numbers of patients studied. Additionally, it is unclear whether the patients had segmental or diffusely abnormal colonic transit studies. More data are needed to judge whether this is a viable option for patients with segmental colonic dysfunction.
Anorectal Outlet Obstruction DYSSYNERGIC DEFECATION Surgical division of the pelvic floor or sphincter muscles has been tried for nonrelaxing or paradoxical puborectalis contraction. However, long-term improvement is seen in few patients, and biofeedback has become the mainstay of treatment for this problem. RECTAL PROLAPSE Rectal prolapse or intussusception can be entirely internal (occult) or external and protrude through the anal sphincter complex. Patients with rectal prolapse and constipation should undergo a complete evaluation before surgery. If diffuse, slowtransit constipation is found, a colectomy with ileorectal anastomosis and rectopexy may be the procedure of choice. Patients with a normal transit and mild constipation may benefit from a sigmoid resection with a colorectal anastomosis and rectopexy. Chapter 27 more fully discusses this condition. RECTOCELE Defecatory dysfunction is commonly associated with rectoceles. This is a condition that results in the protrusion of the posterior vaginal wall and anterior rectal wall into the lumen of the vagina. Patients with a rectocele may complain of various symptoms during defecation, including straining, feeling of incomplete emptying often necessitating the need for digitation to complete a bowel movement, rectal pain, a protrusion from the vagina, and vaginal bulge. Although clinical examination has demonstrated good sensitivity in the detection of rectoceles, there seems to be no correlation between bowel function and the size of the rectocele. Thus, indications for surgical repair of rectocele are variable and not well defined. Because of this, investigators have attempted various tests to provide insight into important dynamic information that may or may not improve with surgery.
Defecography is useful in determining size and position of rectoceles, perineal descent, rectal intussusception, and pelvic floor dyssynergia. However, there are limitations using this imaging modality in patients with rectocele. For instance, data on whether size of a rectocele on defecography correlates with symptoms are conflicting. Although defecography is useful in evaluating how well a person evacuates the rectum, no correlation is found between women who retain contrast and symptoms of defecatory dysfunction or clinical outcome of surgical repair. Defecography may be useful in patients with pelvic floor dyssynergia, but the effects of this on the outcomes of rectocele repair are contradictory. Other studies, such as anorectal manometry, pudendal nerve terminal motor latency, endoanal ultrasonography, and colonic transit studies, have not been helpful in clarifying which patients may benefit from surgery for rectocele in the presence of disorders of evacuation. The approach to surgical repair of rectoceles is presented in Chapter 20. Outcomes of surgical intervention for rectocele suffer from a lack of standardized definitions in the literature. Gynecologists often operate on patients who suffer from the presence of a vaginal bulge or specific symptoms, such as splinting. A thorough history of symptoms of disordered defecation is often ignored, and classification of patients into standardized groups, such as the ROME criteria, is lacking. Although most authors report that constipation improves after surgical repair, the symptoms reported are not specific and do not provide insight into the mechanism of improvement because it appears that most symptoms do not necessarily correlate with anatomic severity. Table 25-1 illustrates the lack of standardized outcomes used for vaginal approaches to rectocele repair, resulting in a wide range of success rates. Investigators need to standardize subjective, anatomic, testing, and global satisfaction outcomes in this area.
CONCLUSION Constipation is a complex constellation of symptoms with unclear pathophysiology that can produce mild or incapacitating symptoms. History and physical examination initiate therapy. Further laboratory, anatomic, and functional testing depend on the history and physical examination and the response to initial therapy. The majority of patients can be helped with dietary improvements and increased fluid consumption. Some patients not helped by simple dietary measures may require laxatives. The bulk-forming laxatives (and dietary fiber) are probably safest for long-term use; however, randomized controlled data are lacking for their long-term effectiveness. For patients with continued constipation, in addition to fiber and bulk laxative supplementation, polyethylene glycol (MiraLax) may be added. Tegaserod maleate (Zelnorm) is effective in women with constipation-predominant IBS. This drug is also effective in the treatment of chronic idiopathic constipation. If constipation continues to be intolerable, the addition of stimulant laxatives on an intermittent basis may be needed, and it is recommended to proceed with physiologic testing or referral. Chronic use of stimulant laxatives should be tempered because of possible colonic neuronal degeneration (especially with the anthraquinones).
Chapter 25
Table 25-1
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Transvaginal Rectocele Repair Symptoms
Author (year)
No. of Patients
Preoperative (%)
Postoperative (%)
Arnold et al. (1990)
29
Constipation (75)
Mellegren et al. (1995)
25
Constipation (96) Rectal bleeding (16) Dyspareunia (4) Vaginal bulge (84) Constipation (22) Dyspareunia (18) Vaginal bulge (64) Constipation (41) Dyspareunia (28) Vaginal bulge (86) Constipation (60) Vaginal bulge (38)
Constipation (54) Anatomic cure (80) Constipation (88) Vaginal bulge (4)
Kahn and Stanton (1997)
231
Kenton et al. (1999)
66
Porter et al. (1999)
125
Glavind and Madsen (2000)
67
Lopez et al. (2001)
25
Paraiso et al. (2001)
102
Sand et al. (2001) Singh et al. (2003)
70 42
Cundiff et al. (2004)
69
Constipation (40) Dyspareunia (12) Vaginal bulge (100) Constipation (96) Dyspareunia (19) Vaginal bulge (84) Straining (76) Manual evacuation (45) Fewer than two bowel movements/week (13) Vaginal bulge (78) Constipation (46) Dyspareunia (29)
For patients unresponsive to these measures, further investigation is warranted using various imaging or physiologic tests. Behavioral or surgical therapy may be offered. Those with outlet-type constipation defecation disorders caused by dyssynergic defecation usually do not benefit from surgical therapy, and biofeedback is the mainstay of treatment for this group. Surgical intervention is mandated for patients with Hirschsprung’s disease and external rectal prolapse. Women with a rectocele present with complex clinical pictures often report mixed gynecologic and anorectal symptoms. Lack of standardized definitions and unclear data regarding testing modalities complicate the appropriate medical or surgical management in these patients.
Bibliography Altman D, Zetterstrom J, Lopez A, et al. Effect of hysterectomy on bowel function. Dis Colon Rectum 2004;47:502. Andorsky RI, Goldner F. Colonic lavage solution (polyethylene glycol electrolyte lavage solution) as a treatment for chronic constipation: a double-blind placebo-controlled study. Am J Gastroenterol 1990;85:261. Arnold MW, Stewart WR, Aguilar PS. Rectocele repair: four year’s experience. Dis Colon Rectum 1990;33:684. Bassotti G, Chistolini F, Sietchiping-Nzepa F, et al. Biofeedback for pelvic floor dysfunction in constipation. Br Med J 2004;328:393. Bharucha AE, Wald A, Enck P: Functional anorectal disorders. Gastroenterology 2006;130:1510. Binder HJ. Use of laxatives in clinical medicine. Pharmacology 1988;36(Suppl 1):226. Cerulli MA, Schuster MM. Medical treatment of constipation and fecal incontinence. In Phillips SF, Pemberton JH, Shorter RG, eds. The
Constipation (33) Dyspareunia (27) Vaginal bulge (24) Improved constipation (43) Dyspareunia (2) Vaginal bulge (9) Constipation (50) Vaginal bulge (14) Anatomic cure (82) Improved constipation (88) Dyspareunia (6) Vaginal bulge (0) Improved constipation (91) Dyspareunia (33) Vaginal bulge (4) Straining (45) Manual evacuation (8) Fewer than two bowel movements/week (6) Anatomic cure (90) Vaginal bulge (7) Anatomic cure (92) Constipation (13) Dyspareunia (19) Vaginal bulge (14)
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52 12 6 3 60 12
12 18 12
Large Intestine Physiology, Pathophysiology, and Disease. Raven, New York, 1991. Connell AM, Hilton C, Irvine G, et al. Variation of bowel habit in two population samples. Br Med J 1965;5470:1095. Cundiff GW, Weidner AC, Visco AG, et al. An anatomic and functional assessment of the discrete defect rectocele repair. Am J Obstet Gynecol 1998;179:1451. Cundiff GW, Fenner D. Evaluation and treatment of women with rectocele: focus on associated defecatory and sexual dysfunction. Obstet Gynecol 2004;104:1403. Dahl J, Lindquist BL, Tysk C, et al. Behavioral medicine treatment in chronic constipation with paradoxical anal sphincter contraction. Dis Colon Rectum 1991;34:769. De Groat WC. Central control of the lower urinary tract. In Neurobiology of Continence. CIBA Foundation Symposium 151. John Wiley & Sons, Chichester, UK, 1990, p. 32. De Looze D, Van Laere M, De Muynck M, et al. Constipation and other chronic gastrointestinal problems in spinal cord injury. Spinal Cord 1998;36:63. DiPalma JA, DeRidder PH, Orlando RC, et al. A randomized, placebo-controlled, multicenter study of the safety and efficacy of a new polyethylene glycol laxative. Am J Gastroenterol 2000;95:445. Drossman DA, Corazziari E, Talley NJ. Rome II. The Functional Gastrointestinal Disorders. Diagnosis, Pathophysiology and Treatment: a Multinational Consensus, 2nd ed. Degnon Associates, McLean, VA, 2000. Drossman DA, Sandler RS, McKee DC, et al. Bowel patterns among subjects not seeking health care. Gastroenterology 1982;83:529. Dubuc MB, Lahaie LC. Nutritive Value of Foods. National Library, Ottawa, 1987, pp. 16–158. Glavind K, Madsen H. A prospective study of the discrete fascial defect rectocele repair. Acta Obstet Gynecol Scand 2000;79:145. Goh JT, Tjandra JJ, Carey MP. How could management of rectoceles be optimized? ANZ J Surg 2002;72:896. Higgins PR, Johanson JF. Epidemiology of constipation in North America: a systematic review. Am J Gastroenterol 2004;241:750.
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Hinds JP, Eidelman BH, Wald A. Prevalence of bowel dysfunction in multiple sclerosis: a population survey. Gastroenterology 1990;98:1538. Hull TL, Milsom JW. Constipation: results of surgical therapy. In Brubaker LT, Saclarides TJ, eds. The Female Pelvic Floor: Disorders of Function and Support. FA Davis, Philadelphia, 1996. Jorge JM, Wexner SD, Ger GC, et al. Cinedefecography and electromyography in the diagnosis of nonrelaxing puborectalis syndrome. Dis Colon Rectum 1993;36:668. Kahn MA, Stanton SL. Posterior colporrhaphy: its effects on bowel and sexual function. BJOG 1997;104:82. Kelvin FM, Maglinte DD, Benson JT. Evacuation proctography (defecography): an aid to the investigation of pelvic floor disorders. Obstet Gynecol 1994;83:307. 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. Kenny KA, Skelly JM. Dietary fiber for constipation in older adults: a systematic review. Clin Effective Nurs 2001;5:120. Kenton K, Shott S, Brubaker L. Outcome after rectovaginal fascia reattachment for rectocele repair. Am J Obstet Gynecol 1999;191:1360. Longstreth GF, Thompson WG, Chey WD, et al. Functional bowel disorders. Gastroenterology 2006;130:1480. Lopez A, Anzen B, Bremmer S, et al. Durability of success after rectocele repair. Int Urogynecol J 2001;12:97. Mathers SE, Kempster PA, Law PJ, et al. Anal sphincter dysfunction in Parkinson’s disease. Arch Neurol 1989;46:1061. Mellegren A, Anzen B, Nilsson BY, et al. Results of rectocele repair: a prospective study. Dis Colon Rectum 1995;38:7. Miller R, Duthie GS, Bartolo DC, et al. Anismus in patients with normal and slow transit constipation. Br J Surg 1991;78:690. Minguez M, Herreros B, Sanchiz V, et al. Predictive value of the balloon expulsion test for excluding the diagnosis of pelvic floor dyssynergia in constipation. Gastroenterology 2004;126:57. Nicholls RJ, Kamm MA. Proctocolectomy with restorative ileo-anal reservoir for severe idiopathic constipation. Dis Colon Rectum 1988;31:968. Novick J, Miner P, Krause R, et al. A randomized, double blind, placebo controlled trial of tegaserod in female patients suffering from irritable bowel syndrome with constipation. Aliment Pharmacol Ther 2002;16:1877. Paraiso MF, Weber AM, Walters MD, et al. Anatomic and functional outcome after posterior colporrhaphy. J Pelvic Surg 2001;7:335. Parkman HP, Rho SS, Reynolds JC, et al. Neurotrophin-3 improves functional constipation. Am J Gastroenterol 2003;98:6. Pemberton JH, Rath DM, Ilstrup DM. Evaluation and surgical treatment of severe chronic constipation. Ann Surg 1991;214:403. Porter WE, Steele A, Walsh P, et al. The anatomic and functional outcomes of defect-specific rectocele repairs. Am J Obstet Gynecol 1999;181:1353. Prior A, Stanley KM, Smith AR, et al. Relation between hysterectomy and the irritable bowel: a prospective study. Gut 1992;33:814. Rao SS, Mudipalli RS, Stessman M. Investigation of the utility of colorectal function tests and Rome II criteria in dyssynergic defecation (Anismus). Neurogastroenterol Motil 2004;16(5):589. Samuelsson EC, Arne Victor FT, Tibblin G, et al. 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.
Sand PK, Koduri A, 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. Sandler RS, Drossman DA. Bowel habits in young adults not seeking health care. Dig Dis Sci 1987;32:841. Schouten WR, Gordon PH. Constipation. In Gordon PH, Nivatvongs S, eds. Principles and Practice of Surgery for the Colon, Rectum, and Anus. Quality Medical Publishing, St. Louis, 1992. Singh K, Cortes E, Reid WM. Evaluation of the fascial technique for surgical repair of isolated posterior vaginal wall prolapse. Obstet Gynecol 2003;101:320. Siproudhis L, Ropert A, Vilotte J, et al. How accurate is clinical examination in diagnosing and quantifying pelvirectal disorders? Dis Colon Rectum 1993;36:430. Sloan S. Medical management of constipation. In Brubaker LT, Saclarides TJ, eds. The Female Pelvic Floor: Disorders of Function and Support. FA Davis, Philadelphia, 1996. Sonnenberg A, Koch TR. Epidemiology of constipation in the United States. Dis Colon Rectum 1989;32:1. Stewart WF, Liberman JN, Sandler RS, et al. Epidemiology of constipation (EPOC) study in the United States: relation of clinical subtypes to sociodemographic features. Am J Gastroenterol 1999;94:3530. Tally NJ, Weaver AL, Zinsmeister AR, et al. Onset and disappearance of gastrointestinal symptoms and functional gastrointestinal disorders. Am J Epidemiol 1992;136:165. Ting KH, Mangel E, Eibl-Eibesfeldt B. Is the volume retained after defecation a valuable parameter at defecography? Dis Colon Rectum 1992;35:762. Tjandra JJ, Ooi BS, Tnag CL, et al. Transanal repair of rectocele corrects obstructed defecation if it is not associated with anismus. Dis Colon Rectum 1999;42:1544. Tramonte SM, Brand MB, Mulrow CD, et al. The treatment of chronic constipation in adults. A systematic review. J Gen Intern Med 1997;12:15. Van Dam JH, Ginai AZ, Gosseling MJ, et al. Role of defecography in predicting clinical outcome of rectocele repair. Dis Colon Rectum 1997;40:201. Van Dam JH, Schouten WR, Ginai AZ, et al. The impact of anismus on the clinical outcome of rectocele repair. Int J Colorectal Dis 1996;11:238. 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;42:204. Vickery G. Basics of constipation. Gastroenterol Nurs 1997;20:125. Wald A, Caruana BJ, Freimanis MG, et al. Contributions of evacuation proctography and anorectal manometry to evaluation of adults with constipation and defecatory difficulty. Dig Dis Sci 1990;35:481. Weber AM, Walters MD, Ballard LA, et al. Posterior vaginal prolapse and bowel function. Am J Obstet Gynecol 1998;179:1446. 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;182:1610. Wexner SD, Cheape JD, Jorge JM, et al. Prospective assessment of biofeedback for the treatment of paradoxical puborectalis contraction. Dis Colon Rectum 1992;35:145. Wexner SD, Daniel N, Jagelman DG. Colectomy for constipation: physiologic investigation is the key to success. Dis Colon Rectum 1991;34:851. Young FE, Heckler MM. Laxative drug products for over the counter human use: tentative final monograph. Fed Regist 1985;50:2124.
Rectovaginal Fistula and Perineal Breakdown
26
Mickey M. Karram
ETIOLOGIES OF RECTOVAGINAL FISTULA 331 Obstetric 331 Inflammatory Bowel Disease 332 Infection 332 Prior Anorectal Surgery 332 Cancer and Radiation Therapy 332 DIAGNOSIS AND PREOPERATIVE EVALUATION 332 SURGICAL TREATMENT 332 Preoperative Preparation 332 High Fistula Repair 333 Midlevel Fistula Repair 333 Low Fistula Repair 334 Fecal Diversion 335 PERINEAL BREAKDOWN 335 SUMMARY 337
Rectovaginal fistula is a congenital or acquired tract between the rectum and the vagina. The communication is lined with epithelium and may occur at any point along the vagina. Most fistulas actually arise in the anal canal distal to the pectinate line. Rectovaginal fistulas are classified according to their location and size; careful attention to both features allows determination of the approach for surgical repair. In a low rectovaginal fistula, the rectal opening is located close to the dentate line, with the vaginal opening just inside the hymen. In a high rectovaginal fistula, the vaginal opening is near the cervix (or apex of the vagina in a posthysterectomy patient); the communication into the intestinal tract may be located in either the sigmoid colon or rectum. These fistulas usually require a laparotomy for repair. Such fistulas may not be readily apparent on physical examination or endoscopy and may require contrast studies for diagnosis. A mid-rectovaginal fistula is found somewhere between the hymen and the cervix. Rectovaginal fistulas range in size from tiny (less than 1 mm in diameter) to large where the rectovaginal defect encompasses the entire posterior vaginal wall. A second method of classification is based on the underlying cause of the fistula, which will be a better predictor of the ultimate success of the repair, as it takes into
consideration the integrity of the local tissue and the health of the patient. A patient with a rectovaginal fistula is usually symptomatic. She most often complains of passage of flatus or stool through the vagina. Occasionally, the presenting complaint is a recurrent vaginal or bladder infection, the result of fecal soilage. A small fistula may be symptomatic only when loose or liquid stool is passed. Determining the status of the anal sphincter mechanism is important when the patient’s complaints are consistent with fecal seepage.
ETIOLOGIES OF RECTOVAGINAL FISTULA Many different causes of rectovaginal fistulas have been identified (Box 26-1); the cause varies with the location of the fistula. Congenital rectovaginal fistulas are rare and are not discussed here.
Obstetric Obstetric injuries are the most common cause of rectovaginal fistulas, occurring in up to 88% of fistulas in published series (Lowry et al., 1988). Episiotomy is commonly performed in the practice of obstetrics. Kozok (1989) reported that approximately 62% of vaginal deliveries in the United States required episiotomy (80% of nulliparous patients and 20% of multiparous patients). Approximately 5% of vaginal deliveries or 20% of episiotomies result in a rectal tear or anal sphincter disruption. Although the majority of perineal injuries are successfully repaired at the time of the delivery, dehiscence of an episiotomy repair can occur and is associated with infection, abscess, fistula, or sphincter disruption. Up to 1.5% of women who undergo an episioproctotomy develop a rectovaginal fistula. Such fistulas present either immediately postpartum from failed recognition of a fourth degree injury or 7 to 10 days following an apparently normal repair. Midline episiotomy with resulting third- or fourth-degree laceration produces the greatest risk for development of a rectovaginal fistula. Mediolateral episiotomy, more common in British obstetric practice, causes fewer tears into the rectum when
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CAUSES OF RECTOVAGINAL FISTULA
Congenital Obstetric Previous anorectal surgery Inflammatory bowel disease Infection Carcinoma Radiation Lymphoproliferative malignancy Endometriosis
compared with midline incision. Rectovaginal fistula following infection and dehiscence of an episiotomy most commonly occurs low in the rectovaginal septum but may extend much higher, especially in the case of a traumatic cloaca. Of paramount importance in these patients is an assessment of their degree of incontinence. Wise et al. (1991) noted that 27% of low rectovaginal fistulas had coexistent fecal incontinence, recommending a careful continence evaluation before embarking on a repair.
Inflammatory Bowel Disease Inflammatory bowel disease (IBD), specifically Crohn’s disease, is the second most common cause of rectovaginal fistulas and should be suspected in any instance where an attempt at repair has failed. Because ulcerative colitis is not a transmural disease, it usually does not cause such problems. Most commonly, a rectovaginal fistula from Crohn’s disease is located in the mid-rectovaginal septum. However, in patients with anorectal Crohn’s disease, a fistula can extend into the most distal aspect of the vagina or perineum. An anovaginal or rectovaginal fistula in Crohn’s disease is more likely to result in proctectomy or a defunctioning stoma than anal Crohn’s disease without rectovaginal fistula.
Infection The most common nonobstetric infection causing a rectovaginal fistula is a cryptoglandular abscess located in the anterior aspect of the anal canal. Extension of such an abscess into the vaginal wall can result in fistula formation. Other infectious processes that may fistulize into the vagina include lymphogranuloma venereum, tuberculosis, and Bartholin’s abscess. Acquired rectovaginal fistula may be an early manifestation of human immunodeficiency virus infection in girls. Colovaginal fistula can result from diverticulitis, is usually located near the vaginal apex or cuff, and usually occurs in women who are postmenopausal and have previously undergone hysterectomy.
Cancer and Radiation Therapy Rectovaginal fistulas can result from invasive cervical or vaginal cancer or from anal or rectal cancer. They also develop in up to 6% of women following pelvic irradiation for endometrial, cervical, and vaginal cancer and are dependent on the radiation dosage. Fistulas that present early, during radiation therapy, are more likely to be caused by destruction of the carcinoma, whereas fistulas that occur later are caused by radiation injury to the tissue. Late fistulas are commonly associated with a rectal stricture. In a patient with a history of pelvic cancer, determining whether the rectovaginal fistula is caused by recurrent cancer is critical. This often requires examination under anesthesia, with biopsies of the margins of the fistula. Rectovaginal fistulas caused by radiation usually occur within 2 years of the completion of the radiation. They are usually located in the mid or proximal vagina. Early warning signs of the development of a radiation-induced fistula include the passage of bright red blood per rectum, nonhealing rectal ulcerations, and anorectal pain.
DIAGNOSIS AND PREOPERATIVE EVALUATION During the history-taking process, determining whether there is a previous history of anorectal surgery, complicated vaginal deliveries, radiation therapy, or IBD is important. Determining the patient’s degree of continence is also important. The perineum and anus should be inspected and palpated. A bidigital examination is performed to palpate the thickness of the perineal body; the majority of rectovaginal fistulas will be appreciated during this maneuver. If the location of the fistula is not obvious with inspection and palpation, a vaginal speculum exam should be performed. Rigid proctoscopy may give information regarding the compliance of the rectum and health of the surrounding tissue. If necessary, the vagina can be filled with water, and the site of the fistula will show the escape of air bubbles. Also, a vaginal tampon can be placed after instilling methylene blue in the rectum. The tampon is withdrawn and inspected for blue staining after 15 to 20 minutes. If the previously described maneuvers still do not demonstrate a fistula, the fistula may be located in the upper rectum, and contrast studies are needed to establish the diagnosis. Vaginography with a water soluble contrast medium has a sensitivity of 79% to 100% (Bird et al., 1993; Giordano et al., 1996). A barium enema is not as sensitive in identifying the fistula but may provide general information as to the health of the colon. A computed tomography (CT) scan of the abdomen and pelvis, using gastrointestinal contrast, may be helpful because it may show contrast in the vagina.
SURGICAL TREATMENT Prior Anorectal Surgery Rectovaginal fistula can occur following surgeries that involve the posterior vaginal wall or the anterior rectal wall. These include procedures, such as vaginal hysterectomy, rectocele repair, hemorrhoidectomy, local excision of rectal tumors, and low anterior resection.
Preoperative Preparation Treatment of a rectovaginal fistula depends on the cause, location, and size of the fistula, as well as the condition of the involved tissues. Rectovaginal fistulas following obstetric trauma may spontaneously heal, whereas those associated
Chapter 26
with Crohn’s disease, cancer, or radiation injury have little chance of healing without surgical intervention. The tissues involved in a rectovaginal fistula should be given adequate time to heal following the acute injury. This allows maximum resolution of inflammation as well as a decrease in size of the fistula tract. Most authors recommend a waiting period of 8 to 12 weeks after the injury before attempting surgical repair, although immediate operative repair of a fourth-degree episiotomy dehiscence is recommended by some (Uygur et al., 2004). Fistulas associated with IBD are unlikely to heal if severe proctitis is present. Inflammation must be controlled by medical treatment, especially if the rectovaginal fistula is low because a reparative procedure is more likely to be successful if the proctitis has been controlled. For most rectovaginal fistulas, especially post-obstetric low fistulas, preoperative evaluation of the anal sphincter with transanal ultrasound should be considered. This allows clear visualization of the sphincter mechanism, which may be very useful in preoperative surgical planning. An assessment of a patient’s degree of fecal incontinence is critical, as a recent study noted that 48% of women with rectovaginal fistula have fecal incontinence (Tsang et al., 1998). Proctoscopy may also be necessary to evaluate for coexisting anorectal disease. Preoperative bowel preparation should be done for all patients. This reduces the fecal and bacterial load, reducing the risk of postoperative infection and dehiscence of repair. Perioperative antibiotics, both oral and intravenous, should be administered. Consideration should be given to the placement of intraoperative ureteral catheters when using a transabdominal approach to repair a rectovaginal fistula in a previously radiated pelvis. Several surgical techniques, alone or in combination, are used for the repair of rectovaginal fistulas. Approaches include transvaginal, transanal, perineal, and abdominal. Most postpartum rectovaginal fistulas are repaired transvaginally.
High Fistula Repair Most surgeons use a transabdominal approach for the repair of a high rectovaginal, or colovaginal, fistula. The cause of high fistulas is usually inflammatory, including diverticulitis and Crohn’s disease. Radiation injury, traumatic injury, and carcinoma must also be considered. Bowel resection with primary reanastomosis, using nondiseased tissue, is the most successful approach.
Midlevel Fistula Repair A midlevel rectovaginal fistula caused by trauma can be repaired successfully transrectally or transvaginally once local tissue inflammation has resolved. For the patient with an intact perineum, an intact external anal sphincter, and a fistula in the lower third of the vagina, most gynecologists would perform a transvaginal fistula excision and layered closure, whereas most colorectal surgeons would perform an endorectal advancement flap repair. Most of these fistulas are secondary to obstetric trauma occurring in the distal third of the vagina. The key to a successful repair is excision of the fistulous tract with a tension-free approximation of the edges of the defect. There
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should be excellent hemostasis, and perioperative antibiotics should be administered to decrease any potential for infection. The following is a description of a vaginal repair of a primary, nonirradiated rectovaginal fistula: 1. The surgeon’s nondominant index finger is placed in the rectum to aid in identification of the fistula to assess the extent of scarification (Fig. 26-1, A). A rectal finger will also facilitate dissection in the appropriate plane. 2. The initial incision depends on the anatomic location of the fistulous tract. A midline incision in the posterior vagina can be used to the level of the fistulous tract, or an inverted U perineal incision may also be beneficial in very low fistulas (Fig. 26-1, B). This allows easy mobilization of the posterior vaginal wall from the anterior rectal wall, as well as rebuilding a perineal body. If the external anal sphincter is intact, there is no reason to disrupt it. If the fistula is higher in the vagina and the perineum is intact, the incision can be made directly into the posterior vaginal wall, over and around the fistula. 3. With traction of the vaginal wall, and a finger in the rectum to provide support to the rectal wall, sharp dissection is used to mobilize the posterior vaginal wall from the anterior rectal wall (Fig. 26-1, C). 4. After the vaginal walls are widely mobilized, the entire fistula tract is excised (Fig. 26-1, D). The rectal wall is cut back until fresh edges are encountered, as noted by fresh bleeding. 5. With the surgeon’s index finger elevating the anterior rectal wall, an initial row of 3-0 or 4-0 delayed, absorbable sutures is placed. These sutures are best placed extramucosally and should include a portion the muscularis and submucosa (Fig. 26-1, E). 6. A second layer of inverted sutures is then placed; this inverts the first suture line into the rectum. Ideally, no sutures penetrate the rectal lumen (Fig. 26-1, F). 7. If possible, a third layer of sutures is placed by plicating the fascia of the posterior vaginal wall over the rectal closure. 8. The vaginal epithelium is closed and the perineum is reconstructed, if necessary. In the endorectal advancement flap procedure, the patient is prone with the hips elevated (Fig. 26-2, A). The fistula is identified through the anus, and a small probe may be used to follow the tract into the vagina (Fig. 26-2, B). A hemostatic solution of 0.5% lidocaine with 1:200,000 epinephrine may be injected submucosally. The rectal ostium is circumscribed by an incision placed 0.5 to 1 cm from the margins of the tract. A broad-based flap of mucosa, submucosa, and circular muscle is developed and advanced distally. Before suturing the flap over the fistula site, the epithelium-lined tract is excised, and the muscular wall of the rectum is reapproximated with absorbable suture (Fig. 26-2, C). The flap is then secured with interrupted absorbable sutures (Fig. 26-2, D). The vaginal side is left open to provide drainage of the surgical site. Several authors report a high rate of success with this approach, even when used for the treatment of rectovaginal fistula in the setting of Crohn’s disease. Care must be taken to ensure that the rectal mucosa is not advanced too far, creating a mucosal ectropion and “wet anus.”
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Figure 26-1 ■ Rectovaginal fistula repair in a patient with an intact perineum. A. A rectovaginal fistula present in the midportion of the posterior vaginal wall. B. The dashed line demonstrates the site of the posterior vaginal wall incision. C. The vaginal wall is mobilized off the anterior rectal wall. D. The fistulous tract is excised. The rectal wall is cut back until fresh edges are encountered.
If the rectovaginal fistula is caused by radiation, local repair is not likely to be successful; healing is impaired by radiation-induced vasculitis. Proctectomy may be required, and, if the anal sphincter mechanism is competent, a coloanal pull-through procedure or coloanal anastomosis can be performed. Proximal diversion of the fecal stream should accompany this technically demanding procedure. A more complex repair has been described by Bricker et al. (1986) but is not commonly used. It involves an onlay patch of wellvascularized intestine and has the advantage of requiring
only anterior mobilization of the rectum; the success rate of this surgery has been difficult to duplicate.
Low Fistula Repair Simple fistulotomy is the treatment of choice for low fistulas lying distal to the anal sphincter mechanism. Caution must be taken when considering a fistulotomy near the anterior anal sphincter mechanism because even a normal sphincter mechanism is attenuated in this region.
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Figure 26-1 ■ Cont’d E. Extramucosal closure of the anterior rectal wall with interrupted, fine, delayed, absorbable sutures. F. The second layer imbricates the muscular portion of the wall of the rectum over the initial layer. The repair is completed by plicating the rectovaginal fascia and closing the posterior vaginal wall.
For rectovaginal fistulas in the lower third of the vagina, especially those that have followed obstetric trauma and have resulted in a damaged perineal body and anal sphincter mechanism, most gynecologists favor conversion of the fistula to an episioproctotomy followed by layered closure. This is done with the patient in supine position via a perineal approach and was described by Nichols (1993). Episioproctotomy permits excision of the entire fistulous tract followed by repair similar to that of a fresh fourth-degree perineal laceration. The technique requires transection and reunification of the external anal sphincter and the lower part of the internal sphincter. An overlapping or end-to-end external anal sphincteroplasty would be required to treat the anal incontinence. A risk of fistula recurrence is present as well as anal incontinence, if the healing is imperfect. For low fistulas above the external anal sphincter, as for lower midlevel fistulas, the approach favored by many colorectal surgeons is transanal repair using an endorectal advancement flap (Fig. 26-2). Repair from the rectal side has the advantage of correction of the defect from the highpressure side, perhaps resulting in less frequent failure of repair. The endorectal advancement flap also has the benefit of the interposition of healthy tissue, which is beneficial in the repair of both complex and recurrent fistulas. The benefit
of a transperineal approach, which would be performed by most gynecologists, is that the perineum can be more appropriately reconstructed.
Fecal Diversion Diversion of the fecal stream is sometimes required to allow adequate healing of the rectovaginal septum. Construction of a stoma is rarely necessary before attempt at primary repair. However, if perineal sepsis is severe, early diversion of the fecal stream may be necessary. Diversion of the fecal stream by construction of a proximal stoma should also be considered following a complex repair of rectovaginal fistula, such as a coloanal anastomosis, a Bricker onlay-type repair, or myofascial grafting. In addition, if previous attempts at repair of a rectovaginal fistula have failed, consideration should be given to construction of a stoma before an additional attempt at surgical reconstruction.
PERINEAL BREAKDOWN Perineal tears are most commonly classified in the following fashion: first-degree is a laceration of the vaginal epithelium
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Figure 26-2 ■ Technique of endorectal advancement flap procedure. A. The patient is placed in prone position with the hips elevated in preparation for a low or midlevel rectovaginal fistula repair. B. With the patient in prone position, the anal speculum is placed posteriorly. The rectovaginal fistula is identified by placing a small probe from the anus into the vagina. The dotted line outlines the incision in the rectal mucosa used to develop the advancement flap. C. The epithelium-lined fistula tract is excised, and the muscular wall of the rectum is reapproximated with absorbable suture. The rectal advancement flap has been mobilized and is ready to be placed over the site of the fistula repair. D. The flap is secured with interrupted absorbable sutures.
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or perineal skin only; second-degree is first-degree with involvement of the perineal muscles and fascia, but not the anal sphincters; third-degree is disruption of the skin, mucous membrane, perineal body, and anal sphincter muscles; and fourth degree is a third-degree tear with disruption of the anal mucosa. The biggest problem with this classification is that it does not incorporate the depth of the external sphincter rupture or involvement of the internal sphincter. If a third-degree tear is incorrectly classified as a seconddegree tear, inappropriate repair could result in suboptimal outcomes. Sultan (2002) has thus proposed that third-degree tears be subclassified into less than 50% thickness of the external sphincter torn, greater than 50% thickness of the external thickness torn, or internal sphincter torn also. Perineal tears most commonly occur at the time of delivery. Although liberal use of episiotomy is not beneficial, the ideal episiotomy rate remains to be established. Midline episiotomy is definitely associated with an increased risk of extension of the laceration to the anal sphincter. To date, unfortunately, there is no consistent, mutually agreed upon approach to reparative techniques is known for obstetric anal sphincter injury. Ultimately, more focused and intensive training of physicians and midwives in perineal anatomy and repair is imperative. Perineal lacerations can occur acutely at the time of delivery or may present more chronically many months or even years after delivery. Most cases of long-standing perineal laceration with disruption of the anterior anal sphincter complex lead to anal incontinence. The severity of symptoms varies with the degree of perineal laceration and sphincter loss. If the puborectalis portion of the levator muscle is well innervated and functional, it will provide some muscular contraction to permit control of feces. These patients often teach themselves a diet that will maintain their stools on the solid side. The technique for appropriate episiotomy repair at the time of delivery should involve complete reconstruction of the perineal body with reapproximation of the external and internal anal sphincters. Either an end-to-end or overlapping sphincteroplasty is appropriate. If the repair at the time of delivery breaks down, traditionally, a second attempt should be deferred for a minimum of 8 weeks to provide sufficient time for resolution of the inflammatory response and return of adequate blood supply to the margins of the defect. Some surgeons have advocated an earlier repair so that the patient can avoid 2 months of uncomfortable symptoms (Uygur, 2004). If the entire perineal body is disrupted, including the internal and external anal sphincters, and the posterior vaginal wall heals directly to the anterior rectal wall above the level of the hymenal ring, the patient is said to have a cloacal deformity (Fig. 26-3). Several techniques have been described for reconstruction of a complete, chronic perineal laceration. They include a layered repair, the Warren’s flap procedure, and the Noble-Mengert-Fish operation. Most commonly, a layered method of repair is performed. The following is the technique for a layered closure of a complete perineal laceration that requires a sphincteroplasty: 1. A transverse or inverted-U perineal incision is made at the junction of the posterior vaginal wall and anal mucosa (Fig. 26-3, A). The incision is extended far enough laterally to access the retracted external sphincter.
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2. A midline incision is then made up along the posterior vaginal wall. Sharp dissection is used to completely mobilize the posterior vaginal wall from the anterior wall of the rectum. Any scar tissue is excised. 3. Any defect in the anal mucosa is closed with interrupted No. 3-0 delayed, absorbable sutures. 4. The edges of viable external anal sphincter are many times identified with the help of a nerve stimulator of lowvoltage cautery. The thickened, downward continuation of the circular, smooth muscle layer of the rectum, which is the internal anal sphincter, appears as a white, smooth layer of tissue between the anorectal mucosa and the external anal sphincter (Fig. 26-3, B). 5. The external anal sphincter is brought together in an endto-end fashion with interrupted No. 0 or 2-0 delayed, absorbable sutures. We prefer to incorporate small bites of the internal anal sphincter in these sutures to reapproximate the internal anal sphincter as well (Fig. 26-3, B). Reapproximating this layer over a length of 3 to 5 cm is important because the internal sphincter is responsible for most of the resting pressure, in what is normally a 4cm high pressure zone in the anal canal. Also, reapproximating the external sphincter in this fashion will close off dead space and decrease any tension on the mucosal layer if the repair involved closure of the anal mucosa. If the defect is small or the external anal sphincter is easily mobilized, an overlapping sphincteroplasty can be considered as well. 6. Once the sphincter is reapproximated, the remainder of the perineal reconstruction should involve further support and elevation of the perineal body by bringing together the disrupted ends of the superficial transverse perineal muscles and bulbocavernosus muscles. At times, because of a widened genital hiatus, a distal levatorplasty can be considered by bringing the puborectalis muscles closer together. One must remember that the arms of the puborectalis muscle do not normally come in contact with each other between the rectum and the vagina, so overzealous plication must be avoided because it can create posterior tissue banding that will lead to dyspareunia. At completion of the repair, the posterior vaginal wall should be perpendicular to the perineal body (Fig. 26-3, C).
SUMMARY Rectovaginal fistula can be congenital or the result of trauma, IBD, carcinoma, radiation, or infection. Most rectovaginal fistulas seen by gynecologists follow traumatic obstetric delivery. The cause, location, and size of the fistula, as well as the competence of the anal sphincter mechanism, must be determined before repair. Repair of fistula resulting from obstetric trauma has a high rate of success, but those from other causes are more difficult to cure and frequently require consultation with a colorectal surgeon. Several different approaches to surgical repair have been described; the best approach is determined by the location, size, and cause of the fistula.
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Figure 26-3 ■ Technique of repair of complete perineal breakdown. A. A cloacal defect is noted in which the posterior vaginal wall and the anterior wall of the rectum are fused. An inverted-U or transverse incision is made (inset). B. The rectovaginal space has been opened, and the posterior vaginal wall has been dissected away from the anterior wall of the rectum. The retracted ends of the external anal sphincter have been identified. Sutures incorporate small bites through the internal anal sphincter as they are passed to the opposite side. The completed end-to-end sphincteroplasty is shown (inset). C. The perineum has been completely reconstructed. The completed repair should show a perpendicular relationship between the posterior vaginal wall and the rebuilt perineum. Note, the anal opening becomes puckered and is no longer patulous.
Bibliography Allen-Mersh TC, Wilson EJ, Hope-Stone HF. The management of late radiation-induced rectal injury after treatment of carcinoma of the uterus. Surg Gynecol Obstet 1987;164:521. Bird D, Taylor D, Lee P. Vaginography—the investigation of choice for vaginal fistulae. Aust N Z J Surg 1993;63:894. Borgstein ES, Broadhead RL. Acquired rectovaginal fistula. Arch Dis Child 1994;71:165. Bricker EM, Kraybill WG, Lopez MJ. Functional results after postirradiation rectal reconstruction. World J Surg 1986;10:249.
Chew SS, Rieger NA. Transperineal repair of obstetric related anovaginal fistula. Aust N Z J Obstet Gynecol 2004;44:68. Coats PM, Chan KK, Wilkins M, et al. A comparison between midline and mediolateral episiotomies. Br J Obstet Gynaecol 1980;87:408. Froines EJ, Palmer DL. Surgical therapy for rectovaginal fistulas in ulcerative colitis. Dis Colon Rectum 1991;34:925. Fry RD, Kodner IJ. Rectovaginal fistula. Surg Ann 1995;27:113. Giordano P, Drew PJ, Taylor D, et al. Vaginography—investigation of choice for clinically suspected fistulas. Dis Colon Rectum 1996;39:568. Goligher JC. Rectovaginal fistula. In Goligher JC, ed. Surgery of the Anus, Rectum and Colon, 4th ed. Spottiswoode Ballantyne, London, 1980.
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Greenberg JA, Lieberman E, Cohen AP, Ecker JL. Randomized comparison of chronic versus fast-absorbing polyglactin 910 for postpartum perineal repair. Obstet Gynecol 2004;103:1308. Homsi R, Daikoku NH, Littlejohn J, et al. Episiotomy: risks of dehiscence and rectovaginal fistula. Obstet Gynecol Surv 1994;49:803. Howard D, DeLancey JO, Burney RE. Fistula-in-ano after episiotomy. Obstet Gynecol 1999;93:800. Kimose H, Fischer L, Spjeldnaes N, et al. Late radiation injury of the colon and rectum: surgical management and outcome. Dis Colon Rectum 1989;32:684. Kodner IJ, Mazor A, Shemesh EI, et al. Endorectal advancement flap repair of rectal, vaginal, and other complicated anorectal fistulas. Surgery 1993;114:682. Kozok LJ. Surgical and non-surgical procedures associated with hospital delivery in the United States: 1980–1987. Birth 1989;16:209. Legino LJ, Woods MP, Rayburn WF, et al. Third and fourth degree perineal tears. Fifty years’ experience at a university hospital. J Reprod Med 1988;33:323. Lowry AC, Thorsen AG, Rothenberger DA. Repair of simple rectovaginal fistulas: influence of previous repairs. Dis Colon Rectum 1988;31:676. Nichols DH. Repair of rectal fistula and of old complete perineal laceration. In Nichols DH, ed. Gynecologic and Obstetric Surgery. Mosby, St. Louis, 1993. Nowacki MP. Ten years of experience with Park’s coloanal sleeve anastomosis for the treatment of post-irradiation rectovaginal fistula. Eur J Surg Oncol 1991;17:563. Parker SL, Thorsen A. Fecal incontinence. Surg Clin North Am 2002;82:1273.
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Radcliffe AG, Ritchie JK, Hawley PR, et al. Anovaginal and rectovaginal fistulas in Crohn’s disease. Dis Colon Rectum 1988;31:94. Rahman MS, Al-Sulerman SA, El-Yahia AR, Rahman J. Surgical treatment of rectovaginal fistula of obstetric origin: a review of 15 years experience in a teaching hospital. J Obstet Gynecol 2003;6:607. Saclarides TJ. Rectovaginal fistula. Surg Clin North Am 2002;82:1261. Scott NA, Nair A, Hughes LF. Anovaginal and rectovaginal fistula in patients with Crohn’s disease. Br J Surg 1992;79:1379. Snyder RR, Hammond TL, Hankins GD. Human papilloma virus associated with poor healing of episiotomy repairs. Obstet Gynecol 1990;76:664. Sultan AH, Thakar R. Lower genital tract and anal sphincter trauma. Clin Obstet Gynecol 2002;16:99. Thacker SB, Banta HD. Benefits and risks of episiotomy: an interpretive review of the English language literature, 1860–1980. Obstet Gynecol Surv 1983;38:322. Tsang CB, Mudoff RD, Wong RD, et al. Anal sphincter integrity and function influences outcome in rectovaginal fistula repair. Dis Colon Rectum 1998;41:1141. Uygur D, Yesildaglar N, Kis S, Sipahi T. Early repair of episiotomy dehiscence. Aust N Z J Obstet Gynecol 2004;44:244. Veronikis DK, Nichols DH, Spira C. The Noble-Mengert-Fish operation revisited: a composite approach for persistent rectovaginal fistulas and complex perineal defects. Obstet Gynecol 1998;179:1411. Wise WE, Aguilar PS, Padmanabtan A, et al. Surgical treatment of low rectovaginal fistulas. Dis Colon Rectum 1991;34:271. Yee LF, Birnbaum EH, Read TE, et al. Use of endoanal ultrasound in patients with rectovaginal fistulas. Dis Colon Rectum 1999;42:1057.
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Rectal Prolapse Alexander G. Heriot and Feza H. Remzi
ETIOLOGY 340 PATHOPHYSIOLOGY 340 EPIDEMIOLOGY 341 CLINICAL FEATURES 341 EVALUATION 341 COMMON SURGICAL REPAIRS FOR PROLAPSE 342 Perineal Repairs 342 Transabdominal and Laparoscopic Repairs 345 OUTCOME AND CHOICE OF PROCEDURE 348
Rectal prolapse is full-thickness intussusception of the rectum toward and sometimes through the anal canal (Fig. 27-1). It can be internal (occult) or external to the anal sphincters and has been known for centuries and described in the medical literature; however, its cause is still unclear. Various operations have been described in the literature, but types of treatment and surgical approach still vary significantly from one institution to another. In this chapter we will discuss the etiology, epidemiology, clinical features, evaluation, common surgical techniques, results, and our experience regarding rectal prolapse.
ETIOLOGY “It is interesting to note that we still know so little about the cause of such a common condition.” —Hugh Lockhart-Mummery, St. Marks’ Hospital, London, 1972 Although some questions have been answered, many aspects of rectal prolapse remain undetermined. Two main theories are known regarding the etiology of prolapse. In 1912, Moschcowitz proposed that rectal prolapse was a sliding hernia that protrudes through a defect in the pelvic fascia at the level of the anterior rectal wall. In 1968, a second theory was proposed by Broden and Snellman, who demonstrated with cinedefecography that full-thickness prolapse starts as an internal intussusception of the rectum with a lead point proximal to the anal verge. This theory was reinforced by
Theuerkauf et al. (1970), who used radiopaque markers applied to the rectal mucosa to demonstrate prolapse secondary to intussusception. Today, rectal intussusception is accepted as the mechanism of rectal prolapse. Various anatomic pathologies related to prolapse include a deep peritoneal cul-de-sac or pouch of Douglas, enterocele, loss of posterior rectal fixation, a patulous anal sphincter, diastasis of the levator ani, redundant rectum and sigmoid colon, and loss of the rectum’s horizontal position, with attenuation of its sacral and pelvic attachments. The ideal rectal prolapse repair should correct as many of these abnormalities as possible. To attain this goal, each abnormality is not addressed individually but addressed in unity by repairing the intussusception itself.
PATHOPHYSIOLOGY Up to 75% of patients with rectal prolapse are incontinent of stool. The precise pathophysiology behind incontinence is not completely defined, although some causative factors have been identified. Parks et al. (1977) demonstrated histologic evidence of denervation in pelvic muscle biopsies taken from patients who underwent postanal repair, the majority of whom also had rectal prolapse. This finding was confirmed by Neill et al. (1981), who performed electromyographic (EMG) studies of pelvic floor musculature and found denervation in incontinent patients, with and without rectal prolapse, but not in continent patients with rectal prolapse. Some patients with rectal prolapse have abnormal rectal sensation, which may improve following repair. Rectal prolapse itself may directly traumatize the anal sphincters. Anal resting pressures improve in some patients following prolapse surgery. Constipation affects between 30% and 67% of patients with rectal prolapse. Constipation may be caused by intussusception of the rectum, colonic dysmotility, slow transit, or inappropriate puborectalis contraction. Prolapse repairs may increase or decrease constipation. Speakman et al. (1991) noted that division of the lateral ligaments during surgery appears to increase postoperative constipation, although whether it is due to colonic denervation remains uncertain.
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Clinic, Tjandra et al. (1993) reported that 18% of patients with prolapse reported straining and 42% had constipation, consistent with the range of 15% to 65% reported in the literature. Solitary rectal ulcer was found in 12% of patients with rectal prolapse. Previous gynecologic surgery is reported with rectal prolapse; we found that 35% of our patients had undergone a previous hysterectomy, and 38% of our patients were incontinent. A complete assessment of female patients with rectal prolapse should include evaluation for constipation, urinary and fecal incontinence, and other pelvic floor disorders, such as rectocele, cystocele, and enterocele. Staged or combined surgical correction of pelvic floor disorders may be needed for resolution of the patient’s symptoms.
EVALUATION
Figure 27-1 Full-thickness rectal prolapse protruding through the anal canal. (Reprinted with the permission of The Cleveland Clinic Foundation.) ■
EPIDEMIOLOGY The incidence and prevalence of rectal prolapse are unknown. It occurs at the extremes of age. Rectal prolapse can be seen in children less than age 3, where malnutrition and cystic fibrosis appear to be predisposing factors. Gender distribution is equal in children. Conservative management is usually successful in treating children with rectal prolapse. In adults, rectal prolapse is more common in women, with a 6:1 female-to-male ratio. Although rectal prolapse can be seen in nulliparous women, it is more common in multiparous women, in whom peak prevalence is after the fifth decade. Men are equally distributed throughout all age groups.
CLINICAL FEATURES Patients with rectal prolapse usually present with fecal soilage, prolapse of tissue through the anal sphincter complex, mucous discharge, and bleeding. The prolapse is covered with mucosa that can secrete a significant amount of mucus, leading to perianal excoriation and itching. Bleeding is caused by trauma or mucosal venous congestion. Patients with internal (occult) prolapse experience incomplete evacuation of rectal contents, tenesmus, and rectal pain. Rectal prolapse is associated with comorbidities, including senile dementia, neurologic disorders, infectious disorders, connective tissue disorders, and bulimia nervosa. In addition, rectal prolapse is associated with straining, constipation, previous gynecologic surgery, and anal incontinence. Straining (or other unknown anatomic abnormalities) in men and younger women may push the anterior wall of the upper rectum against the anal canal and cause trauma, leading to ulceration, irritation, and bleeding. This is known as solitary rectal ulcer. At the Cleveland
Evaluation of patients with rectal prolapse starts with a thorough history and physical examination. The evaluation is important in confirming the diagnosis and in providing information important to decision making for the surgical alternatives. Age, level of activity, comorbid conditions, and living conditions are important issues in determining the type of surgery for an individual. A careful neurologic, obstetric, and surgical history, including hysterectomy and previous prolapse repairs, should be taken in all women. Symptoms related to fecal and urinary incontinence and constipation should be sought. Occasionally, rectal prolapse is not externally visible on initial examination. A Fleet enema along with straining on the commode may be needed to reproduce the prolapse. Differentiating between full thickness rectal prolapse and hemorrhoidal prolapse is important. A thorough anorectal examination starts with inspection of the perianal skin, looking for signs of excoriation from itching or mucous soiling. The anocutaneous reflex should be tested. Digital anorectal examination includes an assessment for anal sphincter defects, along with resting and squeeze pressures. Occasionally, the prolapsing segment can be felt on digital examination. Associated vaginal prolapse, such as rectocele (posterior vaginal prolapse), cystocele (anterior vaginal prolapse), or enterocele (prolapse of small intestine, usually at the vaginal apex or posterior vagina), should be sought. Proctoscopy or flexible sigmoidoscopy is needed to exclude the possibility of a neoplasm and allows the opportunity to perform a biopsy on ulcers or other localized inflammation. Because a significant portion of patients with prolapse have associated constipation, incontinence, or other pelvic floor disorders, it is worthwhile to include certain investigational tools in the workup of these patients, if needed. Such tools could include colon transit marker study, defecography, or anal manometry. These must be individualized, however; patients without associated symptoms may not require any further workup besides proctoscopy. Colonic transit marker studies may be important in patients with severe constipation. This test measures the time it takes for markers to traverse the colon. After patients swallow a set number of radiopaque markers, serial abdominal radiographs evaluate passage of these markers. Patients with
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prolonged colon transit time may benefit from colon resection with rectal preservation and rectopexy. When outlet obstruction or pelvic support disorders are suspected, defecography may be obtained. It may show that the sigmoid colon prolapses into the anal canal with straining, or it may show internal (occult) intussusception that does not go through the anal canal. Anal manometry can be used to evaluate fecal incontinence. Matheson and Keighley (1981) found normal anal pressures in continent patients with rectal prolapse; however, incontinent patients had decreased resting and squeeze anal pressures. Many patients with prolapse-associated fecal incontinence have nerve damage believed to be due to traction injury of the pudendal nerves caused by the rectal prolapse. Continent prolapse patients may not show manometric or EMG signs of denervation. Anal manometry may identify patients who will have improved fecal continence after prolapse repair. Studies from Yoshioka et al. (1989) and Williams et al. (1991) showed that patients who remained incontinent after rectal prolapse repair had significantly lower preoperative resting and squeeze pressures than those whose incontinence improved postoperatively. Other studies, however, dispute the predictive value of anorectal physiology tests. Thus, anal manometry gives preoperative information that may identify patients who will have better outcomes but frequently does not change the clinical approach to the patient.
COMMON SURGICAL REPAIRS FOR PROLAPSE “I have traced in the literature between 30 and 50 operations for prolapse of the rectum and would like to add still one more.” —Charles Wells, 1959 This comment by Wells of the wide variety of operations for rectal prolapse is a reflection that there is no perfect procedure. Decisions about the appropriate procedure depend on surgical morbidity, risk of recurrence, and consideration of function, including fecal incontinence and constipation. The type of surgical procedure is determined by patient characteristics, such as age, comorbid condition(s), degree of prolapse, and associated pelvic disorders. The goals of surgery are to treat the prolapse and to address associated constipation or incontinence. The multiple procedures for rectal prolapse can be classified into two main categories: perineal and transabdominal repairs. Perineal repairs are less invasive and cause less morbidity for patients. They are favored for frail elderly patients, but some institutions favor perineal repairs for their healthy patients too. The perineal approach carries the risk of infection and possible complications related to the suture line or wound. Alternatively, abdominal operations are favored by some because prolapse recurrence is less than with perineal procedures. However, the abdominal approach may have complications, such as anastomotic leak, abdominal sepsis, stricture, and adhesions, and usually requires general anesthesia. Therefore, the abdominal approach is reserved for patients who can tolerate laparotomy. The introduction of laparoscopy in the last decade has added a new dimension to
prolapse surgery and is showing promise in reducing postoperative recovery time after abdominal repairs. Our preference for all repairs is to have patients undergo full mechanical bowel preparation. We give perioperative intravenous antibiotics, such as 500 mg metronidazole and a second-generation cephalosporin. For patients allergic to these medications, alternative broad spectrum antibiotics are used to provide prophylaxis against enteric organisms. All patients have a Foley catheter for bladder drainage and pneumatic compression stockings during prolapse surgery.
Perineal Repairs DELORME PROCEDURE Although the Delorme procedure was first described in 1900, it was not commonly used until Uhlig and Sullivan reported their experience in 1979. Because the technique is simple and can be done under regional or local anesthesia, it is considered optimal for severely debilitated patients. We prefer to perform the operation with the patient in the prone jackknife position; however, it can also be done in lithotomy position. After the patient is positioned, the perineum and vagina are prepared with an aseptic solution. We use sutures applied in four places around the perianal skin to evert the anus. Other surgeons prefer retractors, such as Lone Star or Hill Ferguson, or Pratt bivalve speculums to enhance visualization. The operation is begun by injecting 1:100,000 epinephrine solution circumferentially into the submucosal plane just proximal to the dentate line. This delineates the dissecting plane and diminishes blood loss. Using electrocoagulation, the dissection starts in a circumferential manner 1 to 1.5 cm above the dentate line (Fig. 27-2), creating a plane between the submucosa and the internal anal sphincter. Once this plane is started, the free edge of mucosa and submucosa is tagged with sutures for ease in handling and creating traction for easier dissection. Continuing in a circumferential direction and using liberal amounts of injectable saline in the plane between the submucosa and the muscular cuff, the surgeon uses scissors to divide the attachments (we prefer fistula scissors) and to deliver the submucosa and mucosal cuff out of the rectum and anus. Penetrating blood vessels encountered during the dissection can be treated with electrocoagulation. Maintaining strict hemostasis is important during the dissection to avoid hematomas after the procedure. The dissection continues until the rectal mucosa cannot be pulled down any further. Usually, 10 to 15 cm can be mobilized. During this phase of the operation, we use copious amounts of antibiotic solution, such as tetracycline, to irrigate the surgical field. After the dissection is completed, the rectal muscle is plicated with suture, such as No. 2-0 Polyglactin 910 suture on a UR-6 needle (Vicryl; Ethicon, Inc., Somerville, NJ). A total of eight sutures are spaced circumferentially for this plication. The dissected mucosa is excised, and the proximal line of resection is approximated to the distal incision line. Interrupted sutures of No. 2-0 Vicryl on a UR-6 needle work well for this circumferential suture line (Fig. 27-3). Prolapse recurrence after the Delorme procedure varies from 6.8% to 22% in different series. The procedure is well tolerated in high-risk patients. Fecal incontinence improves in 44% to 83%, perhaps due to the rectal muscular wall
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plication that creates a bulky, doughnut-like circumferential mass around the upper anal canal. Worsened constipation has not been reported. ALTEMEIER PROCEDURE (PERINEAL RECTOSIGMOIDECTOMY)
Figure 27-2 ■ Incision for a Delorme procedure 1 to 1.5 cm above the dentate line. The incision goes initially through the mucosa and submucosa, stripping the tube from the underlying internal anal sphincter and, more proximally, from the rectal muscular cuff. (Reprinted with the permission of The Cleveland Clinic Foundation.)
Figure 27-3 ■ Completed Delorme procedure. Notice that the rectal wall is plicated with sutures in an accordion-type fashion and is situated above the anal sphincters. The anastomosis is just above the dentate line. (Reprinted with the permission of The Cleveland Clinic Foundation.)
Perineal rectosigmoidectomy was first described in 1889 by Mikulicz. In 1952 and in 1971, Altemeier et al. described excellent results in debilitated elderly patients. Many feel that perineal rectosigmoidectomy is the preferred procedure for incarcerated or gangrenous prolapse. The Altemeier procedure removes the rectum via the perineal approach. A potential disadvantage is loss of the rectal reservoir. Additionally, in patients who have undergone previous rectal or sigmoid resections, care must be exercised in performing this operation because the inferior mesenteric vessels may have been previously ligated, and the blood supply to this area may have been altered. The Altemeier procedure can be performed with the patient in either lithotomy or prone jackknife position and under general or regional anesthesia. We prefer the patient to be placed in the prone jackknife position because illumination of the pelvis is superior, and it allows all assistants to see the field. First, the prolapse is recreated by gentle traction with Allis or Babcock clamps. The submucosa is injected with 1:100,000 epinephrine solution. A circumferential incision is made 1.5 to 2.0 cm above the dentate line (Fig. 27-4), with electrocautery or scalpel. The incision is deepened through the muscular layer until perirectal fat is encountered (Fig. 27-5). Mesorectal vessels are ligated (Fig. 27-6), proceeding in a circumferential manner. As the dissection continues in the cephalad direction, a hernia sac may be encountered anteriorly and opened, and the abdominal cavity may be entered. When no additional bowel can be delivered without tension, the bowel is marked, and this will become the line of transection. At this stage, particularly in incontinent patients, a levatorplasty can be performed by anteriorly placing sutures, such as No. 2-0 polypropylene suture (Prolene; Ethicon, Inc., Somerville, NJ), to loosely approximate the levators (Fig. 27-7). Some surgeons prefer to also place
Figure 27-4 ■ Altemeier procedure (perineal proctosigmoidectomy). An incision is made with the Bovie or knife (as shown here) 1 to 1.5 cm above the dentate line. Note that the patient is depicted in the prone jackknife position. (Reprinted with the permission of The Cleveland Clinic Foundation.)
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Figure 27-5 ■ The incision for the perineal proctosigmoidectomy divides all layers of the rectal wall until the perirectal fat is encountered. (Reprinted with the permission of The Cleveland Clinic Foundation.) Figure 27-7 ■ Levatorplasty may be performed posteriorly and/or anteriorly. (Reprinted with the permission of The Cleveland Clinic Foundation.)
sutures are placed using No. 0 Prolene on an SH needle at the proximal and distal lines of resection. The stapling technique is illustrated in Figure 27-10, A–D. The major advantage of the Altemeier procedure is avoiding laparotomy. The rate of postoperative constipation is low. Potential complications include anastomotic leak, infection, and stricture. The postoperative anal incontinence rate is less dramatically improved compared with abdominal procedures, and incontinence may be worsened due to resection of the rectal reservoir. However, eliminating the prolapse may allow the anal sphincters to regain strength and improve continence. Adding levator repair to the Altemeier perineal rectosigmoidectomy can dramatically improve postoperative continence. Williams et al. (1991), at the University of Minnesota, demonstrated improved incontinence in 91% of patients, with addition of levator repair, versus 46% improvement without levatorplasty. The Altemeier perineal rectosigmoidectomy should be considered for patients with severe full-thickness prolapse, which may be associated with incontinence, and who may not tolerate an abdominal procedure. Some clinicians even recommend this approach as the preferred treatment for healthy, young patients with prolapse. Prolapse recurrence varies from 0% to 39%, and complication rates are low. Figure 27-6 ■ The mesorectal vessels are divided and ligated. (Reprinted with the permission of The Cleveland Clinic Foundation.)
sutures posteriorly in the levator muscle. The prolapsed rectal segment is transected (Fig. 27-8). An anastomosis is created with circumferential full-thickness interrupted No. 2-0 Vicryl sutures (Fig. 27-9). A circular stapler can be used as an alternative to the hand-sewn technique. After bowel transection, purse-string
ANAL ENCIRCLEMENT Perineal procedures that narrow the anal orifice by encircling it with an artificial material, such as the Thiersch’s procedure, have high complication rates and do not address the underlying problem. They have a limited place in the current management of rectal prolapse. In high-risk patients, the Delorme procedure and Altemeier perineal rectosigmoidectomy
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Technical aspects of abdominal repairs for rectal prolapse are the degree of rectal mobilization; whether sigmoid resection is indicated; the method of rectal fixation; and which approach, either open or laparoscopic, is indicated. In the last decade, the laparoscopic approach has been used successfully to perform each type of abdominal repair. It has brought a new dimension to the management of rectal prolapse in colorectal surgery. The transabdominal operations can be classified into three groups: (1) rectal mobilization with rectopexy alone, (2) rectal mobilization with rectopexy and resection, and (3) resection alone. The preferred type of transabdominal repair varies greatly from one country to another, one institution to another, and even from one surgeon to another in the same institution. RECTAL MOBILIZATION
Figure 27-8 ■ The prolapsed segment is transected. Note the completed levatorplasty. (Reprinted with the permission of The Cleveland Clinic Foundation.)
Rectal mobilization is performed posteriorly in the presacral space and carried to the coccyx or levators. How the lateral rectal stalks are handled remains controversial. Some surgeons preserve the lateral stalks, whereas others divide them completely or partially. Speakman et al. (1991), in a prospective randomized study of patients who underwent posterior mesh rectopexy, reported that constipation is increased by 50% if the lateral ligaments are divided, but that prolapse recurrence is increased by 33% if the lateral ligaments are not divided. Scaglia et al. (1994) also reported increased constipation with division of the lateral ligaments but no increase in prolapse recurrence. Anteriorly, the rectum is mobilized to the upper third of the vagina. All rectopexies require this degree of rectal mobilization. Although many variations of the rectopexy are known, the same basic principle is to suspend the rectum to the sacrum, either with suture or with the assistance of material, such as Teflon mesh (CR Bard, Inc., Billerica, MA) or polyvinyl alcohol (Ivalon) sponge. Each rectopexy type will be individually discussed. RECTOPEXY FIXATION TECHNIQUES
Figure 27-9 ■ The anastomosis can be sewn by hand with full-thickness circumferential interrupted sutures. (Reprinted with the permission of The Cleveland Clinic Foundation.)
address the underlying problems of prolapse, with acceptable levels of morbidity and mortality.
Transabdominal and Laparoscopic Repairs Transabdominal repairs provide the best outcomes and functional results for the treatment of rectal prolapse by restoring normal anatomy and repairing associated abnormalities.
Ripstein Procedure. In 1963, Ripstein and Lanter described an anterior rectopexy that has since become a commonly performed operation in the United States. After mobilization of the rectum, the rectopexy is performed by placing a long strip of mesh (5 cm × 20 cm) around the rectum and suturing the free ends of the mesh to the presacral fascia with nonabsorbable sutures. The mesh is also secured to the antimesenteric border of the rectum. The rectum is pulled straight out of the pelvis while the sutures are being placed. The mesh is wrapped loosely enough to allow a thumb or two fingers between the rectum and the sacrum. Alternatively, some surgeons secure the mesh to the presacral fascia at the midportion of the mesh and wrap each free end around the rectum, securing the ends to the antimesenteric border of the rectum. This leaves about one third of the antimesenteric surface uncovered with mesh. This modification attempts to decrease the rate of impaction or obstruction seen when the mesh completely encircles the rectum. Indeed, Ripstein himself now uses the posterior rectal sling rather than an anterior sling to decrease problems with constipation. The Ripstein procedure has been praised for its low prolapse recurrence rate and criticized for postoperative
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Figure 27-10 ■ Altemeier procedure using circular stapler. A. Purse-string sutures are placed on the proximal and distal lines of transected bowel. B. The anvil is extruded from the gun, and the proximal purse-string is tied. Note that the anvil and gun remain intact for this anastomosis. C. The proximal resection line is pushed into the pelvis, and the distal purse-string is tied. D. The completed anastomosis. (Reprinted with the permission of The Cleveland Clinic Foundation.)
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obstructive complications. Gordon and Hoexter (1978) polled the members of the American Society of Colon and Rectal Surgeons, obtaining information on 1111 Ripstein procedures. This revealed a prolapse recurrence rate of 2.3%, sling-related complications in 16.5%, and reoperation rate of 4.1%. Postoperative constipation should be interpreted carefully because many patients who undergo prolapse surgery suffer from preoperative constipation. One of the largest series on the Ripstein repair was reported from our institution by Tjandra et al. (1993). Persistence of previous constipation occurred in 57% of patients after the Ripstein procedure (compared with 17% for resection rectopexy), and 15% of patients developed new constipation. The prolapse recurrence rate was 7%. However, 35% of patients were dissatisfied after the Ripstein procedure, based on a personal interview using a standard questionnaire, despite anatomic correction of the prolapse. Because of these results, we tend to not perform Ripstein procedures in patients with preoperative obstructive symptoms or significant bowel dysfunction. Wells Procedure (Ivalon Sponge). Historically, British surgeons have preferred the posterior rectopexy wrap described by Wells, in 1959, versus the Ripstein procedure. In the Wells procedure, an Ivalon sponge of polyvinyl alcohol is used instead of mesh. It is placed posteriorly and wrapped partially around the bowel. This repair was developed to avoid the constipation associated with the traditional anterior Ripstein repair. Nonetheless, constipation rates following the Wells procedure are still relatively high (44%–48%).
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of excessive sigmoid colon with end-to-end anastomosis. The original concept was to suspend the left colon from the splenic flexure to reduce prolapse recurrence. Subsequent studies have demonstrated that recurrence rates are similar with and without sigmoid resection. Resection does, however, significantly alter postoperative function, particularly by reducing constipation. Sayfan et al. (1990) reported reduced constipation in patients who underwent resection and sling rectopexy compared with rectopexy alone. Two randomized trials also confirmed less postoperative constipation in patients who underwent synchronous resection with rectopexy. We perform rectopexy with resection by mobilizing the sigmoid colon and dividing the mesentery. The rectum is mobilized as previously described. We prefer to resect the sigmoid colon and next perform the anastomosis, either as hand-sewn or with the circular stapler. The splenic flexure is mobilized, if needed. The rectopexy is performed by straightening the rectum (pulling it out of the pelvis) and placing two to three sutures from the lateral rectal stalks to the flat portion of the sacrum at the level of S2 or S3 (Fig. 2711). We prefer No. 0 braided polyester (Ethibond; Ethicon, Inc., Somerville, NJ) suture, whereas others at our institution use No. 0 or 1-0 Prolene. Before tying the rectopexy sutures, we place a rigid proctoscope through the anus and above the
Sutured Rectopexy. Some surgeons have argued that the use of foreign material to perform rectopexy is not only unnecessary, but also risky in the event of postoperative complications, such as an abscess. Additionally, in patients with preoperative constipation or extremely redundant sigmoid, colon resection may be contemplated. The use of artificial material in the setting of bowel resection is controversial because the risk of infection may be increased. Because of this concern, sutured rectopexy has been advocated. In fact, excellent results have been obtained in several series suturing the lateral rectal stalks to the presacral fascia. These results are similar, or even superior, to those reported with rectopexy procedures using prosthetic material. However, some patients are severely constipated after sutured rectopexy, ranging from 31% to 87%. Despite considerable debate over the optimum method of rectal fixation, whether anterior or posterior, with or without artificial material, most modern studies of abdominal rectopexy using different methods report low prolapse recurrence rates, often under 5%. RESECTION AND RECTOPEXY Rectopexy with resection was initially described in 1955 by Frykman at the University of Minnesota and includes mobilization of the rectum via the abdominal route, elevation of the rectum as high as possible out of the pelvis, suture fixation of the rectum to the sacral periosteum, obliteration of the cul-de-sac by suturing anteriorly the endopelvic fascia to the rectum, and segmental resection
Figure 27-11 ■ Rectopexy with sigmoid resection. A sigmoid resection with a colorectal anastomosis has been performed. The rectum has been pulled out of the pelvis and straightened. The lateral rectal stalks have been sutured to the sacrum. (Reprinted with the permission of The Cleveland Clinic Foundation.)
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anastomosis to ensure that the sutures are not tied too tightly and contribute to defecation problems. Excellent results have been reported with rectopexy with resection. Watts et al. (1985) reported only 1.9% recurrence in 102 patients. Anastomotic complications occurred in 4%, with half requiring surgical intervention. Other authors have reported low recurrence rates from 0% to 9%. Functional outcomes improve after rectopexy with resection. In 18 patients reported by Tjandra et al. (1993), fecal incontinence rates improved from 28% to 17%, and postoperative constipation rates improved from 37% to 19%. Resection is indicated in patients who have preexisting constipation. However, care must be taken to identify patients with slow-transit constipation who may require subtotal colectomy combined with rectopexy. Resection alone has been advocated with an anastomosis in the mid to low rectum. The Mayo Clinic (Schlinkert et al.) in 1985 reported on 92 patients who underwent this technique. The recurrence rate was 9%; however, there was significant morbidity with the low anastomosis, and postoperative incontinence sometimes increased. LAPAROSCOPIC APPROACH The dilemma when deciding between an abdominal approach and a perineal approach for treatment of rectal prolapse is the balance between the lower recurrence rate of an abdominal approach and the lower surgical morbidity rate of a perineal approach, because many patients with rectal prolapse are elderly and have significant comorbidity. A laparoscopic access is conceptually attractive because it combines the benefits of both approaches. When considering any new procedure, however, it is important to consider several factors: (1) the feasibility of the procedure, (2) its effectiveness (i. e., the risk of prolapse recurrence), (3) whether the procedure is advantageous compared to established procedures, and (4) its cost-effectiveness. Laparoscopic rectopexy was first performed by Berman in 1992. Since then, a number of studies have confirmed its feasibility. Darzi et al. (1995) reported 29 consecutive patients who underwent laparoscopic rectopexy. The operative time ranged between 50 and 190 minutes, with no mortality and low morbidity. Stevenson et al. (1998) reported a series of 34 patients who underwent sutured resection rectopexy via laparoscopy. No conversions to laparotomy occurred, and morbidity occurred in 13%. Operative time and hospital stay decreased with greater surgeon experience. All types of procedures, performed via an open abdominal approach, have been performed laparoscopically. However, the number and overall follow-up for laparoscopic cases are inevitably shorter than for open cases. The prolapse recurrence rate is between 0% and 6%, with similarly improved continence and reduced constipation as open procedures. Recurrence rates have the potential to increase as follow-up time increases, but early results appear equivalent between open and laparoscopic approaches. Studies that compare laparoscopic and open rectopexy have demonstrated consistently reduced postoperative pain, shortened hospital length of stay, and earlier return of bowel function in patients who undergo a laparoscopic approach. Solomon et al. (2002) randomized 40 patients to either laparoscopic or open rectopexy. Operating time was significantly lon-
ger for laparoscopic compared with open cases (153 minutes vs 102 minutes), but the hospital length of stay was shorter (3.9 days vs 6.6 days), and more laparoscopic patients completed an established care pathway (75% vs 35%). No difference was present in prolapse recurrence, but major and minor morbidity were both significantly lower for laparoscopic cases. Delaney et al. (2003) have assessed the cost-effectiveness of laparoscopic over abdominal approach. In a case-matched study of 150 colorectal surgeries, which included several rectal prolapse cases, the cost of laparoscopic cases was significantly lower.
OUTCOME AND CHOICE OF PROCEDURE In this review, different types of surgical procedures for the treatment of rectal prolapse have been discussed. No one “best” operation exists for patients with rectal prolapse. The choice of surgical procedure is tailored to each individual. Associated conditions are considered to provide optimal results, with the lowest morbidity and mortality. To decide which operation is appropriate for each individual, the entire patient must be considered. Perineal repairs are associated with higher recurrence rates, but the morbidity is lower versus an abdominal approach. Therefore, the perineal approach may be the procedure of choice in frail patients with extensive comorbid conditions. If the prolapse is advanced, perineal proctosigmoidectomy is considered. Levatorplasty (posterior and/or anterior) may be added, particularly if the patient is incontinent. In debilitated patients, with previous left colon resections or minimal prolapse, the Delorme procedure may be optimal. Overall, the abdominal approach is favored when considering recurrence rates and improved functional outcomes regarding fecal incontinence and constipation. However, the abdominal approach is associated with higher morbidity and mortality. In young, healthy patients without significant medical risks, this may be the preferred approach. If the patient has no preoperative incontinence, and constipation is a contributing symptom, resection and rectopexy is favored. If the sigmoid is redundant or “kinks” after the rectum is pulled out of the pelvis to perform the rectopexy, resection should be considered. However, in patients with preoperative fecal incontinence, resection may worsen the incontinence. At our institution, the Ripstein procedure is rarely used because of problems with postoperative constipation. Many patients with rectal prolapse have functional defecatory problems. Correcting the prolapse may not change the abnormal defecatory patterns, and the patient must be counseled of this before surgery. Laparoscopic surgery has the potential to fundamentally alter the approach (although not the procedures) for abdominal repair of rectal prolapse, but long-term follow-up of outcomes is required.
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Altemeier WA, Giusefi J, Hoxworth P. Treatment of extensive prolapse of the rectum in aged or debilitated patients. Arch Surg 1952;65:72. 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. Berman IR. Sutureless laparoscopic rectopexy for procidentia: technique and implications. Dis Colon Rectum 1992;35:689. Blatchford GJ, Perry RE, Thorson AG, et al. Rectopexy without resection for rectal prolapse. Am J Surg 1989;158:574. Boccasanta P. Laparotomic vs. laparoscopic rectopexy in complete rectal prolapse. Dig Surg 1999;16:415. Boccasanta P, Rosati R, Venturi M, et al. Comparison of laparoscopic rectopexy with open techniques in the treatment of complete rectal prolapse: clinical and functional results. Surg Laparosc Endosc 1998;8:460. Broden B, Snellman B. Procidentia of the rectum studied with cine radiography: a contribution to the discussion of causative mechanism. Dis Colon Rectum 1968;11:330. Darzi A, Henry MM, Guillou PJ, et al. Stapled laparoscopic rectopexy for rectal prolapse. Surg Endosc 1995;9:301. 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 1999;81:302. Delaney CP, Kiran RP, Senagore AJ, et al. Case-matched comparison of clinical and financial outcome after laparoscopic or open colorectal surgery. Ann Surg 2003;238:67. Delorme E. On the treatment of total prolapse of the rectum by excision of the rectal mucous membranes. Bull Mem Soc Chir Paris 1900;26:499. Duthie GS, Bartolo DC. Abdominal rectopexy for rectal prolapse: comparison of techniques. Br J Surg 1992;79:107. Finlay IG, Atchison M. Perineal excision of the rectum for the prolapse in the elderly. Br J Surg 1991;78:687. Frykman HM. Abdominal proctopexy and primary sigmoid resection for rectal procidentia. Am J Surg 1955;90:780. Gordon SM, Gordon PH, Nivatvongs S. Essentials of Anorectal Surgery. JB Lippincott, Philadelphia, 1980. Gordon PH, Hoexter B. Complications of Ripstein procedure. Dis Colon Rectum 1978;21:277. Graf W, Karlbom U, Pahlman L, et al. Functional results after abdominal suture rectopexy for rectal prolapse or intussusception. Eur J Surg 1996;162:905. Halligan S, Sultan A, Rottenberg G, Bartram CI. Endosonography of the anal sphincters in solitary rectal ulcer syndrome. Int J Colorectal Dis 1995;10:79. Houry S, Lechaux JP, Huguier M, Moihou JM. Treatment of rectal prolapse by Delorme’s operation. Int J Colorectal Dis 1987;2:149. Husa A, Salinio P, von Smitten K. Abdominal rectopexy and sigmoid resection for rectal prolapse. Acta Chir Scand 1988;154:221. Jacobs LK, Lin YJ, Orkin BA. The best operation for rectal prolapse. Surg Clin North Am 1997;77:49. Johansen OB, Wexner SD, Daniel N, et al. Perineal rectosigmoidectomy in the elderly. Dis Colon Rectum 1993;36:767. Kling KM, Rongione AJ, Evans B, et al. The Delorme procedure: a useful operation for complicated rectal prolapse in the elderly. Am Surg 1996;62:857. Kupfer CA, Goligher JC. One hundred consecutive cases of complete rectal prolapse of the rectum treated by operation. Br J Surg 1970;57:481. Lechaux JP, Lechhaux D, Perez M. Results of Delorme’s procedure for rectal prolapse: advantages of a modified technique. Dis Colon Rectum 1995;38:301. Lockhart-Mummery HE. Procidentia: recent experiences in the treatment of rectal prolapse. Dis Colon Rectum 1972;15:347. Lukkonen P, Mikkonen U, Jarvinen H. Abdominal rectopexy with sigmoidectomy vs rectopexy alone for rectal prolapse: a prospective, randomized study. Int J Colorectal Dis 1992;7:219. Madoff RD, Williams JG, Wong WD, et al. Long-term functional results of colon resection and rectopexy for overt rectal prolapse. Am J Gastroenterol 1992;87:101. Madoff RD, Mellgren A. One hundred years of rectal prolapse surgery. Dis Colon Rectum 1999;42:441. Matheson DM, Keighley MR. Manometric evaluation of rectal prolapse and fecal incontinence. Gut 1981;22:126.
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Wells C. New operation for rectal prolapse. Proc R Soc Med 1959;52:602. Williams JG. Perineal approaches to repair of rectal prolapse. Semin Colon Rectal Surg 1991;2:198. Williams JG, Wong WD, Jenson L, et al. Incontinence and rectal prolapse: a prospective manometric study. Dis Colon Rectum 1991;34:209.
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Steven D. Kleeman and Mickey M. Karram
TERMINOLOGY 353 PREVALENCE, EPIDEMIOLOGY, AND ECONOMIC IMPACT OF OVERACTIVE BLADDER 354 NEUROPHYSIOLOGY OF THE LOWER URINARY TRACT 354 Autonomic Pathways 354 Somatic Pathways 355 Central Regulation 355 Afferent Information 355 ETIOLOGY OF OVERACTIVE BLADDER 357 Neurologic Disease 357 Urogynecologic Conditions 360 Psychological or Psychosomatic Causes 362 Idiopathic Detrusor Overactivity 362 EVALUATION 362 Physical Examination 362 Investigations 362 MANAGEMENT 365 Nonpharmacologic Management of Overactive Bladder 365 Pharmacologic Management of Overactive Bladder 367 Surgical Management 369 Conclusion 370 NOCTURIA 370 Causes of Nocturia 371 Clinical Evaluation 371 Treatment Options 372
Overactive bladder (OAB) is a symptom syndrome that comprises urinary urgency, with or without urge incontinence, usually with urinary frequency and nocturia. OAB affects millions of Americans, and growth of the aging population ensures that the number of people who suffer from OAB will increase over time. The symptoms of OAB have a negative impact on social and personal activities and cause significant psychological distress. Despite increased awareness of OAB in recent years, along with improved diagnosis and treatment, it remains underreported. The poorly understood etiology of the syndrome, the variability of symptom presentation and patient characteristics, and
suboptimal patient-physician communication undoubtedly contribute to this problem.
TERMINOLOGY Terminology used to describe OAB has changed numerous times. The International Continence Society (ICS) has historically taken the lead in standardization of terminology. In its most recently published guidelines, the terms detrusor hyperreflexia, detrusor instability, motor urgency, and sensory urgency have been replaced. The ICS recommends the use of symptoms, signs and urodynamic observations for diagnosis. Currently, the ICS uses the following terms: Increased daytime frequency—symptom in which the patient believes that she voids too often during the day. Nocturia—symptom in which the individual feels the need to wake at night one or more times to void. Urgency—symptom of a sudden, compelling desire to pass urine that is difficult to defer. Urgency with or without urge incontinence, usually with frequency and nocturia, can be described as the overactive bladder syndrome, or urgency-frequency syndrome. Urge urinary incontinence—symptom of involuntary leakage accompanied by or immediately preceded by urgency. The ICS uses the following urodynamic observations. Detrusor overactivity is defined as involuntary detrusor contractions that may be spontaneous or provoked. No minimum requirement is known for the amplitude of an involuntary detrusor contraction. Detrusor overactivity is further divided into three types: (1) phasic, (2) terminal, and (3) incontinence. Phasic detrusor overactivity is defined by a characteristic wave form and may or may not lead to urinary incontinence. Terminal detrusor overactivity is defined as an involuntary detrusor contraction that occurs at cystometric capacity, which cannot be suppressed and results in incontinence. Detrusor overactivity incontinence is incontinence caused by an involuntary detrusor contraction. The ICS recommends that the
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terms motor, urge incontinence, and reflex incontinence no longer be used. Detrusor overactivity may be further qualified if the cause is known: neurogenic, when there is a relevant neurologic condition; and idiopathic, when the cause is unknown.
PREVALENCE, EPIDEMIOLOGY, AND ECONOMIC IMPACT OF OVERACTIVE BLADDER The number of individuals affected by OAB is difficult to establish, reflecting the lack of a standard definition and standardized means of diagnosis. Also, the populations studied vary substantially from one publication to another. Many studies report the prevalence of detrusor overactivity incontinence without including symptoms of urgency and frequency. OAB has been estimated to affect up to 33 million women in the United States alone. Only 15% of these patients with incontinence and OAB symptoms have been estimated to seek medical help. The National Overactive Bladder Evaluation (NOBLE) program contacted more than 17,000 households by telephone and found an overall prevalence of OAB of 16.6% in those who responded. Women had urinary urge incontinence more frequently than men. The prevalence of symptoms increased sharply with age in men and women (Fig. 28-1). Recently, the terms OAB dry and OAB wet have been introduced. About two thirds of patients with OAB have symptoms of urgency and frequency without urinary incon-
tinence, which represent OAB dry. One third of patients have symptoms with urinary incontinence, known as OAB wet (Fig. 28-2). This becomes very important when reviewing industry-sponsored trials, because inclusion criteria and severity of disease are significantly different in these two conditions. In 1995, the total economic cost of urinary incontinence for both men and women in the United States, including OAB and stress incontinence, was estimated at $26.3 billion or $3565 per individual of age 65 or older. This included more than $1 billion spent annually on adult disposable products. Forty-eight percent or $12.53 billion of these resources were used to diagnose, treat, care for, and rehabilitate patients with incontinence. The total economic cost of OAB in the United States in 2000 was estimated to be $18.2 billion. The most rapidly growing segment of the U.S. population is women between ages 60 and 80. Up to 50% of women in this age group complain of OAB syndrome. The prevalence of OAB syndrome, as currently defined, is much higher than stress incontinence in the aging female population.
NEUROPHYSIOLOGY OF THE LOWER URINARY TRACT Autonomic Pathways Sympathetic nerves exit between spinal cord levels T1 and L2 and synapse in the paravertebral ganglions. The sympathetic
Figure 28-1 ■ Prevalence of OAB by age and sex in the United States. (Adapted with permission from Stewart WF, Van Rooyen JB, Cundiff GW, et al. Prevalence and burden of overactive bladder in the United States. World J Urol 2003;20[6]:327–336.)
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Figure 28-2 ■ Prevalence of OAB wet and OAB dry. (Adapted with permission from Stewart WF, Van Rooyen JB, Cundiff GW, et al. Prevalence and burden of overactive bladder in the United States. World J Urol 2003;20[6]:327.)
system uses noradrenaline as its neurotransmitter, and the receptors are α- and β-adrenergic. Sympathetic input to the bladder is via the hypogastric nerve (Fig. 28-3). When noradrenaline binds to β-receptors on the bladder, it activates adenylate cyclase, which increases levels of cyclic adenosine monophosphate (AMP), thereby relaxing the detrusor muscle of the bladder (Fig. 28-4). The parasympathetic system originates at spinal cord levels S2, S3, and S4. Parasympathetic input to the bladder is via the pelvic nerve (see Fig. 28-3). The parasympathetic system uses acetylcholine as its neurotransmitter and muscarinic receptors at target organs. Five subtypes of muscarinic receptors are known, with a predominance of M2 and M3 receptor subtypes in the bladder. Release of acetylcholine by postganglionic parasympathetic nerves activates both M2 and M3 receptor subtypes (see Fig. 28-3). M2 receptors make up approximately 80% of the muscarinic receptors in the bladder. Activation of M2 receptors negatively affects adenylate cyclase, thereby decreasing cyclic AMP, and ultimately inhibiting relaxation caused by the sympathetic system (Fig. 28-4). M3 subtypes, which make up the remaining 20% of muscarinic bladder receptors, activates phospholipase C, increases inositol triphosphate, and subsequently causes detrusor muscle contraction (see Fig. 28-4).
Central Regulation Neurotransmitters involved in the central control of micturition include acetylcholine, γ-aminobutyric acid (GABA), glycine, serotonin, dopamine, and noradrenaline. Two regions of the pons are involved in regulating voiding and continence. The pontine micturition center (Barrington nucleus or M region) projects directly to bladder motor neurons and indirectly to urethral motor neurons. The bladder motor neurons are preganglionic and parasympathetic (S2, S3, S4) and located in the intramediolateral cell column of the sacral spinal cord. The urethral motor neurons are located in the sacral ventral horn (Onuf ’s nucleus). With stimulation of the pontine micturition center, urethral pressure decreases via inhibition of the urethral motor neurons and intravesical pressure increases by stimulation of the bladder motor neurons (Fig. 28-5). The pontine continence center, or L region, projects to urethral sphincter motor neurons. With stimulation of the pontine continence center, urethral sphincter tone increases. During the filling phase, the pontine continence center continuously stimulates the urethral sphincter motor neurons to maintain urethral closure (see Fig. 28-5).
Afferent Information Somatic Pathways The neurotransmitter for the somatic nervous system is acetylcholine, and its receptors are nicotinic. The striated muscle of the external urethral sphincter is innervated by motor neurons that originate in Onuf ’s nucleus in the sacral spinal cord and their axons traveling via the pudendal nerve (see Fig. 28-3).
Bladder information is sent from the bladder via the pelvic nerve to the sacral dorsal root ganglia located within the spinal cord. These nerves are primarily made up of myelinated A through D fibers and unmyelinated C fibers. A through D fibers respond to distension and active contraction, whereas C fibers respond to chemical irritation and pain. Several receptors have been identified on these nerves, such as vanilloid,
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Figure 28-3 ■ Neurourology of bladder storage and elimination: (1) Sympathetic nerves exit the spinal cord between levels T1 and L2. They synapse in the paravertebral ganglion, and postganglionic fibers travel to the bladder via the hypogastric nerve. (2) Parasympathetic nerves exit the spinal cord via S2–S4. Preganglionic fibers travel to the bladder via the pelvic nerve and synapse close to the bladder, then send short postganglionic fibers to the bladder. (3) The external urethral sphincter is innervated by motor neurons that originate in Onuf ’s nucleus and travel via the pudendal nerve.
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Figure 28-4 ■ Schematic representation of parasympathetic and sympathetic postjunctional receptors.
tachykinin, purinergic, and prostanoid receptors (Fig. 28-6). These receptors may have a role in the development of OAB syndrome and may be potential pharmacotherapy targets.
ETIOLOGY OF OVERACTIVE BLADDER Although the cause of OAB is not understood, the problem is most likely multifactorial. The process of bladder storage and evacuation can be visualized as complex neurocircuits in the brain and spinal cord that coordinate the activity of smooth and striated muscle in the bladder and urethra. These circuits act as “on/off switches” to alternate the lower urinary tract between its two modes of operation: storage and elimination. Conditions associated with detrusor overactivity are listed in Box 28-1.
Neurologic Disease Detrusor overactivity is associated with neurologic lesions of the suprasacral spinal cord and higher centers. These lesions block the sacral reflex arc from the cerebral cortex and other higher centers that are crucial to both voluntary and involuntary inhibition of the bladder. In this group of patients, involuntary detrusor contractions are usually associated with appropriate relaxation of the urethral sphincter because there is preservation of long tracts from the pontine region. Neurologic conditions resulting in detrusor overactivity include multiple sclerosis, dementia, cerebrovascular disorders, and Parkinson’s disease. MULTIPLE SCLEROSIS Multiple sclerosis (MS) is a disease of unknown etiology that usually affects patients between ages 20 and 40.
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Figure 28-5 ■ Schematic representation of storage and voiding reflexes. A. During bladder storage distension of the bladder causes afferent signals that, in turn, cause efferent signals via the hypogastric nerve (sympathetic system, relaxation) and the pudendal nerve (increased tone of the striated sphincter). B. During bladder elimination, increased afferent activity via the pudendal nerve travels through the periaqueductal gray matter (PAG) through the pontine micturition center and, ultimately, sympathetic outflow (relaxation) and pudendal outflow (urethral tone) while increasing parasympathetic outflow (contraction).
Demyelinating plaques in the white matter of the cerebral cortex, cerebellum, brainstem, spinal cord, and optic nerve produce varied neurologic dysfunction and symptoms. MS is characterized by multiple lesions and usually a progressive course of bladder dysfunction. Plaques in the frontal lobe of the cerebral cortex or in the lateral columns of the spinal cord usually produce lower urinary tract dysfunction. Bladder dysfunction as an initial symptom leading to the diagnosis of MS occurs in only 5% of patients; however, up to 90% of patients with MS have bladder dysfunction during the course of their disease. Approximately 60% of patients with lower urinary tract dysfunction show detrusor contractions on cystometry. Up to half of these patients demonstrate detrusor sphincter dyssynergia, whereas the other half demonstrate adequate and appropriate sphincter relaxation. Approximately 30% of patients have an underactive or areflexic detrusor.
CEREBROVASCULAR DISEASE Based on the 1990–1992 National Health interview surveys, the prevalence of persons in the United States who report a medical history of stroke increases with age from 1.7% for those ages 45 to 64 to 8.1% of those greater than age 75. It is associated with varying degrees of chronic disability, including bladder dysfunction. Atherosclerosis, arteritis, intracranial hemorrhage, and arterial malformations may be etiologic factors. Infarction of discrete areas of the frontal lobe of the cerebral cortex, internal capsule (which sends axons between the thalamus and cerebral cortex), brainstem, or cerebellum can result in bladder dysfunction. During the initial phase of a cerebrovascular accident, urinary retention secondary to detrusor areflexia is common. During recovery, detrusor overactivity with an appropriate sphincteric response usually occurs. Very rarely, detrusorsphincter dyssynergia results.
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Figure 28-6
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Schematic representation of bladder innervation.
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CONDITIONS ASSOCIATED WITH INVOLUNTARY DETRUSOR CONTRACTIONS
Idiopathic detrusor overactivity Congenital Aging Neurogenic detrusor overactivity Multiple sclerosis Cerebrovascular disease Parkinson’s disease Dementia Neoplasia Spinal cord injury Bladder outlet obstruction and pelvic surgery Antiincontinence surgery Advanced pelvic organ prolapse Psychosomatic disease Urine in proximal urethra Inflammation Orgasm Detrusor overactivity with impaired contractility Mixed incontinence
PARKINSON’S DISEASE Parkinson’s disease is estimated to occur in 1 to 2 per 1000 persons in the United States. Onset usually occurs after age 50, and the course of the disease is progressive. The occurrence of bladder dysfunction ranges from 40% to 70%. The extrapyramidal system is believed to inhibit the micturition center, so loss of dopaminergic activity in the substantia nigra, caudate, putamen, and globus pallidus results in loss of detrusor inhibition. However, this theory has been challenged by Malone-Lee et al. (1993), who performed urodynamic studies on 2526 patients, of whom 76 had Parkinson’s disease. They found no evidence of a disease-specific “parkinsonian bladder,” suggesting that changes seen in such patients are age-related phenomena. Obstructive symptoms can occasionally result from therapy with anti-parkinsonian agents. DEMENTIA Dementia is a diffuse deterioration in intellectual function manifested primarily by memory deficits and secondarily by changes in conduct. The causes of dementia include aging, severe head injury, encephalitis, presenile dementias (including Alzheimer’s disease, Pick’s disease, and Jakob-Creutzfeldt disease), hydrocephalus, and syphilis. The mechanism of bladder dysfunction can be direct involvement of the cerebrocortical areas concerned with bladder control. It can also result from the loss or inability to control social appropriate behavior. Detrusor overactivity or areflexia may occur, depending on the cause and severity of the dementia. NEOPLASIA Brain tumors in the superior medial frontal lobe can result in bladder dysfunction, which may manifest as irritative voiding symptoms, including detrusor overactivity. Spinal cord tumors above the level of the conus medullaris and cervical spondylosis can also produce detrusor overactivity.
SPINAL CORD INJURY Spinal cord injury is a common cause of detrusor overactivity. All cord injuries that are complete and spare S2, S3, and S4 segments eventually produce upper motor neuron lesions with resultant detrusor overactivity. However, during the initial phase of spinal shock following suprasacral spinal cord injury, the bladder is areflexic, resulting in urinary retention and overflow incontinence.
Urogynecologic Conditions Various conditions that may present with symptoms of urgency and frequency are listed in Box 28-2. Idiopathic detrusor overactivity is reserved for symptoms of urgency and frequency, with or without incontinence, that cannot be explained by the presence of other conditions. URINARY TRACT INFECTION Inflammation of the bladder epithelium, with or without associated bacteriuria, has been suggested as a cause of bladder overactivity. Bhatia and Bergman (1986) performed urodynamic studies on women with acute urinary tract infections before treatment. Half of those with urodynamic evidence of detrusor overactivity before treatment had stable cystometrograms after the infection was treated. However, Bates et al. (1970) reported on more than 2000 patients examined by videocystography on whom culture and sensitivity studies of midstream urine specimens were performed. They found that of 35 patients infected at the time of the study, only 3 had nonneuropathic detrusor overactivity.
BOX 28-2
CONDITIONS THAT PRODUCE SYMPTOMS OF URINARY FREQUENCY AND URGENCY
Urogynecological Detrusor overactivity Urodynamic stress incontinence Mixed incontinence Interstitial cystitis Urinary tract infection Radiation cystitis Urogenital atrophy Urethral syndrome Pelvic organ prolapse Urethral diverticulum Pregnancy Pelvic mass Intravesical lesion Medical Neurologic diseases Congestive heart failure Diabetes mellitus Diabetes insipidus Diuretics Psychological Habit Anxiety Excessive fluid intake
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HYPERSENSITIVE BLADDER DISORDERS
ORGASM
Pain is not a common symptom of women with OAB. Pain with a full bladder in conjunction with urgency and frequency suggests a hypersensitive bladder condition, such as interstitial cystitis. Women who have had previous pelvic radiation and those with significant urogenital atrophy may also complain of overactive bladder symptoms.
Orgasm may cause detrusor overactivity. The pathogenesis is unknown, but women sometimes experience urgency or urge incontinence with a gush of urine during climax. Treatment is the same as for detrusor overactivity; sexual counseling and education are often helpful. MIXED INCONTINENCE
URODYNAMIC CONDITIONS Urethral instability is defined as a spontaneous fall in maximum urethral pressure exceeding one third of the resting maximum urethral pressure in the absence of detrusor activity. If simultaneous urethrocystometry is performed during filling, the diagnosis of urethral instability or uninhibited urethral relaxation can be made. Resnick and Yalla (1987) noted a subgroup of elderly women with detrusor overactivity resulting in incontinence, who cannot effectively empty their bladders when attempting to void. Urodynamic testing revealed that impaired contractility caused impaired emptying. They named the condition detrusor overactivity with impaired contractility and hypothesized that this may represent the last stage of detrusor overactivity, in which detrusor function deteriorates. STRUCTURAL OR ANATOMIC CONDITIONS At the level of the urethra, urge incontinence can occur with outlet obstruction. This is a well-known problem in men with benign prostatic hyperplasia, and in younger men and women with spinal cord injuries or multiple sclerosis. In women, bladder outlet resistance from previous anti-incontinence surgery can result in irritative symptoms and urge incontinence. Idiopathic bladder outlet obstruction is rare in women. Abnormal voiding is usually caused by poor detrusor function rather than physical obstruction. However, obstructive voiding sometimes occurs with advanced pelvic organ prolapse and after operations for stress incontinence. The correlation between detrusor overactivity and pelvic surgery is confusing and, at times, unexplainable. Studies on patients operated on for stress incontinence who had stable preoperative cystometrograms note that 7% to 27% develop postoperative detrusor overactivity. Women with mixed symptoms of stress incontinence and OAB will have a resolution of their OAB symptoms in approximately 50% of cases after an anti-incontinence procedure. The remaining 50% may have a persistence or worsening of their symptoms. Postoperative detrusor overactivity or a persistence or worsening of symptoms seems to be more common in patients with previous bladder neck surgery and in those with coexistent detrusor overactivity and preoperative sphincteric incompetence. Radical pelvic surgery can result in an unstable bladder. Partial denervation of the bladder during the operative process with subsequent development of detrusor dysfunction is currently the most accepted theory. Other conditions that can impact the lower urinary tract and result in overactive bladder symptoms include pregnancy, pelvic mass, urethral diverticulum, and intravesical lesions.
Detrusor overactivity can coexist with stress incontinence in up to 30% of patients. Whether this is a coincidental finding or some underlying relationship between these two conditions is unknown. In women with mixed stress and urge incontinence, a deficient urethral sphincter may result in urge incontinence, if leakage of urine into the proximal urethra stimulates urethral afferents that induce involuntary voiding reflexes. Interestingly, after anti-incontinence surgery, detrusor overactivity may disappear, remain the same, or worsen. In a matched control study, Colombo et al. (1996) noted that 95% of their patients were cured of stress incontinence after a Burch urethropexy was performed if they had a stable preoperative cystometrogram. On the other hand, only 75% were cured if, preoperatively, they had low compliance or uninhibited bladder contractions. Women may condition themselves to have urgency and frequency by becoming habitual frequent voiders. This can be seen in women with long-standing stress incontinence because these women will consciously or subconsciously void more frequently to avoid or reduce leakage. Over time, it has been proposed that functional bladder capacity is reduced, and the bladder becomes more sensitive at lower volumes of urine, thus resulting in frequency and urgency (OAB dry). This same phenomenon can occur in women with urge incontinence, resulting in more severe frequency. This can be viewed as a cycle in which symptoms continue to worsen unless intervention is undertaken (Fig. 28-7).
Figure 28-7
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Cycle of bladder dysfunction.
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Psychological or Psychosomatic Causes The psychological status of women with detrusor overactivity has been investigated by several authors with conflicting results. Norton et al. (1990) performed psychiatric evaluations on 117 women and found no more psychiatric morbidity in women with detrusor overactivity than in women with stress incontinence. Interestingly, women in whom no urodynamic abnormality could be detected had the highest scores for anxiety and neuroticism. Moore and Sutherst (1990) analyzed the response to treatment of idiopathic detrusor overactivity, relative to “psychoneurotic” status in 53 women. Women who responded poorly to treatment had higher psychoneurotic mean scores than those who responded, although one third of poor responders had a normal psychoneurotic score. Patients who responded well to therapy had scores similar to those of normal urban women. These studies emphasize the need for future research in this area.
Idiopathic Detrusor Overactivity With our current diagnostic capabilities, more than 90% of women with detrusor overactivity have no other recognizable disorder. Various theories have been proposed to explain detrusor overactivity, such as detrusor hypersensitivity or deficient inhibitory activity, but no one theory has been identified that adequately explains all or most detrusor overactivity, so it remains idiopathic at this time. Kinder and Mundy (1987) studied detrusor muscle strips in vitro from patients with detrusor overactivity and from normal continent subjects. The unstable muscle strips showed an increased response to direct electrical stimulation and increased sensitivity to stimulation with acetylcholine. In vivo, this response would correspond to a higher sensitivity of efferent neurologic activity or to a lower level of acetylcholine release necessary to initiate a detrusor contraction. However, it is not clear whether this detrusor supersensitivity is caused by a relative cholinergic denervation or by reduced inhibitory or modulatory neurologic activity, possibly mediated by vasoactive intestinal polypeptide (VIP). VIP is a 28-amino-acid neuropeptide with powerful relaxant effects on smooth muscle. VIP is abundant in normal human bladders and markedly decreased in the bladders of patients with detrusor overactivity. Elbadawi et al. (1993) suggested that spontaneous trigger and subsequent spread of contractile signals via increased cell-to-cell coupling were the likely mechanisms for the development of idiopathic detrusor overactivity.
dysfunction are important. A thorough medical history should be taken, as well as a surgical history with emphasis on previous bladder or gynecologic surgery. A review of all current prescription medication that the patient is taking is vital (see Chapter 6).
Physical Examination A physical examination should include a general physical, neurologic, and pelvic examination. Neurologic studies should include a brief mental status examination and evaluation of cranial nerves and deep tendon reflexes. Muscle strength can be assessed by having the patient actively move against resistance, such as shrugging her shoulders against downward pressure. Specifically testing the sacral spinal cord involves evaluating the patient’s ability to extend and flex her hip, knee, and ankle, and invert and evert her foot. Deep tendon reflexes should be checked at the biceps (C5–C6), triceps (C7), knee (L3–L4), and Achilles tendon (L5–S2). Spinal cord segments S2, S3, and S4 contain important neurons involved with micturition. The anal sphincter and pelvic reflexes are important indicators of sacral cord integrity. Voluntary contraction of the external anal sphincter indicates a minimum level of integrity of pelvic floor innervation. Stroking the skin lateral to the anus elicits a reflex anal sphincter contraction. The bulbocavernosus reflex involves tightening of the bulbocavernosus and ischiocavernosus muscles by tapping or squeezing the clitoris. The cerebellum should also be tested, because it has major functions in the control of micturition. The cerebellum can be tested by evaluating finger/nose and heel/shin coordination and examining the patient’s gait. A pelvic examination should include a thorough inspection of the perineal area and vulva, looking for excoriation, vaginal discharge, or atrophy, suggesting estrogen deficiency. Vaginal examination should include assessment for pelvic organ prolapse, pelvic muscle function, atrophy, and anatomic abnormalities. The urethra can be palpated through the anterior vagina, checking for a mass or purulent discharge from the urethral meatus consistent with urethral diverticulum. Pelvic floor muscle function should be described by pelvic muscle tone at rest and by the strength of voluntary contraction. Muscle tone and strength can be subjectively described as strong, weak, or absent; or described by a validated graded system, such as the Oxford system, usually on a scale from 1 to 5. Pelvic organ prolapse should be evaluated, specifically, support of the anterior, apical, and posterior vagina. Rectal examination should also be performed to rule out fecal impaction and rectal mass and to assess sphincter tone.
EVALUATION Investigations An important aspect of the evaluation is appreciating the quality-of-life impact that these symptoms are creating. Standardized quality-of-life questionnaires are available and can be administered. In addition, specific questions about pelvic organ prolapse, defecatory dysfunction, and sexual
URINALYSIS AND CULTURE Because the symptoms of urinary tract infection and other irritative bladder conditions commonly mimic OAB, urinalysis should be performed before further investiga-
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tion is initiated. As previously mentioned, bacteriuria may cause detrusor overactivity, which sometimes resolves after the infection has been treated. Urine cytology should be performed to rule out neoplasia in patients with chronic irritative bladder symptoms, particularly in elderly patients and those with microscopic hematuria. VOIDING DIARY In addition to history-taking, patients can be mailed or given a voiding diary to fill out 48 hours before their office visit, usually over a weekend to avoid the possible interference of work. A chart of the timing and volume of intake and output is indispensable for corroborating the patient’s history and symptoms. Patients’ interpretation of problems do not always correlate with their voiding diary. Also, significant changes can be made with daily fluid intake and medication to decrease urinary loss. Follow-up charts are useful to provide evidence to both patient and clinician of treatment response, particularly when bladder retraining is used. URODYNAMIC TESTS Cystometry Cystometry is the mainstay of investigation for bladder storage function and is the only method of objectively
Figure 28-8 ■ Various cystometric patterns noted in patients with detrusor instability. A. Normal filling cystometry with voluntary terminal contraction. B. Phasic involuntary detrusor contractions that return to baseline. C. Cough-provoked detrusor instability (intravesical instead of true detrusor pressure is depicted here). D. Phasic contractions with steady rise in detrusor pressure. E. Steady rise in detrusor pressure (low-compliance bladder). F. Subthreshold detrusor instability with voluntary terminal contraction.
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diagnosing detrusor contractions. Figure 28-8 reviews the various cystometric patterns that may be seen in patients with detrusor overactivity. During the cystometric evaluation of patients with suspected OAB, one must use provoking stimuli if detrusor contractions are not elicited during filling. Sometimes the provocation needed to reproduce a detrusor contraction cannot be performed in a laboratory setting. This problem has been demonstrated in numerous ambulatory monitoring studies in which symptomatic patients had normal bladder filling in the urodynamic laboratory but had uninhibited contractions when monitored on a continuous basis. Testing should always be performed with the patient in a sitting or erect position because supine filling cystometry alone fails to uncover a significant proportion of bladder overactivity. Other provoking factors are coughing, straining, heel-bouncing, jogging in place, listening to running water, and placing the patient’s hands under running water. (See Chapter 7 for more details on cystometry.) Urethral Pressure Studies Urethral pressure studies add little to the diagnosis of detrusor overactivity or to the differentiation of patients with stress incontinence from those with urge incontinence. Detrusor contractions are almost always preceded by a drop in urethral pressure (Fig. 28-9). Bergman et al. (1989)
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Figure 28-9 ■ Multichannel substracted urethrocystometry showing detrusor instability. Note urethral relaxation and quieting of EMG activity.
studied urethral pressure tracings in 72 women with detrusor overactivity to learn whether urethral pressure changes may be the cause, rather than the effect, of bladder contractions. Patients who had urethral relaxation before detrusor contractions responded better to α-sympathomimetic drugs, whereas patients without urethral pressure changes responded more favorably to anticholinergic drugs. In another study, urethral instability occurred in 42% of patients with detrusor overactivity and was strongly associated with the sequence of urethral relaxation before an unprovoked contraction. This study concluded that, based on a urethral response, two subgroups of detrusor overactivity may exist. Electromyography Electromyography (EMG) gives information on the activity of the external striated urethral sphincter muscles. Its potential value in patients with
detrusor overactivity is to document voluntary control of this sphincter, as well as to demonstrate that the external sphincter and detrusor muscle function in a coordinated fashion (see Fig. 28-9). Mayo (1978) found that 48% of patients with idiopathic detrusor overactivity exhibited reflex relaxation of the sphincter at the time of a detrusor contraction. This observation is important because these patients are probably unable to voluntarily contract the external sphincter at the moment of the detrusor contraction, thus they are unable to inhibit urine loss. Spontaneous sphincter relaxation can also be detected during EMG studies, leading to the diagnosis of uninhibited urethral relaxation. External sphincter EMG studies are used for the diagnosis of detrusor-external sphincter dyssynergia, which is a rare condition and occurs in only patients with neurologic disease (Fig. 28-10). EMG adds little to the evaluation and management of neurologically intact women.
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Figure 28-10 ■ Multichannel urodynamic tracing showing detrusor– external sphincter dyssynergia. As patient tries to void, an increase in EMG activity is associated with a strong bladder contraction, rise in urethral pressure, and minimal urine flow.
Endoscopy. The role of cystourethroscopy is questionable in the patient with detrusor overactivity. Definitive indications include microscopic hematuria and abnormal urine cytology. Cystoscopy should also be considered if the diagnosis is in doubt or if the patient shows no response to appropriate behavioral and pharmacologic therapy.
MANAGEMENT Detrusor overactivity is treated in several different ways. The following is a discussion of various treatments (Box 28-3).
Nonpharmacologic Management of Overactive Bladder BLADDER RETRAINING DRILLS This therapy institutes a program of scheduled voiding with progressive increases in the interval between each void, based on the assumption that conscious efforts to
suppress sensory stimuli will reestablish cortical control over an uninhibited bladder, thus reestablishing normal voiding patterns. This therapy has been studied by Frewen (1982), Fantl et al. (1981), and others. In several studies, Frewen reported success rates of approximately 80%. However, his protocol included primarily in-hospital behavioral management and concurrent pharmacologic therapy. Fantl et al. reported on 92 patients with objective evidence of detrusor overactivity treated by bladder drill, with or without anticholinergic therapy. Cure rates were the same in both groups: 83% in patients treated with bladder drill and drugs, and 79% in patients treated with bladder drill alone. These high cure rates with bladder retraining drills have been substantiated by other authors. The technique used for bladder retraining involves giving the patient insight into the nature of her dysfunction. Drawings demonstrating cerebral cortical inhibitory effects over bladder reflexes can be shown to the patient to assist in explaining lower urinary tract dysfunction. The patient’s own cystometric tracing can be shown to her to illustrate the dysfunction. The patient is taught scheduled voiding at
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TREATMENT OPTIONS FOR OVERACTIVE BLADDER
Treatment of associated conditions Stress incontinence Outlet obstruction Treatment of detrusor overactivity Behavioral treatment Bladder drill Biofeedback Pharmacologic treatment Anticholinergics Adrenergic Afferent mechanisms Central mechanisms Botulism toxin Tricyclic antidepressants Electrical stimulation Surgical treatment Phenol injections Sacral blockade Sacral neurectomy Sacral electrical stimulation Transvaginal denervation Bladder transaction Augmentation cystoplasty Detrusor myomectomy Urinary diversion
timed intervals, varying from 15 minutes to 1 hour, based on the patient’s own frequency or incontinence intervals. We usually start patients at voiding intervals of 30 to 60 minutes. Patients are given preprinted cards, on which they record voiding (daily and nightly), involuntary leaking episodes, and occurrences that precipitate incontinence. Patients are instructed to make an earnest effort to follow the schedule during the day, attempting to suppress urgency and voiding only at the scheduled times regardless of the presence or absence of urinary urgency. Patients are instructed to contract their pelvic floor muscles when they feel urgency and impending urge incontinence, to suppress involuntary bladder overactivity. Schedules are not followed during sleeping hours. Follow-up visits are scheduled every 1 to 2 weeks, at which time the cards are reviewed with the patient. Voiding intervals are increased periodically by 15 to 60 minutes, according to the patient’s response in reducing urgency and urge incontinence episodes. A 6- to 12-week treatment program is anticipated in most cases. Enthusiastic patient contact, reassurance, good longterm support, and follow-up are important. Patients must be highly motivated to improve with this therapy. The degree of patient compliance determines success. Because the success rate is so good and the therapy involves low cost, bladder retraining drills should be the first line of therapy in patients with detrusor overactivity. BIOFEEDBACK Biofeedback is a form of patient reeducation, such that normally unconscious physiologic processes are made accessible
by auditory, visual, or tactile signals, while attempts are made to modify the process by manipulating the signal presented to the patient. This method has been used with some success in the treatment of autonomic dysfunctions, hypertension, and cardiac dysrhythmias. As an example of how biofeedback can be used to treat detrusor overactivity, after cystometry is explained to the patient, bladder filling begins and an audible signal is used to let the patient know that her bladder pressure is rising. The tone of the signal varies by the change in bladder pressure. The patient also visualizes the urodynamic tracing throughout the test. The bladder is repeatedly filled while the patient attempts to inhibit detrusor contractions. Individual treatment sessions are approximately 1 hour and are repeated weekly for up to 8 weeks. Cardozo et al. (1978) have reported 81% subjective and objective improvement with biofeedback. They noted that biofeedback was not as successful in patients with severe detrusor overactivity, particularly in women with high-amplitude detrusor contractions occurring at small bladder volumes. Burgio et al. (1998) randomized patients to biofeedback-assisted behavioral training, drug treatment, or placebo. Behavioral treatment was significantly better than drug treatment or placebo. In a follow-up study, Burgio et al. (2000) found that drug treatment along with biofeedback-assisted behavioral therapy were superior to either modality alone. Many investigators use biofeedback techniques aimed at identifying and strengthening pelvic floor muscles. In addition, appropriate control of the external urethral sphincter mechanism may enhance the urethrovesical inhibitory reflex. ACUPUNCTURE Acupuncture is thought to act by increasing levels of endorphins and enkephalins in the cerebrospinal fluid and via neuromodulation. One of the first studies using Chinese acupuncture, published in Western literature, was carried out by Philip et al. (1981), who reported improvement in 77% of 20 patients with detrusor overactivity. Minni et al. (1990) found acupuncture effective in 18 of 20 children with enuresis and detrusor overactivity. Cheng et al. (1998) reported on acupuncture in 80 patients with spinal cord injury and neurogenic detrusor overactivity. Results were better if treatment started within 3 weeks of surgery, but they also reported that complete spinal cord injury was not affected by acupuncture. Honjo et al. (2000) reported on 13 patients with spinal cord injury treated with acupuncture, with complete resolution of symptoms in 2 patients and 50% reduction in 6 others. FUNCTIONAL ELECTRICAL STIMULATION Functional electrical stimulation (FES) stimulates the afferent limb of the pudendal reflex arc, increasing pelvic floor muscle and urethral striated muscle contractility, and possibly stimulating reflex inhibition of detrusor contractility. Some patients who are refractory to behavioral and pharmacologic therapies respond to FES. The main difficulty with FES is patient acceptance of intravaginal or transrectal stimulation. Originally, patients were required to use the devices for several hours daily. The results of Leach and Bavendam
Chapter 28
(1989) clearly point out these limitations—94% dropout rate in a study of 36 patients using a transrectal stimulating device. To overcome the requirement for long treatment sessions, investigators have studied the efficacy of intermittent maximal electrical stimulation in treating incontinence. With this therapy, the patient receives a short period of stimulation (for example, 30 minutes) at maximum tolerable intensity. Treatment is continued over several weeks. Eriksen et al. (1989) reported short-term maximal pelvic floor electrical stimulation in 48 patients with idiopathic detrusor overactivity. Each patient received 20 minutes of simultaneous vaginal and anal electrical stimulation for an average of seven treatments. Initial clinical and urodynamic cures were observed in 50% of patients, with significant improvement in an additional 33%. At 1-year follow-up, persistent positive therapeutic effects were found in 77% of patients. In another study, Plevnik et al. (1986) treated 30 patients with detrusor overactivity with maximal electrical stimulation at home for 20 minutes per day for 30 days. Cure was noted in 29%; an additional 22% reported improvement. Bent et al. (1989) noted significant subjective improvement in 69% of patients with detrusor overactivity, using a regimen of 15 minutes of maximal stimulation twice daily for 6 weeks. Wise et al. (1992) compared maximum electrical stimulation with oxybutynin therapy. With either treatment, symptoms were significantly reduced on visual analog scales, and diurnal frequency was reduced by voiding diary. Spruijt et al. (2003) randomized 24 postmenopausal women with urinary incontinence to
Table 28–1
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intravaginal electrical stimulation or a daily Kegel exercise program. The effectiveness of FES was similar to Kegel exercises (29.2% vs 36.4%, for objective improvement, and 29.2% vs 27.3% for subjective improvement, respectively). Wang et al. (2004) evaluated pelvic floor muscle training with and without biofeedback-assistance and FES for 103 women with OAB. OAB symptoms were reduced in about half of women treated with FES and biofeedback-assisted pelvic muscle training, compared to 38% treated with pelvic muscle training alone (although this difference was not statistically significant). The role of FES as therapy for detrusor overactivity is still evolving. Although currently not a first-line therapy, it may benefit certain groups of patients who have failed multiple treatments.
Pharmacologic Management of Overactive Bladder The mainstay of pharmacologic therapy for OAB to date has been antimuscarinic medications. In addition, other medications that work on different aspects of the neurophysiology of micturition will be reviewed. See Table 28-1. ANTIMUSCARINIC AGENTS As previously mentioned, there are five different subtypes of muscarinic receptors in the bladder, with a predominance of M2 and M3 subtypes. Because of these, antimuscarinic agents have been developed to modify the activity of these
Drug Classification and Mechanism of Action
Classifications
Mechanism of Action/Comments
Drugs
Dosage
Anticholinergic
Inhibit muscarinic receptors
Oxybutynin
2.5–5 mg tid IR 5–15 mg qd ER 3.9 mg/4 days TD 1–2 mg bid IR 4 mg qd ER 15 mg bid to 30 mg qid 20 mg bid 5–10 mg qd 7.5–15 mg qd 25 mg PO qid Nonextended release: 60 mg PO qid Extended release: 120 mg PO bid Investigational Investigational 25 mg qd to 75 mg bid 10 mg/d PO; titrate prn by 10 mg/wk until maximum dose of 150 mg is reached, urinary symptoms disappear, or adverse effects become intolerable 200–300 units injected cystoscopically Investigational
Tolterodine Propantheline Trospium Solifenacin Darifenacin Ephedrine Pseudoephedrine
α-Adrenergic agonists
Increases urethral closure pressure
Afferent nerve inhibitors
Blocks sensory input to bladder
Tricyclic antidepressant
Some anticholinergic properties, smooth muscle relaxation, and norepinephrine reuptake inhibition
Botulinum toxin
Inhibit release of acetylcholine
Toxins A and B
Central-acting
Serotonin and norepinephrine reuptake inhibitor
Duloxetine
IR, Immediate release; TD, transdermal; ER, extended release.
Capsaicin Resiniferatoxin Imipramine Amitriptyline
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receptors. The two most commonly prescribed medications are oxybutynin and tolterodine. Oxybutynin has some selectivity for M3 receptors to inhibit bladder contractions, but, because of muscarinic blockade in other parts of the body, it can have bothersome side effects. Oxybutynin has a higher affinity for muscarinic receptors in the parotid gland compared to the bladder, leading to the side effect of dry mouth. Additionally, levels of the active metabolite of oxybutynin, N-desethyl-n-oxybutynin, can be sixfold higher than the parent compound after oral administration. Other side effects include constipation, gastrointestinal upset, and blurry vision. Alternative approaches have been developed to improve tolerability, including extended-release oral formulations, rectal or intravesical administration, and a transdermal patch. The extendedrelease form of oxybutynin, marketed as Ditropan-XL, uses a push/pull osmotic system. In trials that compare extended release with immediate release, extended-release oxybutynin had similar efficacy but reduced side effects. Absorption of extended-release oxybutynin may occur more in the large intestine, rather than the stomach and proximal small intestines, thereby decreasing conversion to N-desethyl-noxybutynin. Transdermal oxybutynin, in theory, offers potential therapeutic advantages, including more stable plasma concentrations and less presystemic metabolism that may decrease levels of the primary active metabolite, N-desethyl-n-oxybutynin. In a study of transdermal oxybutynin 3.9 mg per day and extended-release oxybutynin 10 mg once a day, the transdermal drug showed greater systemic availability with less metabolism to N-desethyl-n-oxybutynin and greater salivary output. Dmochowski et al. (2002) studied 361 adults, with OAB symptoms, who were randomly assigned to transdermal oxybutynin, extended-release tolterodine 4 mg, or placebo. Transdermal oxybutynin and extended-release tolterodine were superior to placebo by reduced daily incontinent episodes and improved quality of life. Localized pruritus occurred in 14% of patients using transdermal oxybutynin. Under certain circumstances, it may be beneficial to increase oxybutynin above the recommended dose. In a study by Bennett et al. (2004), patients with neurogenic detrusor overactivity were treated with extended-release oxybutynin up to 30 mg per day. Tolterodine is a potent muscarinic receptor antagonist without selectivity for particular receptor subtypes. Tolterodine is marketed in immediate release and extended release formulations. The major active metabolite shows a similar pharmacologic profile to its parent compound. A study compared extended-release to immediate-release tolterodine and placebo in 1529 adults with OAB symptoms, with the primary outcome of change in weekly incontinent episodes. Both medications showed a significantly better response than placebo. Dry mouth was significantly lower with extended-release tolterodine compared with immediate-release tolterodine and placebo. Several comparative studies of oxybutynin and tolterodine are known. The OBJECT trial, sponsored by the manufacturer of extended-release oxybutynin, was a prospective, randomized, double-blind parallel group study in
which 378 patients were randomized to receive extendedrelease oxybutynin 10 mg a day or immediate-release tolterodine 2 mg twice a day. Although both medications decreased detrusor overactivity, extended-release oxybutynin had better efficacy and a small but statistically significant advantage for mixed incontinence and urinary frequency, compared with immediate-release tolterodine. Dry mouth and central nervous system side effects were similar for both treatment groups. The OPERA study, also sponsored by the manufacturer of oxybutynin, was a randomized, double-blind, parallel group study of 790 women; the study compared extendedrelease oxybutynin 10 mg a day with tolterodine 4 mg once a day. Inclusion criteria included detrusor overactivity of 21 to 60 episodes per week and frequency greater than 10 episodes per 24 hours. Both medications were similar in decreasing detrusor overactivity episodes and total incontinence episodes. However, 23% of women taking oxybutynin reported no episodes of incontinence, compared with 16.8% of women taking tolterodine, a statistically significant difference. Oxybutynin was significantly more effective in reducing frequency, although it was also more likely to cause dry mouth. The ACET trial, which was sponsored by the manufacturer of tolterodine, involved two separate trials conducted in parallel with individual centers evaluating one study drug only. Patients were randomly assigned to open label treatment with either 2 or 4 mg extended-release tolterodine; in the other trial, patients were randomized to 5 or 10 mg extended-release oxybutynin. Investigators were blinded to the existence of the other trial. A total of 1289 patients with symptoms of urinary frequency and urgency with or without incontinence (OAB wet and OAB dry) were enrolled. Although not designed to make direct comparisons between the two study populations, the authors reported that after 8 weeks, extended-release tolterodine 4 mg was significantly better than extended-release oxybutynin 5 and 10 mg. Extended-release tolterodine 2 mg once daily was similar to extended-release oxybutynin 5 and 10 mg once daily. Using a visual analog scale, subjects taking extended-release tolterodine 4 mg had significantly less dry mouth than extended-release oxybutynin 10 mg. Interpretation of this study’s results was hampered because no data were supplied on the number of patients with isolated frequency and urgency versus those with detrusor overactivity, resulting in urge incontinence. Also, no objective parameters, such as a voiding diary, were used for outcome measures. Trospium is a quaternary amine with some antimuscarinic activity. Because of its structure, it does not cross the brain barrier well and may, therefore, have fewer central side effects. Zinner et al. (2004) performed a multicenter, parallel, double-blind, placebo-controlled trial with 523 patients and found trospium 20 mg twice daily to be superior to placebo in decreasing the number of voids and incontinence episodes. Darifenacin shows high selectivity for M3 receptor subtypes, with an 11-fold higher affinity for M3 than M2 receptors. Haab et al. (2004) studied 561 patients with detrusor overactivity and found that doses of darifenacin at 7.5 and
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15 mg were superior to placebo for reducing incontinent episodes. Solifenacin is another M3-selective antagonist with selectivity for the bladder over salivary glands. Chapple et al. (2004) published results of a phase III trial that compared solifenacin and tolterodine with placebo. With tolterodine 2 mg twice daily, patients experienced a statistically significant decrease in the number of voids per 24 hours, but the decrease in incontinence and urgency episodes per a 24-hour period was not statistically significant. In contrast, solifenacin showed statistically significant decreases for the number of voids, incontinent episodes, and urgency episodes per 24 hours. Dry mouth was seen in 18.6% of patients using immediate-release tolterodine and in 14% and 21.3% using solifenacin 5 and 10 mg, respectively. ADRENERGIC MEDICATIONS In addition to antimuscarinic medications, adrenergic agonists and antagonists are also used. Because the bladder and urethra contain α- and β-adrenergic receptors, stimulation of these receptors can influence bladder and urethral function. Alpha-adrenergic antagonists are used for benign prostatic hyperplasia, including alfuzosin, doxazosin, prazosin, tamsulosin, and terazosin. Ephedrine, phenylpropanolamine, and pseudoephedrine act via direct stimulation of α-adrenergic receptors to increase urethral tone and closure pressure. Beta-adrenergic agonists, including isoproterenol and terbutaline, induce bladder relaxation and decreased intravesical pressure. The Cochrane Database (2003) reviewed adrenergic drugs for urinary incontinence in adults. In 15 randomized trials, weak evidence suggested that adrenergic agonists were better than placebo for urinary incontinence. DRUGS THAT ACT ON AFFERENT MECHANISMS Two medications that affect receptors on afferent nerves have been identified for potential use as therapeutic interventions: capsaicin and resiniferatoxin (RTX). Both medications are dissolved in ethanol and instilled into the bladder. Capsaicin may initially produce some discomfort when instilled, whereas RTX does not. RTX is 1000 times more potent than capsaicin such that the nerve may be “burned out” before it can cause excitation. Kim et al. (2003) treated 36 patients with refractory neurogenic detrusor overactivity with intravesical RTX. Improvements were seen in mean cystometric capacity and incontinence episodes. Some patients had an increase in cystometric capacity of 500%. These agents are currently available for use in research investigations only. TRICYCLIC ANTIDEPRESSANTS Tricyclic antidepressants, including amitriptyline and imipramine, produce smooth muscle relaxation, inhibit norepinephrine reuptake, and have anticholinergic properties. Woodman et al. (2001) reported that imipramine was an effective treatment in 25 patients with detrusor overactivity. Incontinent episodes were reduced and quality of life was improved; however, 41% of patients experienced side effects and, ultimately, 14% withdrew from the study.
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CENTRAL MECHANISMS Potential neurotransmitter targets in the central mechanisms include serotonin, GABA, glycine, dopamine, and noradrenaline. Both sympathetic and parasympathetic autonomic nuclei, as well as urethral sphincter motor nuclei, receive serotonergic input from the Raphe nuclei in the caudal brainstem. Serotonergic pathways promote urine storage by activating sympathetic pathways and inhibiting parasympathetic pathways. Duloxetine is a selective serotonin and norepinephrine reuptake inhibitor that shows promise for the treatment of both urge and stress incontinence. Although phase III studies have shown duloxetine to be superior to placebo in the treatment of stress incontinence, Bump et al. (2003) recently analyzed a subset of women with mixed incontinence and found that duloxetine showed equal efficacy in women with either mixed incontinence or pure stress urinary incontinence. Duloxetine is currently awaiting approval from the U.S. Food and Drug Administration (FDA). BOTULINUM TOXIN Botulinum neurotoxin causes muscle paralysis by blocking release of acetylcholine at the nerve terminal. Case series of cystoscopic injection of botulinum toxin into detrusor muscle have been reported. Schurch et al. (2000) reported on 21 patients with severe neurogenic detrusor overactivity secondary to spinal cord injury. Of 19 patients available at 6 weeks follow-up, 17 became continent and significantly decreased anticholinergic medication use. Reitz et al. (2004) retrospectively reviewed results of 231 patients with neurogenic detrusor overactivity secondary to spinal cord injury and showed increased cystometric capacity, increased voided volume, and decreased voiding pressure.
Surgical Management Sacral neuromodulation involves inserting an insulated wire into the S3 foramen and connecting the wire to a stimulation device called InterStim, which is produced and marketed by Medtronic (Medtronic, Inc., Minneapolis, MN). For more information on neuromodulation therapy, see Chapter 31. More invasive surgery is reserved for the treatment of associated urologic conditions and in the uncommon case in which intractable symptoms of detrusor overactivity persist, despite exhausting all conservative and less invasive measures previously discussed. Historically, many different surgical procedures have been used, but only a few have stood the test of time. Bladder transection was initially described by TurnerWarwick and Ashken in 1967. This operation involved complete transection of the bladder above the trigone and ureteric orifices and division of all inferior lateral communications. The largest series was reported by Mundy (1983), who noted a 74% subjective cure rate at 1-year follow-up. Transvaginal infiltration of the pelvic plexus with phenol was described by Ewing et al. (1982) as a less traumatic alternative to bladder transection. Initial studies reported success rates around 60% for refractory detrusor overactivity. Wall
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and Stanton (1989) reported on a series of 28 patients, with refractory detrusor overactivity, who underwent a total of 40 transvesical phenol injections. Only eight patients (29%) achieved a significant response, and all relapsed during the 22-month follow-up period. A similar denervation procedure is selective blockade of the sacral pelvic nerves, which involves the injection of a local anesthetic into the foramina of sacral segment S3. Permanent neurolysis can be obtained by the injection of 6% aqueous phenol. The few studies on this procedure have reported variable results. Awad et al. (1987) developed a similar technique using a cryoprobe instead of phenol injections. They reported good or excellent results in 16 of 17 patients with idiopathic detrusor overactivity. Mean duration of follow-up was 4.8 months. The technique was safe, and temporary sensory disturbances were the only side effects. The Ingelman-Sundberg procedure is a transvaginal partial denervation of the bladder originally described in 1959 (Ingelman-Sundberg, 1978). In this procedure, the inferior hypogastric pelvic nerve plexus is resected after a preliminary local anesthetic block has indicated the likelihood of a symptomatic response. Successful outcomes have been reported in 50% to 80% of patients. Augmentation cystoplasty has been used for cases of resistant detrusor overactivity. The bladder is bisected almost completely, and a patch of gut, usually ileum, equal in length to the circumference of the bisected bladder (approximately 25 cm), is sewn in place. The operation often cures the symptoms of detrusor overactivity but results in inefficient voiding. Patients may have to learn to strain to void or resort to clean intermittent self-catheterization. Mundy and Stephenson (1985) reported on a series of 40 patients treated by “clam” ileocystoplasty. Thirty-six (90%) were cured of their symptoms, and 30 were able to void spontaneously and efficiently. Recent concerns regarding the possible long-term untoward sequelae of enterocystoplasty have led to a search for an alternative. Detrusor myomectomy may achieve the same improvement in bladder compliance and is currently under study in various clinical situations. For women with severe detrusor overactivity in whom all other methods of treatment have failed, urinary diversion via an ileal conduit may be considered as a last resort. This therapy is particularly useful in young disabled patients with severe neurologic dysfunction.
Conclusion OAB symptoms are prevalent in our society, and we are just beginning to have a full understanding of the impact of this condition. The mainstay of treatment has been antimuscarinic medications along with behavior modification. A tremendous amount of resources have been spent marketing and comparing different anticholinergic agents. Hay-Smith et al. (2005) reviewed 32 randomized controlled trials but found little clinical difference between anticholinergic medication and placebo. In all trials, the placebo effect is quite dramatic. This underscores the importance of education when treating patients with this syndrome. Research must continue and hopefully lead to
new approaches of therapy for this syndrome. Additional anticholinergic medications will probably add little to currently available treatments.
NOCTURIA Nocturia is a symptom in which the individual feels the need to wake at night one or more times to void. Nocturia, as a condition, has only recently begun to be recognized in its own right rather than as a symptom of some other disorder. Nocturia is a very common condition, particularly affecting older age groups. Four percent of children ages 7 to 15 experience habitual nocturia (Mattsson, 1994), whereas the prevalence is as high as 58% in women between ages 50 and 60 and 72% in women over age 80. Diokno et al. (1986) noted the prevalence of nocturia (defined as more then three voids per night) to be 7.3% in women who complain of urinary incontinence, 25% in women with irritative voiding symptoms, and 24% in women with difficulty emptying. Patients with nocturia will present not only to the gynecologist or urologist, but also to the geriatrician, neurologist, sleep expert, endocrinologist, and general practitioner. As each specialist approaches patients from a different perspective, it is important that some of the basic terms surrounding nocturia have specific definitions so that physicians are referring to the same condition and managing it appropriately. The following are standardized definitions for various terms associated with nocturia. The basis for these values is an average 70-kg individual who sleeps 8 hours a night; the normal range is generally considered to be within two standard deviations of the average values. Nocturia—the number of voids recorded during a night’s sleep. Each void is preceded and followed by sleep. Nocturnal urine volume—the total volume of urine passed during the night, including the first morning void. Rate of nocturnal urine production—nocturnal urine volume divided by the amount of time asleep, reported in milliliters per second. Nocturnal polyuria—nocturnal urine volume greater than 20% to 30% of total 24-hour urine volume (agedependent). Twenty-four hour urine voided volume—total volume of urine voided during a 24-hour period (first void to be discarded—24 hours begin at the time of the next void). Polyuria—24-hour voided volume in excess of 2800 mL (i.e., in an average 70-kg person, >40 mL/kg). Night—the period of time between going to bed with the intention of sleeping and waking up with the intention of rising. Nighttime frequency—the number of voids recorded at night, that is, from the time that the individual goes to bed, with the intention of sleeping, to the time that the individual wakes up, with the intention of rising.
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First morning void—the first void after waking, with the intention of rising. Maximum voided volume—the largest single voided volume measured in a 24-hour period.
Causes of Nocturia The causes of nocturia are largely the same for men and women. The underlying causes are well described in the ICS document on nocturia terminology by van Kerrebroeck et al. (2002). Possible contributing factors are reviewed in Box 28-4. Although nocturia stems from a combination of causes in most individuals, nocturnal polyuria is probably a contributing factor in a large proportion of women. In elderly patients, sleep-related issues are important, sleep disturbances and hyposedative use being quite prevalent in this age group. Often difficult to tell is whether patients are waking to void or voiding because they are awake. At times, nocturia may simply be a consequence of spending too much time in bed. In the aging population, bladder capacity may decrease. Thus, voiding more fluid at night is commonly coupled with a bladder that is holding less fluid. In addition, most elderly patients with nocturia have existing comorbidities, which can make treatment very complex.
Clinical Evaluation When assessing a patient for nocturia, determining whether the patient feels that her nocturia is a problem to her is important. The initial evaluation starts with a detailed history, including questions about voiding behavior; previous urinary tract infections; medical and surgical history; and
BOX 28-4
CAUSES OF NOCTURIA
A. Behavioral, psychological, and/or environmental issues B. Diurnal polyuria or polyuria/polydipsia syndromes 1. Diabetes mellitus 2. Primary polydipsia 3. Central or nephrogenic diabetes insipidus 4. Hypercalcemia C. Nocturnal polyuria 1. Daytime fluid retention 2. Venous insufficiency 3. Hypoalbuminemia 4. Diuretic therapy 5. Congestive heart failure 6. Renal disease 7. Neurologic dysfunction D. Bladder storage or emptying problems 1. Infection 2. Urogenital altrophy 3. Overactive bladder E. Sleep-related issues 1. Sleep disturbance 2. Sleep apnea 3. Time spent in bed 4. Hyposedative use F. Combined factors
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possible sleep disturbances. A physical examination should be performed, and urinary tract infection should be ruled out. Assuming that the patient desires treatment, behavioral changes that include reducing caffeine and alcohol intake, and fluid management to limit fluid intake before bedtime, may be initiated. In some cases, this may be sufficient to manage the patient’s nocturia. If patients are still symptomatic after simple measures, further evaluation should be performed. Care must be taken not to impose a general fluid restriction before further evaluation is carried out, because this could have serious consequences in women with undiagnosed diabetes insipidus. Further evaluation includes asking the patient to keep a frequency-volume chart for 24 to 72 hours, in which she records the volume and type of fluid ingested, as well as the volume and time of each void. It should also include the time she retires to bed, what time she wakes up, and her subjective assessment of whether she felt that the night was good or bad in terms of her sleeping pattern. If a sleep disorder is suspected, a nocturnal polysomnograph should be ordered. Sleep disorders potentially related to nocturia include insomnia, obstructive and central apnea syndrome, restless legs syndrome, periodic legs syndrome, parasomnias, sleep disorders related to medical conditions, such as chronic obstructive lung disease, and sleep disorders related to neurologic diseases, such as Alzheimer’s disease. If a patient’s urine output exceeds 40 mL/kg body weight during a 24-hour period, this meets the definition of polyuria and should be investigated further. The patient may have solute diuresis (e.g., diabetes mellitus) or diabetes insipidus. The various types of diabetes insipidus (pituitary, renal, gestational, and primary polydipsia) can be differentiated by measuring the glucose, specific gravity and osmolality of a 24-hour urine collection, followed by various more specialized tests best undertaken by the appropriate subspecialist (Robertson, 1995). Patients with nocturia without polyuria will most likely have reduced voided volume or a sleep disorder. Nocturnal polyuria (production of an abnormally large volume of urine during sleep) is measured by including all urine produced after going to bed and the first void after arising. This value varies considerably from person to person and normally increases with age. Causes of nocturnal polyuria include congestive heart failure, autonomic dysfunction, sleep apnea syndrome, renal insufficiency, estrogen deficiency, and circadian defect in secretion or action of antidiuretic hormone. Bladder storage problems can be suspected from the frequency-volume chart by comparing each nighttime voided volume with the patient’s maximum bladder capacity. However, there is no definitive range of normal or abnormal volumes, and clinical judgment is required in reviewing the patient’s frequency-volume chart. Some patients who could be suspected of having a bladder storage problem, based on the frequency-volume chart, in reality, may have a sleep disturbance. Patients who wake frequently at night for other reasons may feel the need (or habit) to void each time they wake, voiding a small volume. Further investigation in a sleep laboratory may be necessary to determine the cause of nocturia in these patients.
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Treatment Options Depending on the diagnosis and underlying cause(s), treatment options for nocturnal polyuria may include restriction of fluids in the evening, time-release diuretics, afternoon naps, elevation of the legs, compression stockings, and antidiuretic hormone. Fluid restriction should be avoided in patients who have accumulations of fluid in the lower extremities. Swelling in the legs or presacral area may improve with diuretics, assuming that they are administered well before bedtime. Bumetanide, furosemide, and, recently, imipramine have all proved effective in reducing polyuria (Hunsballe, 1997). Desmopressin has also reduced or eliminated nocturia in patients with diabetes insipidus, autonomic dysfunction, multiple sclerosis, and Parkinson’s disease. (Cannon, 1999; Hilton, 1983). Symptoms of nocturia may also improve after a 6-month continuous regimen of combined hormone replacement therapy (Kok, 1999).
Bibliography PREVALENCE AND INCIDENCE Abrams P. Detrusor instability and bladder outlet obstruction. Neurourol Urodyn 1985;4:317. Arnold EP, Webster JR, Loose H, et al. Urodynamics of female incontinence: factors influence the results of surgery. Am J Obstet Gynecol 1973;117:805. Couillard DR, Webster GD. Detrusor instability. Urol Clin North Am 1995;22:593. Diokno AC, Brown MB, Brock BM, et al. Clinical and cystometric characteristics of continent and incontinent noninstitutionalized elderly. J Urol 1988;140:567. Hodgkinson CP, Ayers MA, Drukker BH. Dyssynergic detrusor dysfunction in the apparently normal female. Am J Obstet Gynecol 1963;87:717. Milsom I, Stewart W, Thuroff J. The prevalence of overactive bladder. Am J Manag Care 2000;6(11 Suppl):S565. Payne CK. Epidemiology, pathophysiology and evaluation of urinary incontinence and overactive bladder. Urology 1998;51(2A Suppl):3. Sand PK, Hill RC, Ostergard DO. Supine urethroscopic and standing cystometrogram as screening methods for the detection of detrusor instability. Obstet Gynecol 1987;70:57. Stewart WF, Van Rooyen JB, Cundiff GW, et al. Prevalence and burden of overactive bladder in the United States. World J Urol 2003;20(6):327. Turner-Warwick RT. Observations on the function and dysfunction of the sphincter and detrusor mechanism. Urol Clin North Am 1979;6:13. Wagner TH, Hu TW, Bentkover J, et al. Health-related consequences of overactive bladder. Am J Manag Care 2002;8(19 Suppl)S598. 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. Webster GD, Sihelnik SA, Stone AR. Female urinary incontinence: the incidence, identification and characteristics of detrusor instability. Neurourol Urodyn 1984;3:235. Wein AJ, Rovner ES. Definition and epidemiology of overactive bladder. Urology 2002;60(5 Suppl 1):7–12; discussion 12.
ETIOLOGY Anderson JT, Bradley WE. Bladder and urethral innervation in multiple sclerosis. Br J Urol 1976;48:193. Awad SA, Gajewski JB, Sogbein SK, et al. Relationship between neurological and urological status in patients with multiple sclerosis. J Urol 1984;132:499. Barrington FJ. The component reflexes of micturition in the cat. Brain 1931;54:177. Bauer SB, Retic AB, Colodny AH, et al. The unstable bladder of childhood. Urol Clin North Am 1980;7:321.
Beck RP, Armsch D, King C. Results in treating 210 patients with detrusor overactivity incontinence of urine. Am J Obstet Gynecol 1976;125:593. Beck RP, Warren KG, Whitman P. Urodynamic studies in female patients with multiple sclerosis. Am J Obstet Gynecol 1981;139:273. Bhatia NN, Bergman A. Cystometry: unstable bladder and urinary tract infection. Br J Urol 1986;58:134. Blaivas JG, Bhimani G, Labib KB. Vesicourethral dysfunction in multiple sclerosis. J Urol 1979;122:342. Bradley WE, Logothetis JL, Timm GW. Cystometric and sphincter abnormalities in multiple sclerosis. Neurology 1973;23:1131. Cardozo LD, Stanton SL, Williams JE. Detrusor instability following surgery for genuine stress incontinence. Br J Urol 1979;51:204. Cucchi A. Detrusor instability and bladder outflow obstruction. Evidence for a correlation between the severity of obstruction and the presence of instability. Br J Urol 1988;61:420. Elbadawi A, Yalla SV, Resnick NM. Structural basis of geriatric voiding dysfunction. III. Detrusor. J Urol 1993;150:1668. Frewen WK. An objective assessment of the unstable bladder of psychosomatic origin. Br J Urol 1978;50:246. Goldstein I, Siroky MB, Sax DS, et al. Neurourologic abnormalities in multiple sclerosis. J Urol 1982;128:541. Gonor SE, Carroll DJ, Metcalfe JB. Vesical dysfunction in multiple sclerosis. Urology 1985;25:429. Gu J, Restorick JM, Blank MA, et al. Vasoactive intestinal polypeptide in the normal and unstable bladder. Br J Urol 1983;55:645. Hassouna M, Lebel M, Elhilali M. Neurologic correlation in multiple sclerosis. Neurourol Urodyn 1984;3:73. Hilton P. Urinary incontinence during sexual intercourse: a common, but rarely volunteered, symptom. Br J Obstet Gynaecol 1988;95:377. Hodgkinson CP, Ayers MA, Drukker BH. Dyssynergic detrusor dysfunction in the apparently normal female. Am J Obstet Gynecol 1963;87:717. Ketelaer P, Leruitte A, Vereecker RL. Striated sphincter urethral and anal sphincter electromyography during cystometry in multiple sclerosis. Electromyogr Clin Neurophysiol 1977;17:427. Khan Z, Bhola A, Starer P. Urinary incontinence during orgasm. Urology 1988;21:279. Kinder RB, Mundy AR. Inhibition of spontaneous contractile activity in isolated human detrusor muscle strips by vasoactive intestinal polypeptide. Br J Urol 1985;57:20. Kinder RB, Mundy AR. Pathophysiology of idiopathic detrusor instability and detrusor hyper-reflexia: in vitro study of human detrusor muscle. Br J Urol 1987;60:509. Kinder RB, Restorick JM, Mundy AR. Vasoactive intestinal polypeptide in the hyper-reflexic neuropathic bladder. Br J Urol 1985;57:289. Petersen T, Pederson E. Neurourodynamic evaluation of voiding dysfunction in multiple sclerosis. Acta Neurol Scand 1984;69:402. Philp T, Read DJ, Higson RH. The urodynamic characteristics of multiple sclerosis. Br J Urol 1981;53:672. Piazza DH, Diokno AC. Review of neurogenic bladder in multiple sclerosis. Urology 1979;14:33. Rees DL, Whickham JE, Whitfield HN. Bladder instability in women with recurrent cystitis. Br J Urol 1978;50:524. Resnick NM, Yalla SV, Laurino E. The psychophysiolog y of urinary incontinence among institutionalized elderly persons. N Engl J Med 1989;320:1. Resnick NM, Yalla SV. Detrusor hyperactivity with impaired contractile function. JAMA 1987;257:3076. Schoenberg HW, Gutrich J, Banno J. Urodynamic patterns in multiple sclerosis. J Urol 1979;122:648. Sutherst JR, Brown M. The effect on the bladder pressure of sudden entry of fluid into the posterior urethra. Br J Urol 1978;50:406. Van Poppel H, Vereecken RL, Leruitte A. Neuro-muscular dysfunction of the lower urinary tract in multiple sclerosis. Paraplegia 1983;21:374. Wise BG, Cardozo LD, Cutner A, et al. Prevalence and significance of urethral instability in women with detrusor instability. Br J Urol 1993;72:26.
MIXED INCONTINENCE Colombo M, Zanetta G, Vitobello D, et al. The Burch colposuspension for women with and without detrusor over activity. Br J Obstet Gynaecol 1996;103:255.
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Karram MM, Bhatia NN. Management of coexistent stress and urge urinary incontinence. Obstet Gynecol 1989;73:4. Lockhart JL, Vorstman B, Politano VA. Anti-incontinence surgery in females with detrusor instability. Neurourol Urodyn 1984;3:201. McGuire EJ, Savastano JA. Stress incontinence and detrusor instability urge incontinence. Neurourol Urodyn 1985;4:313. McGuire EJ. Bladder instability and stress incontinence. Neurourol Urodyn 1988;7:563.
DIAGNOSIS Awad SA, McGinnis RH. Factors that influence the incidence of detrusor instability in women. J Urol 1983;130:114. Bates CP, Whiteside CG, Turner-Warwick RT. Synchronous cine pressure flow cystourethrography with special reference to stress and urge incontinence. Br J Urol 1970;42:714. Bent AE, Richardson DA, Ostegard DR. Diagnosis of lower urinary tract disorders in postmenopausal patients. Am J Obstet Gynecol 1983;145:218. Bergman A, Koonings PP, Ballard CA. Detrusor instability. Is the bladder the cause or the effect? J Reprod Med 1989;34:834. Bhatia NN, Bradley WE, Haldeman S. Urodynamics: continuous monitoring. J Urol 1982;128:963. Bradley WE, Timm GE. Cystometry VI. Interpretation. Urology 1976;2:231. Cantor TJ, Bates CP. A comparative study of symptoms and objective urodynamic findings in 214 incontinent women. Br J Obstet Gynaecol 1980;87:889. Cardozo LD, Stanton SL. Genuine stress incontinence and detrusor instability: a review of 200 cases. Br J Obstet Gynaecol 1980;87:184. Coolsaet BL, Blok C, van Venrouij GE, et al. Subthreshold detrusor instability. Neurourol Urodyn 1985;4:309. Coolsaet BL. Bladder compliance and detrusor activity during the collection phase. Neurourol Urodyn 1985;4:263. Diokno AC, Wells TJ, Brock BM, et al. Urinary incontinence in elderly women: urodynamic evaluation. J Am Geriatr Soc 1987;35:940. Eastwood HD, Warrell R. Urinary incontinence in the elderly female: prediction in diagnosis and outcome of management. Age Ageing 1984;13:230. Farrar DJ, Whiteside CG, Osborne JL, et al. A urodynamic analysis of micturition symptoms in the female. Surg Gynecol Obstet 1975;141:875. Griffiths CJ, Assi MS, Styles RA, et al. Ambulatory monitoring of bladder and detrusor pressure during natural filling. J Urol 1989;142:780. Haylen BT, Sutherst JR, Frazer MI. Is the investigation of most stress incontinence really necessary? Br J Urol 1989;61:147. Hilton P, Stanton SL. Algorithmic method for assessing urinary incontinence in elderly women. Br Med J 1981;282:940. Jeffcoate TN, Francis WJ. Urgency incontinence in the female. Am J Obstet Gynecol 1966;94:604. Korda A, Krieger M, Hunter P, et al. The value of clinical symptoms in the diagnosis of urinary incontinence in the female. Aust N Z J Obstet Gynaecol 1987;27:149. Kulseng-Hanssen S, Klevmark B. Ambulatory urethro-cysto-rectometry: a new technique. Neurourol Urodyn 1988;7:119. Lockhart JL, Sherrel F, Weinstein D, et al. Urodynamics in women with stress and urge incontinence. Urology 1982;20:333. Low JA, Mauger GM, Drajovic J. Diagnosis of the unstable detrusor: comparison of an incremental and continuous infusion technique. Obstet Gynecol 1985;65:99. Malone-Lee JG, Saadu A, Lieu PK. Evidence against the existence of a specific parkinsonian bladder. Neurourol Urodyn 1993;12(4):341. Mayo ME. Detrusor hyperreflexia: the effect of posture and pelvic floor activity. J Urol 1978;119:635. Ouslander J, Leach G, Abelson S, et al. Simple versus multichannel cystometry in the evaluation of bladder function in an incontinent geriatric population. J Urol 1988;140:1482. Sutherst JR, Brown MC. Comparison of single and multichannel cystometry in diagnosing bladder instability. Br Med J 1984;288:1720. Turner-Warwick RT. Some clinical aspects of detrusor dysfunction. J Urol 1975;113:539. Webster GE, Older RA. The value of subtracted bladder pressure measurements in routine urodynamic studies. Urology 1980;16:656.
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TREATMENT: BEHAVIORAL, PSYCHOTHERAPY, AND ACUPUNCTURE 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(18):2293. Burgio KL, Locher JL, Goode PS, et al. Behavioral vs drug treatment for urge urinary incontinence in older women: a randomized controlled trial. JAMA 1998;280(23):1995. Burgio KL, Locher JL, Goode PS. Combined behavioral and drug therapy for urge incontinence in older women. J Am Geriatr Soc 2000;48(4): 370–374. Burgio KL, Whitehead WE, Engel BT. Urinary incontinence in the elderly: bladder-sphincter biofeedback and toileting skills training. Ann Intern Med 1985;103:507. Cardozo LD, Abrams PD, Stanton SL, et al. Idiopathic bladder instability treated by biofeedback. Br J Urol 1978;50:512. Cardozo LD, Stanton SL, Hafner J, et al. Biofeedback in the treatment of detrusor instability. Br J Urol 1978;50:250. Cardozo LD, Stanton SL. Biofeedback: a 5-year review. Br J Urol 1984;56:220. Cheng PT, Wong MK, Chang PL. A therapeutic trial of acupuncture in neurogenic bladder of spinal cord-injured patient. A preliminary report. Spinal Cord 1998;36:476. Fantl JA, Hurt WG, Dunn LJ. Detrusor instability syndrome: the use of bladder retraining drills with and without anticholinergics. Am J Obstet Gynecol 1981;140:885. Fantl JA, Wyman JF, McClish DK, et al. Efficacy of bladder training in older women with urinary incontinence. JAMA 1991;26(55):609. Ferrie BG, Smith JS, Logan D, et al. Experience with bladder training in 65 patients. Br J Urol 1984;56:482. Frewen WK. A reassessment of bladder training in detrusor dysfunction in the female. Br J Urol 1982;54:372. Hadley EC. Bladder training and related therapies for urinary incontinence in older people. JAMA 1986;256:372. Hafner RJ, Stanton SL, Guy J. A psychiatric study of women with urgency and urgency incontinence. Br J Urol 1977;49:211. Hunjo H, Naya Y, Ukimura D, et al. Acupuncture on clinical symptoms and urodynamic measurements in spinal core injured patients with detrusor hyperreflexia. Urol Int 2000;65:190. Jarvis GJ. A controlled trial of bladder drill and drug therapy in the management of detrusor instability. Br J Urol 1981;53:565. MacCaulay AJ, Stern RS, Holmes DM, et al. Micturition and the mind: psychological factors in the etiology and treatment of urinary symptoms in women. Br Med J 1987;294:540. Millard RJ, Oldenburg BF. The symptomatic, urodynamic, and psychodynamic results of bladder re-education programs. J Urol 1983;130:715. Minni B, Capozza N, Creti G, et al. Bladder instability and enuresis treated by acupuncture and electrotherapeutics: early urodynamic observations. Acupunct Electrotherap Res 1990;15:19. Moore KH, Sutherst JR. Response to treatment of detrusor instability in relation to psychoneurotic status. Br J Urol 1990;66:486. Norton KR, Bnat AV, Stanton SL. Psychiatric aspects of urinary incontinence in women attending an outpatient clinic. Br Med J 1990;301:271. Pengelly AW, Booth CM. A prospective trial of bladder training as treatment of detrusor instability. Br J Urol 1980;52:463. Philip T, Shah PJ, Worth PH. Acupuncture in the treatment of bladder instability. Br J Urol 1988;1:490.
TREATMENT: FUNCTIONAL ELECTRICAL STIMULATION Bent AE, Sand PK, Ostergard DR. Transvaginal electrical stimulation in the treatment of genuine stress incontinence and detrusor instability. Neurourol Urodyn 1989;8:363. Eriksen BC, Bergmann S, Eik-Nes SH. Maximal electrostimulation of the pelvic floor in female idiopathic detrusor instability and urge incontinence. Neurourol Urodyn 1989;8:219. Fall M, Ahlstrom K, Carlsson C, et al. Contelle: pelvic floor stimulation for female stress-urge incontinence: a multicenter study. Urology 1986;27:282. Fall M. Does electrostimulation cure urinary incontinence? J Urol 1984; 131:664. Fossberg E. Urge incontinence treated with maximal electrical stimulation. Neurourol Urodyn 1988;7:270.
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Leach GE, Bavendam TG. Prospective evaluation of the Incontan transrectal stimulator in women with urinary incontinence. Neurourol Urodyn 1989;8:231. McGuire EJ, Shi-Chun Z, Horwinski R, et al. Treatment of motor and sensory detrusor instability by electrical stimulation. J Urol 1983;129:78. Merrill D. The treatment of detrusor incontinence by electrical stimulation. J Urol 1979;122:515. Plevnik S, Janez J, Vrtenik P, et al. Short-term electrical stimulation: home treatment for urinary incontinence. World J Urol 1986;4:24. Plevnik S, Janez J. Maximal electrical stimulation for urinary incontinence. Report of 98 cases. Urology 1979;14:638. Spruijt J, Vierhout M, Verstraeten R, et al. Vaginal electrical stimulation of the pelvic floor. A randomized feasibility study in urinary incontinent elderly women. Acta Obstet Gynecol Scand 2003;82:1043. Wang AC, Wang YY, Chen MC. Single-blind, randomized trial of pelvic floor muscle training, biofeedback assisted pelvic floor muscle training, and electrical stimulation in the management of overactive bladder. Urology 2004;63:61. Wise BG, Cardozo LD, Cutner A, et al. Maximal electrical stimulation: an acceptable alternative to anticholinergic therapy. Int Urogynecol J 1992;(3)3:270.
TREATMENT: DRUG THERAPY Abrams P, Freeman R, Anderstrom C, et al. Tolterodine, a new antimuscarinic agent: as effective but better tolerated than oxybutynin in patients with an overactive bladder. Br J Urol 1998;81:801. Abrams P, Freeman R, Anderstrom C, Mattiasson A. Tolterodine, a new antimuscarinic agent: as effective but better tolerated than oxybutynin in patients with an overactive bladder. BJU Int 1998;81(6):801. Alhasso A, Glazener CM, Pickard R, N’Dow J. Adrenergic drugs for urinary incontinence in adults. Cochran Database Syst Rev 2003(2): CD001842. Anderson RU, Mobley D, Blank B, et al. Once daily controlled versus immediate release oxybutynin chloride for urge urinary incontinence. OROS Oxybutynin Study Group. J Urol 1999;161(6):1809. 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 Clinic Proc 2001;76(4):358. Appell RA. Clinical efficacy and safety of tolterodine in the treatment of overactive bladder: a pooled analysis. Urology 1997;50(6A Suppl):90–96; discussion 97. Appell RA. Clinical efficacy and safety of tolterodine in the treatment of overactive bladder: a pooled analysis. Urology 1997;50(Suppl 6A):90. Barker G, Clenning PP. Treatment of the unstable bladder with propantheline and imipramine. Aust N Z J Obstet Gynaecol 1987;27:152. Bennett N, O’Leary M, et al. Can higher doses of oxybutynin improve efficacy in neurogenic bladder? J Urol 2004;171:749. Blaivas JG, Labib KB, Michalik SJ, et al. Cystometric response to propantheline in detrusor hyperreflexia: therapeutic implications. J Urol 1980;124:259. Bodner DR, Lindan R, Leffler E, et al. The effect of verapamil on the treatment of detrusor hyperreflexia in the spinal cord injured population. Paraplegia 1989;27:364. Briggs RS, Castleden CM, Asher MJ. The effect of flavoxate on uninhibited detrusor contractions and urinary incontinence in the elderly. J Urol 1980;123:665. Brooks ME, Braf ZF. Oxybutynin chloride (Ditropan): clinical uses and limitations. Paraplegia 1980;18:64. Cannon TW, Chancellor MB. Pharmacotherapy of the overactive bladder and advances in drug delivery. Clin Obstet Gynecol 2002;45(1):205. Cardozo LD, Stanton SL, Robinson H, et al. Evaluation of flurbiprofen in detrusor instability. Br Med J 1980;280:281. Cardozo LD, Stanton SL. A comparison between bromocriptine and indomethacin in the treatment of detrusor instability. J Urol 1980;123:399. Cardozo LD, Stanton SL. An objective comparison of the effects of parenterally administered drugs in patients suffering from detrusor instability. J Urol 1979;122:58. Castleden CM, Duffen CM, Gulati RS. Double-blind study of imipramine and placebo for incontinence due to bladder instability. Age Ageing 1986;15:299. Chancellor M, Freedman S, Antoci J, et al. Tolterodine, an effective and well tolerated treatment for urge incontinence and other overactive bladder symptoms. Clin Drug Invest 2000;19(2):83.
Chapple CR, Rechberger T, Al-Shukri S, et al. Randomized double-blind placebo- and tolterodine-controlled trial of the once-daily antimuscarinic agent solifenacin in patients with symptomatic overactive bladder. BJU Int 2004;93:303. Davila GW, Daugherty CA, Sanders SW, for the Transdermal Oxybutynin Study Group. 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. Detrol® LA (tolterodine tartrate extended release capsules) prescribing information. Pharmacia & Upjohn Company, Kalamazoo, MI. Diokno A, Appell R, Sand P, 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. Diokno AC, Lapides J. Oxybutynin: a new drug with analgesic and anticholinergic properties. J Urol 1977;108:307. Ditropan XL® (oxybutynin chloride extended release tablets) prescribing information. ALZA Corporation, Mountain View, CA. Dmochowski RR, Davila GW, Zinner NR, et al., for the Transdermal Oxybutynin Study Group. Efficacy and safety of transdermal oxybutynin in patients with urge and mixed urinary incontinence. J Urol 2002;168(2):580. Fantl JA, Wyman JF, Anderson RL, et al. Postmenopausal urinary incontinence: comparison between nonestrogen supplemented and estrogen supplemented women. Obstet Gynecol 1988;71:823. Farrar DJ, Osborne JL. The use of bromocriptine in the treatment of the unstable bladder. Br J Urol 1976;48:235. Finkbeiner AE, Bissada NK, Welch LT. Uropharmacology: part VI. Parasympathetic depressants. Urology 1977;10:503. Fischer-Rasmussen W, Korhonon M, Bossberg E, et al. Evaluation of longterm safety and clinical benefit of terodiline in women with urgency urge incontinence: a multicentre study. Scand J Urol Nephrol Suppl 1984;87:35. Gajweski JB, Awad SA. Oxybutynin versus propantheline in patients with multiple sclerosis and detrusor hyperreflexia. J Urol 1986;135:966. Gleason DM, Susset J, White C, et al. 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. Gruneberger A. Treatment of motor urge incontinence with Clenbuterol and flavoxate hydrochloride. Br J Obstet Gynaecol 1984;91:275. Gupta SK, Sathyan G. Pharmacokinetics of an oral once-a-day controlledrelease oxybutynin formulation compared with immediate-release oxybutynin. J Clin Pharmacol 1999;39(3):289. 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. Harvey MA, Baker K, Wells GA. Tolterodine versus oxybutynin in the treatment of urge urinary incontinence: a meta-analysis. Am J Obstet Gynecol 2001;185(1):56. Hay-Smith J, Herbison P, Ellis G, Morris A. Which anticholinergic drug for overactive bladder symptoms in adults. Cochrane Database Syst Rev 2005;Jul 20(3):CD005429. Holmes DM, Montz FJ, Stanton SL. Oxybutynin versus propantheline in the management of detrusor instability. A patient-regulated variable dose trial. Br J Obstet Gynaecol 1989;96:607. Kim JH, Rivas DA, Shenut PF, et al. Intravesical resiniferatoxin for refractory detrusor hyperreflexia: a multicenter, blinded, randomized, placebocontrolled trial. J Spinal Cord Med 2003;26:358. Kohler FP, Morales P. Cystometric evaluation of flavoxate hydrochloride in normal and neurogenic bladders. J Urol 1968;100:729. Larsson G, Hallen B, Nilvebrant L. Tolterodine in the treatment of overactive bladder: analysis of the pooled phase II efficacy and safety data. Urology 1999;53(5):990. Levin RM, Staskin DR, Wein AJ. The muscarinic cholinergic binding kinetics of the human urinary bladder. Neurourol Urodyn 1982;1:221. Macfarlane JR, Tolley D. The effect of terodiline on patients with detrusor instability. Scand J Urol Nephrol 1984;87(Suppl):51. Massey JA, Abrams P. Dose titration in clinical trials. An example using emepronium carrageenate in detrusor instability. Br J Urol 1986;58:125. Moisey CV, Stephenson TP, Brendler CB. The urodynamic and subjective results of treatment of detrusor instability with oxybutynin chloride. Br J Urol 1980;52:472.
Chapter 28
Ramsden PD, Hindmarsh JR, Price DA, et al. DDAVP for adult enuresis—a preliminary report. Br J Urol 1982;54:256. Reitz A, Schurch B. Botulinum toxin type B injection for management of type A resistant neurogenic detrusor overactivity. J Urol 2004;171:804. Rentzhog L, Stanton SL, Cardozo L, et al. Efficacy and safety of tolterodine in patients with detrusor instability: a dose-ranging study. Br J Urol 1998;81(1):42. Schurch B, Stohrer M, Kramer G, et al. 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. Stanton SL. A comparison of emepronium bromide and flavoxate hydrochloride in the treatment of urinary incontinence. J Urol 1973;110:529. Sussman D, Garely A. Treatment of overactive bladder with once-daily extended release tolterodine or oxybutynin: the Antimuscarinic Clinical Effectiveness Trial (ACET). Curr Hosp Res Opin 2002;18(4):177. Tapp A, Fall M, Norgaard J, et al. Terodiline: a dose-titrated, multicenter study of the treatment of idiopathic detrusor instability in women. J Urol 1989;142:1027. Thompson IM, Lauvetz R. Oxybutynin in bladder spasm, neurogenic bladder, and enuresis. Urology 1976;8:452. Thuroff JW, Chartier-Kastler E, Corcus J, et al. Medical treatment and medical side effects in urinary I continence in the elderly. World J Urol 1998;16 Suppl 1:S48. Ulmsten U, Ekman G, Andersson KE. The effect of terodiline treatment in women with motor urge incontinence. Results from a double-blind study and long-term treatment. Am J Obstet Gynecol 1985;153:619. Van Kerrebroeck P, Amarenco G, Thuroff JW, et al. Dose-ranging study of tolterodine in patients with detrusor hyperreflexia. Neurourol Urodyn 1998;17(5):499. Van Kerrebroeck P, Kreder K, Jonas U, et al., on behalf of the Tolterodine Study Group. Tolterodine once-daily: superior efficacy and tolerability in the treatment of the overactive bladder. Urology 2001;57(3):414. Versi E, Appell R, Mobley D, et al. Dry mouth with conventional and controlled-release oxybutynin in urinary incontinence. The Ditropan XL Study Group. Obstet Gynecol 2000;95(5):718. Wein AJ. Pharmacologic options for the overactive bladder. Urology 1998;51(2A Suppl):43. Wein AJ. Drug therapy for detrusor instability: where are we? Neurourol Urodyn 1985;4:337. Yarker YE, Goa KL, Fitton A. Oxybutynin: a review of its pharmacodynamic and pharmacokinetic properties, and its therapeutic use in detrusor instability. Drugs Aging 1995;6(3):243. Zinner NR. Trospium chloride: an anticholinergic quaternary ammonium compound for the treatment of overactive bladder. Expert Opin Pharmacother 2005;6;1409. Zobrist RH, Quan D, Thomas HM, et al. Pharmacokinetics and metabolism of transdermal oxybutynin: in vitro and in vivo performance of a novel delivery system. Pharm Res 2003;20(1):103. Zobrist RH, Schmid B, Feick A, et al. Pharmacokinetics of the R- and S-enantiomers of oxybutynin and N-desethyloxybutynin following oral and transdermal administration of the racemate in healthy volunteers. Pharm Res 2001;18(7):1029.
TREATMENT: SURGERY Awad SA, Flood HD, Acker KL, et al. Selective sacral cryoneurolysis in the treatment of patients with detrusor instability hyperreflexia and hypersensitive bladder. Neurourol Urodyn 1987;6:307. Blackford HN, Murray K, Stephenson TP, et al. Results of transvesical infiltration of the pelvic plexuses with phenol in 116 patients. Br J Urol 1984;56:647. Clarke SJ, Forster DM, Thomas DG. Selective sacral neurectomy in the management of urinary incontinence due to detrusor instability. Br J Urol 1979;51:510. Diokno AC, Brock BM, Brown MB, Herzog AR. Prevalence of urinary incontinence and other urological symptoms in the noninstitutionalized elderly. J Urol 1986;136:1022. Ewing R, Bultitude MI, Shuttleworth KE. Subtrigonal phenol injection for urge incontinence secondary to detrusor instability in females. Br J Urol 1982;54:689. Hunsballe JM, Rettig S, Pedersen EB, et al. Single dose imipramine reduces nocturnal urine output in patients with nocturnal enuresis and nocturnal polyuria. J Urol 1992;158:830.
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Ingelman-Sundberg A. Partial bladder denervation for detrusor dyssynergia. Clin Obstet Gynecol 1978;21:797. Lucas MG, Thomas DG, Clarke S, et al. Long-term follow-up of selective sacral neurectomy. Br J Urol 1988;61:218. McGuire EJ, Savastano JA. Urodynamic findings and clinical status following vesical denervation procedures for control of incontinence. J Urol 1981;132:87. Mundy AR, Stephenson TP. “Clam” ileocystoplasty for the treatment of refractory urge incontinence. Br J Urol 1985;57:641. Mundy AR. Long-term results of bladder transection for urge incontinence. Br J Urol 1983;55:642. Mundy AR. The surgical treatment of detrusor instability. Neurourol Urodyn 1985;4:352. Mundy AR. The surgical treatment of urge incontinence of urine. J Urol 1982;128:481. Opsomer RJ, Klarskov P, Holm-Bentzen M, et al. Long-term results of superselective sacral nerve resection for motor urge incontinence. Scand J Urol Nephrol 1984;18:101. Rosenbaum TP, Shaw PJ, Worth PH. Trans-trigonal phenol failed the test of time. Br J Urol 1990;66:164 Torrens MJ. The role of denervation in the treatment of detrusor instability. Neurourol Urodyn 1985;4:353. Turner-Warwick RT, Ashken MH. The functional results of partial, subtotal and total cystoplasty with special reference to ureterocaecocystoplasty, selective sphincterotomy, and cystocystoplasty. Br J Urol 1967;39:3. Van Kerrebroeck P, Abrams P, Chaiken D, et al. The standardization of terminology in nocturia: report from the Standardization Subcommittee of the International Continence Society. BJU Int 2002;90:11. Wall LL, Stanton SL. Transvesical phenol injection of pelvic nerve plexuses in females with refractory urge incontinence. Br J Urol 1989;63:465.
NOCTURIA Asplund R. The Nocturnal Polyuria Syndrome (NPS). Gen Pharmacol 1995; 26(6):1203. Cannon A, Carter PG, McConnel AA, Abrams P. Desmopressin in the treatment of nocturnal polyuria in the male. BJU Int 1999;84:20. Carter PG. The role of nocturnal polyuria in nocturnal urinary symptoms in healthy elderly males. MD Thesis, Bristol, 1992. Chute CG, Panser LA, Girman CJ, et al. The prevalence of prostatism: a population based survey of urinary symptoms. J Urol 1993;150:85. Donovan JL, Abrams P, Peters TJ, et al. The ICS “BPH” Study: the psychometric validity and reliability or the ICS male questionnaire. Br J Urol 1996;77:554. Hald T, Nordling J, Andersen JT, et al. A patient weighted symptom score system in the evaluation of uncomplicated benign prostatic hyperplasia. Scand J Urol Nephrol Suppl 1991;138:59. Hay-Smith J, Herbison P, Ellis G, Murvis A. Which anticholinergic drug for overactive bladder symptoms in adults. Cochrane Database Syst Rev 2005;20:CD005429. 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. Jackson S, Donovan J, Brookes S, et al. The Bristol Female Lower Urinary Tract Symptoms questionnaire: development and psychometric testing. Br J Urol 1996;77:805. Kok AL, Burger CW, van de Weijer PH, et al. Micturition complaints in postmenopausal women treated with continuously combined hormone replacement therapy: a prospective study. Maturitas 1999;31:143. Kirkland JL, Lye M, Levy DW, Banerjee AK. Patterns of urine flow and electrolyte excretion in healthy elderly people. Br Med J 1983; 287(6406):1665. Mattiasson A. Nocturia: current knowledge and future directions. BJU Int 1999;84(Suppl 1):33. Mattsson S. Urinary incontinence and nocturia in healthy schoolchildren. Acta Paediatr 1994;83:950. Malmsten UG, Milsom I, Molander U, Norlen LJ. Urinary incontinence and lower urinary tract symptoms: an epidemiological study of men aged 45 to 99 years. J Urol 1997;158:1733. Middlekoop HA, Smilde-van den Doel DA, Neven AK, et al. Subjective sleep characteristics of 1485 males and females aged 50–93: effects of sex and age, and factors related to self evaluated quality of sleep. J Gerontol A Biol Sci Med Sci 1996;51:108.
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Rembratt A, Robertson GL, Norgaard JP, Andersson KE. Pathogenic aspects of nocturia in the elderly: differences between nocturics and non-nocturics. ICS meeting, 2000. Robertson GL. Diabetes insipidus. Endocrinol Metab Clin North Am 1995; 24(3):549. Robertson GL, Rittig S, Kovacs L, et al. Pathophysiology and treatment of enuresis in adults. Scand J Urol Nephrol Suppl 1999; 202:36. Swithinbank LV, Donovan J, James MC, et al. Female urinary symptoms: age prevalence in a community dwelling population using a validated questionnaire. Neurourol Urodyn 1998;16:432. Thorpy MJ. International classification of sleep disorders: diagnostic and coding manual. American Sleep Disorders Association (Chairman), Rochester, MN, 1990.
van Kerrebroeck P, Abrams P, Chaiken D, et al. The standardization of terminology in nocturia: report from the Standardization Sub-committee of the International Continence Society. Neurourol Urodyn 2002;21(2): 179. van Kerrebroeck P, Weiss JP. Standardization and terminology of nocturia. In Mattiasson A, ed. Nocturia Towards a Consensus. BJU 1999;84 (Suppl 1):1. Weiss JP, Blaivas JG, Stember DS, Brooks MM. Nocturia in adults: etiology and classification. Neurourol Urodyn 1998;17:467. Weiss JP, Blaivas JG. Nocturia. J Urol 2000;163:5.
29
Painful Bladder Syndromes Raymond A. Bologna and Kristene E. Whitmore
INTERSTITIAL CYSTITIS 377 Epidemiology 377 Diagnosis 379 URETHRAL SYNDROME 382 MANAGEMENT OF PAINFUL BLADDER SYNDROME Hydrodistention of the Bladder 383 Pharmacologic Therapy 383 Bladder Instillations 385 Sacral Neuromodulation 386 Refractory Symptoms 386 FUTURE DIRECTIONS 386
383
Hypersensitivity or sensory disorders of the lower urinary tract in women have been poorly elucidated, and management has been mandated by anecdotal evidence. Reliable and standardized testing to make an accurate diagnosis remains elusive. These disorders represent a spectrum of symptoms and conditions that include chronic bacterial cystitis, urgency and frequency syndrome, “sensory urgency,” and urethral syndrome. The International Continence Society (ICS) recognizes this syndrome as genitourinary pain syndromes and syndromes suggestive of lower urinary tract dysfunction. This definition would include painful bladder syndrome, urethral pain syndrome, vulvar pain syndrome, vaginal pain syndrome, perineal pain syndrome, and pelvic pain syndrome. Ultimately, hypersensitivity disorders, pelvic pain syndrome, and interstitial cystitis (IC) remain diagnoses of exclusion. This chapter focuses on what may be the ultimate expression of this disease process: IC. Anatomically, the short female urethra lends itself to infectious invasion. Childbirth and sexual activity cause displacement and trauma to the bladder neck. The postmenopausal state subjects the female lower urinary tract to the effects of chronic estrogen deprivation. This leads to ischemia, with a decrease in the urethral mucosal cushion and increased susceptibility of the bladder to bacterial adherence. The result is potential exposure of the neurovascular elements of the bladder wall to urinary toxins and infectious
agents. The physiologic ramifications of chronic overstimulation of the sensory nerve components of the lower urinary tract are under investigation. Hypersensitivity disorders affect most physicians’ practices. An estimated 15% of the 7 million women who experience a urinary tract infection (UTI) annually will have recurrences (greater than two episodes in 6 months or greater than three in 1 year). Of the 8.5 million women with urinary incontinence, about 40% have detrusor overactivity. More than 750,000 women have IC, and their quality of life is often lower than that of age-matched patients on renal dialysis. Significant clinical depression is present in 68% of these patients. In the absence of infection, patients with frequency, urgency, and pain are often classified as having one or more of the following: painful bladder syndrome, urethral syndrome, frequency and urgency syndrome, urethral instability, “sensory urgency,” or IC. These terms may represent one disease process in different phases or degrees of severity (Fig. 29-1). Appropriate classification is forthcoming, with current research efforts working toward defining etiology.
INTERSTITIAL CYSTITIS IC is the most challenging and encompassing hypersensitivity disorder. Tremendous efforts have been made to gain an understanding of this disease, but the etiology remains unclear. This section presents the current understanding of the pathogenesis and diagnostic approach to IC.
Epidemiology Skene first suggested the term interstitial cystitis in 1887. In 1907 Nitze described a painful bladder condition associated with urinary frequency and bladder ulcerations. In 1915 Hunner reported the classic ulcer associated with a contracted fibrotic bladder, mucosal congestion adjacent to the ulcers, and hemorrhage following bladder hydrodistention. Although IC was described early in the century, it was not until the 1970s that epidemiologic studies were done to evaluate and characterize this disease.
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Severity of symptoms
Recurrent UTI diagnosis
Urethral syndrome
Mild interstitial cystitis
NIH cases
Advanced interstitial cystitis
Figure 29-1 ■ Spectrum of interstitial cystitis. NIH, National Institutes of Health; UTI, urinary tract infection.
study group established in 1991, was sponsored to study the natural history of the disease and was based on a large population with symptoms consistent with IC. In 1999 the ICDB reported that the NIH guidelines were too restrictive to be used by clinicians. If the initial criteria were used, up to 60% of symptomatic women would not be diagnosed. Following an International Consensus in Kyoto, Japan, in April, 2003, the NIH assigned a panel to update the definition and management of IC. The guidelines are pending. ETIOLOGY
The reported prevalence of IC varies greatly. Population prevalence estimates of IC have ranged from 30 in 100,000 to 501 in 100,000 of the total population (as many as 1 million Americans). Many of these studies were self-reported questionnaires and were not confirmed by medical record review. It is also important to note that diagnostic criteria were not established until 1987. In 1987, for research purposes, the National Institutes of Health (NIH) established standardized diagnostic criteria for IC (Box 29-1). The National Interstitial Cystitis Data Base (ICDB), a cooperative multicenter longitudinal observation
BOX 29-1
NIH-NIDDK DIAGNOSTIC CRITERIA OF INTERSTITIAL CYSTITIS
Category A: At least one of the following findings on cystoscopy: ●
●
Diffuse glomerulations (at least 10 per quadrant) in at least 3 quadrants of the bladder A classic Hunner’s ulcer
Category B: At least one of the following symptoms: ● ●
Pain associated with the bladder Urinary urgency
Exclusion criteria: ● ● ● ● ●
●
● ●
● ● ● ● ● ● ●
●
Age <18 years* Urinary frequency while awake <8 times per day Nocturia fewer than two times per night Maximal bladder capacity >350 mL while patient is awake Absence of an intense urge to void with bladder filled to 150 mL of water with medium filling rate (30–100 mL/min) during cystometry Involuntary bladder contractions on cystometry using medium filling rate Duration of symptoms <9 months* Symptoms relieved by antimicrobial agents (antibiotics, urinary antiseptics), anticholinergics, or antispasmodics* Urinary tract or prostatic infection in the past 3 months* Active genital herpes Vaginitis* Uterine, cervical, vaginal, or urethral cancer within the past 5 years* Bladder or ureteral calculi* Urethral diverticulum* History of cyclophosphamide or chemical cystitis or tuberculosis or radiation cystitis Benign or malignant bladder tumors
note: These are the original criteria and are changing. Gillenwater JY, Wein AJ. Summary of the National Institute of Arthritis, Diabetes, Digestive and Kidney Diseases Workshop on Interstitial Cystitis, National Institutes of Health. Bethesda, MD, August 28–29, 1987. J Urol 1988;140:203. *Relative exclusion criteria.
The etiology of IC is currently unknown. Most authors believe it is multifactorial. Currently proposed causes include infectious agents, quantitative glycosaminoglycan (GAG) layer deficiency, ultrastructural abnormality of the lamina propria or interstitium of the bladder, mast cells, and neurogenic inflammation. The development and complete characterization of a promising urinary marker, antiproliferative factor (APF) may aid in our understanding of the etiology, diagnosis, and management of IC. INFECTIOUS AGENTS Extensive efforts have been made, with limited success, to establish an infectious agent as the cause of IC. Hunner (1915) first suggested a hematogenously disseminated bacterial cystitis as the cause. Most patients with IC report a history of UTI and have received several courses of antibiotics based on their symptoms, not on positive urine cultures. To date, no single bacterium, virus, fungus, or fastidious microorganism has been isolated as an etiologic factor in IC. Some authors believe that a low bacterial count, bacterial antigens, or by-products, such as endotoxins or P-fimbriae, may be involved. These substances can activate an autoimmune response or cause sensory nerve stimulation, thus activating the neurogenic inflammation model of IC. DNA sequencing of bladder biopsies searching for bacteria or their by-products has demonstrated controversial results. GAG LAYER DEFICIENCY The concept of a defective urothelium resulting from a quantitative deficiency of its surface coat of GAGs, and thereby allowing access of a toxic urothelial substance into the interstitium of the bladder, was once the leading theory of the pathogenesis of IC. Current research is focusing on biochemical and ultrastructural studies of the surface layer of urothelium, of the umbrella cells, and intra-adhesion molecules. This may provide a more comprehensive understanding of the pathogenesis of IC. ULTRASTRUCTURAL ABNORMALITIES Ultrastructural studies of bladder biopsy specimens following hydrodistention have revealed several distinct features. Abnormalities are observed in all tissue components of the bladder wall, including tissue cells, interstitial tissue, blood vessels, and intrinsic nerves. These features include urothelium with disrupted permeability barrier and accelerated turnover, abnormal profiles of detrusor muscle cells, and damage of intrinsic nerves and blood vessel walls. Significant fluid engorgement, with diffuse or loculated edema of tissue
Chapter 29
cells and extracellular tissue, is also seen. Lymphocytes are the predominant component, distributed unevenly throughout the tissue. Activated mast cells are readily identified adjacent to intrinsic nerves, but they are less commonly seen near blood vessels and in the suburothelium. These distinctive features are most prominent and extensive in biopsies from areas of glomerulations (submucosal hemorrhages) following diagnostic hydrodistention. These features, although recognizable, are less dramatic in severity and extent of distribution in biopsies from cystoscopically normal-appearing areas of the bladder lining. Further research has identified that urine from IC patients has a decreased level of heparin-binding epidermal growth-like factor (HB-EGF) and an increase in a putative antiproliferative factor. HB-EGF has been shown to increase toward normal values with hydrodistention. Antiproliferative factor and HB-EGF normalize following sacral neuromodulation. The abnormality in epithelial permeability/transitional dysfunction led to the development of the potassium sensitivity test. MAST CELLS Mast cells examined ultrastructurally in IC are intimately associated with nerve fibers and terminals in the suburothelium and are found in the interstitium of the detrusor, often next to nerves and blood vessels. Mast cells are essential for the development of allergic hypersensitivity reactions. Their activation and subsequent degranulation trigger the secretion of many biologically active chemicals. These substances include histamine, serotonin, cytokines, neuropeptides (substance P), and vasoactive intestinal peptide. These mediators, especially histamine, play a role in stimulating reactions, such as vasodilation, leukocyte infiltration, and angiogenesis. An elevated mast cell count in the bladder muscularis has been promoted as a diagnostic histopathologic feature of IC, and detrusor mastocytosis has been advocated as a more appropriate name for IC. Different values for mast cell counts in the detrusor layer have been proposed as a diagnostic marker. These values and their validity are debated. Detrusor mastocytosis has been found in 20% to 65% of patients with IC; patients with classic ulcer-type or late-stage IC have demonstrated an even higher percentage. Recently, investigators have attempted to compare the ratio of detrusor to mucosal mast cells and the relationship of nerve fibers to mast cells. The ultrastructure of the mast cell, demonstrated by electron microscopy, has shown the proximity of nerves and activated mast cells. Researchers are investigating mast cell activation and the subsequent mediator release as an origin of some of the symptoms and cystoscopic findings seen with IC. Current research involving the role of mast cells in IC has brought forth three findings: (1) the intimate association and interaction of mast cells with intrinsic nerves in the bladder wall; (2) the unlikeliness, if not incompatibility, of an immunologic pathogenetic mechanism of immunoglobulin E–mediated immediate hypersensitivity; and (3) the relationship of stress and female hormones to IC.
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inflammation may be implicated include irritable bowel syndrome, vulvodynia, migraines, fibromyalgia, and multiple sclerosis. Mast cells are located in close proximity to the peripheral and central nervous systems. In addition, an intimate association between mast cells and sensory nerve fibers has been demonstrated in the integumentary, pulmonary, and gastrointestinal systems. Excitation of sensory nerves, especially small pain C-fibers, triggers an inflammatory process through release of neuropeptides (substance P) and calcitonin gene-related peptide. Substance P causes vasodilation and increased vasopermeability and activates mast cells, causing injury with increased permeability of epithelial surfaces. Multiple events or factors trigger neurogenic inflammation. These include (1) bacterial cystitis or the antigen from the organism, (2) an increased level of estrogen, (3) toxins of endogenous and exogenous origin, including drugs, their metabolites, and certain foods, and (4) a potent mediator, such as the histamine released by activated mast cells. As our understanding of neurogenic inflammation and the role of mast cell activation progresses (Fig. 29-2), the diagnosis and treatment of IC will evolve.
Diagnosis Painful bladder syndrome is a diagnosis of exclusion (see Box 29-1). Patients cannot have evidence of cystitis caused by infection, use of cyclophosphamide or other chemical agents, radiation, or tuberculosis. Other infections, such as vaginitis, urethritis, urethral Ureaplasma, or genital herpes, cannot be present. Also, urethral diverticulum, bladder carcinoma, and carcinoma-in-situ must be excluded. However, patients with painful bladder syndrome may have concomitant lower urinary tract or pelvic floor disorders. HISTORY Frequency (greater than eight voids during waking hours), nocturia (greater than two voids during sleeping hours), urgency, suprapubic pressure on bladder filling, bladder pain, and dyspareunia are the most common symptoms.
Bladder insult
More injury
Activation of C-fibers Substance P release
Potassium leak into interstitium
Mast cell activation and histamine release
NEUROGENIC INFLAMMATION Neurogenic inflammation may provide the nidus for induction, establishment, and chronicity of the various tissue changes seen in IC. Other conditions in which neurogenic
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Epithelial layer damage Figure 29-2
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Pathogenesis of interstitial cystitis.
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Secondary symptoms include burning during or after urination; a feeling of decreased bladder emptying; hesitancy; interruption of urinary stream; double voiding; referred pain to the abdomen, lower back, or medial thighs; abdominal bloating; postvoid urethral pain; incontinence without sensation; or detrusor overactivity. The severity and duration of each flare over the previous year should be recorded. The physician should also inquire about previous UTI, types of incontinence, parity, previous pelvic surgery, radiation therapy, chemotherapy, previous treatments, menstrual history, history of endometriosis, central nervous system trauma, and dyspareunia. Commonly, patients initially present with one symptom only, urinary urgency/frequency, nocturia, or pain. All patients should be asked to do a voiding diary (see Fig. 14-1) and fill out the O’Leary-Sant symptom and problem index (Fig. 29-3). The recently validated pelvic pain urgency and frequency (PUF) questionnaire may also be used. A medical history should include associated diseases, such as migraines, fibromyalgia, sinusitis, drug hypersensitivity, sicca syndrome (dry eyes, dry mouth), Sjögren’s syndrome, vulvodynia, and irritable bowel syndrome. PHYSICAL EXAMINATION The abdominal and back examinations detect the presence of costovertebral tenderness and abdominal tenderness or mass. The external genitalia are examined for signs of infection and vulvar vestibulitis (tenderness over the vulvar vestibular or Bartholin’s glands). The pelvic examination includes a vaginal and urethral culture, if appropriate, evaluation for signs of atrophic vaginitis or a urethral caruncle, and a Pap smear if indicated. Careful palpation and perineometry may help evaluate the pelvic floor muscles to rule out pelvic floor dysfunction (the inability to optimally contract and relax the pelvic floor muscles). Evaluation of bladder and pelvic organ support is done in the dorsal lithotomy and standing positions to determine and grade bladder neck hypermobility, cystocele, enterocele, uterine prolapse, rectocele, and perineal descent. The posterior bladder wall and urethra should be palpated to check for tenderness and masses, and a bimanual examination should be performed to detect pelvic or adnexal masses and tender nodules. A rectovaginal examination is performed to evaluate tenderness along the uterosacral ligaments. Finally, a neurourologic examination ascertains the presence of the bulbocavernosus reflex and grades perineal sensation and anal sphincter strength. LABORATORY AND RADIOGRAPHIC EVALUATION Initial laboratory examination should include urinalysis, urine culture and sensitivity, and measurement of postvoid residual urine volume (catheterized or with bladder ultrasound). Urine cytology is indicated in the presence of hematuria and persistent urgency. A 24-hour voiding diary measures input and output, number and quantity of voids, and number and severity of leakage episodes. A renal ultrasound, intravenous pyelogram (IVP), or computed tomography (CT) scan is indicated in the presence of hematuria, history of recurrent UTI, or history of pelvic surgery. A voiding cystourethrogram (VCUG) is useful in ruling out vesicoureteral reflux and evaluating the bladder neck in patients with concomitant incontinence or suburethral diverticulum. Magnetic resonance imaging (MRI)
may further delineate the urethra when evaluating for a urethral diverticulum. Awake cystoscopy is indicated in the presence of hematuria, persistent or recurrent UTI, or suspected fistula or urethral diverticulum. POTASSIUM SENSITIVITY TEST Parsons (1996) designed the potassium sensitivity test (PST) to measure epithelial permeability. Instilling a solution of potassium chloride (KCl) into a normal bladder will not promote urgency or pain (Box 29-2). If a patient’s bladder has a leaky epithelium, the KCl mixture readily diffuses across the transitional cells and stimulates sensory nerves, causing urgency and pain. Parsons demonstrated that 70% of patients with IC had provocation of symptoms, whereas only 4% of normal subjects responded with pain. A recent study showed that 84% of patients with a score of >14 of the PUF questionnaire had a positive PST. CYSTOSCOPY Cystoscopy is both diagnostic and therapeutic. Cystoscopy with hydrodistention of the bladder traditionally has been performed under general or regional anesthesia. Our experience has been that intravenous sedation, bupivacaine hydrochloride (Marcaine) bladder instillation, and pudendal nerve block are effective diagnostic and therapeutic alternatives with minimal morbidity and increased postoperative patient satisfaction. Cystoscopy is performed to eliminate other causes of persistent patient symptoms and hematuria and to examine for typical findings of IC (Table 29-1). The classic Hunner’s ulcer, an area of erythema with small vessels radiating to a central, pale scar after bladder filling, is found in only 8% of patients with IC. Previous biopsy sites and carcinoma in situ can be confused with ulcers. Before hydrodistention, an inclusive evaluation of the bladder is performed, and the degree of hypervascularity and linear scarring (mild, moderate, severe) is assessed. Hydrodistention is performed by filling the bladder under gravity at 80 cm H2O with urethral compression for 2 to 7 minutes. The bladder is then drained, looking for a terminal bloody effluent, and the capacity is measured (>350 mL is defined as early-stage IC and ≤350 mL as late-stage IC). The average bladder capacity for patients with IC has been reported as 575 mL and as 1115 mL for patients without persistent irritative voiding symptoms. On redistention of the bladder, the presence and severity of glomerulations, strawberry-like petechial hemorrhages, are determined. Not all patients with significant symptoms have glomerulations or a reduced bladder capacity. Bladder biopsy is performed after hydrodistention to reduce the risk of perforation. The biopsy eliminates the presence of carcinoma in situ and infection, and it can quantitate the number of mast cells in the lamina propria and detrusor muscle. The diagnosis of IC cannot be ruled out based on normal cystoscopic findings; the findings of glomerulations and a terminal bloody effluent suggest the diagnosis of IC. A capacity below 350 mL or the presence of a Hunner’s ulcer confirms the diagnosis of late IC. Concomitant laparoscopy may be performed when there is tenderness in the adnexa, a history of previous pelvic surgery, infertility, an abnormal pelvic ultrasound, suspected endometriosis, dysmenorrhea, or dyspareunia in the absence of vulvodynia.
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381
Check the one best answer for each question. 1. During the past month, how often have you felt the strong need to urinate with little or no warning? [ ] Not at all
Score [0]
[ ] About half the time
Score [3]
[ ] Less than 1 time in 5
[1]
[ ] More than half the time
[4]
[ ] Less than half the time
[2]
[ ] Almost always
[5]
2. During the past month, have you had to urinate less than 2 hours after you finished urinating? [ ] Not at all
Score [0]
[ ] About half the time
Score [3]
[ ] Less than 1 time in 5
[1]
[ ] More than half the time
[4]
[ ] Less than half the time
[2]
[ ] Almost always
[5]
3. During the past month, how often each night did you most typically get up at night to urinate? [ ] None
Score [0]
[ ] 3 times per night
Score [3]
[ ] Once per night
[1]
[ ] 4 times per night
[4]
[ ] 2 times per night
[2]
[ ] 5 or more times per night
[5]
4. During the past month, have you experienced pain or burning in your bladder? [ ] Not at all
Score [0]
[ ] Usually
Score [3]
[ ] A few times
[1]
[ ] Almost always
[4]
[ ] Fairly often
[2] Interstitial Cystitis Problem Index (ICPI)
During the past month, how much has each of the following been a problem for you? 1. Frequent urination during the day? [ ] No problem
Score [0]
[ ] Medium problem
Score [3]
[ ] Very small problem
[1]
[ ] Big problem
[4]
[ ] Small problem
[2]
2. Getting up at night to urinate? [ ] No problem
Score [0]
[ ] Medium problem
Score [3]
[ ] Very small problem
[1]
[ ] Big problem
[4]
[ ] Small problem
[2]
3. Need to urinate with little warning? [ ] No problem
Score [0]
[ ] Medium problem
Score [3]
[ ] Very small problem
[1]
[ ] Big problem
[4]
[ ] Small problem
[2]
4. Burning, pain, discomfort, or pressure in your bladder? [ ] No problem
Score [0]
[ ] Medium problem
Score [3]
[ ] Very small problem
[1]
[ ] Big problem
[4]
[ ] Small problem
[2]
(Patients without IC will score less than 6 on either index.)
Figure 29-3
■
O’Leary-Sant Interstitial Cystitis Symptom Index.
URODYNAMIC TESTS Urodynamic evaluations are performed on patients with hypersensitivity symptoms to evaluate the following features: volume at first sensation of bladder filling, first desire to void, strong desire to void, increased bladder sensation,
maximum cystometric capacity, detrusor compliance, the presence or absence of detrusor overactivity, and reproduction of bladder pain and/or patients’ symptoms. Patients with IC often have symptoms suggestive of an overactive bladder. The ICS refers to the term overactive bladder as a storage phase disease diagnosed by urodynamics. Detrusor
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BOX 29-2
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POTASSIUM SENSITIVITY TEST
Measure of epithelial permeability: KCl solution (40 mL; 400 mEq/L) Normal bladder intact epithelium: KCl provokes no symptoms Epithelial dysfunction: K+ diffuses across transitional cells and stimulates sensory nerves, causing urgency or pain Positive response: no response to H2O; ≥2 response to KCl (scale 0–5)
overactivity is a urodynamic observation characterized by involuntary detrusor contractions during the filling phase that may occur spontaneously or may be provoked. Patients with hypersensitivity disorders often demonstrate increased bladder sensation and bladder pain during filling cystometry. Increased bladder sensation is a new ICS urodynamic observation during filling cystometry and is defined 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. Jarvis (1982) defined sensory urgency as an abnormal first sensation on bladder filling less than 75 mL and a bladder capacity less than 400 mL in the absence of involuntary bladder contractions. Normal first sensation of filling occurs between 50 to 150 mL, with a first urge to void between 200 and 500 mL and a maximum capacity between 400 and 700 mL. Kirkemo et al. (1997) found that patients enrolled in the NICDB had a correlation between reported daytime, nighttime, and 24-hour frequency and both volume at first sensation to void (VFSV) and volume at maximum cystometric capacity (VMCC). VFSV decreased as awake frequency increased. Patients who voided equal to 5 times during awake hours had a mean VFSV of 114 ± 81 mL versus 74 ± 61 mL for those voiding greater than 15 times. Similarly, this was seen with VMCC with mean volumes of 244 ± 149 mL versus 184 ± 114 mL, respectively, for those voiding equal to 5 times and those voiding greater than 15 times. This same trend was seen with nocturia and 24-hour voiding frequency. Patients with a 24-hour voiding frequency of greater than 15 times per day had a mean VFSV of 70 ± 59 mL and a VMCC of 190 ± 112 mL. In addition to comparing a patient’s symptoms to urodynamic findings, a correlation has been made between urodynamic findings, cystoscopic findings, and a patient’s severity of disease. Most authors have noted a decrease in volume at first sensation to void and maximum cystometric capacity. Nigro et al. (1997) compared the findings of 150 women involved in the NICDB who underwent cystoscopy, bladder overdistention, and urodynamics. The mean volume
Table 29-1
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at first sensation to void was 81 ± 64 mL, and a mean volume at maximum capacity was 198 ± 107 mL. Many authors feel that patients with a Hunner’s ulcer have a more severe form of IC. The NICDB noted that patients with a Hunner’s ulcer had a mean volume at first sensation of 34.7 ± 20.5 mL. This was statistically lower than the volume at first sensation of patients without a Hunner’s ulcer. None of the urodynamic criteria were statistically significant when related to the presence or absence of bloody effluent, presence and degree of glomerulations, presence of involuntary bladder contractions, or end-filling pressures. Twenty-six patients (17.5%) in this study had involuntary bladder contractions. Other studies have found that 5% to 26% of patients with the symptom complex of IC had involuntary bladder contractions. The original exclusion criteria for IC included involuntary bladder contractions; this is now a debatable issue. However, there does appear to be a relationship between the severity of a patient’s symptoms and the urodynamic findings. Currently, no specific urodynamic values are known that diagnose IC or predict the characteristic cystoscopic findings of the disease. Patients with the symptom complex of a hypersensitive lower urinary tract tend to have an early first sensation of bladder filling, a decreased volume at first sensation to void, and a decreased maximum capacity during urodynamic studies.
URETHRAL SYNDROME Urethral syndrome, part of the spectrum of painful bladder syndrome, was once considered a separate diagnosis. Now it appears to be a mild or early stage of IC (see Fig. 29-1). Urethral pain syndrome is defined by the ICS as 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. Urethral syndrome is characterized by symptoms similar to those of IC: frequency, urgency, nocturia, dysuria, urethral pain, and a feeling of decreased bladder emptying. Certain subgroups of patients specifically isolate urethral pain from bladder pain. As with other hypersensitivity disorders, all other diagnoses must be excluded. Of particular importance with urethral pain is the exclusion of cystitis, including bacterial and tuberculosis, as well as various sexually transmitted diseases, including Chlamydia, Trichomonas vaginalis, Gardnerella, genital mycoplasmas, genital herpes, and human papilloma virus. A hypoestrogenic state can produce symptoms of urethral syndrome. Symptoms of urethral syndrome can also be caused by allergic hypersensitivity reactions related to personal hygiene products and other external
Most Common Cystoscopic Findings in Interstitial Cystitis
Early
Late
Glomerulations (petechial submucosal hemorrhages) Hypervascularity and linear scarring Bloody terminal effluent after hydrodistention
Bladder capacity <300 mL Hunner’s ulcers
Chapter 29
chemical exposure, including chlorine and spermicides. A urethral stricture, diverticulum, or other anatomic abnormality can be found at the time of cystoscopy. Finally, many patients with early IC or urethral syndrome have pelvic floor dysfunction or pelvic muscle spasticity that may respond to biofeedback or physical therapy. Diagnosis and treatments are similar to those for IC. Historically, urethral dilation was felt to help by relieving infected urethral glands. No controlled studies are found in the literature to establish the benefit of urethral dilation. Typically, these patients respond to treatment of the underlying disorder. Once all other disorders are excluded, patients benefit from conservative measures similar to those for earlystage IC.
MANAGEMENT OF PAINFUL BLADDER SYNDROME After the exclusion of all other diagnoses, painful bladder syndrome can be managed successfully in over 85% of patients by using a combination of anecdotal and conventional modalities. A multidisciplinary approach and patient self-care regimens are most successful. Initial management should promote bladder retraining, relieve irritative voiding symptoms, enhance healing of potential bladder lining defects, and correct high tone pelvic floor dysfunction. Learning how to keep a voiding diary, with emphasis on the time and amount of fluid intake, amount and time between voids, and comments about exacerbation of symptoms with food and fluid intake and activity, aids in formulating intake and voiding schedules in a 24hour period. Adequate hydration with frequent sips of water during waking hours aids in urinary dilution. Voiding on a regular schedule can significantly decrease leakage and pain. For example, voiding every 2 hours is recommended if pain or leakage occurs at intervals greater than every 2 hours on the voiding diary. On the other hand, if the patient is a frequent voider, bladder holding to increase the voiding interval by 10 to 15 minutes per week over a 3-month period can significantly decrease frequency, especially if pain is controlled. A low-potassium, low-acid diet (Box 29-3) and an acid neutralizer, calcium glycerophosphate (Prelief), may decrease symptoms in 40% to 65% of patients (Table 29-2). The addition of bladder analgesics or antispasmodics may further decrease hypersensitivity symptoms. Anticholinergic medications, such as tolterodine tartrate or oxybutynin chloride, may also help decrease symptoms. If these conservative measures fail, the patients proceed to diagnosis with cystoscopy, bladder hydrodistention, bladder biopsy, and video or office urodynamics, depending on the symptoms and history (Fig. 29-4).
Hydrodistention of the Bladder Hydrodistention of the bladder under anesthesia improves symptoms in 30% to 54% of patients. Patients who have significant improvement for 6 months or more are candidates for a repeat hydrodistention. The physiology of how this improves symptoms is not known. In patients with a capacity
BOX 29-3
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ANTI-INFLAMMATORY DIET
*Alcoholic beverages Apples Apple juice Cantaloupe *Carbonated beverages Chili and other spicy foods *Citrus fruits, including lemons, limes, oranges, and grapefruit *Coffee (may use decaf or Kava) Cranberries Grapes Peaches *Pineapple Plums *Berries *Tea Herbal tea *Tomatoes *Vinegar and other condiments Avocado Bananas *Cheeses, particularly hard and soft brie-type cheeses *Chocolate (may use white chocolate) Corned beef Beans Nuts Prunes and raisins Rye bread Yogurt and sour cream *Aspartame and saccharin *Onions *Pepper Vitamins buffered with aspartame *Foods to be avoided by patients with IC and vulvodynia. Nonasterisk entries may be ingested in moderation only. Asterisk entries should be avoided altogether whenever possible. The acid-restricted diet is most effective when 64 oz of water is ingested daily and urine is alkalinized.
of less than 600 mL under anesthesia, the therapeutic result was excellent in 26% and fair in 29%, compared with 12% with an excellent response and 43% with a fair response in patients whose capacity was greater than 600 mL. Patients for whom hydrodistention fails are begun on oral medications. Oral therapy includes pentosan polysulfate (PPS; Elmiron), antidepressants (amitriptyline), antihistamines (hydroxyzine), α-blockers, anticonvulsants, muscle relaxants, and narcotics (Fig. 29-5).
Pharmacologic Therapy PENTOSAN POLYSULFATE (PPS) PPS (Elmiron) is a synthetic sulfated polysaccharide with properties of sulfated GAGs and an affinity for mucosal membranes. Its use is based on the concept of stabilizing urothelial permeability (the GAG layer) to prevent irritating solutes in the urine from reaching the bladder interstitium. Elmiron is excreted in the urine and attempts to correct the permeability defect in the GAG layer. A randomized clinical trial noted a 38% improvement in symptoms (predominantly
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Table 29-2
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Food Sensitivity in Interstitial Cystitis Patients*
Diet
Exacerbation N (%)
Worst Symptoms (hours)
Dietary Quantity
Pizza Tomato Spicy foods Coffee Acidic juice or fruit Carbonated drink Alcohol Chocolate
91 125 111 119 125 114 106 82
0–4 0–2 0–2 0–2 0–2 0–2 0–2 0–2
1–2 slices 1 serving 1 serving 1 cup 1 serving or glass 1 glass 1 glass 1 piece
(45.5) (62.5) (55.5) (59.5) (62.5) (57.0) (53.0) (41.0)
*Reflects the results of a survey of 200 patients with the symptom complex of IC. Patients were asked a series of questions regarding foods and events that exacerbate their symptoms. This table demonstrates the type of foods that most commonly exacerbated the patients’ symptoms, the time to exacerbation, and the amount of food required for exacerbation.
Hypersensitivity disorders of the lower urinary tract Urgency/frequency
urethral syndrome
interstitial cystitis
Figure 29-4 ■ Diagnostic algorithm for women with hypersensitivity disorders of the lower urinary tract. ICDB, Interstitial Cystitis Data Base; PMH, past medical history.
History: Urgency—strong desire to void accompanied by a fear of leakage or pain Frequency; nocturia; pelvic, suprapubic, perineal, or urethral pain; dyspareunia Symptoms > 6 months, feeling of incomplete emptying, pain with bladder filling Dysuria, bowel function, voiding diary ICDB—frequency > 8 during waking hours, nocturia > 2 sleeping hours PMH:
Inclusion: previous pelvic surgery Exclusion: cystitis (radiation, bacterial, chemical); previous genitourinary or gynecologic malignancy
Labs: X-ray:
Negative urine culture and cytology Unexplained microhematuria and/or previous pelvic surgery Upper tract imaging, intravenous pyelogram (IVP) or ultrasound and cystoscopy
Pelvic exam: Bladder, urethral tenderness; pelvic floor dysfunction; prolapse Exclude: urethral diverticulum, genital herpes, vaginitis, urethritis, adnexal mass
Conservative therapy Improved
Low-acid diet, urinary alkalinization, anticholinergics, analgesics
Follow Not improved Diagnosis Cystoscopy, hydrodistention, bladder biopsy No evidence of tumors or calculi Positive glomerulations after hydrodistention, and terminal bloody efflux Urodynamics: sensory urgency Potassium sensitivity test: positive
pain) compared with an 18% response in the placebo group during a 3-month treatment period. A subsequent review of the long-term therapy (up to 3 years) with Elmiron showed that patients had a 42% to 62% improvement in their overall symptoms (pain and urgency). This study also demonstrated that the medication is safe and effective for 3 years. The recent IC Clinical Trials Group (NIH sponsored) found no clinical benefit of PPS versus placebo in a randomized pilot study. Side effects occur in less than 5% of patients and include
alopecia, diarrhea, nausea, and headache. Elmiron should be taken for 6 months or longer to achieve effectiveness. ANTIDEPRESSANTS Most patients with IC suffer from anger, anxiety, depression, or fatigue caused by the lack of sleep and chronic pain. Tricyclic antidepressants work as central and peripheral anticholinergic agents that block the reuptake of serotonin and
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385
Treatment for painful bladder syndrome
Improved
Low-acid diet, urinary alkalinization, anticholinergic medication, biofeedback, stress management, correction of bowel problems, nutritionist Not improved
Follow Improvement lasting 6 months
Cystoscopy and hydrodistention Not improved
Repeat therapeutic overdistention
Antidepressants Amitriptyline 10-75 mg qhs Doxepin 10-75 mg qhs Paxil 10-20 mg qhs Prozac 20 mg qd
Antihistamines Hydroxyzine 25-75 mg qd
Other agents
Mucosal building Elmiron 100 mg tid
L-Arginine
1.5 g/day Anticonvulsants, benzodiazepines, Opioids with the assistance of a pain clinic or neurologist
Improved Not improved
Follow
Bladder instillations Failure of oral medication or flare while on oral medications DMSO 50 ml, heparin 10,000 units, triamcinolone 10 mg, 44 mEq NaHCO3 Heparin 10,000 U daily Bupivacaine 0.5%, hydrocortisone, NaHCO3, gentamicin, heparin
Research protocols Neuromodulation Botox Amitriptyline Biomarkers
Figure 29-5
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Treatment for women with hypersensitivity disorders of the lower urinary tract. BCG, Bacillus Calmette-Guérin.
norepinephrine, and they have antihistaminic properties. Amitriptyline is usually started at a low dosage, 10 to 25 mg before bedtime and titrated up to 75 mg and taken 1 hour before bedtime (patients should be advised that they will feel tired for 12 hours after taking the medication). Substitutes may be given, if side effects are unacceptable. They include doxepin hydrochloride, 10 to 75 mg at 1 hour before bedtime, paroxetine hydrochloride (Paxil) 10 to 20 mg before bedtime, or fluoxetine hydrochloride (Prozac) 20 mg a day. ANTIHISTAMINES Hydroxyzine has been shown to provide symptomatic relief, especially in patients with a history of allergies or biopsyproven mast cell activation. In a study of 90 patients, 40% were noted to have a reduction in symptom scores using hydroxyzine up to 75 mg per day. The reason that hydroxyzine is effective is not completely understood; theories include stabilization of mast cells, anticholinergic properties, and a sedative effect. OTHER ORAL AGENTS Between 10% and 15% of patients with IC have severe, unrelenting pain. l-Arginine, a nitric oxide synthetase inhibitor and dietary supplement, significantly decreased pain when
taken daily for 6 months at 1.5 g per day. After appropriate functional assessment, anti-inflammatory agents, opioids, anticonvulsants, or muscle relaxants may be administered and titrated often in coordination with a pain specialist.
Bladder Instillations Bladder instillations are reserved for patients who are not responding to oral therapy and for those who are doing well on oral therapy and have a flare in their symptoms. A common instillation mixture includes 50 mL dimethyl sulfoxide (DMSO), 10,000 units heparin, 10 mg triamcinolone, and 44 mEq NaHCO3 instilled once a week for 6 weeks. The pharmacologic properties of DMSO include anti-inflammatory and analgesic effects, collagen dissolution, muscle relaxation, and mast cell histamine release. Heparin is a GAG that is thought to mimic the activity of the bladder’s mucopolysaccharide lining. An improvement in symptoms for up to 6 months has been achieved using the DMSO cocktail in 78% of patients receiving six weekly treatments. Intravesical heparin (20,000 units in 10 mL of sterile water), self-administered daily for 4 to 12 months, has resulted in a 60% or better response rate. A combination of 0.5% bupivacaine, heparin, hydrocortisone, NaHCO3, and gentamicin (pH 6.5), given to patients with IC and a history of recurrent UTI, resulted
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in an improvement in 78% of patients that lasted up to 6 months. Intravesical hyaluronic acid, a GAG, showed a 71% response rate that was sustained for up to 6 months. Two recent, randomized controlled trials, however, showed no clinical benefit. Bacillus Calmette-Guérin (BCG), an immunogenic agent used to treat superficial transitional cell carcinoma of the bladder, is under investigation as an alternative for instillation therapy. Preliminary studies in patients with IC showed a response rate of 60% (compared with a 27% placebo response rate) that lasted for at least 6 months. Resiniferatoxin (RTX), a vanilloid receptor agonist, recently showed no significant benefit over controls in a randomized controlled trial.
Sacral Neuromodulation Sacral neuromodulation has been demonstrated in prospective studies to help decrease the symptoms associated with urgency-frequency syndrome and voiding disorders. Multiple small studies demonstrated that patients are achieving a significant reduction in their symptoms with S3 neuromodulation. Recent studies have demonstrated a 60% to 70% reduction in pain and lower urinary tract symptoms that is sustained in excess of 2 years. Refer to Chapter 31 for an in-depth description of neuromodulation therapy.
The currently accepted modality of surgical therapy is urinary diversion (ileal loop or conduit, continent diversion, or pouch), with or without cystectomy. Before urinary diversion is chosen as therapy for intractable pain, a psychological evaluation is recommended. A differential epidural block may help distinguish between psychogenic, sympathetic, and somatic pain. Reported success rates of urinary diversion have been approximately 70%. The physician and patient choose between a continent diversion (pouch) or ileal loop (conduit). Several reports of recurrent symptoms (pouchitis) have led surgeons to recommend an ileal loop. Urinary diversion without cystectomy is particularly attractive in younger patients with the hope of finding a cure and possible undiversion. Morbidity from the in situ bladder has been reported in up to 80% of patients. These complications include pyocystis (67%), hemorrhage (23%), severe pain (13%), and intractable spasm (17%). Many of these patients will require cystectomy. Our own experience has shown that patients with continent diversions experience significant pouch spasms. Total cystourethrectomy is indicated in patients with urethral pain to avoid persistent pain from the urethral remnant. Patients must be informed that their pelvic pain may persist with urinary diversion, with or without cystectomy.
FUTURE DIRECTIONS Refractory Symptoms Patients with intractable pain, despite an adequate trial of conservative interventions, such as physical therapy, biofeedback, and oral and intravesical therapies, may benefit from evaluation at a pain clinic. Pain diversion with the use of transcutaneous electrical stimulation may be helpful. Studies report a 26% improvement in pain symptoms for patients with nonulcer IC and a 54% improvement for ulcer IC patients. Epidural nerve blocks have been used in the management of chronic pain. Continued neurogenic inflammation of the bladder may lead to fibrosis and neurologic ischemia or reflex sympathetic dystrophy. Refractory IC pain may respond to a series of epidural nerve blocks. Peripheral denervation (cytolysis) and central denervation (presacral neurectomy or rhizotomy) techniques were popular in the 1970s and 1980s. Unfortunately, the duration of results was short, and complication rates were high. Surgery is considered a last resort for patients with IC. Neuromodulation may be the most appropriate step before invasive surgery. Less than 10% of patients are unresponsive to all other therapeutic modalities and undergo surgery. Augmentation cystoplasty, using ileum, cecum, or colon with a supratrigonal cystectomy, was popularized in the early 1980s. The fate of the augmented bowel remains undetermined. These patients can experience recurrent symptoms or pain, and self-catheterization (necessary in up to 80% of the patients) of the patient’s inflamed bladder and urethra may be painful. The bowel segment may develop mast cell infiltration and contraction. Therefore, the use of augmentation cystoplasty should be reserved for the rare IC patient with a small-capacity bladder and no pain.
A multidisciplinary approach to treating patients with pain disorders of the lower urinary tract is comprehensive and cost-effective (Box 29-4). A pelvic floor team provides a detailed history, physical examination, and management, based on input from several specialties. The urologist, urogynecologist, or pelvic floor specialist initially evaluates the patient. A gastroenterologist or colorectal surgeon is helpful because many patients have irritable bowel syndrome or constipation. A rheumatologist or internist should evaluate the patient’s general medical and autoimmune status because many patients are chronically debilitated or have the systemic features of IC (fibromyalgia, migraines, sinusitis, drug hypersensitivity). Up to 70% of patients with severe symptoms have pelvic floor dysfunction, which is conservatively treated with physical therapy (exercise, myofascial massage, and manual
BOX 29-4
MEMBERS OF A MULTIDISCIPLINARY IC TEAM
Urologist Urogynecologist Gastroenterologist Colorectal surgeon Rheumatologist or internist Nutritionist Psychologist (stress, behavioral, and sex therapy) Physical therapist (biofeedback) Neuropsychiatrist Chemical and invasive pain management specialist Acupuncture or herbal therapy specialist
Chapter 29
therapy) or biofeedback, with or without electrical stimulation. A psychologist is invaluable in providing stress reduction techniques, such as self-visualization, self-hypnosis, baths, deep breathing, and meditation. Behavioral therapy, including the development of coping mechanisms, problem solving, and sex therapy, is also very useful. Nutritional counseling is beneficial to any patient with a painful or chronic illness. A chemical pain manager (neuropsychiatrist) and invasive pain manager (anesthesiologist) make intractable pain tolerable for most patients. Complementary medicine has been effective in the treatment of IC. Acupuncture reduced pain by at least 50% in more than 60% of patients after an average of 12 treatments. Anecdotally, herbal therapy may be useful in up to 75% of patients. Nutritional supplements may be useful in boosting the immune system in patients with long-standing disease. A multidisciplinary approach to research will improve our ability to study the epidemiology, diagnosis, and management of IC. Procurement of increased funding for clinical and basic science research will aid in defining the hypersensitivity pelvic floor disorder population, finding markers for etiology and treatment efficacy, determining the effect of hormones on these disorders, and defining outcome measures for treatment protocols. Unbiased, randomized controlled trials for the prevention of IC, by treating lower urinary tract hypersensitivity disorders appropriately and in a timely fashion, will improve the quality of women’s pelvic health. Increased funding for public education, medical student and resident education, and education of primary care providers will allow access to treatment at an earlier point in the hypersensitivity and pain spectrum.
BIBLIOGRAPHY HISTORY AND EPIDEMIOLOGY Christmas TJ. Historical aspects of interstitial cystitis. In Sant GR, ed. Interstitial Cystitis. Lippincott, Philadelphia, 1997. Curhan GC, Speizer FE, Hunter DJ, et al. Epidemiology of interstitial cystitis: a population based study. J Urol 1999;161:549. Erickson DR, Morgan KC, Ordille S, et al. Nonbladder related symptoms in patients with interstitial cystitis. J Urol 2001;166:557. Gillenwater JY, Wein AJ. Summary of the National Institute of Arthritis, Diabetes, Digestive and Kidney Diseases Workshop on Interstitial Cystitis, National Institutes of Health. Bethesda, MD, August 28–29, 1987. J Urol 1988;140:203. Hanash KA, Pool TL. Interstitial and hemorrhagic cystitis: viral, bacterial, and fungal studies. J Urol 1970;104:705. Hunner GL. A rare type of bladder ulcer in women: report of cases. Boston Med Soc J 1915;172:660. Jones CA, Nyberg L. Epidemiology of interstitial cystitis. Urology 1997; 49S(5A):2. Nitze M. Lehrbuch de cystoscopie: ihre technik und kinsche bedeutung. JE Bergman, Berlin, 1907. O’Leary MP, Sant GR, Fowler FJ, et al. The interstitial cystitis symptom index and problem index. Urology 1997;49S(5A):58. Rothrock NE, Lutgendorf SK, Hoffman A, Kreder KJ. Depressive symptoms and quality of life in patients with interstitial cystitis. J Urol 2002;167:1763. Skene AJ. Diseases of Bladder and Urethra in Women. William Wood, New York, 1887.
ETIOLOGY Alagiri M, Chottiner S, Ratner V, et al. Interstitial cystitis: unexplained associations with other chronic disease and pain syndromes. Urology 1997;49S(5A):52.
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Aldenborg F, Fall M, Enerback L. Proliferation and transepithelium migration of mucosal mast cells in interstitial cystitis. Immunology 1986;58:411. Boucher W, El-Mansoury M, Pang X, et al. Elevated mast cell tryptase in the urine of patients with interstitial cystitis. Br J Urol 1995;76:94. Buffington CT, Wolfe SA. High affinity binding sites for [3H] substance P in urinary bladders of cats with interstitial cystitis. J Urol 1998;160:605. Chai TC, Zhang C, Shoenfelt JL, et al. Bladder stretch alters urinary heparinbinding epidermal growth factor and antiproliferative factor in patients with interstitial cystitis. J Urol 2000;163:1440. Christmas TJ, Rode J, Chapple CR, et al. Nerve fiber proliferation in interstitial cystitis. Virchow Arch Pathol Anat 1990;416:447. Collan Y, Alfthan O, Kivilaakso E, et al. Electron microscopic and histologic findings on urinary bladder epithelium in interstitial cystitis. Eur Urol 1976;2:242. Domingue GJ, Ghoniem GM, Bost KL, et al. Dormant microbes in interstitial cystitis. J Urol 1995;153:1321. Domingue GJ, Ghoniem GM, Human L, et al. Bacteriology of urinary bladder tissue and urine in interstitial cystitis. J Urol 1996;155S(5A):432. Elbadawi A. Interstitial cystitis: a critique of current concepts with a new proposal for pathologic diagnosis and pathogenesis. Urology 1997;48S(5A):14. Elbadawi A, Light JK. Distinctive ultrastructural pathology of nonulcerative interstitial cystitis: new observations and their potential significance in pathogenesis. Urol Int 1996;56:137. Elliott TS, Slack RC, Bishop MC. Scanning electron microscopy of the human bladder mucosa in acute and chronic urinary tract infection. Br J Urol 1984;56:38. El-Mansoury M, Boucher W, Sant GR, et al. Increased histamine and methylhistamine in interstitial cystitis. J Urol 1994;152:350. Erickson DR. Inflammatory cell types and other clinical features of interstitial cystitis. J Urol 1995;155S(5):440A. Fall M, Johasson SL, Vahlne A. A clinicopathological and virological study of interstitial cystitis. J Urol 1985;133:771. Haarla M, Jalava J, Laato M, et al. Absence of bacterial DNA in the bladder of patients with interstitial cystitis. J Urol 1996;156:1843. Hampson S, Christmas T, Moss M. Search for mycobacteria in interstitial cystitis using mycobacteria-specific DNA probes with signal amplification by polymerase chain reaction. Br J Urol 1993;72:303. Hanno PM, Landis JR, Matthews-Cook Y, et al. The diagnosis of interstitial cystitis revisited: lessons learned from the National Institutes of Health Interstitial Cystitis Database study. J Urol 1999;161:553. Hanno PM, Levin RM, Monson FC, et al. Diagnosis of interstitial cystitis. J Urol 1990;143:278. Hedelin HH, Mardh PA, Brorson JE, et al. Mycoplasma hominis and interstitial cystitis. Sex Trans Dis 1980;10S:327. Hofmeister MA, He F, Ratliff TL, et al. Mast cells and nerve fibers in interstitial cystitis: an algorithm for histologic diagnosis via quantitative image analysis and morphometry. Urology 1997;49:41. Hohenfellner M, Nunes L, Schmidt RA, et al. Interstitial cystitis: increased sympathetic innervation and related neuropeptide synthesis. J Urol 1992;147:587. Holm-Bentzen M, Sondergaard I, Hald T. Urinary excretion of a metabolite of histamine (1,4 methyl-imidazole, acetic-acid) in painful bladder disease. Br J Urol 1987;59:230. Hurst RE, Roy JB, Min KW, et al. A deficit of chondroitin sulfate proteoglycans on the bladder uroepithelium in interstitial cystitis. Urology 1996;48:817. Johansson SL. Interstitial cystitis. Mod Pathol 1993;6:738. Kastrup J, Hald T, Larsen S, et al. Histamine content and mast cell count of detrusor muscle in patients with interstitial cystitis and other types of chronic cystitis. Br J Urol 1983;55:495. Keay S, Schwalbe RS, Warren JW, et al. A prospective study of microorganisms in urine and bladder biopsies from interstitial cystitis patients and controls. Urology 1995;45:223. Keay S, Szekely Z, Conrads TP, et al. Complete characterization of an antiproliferative factor from bladder epithelial cells of interstitial cystitis patients. J Urol 2004;171:94S. Larsen S, Thompson SA, Hald T, et al. Mast cells in interstitial cystitis. Br J Urol 1982;54:283. Leon A, Buriani A, Dal Toso R, et al. Mast cells synthesize, store, and release nerve growth factor. Proc Natl Acad Sci U S A 1994;91:3739. Letourneau R, Pang X, Sant GR, et al. Intragranular activation of bladder mast cells and their association with nerve processes in interstitial cystitis. Br J Urol 1996;77:41.
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Lundenberg T, Lieberg H, Nordling L, et al. Interstitial cystitis: correlation with nerve fibers, mast cells and histamine. Br J Urol 1993;71:427. Lynes WL, Flynn SD, Shortliffe LD, et al. The histology of interstitial cystitis. Am J Surg Pathol 1990;14:969. Marshall JS, Wasserman S. Mast cells and the nerves: potential interactions in the context of chronic disease. Clin Exp Allergy 1995;25:102. Messing EM, Stamey TA. Interstitial cystitis. Early diagnosis, pathology and treatment. Urology 1987;12:381. Miller CH, MacDermott JP, Quattrocchi GA, et al. Lymphocyte function in patients with interstitial cystitis. J Urol 1992;157:592. Myers G, Donlon M, Kaliner M. Measurement of urinary histamine: development of methodology and normal values. Clin Allergy Immunol 1981;67:305. Newson B, Dahlstrom A, Enerback L, et al. Suggestive evidence for a direct innervation of mucosal mast cells. Neuroscience 1983;10:565. Ochs RL, Stein TW, Peebles CL, et al. Autoantibodies in interstitial cystitis. J Urol 1994;151:587. Pang X, Boucher W, Triadafilopoulos G, et al. Mast cell and substance P-positive nerve involvement in a patient with both irritable bowel syndrome and interstitial cystitis. Urology 1996;47:436. Pang X, Marchand J, Sant GR, et al. Increased number of substance P positive nerve fibers in interstitial cystitis. Br J Urol 1995;75:744. Parsons CL. Potassium sensitivity test. Tech Urol 1996;2:171. Purcell WM, Aterwill CK. Mast cells in neuroimmune function: neurotoxicological and neuropharmacological perspectives. Biochem Res 1995;20:521. Saban R, Keith IM, Bjorling DE. Neuropeptide-mast cell interaction in interstitial cystitis. In Sant GR, ed. Interstitial Cystitis. Lippincott, Philadelphia, 1997. Sant GR, Theoharides TC. The role of the mast cell in interstitial cystitis. Urol Clin North Am 1994;21:41. Stead RH, Dixon MF, Bramwell NH, et al. Mast cells are closely apposed to nerves in the human gastrointestinal mucosa. Gastroenterology 1989; 97:575. Steers W, Tuttle JB. Neurogenic inflammation and nerve growth factor: possible roles in interstitial cystitis. In Sant GR, ed. Interstitial Cystitis. Lippincott, Philadelphia, 1997. Theoharides TC, Sant GR. Bladder mast cell activation in interstitial cystitis. Semin Urol 1991;9:74. Theoharides TC, Sant GR, El-Mansoury M, et al. Activation of bladder mast cells in interstitial cystitis: a light and electron microscopic study. J Urol 1995;153:629. Warren JW. Interstitial cystitis as an infectious disease. Urol Clin North Am 1994;21:31. Yun SK, Laub DJ, Weese DL, et al. Stimulated release of urine histamine in interstitial cystitis. J Urol 1992;148:1145.
DIAGNOSIS Abrams P, Cardozo L, Fall M, et al. The standardization of terminology in lower urinary tract function. Report from the Standardization Subcommittee of the International Continence Society. Neurourol Urodyn 2002;21:167. Alagiri M, Chottiner S, Ratner V, et al. Interstitial cystitis: unexplained associations with other chronic disease and pain syndromes. Urology 1997;49S(5A):52. Chambers GK, Fenster HN, Howard N, et al. An assessment of the use of intravesical potassium in the diagnosis of interstitial cystitis. J Urol 1999; 162:699. Driscoll A, Teichman JM. How do patients with interstitial cystitis present? J Urol 2001;166:2118. Ito T, Tomoe H, Ueda T, et al. Clinical symptoms scale for interstitial cystitis for diagnosis and for following the course of the disease. Int J Urol 2003;10(Suppl):S24. Jarvis GJ. The management of urinary incontinence due to primary vesical sensory urgency by bladder drill. Br J Urol 1982;54:374. 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;49S(5A):76. Koziol JA, Clark DC, Gittes RF, et al. The natural history of interstitial cystitis: a survey of 374 patients. J Urol 1993;149:465. Lutgendorf SK, Kreder KJ, Rothrock NE, et al. Diurnal cortisol variations and symptoms in patients with interstitial cystitis. J Urol 2002;167:1338. Messing EM, Pauk D, Schaeffer A, et al. Associations among cystoscopic findings and symptoms and physical examination findings in women
enrolled in the interstitial cystitis data base (ICDB) study. Urology 1997;49S(5A):81. Nigro DA, Wein AJ, Foy M, et al. Associations among cystoscopic and urodynamic findings from women enrolled in the interstitial cystitis data base (ICDB) study. Urology 1997;49S(5A):86. O’Leary MP, Sant GR, Fowler FJ, et al. The interstitial cystitis symptom index and problem index. Urology 1997;49:58. Parsons CL. Interstitial cystitis: clinical manifestations and diagnostic criteria in over 200 cases. Neurourol Urodyn 1990;9:241. Parsons CL, Stein PC, Bidair M, et al. Abnormal sensitivity to intravesical potassium in interstitial cystitis and radiation cystitis. Neurourol Urodyn 1994;13:515. 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. Parsons CL, Dell J, Stanford EJ, et al. Increased prevalence of interstitial cystitis: previously unrecognized urologic and gynecologic cases identified using a new symptom questionnaire and intravesical potassium sensitivity. Urology 2002;60:573. Ratner V, Salde D, Whitmore KE. Interstitial cystitis: a bladder disease finds legitimacy. J Women’s Health 1992;1:63. Simmon LJ, Landis JR, Erickson DR, et al. The interstitial cystitis data base (ICDB) study: concepts and preliminary baseline descriptive statistics. Urology 1997;49S(5A):64. Waxman JA, Sulak PJ, Kuehl TJ. Cystoscopic findings consistent with interstitial cystitis in normal women undergoing tubal ligation. J Urol 1998; 160:1663. Whitmore KE. Self-care regimens for patients with interstitial cystitis. Urol Clin North Am 1994;21:121.
URETHRAL SYNDROME Bodner DR. The urethral syndrome. Urol Clin North Am 1988;15:699. Bump RC, Copeland WE. Urethral isolation of genital mycoplasmas and chlamydia trachomatis in women with chronic urologic complaints. Am J Obstet Gynecol 1985;152:38. Hamilton-Miller JT. The urethral syndrome and its management. J Antimicrob Chemother 1994;33S:63. Ishigooka MH. Effect of hormonal replacement therapy in postmenopausal women with chronic irritative voiding symptoms. Int Urogynecol J 1994;5:211. Wilkens EG, Payne SR, Pead PJ, et al. Interstitial cystitis and the urethral syndrome: a possible answer. Br J Urol 1989;64:39.
MANAGEMENT OF HYPERSENSITIVITY DISORDERS Bade JJ, Peeters JM, Mensink HJ. Is the diet of patients with interstitial cystitis related to their disease? Eur Urol 1997;32:179. Bardot SF, Weigel JW, Krueker DC. Treatment of intractable interstitial cystitis with cystourethrectomy and continent urinary diversion. J Urol 1990;143:375A. Baskin LS, Tanagho EA. Pelvic pain without pelvic organs. J Urol 1992; 147:683. Brookoff D. The causes and treatment of pain in interstitial cystitis. In Sant GR, ed. Interstitial Cystitis. Lippincott, Philadelphia, 1997. Chaiken DC, Blaivas JG, Blaivas ST. Behavioral therapy for the treatment of refractory interstitial cystitis. J Urol 1993;149:1445. Comiter CV. Sacral neuromodulation for the symptomatic treatment of refractory interstitial cystitis: a prospective study. J Urol 2003;169:1369. Eigner EB, Freiha FS. The fate of the remaining bladder following supravesical diversion. J Urol 1990;144:31. Fall M. Transcutaneous electrical nerve stimulation in interstitial cystitis. Urology 1987;29:40. Fall M, Lindstrom S. Transcutaneous electrical nerve stimulation in classic and nonulcer interstitial cystitis. Urol Clin North Am 1994;21:131. Galloway NT, Gabale DR, Irwin PP. Interstitial cystitis or reflex sympathetic dystrophy of the bladder? Semin Urol 1991;9:148. Hanno PM. Amitriptyline in the treatment of interstitial cystitis. Urol Clin North Am 1994;21:21. Hanno PM. Analysis of long-term Elmiron therapy for interstitial cystitis. Urology 1997;49S(5A):99. Hanno PM, Fritz R, Wein AJ, et al. Heparin as an antibacterial agent in rabbit bladder. Urology 1978;12:411.
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Hanno PM, Wein AJ. Conservative therapy of interstitial cystitis. Semin Urol 1991;9:143. Hohenfellner M, Lin JF, Hampel C, et al. Surgical treatment of interstitial cystitis. In Sant GR, ed. Interstitial Cystitis. Lippincott, Philadelphia, 1997. Irwin P, Galloway NT. Surgical management of interstitial cystitis. Urol Clin North Am 1994;21:145. Keselman I, Austin P, Anderson J, et al. Cystectomy and urethrectomy for disabling interstitial cystitis: a long term follow-up. J Urol 1995;153:290A. Kirkemo AK, Miles BJ, Peters JM. Use of amitriptyline in the treatment of interstitial cystitis. J Urol 1990;143:279A. Kisman OK, Lycklama AB, Nijeholt A, et al. Mast cell infiltration in intestine used for bladder augmentation in interstitial cystitis. J Urol 1991;146:1113. 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. MacDermitt JP, Charpied GL, Tesluk H. Recurrent interstitial cystitis following cystoplasty: fact or fiction? J Urol 1990;144:37. Morales A, Emerson L, Nickel JC. Intravesical hyaluronic acid in the treatment of refractory interstitial cystitis. Urology 1997;49S(5A):111. Nielsen KK, Kromann-Andersen B, Steven K, et al. Failure of combined supratrigonal cystectomy and Mainz ileocecocystoplasty in intractable interstitial cystitis: is histology and mast cell count a reliable predictor for the outcome of surgery? J Urol 1990;144:255. Nurse DE, Parry JW, Mundy AR. Problems in the surgical treatment of interstitial cystitis. Br J Urol 1991;68:153. Parsons CL. A quantitatively controlled method to prospectively study interstitial cystitis and demonstrate the efficacy of pentosan polysulfate. J Urol 1993;150:845. Parsons CL. Epithelial coating techniques in the treatment of interstitial cystitis. Urology 1997;49S(5A):100. Parsons CL, Housley T, Schmidt JD, et al. Treatment of interstitial cystitis with intravesical heparin. Br J Urol 1994;73:504. Peters KM, Carey JM, Konstandt DB. Sacral neuromodulation decreases narcotic requirements in refractory interstitial cystitis. Br J Urol 2004; 95:777. Peters KM, Carey JM, Konstandt DB. Sacral neuromodulation for the treatment of refractory interstitial cystitis: outcomes based technique. Int Urogynecol J 2003;14:223.
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Peters KM, Diokno A, Steinert B, et al. The efficacy of intravesical Tice strain bacillus Calmette-Guérin in the treatment of interstitial cystitis: a double-blind, prospective, placebo controlled trial. J Urol 1997;157:2290. Pontari MA, Hanno PM, Wein AJ. Logical and systematic approach to the evaluation and management of patients suspected of having interstitial cystitis. Urology 1997;49S(5A):114. Sant GR. Intravesical 50% dimethylsulfoxide (DMSO-50) in treatment of interstitial cystitis. Urology 1987;29:17. Sant GR. Interstitial cystitis. Monogr Urol 1991;12:37. 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. Schwartzman R, McLellan R. Reflex sympathetic dystrophy: a review. Arch Neurol 1987;44:555. Smith SD. Improvement in interstitial cystitis syndrome scores during treatment with oral L-arginine. J Urol 1997;158:703. Theoharides TC. Hydroxyzine for interstitial cystitis. J Allergy Clin Immunol 1993;91:686. Theoharides TC, Sant GR. Hydroxyzine therapy for interstitial cystitis. Urology 1997;49S(5A):108. Torens M, Hald T. Bladder denervation procedures. Urol Clin North Am 1978;6:283. van Ophoven A, Oberpenning F, Hertle L. Long-term results of trigone-preserving orthotopic substitutional enterocystoplasty for interstitial cystitis. J Urol 2002;167(2 Pt 1):603. Webster GD, MacDiarmid SA, Timmons SL, et al. Impact of urinary diversion procedures in the treatment of interstitial cystitis and chronic bladder pain. Neurourol Urodyn 1992;11:417. Whitmore KE, Tu LM, Gordon DA, et al. Self-care and interstitial cystitis: identification of the food-sensitive IC patient. Inter Research Symposium on IC, Washington, DC, October 1997. Worth PL. The treatment of interstitial cystitis by cytolysis with observation on cystoplasty. A review after 7 years. Br J Urol 1980;52:232. Worth PL, Turner-Warwick R. The treatment of interstitial cystitis by cytolysis with observation on cystoplasty. Br J Urol 1973;45:65.
Voiding Dysfunction and Urinary Retention
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Victor W. Nitti and Nicole Fleischman
NEUROPHYSIOLOGY OF MICTURITION 390 EVALUATION OF VOIDING DYSFUNCTION 392 CLASSIFICATION OF VOIDING DYSFUNCTION 393 SPECIFIC CAUSES OF VOIDING DYSFUNCTION: DIAGNOSIS AND MANAGEMENT 393 Neurogenic Voiding Dysfunction 394 Nonneurogenic Voiding Dysfunction 397 CONCLUSION 400
Voiding dysfunction or lower urinary tract dysfunction are terms used to describe various problems related to the bladder’s ability to store or empty urine. Urinary retention is the inability to complete the voiding phase of the micturition cycle and, often times, represents the end stage of voiding dysfunction. Physiologically, a problem may be present with either the bladder or the outlet, or both. Voiding dysfunction is manifest clinically in lower urinary tract symptoms (LUTS), which may be characterized as storage symptoms (frequency, urgency, nocturia, and urge incontinence) or emptying symptoms (decreased force of stream, incomplete emptying, hesitancy, straining to void, and urinary retention). Symptoms do not always correlate with the underlying pathology, and numerous conditions may exist that can have similar presentations. Thus, an often challenging task is to determine the specific etiology involved. In many cases, voiding dysfunction can be explained by neurologic disease, learned behavioral patterns, congenital, acquired, or by iatrogenic bladder outlet obstruction. In this chapter, we discuss normal voiding and the pathophysiologic events that lead to abnormal voiding as well as the evaluation, management, and treatment of women with specific types of voiding problems.
NEUROPHYSIOLOGY OF MICTURITION Normal voiding is accomplished by activation of the “micturition reflex” (Fig. 30-1). This is a coordinated event characterized by relaxation of the striated urethral sphincter,
contraction of the detrusor, opening of the vesical neck and urethra, and onset of urine flow (Fig. 30-2). This reflex is integrated in the pontine micturition center, which is located in the rostral brainstem. Also, a sacral micturition center is located at S2–S4, through which the bladder can contract independently of cortical and pontine input. However, the pontine micturition center, through its neural pathways to the sacral micturition center, is responsible for coordinated and voluntary voiding. Both the autonomic and somatic nervous systems play a crucial role in lower urinary tract function. Normal voiding occurs when the bladder responds to threshold tension via its mechanoreceptors. To avoid a random occurrence, central nervous system inhibitory and facilitatory pathways are involved in coordination of urine storage and micturition. Micturition depends on a spinobulbospinal reflex that is relayed through the pontine micturition center, which receives input from the cerebral cortex, cerebellum, basal ganglia, thalamus, and hypothalamus, and is the final common pathway to the bladder motor neurons. Much of the input from suprapontine centers appears to be inhibitory, although some facilitatory influences are involved. The central facilitatory areas are the anterior pons and the posterior hypothalamus, and the inhibitory areas include the cerebral cortex, basal ganglia, and cerebellum. The cerebellum is also implicated in the maintenance of tone in the pelvic floor striated musculature and coordination between bladder contraction and periurethral striated muscle relaxation. Because most the suprapontine input to the pontine micturition center is inhibitory, interruption of this input (e.g., cerebrovascular accident, cerebral atrophy, Parkinson’s disease, brain tumor, or trauma) often results in uncontrolled detrusor activity, or hyperreflexia, but the “micturition reflex” is intact. When micturition is affected by suprapontine lesions, it is usually characterized by loss of voluntary control. Uninhibited detrusor contractions may result in urinary frequency, urgency, and urge incontinence. Little risk is present for developing urologic complications because voiding is coordinated, even if not voluntary. Anatomically, the two areas of the spinal cord responsible for transmitting afferent input from the lower urinary tract are the lateral spinothalamic tracts and the posterior
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Figure 30-1 ■ Diagram of reflex pathways involved in micturition (according to deGroat). Plus and minus signs indicate, respectively, excitatory and inhibitory synaptic actions. The connection of the pontine micturition center to the cerebral cortex and other suprapontine areas in not pictured. (From deGroat WC and Booth AM: Physiology of the urinary bladder and urethra. Ann Intern Med 1980;92[part 2]:312.)
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Micturition “center”
Lumbar cord
Sympathetic ganglion
Sacral cord
Urinary bladder
Parasympathetic ganglion
Pudental nerve
columns. The lateral spinothalamic tracts contain ascending routes responsible for transmitting bladder sensation and triggering voiding. Proprioceptive sensory impulses generated in bladder muscle and periurethral striated muscle travel in the posterior columns. The pontine micturition center controls efferent input to the bladder and external sphincter via two separate regions. The medial region is responsible for motor input to the bladder detrusor muscle via the reticulospinal tracts to the sacral intermediolateral cell groups, which contain preganglionic parasympathetic neurons that form the motor supply of the bladder detrusor muscle. Electrical stimulation of this region results in a prompt decrease in pelvic floor electromyography (EMG) and urethral pressure followed by an increase in intravesical pressure (normal voiding). The lateral region has specific projections via the corticospinal tracts to the nucleus of Onuf in the sacral cord that contains motor neurons innervating the pelvic floor, including the urethral and anal sphincters. Electrical stimulation of this region results in a rapid increase in urethral pressure and pelvic floor EMG but little increase in intravesical pressure (normal storage). Storage and evacuation of urine depend on neural integration at the peripheral, spinal cord, and central levels. Normally, bladder distension will cause low-level firing of afferent nerves. This will cause reflex inhibitory response
Urethral sphincter
to the bladder via the hypogastric nerve and stimulatory response to the external sphincter from the pudendal nerve. With further distension, myelinated A-delta fiber afferents are activated. Afferents travel up the spinal cord to the pontine micturition center. Here central input, mostly inhibitory, is received from suprapontine centers. If voiding is not desired, the voiding reflex can be interrupted. If voiding is desired, efferent output to the pelvic plexus at S2–S4 via the spinal cord is initiated. Ultimately, the stimulatory message is sent to the bladder via the pelvic nerve. At the same time, inhibitory messages are sent to the hypogastric and pudendal pathways to allow for relaxation of the sphincter mechanisms and coordinated voiding. Peripheral innervation to the bladder, internal, and external sphincters is provided by the pelvic, hypogastric, and pudendal nerves. Parasympathetic efferent input to the bladder arises from the intermediolateral cell column of S2–S4 and travels as preganglionic fibers via the pelvic nerve to the pelvic plexus located on both sides of the rectum, from which postganglionic fibers innervate the bladder. Efferent sympathetic nerves to the bladder and urethra arise from the intermediolateral cell column of T10–L2 as preganglionic fibers that travel to ganglia located in the superior hypogastric plexus, from which arises the hypogastric nerve that contains the postganglionic sympathetic efferents to the
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Figure 30-2 ■ Urodynamic representation of the micturition cycle. Note that during filling, there is an involuntary detrusor contraction (arrow) accompanied by an increase in external sphincter activity as portrayed by increased EMG activitiy (guarding reflex). The contraction abates and then normal voiding ensues (large arrow). First there is relaxation of the external sphincter followed by a voluntary detrusor contraction and initiation of flow.
bladder and urethra. The pudendal nerve carries the somatic input from S2–S4 to the external sphincter. Injury to any one of these nerves or their branches can result in a partial or complete denervation to the involved end organ. In addition to the neurophysiologic pathways, other pharmacologic factors are responsible for normal voiding. The lower urinary tract is rich in both cholinergic and adrenergic receptors. Muscarinic receptors are located in the body of the bladder, and they are activated by parasympathetic release of acetylcholine to induce bladder contraction. Also, β-adrenergic receptors in the detrusor cause relaxation in response to increasing levels of cyclic adenosine monophosphate (AMP). In the bladder neck and urethra, α-adrenergic receptors are responsible for the increase in urethral tone and rise in intraurethral pressure during sympathetic stimulation via the hypogastric nerve. Each of these receptor types have been the basis for pharmacologic therapy of the lower urinary tract. Anticholinergic medications are able to cause bladder relaxation by inhibiting parasympathetic pathways; α-agonists have been used in the treatment of stress incontinence.
EVALUATION OF VOIDING DYSFUNCTION The evaluation of LUTS in women starts with a thorough history. This should focus on the type and duration of
symptoms and voiding habits over time. Typically, voiding (obstructive) symptoms are not a common complaint in women. Although it is true that many women with obstruction complain of significant storage (irritative) symptoms, voiding symptoms should not be overlooked. Two recent studies showed that with a high index of suspicion and careful questioning, voiding symptoms are noted in 71% to 76% of women with obstruction. Storage symptoms were a bit more common with 79% to 92% of obstructed women complaining of these. A complete medical, surgical, obstetric/gynecologic, neurologic, and urologic history may uncover possible causes of voiding dysfunction. If symptoms are acute, and the cause of acute obstruction is clear, treatment should be directed toward alleviating the obvious cause. A complete physical examination is the next part of the evaluation. Particular attention should be paid to a systematic examination of the vagina and pelvis. One should first inspect the mucosa for atrophic changes as well as signs of previous surgery. Also, the position of the urethra, bladder neck, and bladder can be observed at rest and with straining to determine the degree of anterior vaginal wall prolapse (urethral hypermobility and cystocele). We like to use the posterior blade of a small vaginal speculum to retract the posterior vaginal wall to view the anterior wall. A Q-tip test can be used to quantify urethral hypermobility. The patient should also be assessed for stress urinary incontinence (SUI). An assessment of the uterus should be done to determine
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its support and position. In cases of previous hysterectomy, vaginal apex support and position are important. Uterine or apical prolapse are potential causes of obstruction. After examination of the anterior vaginal wall is completed, the blade of the speculum is rotated and the posterior wall and apex are inspected. Similar to other forms of prolapse, posterior vaginal wall prolapse, including rectocele and posterior enterocele, can cause obstruction and voiding dysfunction. Bimanual examination is performed to determine the presence of pelvic masses, including fibroids, which may also cause or contribute to voiding dysfunction. In patients with LUTS, a neurourologic examination should also be performed. Attention should be paid to the sensory and motor functions of the sacral nerves, including anal sphincter tone, perineal sensation, bulbocavernosus and anal wink reflex, strength of lower extremities, and deep tendon reflexes (knee and ankle). A careful neurologic examination may help to confirm suspected disease or uncover an unknown lesion. In addition to history and physical examination, several simple tests can give insight to the cause of LUTS. Urine analysis (and culture, if indicated) is done routinely. Intake and voiding diaries are helpful in quantifying symptoms, voiding habits, and urine production. In addition, several incontinence episodes and type (stress, urge, unconscious) should be noted. Noninvasive uroflow and postvoid residual (PVR) volume determination give a good idea of how well a patient empties her bladder. Although these tests cannot determine why voiding and/or emptying are abnormal (e.g., impaired detrusor function versus obstruction), they may prompt more thorough evaluation with urodynamics. Thus, we consider uroflow and PVR to be good “screening tests” for a woman with LUTS. Urodynamic testing can be an important part of the evaluation of female voiding dysfunction. However, it must always be kept in mind that it is only part of the evaluation to be used in conjunction with the rest of the assessment. Urodynamic findings inconsistent with patient symptoms or events occurring during testing that are uncharacteristic for patients during normal activity outside of the urodynamics lab should be interpreted with caution. We always advocate the use of multichannel urodynamics with simultaneous measurement of vesical and abdominal pressure and “subtracted” detrusor pressure during filling and voiding (see Fig. 30-2). The filling phase (cystometry) evaluates the ability of the bladder to effectively store urine by assessing bladder stability, compliance, and capacity. Pressure-flow analysis during voiding assesses bladder contractility and bladder outlet resistance. EMG may be added to assess the pelvic floor musculature and external sphincter. We have found videourodynamics to be particularly helpful in confirming and localizing anatomic or functional obstruction. The addition of simultaneous fluoroscopy of the bladder outlet will often discover an obstruction that would not have been made on the basis of multichannel urodynamics alone. When videourodynamics are not available, radiographic evaluation may still be useful in evaluating incomplete emptying. A standing cystogram in the anterior–posterior, 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 will examine the bladder, bladder neck, and urethra during voiding and is important in uncovering anatomic abnormalities.
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The final component of the evaluation is cystourethroscopy, when indicated. Scarring, kinking, or deviation of the urethra, especially after previous surgery, may be responsible for incomplete emptying. Rarely, a urethral lesion responsible for obstruction may be found. Examination of the bladder may uncover a lesion, such as a tumor or stone, and may also identify some of the changes associated with obstruction or retention.
CLASSIFICATION OF VOIDING DYSFUNCTION Many complex classification systems for voiding dysfunction have been proposed in the past; however, they failed to be diagnostically and therapeutically oriented. We have found the functional classification system, proposed by Wein (1981) and reviewed in Chapter 5, to be the most useful. This simple and practical classification system can be easily applied to our diagnostic criteria (e.g., urodynamics). Of equal importance is that treatment options can be chosen based on the classification. Wein’s functional classification is based on a simple understanding of urine storage and micturition. For normal urine storage and voiding to occur, there must be proper and coordinated functioning of the bladder and the bladder outlet. Therefore, in simple anatomic terms, voiding dysfunction can be divided into: 1. Bladder dysfunction 2. Bladder outlet dysfunction (bladder neck, urethra, external sphincter) 3. Combined bladder and outlet dysfunction Similarly, the effects of these problems can be classified as: 1. Failure to store urine 2. Failure to empty urine 3. Failure to store and empty urine In this chapter we will divide voiding dysfunction into neurogenic and nonneurogenic. Furthermore, nonneurogenic voiding dysfunction and obstruction can be classified as functional or anatomic.
SPECIFIC CAUSES OF VOIDING DYSFUNCTION: DIAGNOSIS AND MANAGEMENT Treatment of voiding dysfunction is dictated by several factors. First and foremost is the potential danger to the upper urinary tract associated with high storage pressures or the inability to empty the bladder. Although this is less common in nonneurogenic voiding dysfunction, any evidence of upper tract decompensation (hydronephrosis, elevated blood urea nitrogen [BUN], and creatinine) should be given immediate attention. Second is the degree of bother of the patient’s symptoms. In many cases, empirical therapy is an appropriate first step for patients with symptoms of voiding dysfunction. In patients without neurologic disease whose primary complaints are storage symptoms, such as urge incontinence, and who demonstrate an ability to empty,
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a course of anticholinergic therapy and/or bladder training programs (with or without biofeedback) is effective in relieving overactive bladder symptoms. In cases in which the diagnosis is not clear, or when abnormal emptying and storage coexist, a more comprehensive workup is necessary. The same can be said when empirical therapy fails and for cases of voiding dysfunction associated with neurologic disease. In all such cases further investigation with urodynamic testing is usually indicated. In these instances, the specific cause for the voiding dysfunction will direct treatment. Distinguishing neurogenic from nonneurogenic voiding dysfunction is important. The latter category is often caused by bladder outlet obstruction, and this may be functional, as in the case of dysfunctional voiding and primary bladder neck obstruction (PBNO), or anatomic, as in the case of pelvic floor prolapse or post-surgical obstruction. A complete list of causes for bladder outlet obstruction in women is shown in Table 30-1.
Neurogenic Voiding Dysfunction Neurologic disease can have a profound effect on the urinary system, including both the upper and lower urinary tracts. The term neurogenic bladder is often used loosely by many clinicians to describe a bladder that is not functioning normally. However, in the evaluation of neurogenic voiding dysfunction, it is critical to be more precise in assessment and classification. Ideally, this should be done in such a way that
Table 30-1
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it is practical for diagnostic and therapeutic purposes. Thus, the goals in assessing patients with neurogenic voiding dysfunction are to determine the effects of the neurologic disease on the entire urinary tract (not just the bladder) in such a way that treatment can be implemented to relieve symptoms and prevent damage to the upper and lower urinary tracts. For the patient with neurologic disease, it is important to keep in mind that symptoms do not always indicate the magnitude to which the disease is affecting the urinary tract. Pathologic processes at each level of innervation must be considered when evaluating neurogenic voiding dysfunction (Box 30-1). For example, suprapontine lesions (e.g., cerebral atrophy, cerebrovascular accident, brain tumor) cause a loss of inhibitory input to the pontine micturition center and subsequent uninhibited bladder contractions, a condition known as neurogenic detrusor overactivity. Sphincter reflexes are not affected, and coordinated uninhibited voiding can result. Clinically, interruption of the neural pathways connecting the pontine micturition center to the sacral micturition center (e.g., spinal cord injuries or lesions) usually results in uninhibited bladder contractions (neurogenic detrusor overactivity) and a dyscoordination of the bladder and external sphincter or detrusor-external sphincter dyssynergia (DESD). DESD is characterized by simultaneous contractions of the detrusor and external sphincter. The involuntary detrusor contractions cause incontinence and the involuntary sphincter contractions bladder outlet obstruction and retention of urine. DESD is commonly seen in suprasacral spinal cord
Anatomic and Functional Causes of Bladder Outlet Obstruction in Women
Anatomic Obstruction
Functional Obstruction
A. Inflammatory processes 1. Bladder neck fibrosis 2. Uretheral stricture 3. Atrophic vaginitis/urethritis 4. Meatal stenosis 5. Urethral caruncle 6. Skene’s gland/cyst abscess 7. Urethral diverticulum
A. Detrusor-sphincter dyssynergia
B. Pelvic prolapse 1. Anterior vaginal wall 2. Posterior vaginal wall 3. Apical (uterine prolapse/enterocele)
B. Dysfunctional voiding
C. Neoplastic 1. Urethral carcinoma 2. Bladder carcinoma
C. Primary bladder neck obstruction
D. Gynecologic (extrinsic compression) 1. Retroverted uterus 2. Lower segment uterine or vaginal leiomyoma 3. Vaginal carcinoma 4. Cervical carcinoma E. Iatrogenic obstruction 1. Anti-incontinence procedures 2. Multiple urethral dilations 3. Urethral excision/reconstruction F. Miscellaneous 1. Urethral valves 2. Ectopic ureterocele 3. Bladder calculi
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BOX 30-1
SUMMARY OF LESIONS FOUND IN COMMON NEUROGENIC VOIDING DYSFUNCTIONS
Suprapontine Lesions Cerebrovascular disease Parkinson’s disease Multiple sclerosis Concussion Brain tumor Shy-Drager syndrome Normal pressure hydrocephalus
Pontine–Sacral Spinal Cord Lesions Spinovascular disease Spinal cord injury Multiple sclerosis Spinal dysraphism Tabes dorsalis Spinal stenosis Disk herniation
Infrasacral/Peripheral Lesions Sacral agenesis Spinal cord injury Cauda equina syndrome Herpes zoster Tables dorsalis Radical pelvic surgery
lesions, multiple sclerosis, and, less commonly, myelodysplasia and lumbosacral lesions. Untreated DESD can result in high storage pressures (loss of bladder compliance) and resultant vesicoureteral reflux, hydronephrosis, urolithiasis, and urosepsis. Suprasacral spinal cord lesions also result in loss of supraspinal input; however, the complexity of the resulting voiding dysfunction depends on the level and completeness of the lesion. Also, input to the sphincters may be disrupted, resulting in DESD. A complete spinal cord lesion will result in the development of a spinal micturition reflex. Unmyelinated C-fiber afferents excite sacral neurons and trigger a bladder contraction. In addition, incomplete relaxation of the external sphincter results in a contraction against a closed outlet with subsequent incontinence, retention, and eventual loss of bladder compliance. Infrasacral cord and peripheral nerve lesions generally result in loss of sensation and contractility, leading to a large, super compliant, areflexic bladder. The external sphincter may also be deficient of contractility and tone. Neurologic lesions that interfere with the sacral reflex arc are most often seen in patients with myelodysplasia, diabetic cystopathy, ruptured discs, and low spinal cord tumors. These can take away reflex voiding and result in various degrees and combinations of detrusor areflexia, intrinsic urethral sphincter deficiency, and paralysis of the external urethral striated sphincter. The previous information is useful when evaluating patients with particular neurologic diseases. However, the clinician must always keep in mind that neurologic lesions can be “complete” or “incomplete.” Therefore, the exact manifestations of a particular disease or lesion on a given patient are not absolutely predictable. A complete urologic evaluation
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for patients with neurogenic voiding dysfunction is therefore recommended. A good example of a disease that can affect the lower urinary tract in various ways is multiple sclerosis (MS), a disease common in young and middle-aged women. Because it can affect multiple areas of the central nervous system (CNS), urologic presentations include detrusor overactivity, detrusor overactivity with DESD, and impaired or absent detrusor contractility. The latter two presentations can lead to problems with bladder emptying. The urodynamic evaluation is integral to the evaluation of patients with suspected neurologic voiding dysfunction (Fig. 30-3). Incontinence, which is a common complaint of these individuals, can be secondary to neurogenic detrusor overactivity, decreased compliance, or sphincteric incompetence. Only multichannel urodynamics will demonstrate the underlying pathology. Incontinence secondary to bladder dysfunction may be measured by the detrusor leak point pressure (DLPP). The DLPP is the amount of detrusor pressure, in the absence of an increase in abdominal pressure, required to cause incontinence. The DLPP is a direct reflection of the amount of resistance provided by the external sphincter; the higher the resistance, as with DESD, the higher the DLPP. High storage pressures are potentially dangerous to the upper urinary tract. McGuire et al. (1981) have shown that storage pressures of greater than 40 cm H2O are associated with upper tract deterioration. Incontinence secondary to sphincteric dysfunction can be measured by the Valsalva or abdominal leak point pressure (ALPP). The ALPP is the amount of abdominal pressure, in the absence of a rise in detrusor pressure, that is required to cause incontinence. The ALPP is commonly used to evaluate sphincteric function in women with SUI. Normally, no physiologic abdominal pressure will cause incontinence and therefore there is no normal ALPP. Unlike the DLPP, a high ALPP does not indicate potential danger to the upper tracts. The evaluation of upper urinary tract function is extremely important in women with neurogenic voiding dysfunction, especially in those who are at risk for developing upper tract problems (see earlier text). A renal ultrasound can be performed to assess hydronephrosis. Renal scans are best to evaluate renal function. When videourodynamic studies are not available, it may be necessary to perform a cystogram or voiding cystourethrogram to assess for vesicoureteral reflux. Also, patients with neurogenic voiding dysfunction, especially if not properly managed in the past, are at risk for developing calculi. Calculi have been reported to occur in over 30% of patients managed with an indwelling catheter. The main goal in the treatment of neurogenic voiding dysfunction, first and foremost, is to protect the upper urinary tract from damage. This is accomplished by maintaining low storage pressures in the lower urinary tract. Second, the goal is to alleviate the patient’s bothersome LUTS. Treatment should be directed at the specific problems uncovered during the evaluation, regardless of the neurologic disease associated with those problems. For detrusor overactivity and impaired compliance, anticholinergic medications are the first line of therapy and, in many cases, are sufficient to lower storage pressures and reduce or abolish involuntary detrusor contractions. Sometimes, especially in cases of outlet dysfunction, like
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Figure 30-3 ■ Urodynamic tracing of a young woman with incontinence and a tethered cord. Note the first involuntary detrusor contraction (IDC) accompanied by increased EMG activity and incontinence as registered on the flow curve. The second IDC is also accompanied by increased EMG activity that does not abate when the patient is asked to voluntarily void. Diagnosis: neurogenic detrusor overactivity with detrusor-external sphincter dyssynergia.
DESD, anticholinergic medication will also produce urinary retention, necessitating the patient to perform intermittent self-catheterization. Recently, second-line therapies have been developed for use in cases where medical therapy is not effective in treating detrusor overactivity. These include intravesical botulinum toxin-A injection and neuromodulation. Schurch et al. (2000) reported their series of 21 patients with spinal cord injury who were doing clean intermittent catheterization (CIC) for severe detrusor overactivity and incontinence unresponsive to anticholinergic therapy. They transurethrally injected 200 to 300 U of botulinum toxin-A in the detrusor muscle in 30 places, avoiding the trigone. At 6 weeks, 17 of the 19 patients were continent, and all medications were withdrawn. The effects of the drug lasted for at least 9 months, and repeat injections were required after this time period. A study by Reitz et al. (2004) on 200 patients with neurogenic incontinence showed that at 36 weeks, urodynamic parameters, such as bladder capacity, mean voiding pressure and bladder compliance, were significantly improved. Although botulinum toxin-A appears to hold great promise for the treatment of detrusor overactivity, further confirmatory studies as well as trials on dose, concentration, and technique are needed in the future. Neuromodulation must be considered investigational for neurogenic bladder dysfunction. Although there have been many studies on the use of sacral nerve modulation for
refractory overactive bladder, secondary to nonneurogenic causes, there have been only anecdotal reports of improved symptoms in patients with neurogenic detrusor overactivity, primarily on patients with MS. Further investigation in this area is needed. Finally, in patients who do not respond to any of the first- or second-line therapies for neurogenic detrusor overactivity, augmentation cystoplasty, with or without continent catheterizable stoma or complete urinary diversion, can be considered. These operations are indicated in patients with functionally decreased bladder capacities and refractory filling/storage symptoms. They are, however, major operations with obvious risks and, with the exception of an ileal conduit, they require the use of upper extremities for chronic self-catheterization. In patients who have a problem with emptying, either secondary to DESD (or detrusor-internal sphincter dyssynergia) or impaired contractility, emptying must be facilitated in many cases. For DESD, CIC has been a mainstay of therapy and is most effective when detrusor overactivity is controlled by one of the means described previously. The same is true for retention secondary to impaired contractility. In some cases, a catheterizable stoma can facilitate independence when neurologic disease is advanced and urethral catheterization cannot be performed independently. Botulinum toxin has been injected transurethrally for the treatment of DESD, and both open label and controlled randomized studies have shown benefit. De Seze et al. (2002) performed a randomized
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controlled study to compare 100 U of botulinum toxin versus 4 mL of 0.5% lidocaine injected endoscopically in 13 patients with urinary retention secondary to DESD. Results showed an immediate improvement in ability to void, as measured by decreased PVR volumes in the botulinum toxin group. Chronic indwelling catheters are generally not recommended for treatment of chronic retention but may be used as a last resort in select patients. A propensity exists for chronic infections stone formation, bladder neck erosions, and the development of squamous cell carcinoma. In situations in which this form of management is desirable and necessary, appropriate catheter care with frequent changing of the catheter is recommended.
Nonneurogenic Voiding Dysfunction DYSFUNCTIONAL VOIDING Dysfunctional voiding is an abnormality of bladder emptying in neurologically normal individuals in which there is increased activity of external sphincter during voluntary voiding. It is a learned behavior, which differentiates it from true DESD that was described earlier (Fig. 30-4). Thus, the terms pseudodyssynergia and learned voiding dysfunction have also been used to describe the condition. Dysfunctional voiding may result in various LUTS, both storage and emptying symptoms. It may also be respon-
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sible for recurrent urinary tract infections, acute or chronic urinary retention, and, in severe cases, upper and lower urinary tract decompensation. In 1973, Hinman and Bauman popularized the concept of dyscoordination between the detrusor and the activity of the pelvic floor-external sphincter complex in neurologically normally individuals. Much of the literature describes this phenomenon, also known as the nonneurogenic neurogenic bladder, or Hinman’s syndrome, as occurring in children and adolescents who typically present with enuresis, recurrent urinary tract infections, and sometimes hydronephrosis. In 1978, Allen and Bright used the term dysfunctional voiding to describe failure to coordinate detrusor and sphincter activity in children. The literature is replete with reports of this condition in children; in adults, however, much less has been written, although it has been reported to cause various LUTS, incomplete emptying, incontinence, and recurrent urinary tract infections. In 1999, Nitti et al. found dysfunctional voiding to be the most common abnormality of the voiding phase in women presenting with LUTS. Dysfunctional voiding in children was originally thought to be a response to psychosocial problems. The condition is now recognized as a developmental abnormality, whereby there is persistence of the transitional phase between infantile reflexogenic voiding and normal volitional voiding of adulthood. Several theories are known on why dysfunctional voiding occurs in adults. The most plausible is that it represents
Figure 30-4 ■ Videourodynamic study of a 23-year-old woman with urge incontinence and incomplete emptying. Note the high-pressure detrusor contraction to void, accompanied by decreased flow and increased EMG activity. Fluoroscopic image taken during voiding shows a spinning top urethraî with obstruction at the level of the external sphincter. Neurologic evaluation was negative. Diagnosis: dysfunctional voiding.
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a learned behavior in response to an adverse event or condition, such as inflammation, irritation, infection (cystitis, urethritis, vaginitis), urethral diverticulum, pelvic inflammatory disease, anorectal disease, or trauma. Other authors have suggested that dysfunctional voiding may result from voluntary withholding of urination in individuals who work long hours. Kaplan et al. (1980) proposed that “the stress of modern society may manifest itself in this region of the body.” McGuire and Savastano (1984) attributed the behavior to a primary abnormality of detrusor overactivity with the dyssynergic sphincter response developing as a result of sudden unanticipated detrusor contractility. Contraction of the pelvic floor-external sphincter complex is a normal response to control urgent urination and results in a reflex inhibition of the detrusor. When this becomes habitual over time, the abnormal incoordination carries over to voluntary voiding, resulting in an intermittent urinary stream and residual urine. The treatment of dysfunctional voiding has evolved over the years. Kaplan et al. (1980) reported success with diazepam in six women with “urethral syndrome” who demonstrated a staccato voiding pattern with increased external sphincter or pelvic floor EMG activity during voiding. As in children, biofeedback and behavioral modification have become our recommended treatment for women with dysfunctional voiding. Biofeedback has also been proven to be successful in adult men. In cases where there is also detrusor overactivity or impaired compliance, anticholinergic medications can be used in addition to biofeedback. Interestingly, in the study by Deindl et al. (1998), biofeedback was successful in cases of pubococcygeus dysfunction but not in cases of true external urethral sphincter dysfunction. Several clinicians, including ourselves, have had anecdotal success with amitriptyline. Just as in the treatment of DESD, endoscopic and transperineal urethral injections of botulinum toxin-A have been performed in women with dysfunctional voiding. In a study by Kuo (2003) on 103 women with urinary retention and voiding complaints, of whom 39 had dysfunctional voiding, there was an 84.5% 4-week success rate with 50–100 U intraurethral injection of botulinum toxin-A. Finally, the role of neuromodulation, which has been described for the treatment of idiopathic urinary retention, needs to be defined specifically with respect to dysfunctional voiding. PRIMARY BLADDER NECK OBSTRUCTION (PBNO) PBNO is characterized by failure of the bladder neck to open properly in the presence of a detrusor contraction of normal or increased pressure and duration (Fig. 30-5). Marion (1933) originally described it in a male patient, but its presence in women has only recently been emphasized. In a group of women who underwent videourodynamic tests for nonneurogenic voiding dysfunction, Nitti et al. (1999) found PBNO in 0.5% of women overall and in 16% of obstructed women. The exact etiology of PBNO is unknown. One theory is that it is caused by smooth muscle hypertrophy or an increase in collagen deposition at the bladder neck. Another is that a continual high tonus in the smooth muscle of the posterior urethra causes rigidity of the bladder neck. A theory that an increased number of α-adrenergic receptors resulting in nonrelaxation during voiding has also been suggested.
Figure 30-5 ■ Videourodynamic study of a 36-year-old woman with obstructive voiding symptoms and intermittent urinary retention. There is a sustained detrusor contraction of > 50 cm H2O with failure of the bladder neck to open. Diagnosis: primary bladder neck obstruction.
Women with PBNO typically present initially with storage symptoms and are often treated for bladder overactivity. Voiding symptoms may then become more prominent, and patients may even progress to periodic urinary retention and have high PVR volumes. Recurrent urinary tract infections can commonly result. The treatment options for PBNO in women are the same and include watchful waiting, pharmacotherapy, and surgical intervention. Watchful waiting is an option for patients whose symptoms are not that bothersome and who do not have clinical or urodynamic evidence of upper and/or lower urinary tract decompensation. Unfortunately, little is known about the natural history of PBNO in men and women. The number of those who elect observation and have progressive symptoms, decompensation, or even go on to receive treatment is unknown. Most treatment options are based on “expert opinion,” with only a few small series available for review. Most opinion leaders recommend α-blockers, but this is based primarily on anecdotal experience. One published study by Kumar et al. (1999) documents that 24 women with PBNO were treated. This was a highly symptomatic group, all with significantly elevated PVR volumes, and stringent urodynamic criteria were used to make the diagnosis. All women were treated initially with phenoxybenzamine, prazosin, or terazosin, and 50% responded to α-blockade with decreased symptoms, increased flow, and decreased residual volumes. Specifically in responders Qmax increased from 9.5 mL/sec to 15.1 mL/sec, and PVR decreased from 277 mL to 27 mL. No validated symptom assessment was used to assess symptom response. PBNO can be treated surgically with transurethral incision of the bladder neck. This can be done either unilaterally or bilaterally. The main concern of bladder neck incision is the development of postoperative stress incontinence. Axelrod and Blaivas (1987) made bilateral incisions at the 5 o’clock and 7 o’clock positions in three women and reported success in all, of whom none developed incontinence. A recent study by Blaivas et al. (2004) included seven women with PBNO and had similar results. Gronbaek et al. (1992) initially performed a single incision and a second incision, as needed, in 38 women. A 76% success rate at mean follow-up of 55 months was obtained;
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one patient (3%) developed incontinence. Kumar et al. did a single incision at the 12 o’clock position, using a pediatric resectoscope in six women who failed α-blockade (from the group described previously). Success was reported in all six women with Qmax increasing from 8.5 mL/sec to 15.5 mL/sec and PVR volumes decreasing from 256 mL to 40 mL. “Mild SUI” was reported in 2 (33%) patients. PELVIC PROLAPSE Prolapse of pelvic organs can have a profound effect on lower urinary tract function. In addition to the common symptoms of urinary frequency, urgency, and incontinence, bladder outlet obstruction and varying degrees of urinary retention are possible. Patients may report the need to position themselves in a certain way to void (e.g., leaning backward or squatting) or may need to manually reduce the prolapse to void. Obstruction from prolapse can be caused by kinking of the urethra in cases of anterior vaginal wall prolapse (cystocele) or by direct compression of the prolapsing organ on the urethra. It can be demonstrated urodynamically by evaluating patients with the prolapse unreduced. The effect of the prolapse on voiding function can be seen further by reducing the prolapse (with a pessary, vaginal retractor, or vaginal packing) and repeating the study. Using this technique, Romanzi and Blaivas (1999) found obstruction in 4% of the grades 1 and 2 cystoceles and 58% of the grades 3 and 4 cystoceles. After pessary placement, 94% reverted to free flow. Reduction of prolapse can unmask intrinsic sphincter deficiency and stress incontinence (occult or potential stress incontinence) and should be done as part of the preoperative urodynamic evaluation in women, with prolapse, who are undergoing surgery. Voiding dysfunction caused by pelvic prolapse can be treated by a pessary or surgical repair. IATROGENIC POST-SURGICAL OBSTRUCTION Surgical procedures for the correction of SUI are designed to restore support to the urethrovesical junction and/or improve coaptation of the urethra (in cases of intrinsic sphincter deficiency). This can be accomplished in various ways, including retropubic colposuspension, transvaginal bladder neck suspension (e.g., needle suspension), and sling procedures. A potential complication of all these procedures is iatrogenic outlet obstruction leading to voiding dysfunction. The incidence of iatrogenic urethral obstruction varies widely in the literature, from 2.5% to 24%. The wide discrepancy in reported rates may be explained by various factors, such as underdiagnosis and incomplete evaluation and follow-up of patients. Obstruction after incontinence surgery is typically a result of technical factors, such as improper placement or excessive tensioning of sutures or slings. Even tension-free procedures like the tension-free vaginal tape (TVT) have a reported iatrogenic obstruction rate of 2% to 3%, which is similar to the pubovaginal sling. Some additional indirect factors may affect a patient’s ability to empty after anti-incontinence surgery. Obstruction may be indirectly caused by a cystocele or other prolapse that was either uncorrected at the time of surgery or had occurred postoperatively. Prolapse of sufficient size may kink the urethra. Impaired detrusor contractility, a condition that should have been present preoperatively, in the face of increased
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urethral resistance by an anti-incontinence procedure, may cause obstruction. Finally, the patient who habitually voids by abdominal straining may have difficulty emptying after pubovaginal sling surgery because the sling acts to increase urethral resistance with increases in abdominal pressure. The evaluation of the post-surgical patient is a unique situation. Transient voiding dysfunction is frequent and expected after many types of anti-incontinence surgery and is the rationale behind concomitant placement of suprapubic tubes or preoperatively teaching patients clean, intermittent catheterization. Most women will begin voiding sufficiently on their own within a few days to weeks, whereas others may take longer to resume normal voiding. Return to normal voiding may take longer in patients who have been obstructed chronically. Irritative symptoms, such as urgency, frequency, and urge incontinence, are often more refractory than retention because they can be related to bladder changes. Irritative symptoms may resolve as late as 6 months after surgery. It is common to delay evaluation of the patient with urinary retention or severe irritative symptoms after incontinence surgery for up to 3 postoperative months. Although this time frame is arbitrary, most data in the literature are based on a waiting period of at least 3 months to ensure adequate time for retention from obstruction to resolve and to minimize the risk of recurrent stress incontinence. After 3 months, a very low probability is present that any persistent retention will resolve without intervention. In the case of TVT, some have advocated quicker intervention, within 7 to 10 days, when obstruction is suspected. Because of the immobility of the polypropylene mesh and the ingrowth of fibroblastic tissue at 1 to 2 weeks, patients with severe symptoms or urinary retention are less likely to improve after this period. 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 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. 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. It is well established that urodynamic tests may fail to diagnose obstruction in a significant number of women obstructed from anti-incontinence procedures. Additionally, patients with nondiagnostic urodynamic studies, or those who fail to produce a detrusor contraction during urodynamics, have the same outcomes as those with urodynamic findings that are classic for obstruction. However, in cases of de novo or worsened irritative symptoms, including urge incontinence without a significantly elevated PVR, a formal urodynamic evaluation is preferred. The physical examination may reveal a hypersuspended urethra or significant prolapse that could point to the cause of obstruction, but often the exam is normal. Treatment is dictated by the degree of bother of postoperative symptoms. In some cases, an obstructed patient, at least temporarily, will opt for conservative management with CIC. Occasionally, a woman who had severe SUI before surgery and is not very bothered by catheterization may prefer CIC to repeat surgery and a risk of recurrent SUI. Most patients with
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significant symptoms from iatrogenic obstruction, however, choose definitive treatment. The role for urethral dilation in such cases is not known, but we feel it is of limited use. The same uncertainty exists for cutting suspension or sling sutures from above. Although some have reported anecdotal success, no peer-reviewed series exist. Surgery by formal urethrolysis or sling incision is the most definitive treatment available. Urethrolysis, whether by retropubic, transvaginal, or suprameatal approach, appears to have similar success ranging from 65% to 93%. Sling incision has similar success rates. The type of urethrolysis (or sling incision) chosen will depend on several factors, including patient presentation, type of incontinence procedure performed, whether she had a previously failed urethrolysis, and surgeon preference. It has been our practice to perform a transvaginal procedure—usually a sling incision or urethrolysis when a sling cannot be identified—as a primary operation. Retropubic urethrolysis is reserved for a previously failed transvaginal procedure or, in special circumstances, based on the incontinence procedure, such as retention after a Burch colposuspension. Our experience with sling incision, including for TVT, has shown results equivalent to formal urethrolysis. In the case of TVT, we have also performed sling “adjustment” by pulling the sling down at 1 week, either as an office procedure or in the operating room with local anesthesia. IMPAIRED DETRUSOR CONTRACTILITY Several conditions can result in impaired detrusor contractility of nonneurogenic origin. They include structural changes that affect the detrusor, such as radiation cystitis, tuberculosis, and other conditions that produce fibrosis; chronic outlet obstruction causing detrusor failure; and idiopathic processes. In addition, diabetic cystopathy, a myogenic phenomenon resulting from chronic overdistension secondary to sensory neuropathy, can cause impaired contractility. The treatment for impaired contractility of nonneurogenic origin is similar to that mentioned for neurogenic origin. CIC is the mainstay for patients with significant retention. It is reasonable to try techniques, such as Credé and/or doublevoiding, provided there is no obstruction. Pharmacotherapy with cholinergic agonists, such as bethanecol, has not proven to be successful in randomized controlled trials, though it is used anecdotally by some.
CONCLUSION The evaluation, management, and treatment of female patients with voiding dysfunction and urinary retention is often complex and must take multiple factors into consideration, including the degree to which the patient’s symptoms are bothersome and whether the upper tracts are in jeopardy. A patient-specific diagnostic approach is recommended, depending on symptoms, degree of bother, and whether there is a history or suspicion of neurologic disease. In certain cases, empirical treatment is appropriate. However, when a formal diagnosis is indicated, specific therapy can be directed based on urodynamics and other tests.
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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. Leippold T, Reitz A, Schurch B. Botulinum toxin as a new therapy option for voiding disorders: current state of the art. Eur Urol 2003;44:165. Lyon RP, Smith DR. Distal urethral stenosis. J Urol 1963;89:414. Marion G. Surgery of the neck of the bladder. Br J Urol 1933;5:351. Mayo ME. Primary bladder neck obstruction. Surg Rounds 1982;5:66. McGuire EJ, Woodside JR, Borden TA, Weiss RM. The prognostic significance of urodynamic testing in myelodysplastic patients. J Urol 1981; 126:205. McGuire EJ, Savastano JA. Urodynamic studies in enuresis and the nonneurogenic neurogenic bladder. J Urol 1984;132:299. Morgan TO, Westney OL, McGuire EJ. Pubovaginal sling: 4-year outcome and quality of life assessment. J Urol 2000;163:1845. Nathan PW. The central nervous connections of the bladder. In Williams DI, Chisholm GD, eds. Scientific Foundations of Urology. Yearbook Medical Publishers, Chicago, 1976;2:51–58. Nitti VW, Fiske J. Cystometrogram v
